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2020

Essential Notes on Pathophysiology for Advanced Practice

Nurses
Alex Sargsyan
East Tennessee State University, [email protected]

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https://dc.etsu.edu/etsu-oer/3

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 ESSENTIAL NOTES ON
PATHOPHYSIOLOGY FOR
ADVANCED PRACTICE NURSES

Alex Sargsyan, DNP, ANP-BC, RN

Table of Contents
Preface .................................................................................................................................... 6
Genes and Genetic Diseases .................................................................................................... 7
RNA and DNA ........................................................................................................................................................7
Genetics ................................................................................................................................................................7
Genomics ..............................................................................................................................................................7
Transcription .........................................................................................................................................................7

Mitosis and Meiosis ......................................................................................................................... 8

Mitosis ..................................................................................................................................................................8
Meiosis ..................................................................................................................................................................9

Inheritance and Mendel’s Law ......................................................................................................... 9

Genotype versus Phenotype .......................................................................................................... 10
Genotype ............................................................................................................................................................10
Gene Expression .................................................................................................................................................10

Mutations ...................................................................................................................................... 10
Point mutations ..................................................................................................................................................10
Mutagens ............................................................................................................................................................11
Consequences of mutations ...............................................................................................................................11

Alterations in Chromosome Structures ........................................................................................... 12

Translocation ......................................................................................................................................................12
Failure to thrive...................................................................................................................................................13
Fragile sites .........................................................................................................................................................13
Mendel and Mendelian Laws ..............................................................................................................................14
Genotype vs Phenotype ......................................................................................................................................14
Penetrance ..........................................................................................................................................................14
Expressivity .........................................................................................................................................................15

Aneuploidies .................................................................................................................................. 15
Autosomal Aneuploidy........................................................................................................................................15
Turner syndrome ................................................................................................................................................17
Klinefelter's syndrome ........................................................................................................................................17
Deletion ..............................................................................................................................................................18
Robertsonian translocation ................................................................................................................................18
Ring chromosome ...............................................................................................................................................18
Duplication ..........................................................................................................................................................18
Fragile sites .........................................................................................................................................................19

Inflammation and Infection ................................................................................................... 19

Inflammation ......................................................................................................................................................20
Phagocytosis .......................................................................................................................................................21
Infection ..............................................................................................................................................................21
Normal flora ........................................................................................................................................................22
Staphylococcus ...................................................................................................................................................22
Pseudomonas......................................................................................................................................................23
Viruses ................................................................................................................................................................23

1
 Fungi ...................................................................................................................................................................23
Ricketsiae ............................................................................................................................................................23
Protozoan infections ...........................................................................................................................................24
Giardia.................................................................................................................................................................24
Helminths ............................................................................................................................................................24
Testing for bacterial or viral infections ...............................................................................................................24
Skin testing ..........................................................................................................................................................24

Cancer ................................................................................................................................... 25
Common Cancers ................................................................................................................................................25
Benign neoplasms ...............................................................................................................................................25
Malignant neoplasms..........................................................................................................................................25
Epithelial vs Connective Tissue Malignancies .....................................................................................................26
Carcinogen ..........................................................................................................................................................26
Oncogenesis ........................................................................................................................................................27
Growth factors ....................................................................................................................................................27
Malignant Transformation ..................................................................................................................................28
Grading and Staging ............................................................................................................................................29
The TNM system .................................................................................................................................................29
Distant metastasis...............................................................................................................................................29

Neurologic System Disorders ................................................................................................. 30

Seizures ...............................................................................................................................................................30
Clonic seizures.....................................................................................................................................................30
Idiopathic epilepsy ..............................................................................................................................................30
Mental Confusion and Dementia ........................................................................................................................31
Alzheimer's disease .............................................................................................................................................31
Cerebral vascular accidents (CVA) ......................................................................................................................33
Aneurysms ..........................................................................................................................................................33
Vascular malformations include .........................................................................................................................33
Venous angioma .................................................................................................................................................33

Headaches ..................................................................................................................................... 34
Meningitis ...........................................................................................................................................................35
Encephalitis .........................................................................................................................................................35
Lyme disease .......................................................................................................................................................36
Multiple sclerosis ................................................................................................................................................36
Amyotrophic lateral sclerosis..............................................................................................................................37
Neuropathies ......................................................................................................................................................38
Myasthenia Gravis ..............................................................................................................................................38

Mental Health Disorders ................................................................................................................ 39

Schizophrenia......................................................................................................................................................39
Affective disorders ..............................................................................................................................................39
Depression ..........................................................................................................................................................39
Situational depression ........................................................................................................................................40
Substance abuse .................................................................................................................................................40
Anxiety disorders ................................................................................................................................................41
Panic disorder .....................................................................................................................................................41
Post-traumatic stress disorder ............................................................................................................................41

2
 Obsessive-compulsive disorder ..........................................................................................................................42

Musculoskeletal Disorders ..................................................................................................... 42

Trauma ................................................................................................................................................................42
Pathologic fractures ............................................................................................................................................43
Open reduction ...................................................................................................................................................44
Dislocation and Subluxation ...............................................................................................................................44
Support structure injuries ...................................................................................................................................46
Disorders of the tendons ....................................................................................................................................46
Muscle strain.......................................................................................................................................................47
Rhabdomyolysis ..................................................................................................................................................47
Osteoporosis .......................................................................................................................................................47
Postmenopausal osteoporosis ............................................................................................................................48
Osteomalacia ......................................................................................................................................................48
Paget’s disease ....................................................................................................................................................49
Osteomyelitis ......................................................................................................................................................49
Joint disease ........................................................................................................................................................49
Arthritis ...............................................................................................................................................................50
Rheumatoid arthritis ...........................................................................................................................................50
Ankylosing spondylitis.........................................................................................................................................51
Gout ....................................................................................................................................................................51
Fibromyalgia .......................................................................................................................................................51

A brief Overview of Integumentary Disorders ........................................................................ 52

Psoriasis ..............................................................................................................................................................52
Hyperkeratosis ....................................................................................................................................................52
Skin cancers. .......................................................................................................................................................52
How to describe lesions on the skin: ..................................................................................................................52
Actinic Keratosis ..................................................................................................................................................53
Seborrheic Keratosis ...........................................................................................................................................53
Xanthelasma .......................................................................................................................................................53

Hematologic Disorders .......................................................................................................... 53

Hematologic Cancers ...................................................................................................................... 53
Leukemia .............................................................................................................................................................53
Lymphomas .........................................................................................................................................................53

Hematopoiesis ............................................................................................................................... 55
Neutrophils, Eosinophils, and Basophils .................................................................................................55
Monocytes ..........................................................................................................................................................55

RBC development........................................................................................................................... 56
Hemostasis .................................................................................................................................... 57
Hemostasis ..........................................................................................................................................................57
Coagulation Factors ............................................................................................................................................58
Plasminogen........................................................................................................................................................58
Antithrombin ......................................................................................................................................................59
Thrombocytopenia .............................................................................................................................................59
Disseminated intravascular coagulation .............................................................................................................59

3
 Red Blood Cells Disorders ............................................................................................................... 60
Mean corpuscular volume ..................................................................................................................................60
Megaloblastic anemias .......................................................................................................................................61
Hemolytic anemias .............................................................................................................................................61

Hemoglobinopathies, Thalassemia and Sickle -Cell Anemia ............................................... 61

Sickle cell anemia ................................................................................................................................................61
Thalassemia ........................................................................................................................................................62

Cardiovascular Disorders ....................................................................................................... 62

Hypertension ......................................................................................................................................................63
Arteriosclerosis and atherosclerosis ...................................................................................................................63
Peripheral vascular disease.................................................................................................................................63
Coronary artery disease ......................................................................................................................................64
Unstable angina ..................................................................................................................................................64
Congestive heart failure ......................................................................................................................................65
Cardiomyopathies ...............................................................................................................................................66
Valvular heart disease .........................................................................................................................................66
Rheumatic heart disease.....................................................................................................................................66
Cardiomyopathy .................................................................................................................................................67

Adult Respiratory Disorders ................................................................................................... 67

Respiratory Symptom Evaluation ................................................................................................... 67
Rhinovirus ...........................................................................................................................................................67
Laryngopharyngitis..............................................................................................................................................68
Treatment for upper respiratory infections........................................................................................................68
Influenza .............................................................................................................................................................68
Chronic Obstructive Pulmonary Disease.............................................................................................................69
Chronic bronchitis ...............................................................................................................................................70
Emphysema.........................................................................................................................................................70
Pneumonia ..........................................................................................................................................................70
Tuberculosis (TB).................................................................................................................................................71

Renal Disorders ..................................................................................................................... 72

Kidney stones ......................................................................................................................................................72
Struvite stones ....................................................................................................................................................72
Urinary tract infections (UTI) ..............................................................................................................................73
Cystitis .................................................................................................................................................................74
Pyelonephritis .....................................................................................................................................................74
Glomerulonephritis .............................................................................................................................................74

Renal Failure .................................................................................................................................. 75

Post renal failure .................................................................................................................................................75
Acute renal failure ..............................................................................................................................................75
Chronic renal failure ...........................................................................................................................................75
Renal insufficiency ..............................................................................................................................................76

Endocrine Disorders ............................................................................................................... 77

Hormonal Regulation ..................................................................................................................... 77

4
 Thyroid and Parathyroid Functions ................................................................................................. 78
Hyperthyroidism .................................................................................................................................................79
Hypoparathyroidism ...........................................................................................................................................79

Adrenal gland disorders ................................................................................................................. 79

Addison disease ..................................................................................................................................................80

Diabetes ....................................................................................................................................... 80
Diabetes ketoacidosis (DKA) ...............................................................................................................................81
Hyperosmolar hyperglycemic non-ketonic state ................................................................................................81

Gastrointestinal Disorders Part 1 ........................................................................................... 82

Disorders of the Digestive System .................................................................................................. 82
Dysphasia ............................................................................................................................................................82
Achalasia .............................................................................................................................................................82
Gastroesophageal reflux disorder.......................................................................................................................82
Peptic ulcer disease ............................................................................................................................................83
Duodenal ulcers ..................................................................................................................................................83
Gastric ulcers ......................................................................................................................................................83

Liver disorders ............................................................................................................................... 83

Hepatic liver ........................................................................................................................................................84
Viral Hepatitis. ....................................................................................................................................................84
Hepatitis B ...........................................................................................................................................................84
Hepatitis C ...........................................................................................................................................................84
Hepatitis D ..........................................................................................................................................................85
Cirrhosis ..............................................................................................................................................................85
Primary Biliary cirrhosis ......................................................................................................................................85
Pancreatitis .........................................................................................................................................................86

5
Preface
This text is a compilation of lecture notes from pathophysiology courses I have taught over the
last ten years. The goal of the text is to equip future advanced practice nurses with knowledge
of pathophysiology for common diseases and disorders they may encounter in the primary care
setting. The creation of this text was possible because of the Open Educational Resources
Awards Program at East Tennessee State University.

Copyright

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0

International License.
For ease of adapting the materials, the Word document of this PDF is available at
https://dc.etsu.edu/etsu-oer/3/

6
Genes and Genetic Diseases
RNA and DNA
Genetics is the study of inheritance of biologic heredity. A gene is the basic unit of
heredity, which means that a gene carries enough information, to transfer or to pass one or
more traits; the traits will be passed based on genetic composition. Don't confuse genes with
chromosomes, a unit of heredity or codons- codons alone, don't have enough information to
transfer traits, and chromosomes contain multiple genes. Usually, in order to pass one trait,
only a single gene is required.
Genomics is the field of genetics, that studies the structure of the genome. A genome is
the DNA that represents all the genes for a given type of species. A genome will be
representing the complete genetic information - all types of genes for the type of species. This
pertains to not only human physiology and human pathophysiology, but also to animals and
plants, or even microbial world. Heredity information is controlled by genomes, genetics and
genes that carry the information in living structures.
When discussing heredity, a focus is on DNA and genes. Genes are the sections or
sequences of DNA that have the instructions to make a single protein. One strand of DNA may
contain a multitude of genes. The building blocks that make up genes are called bases. There
are four bases that make up DNA:
Adenine
Thymine --------- Uracil in RNA
Guanine
Cytosine.
RNA consists of similar bases; however, thymine is replaced by uracil in RNA. The amino
acids are strung together and attach to one another to make a protein. Protein is a polypeptide
chain, a polymer molecule that consists of peptides or amino acids. The DNA resides in the
nucleus and contains codes for future protein. DNA has a double-stranded structure, but one of
the strands has no function at all, but to compliment the other strand. The main strand, the
meaningful strand, carries the genetic information while the meaningless strand just acts as a
complement.
The main strand is complemented with meaningless strand to give a structure to DNA.
However, when DNA replicates, the result is two identical molecules of DNA. During the
replication the DNA “unzips.” The original meaningful strand attaches to another new
meaningless strand, and meaningless strand attaches to a new meaningful strand.
Transcription is the initial step to get the genetic information out of the nucleus and
move it to the cytoplasm for the creation and construction of the proteins. Transcription occurs

7
inside of the nucleus. This process can only occur in eukaryotic cells because eukaryotic cells are
the only cells that have a nucleus, and the nucleus contains DNA. Prokaryotic cells do not
contain a nucleus.
Human cells are all eukaryotic, in this situation messenger RNA will create a copy of
complementary strand of DNA will move to the cytoplasm. The main players in this concept are
the stop codons. The stop codon marks the point where the transcription will end. However,
before the messenger RNA moves into cytoplasm, some other changes have to occur.
Initially the transcribed RNA is immature. Immature in this context applies to the fact
that the RNA contains a combination of two different nucleotide sequences: exons and introns.
Only exons carry the information necessary for protein synthesis. Introns and exons are
nucleotide sequences within a gene. The immature RNA will be modified and eventually the
introns will be removed. This process is called splicing. After removal of the introns, the RNA is
reassembled and sent out from the nucleus to cytoplasm.
In the cytoplasm the RNA seeks the ribosome, you may view the ribosome as the
assembling production line where protein synthesis occurs. In the ribosome the messenger
RNA will attach to ribosomal RNA and will start running through the ribosome. Simultaneously,
the amino acids are carried into the ribosome by the transfer RNA. The transfer RNA continues
to carry the amino acids and the whole process creates a chain of proteins or a polypeptide
chain. Everything in this process works like an assembly line. There are 20 amino acids and 20
different types of transfer RNAs; they all work to assemble proteins.
After the protein is assembled, it must be folded and transported to an appropriate
place in the cells. The folding process occurs with the help of particles called molecular
chaperones. The chaperones oversee the protein and control the proteins behavior; the
chaperones act as need to make sure the protein does not unfold. However, it is possible that
eventually the protein may unfold. In this case, the protein may contribute and attach to
another protein. This process of attaching and unfolding of proteins is known as denaturation.
This process can lead to many diseases; an example of this may be Alzheimer’s disease. Heat,
chemical exposure may lead to the denaturation of the proteins. You may see the denaturation
of the proteins in your everyday life: when cooking a raw egg the proteins in the translucent
egg white denaturate resulting in a solid white color of the cooked egg white.
In review, when the cell divides, it needs the duplication of DNA. Ribosomal RNA moves
along the messenger RNA and then moves the transfer RNAs into position. However, even
though this process involves teamwork of three different RNAs, the only RNA that goes into the
nucleus is the messenger RNA. The other two work only in the cytoplasm.
Mitosis and Meiosis
Mitosis is a regular cell division. Mitosis is needed for the for the replenishment of some
wear and tear, such as creating new blood cells or skin cells.

8
 Meiosis leads to the creation or production of gametes, or sex cells, or otherwise called
sperm or ovum. In meiosis, the chromosomes duplicate, and one pair will go to each daughter
cell on the first division, however, one chromosome of each pair, will go to the daughter cell, on
the second division.
This is important in relevance to genetic disorders and the phenomenon of crossing-
over. When chromosome pairs are lining up during meiosis, and then they will exchange ends.
This will result in gametes or sex cells. The gametes will have different combination of genes
where the tips are exchanged. This results in richer, broader, genetic variety. Another
phenomenon is linkage, when two genes are standing close together that the chromosome
become linked; they will be very inseparable and have difficulty separating in the crossing-over
stage. This results in the genes being inherited together.
Inheritance and Mendel’s Law
A Punnet Square describes the genetic inheritance process, by using probability of
inheriting each trait. The capital 'D' represents a dominant allele and a small 'd' represents a
recessive allele.
D d

D DD Dd

d Dd dd

If two dominant traits interact together to create a new cell, it will result in dominant traits. If a
dominant trait interacts with a recessive trait to create a new cell, it will result in a dominant
trait. If two recessive traits interact to create a new cell, it will result in recessive trait. It is much
harder to develop recessive traits. Two recessive traits must be supplied from each parent in
order to inherit a recessive trait; it is much easier to inherit dominant traits. Each square
represented in a Punnet Square with four squares represents a 25% of inheritance. In cases of
phenomenon’s, such as inbreeding, the supply of recessive material or genes increases. This
raises concern about these types of relations because recessive genes can sometimes be
related to diseases. This is way off-springs of partners close in familial relations may have health
problems or cognitive or physical deficits. Alleles are the copies of a genes. If the copies of
genes are alike it is homozygous; if the copies are different, they are considered heterozygous.
If the allele is heterozygous, the recessive trait is not shown, however, the individual is still a
carrier of the recessive trait. If only one copy of the gene is present, it is considered
hemizygous. Only dominant genes will be expressed.

9
Genotype versus Phenotype
Genotype is the genetic material and phenotype is the appearance of actual physical
characteristics. For example, blue eyes this is a recessive trait and brown eyes are a dominant
trait. A person with brown eyes may have genotype of two genes supplied, one from the
mother and father both dominant, or he or she may have a genotype of one set of blue eyes,
recessive gene, from one parent and brown eyes, dominant gene, from the other. The person
will have brown eyes, but may be a carrier of a recessive gene for blue eyes.
Gene Expression refers to the process of genes being turned on or turned off, induction
and repression. During induction there must be a trigger or external factor present to start a
gene or turn a gene on. Repression refers to a factor that turns the gene off. If a gene is turned
off, the code for the protein is not. Gene expression simply refers to the gene being expressed
when trait is visible. However, if the gene is turned off, the protein is not. If a recessive gene is
expressed, it is called intermediate penetrance.
If a person exhibits a trait, and the trait is secondary to many genes it is polygenic. If
trait is expressed secondary to genes and the environment can also influence it, it is a
multifactorial expression. Multifactorial refers to several factors having an influence on
something. Very early events can be secondary to a single factor. When one gene masks the
effect of another one, it is referred to as epistasis; one of the genes will never be expressed.
When genes depend on each other, they work collaboratively and complementary. Two genes
may work together to create a new phenotype; this is referred to as collaborative. The
difference between complementary and collaborative is that in a complementary type the
genes depend on another; they cannot work separately.
Mutations
A mutation is always a change; however, it may not be a positive change. A mutation
may occur at any time, and the changes in the organism may not be apparent in behavior,
appearance or in function. Mutations can be transmitted to offspring, only in gametes. When
gametes are mutated, there is a generation of transmissions, and the children or offspring will
present with the mutations already that occurred in the parent in somatic cells. The harm of a
mutation can have effect on the parent, however somatic cell mutation will not be transmitted
to the offspring. In order to produce a healthy new generation, mutations in gametes should be
prevented.
Point mutations is a type of mutation that is caused by a single nucleotide base pair
change, in the DNA's. When a single nucleotide base pair changes in DNA, there may be no
consequence because of the repetition in the DNA. Point mutations may not have any
consequences; rates of spontaneous mutation may vary and vary per gene; and is dependent
on the factors that can also influence the genes at a given point of time. A mutation can be
described as anything that alters the genetic materials, chromosome aberrations, or base pair
substitution. This definition applies to all types of mutations. Substitution of the base pair may
result in the change of amino acid sequence. This substitution causes the protein to not be
produced the way it was designed. This can result in drastic consequences if a change in the

10
protein occurs. If a silent substitution occurs, it may not result in an amino acid change because
of the redundancy of the genetic code. When the amino acid sequence is changed by a base
pair substitution, drastic consequences can occur because a change in the base pair causes a
change in the amino acid sequence which results in a change in the protein synthesis.
Mutagens are the agents that are known to cause or increase the frequency of
mutations, agents, or influencing factors. These terms can be used interchangeably, but a
mutagen is something that will cause the DNA to mutate. Radiation is a very well-known and
studied 20th century cause of mutation. Chemicals can also cause mutations. Some chemicals
can be extremely harmful, while others can cause mild or insignificant mutations. Chemicals
such as pesticides, herbicides and fertilizers have a very low rate of related mutations. Sodium
nitrate is also a relatively harmless chemical that is widely used in fertilizer.
A silent mutation is a DNA sequence change that does not change the amino acid
sequence of the gene. Missense mutation is a type of mutation that results in a single amino
acid change in the translated gene product. A protein is a polypeptide chain of amino acids
which are peptides. If only one of the amino acids is changed, then a missense mutation has
occurred, and the consequences can be drastic. The change in the amino acid may result in a
significant change in the protein due to a missense mutation or a consequence of a missense
mutation. A nonsense mutation is a type of mutation in which the messenger RNA stop codon
and the produced protein will have a premature termination of the sequence or production of
the long protein. The nonsense mutation will affect the messenger RNA stop codon and result
in a protein that is too short or too long. This results in a different protein being created.
Frameshift mutation occurs when the DNA is altered, and an addition or deletion of base pair
takes place. The shift causes the entire frame to become transposed and changed. If one base is
inserted into a DNA molecule, every base beyond that one inserted is now changed, and as a
result every codon and base is incorrect. The consequences of the addition or deletion will be
apparent because everything has been shifted in the strand. A frame shift mutation can result
in an entire change in the protein appearance and protein amino acid sequence.
Consequences of mutations
A mutation can result in either a gain of function or loss of function. An overproduction
of protein can cause and over expression, under expression, or inappropriate expression on a
gene. DNA is read and protein is produced secondary to DNA composition. Gain of function
disorders can be a consequence of mutations. Although there is a gain in function, this still may
not be a positive change and can still be taking on the organism. Loss of function can also occur
and is associated with recessive disorders.
Chromosomal abnormalities can be quite widespread; the most common chromosomal
abnormality presentation is early miscarriage. Most of the early miscarriages, occur secondary
to chromosomal abnormalities; sometimes they are not detected as a pregnancy because it is
so early in the gestation period. Euploid cells ('eu' prefix in Greek means normal or true) have a
stable, correct number of chromosomes; these are also known as diploid cells. Haploid cells
have the half number of chromosomes. Gametes, sex cells (sperm and eggs), are considered
both haploid and euploid; they have 23 unpaired chromosomes. Diploid cells have paired

11
chromosome- human cells have 46 total chromosomes and 23 chromosome pairs. When a
euploid cell has more than double number of chromosomes, it is a polyploid cell. Triploid cells
occur when a zygote contains three copies of each chromosome, 69 chromosomes total. A
tetraploid cell contains four copies of each chromosome, 92 chromosomes total. Triploid and
Tetraploid fetuses don't survive.
A lack of the normal number of chromosomes is referred to as aneuploid cells- a lack of
normal cells in contrast to euploid. Euploid cells contain multiple of normal 23 chromosomes.
Euploid cells can be tetraploid, which is abnormal and has no chances to survive, but still it's
euploid. Aneuploid refers to a lack of number of chromosomes that is a multiple of 23- the
number of chromosomes cannot be divided by 23. Monosomy cells only have one copy of the
chromosome; there is a missing member of the pair of the chromosome. Monosomy is quite
commonly fatal. If there is a chromosome missing from the pair and an extra copy of the
chromosome is present, the infant may survive and lead a relatively normal life. One well
known example is trisomy 21 (Down Syndrome). Individuals with Down Syndrome may develop
mentally and physically and progress in their development. It is better to have extra copies of a
chromosome than to have a missing chromosome. If there is extra genetic material, chances of
survival increase with genetic abnormality. If there is missing genetic material, chances of
survival decrease.
When chromosomes separate normally during cell division, they go through disjunction.
Chromosome abnormalities are due to nondisjunction. Nondisjunction is a non-division or non-
separation; it usually results in aneuploid cells or and aneuploid chromosome number. A
member of a chromosomal pair disappeared or separated to a different place. This missing pair
may cause trisomy or monosomy. If the homologous chromosomes are failing to separate
normally during the division in either meiosis or mitosis, it can lead to nondisjunction and
resulting in aneuploid cells.
Alterations in Chromosome Structures
Translocation can be described as an exchange of genetic material between
chromosomes. The genetic material from one chromosome is transferred to another. There are
many types of translocations. Robertsonian translocation is when the long arms of two
chromosomes fuse at the centromere and form single chromosome. Robertsonian translocation
can happen in chromosomes 13, 14, 15, 2, and 22 because the short arms of these
chromosomes are very small and they don't have any essential genetic material. When the
translocation happens in Robertsonian, the short arms are lost completely during the next cell
division. This can result in a loss of no important genetic material and only 45 chromosomes in
each cell. When this occurs, the individual will present as normal with no disorders because
there is no essential genetic material lost. However, monosomies and trisomies are common in
this occurrence. The fusion of the arms of chromosome 21 and 14 when a baby is born from a
parent who has this, the child can receive an extra copy of the long arm of chromosome 21
resulting in Down Syndrome.

12
 A ring chromosome occurs when the telomers of each chromosomal arm have been
deleted, and the broken arm joins together and form a ring. A ring chromosome can actually
trigger series of breakage and fusion bridge events which will cause continuous DNA breakage.
It is a chain reaction and recombination of chromosomal material. The ring itself is not a big
danger, but because of the chain reactions, it can cause ring syndrome to display very diverse
symptoms resulting from DNA breakage and recombination. The deletions of the chromosomal
material will occur, and duplications and the diverse presentation will exist. However, all
individuals with congenital ring chromosome will show signs of failure to thrive.
Failure to thrive is a consequence of cells not proliferating normally and suggests that
mitotic instability of the ring is the cause. Again, the ring itself is not the danger, but the
consequences may cause diverse presentation of symptoms. When chromosomal breakage
occurs, physiological mechanisms try to repair the break, however, the break would heal
differently than the original chromosome. The effects of a ring chromosome can be very mild or
drastic. Ionizing radiation, chemicals, and viruses can may all have an effect on the
chromosomes in autosomal structures rather than in sex cells. When these factors have an
effect on the cell, they cause breakage and the healing process results in distortion of the
chromosome and DNA. The healing process continues to alter the structure of the
chromosome. Duplication is a relatively rare occurrence in alteration in chromosomal
structures. When a repeated gene or gene sequence occurs as a result of duplication, the
consequences are more severe compared to deletion. The reason for this is because more
genetic material better than less, so when deleting something of occurs the result is a viable
infant. It is more difficult to add something like trisomy 21 to a viable fetus. Examples of
duplications include Cri-du-chat syndrome. This syndrome is a result of a short arm on
chromosome five and results in intellectual disabilities and several physical abnormalities such
as microcephaly. If duplication occurs in the short arm of chromosome 5, there will be no
physical presentation, but the infant will present with intellectual disabilities.
Fragile sites are sites that the breaks or gaps within chromosome. Fragile sights can be
seen by a microscope when the cells are cultured or developed. There is no evidence that this
may be related to some disorder. Fragile chromosome X syndrome, or fragile X syndrome does
present with severe intellectual disabilities. It is fairly prevalent in the population: one in 4,000
males will develop it, and one in 8,000 females. The distinct ratio between male and female is
due to females having two x chromosomes and males only having one. Females who inherit the
chromosome mutation associated with fragile x syndrome, will not express the disease, but
males will express the symptoms. The female may or may not express the symptoms of the
disease but can pass it down to her children. Most of the fragile sites will not be present with
any relation to the disease, fragile X chromosome is the exception. When the mutation of the
fragile X chromosome occurs, it occurs on the long side of the X chromosome. The mutation is
related to intellectual disabilities. It is one of the most common genetic disorder, second
compared to Down Syndrome, and has a higher occurrence in males due to one x chromosome.

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 Mendel and Mendelian Laws
Gregor Mendel was an Austrian monk, who started a garden pea experiment. Mendel
had no formal knowledge or education about genetics health or medicine. During his
experiment, he noticed that different varieties of peas, and how when the different peas were
crossed, they were present differently. His observations were not the first examples of
hybridization. The notion of hybridization had been around for generations. However, Mendel
is noted as the father of discovery because he was the first to notice some kind of law or
regularity in crossbreeding his plants. Before Mendel, the breeding of the plants and animals
was considered a rather random process, but after Mendel’s discovery the notion of a rule or
Mendelian Laws appeared.
Locus refers to the location occupied by a gene on the chromosome, and an allele is the
alternative version of a gene at the locus. Each individual has two alleles for each gene. A
homozygous gene has two identical alleles. A heterozygous gene will possess two different
alleles of the given gene. The allele is the same gene, which is responsible for the same trait,
but it is the alternative version. For example, eye color is controlled by the same gene, but by a
different allele. Polymorphism occurs when the locus has two or more alleles that will occur
with a certain frequency. Loci on a pair of a chromosome are homozygous if the alleles are
identical. If the loci on a pair of chromosomes have different alleles, it is heterozygous.
Genotype vs Phenotype
A genotype is the genetic makeup of the organism. The phenotype is what the
individual will demonstrate or show; it is the visible physical trait or traits that can be detected
through other measures. The phenotype determines the appearance of the organism. An
example of a genotype is blood type. I person with type A blood can have AA or AO; A is the
phenotype, but AA or AO is the genotype. When two alleles are found together, and one of
them will be dominant.
The dominant allele will be the one that' will be the presentation of the feature or is
observable. The allele that is not expressed is the recessive. The dominant allele is always
represented by a capital letter and the recessive is always lower-case letter. Alleles can appear
together and be called dominant- this is referred to as codominant alleles. When the individual
has a recessive gene that is not expressed, he or she is a carrier of that allele. When a recessive
disease is presented, and patient demonstrates the recessive disease, both genes in the pair are
recessive. For example, in the case of sickle-cell anemia, a capital ‘S’ would represent no sickle-
cell trait and the lower case ‘s’ does. Only the patient that has both lowercase ‘s’ will
demonstrate the disease. If the patient has two capital ‘S’, the patient is neither a carrier nor
presents with the disease. This patient can not pass the disease to his or her offspring.
Penetrance is a term that refers to the percentage of people with a specific genotype
who may express an expected phenotype. For example, retinoblastoma has incomplete
penetrance. This means that 10% of affected children with the gene will have not have the
disease.

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 Expressivity is the variation of a phenotype associated with the genotype. Expressivity is
the rate of presentation of a disease, disorder, or trait. This can be caused by modifier genes
and can vary in degree of how it affects the individual. Modifier genes at other loci can modify
the expression of the disease-causing genes. Environmental factors can influence the
expression of the disease-causing gene and result in mutations at the locus. Hemophilia A is an
example of when a mutation alters just one amino acid at the factor eight gene, and it will
result in milder hemophilia A. If a stop codon is introduced, it will terminate the translation
prematurely resulting in a severe form of hemophilia. Von Recklinghausen disease is an
autosomal dominant disorder that affects the long arm of chromosome 17. The expressivity can
vary significantly and may have a dramatic appearance of the disease. Single gene disorders are
autosomal dominant disorders and autosomal recessive disorders. Abnormal allele is dominant,
and the normal allele is recessive. Only one allele is needed to express the disease an
autosomal dominant disorder. Autosomal dominant disorders may present equally in males and
females because it's not sex related. Approximately half of the children affected heterozygous
individuals will show the condition; homozygous affected individuals are rare. Homozygous
refers to two copies of the allele that carry and are responsible for the disease. The probability
of generational skipping is fairly low. However, generational skipping can happen with recessive
traits.
In homozygous affected individuals, both parents have the trait. The probability of the
offspring having the disease is 75%. More commonly, one parent will have the disease and one
will not. The probability of the offspring having the disease is only 50% one parent will donate
the affected gene and the other will donate an unaffected. If the affected parent is
heterozygous and presents with disease, the affected parents still have one gene that's normal.
If one recessive gene can pair with a normal gene, the disease may be eradicated. Traits can do
these as well. Autosomal recessive disorders are not linked to sex and will be expressed equally
in males and females. Most often, offspring have parents who are carriers, but don’t have the
disease, and are unaware of the disease.
For the condition to be expressed, the individual will be homozygous - two disease
genes will be present. Generational skipping can occur. Probability of an autosomal recessive
disorder can be increased significantly if two related individuals’ mate and have offspring. This
can dramatically will increase the recurrence of recessive disorders. If both related individuals
have the recessive gene, the probability of having an offspring with an autosomal recessive
disorder increases significantly. Therefore consanguinity may present such a risk for
development of autosomal recessive disorders. Like autosomal dominant diseases, autosomal
recessive diseases are fairly rare because two recessive genes must connect to create the
recessive disorder expression.
Aneuploidies
Autosomal Aneuploidy is when the cell doesn't contain a multiple of 23 chromosomes
and results in aneuploid cells. Aneuploidy can occur in any chromosome. However, only the
13th,18th, and 21st chromosome can be presented in live births, otherwise the chromosomes
aneuploidy will result in a still birth. For example, trisomy 16, is quite common, unfortunately
the baby is not viable, and the birth isn't live.

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 The most common example of Aneuploidy is Down syndrome; the frequency is one out
of 800 life births. Down syndrome was first described by Langdon Down who described the
disease in 1866.Since then, extensive research has been conducted on Down syndrome. One of
the most significant findings is that the incidence of Down syndrome vastly increases with
maternal age. After the maternal age of 45 years old, the risk can be as high as 5% probability of
having baby with Down syndrome. Because women are born with all maternal egg cells, the
eggs are held in a dormant state. During the dormant state, the eggs may acquire damage from
external factors. Damage also occurs from cellular proteins that govern meiosis. Nondisjunction
may occur resulting in trisomy 21 or Down syndrome.
Speculation that paternal age plays a role in development of Down syndrome, however,
there is no steady evidence that will point on paternal age. The famous Columbia University
conducted research in 2003. Data was collected on births of infants from 1983 to 1997.
Approximately 3,400 cases were examined. A similar study was conducted at New York State
University and paternal age was linked to influence the baby having Down syndrome. When
babies born with Down syndrome, there is a chance of intellectual disabilities- the degree may
vary significantly. Individuals with Down syndrome may present with significantly high IQ, and
there were cases described in literature that persons diagnosed with Down syndrome were
able to enter and complete the college and be successful in professional employment.
However, majority of individuals with Down syndrome may present with relatively low IQ.
Physical features will include, low nasal bridge, epicanthal folds will be present, protruding
tongue, and poor muscle tone. Patients with Down syndrome may present with increased risk
of heart disease and congenital heart disease. It's important to screen a baby for congenital
heart disease. Individuals may also have GI disorders and a higher risk of developing leukemia.
Because of the development of the health sciences, the management of Down syndrome and
consequences is much more elaborate. Today, the quality of life is much higher compared to
decades ago. Trisomy 13 and 18 or other trisomies that can be present in live births, but
unfortunately the patients with trisomy 13 and 18, will present with much more significant and
severe complications, than the person with trisomy 21. In these cases, the probability of having
more profound deficits is much higher. Intellectual disabilities can be present, as well as the
physical disorders may be present. The chromosomal trisomies will not survive to term. Trisomy
16 is the most common one in spontaneous abortions- it never results in live births. Partial
trisomies may also occur when an extra portion of chromosome is present in each cell. The
consequences of a partial trisomy is not as severe as a complete trisomy.
Individuals who are partial trisomy are considered chromosomal mosaics; this means
the individual organism has several cell lines. Each cell line has a different karyotype, and
mosaics are formed by early mitotic nondisjunction. This can occur in one embryo cell, but not
in other embryos cells. Partial trisomy is not as severe because a portion of a chromosome is
present in the cell. If a portion of the chromosome is left, it is not a complete trisomy. A
missing chromosome is worse than having a portion of a chromosome missing. Sex
chromosome aneuploidy is similar to autosomic chromosomal aneuploidy. However, the

16
consequences are less severe. For example, when there is an abnormality related to Y
chromosome the consequences may be relatively insignificant. This is due to the small amount
of genetic material carried by the Y chromosome, and the approximate location on the gene.
When X chromosome aneuploidy occurs, more serious consequences may occur. For instance,
when there is no X chromosome, and only Y chromosome the chances of survival are non-
existent. The zygote won't survive if there is no X chromosome. Instead of two X chromosomes,
some females may have three x chromosomes or even four X chromosomes. This is called
metafemale. No physical abnormalities occur, but a female with three X chromosomes may
have sterility, menstrual irregularity, abnormal menstrual cycle, and may have intellectual
disabilities. When the number of X chromosome increases, the chances of developing disorders
especially intellectual disabilities increases, and with five chromosomes the chances are even
higher. The presentation of the disorders will increase, and the consequences will be more
severe with each additional X chromosome.
Turner syndrome is a disorder when only one X chromosome present. With only one X
chromosome, survival is still possible, but without X chromosome the survival is impossible.
When an individual only has 45 chromosomes in Turner syndrome, and only one X chromosome
there is no corresponding X chromosome or Y chromosome. The gender of the individual will be
female, but she will be presenting with absence of ovaries and sterility. Short height and
webbing of the neck is also a characteristic, and individuals may have some edema. They can
also have coarctation of the aorta. Newborns will have edema in lower extremities and gonadal
streaks. Gonadal streaks are similar to undeveloped ovaries; they are not fertile, but can still
can be susceptible to neoplasm. This should be monitored and treated of if there is a suspicion
for cancer. Turner syndrome will have relatively high mortality rate presented as spontaneous
abortion, but survival rate is relatively high, and the individual will present with all the
symptoms described. The X chromosome will be inherited from mother; the paternal X
chromosome will not be present. The father, in this case, does not donate anything. Turner
syndrome is possible with only one X chromosome.
Klinefelter's syndrome is another sex chromosome aneuploidy and results in the
individual having at least two X chromosomes and one Y chromosome. The individual will have
a male appearance and karyotype can be described as 47 XXY karyotype. The individual will
have all the consequences of having excess in X chromosomes. Some individuals will have
symptoms of sterility, they will have still testicles, but they won't be developed. The individual
may have gynecomastia, long limbs, and sparse body hair. Some individuals may have 3 X
chromosomes, or even 4 X chromosomes, but the more X chromosomes, the increase in
abnormality rate.
In addition to, when losing or gaining a chromosome, sometimes, parts of chromosome
can be lost, or interchanged, or duplicated. When the sex cells are formed the arrangement
may be altered, because of the small amount of genetic material involved. Consequences may
not be as serious as changes that involve an entire chromosome or may not even be present at

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all. If abnormalities of the chromosome are present, they can produce a serious disease in some
cases, and may influence the children. If it is some type of sex transfer trait, it may show up in
the next generation.
Deletion is when a chromosome loses part of the DNA. When a gamete with deletion is
present, the probability of uniting with another gamete with deletion is very low. In most cases,
the gamete with deletion unites with a normal gamete. Inversion is another type of alteration
in chromosomal structure. It occurs when there is a rearrangement of a segment of the
chromosome; the segment flips around and is reversed end to end. The deletion can result in
Cri du chat syndrome. Translocation can be described as an exchange of genetic material
between chromosomes. Robertsonian translocation occurs when the long arms of two
chromosomes fuse at the centromere to form a single chromosome.
Robertsonian translocation can occur on chromosomes 13, 14, 15, 21 and 22 because
short arms of these chromosomes are very small and do not have any essential genetic
material. When the translocation happens in Robertsonian translocation, the short arms are
lost completely during the next cell divisions. In this type of translocation, there is no loss of
important genetic material. The individual will have 45 chromosomes in each cell and present
at typical developing with no disorders. In other cases, the individual can have monosomies and
trisomies. It is common in Robertsonian translocation for the fusion of the arms of
chromosome 21 and 14 to occur and result in an extra copy of the long arm of chromosome 21.
Chromosome 21 is the chromosome related to Down syndrome, and this can result in the
disorder.
Ring chromosome occur when the telomers of each chromosomal arm have been
deleted, and the broken arm joins together to form a ring. This can trigger a series of breakage,
fusions, and bridge events that will cause continuous DNA breakage. It occurs like a chain
reaction of recombination of chromosomal material. The ring itself is not the danger, however,
the chain reactions have severe consequences. Individuals with ring syndrome may display very
diverse symptoms as a result from DNA breakage and recombination. Deletions of the
chromosomal material will occur as well as duplications and the diverse presentation.
Individuals will show failure to thrive. Failure to thrive is a consequence of cells not proliferating
normally and is suggested to be due to mitotic instability of the ring that prevents the forming
of somatic cells. Chromosomal breakage occurs and physiological mechanisms trying to repair
the break. Unfortunately, the break heals differently than the original chromosome, and this
may result in diverse presentation of different abnormalities. The abnormalities can be very
mild or drastic. Ionizing radiation, chemicals, and viruses may affect chromosome in autosomal
structures.
Duplication is a relatively rare occurrence that alters the chromosomal structure. When
a repeated gene sequence occurs, the consequences are less severe than deletion. Duplication
can occur in the short arm of chromosome 5 and result in Cri du chat syndrome. This syndrome
results in several physical abnormalities such as microcephaly and intellectual disabilities.

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 Fragile sites are sites that the breaks or gaps within a chromosome. They can be seen by
a microscope when the cells are cultured or developed. There is no evidence that this may be
related to some disorder in most of the fragile sites. However, Fragile chromosome X
syndrome or fragile x syndrome can occur. It presents with intellectual disabilities and is
prevalent in the population. The ratio is 1:4,000 males a 1:8,000 females. The distinct ratio
between male and females is due to females having two X chromosomes and males only having
one. If a female inherits the mutation, they may not express the disease, but a male because of
only having one chromosome. Therefore, the prevalence is so much higher in males. So, that's
why the prevalence is two times more in males. A female may have mutation and not present
with the disease, but she can still pass the mutation along to her offspring. Fragile sites will not
be presenting any relation to the disease except for fragile X chromosome. When fragile X
chromosome occurs, it occurs on the long side of X chromosome and will be related to
intellectual disabilities. Fragile X syndrome is one of the most common genetic disorder second
to Down syndrome.

Inflammation and Infection

Immune response and inflammation are a part of defense mechanism created to protect
the body against the foreign invaders. There are three types of protective barriers. Physical and
surface barriers, such as intact skin, is the first line of defense. The skin by itself is a physical
barrier and at the same time skin surface is acidic. This makes it an antimicrobial barrier against
infection. However, this does not always happen, and sometimes it’s possible to have skin
infections, but if everything functions well skin can be an efficient barrier against infection.
Thousands of microorganisms are on the skin’s surface. Some sources cite that more than 100
trillion microorganisms are carried by one individual. This is a normal bacterial flora on the
skin. It prevents opportunistic infections by other bacteria. So, on the other Skin has sebaceous
glands that secretes sweat. This creates an acidic environment and antibacterial enzymes.
Mucus membranes can serve as another physical barrier and serves to trap and destroy
invaders. Besides physical barriers, the human body also uses inflammation and immune
response. Inflammation is a nonspecific response. When a physical barrier is broken by a
scratch, stab knife wound, or a simple splinter the bacteria or other microorganisms penetrate
the tissues causing a trigger in inflammatory response. This process begins with a vascular
response. The vascular response happens within seconds of the physical barrier being broken.
It is an unspecific process that follows the same pattern regardless of what caused the break.
An immune system response is a specific response; it is even referred to as “a third line of
defense.” Every cell has proteins that we are called antigens on the surface that can identify the
cell. When a response occurs, the body’s immune system identifies the invader by the antigen
and the lymphocytes produce antibodies. The antibodies link to the antigen and either kill the
cell or disable it. The immune system has the ability to remember the invader and produce
antibodies to fight against it.

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 Inflammation is a nonspecific response in which the process does not distinguish they
type of invader that is attacking the body. The invader is usually a reaction to distortion in
tissue integrity, destruction in tissue integrity, trauma, injury, or a burn. Inflammation will not
occur if there is no blood supply. The blood supply creates the vascular and cellular component
of the inflammation. Inflammation cannot occur in necrotic tissue, however if there is a
decubitus ulcer, an inflammation response may occur around borders of the ulcer. If there is
inflammation in a tissue, an injury occurred when the individual was alive. If an injury has
occurred after the person is already deceased, there will be no evidence of inflammation
because blood supply is needed for the inflammatory response. Inflammation benefits as a
second line of defense. However, it may be harmful to the individual and destructive to the
tissues and severe inflammation can even be deadly. Type 1 and anaphylactic shock reactions
are an example. Inflammation by itself is a blind mechanism and its nonspecificty can make it
harmful. When inflammation occurs, there are several signs and symptoms including redness,
heat, edema and pain. For redness, heat, edema and pain, Latin equivalents can be used: heat
is calor, edema is tumor, pain dolor, and redness is rubor. These are the signs of inflammation,
that visible and reported. Some types of inflammation are acute and chronic.
Acute refers to the inflammation lasting less than ten days; it is a relative term, so if
inflammation lasts elven days it is still acute but two weeks is usually the cut off point. If
inflammation last more than two weeks, it is considered to be chronic. When a inflammation
occurs, basophils or mast cells are involved. When the injury is detected, the inflammatory
response is triggered, and mast cells may release histamine. Histamine will cause dilation
vasodilation in local capillaries. Dilation will increase the blood flow to the area and cause rubor
or erythema and heat in the area. When this happens, dilation also works to bring neutrophils
into the area. Neutrophils lines the endothelium of the vessels and wait for an opportunity to
move inside of the tissue. When this happens, the neutrophil influx is a short-term process. It
cannot be caught in lab work unless interval blood drawls are done. Interval blood draws should
be done every few hours because neutrophils will move into the tissues within a 24-hour
period. When the capillaries dilate, because of the histamine and other substances, vascular
permeability will increase. Permeability is when the capillaries leak and cells in the endothelium
are stretched. The blood then begins to produce exudate. The fluid from the blood leaks into
the tissue and causes edema. Edema is a sign of inflammation. As the edema increase, the
pressure build-up causes pain. Swelling can prevent functioning of the organs. An individual will
lose mobility if the swelling happens in an extremity due to pain- like a sprain or strain.
Vascular permeability helps the neutrophils to run into the tissues. Diapedesis is the
process by which the neutrophils squeeze between the epithelial cells; it is a very effective
process that happens very rapidly in which millions of neutrophils will invade and area within a
few hours. Neutrophils are the first cell that attack the inflammatory process. These cells are
attracted to the injured area by chemotaxis force or the process of chemotaxis. The
chemoreceptors are located on the neutrophils. The detect the source of the release of

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chemically active substances, and make the neutrophils move toward the site of the injury.
When neutrophils arrive to the site of the injury, phagocytosis begins.
Phagocytosis is the “eating” process of the cells. This process starts with the destroying
the foreign materials, and the cells start dying because neutrophil cells do not live long. As the
cells are dying, they produce the purulent exudate or pus. Another type of exudate is fibrinous
exudate. This occurs in a larger injury with more severe inflammation. The fibrinous exudate is
composed of fluids and a large amount of fibrinogen. When comparing two serous exudates,
the leakage of the fibrinogen will signify more severe inflammation. The presence of fibrinogen
is observed, in streptococcal laryngopharyngitis, pneumonia, other infections with bacterial
origin. In these cases, the lesion will have a mesh like structure. The superficial wound may be
covered with dried fibrinogen exudate or a scab; it is a collection of dead neutrophils.
Approximately three to four days after the inflammatory process begins, monocytes will
appear. Monocytes leave the bloodstream and move into the tissue, become phagocytic cells,
and then turn into macrophage cells. Monocytes remain the same, but the name changes
because it moves from the blood into the tissue. Neutrophils, may be dead, is still present at
the location and the injury and may create an abscess.
An abscess is a collection of pus; it typically needs to be drained and may cause
significant pain and/or trigger further inflammation and infection. Empyema is the
accumulation of pus in body cavity. Ulcers can happen secondary to inflammation. An ulcer is
the absence of the tissue. It is a result of the injury and the inflammatory response that follows
the injury. An ulcer is the result of necrotic tissue sloughing off and leaving a crater or
excavated area. Examples of ulcers include stomach ulcers or duodenum, gastric or duodenal
ulcers or peptic ulcer disease. Cellulitis is a diffuse and widespread acute inflammation that
can be seen in tissue on the surface, like skin, and subcutaneous tissue. Cellulitis is caused often
by of streptococcus or Staphylococcus bacteria, or failure of immune system. When
opportunistic infection takes over and the immune system fails to protect the surface
pathogen, cellulitis can be very dangerous and spread. If an antibiotic treatment is introduced
or intravenously in severe cases it is usually treated effectively.
Infection is an invasion of the organism or microorganism that can cause cell and tissue
injury. Injury or damage is a part of the infection process. If colonization occurs with no injury,
then the term 'infection' cannot be used. When discussing microorganisms that have the
potential to cause pathology or pathogenesis, normal flora will become pathogenic under
certain conditions. An example includes the e.coli infection, which can be considered an
opportunistic infection under certain conditions, but in other cases, it may be just considered a
normal flora of the gut. The resistance of the pathogen to the barriers, physical barriers to
immune barriers, and the number of pathogens invading, and area are factors to be considered.
In order for the normal flora to become pathogenic, the barrier must first be broken and create
a port of entry. The pathogens must be somewhat resistant to the defenses of the host. The
number of pathogens along with the types of comorbidities that are present in the host will

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facilitate the invasion of the pathogens. Infectious diseases are the leading cause of death
worldwide, in the United States next to cancer and heart disease. Infectious diseases are not as
rampant in the United States because of the country’s ability to identify, track, and control the
spread of diseases. The Center for Disease Control and Prevention (CDC) can provide the
services and is providing the services in the United States.
There are many pathogens that may cause infection. Bacterial infections may occur as a
primary infection or a secondary infection. When this occurs, the person is exposed to a
pathogen and is considered a primary infection. A secondary bacterial infection occurs when
there is some type of other disease present. It can be viral disease or mechanical factor, which
may result in a bacterial infection afterwards. For example, a person has a nasal obstruction of
some kind. This leads to sinusitis, and because of bacterial influx, it is secondary infection.
Eustachian tubes obstruction mechanically, or again secondary to other infective organisms,
and may lead to otitis media.
Normal flora is the bacteria that occupies the skin, lives on the skin, and is usually
harmless. It is also found in the intestinal tract, genital tract, and mucous membranes in mouth
and nose. The bacteria that is harmless and creates normal flora can become pathogenic under
certain conditions. When the resistance or body defenses are weakened, these bacteria can
take over.
Staphylococcus is an infection on the skin and can be a very devastating. If the skin
barrier is broken, the microorganism can enter, and may infect any organ. Staphylococcus
aureus is a bacterium that can be very devastating and harmful, especially the Methicillin
resistant forms such as MRSA or MRSA. MRSA is resistant to penicillin and other antibiotics. It
is a consequence of widespread antibiotic use, treatment, and overuse of antibiotics mostly in
primary care, as well as in acute care. A significant number of people with viral diseases, such as
bronchitis are treated by antibiotics, in which there is no indication for that. Bronchitis often
has a viral origin, and signs and symptoms aren't recognized. For instance, if patient has
productive cough, and a yellow greenish sputum, the chest x-ray will be negative for
pneumonia, a patient is febrile, and everything points on viral infection. However, a primary
care provider may go ahead and prescribe antibiotics. This creates the resistance of the normal
flora, that can be invasive and become an invasive pathogen and MRSA.
In regions that the over-prescription of the antibiotics is very low, the MRSA and other
type of Streptococcal bacteria can normally live on the skin and in the throat, Common
infections caused by streptococcus will include streptococcal laryngopharyngitis, or commonly
called strep throat, scarlet fever, pneumonia and even meningitis. Some people may develop as
the sequel of streptococcal laryngopharyngitis, rheumatic fever and glomerulonephritis. Enteric
bacteria in the intestines includes E.coli, Klebsiella, Pseudomonas, Shigella, and Salmonella.
E.coli can cause enteritis in infants and adults. It is also associated with “travelers diarrhea”
because when people travel to different regions the are infected with an E.coli strain the local

22
dwellers are susceptible against, but the travels are not and results to some type of colitis.
Pseudomonas is notorious for infecting wounds.
Pseudomonas infection will result in a green exudate, pus exudate production, and a
foul odor. Although, Shigella and Salmonella, are not usually found in the intestinal tract,
Shigellosis can still happen, and Salmonella infection can occur. Salmonella can cause severe
food poisoning especially if the cause is from eggs.
Viruses are the smallest infective particle. Viruses have properties of a living organism;
however, it needs another living organism to replicate. In the healthcare field, it is important to
recognize and treat viral infections. Viruses need a host cell to reproduce and are not easily
treated. Antibiotics again are not effective, but when pneumonia is a sequel of a viral infection
antibiotics will be needed to combat secondary infection. Immunizations are still an effective
way to prevent certain viral infections, such as measles, mumps, rubella, smallpox, chicken pox.
Latent viruses may lay dormant in cells and replicate. Varicella can present later in life as the
shingles infection. Shingles is not only disease of elderly people but can affect younger people
in their twenties and thirties who present with shingles.
Fungi are different in that fungus is bigger than bacteria but is not as deadly or harmful
as bacteria- only very few types are pathogenic. Most of the fungal growth is harmless, and
fungus plays a significant role in nature. It helps to restore the balance in nature by destroying
already dead tissues and debris. They are a few fungal infections or types of fungus that can be
harmful to humans. Tinea infections are fungal infections on the skin; the skin is a cooler
environment than inside the body and fungus often choose cold environments. Tinea infections
are commonly described as ringworm, athlete’s foot, or jock itch. They are common and very
infective and can be transferred from one person to another. Another type of fungal infection
is Candida infections. It is a superficial infection of skin and mucous membranes. In an adult,
Candidal infection in the oral cavity or thrush is not an expected finding, but in this case, oral
Candida in an adult or thrush may signify immunocompromised status. Children may often
develop Candida and it may be considered quite an expected finding. Adult candidiasis may
signify an HIV infection. Also, candidal infection can cause vaginitis and/or yeast infection which
is easily treatable. Other fungal infections may cause histoplasmosis; histoplasmosis can be tied
to certain geographic locations and certain behavioral factors, such as 'having the cat and
emptying the litter box,’ and is not common in general population, but still the damage can be
devastating. Fungal infections can be treated with antibiotics and certain fungal medications.
Some fungal infections are extremely difficult to cure, such as nail fungus, or even ringworm
infections; they may require long-term therapy. For example, nail fungus may require the
Sporanox-pulse therapy and other type of antifungal medication. Antifungal medications may
cause liver damage in some cases, but other fungal infections like vaginitis or even candidiasis
are easy to treat and cure.
Ricketsiae is a microscopic organism, that is an intermediate between bacteria and
viruses. Like a virus, it needs a living host so to multiply. It can be spread by a vector organism

23
like flea, tick mites’ lice, something that can bite. The most common disease that may have
devastating consequences is Rocky Mountain spotted fever which is spread by the tick. A
regular tick that you may find on a dog is not the carrier of Rocky Mountain spotted fever. The
carrier will be much smaller brown tick. If there is suspicion of the infection of Rocky Mountain
spotted fever caused by a tick, the tick should be preserved in some way and presented a
healthcare provider for identification and treatment.
Protozoan infections are caused by a single-cell microscopic organism and can be found
in the soil in dead or decaying material. Ingestion of spores or infection can be caused by insect
bites. Malaria can be spread by mosquitoes and is a protozoal infection It is the most prevalent
of the protozoa infections worldwide. However, in the United States, it is very uncommon. The
malarial infection is a result of the protozoa living in the red blood cells of the host and causing
destruction of red blood cells.
Giardia is another type of protozoal infection and usually is not as devastating as
malaria. It can be caused by drinking infected water and can results diarrhea. It is often can
resolve by itself or if detected early can be treated by antibiotic therapy.
Helminths is another class of infection that includes roundworms, flatworms,
tapeworms. The helminths are very common worldwide, but not common in developed
countries. Pinworms or tapeworms are the most common helminths in the United States.
Pinworms are usually causing anal itching. Tapeworms may cause certain symptoms such as
pain and diarrhea; they usually are a result of consuming inadequately cooked meat especially
in hamburger meat. Treatment can include anti helminthic agents; this type of treatment is
very effective, and is one of the reasons that these infections were under control in the United
States. However, with the influx of immigrants from developing countries, it is typical to have
the reemergence of these infections, but these types of infections are easily treatable.
Testing for bacterial or viral infections may include testing blood for increase white
blood cells. Bacterial infections will cause a left shift and viral infection-right shift. The left shift
is most commonly observed. The left shift signifies the increase in numbers of neutrophils while
the right shift signifies an increase in the number of lymphocytes. Another test that can be
done, is a culture and sensitivity for blood or urine. This involves culturing the invading
organisms and then check the sensitivity of that organism against certain antibodies.
Skin testing is also used to determine antibody presence for a pathogen. It is one of the
common tests done as well as the Mantoux test to determine tuberculosis presence. The tests
involve intradermal injections- injections of antigens of tuberculosis. If the patient is exposed to
TB and developed tuberculosis antibody, the antibody will attack the antigen and cause
induration. In severely immunocompromised patients, the size of induration is smaller because
they cannot mount an immune response. The size of induration for different categories of
population is constantly changing, but currently 15 millimeters is for people who do not have
any potential for exposure for TB. 10 millimeters is for healthcare workers, and 5 millimeters for

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immunocompromised people with HIV. There are many other types of testing for the
infections, but there are three major types.
In general, the immune system will be able to control the invasion of foreign organisms
or foreign particles. When the barriers of defense are broken and inflammation doesn't occur,
infection may occur. Many different organisms can cause infection, but most common types are
bacteria and virus. These two can be diagnosed and treated in many different ways.
Immunization is an important consideration for the prevention of viral infection, and beneficial
for treatment in many types of viral infections.

Cancer
Neoplasms and cancers are very important topics for everyone involved in healthcare,
either someone in clinical practice, clinical education, or research. Thousands or even millions
of people worldwide are diagnosed with neoplasms every year. To many, the news can be the
equivalent to death sentence, however, many neoplasms and cancers are treatable. Research is
continuing to find ways to treat most of the common neoplasms. Neoplasm and tumor are
terms that may be used interchangeably. Tumor is a more colloquial term and neoplasm refers
to a new growth; the new growth can be cancerous or benign. Not all the tumors and
neoplasms are deadly or malignancies.
Common Cancers
For men, prostate cancer is the most commonly diagnosed. Women are most
commonly diagnosed with breast cancer. Cancers are diagnosed in many different ways, and
the earlier the cancer is detected the treatment outcomes increase. Cancers are classified
according to their appearance, growth patterns, type of body tissue, and where is started.
Benign neoplasms are the neoplasms that are confined to a certain localized area and
will not spread. The term tumor most often refers to benign neoplasms, however some can
refer to malignant tumors. One important characteristic of benign neoplasm is that they are
encapsulated, localized, don’t metastasize or spread. Most of the time, these types of tumors
are harmless unless they grow in some type of confined space such as the cranium or proved
pressure on important blood vessels and cut off the blood supply, nutrients, and oxygen to the
certain areas of the body. Benign neoplasms are usually harmless and can be considered a
cosmetic defect that can be removed.
Malignant neoplasms or cancers present with two main characteristics - invasions and
metastasis. Invasion will involve spreading of the neoplasm into local or surrounding tissue.
Metastasis will be involve spreading of the neoplasm to distant sides. Metastasis can happen

25
via lymphatic venule or via the blood stream. When differentiating the neoplasm, focus should
involve the tissue of origin. Neoplasms are classified into tissue type related classification or
classification based on the tissue from which they grow. Depending on the location of the
tumor and origination site of the tumor, the tumors may have different names. Benign tumors
usually take the tissue name and the suffix-oma for tumor. For example, lipoma is a tumor of
fatty tissue. Malignancies will have terms carcinoma or sarcoma added to the type of the tissue.
Epithelial vs Connective Tissue Malignancies
If an epithelial tissue is harboring a neoplasm, it is a non-malignant tumor and will be
named adenoma. If it is a malignant tumor, the name will be adenocarcinoma. In general, the
epithelial tissue neoplasm, a malignant neoplasm will be named carcinoma. Depending on the
original tumor site and tissues where tumor originated the name of the tumor changes. A
benign tumor of connective tissue such as bone will be named osteoma. If the tumor becomes
malignant, the name will change osteosarcoma. Sarcoma is a term is used in connective tissue
disorders such as muscle, fat, and bone; sarcomas are less common than carcinomas and will
also spread more rapidly.
Lymphatic and blood forming organs and lymphatic tissues do not produce benign
neoplasms, neoplasms in these tissues are always malignant. Malignancies do not have to have
a benign variety or benign counterparts, for malignant transformation to occur. Lymphomas
and leukemias are malignant neoplasms of lymphatic and blood forming organs and lymphatic
tissues. The leukemias and lymphomas, can be deadly and have a high degree of mortality, but
depending on the variety they may be predictable and may result in a favorable course of
treatment and remission dependent on the type of cancer.
In other tissues, the naming process is different. For example, melanoma is a
malignancy of melanocytes. The tern carcinoma is not added to the name; melanoma is the
specific term used. Also in brain tumors, which originate in the glial cells of the brain, is referred
to as gliomas. Gliomas are benign in appearance and do not metastasize, but they are still
considered malignant because most gliomas are fatal. Adenoma will come up from the granular
epithelium and will be a benign neoplasm. If something comes out from the squamous
epithelium it is an epithelioma, and if something comes from the fat tissues it is a lipoma. If fat
tissue turns into a malignant neoplasm, it is liposarcoma. When malignant neoplasm appears,
usually some type of genetic mutation is to blame. Genetic mutation can take place secondary
to disruption of genetic code by radiation, viruses, different carcinogens, or different chemicals.
There is a big list of household chemicals, pesticides, herbicides, insecticides, they all may be
presenting themselves as carcinogens. Research has also determined many other possibilities of
carcinogens, such as burnt cooking oils, excess in certain dietary, certain dietary ingredients
such as fat and trans fats and all.
Carcinogen refers to chemical structures that are considered cancer-causing. Viruses
and radiations are separate entities because they are not chemical structures and cause genetic

26
mutation by a different mechanism that results in a disruption of the genetic code and
development of a malignant neoplasms. Malignant neoplasms do not have the structure and
the purpose of the normal cells. Normal cells have a purpose and have controlled division, but
cancer cells do not follow any pattern. This can cause difficulties in determining the location of
the metastasis and the tissue of origin.
Oncogenesis occurs when cancer tissues grow and is a genetic mechanism where
normal cells are transformed into cancerous cells. Carcinogenic agents affect the DNA of the
cell and leads to DNA damage which eventually will result in malignancy. Unregulated cell
differentiation and growth is main problem with cancer. The malignant neoplasm steals
nutrients, oxygen, and blood supply form other places in the body and grow uncontrollably. A
malignant tumor can take over the body and result in death if not treated. Another concern
with cancerous tissues is invasion and metastasis. Invasion into the surrounding tissue may
damage vital organs and vital function. Invasion occurs by the process of growing endings from
the original tumor as well as the process of metastasis. Metastasis involves seeding the cancer
cells into remote location by using lymphatic supply or blood supply. Proto-oncogenes are
normal genes that regulate cell growth. Oncogenes are mutations that lead to uncontrolled cell
growth; the growth is autonomous because the cell grows by itself. The growth is not regulated
by any factors from the body and does not obey the uniform program that entire body obeys.
Oncogenes include growth factors, receptors, different enzymes and transcription factors.
Growth factors will bind to receptors on cell structure which will activate signaling
enzymes inside the cell. This activates special proteins called transcription factors inside of cell
nucleus. The activated transcription factor will facilitate the turning on of the genes required
for cell growth and proliferation. This will also promote autonomous cell growth in cancer cells
in the absence of normal growth promoting signals because of the point mutations,
chromosome translocations, or chromosome applications. For the cell to grow autonomously
and uncontrollably, the oncogenes must be present, and these oncogenes are factors such as
growth factors signaling enzymes, transcription and factors that would disrupt or turn on the
genes are required for growth and proliferation. The whole process promotes uncontrolled
growth. Tumor suppressor genes are “brakes” that the body uses stop the cancerous or
malignant growth. There are numerous suppressor genes that have been identifies. One
example is the p53 gene; mutation in the gene can result in lung, breast, an colon cancer. This
specific gene mutation is blamed for the three leading types of cancer. A single genetic event
can activate an oncogene. There are two copies of each gen from each parent, if both genes are
mutated, both copies of the suppressor gene will become inactive. Two mutations must occur
for the loss of both alleles of a gene to be inactive- this is referred to as a loss of
heterozygosity. Loss of heterozygosity (LOH) must occur for the process of genetic mutation of
suppressor gene to occur. DNA repair occurs secondary to the presence of cyclins. Cyclins are
important for making sure that the cell has produced the proteins needed for separation of the
chromosomes. Cyclins will check that the DNA has been correctly duplicated and the cyclin
proteins to measure whether cells have grown large enough to divide. Cyclins regulate the

27
process as a whole and serve as checkpoints. They check the presence of the proteins necessary
for chromosome separations and check the duplication of the DNA to make sure it is correct,
and they measure if the cell is large enough to divide.
The earlier the cancer is detected the likelihood of better treatment outcomes
increases. Cancers are classified according to their appearance, growth patterns, type of body
tissue, and origin. Normal cells undergo apoptosis while cancerous cells divide indefinitely.
Apoptosis does not occur in cancerous cells; these cells not only survive but replicate. When the
telomers shorten with each replication in a normal cell, it eventually the cell will no longer be
able to divide. In cancerous cells, the enzyme telomerase is activated, and it keeps repairing the
telomers until indefinitely; the cancerous cells are able to replicate because the telomers are
maintaining their length. HeLa cells are cancerous cells that were obtained from a young
woman, a 31-year-old named Henrietta Lacks, upon her death from cervical cancer. The cells
were collected in 1951 and the cells are still living and multiplying. These HeLa cells were used
for polio research, and in 1955 the vaccine was created that was helped to nearly erase the
polio disease. The HeLa cells are slightly different from other cancer cells. When the cancer cell
samples were obtained in the early fifties, they would replicate for a short time and then die
outside of the host organism. However, the HeLa cells would multiply uncontrollably, and some
scientists speculated that the total weight of all cells that multiplied from the original HeLa cell
sample is about 20 tons. This experiment raises an issue of bioethics. The tissue samples were
obtained from Henrietta Lacks without her consent.
When the telomerase is activated in cancer cells, they continue to divide. Normally with
all genetic abnormalities, tumors cannot grow without blood supply. Blood supply is needed for
tumor growth and metastasis. In a healthy body, angiogenesis (development of new blood
vessels) only occurs in two cases- wound healing, secondary and primary wound healing, and in
the uterus during the proliferation state of the menstrual cycle. With the expectation of these
two processes, angiogenesis will be one of the signs of tumors and tumor growth. In one
research study, Thiabendazole (TBZ), a common antifungal drug, was shown to inhibit
angiogenesis in vivo, and Xenopus embryos.
Malignant Transformation
The first step in the malignant transformation process involves the initiation phase. In
this phase, cell damage occurs resulting in changes to the tumor suppressor genes. Apoptosis
agents transform to a promotion period or a latency period. The latency period is the time
between the cell initiation into a detectable tumor. During this phase, the growth is still
occurring, but cannot be detected. The last phase includes the occurrence or emergence of the
detectable tumor. The tumor is still small, approximately one centimeter in size. Even though
the tumor is small, 1 billion cells have already been replicated; the growth is exponential, and
the cells rapidly divide. In reference to the HeLa cells, their growth doubled in only 24 hours
compared to the growth of normal cells in 36 hours. The malignant cells have, in addition to
uncontrolled growth, a faster growth time compared to normal cell.

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 Grading and Staging are two important concepts in cancer diagnostics and treatment.
The factors allow for the determination of the development of the disease, the extent to which
the disease is developed, how to plan treatment accordingly, and predict the possibility of a
cure.
Grading is the degree of differentiation. If tissue is well differentiated, like a normal
tissue, there is a lower grade. If tissue is very similar to normal tissue, it is a grade 1. When
differentiation starts to disappear, the grading will increase. Grade 4 will be less differentiated
than grade 2. Grading is typically numbered by Roman numerals from one to four. However, in
regard to prostate cancer, five gradings of malignancy may be used; these are obtained by using
the Gleason grading.
Staging of the cancer determines the extent of spread of neoplasm. Stating can be
developing from clinical examination, imaging studies, biopsies, and even surgical exploration
with biopsies. Staging is also categorized by numerical numbers, from one to four, and the
system is very similar to grading, but is spread. Staging will show how well spread the cancer is.
The TNM system can be used for staging; in this system, tumors are staged according to the size
of expand of primary tumor, number of lymph nodes involved, and metastases present in the
other remote sites. The staging depends on an extent of metastasis and invasion of the tissues.
In this staging system, stage zero will signify carcinoma in situ, stage 1, and stage 2 and stage 3,
basically reflect the extent of the disease. Things to consider when determining the stage
include how big or small the tumor is, if it spread beyond the organ in which it first developed
and is it in lymph nodes and organs that are adjacent to the location of primary tumor. Stage 4
cancer will be a result of the cancer spreading to the other organs.
The TNM system is an important classification system, and it provides a better idea of
what's going on compared to a simple staging system. For TNM, under T, the primary tumor is
being examined. If its size prevents the tumor from being evaluated or there is no evidence of a
primary tumor like carcinoma in situ, the stage will be T’0’. N stands for regional lymph nodes; if
a carcinoma is present in situ, the state will be T '0' N '0'. CIS will also be added to this stage if
abnormal cells are present but have not spread. When carcinoma in situ becomes cancer, the
size of the primary tumor is described by as T 1, T 2, T 3, T 4 size, and extent of primary tumor.
So, T always presents the primary tumor, and N also refers to the lymph nodes. If there is
nothing in the lymph nodes, you may N0 may be used; if there is some involvement, number
like N 1 , N 2, may be used to reflect the number of lymph nodes and the extent of spread.
Distant metastasis has no way of being evaluated, so it is represented by M0 there is no
way to evaluate this, it's M0. For example, breast cancer may be represented by T3 N2 M0. T3
reflects a relatively large tumor that has spread to nearing lymph nodes, but not to other parts
of the body- there is no metastasis. Another example includes prostate cancer represented by
T2 N0 M0. This involves a tumor that is located only in the prostate, has is no signs of lymphatic
spread or metastatic spread. The result in a good prognosis for the patient. No set standard is
used for measuring staging and grading. They are both interpretations that reflect the condition

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of what happens and the condition of the patient. Staging refers to what has happened to the
tumor, and grading refers to how bad the tumor has become. Zeros in TNM system are good,
and the greater the numerical values the worse the prognosis usually is.

Neurologic System Disorders

Seizures are abnormal and sudden; they are an uncontrolled electrical discharge that
occurs in the brains. The neurons are the particles that release the charge. A seizure may result
of alteration and consciousness, motor and sensory ability, or even behaviors. There is a
differentiation between seizures and epilepsy. Epilepsy is a chronic disorder and the seizures
are unprovoked. Every individual has a seizure threshold. Seizures are the result of resting
potential instability and is a burst of action potential. It is a significant discharge of electrical
energy and determines hyper synchronization. Seizures do not start and affect the entire brain;
however, they start at an epileptogenic focus. The term focus refers to a certain group of
neurons that are sensitive to a trigger. The trigger can be depolarization, an external or internal
agent, or an intervention that may cause a seizure.
Clonic seizures are generalized seizures with area of hyper excitable neurons that define
the epileptogenic focus. The epileptogenic focus will be the source or the place where seizure
starts taking place. The tonic phase is accompanied by laryngeal spasm. The autonomic
reaction may occur at this time; pulse and blood pressure may change, and the patient may
have increased mucus secretion. The tonic phase will last approximately 15-20 seconds. The
clonic phase will follow and is characterized by Antonia and spasms. During the clonic phase,
the patient may become incontinent and my have urination and defecation. Normally, tonic-
clonic seizures will not exceed 1 to 2 minutes. The postictal phase will follow the seizure. During
this phase, the patient is questioned, and patients may experience amnesia of the seizure
event, confusion, lethargy, muscle cramping. Psychosocial side effects may also occur, such as
embarrassment. Consideration of the person who has history of seizures must occur. The
patient may be embarrassed of the episode if they seizure happened in a public or hospital
setting. Muscle pain is the result of the severe spasming of the muscles. The consequences of
seizures may be severe. The status epilepticus is due to a tremendous increase in adenosine
triphosphate (ATP). The cerebral oxygen consumption and blood flow increases, and the
available sources of glucose and oxygen are depleted. The severe seizure may also produce
hypoxia, acidosis, and lactic acid or lactate accumulation. This may result in brain injury and
destruction and cellular exhaustion and destruction. Other consequences of status epilepticus,
besides injury to the brain, injury to the body may occur from trauma. Patients may
unconsciously bite lips or tongue and may experience vertebral fracture. Psychosocial
consequences of the disease may result in strain on the relationship and alienation of the
patient because of their disorder. Epilepsy can be classified into three different types.
Idiopathic epilepsy is characterized by neurogenic abnormalities or genetic
abnormalities; however, the exact cause is not identified. Patients with idiopathic epilepsy may

30
have a family history or family members with this type of epilepsy Symptomatic epilepsy is
related to some type of lesion and cryptogenic. Epilepsy is characteristic with an aura. An aura
is a sensation that the patient may experience that predicts that an epileptic episode may occur
soon. Some patients may not experience the aura and the seizure may start quite suddenly. The
aura is some type of warning to the patient and some patients will choose to take protective
measures especially if they are alone to avoid the seizure. This could include medication to safe
positions.
Mental Confusion and Dementia. Acute confusional states occur secondary to external
factors such as drug intoxication, some type of metabolic disorders, or a neurologic system
disease. Confusion may also present with a urinary tract infection. When a disruption of the
reticular activating system of upper brainstem occurs, the patient may experience acute
confusion. The acute confusional state may have abrupt onset and is a differentiation from a
disease that manifests itself over long period of time such as dementia. The acute confusional
state may happen to a patient who has no previous history or have no symptoms. The abrupt
onset is one of the main characteristics of that concludes no organic disease, but a secondary
consequence such as a urinary tract infection or metabolic disturbance. When talking about
dementia, this is a progressive failure or progressive disturbance of cerebral functions. There is
no impaired level of consciousness or altered mental status at this point may not be so
significant. In the beginning of the disease especially there is no impaired level of
consciousness. There is cortical classification that include Alzheimer’s and Picks disease, and
subcortical classifications such as Parkinson’s Disease and Huntington disease. A mix type of
cortical and subcortical classification includes infection and Creutzfeldt Jakob disease. For
individuals with cortical dementia such as Pick disease, they may have abnormal tangles or
substances called Pick bodies or Pick cells inside neurons in the areas of the brain that sustained
damage. Pick cells are cells that contain abnormal protein called tau- this can be found in all
types of cells. However, persons with Pick’s disease has and abnormal production of this
protein. Pick disease is very rare and is much more devastating than Alzheimer's because it
affects younger group of population. The disease can start as early at 20, but the average age is
around mid-50's and has progressive characteristics. The patients may experience symptoms or
behaviors that may be typical for Alzheimer’s disease as well as difficulty in social settings,
keeping a job, inappropriate behavior. Unlike Alzheimer’s disease, Picks disease results in
personality changes while Alzheimer’s results in memory loss.
Alzheimer's disease can be divided into familial, early and late onset, and non-
hereditary sporadic or late onset. In a familial type of disease, there is a strong genetic
component compared to a non-hereditary there is no evidence that anyone in family had onset
of the disease, but the genetic component is still present. Alzheimer's disease is a combination
of genetics, lifestyle, and environmental factors unlike to popular belief that Alzheimer's is only
the reflection of genetic predisposition. Popular belief is that Alzheimer's is a combination of
the above factors, such as environment, lifestyle and genetic composition. The chances of
developing Alzheimer's, despite genetic predisposition, is relatively low at a 5%. Patient also will

31
have a lifestyle, history, and also environmental factors or combination. To develop Alzheimer’s
disease, an accumulation of clumps of beta amyloid protein will occur. These proteins will
destroy cells resulting in an interference with intracellular communication and will cause
destruction to the cell communication link. The tangles of the tau protein will also occur and
lead to the cell death. The trademark of Alzheimer’s disease is the presence of the beta amyloid
proteins. Theories regarding the alteration of apolipoprotein E and pathologic activation at
MNDA exist.
Senile plaques and neurofibrillary tangles from tau proteins, and plaques, beta amyloid
plaques can hinder the functioning of the brain and result in the development of forgetfulness.
In Alzheimer's disease, the first symptom is the memory changes, memory loss, and then
personality change, problem-solving abilities, and judgment will decline. A classic example of a
declining task is balancing a checkbook. When balancing a checkbook, a person must use
complex thought to complete the task, even if it is a task that they have done before. If a
patient cannot balance a checkbook, this may be a sign of the onset of Alzheimer’s disease.
However, with the development of online banking, the universal balancing a checkbook test,
may not be an appropriate screening for testing the onset of Alzheimer’s disease. Alzheimer's
disease is a diagnosis of exclusion and can be made by ruling out other causes of dementia.
However, a true diagnosis can be made only by autopsy when the neurofibrillary tangles are
present in the brain. It can be easy to describe a patient as having Alzheimer’s disease because
of their age. However, the cause can be several different things especially when the onset of
mental confusion is rapid. The patient deserves and warrants a thorough evaluation of other
causes that can be metabolic or other neurologic diseases such as Parkinson’s disease.
Another type of dementia is HIV related dementia. This type of dementia may affect
anyone who has history of HIV. This disease runs somewhat similar to Alzheimer’s disease in
the way that it is very unpredictable. While in Alzheimer's disease, there is stages of
development and a timeline of progression, but with HIV related dementia the development
may be very rapid, but the result will be the same- the patient will present with cognitive
system deficits. Memory is one of the deficits, and it is similar to memory loss in Alzheimer's
disease as well as the loss of balance, ataxia, and generalized hyperreflexia. Parkinson disease is
a result of degeneration of basal ganglia and corpus striatum and involves a dopamine
deficiency. The patient will have a dopamine deficiency and treatment may be focused on
several different agents that may replenish the dopamine deficiency or make dopamine
production or availability higher. The patient will present with rigidity, brady kinesia, tremor,
postural abnormalities, shuffling gait, autonomic and neuro endocrine disorder. The endocrine
disorder is one of the autonomic disorders that may result in abnormal sweating and cognitive
affective symptoms.
Patients with Parkinson’s are also very prone to developing depression. Treatment
involves treating the dopamine deficiency and trying to alleviate the symptoms. Parkinson may
lead to development of dementia. Approximately half of the people who are diagnosed with

32
Parkinson’s disease may have depression. Depression may not improve because some of
antidepressants may work on dopamine re-uptake, and other patients may develop dementia.
Some patients are institutionalized in skilled nursing facilities. The progression of the disease
leads to disorientation, confusion, and memory changes. Patients can be distracted, have
difficulty with the concept of judgment, and thinking. The dementia related to Parkinson’s
disease may be similar to Alzheimer’s disease. When a patient with Parkinson’s disease
develops dementia, there is no steady progression to a worse state, but eventually, symptoms
will worsen. The patient may have better days or worse days. The patient may also have anxiety
disorders or impulse control disorders. These disorders may be related to dopamine deficiency.
Motor behavior is also impaired, and patients will develop stereotypic motor behavior that
includes a fascination with repetitive handling and examining mechanical objects. Daytime
sleepiness can also be a symptom. Gait can also be affected.
Cerebral vascular accidents (CVA) can be divided into three main categories:
Thrombotic stroke, embolic stroke and hemorrhagic stroke. A thrombotic stroke occurs within
the brain and is due to a blockage formed within the brain, arteries supplying blood to the
brain, or in the intracranial vessels. A transient ischemic attack (TIA) is a small thrombotic
stroke that resolves itself within 24 hours. An embolic stroke is very similar to thrombotic
stroke, but embolic stroke is the consequence of traveling thrombus or traveling clot which
called an embolus. When the thromb is dislodged from another place in the body, such as in
deep veins in lower extremities, it travels to the brain. A thrombotic stroke is due to a clot
formed inside of brain and an embolic stroke is due to a clot that comes from somewhere else.
A hemorrhagic stroke is a stroke that is caused by excessive bleeding in the brain and damage
to the blood vessels secondary to hypertension, or any other factor that may disturb the blood
flow. The main concern with a hemorrhagic stroke is ischemia caused by excessive pressure
that can lead to infarction. Lacunar strokes are typically small strokes, and the lacunae is a
small absent matter in the brain. The lacunar infarcts are silent, but on radiographic
examination they are possible to see.
Aneurysms are formed in the vessels in the brain and result in a rupture. Aneurysms are
diagnosed by imaging studies and treatment will include prevention of the rupture and stroke.
One treatment included using a small clip in attempt to isolate the aneurysm.
Vascular malformations include cavernous angiomas, capillary tangel ectasias, venous
angiomas and arteriovenous malformations or AVM s. Vascular malformation is not as common
an occurrence as aneurysms, cavernous angiomas, or collections of blood vessel. Cavernous
angiomas has n o interference with normal brain tissue and rarely results in a hemorrhage.
Telangiectasiasis is dilated capillaries; it can be seen on the integumentary covering on the
skins, and when in the brain it may interfere or intercept with normal brain tissue, however,
hemorrhage is rare.
Venous angioma can present as a vascular malformation and rarely will result in a
hemorrhage. This is one of the most commonly found disorder or venous malformations or

33
vascular malformation when an autopsy is performed. AVM, arteriovenous malformation, can
occur in the brain or in other parts of the body such as gastrointestinal tract. The arterial
vascular malformation is arteries tangled into the vein and is malformed vessels. There is no
capillary network, but the veins are fed into the artery or vice versa. This formation may
rupture and cause a hemorrhagic stroke. On evaluations, AVMs will be remarkable for systolic
bruit and when the carotid arteries are auscultated bruit may be experienced. Other sources
recommend to acetate the eyeball; if you hear the bruit, this may be a sign of AVM. Treatment
includes surgical excision, embolization and radiotherapy. Treatments are effective and reduce
risk of a hemorrhage. A subarachnoid hemorrhage is a condition that should be treated rapidly.
If a rupture of the blood vessel occurs, blood can escape into the subarachnoid space and settle
causing an inflammation response by irritating the meningeal and other tissues in the brain.
Intracranial pressure (ICP) will also significantly increase because of the pumping action of the
heart. At some point the ICP will reach diastolic levels which is high and will eventually return to
normal. Patients with a subarachnoid hemorrhage may present with infarctions in the brain on
a radio graphic examination. The patient may have an altered mental status, nausea, vomiting,
neurologic deficits, knuckle rigidity and complaints of a throbbing or explosive headache. The
patient may also present with positive Kernig sign and Brudzinski sign. The Kernig sign refers to
the producing pain in the back neck from straightening the knee with the hip. The Brudzinski
sign is a passive flexion of the neck that produces neck pain and rigidity. Treatment of a
subarachnoid hemorrhage is directed to prevention of a cerebral ischemia and may include
surgical treatment to correct the vessel dysfunction or abnormality. Risk factors may include
familial history.
Headaches are one of the most commonly diagnosed condition. There are four types of
headaches. Migraine headaches present with trigger factors and may have an aura or warning.
Migraines are usually unilateral and may be severe. They can also be sensitive to noise and
light, and patient may also have nausea and vomiting. Cluster headaches are most common in
male patients, while migraines are most common in females. Cluster headaches are typically
unilateral and may also have a trigger. However, cluster headaches will not have an aura and
may spontaneously resolve; the patient may have several attacks in one day and then
experience a period of remission. Some of the most common triggers of cluster headaches
include hunger. Chonic paoxysmal hemicrania is a type of cluster headache that occur in a
higher frequency, but it will have shorter duration, and unlike a typical cluster headache this
may be experienced more often by women. Tension type headaches are the most common and
are bilateral. If a patient complains of having a headache or migraine in which the whole head
or forehead hurts, it is most likely a tension headache. Triggers may be present and have
chronic characteristics. Chronic characteristics are diagnosed if the headache occurs at least 15
days a month or half of the time during the month. A patient can be diagnosed with a chronic
condition if it occurs over a long duration of time. Headaches can be treated by NSAIDS, over-
the-counter medications, and prescription preparation. Tension headaches have a relation to
the contraction of the jaw and neck muscles. The exact mechanism is unknown, but some

34
treatments include Botox to paralyze the muscle and prevent headaches. Many medications
available over the counter and prescriptions on the market to treat headaches, but again this is
one of the most common conditions diagnosed. In review, migraine headaches are usually
unilateral have an aura, sensitivity to light, nausea, and vomiting. Cluster headaches are
unilateral and have no aura. Tension headaches are bilateral and usually related to some type
of muscle tension.
Meningitis is an acute inflammation of arachnoid and Pia matter that surrounds the
brain and spinal cord. It may lead to increased cerebrospinal fluid production and increase in
intracranial pressure. Bacterial meningitis or meningococcal may be considered a medical
emergency; the mortality rate is relatively high at 25 percent. Viral meningitis is a limiting
condition that will not require treatment. Meningitis can be caused by again bacteria, viruses,
micro bacterial fungal infections, amoebas, cancer, or other known infectious sources. The
most common entry way is respiratory system. Symptoms that may occur include headache,
nausea, vomiting, and constitutional symptoms like fever, loss of appetite, and phobia.
Headaches are a result of an increase in intracranial pressure. Patients may also have nuchal
rigidity and resistance to flexion of the neck; these are the positive Kernig and Brudzinski's sign.
The patient may even develop seizures and petechiae with meningococcal meningitis.
Meningococcal meningitis is one of the less common types of meningitis but has a high rate of
mortality. Treatment should include a cure for the meningitis and treating the Brudzinski sign. If
a patient presents with a headache, nuchal rigidity, and carrying Brudzinski's signs positive, they
have petechiae. The brain can tolerate this for some time, but unfortunately, if the treatment
isn't initiated fast enough the patient may have devastating consequences. Changes in level of
consciousness may also occur; this may be the first initial sign followed by headache, nuchal
rigidity, and petechiae. These symptoms can occur simultaneously and result in strange
behavior form the patients or levels of consciousness affected. Vaccination is important and
recommended for bacterial meningitis especially for individuals living in crowded conditions.
For bacterial meningitis, antibiotics and antipyretics may be required depending on the cause.
Some patients may need treatment for pain management. Surgical intervention including
drainage is rarely needed.
Encephalitis is an inflammation of the brain parenchyma. Often, the meninges are also
involved as well as the cerebrum, brain stem, and cerebellum. In the case of encephalitis,
hemorrhage edema and necrosis may occur in cerebral hemispheres. Encephalitis is different
from meningitis because the cerebral function changes. Encephalitis is most commonly caused
by arthropod borne viruses, herpes, simplex viruses. Viral encephalitis is due to the vector, and
the patient may experience fever, headache, nausea, vomiting, altered cerebral functioning,
altered mental status, motor deficits, and weakness or paralysis. Encephalitis may result in an
altered mental status confusion but does not affect the level of consciousness like meningitis.
Patients with encephalitis may need antipyretics, analgesics, sedatives, and corticosteroids. The
patient will require ICP monitoring and may need other invasive methods to introduce antiviral
treatments if a viral infection is the cause. If a viral infection is present, it is most likely the West

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Nile virus infection. The patent may present with brain herniation as a complication and needs
to be treated rapidly. The patient will require continuous monitoring of intracranial pressure,
lab values such as CBC and ICP measures, may need extensive interventions. Patient may have a
severe or mild case. This may also result in a rather challenging period for the family and
patient while the rapid decrease in cerebral function and altered mental status occur.
Lyme disease is a disease that was discovered in 1975 in the town of Lyme, Connecticut.
The disease is most prevalent in the Northeast. It has become the most common tick-borne
disease in the United States. When diagnosed it is often a consequence of tick bite. The tick
does not cause the disease, but the tick is a vector and carrier of the Borrelia burgdorferi
bacterium. The tick transmits the borrelia burgdorferi to humans. The time it takes for the
bacteria to incubate can be on average 3 to 32 days. The bacteria can affect any organ and can
cause a variety of symptoms such as flu like symptoms, constitutional symptoms such as chills,
fever, and malaise. The patient may also develop arthralgia. The most common sign of Lyme
disease is the bullseye which is a reddened circle with a light-colored center that appears within
days or weeks of the bacteria incubating. The bullseye rash is the first state of the disease.
During the second stage, the patient may develop cardiac and neurological manifestation and
complain of chest pain or soreness, rib soreness, and shortness of breath. The patient may also
complain of palpitation, develop arrhythmias, cardiac blocks, murmurs, and valvular prolapse.
Cardiac echocardiogram may be necessary for diagnosis. Neurological symptoms such as
twitching of the face, spontaneous tremors, Bell’s palsy development of facial paralysis,
paresthesias, headaches, confusion, cognitive difficulties, difficulty in concentrating, reading,
poor short-term memory, and disorientation may occur.
Multiple sclerosis is a disease characterized by the degeneration of the myelin sheath in
the central neural system. It is the most common case of neurologic disability among young and
middle-aged adults; typical onset is between ages 20 and 45. There is some genetic component
in multiple sclerosis inheritance, however, there is no direct inheritance. It has been suggested
that second- and third-degree relatives of person with multiple sclerosis are at increased risk of
developing MS. When the demyelination of subsequent degeneration of neural fibers in SNS
happens, the patient may start experiencing symptoms. Symptoms are a result of the nerve
being demyelinated and resulting in the improper conduction of electrical signals. Different
conduction abnormalities can occur and are measured by testing changes or decreases in
conduction velocity and conduction blocks. The location and size of the lesion can also have an
effect. The abnormality of demyelination causes a disappearing or decreased sped of the
neuron’s signal. The signal either will slow down or be completely will be blocked.
Multiple sclerosis is an autoimmune disorder. A lymphocytic invasion of the lesion
occurs as well as demyelination. Lymphocytes may invade the lesions resulting in evidence of
antibody mediated damage and damage to the myelin proteins. When examining the nerve,
hard or sclerotic patches are visible in the white matter even without a microscope. The
patches are called plaque, and they can appear anywhere in the brain, brain stem, cerebellum,

36
and spinal cord. If the plaque is fresh, evidence for an active myelin breakdown may be present.
An MRI is one way to diagnose and evaluate for MS. It may show two types or two states of
lesions. It may also show the inflammatory component found in stage one and they formation
of scars from the demyelinated nerve that occurs in the second stage. The demyelination
prevents nerves from conducting a signal normally. This results in neurologic symptoms as well
as speech and swallowing problems, visual problems, abnormalities in gait, paresthesia’s,
disturbance of visual field, and diplopia. The patient will progressively worsen. There are
several types of multiple sclerosis. Remitting of the disease is characterized by episodes. The
patient present with acutely worsening symptoms and then experience a relapse or fairly stable
period of time. In the secondary progressive disease, gradual deterioration, neurologic
deterioration, and possibility of relapse may occur. In the primary progressive disease, there is
a continuous neurologic deterioration from the time the symptoms start. Remitting includes a
patient having episodes of acute worsening symptoms and then returning to a stable phase,
and then worsening. Secondary progressive disease is a gradual worsening with the possibility
of a relapse. Primary progressive disease is the continuous neurologic progressive worsening
from the time that symptoms appear.
Amyotrophic lateral sclerosis is a devastating neurodegenerative disease. It is also
referred to Lou Gehrig's disease, and named after the famous baseball player. This disease
effects individuals in their late adult years around 50 to 60 years of age. The disease is very
progressive and from the time of onset of symptoms the life expectancy is approximately two
to five years. The disease is characterized by the death of the lower motor neurons. As the
lower motor neuron is dying, innervation occurs and results in no nerve connection to the
muscles. This causes muscle mas or the muscle fibers to shrink and results in atrophy. This type
of atrophy is secondary to the death of the nerves. Denervation is referred to as Amyotrophy,
and therefore the disease’s name is Amyotrophic lateral sclerosis. The term lateral sclerosis
reflects the structure of the nerve fibers in lateral columns of white matter of the spinal cord
which are affected and lost. The disease does not affect intellectual abilities, regulatory
mechanisms of coordination, or control of movement and sensory systems. The neurons of the
ocular system are also parasympathetic neurons. The ocular mobility in the parasympathetic
neurons in the spinal column is also spared. The cause of this disease is uncertain; some
evidence of familial history has been shown. There are several mechanisms of ALS that occur
and lead to a possibility of injury to the nerves through the glutamate gated ion channels. These
channels are distinguished by sensitivity to the N-Methyl D aspartic acid. One theory disclaims
this a cause of the disease, but other immune sources describe or suggest evidence that disease
will not respond to a suppressant and may not be autoimmune. However, there is no cure for
the disease. Care is palliative and includes rehabilitation techniques. Patients who cope and
maintain independence as long as possible will prolong survival. An anti glutamate drug such as
Riluzol is FDA approved for treatment of the disease, but the drug only prolongs survival by
three to six months. Patients will experience atrophy of the muscles, but intellectual abilities
will not be affected. Symptoms of ALS will result in muscle deficits and patient develop

37
dysphasia or dysarthria. Dysarthria is an inability to talk or articulate speech movement due to
too weak muscle tone or too high. In rehabilitation, during evaluation and treatment it is
important to involve an entire healthcare team that includes auxiliary services such as speech
therapy and physical therapy. The goal of treatment is to prolong the survival time and improve
or maintain quality of life.
Neuropathies are peripheral nervous system disorders. Neuropathy is not a single
disorder, but a collection or cluster of disorders that result in neuropathy. Guillain-Barre
syndrome is an acquired inflammatory disease that can be described as an acute immune
mediated polyneuropathy. It is clinically defined as a rapid progressive weakness of the limbs
and loss of tendon reflexes. The syndrome is the most common cause of acute paralysis. There
are several types of Guillain-Barre syndrome, but the most common has an immune
component. It is due to some type of exposure to virus or an offending. To determine
diagnosis, a epidemiology study is done to link the infection to Campylobacter, Cytomegalovirus
Epstein-Barr, and Mycoplasma. Often, patients will report having flu-like illness. Prior to the
onset of symptoms, some patients will have antibodies against gangliosides which may be
consistent with infections or campylobacter. The disease results in a progressive ascending
muscle weakness of the limbs that produces symmetric flaccid paralysis. Paresthesia will occur
as well as a rapid loss of motor function, however, progress of progression may vary.
Disproportionate involvement of upper or lower extremities may occur. Paralysis in ascending
cases will progress upwards. This can present with symptoms involving the respiratory muscles.
The autonomic nervous system may also be affected and result in cardiac arrhythmias.
Autonomic dysfunction symptoms such as sweating and facial flushing, urinary retention,
postural hypertension may also occur. Patients may have a significant amount of pain. Guillain-
Barre syndrome is a medical emergency, but it is treatable. Approximately 90% of individual
effected achieve a full recovery. Recovery may take up to a full year to recover. The patient
may require ventilator support and support of other vital functions as treatment.
Myasthenia Gravis is a chronic autoimmune disease that effects neuromuscular
junction. This disease results in a breakdown in communication between motor neuron and
the innervated muscle cells. The disease effect individuals who are in their twenties and thirties
and is more common in women. Because it is an autoimmune disease, it is caused by antibody
mediated destruction of acetylcholine receptors. The receptors are located in neuromuscular
junction. The exact mechanism is unknown, but the cause is believed to be related to abnormal
T lymphocyte function. Often individuals will also present wit thymus abnormalities. The
symptoms of Myasthenia Gravis will involve the patients having less acetylcholine receptors in
postsynaptic membrane. The release of acetylcholine from the presynaptic membrane will
result in lower end plate potential. The muscle will present with weakness and fatigue when the
patient I trying to make a movement or use the muscle. First symptoms may occur in the ocular
muscle. Myasthenia Gravis may present with sudden exacerbation of symptoms. This is
referred to as a Myasthenia Crisis. A crisis is a condition when the ventilation is affected due to
stress. This can include emotional stress, infection, excessive alcohol, or surgical intervention.

38
Treatment involves a replenishment of acetylcholine. If stress is too high, acetyl-choline
esterase drugs may not be enough. If the patient receives an acetyl-choline esterase test,
Tensilon will be used. Tensilon is a drug that inhibits acetyl cholinesterase. It is used for
treatment of Myasthenia Gravis and clears symptoms completely. A positive Tensilon test is a
diagnostic method for Myasthenia Gravis. Electrophysiology studies can also be done to
demonstrate how muscles do not respond to stimulation of motor nerves to diagnosis.
Pharmaceutical treatments involve immunosuppressive therapy and corticosteroids. This
involves using mediation that affect cholinesterase such as Tensilon. Removal of the thymus
gland may be a treatment method; however, it is controversial due to its unproven link to the
disease.
Mental Health Disorders
Schizophrenia is a type of psychosis and is a collection of thought disorders. Psychotic
individuals may have delusions, hallucinations, impaired coping skills, and impaired
communication. Swiss psychiatrist Eugen Bleuler used the term schizophrenia first time in 1911,
but the disease itself was first described and distinguished as separate mental illness by Dr. Emil
Kraepelin in 1887. During that period, the term was Dementia Praecox, and Kraepelin described
the symptoms of Schizophrenia. Through the centuries, people have described symptoms of
Schizophrenia. Sources begin with ancient Egypt, and there are descriptions of symptoms that
are similar to symptoms of Schizophrenia. Symptoms often appear in an individual’s teenage
years to mid-twenties. However, it is not uncommon if a patient in diagnosed with
Schizophrenia at an older age. The patient develops the disease and will lose touch with reality.
Individuals will replace reality with an imagined or fantasy realty. The patient truly believes in
this reality and will have mood or affective disorders.
Affective disorders involve emotions and the outward representation of emotions.
When discussing and person’s emotions that is referred to as a mood, but the representation of
those emotions if the effect. Effective states are brief emotional feelings that are somewhat
visible and manifest within the patient. Effective states can be observed in the patient, but their
mood is a result form the sustained emotional state. Often healthcare professionals fail to
recognize that people experience times of sadness and extreme happiness during appropriate
events and may misdiagnosis. For instance sadness after the death of beloved family member.
However, if an individual’s displays emotions that are not appropriate for an event, or the
mood lasts for very long duration of time, or mood changes are extreme in nature then a mood
disorder may be suspected. Every individual reacts differently, but extremes in mood changes
can be diagnostic for mood disorders. An example of a mood disorder is manic depressive
disorder or bipolar disorder which alternates between a manic and depressive state.
Depression is a prolonged feeling of extreme sadness, and unhappiness, despair, and
discouragement. Healthcare providers need to differentiate depression from grief. Grief is a
realistic sadness related to a loss. This can include a personal loss of another person or animal.
A patient may grieve because of a loss of function or loss of limb. Prolonged grief may become

39
depression, and if a person is not able to cope with their loss, they may experience symptoms
of depression. Genetic manifestations may also be a factor as well as biological and
environmental factors. In some cases, depression can be caused by a single factor and in others
it is multiple factors. The exact cause of why an individual develops depression is unknown.
Heredity personality may be a cause along with environmental factors.
Situational depression is a different type of depression. It occurs as a reaction to a
situation. If an individual’s reaction to a situation is prolonged, this could be due to situational
depression. Medical conditions can affect development of depression. Hypothyroidism is an
example. When people develop this condition, they often develop depression and suicidal
thoughts are common. The symptoms are reversed with levothyroxine or Synthroid is used
treatment. There is a strong correlation between hypothyroid state and depression.
Substance abuse can be another source of depression. Dietary deficiencies such as Folic
acid and B12 and gender is a risk factor for depression. Females are at more risk to developing
depression than males. Elderly-age, socioeconomic status, income level may also be factors of
depression. Extreme weight loss can result in depression as well as social isolation. The cause
and consequence of social isolation are hard to identify but may accompany individuals who
live alone. Individuals who experience depression have feelings of rejection, helplessness, and
worthlessness. These individuals will be uninterested in their surrounding or in events that
were once pleasurable.
Anhedonia is a term used to describe the patient’s loss of interest in previously
pleasurable activities. Irritability, suicidal thoughts, easily crying, and lack of or excessive sleep
are symptoms of depression. Depression may occur during critical periods in life. It can occur
and affect puberty in adolescence, during menopause, retirement, or entering into new work
environment. Diagnosis of depression includes a medical physical examination, a questionnaire,
and lab work. Depression is a Diagnosis is of Exception, and any organic source of depression
must be ruled out.
Besides the depression, the cohort of mood disorders can include seasonal affective
disorders. This is speculated to be related to circadian rhythms of the person, and treatment
usually is the same as depression. Some activities for treatment may involve mimicking the
longer duration of daylight, especially during the winter months. Bipolar disorders are due to a
genetic component, and treatment may include mood stabilizers as well as antidepressants.
The use of antidepressants in bipolar treatment is somewhat controversial because they may
exacerbate the manic episode.
The antidepressant medications work by altering a pathway of communication between
the synaptic cleft and as a result different neurotransmitter may be affected. The SSRI interrupt
neurotransmitters' reuptake in the synaptic cleft. The sufficient amount of neurotransmitter
provides the halting of the depressive symptoms. There are three major classes of
antidepressants. Medications that are Monoxidase inhibitors are very seldom prescribed

40
because of the side effects and possibility of adverse effect such as overdose. Amitriptyline is a
medication that is often not prescribed. This medication is often prescribed for sleep disorders.
Selective serotonin reuptake inhibitors (SSRI) is the main treatment for anti-depressive
therapy. These medication work in a single synaptic cleft and inhibit the reuptake of serotonin.
SNRI is a subcategory of SSRIs, but it is a drug that acts similarly by affecting the reuptake of the
neurotransmitter, but this drug affects several neurotransmitters. SNRI can cover
norepinephrine serotonin as well as dopamine. As a result, they are used to treat not only
depression but also anxiety.
Anxiety disorders is the condition that can be considered as a deviation from a normal
anxiety presentation. Normally anxiety is a response to stress which induces a fight-or-flight
response in some individuals, but for others, anxiety may become a chronic problem. The
individual may experience anxiety that is exaggerated or inappropriate to the situation. Anxiety
disorder was previously referred to as neurosis. Anxiety affects the largest number of people of
any mental health disorder It's truly the largest mental health disorder in the United States. The
cause of the anxiety disorder is unknown, but genetic factors, stress, environment, chemical
alterations, and physical factors may be causes. Physical causes of anxiety can be better
studied. For example, Hyperthyroidism can have an effect on the development of anxiety in a
patient. Anxiety has several types and different manifestations. An extreme manifestation of
anxiety disorder is panic disorder.
Panic disorder is a state of extreme and uncontrollable fever which may be referred to
as a panic attack. It is usually a very sudden onset and peaks in minutes. The patient may
experience a feeling of impending doom and may want to escape of run away. Psychosomatic
manifestation may also be present and present with diaphoresis, chest pain, and tachycardia.
The patient may also have a sense nausea and disassociation. In a generalized anxiety disorder
(GAD), feelings of excessive worry are a continuous state of mind. Intense anxiety is not related
to a specific event. GAD is characterized by a state of constant anxiety that may lead to somatic
manifestations such as nausea, vomiting, diarrhea, dryness of mouth, tachycardia. In these
exaggerated states, patients live on the edge and are always anticipating some impending
drastic event.
Post-traumatic stress disorder (PTSD) is the development of the reaction as a response
to psychologically stressful event or an event that the person could not control and was outside
of normal human experiences. PTSD is a relatively new addition to the classification of anxiety
disorders. It may be observed in war veterans, victims of rape abuse, or survivors of natural
disaster. Individuals who are often in extreme situations such as policemen and firemen are at a
higher risk for developing PTSD. Symptoms may occur immediately after the event or dormant
until several months after the trauma. Diagnosis in a post-traumatic stress disorder includes a
thorough physical examination to rule out other physical or organic conditions that may result
in the development of similar symptoms. Diagnosis is established also by confirming the history
of symptoms and confirming no other conditions are present. Treatment may include stress

41
reduction, hypnosis, relaxation, exercise therapy, biofeedback, and medications. Treatment
with antidepressants may be beneficial. Some studies suggest that rapid debridement after
being exposed to a traumatic event, will have higher results versus debridement after a few
days when the event occurred.
Obsessive-compulsive disorder is an anxiety disorder with two major components.
Obsession is a repetition of a thought or emotion and compulsion is repetitive act. This
disorder affects the individual in a way that person cannot resist not performing that act or get
rid of the thought. With OCD, the person is unable to stop the thought, or the action resulting
in the behavior becoming some type of ritual. Thoughts or attempts to stop the ritual may
result in extreme anxiety. The behavior may become time consuming. In some health care
providers, handwashing can become obsessive compulsive behavior, and may become
disruptive to job activities. Treatment will include anti-anxiety agents, and sometimes SSRIs or
even SNRI'S may be prescribed. The results can be reassuring with treatment of SSRIs.
Psychotherapy may also be beneficial.

Musculoskeletal Disorders
Trauma is the leading cause of death among young people, ages one to forty-four years
old. Trauma is not discriminative based on race, socio-economic status, or national origin. Other
alternation can happen in the bones, joints, and muscles. These disorders are not caused by
external factors like trauma and other musculoskeletal injuries but are caused by internal
factors. These factors may include distorted metabolism, infections, inflammatory, non-
inflammatory disease, malignancies, tumors, and non-malignant tumors. A fracture is a break in
the continuity of the bone; the bone is not completely broken, but there is complete
detachment. A break can be a greenstick fracture where part of the bone is still attached with
some type of crack. In some types of breaks, a distortion or disruption may be present in the
continuity of the bone. A diagnosis of a cracked bone is colloquially an incomplete fracture. A
fracture will occur when force is applied that exceeds the tensile or compressive strength of the
bone. The term tensile refers to tension or compression that the bone cannot sustain. Elderly
individuals may develop features than those who are younger. The causes may be benign like
falling that may result in a femoral fracture. Younger athletes may sustain numerous falls and
have no trauma. This is attributed to the aging process. Different age population will have
different strengths in bone and a different ability to sustain trauma. Fractures can be classified
in several ways. They can be classified as conditions based on the condition of the overlying
skin- closed, open, complete, or incomplete.
A closed fracture is when no visible bone is puncturing the skin. If the bone is protruding
through the skin or if an object has punctured the skin resulting in an opening that hits the
fracture site, it is an open fracture. An open fracture is not just characterized by a bone coming
out. Open fractures are also referred to as compound fractures because they are not only a

42
fracture but open skin. When the skin is no longer intact, it is a compound fracture. A complete
fracture occurs when the fracture goes completely through the bone. An incomplete fracture is
when the bone is not fractured in two and is still connected. If there are more than two ends of
the fragments, the break is a comminuted fracture. If the bone is somehow sustained, like a
nice clear-cut break, it is a linear fracture. An oblique fracture runs in a transverse pattern, a
spiral fracture will twist around the bone. A spiral fracture is a disturbing sing if found on an
infant or toddler; it typically is a sign of abuse. Fractions can also be classified by differentiate of
location and how the fracture goes through the bone.
A transverse fracture will cut across at a 90-degree angle. It is opposite of a longitudinal
fracture that runs the length of the bone. A greenstick fracture or call it Torus fracture is an
incomplete bone break and is a bowing of the bone without visible breaks. Cracks and changes
occur in the bone. Torus fracture is a greenstick fracture that usually occurs in children because
of their soft, non-completely calcified bones. It is more difficult to break a bone completely
resulting in a transverse fracture.
Pathologic fractures are typically related to a pathologic process such as hypercalcemia.
This condition results in calcium being stolen from the bones and can result in a deficiency of
vitamins such as vitamin D. Pathologic fractures have some underlying cause such as a cancer,
tumor, or other conditions. Stress fractures are another class of fractures that are repetitive.
With repetitive use, tiny cracks will occur in the bone. Transchondral fractures are a type of
stress fracture of the articular surface of the bone. It is a result of force that is transmitted from
the articular surface of the bone, across the joint, through the articular cartilage, and to the
subchondral trabecula of the fractured bone.
Open fractures are an important physiological or paraphysiological phenomenon
because the continuity of the skin is disturbed and allows open access to the bone. This can
result in an osteomyelitis if not treated rapidly. A pathologic fracture is due to some type of
tumor or degeneration of the bone. When segment of the bone is present, it may be more
difficult to repair the fracture. The healing process is dependent upon the number of segments
present, but because of modern technology such as open reduction and internal fixation repair
is possible. Spiral fractures, transverse fractures, greenstick fractures, and impact fractures are
the most difficult fractures to heal because the femoral head is affected. In the past, these
types of fractures resulted in a severe handicap or loss of mobility, but because of modern
technology treatment is possible. Treatment may include a partial or total hip replacement that
can result in a sufficient degree of mobility; however, baseline level of mobility may not be
achieved.
Bone fractures may also cause damage to surrounding tissues, periosteum blood
vessels, and the cortex and bone marrow. This damage can result in hematoma formation and
initiation of the inflammatory response. Procallus formation may also occur and result in
incorrect healing. For healing, the bone or fractures needs to be set correctly by a cast splint or
surgical procedures such as open reduction internal fixation. A patient with bone fractures may

43
present with unnatural alignment, edema, swelling, muscle spasms, tenderness, pain, impaired
sensation. Impaired sensation is a consequence of nerve compression. Nerve compression is
the consequence of edema or trauma to the nerve from a broken bone.
Treatments for a bone fracture may involve manipulation or closed manipulation which
includes aligning the bone, with a cast or splint. When the bones are severely misaligned, the
bones may need to be pulled apart due to a union in an inappropriate angle.
Open reduction is another treatment option that involves creating and incision and
fixating the bone with an internal device such as plates, screws, or rods. Open reduction
typically results in a quicker recovery time and improved functionality after surgery. If the
reduction is improper, complications such as non-union, delayed union, or malunion may occur.
All these complications may result in severe impairment of mobility and severe reduction of the
quality of life of the patient. When non-union occurs, the edges of the bone fail to grow
together. This results in a gap between the broken ends of the bone that will fill with fibrous
and cartilaginous tissue. The gap will not be functional. A fluid-filled sac may also fill the space
and create a pseudo joint, pseudarthrosis, or false joint. A fiber will be created, and the fluid
will act as a synovial fluid and fill the space. Because it is not a joint, it will not have a function,
but will cause complications. Malunion occurs when a fracture results in the bones uniting an
inappropriate angle. Malunion will result in no function of sustaining mobility. A delayed union
of the bone occurs when the time of the union takes longer than usual.
Dislocation and Subluxation are displacements of the bones, but dislocation results in
displacement and loss of contact between articular cartilage and articular surfaces. Subluxation
results in a partial loss contact between articular cartilage and articular surfaces. Both,
dislocation and subluxation occur with fractures, muscle imbalance, joint instability,
Rheumatoid arthritis, and other causes of joints becoming more or less lax. Trauma, a fall, and
excessive force in an individual, who otherwise has strong bones and not prone to fractures,
may cause dislocation.
The picture and x-ray below are of an individual who sustained trauma on his ring finger.
The picture was taken in the emergency room and does not look like a severe trauma.
However, the x-ray shows the complete dislocation of the joint. The bone is completely
dislocated and there is no connection of the articular cartilage and bones. From the lateral
view, the dislocation is easily seen compared to the posterior view. On the lateral view of the x-
ray, there is a significant amount of swelling.

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 Images are cortesy of M. Parsons, Esq.

45
 Support structure injuries include sprains, strains and avulsions. A strain is a tear or
injury to a tendon and a sprain is a tear or injury to a ligament. These terms are sometimes
used interchangeably. Avulsion is the complete separation of the tendon or ligament from
wherever the bone. A strain is one of the most common injuries and is an over stretching injury
of the muscles. For example, a patient may have a lumbar strain from lifting too much weight,
inappropriate lifting techniques, or repetitive lifting. The back is the most common muscle
strain. A complete sprain or complete tear will be avulsion. Sprains most commonly occur
during sports activities because of an intense overload of the joints incurs overload of the
ligament. The ankle joint is most commonly affected. The pain can become unbearable and
result in the ankle not being used. The pain is a protective mechanism that prevents the use of
the injured extremity or body part to facilitate healing. Swelling, pain, erythema, ecchymosis
due to damage to the capillaries, and hemorrhaging are signs and symptoms of a sprain.
X-rays are used not as a tool for diagnosis of support structure injuries, but to rule out a
fracture. A sprain will be diagnosed by exclusion. If there is a suspicion of something else or a
complicated sprain, an MRI or arthroscopy may be ordered. If an arthroscopy is ordered it will
most likely be a repair procedure. Sprains and strains can be treated, especially when mild, by
using the RICE principle (Rest Ice Compression and Elevation). Compression is typically an Ace
bandage. All these interventions benefit the patient by reducing or eliminating the use of the
affected ligament and result in healing. In severe cases, surgical intervention may be needed. It
is important to evaluate for fracture if patient presents with sprain because the presentation
will be similar with same edema, pain, ecchymosis, and tenderness on touch. So, it's all the
same. An x-ray should be done if the patient does not have a severe sprain. If the patient has
typical function in the extremity, the RICE principle may be applied. If there is suspicion of a
complete avulsion, a referral to an orthopedics or emergency services is needed for further
evaluation and treatment.
Disorders of the tendons may vary from tendinitis, which is inflammation of the
tendon, to bursitis which is inflammation of the bursa. Tendinosis is a painful degradation of
collagen fibers. When the tendon by itself is degrading, it may also cause pain. Tendinitis is
inflammation of the tendon. The tendon is a connective tissue that may attach the muscle to
the bone. Any of these conditions can occur in any tendon, but tendinitis most commonly
occurs in the shoulder. It may be caused from overuse, age, and calcium deposits. It may also
be associated with bursitis. A patient with tendinitis will present with tenderness over the
affected tendon and pain when the muscle is in use or against resistance. Treatment includes
RICE, analgesic medications, anti-inflammatory, and NSAID. The patient will benefit from
physical therapy and range of motion exercises once the pain is under control. Some individuals
will develop adhesions in joints that often require surgical interventions to destroy the
adhesions. Strengthening exercises that avoid overuse will prevent this type of injury and
tendonitis. Bursitis is inflammation of bursal sac. It is caused by a repetitive motion or overuse.

46
The joint will be affected. This also most often occurs in the shoulder. Severe pain, immobility
due to pain, location, tenderness on palpation are symptoms of bursitis. X-ray testing is used to
do a diagnosis of exclusion. The same rules for a fracture apply, but heat is recommended in
place of rest. Corticosteroid treatments and surgical treatments can be used in extreme cases.
Physical therapy may also strengthen the affected area. Colloquially, bursitis is most commonly
referred to as tennis elbow, however, tennis elbow is epicondylitis. Epicondylitis is a type of
tendinitis and is inflammation of the tendon in the place where it is attached to the bone. This
is an overuse injury and same principles may apply. Rest, physical therapy, steroid injections,
and muscle strengthening may help.
Muscle strain is one of the most common injuries and is a severe stretch that stretches
beyond normal capacity. It is local muscle damage. It is difficult to distinguish between muscle
or tendon strain. A muscle relaxant may or may not be prescribed. Principles of rest, correct
techniques of use or movement and lifting can avoid muscle strains.
Rhabdomyolysis is a life-threatening condition that may be related to severe muscle
trauma and cell loss. When the content of the damaged muscle is released into circulation
(Myoglobin), it will clog the kidneys and tubules resulting in kidney damage. Once reaching this
stage, it is an emergency and requires immediate treatment. For individuals who are prone to
injuries, such as falls, it is important to reduce the risk for prevention. Other risk factors include
alcoholism, use of cocaine, heat stroke, and ischemia.
Osteoporosis is a metabolic bone disease that causes porous bone appearance. The
bone loses mineralization and strength and bone density decreases. Osteoporosis is a disease
of multifactorial origin. It is also an age-related bone loss will happen in men and women, but
mostly women experiencing severe negative consequences of osteoporosis. These
consequences include fractures, and during post menopause the risk for a fracture increase.
Immobility is another factor that can affect the development of osteoporosis. If patient has a
decreased activity level, they may experience osteoporosis. When a woman becomes estrogen
deficient after menopause, it may result in loss of density and the inability to retain and absorb
calcium resulting in osteoporosis. Hormone therapy is a controversial therapy; however,
weight-bearing exercise can slow the progression of osteoporosis. When osteoporosis occurs,
the patient may experience consequences related to compression and vertebral fracture in the
spine may occur as well as tiny wrist fractures. Compression fractures are common.
Compression fractures in the spine may result in a decrease of height or the development of a
hump.
A Dowager’s hump is an abnormal curvature in the upper thoracic spine. Wrist fractures
may occur as the disease progresses. Patients may also experience an increased risk for
fractures of the hip, femur, and distal radius. Approximately 1 million hip fractures occur
annually in the United States despite the introduction of medications such as Boniva and
Fosamax. Hip fractures will occur in older women and increase mortality. Advanced techniques
of hip replacement may result in regaining mobility and preserving and providing quality of life.

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 Treatment includes leveling the bone mass to maintain adequate levels of bone mass.
Medications such as Fosamax, Actonel, Boniva, and Reclast may be used for treatment. Reclast
is a once a year injection and Boniva can be done every three months. Fosamax and Actonel are
dependent on a daily or weekly regimen. Treatment can prevent osteoporosis development.
Adequate consumption of calcium is also important for prevention and treatment. Besides
calcium, adequate vitamin D intake and weight bearing exercise is needed. Estrogen therapy
may be a benefit but is controversial because of the strong correlation to breast cancer. The
decision for hormone therapy should be made case-by-case and the patient should be involved
in the decision-making process.
Postmenopausal osteoporosis is one of the most common types. Postmenopausal
women are more commonly affected the males of the same age. Serum androgens will affect
bone density and cause it to increase. Androgens such as Testosterone or Dihydrotestosterone
will stimulate bone formation. A decrease level of Estrogen will cause an increase of Aromatase
which is the enzyme that converts testosterone to estradiol. This will result in losing the
intensity of bond formation compared to a female who does not have significant amounts of
aromatase. Another cause of osteoporosis is a progesterone deficiency. This may be due to
changes in osteroprotegerin and insulin growth factor (IGF). Osteoporosis is a combination of
deficiency in osteoprotegerin, deficiency of calcium intake, deficiency in vitamin D, magnesium
deficiency, and not enough weight-bearing exercise. Dropping estrogen levels and family
history are also factors. Excessive consumption of sodas is also linked to osteoporosis. Sodas
are laced with phosphorous that will interfere with the calcium phosphorus balance and result
in osteoporosis.
Osteomalacia is a softening of the bone due to a calcium deficiency. A deficiency of
vitamin D may lower the absorption of calcium from the gut. Osteomalacia will occur if not
enough vitamin D is present. Vitamin D is needed to facilitate the bone mineralization that gives
structural integrity and hardness to the bone. Without appropriate mineralization or delayed
mineralization, the bone formation will not advance. During the bone formation, the bone will
progress to osteoid formation, but if calcification does not occur is will result in a soft bone. A
vitamin D deficiency in an adult may be secondary to low nutrition intake or malabsorption
problem. A patient with osteomalacia will have bone pain, may develop small fractures, may
have vertebral collapse and bone malformation. Bones that have weight-bearing roles will be
affected the most and will show deformity if in the spine, vertebra bones, pelvic, girdle, or
bones in the lower extremities. Treatment will include the correction of the deficiency, vitamin
D. The patient may be required to consume significant amounts, approximately two hundred
thousand international units weekly of vitamin D, for a month or month and a half. This may be
followed by daily doses of vitamin D. If damage such as bowing of the bones, shortening,
flattening, these treatments will not help, and baseline will not be achieved. Recommendations
for prevention included sunlight. It is important to discuss the minimal risk of skin related
malignancies due to UV ray exposure. Dietary intake of vitamin D is important for prevention.

48
Fish such as salmon, eggs like egg yolks are rich in vitamin D. Supplements may also be
recommend.
Paget’s disease is a relatively rare disorder and is also known as Osteitis Deformans. It is
a chronic metabolic disorder that affects bone formation. Excessive resorption of spongy bone
will cause accelerated formation of softened bone. So, normally bone is broken down and
replaced. Osteoclasts and osteoblasts work together. Remodeling is the constant rate in which
this occurs. Paget's disease is characterized by an overgrowth of a new bone that out places the
breakdown of the old bone. The new bone is thicker than the old but is weaker resulting in an
increased possibility of rupture. There is a change in the bone into something spongy and brittle
while becoming a new structure that is thicker but not as strong. When an x-ray is done, the
mosaic bone pattern is revealed, and Paget’s disease can be diagnosed. Paget's disease will
affect the axial skeleton, and it will affect the pelvis and long bones of lower extremities. It
typically occurs after the age of 40 and becomes more common with advancing age. Thickened
bones can cause abnormal bone shapes which can be a cosmetic defect or functional defect.
They can also result in brain compression, impairment of motor function, deafness, and atrophy
of the optic nerve. Deafness occurs because the bones in the ear are affected. The
development of osteosarcoma is more prevalent in individuals with Paget’s disease. The
etiology of Paget’s disease is unstudied, but there is a theory of an idiopathic source. Treatment
includes calcium and vitamin D supplements.
Osteomyelitis is an infection of the bone. Th most common causative organism is
Staphylococcus. If the infection is due to an open wound it is exogenous osteomyelitis. The
infection can also be due to blood-borne and is considered endogenous. The infection will be
acute and chronic inflammation will cause symptoms such as fever, weight loss, severe pain,
and bone pain. If not treated, a necrotic bone may be the result causing necrosis of the bone.
Treatment may include antibiotics, debridement, surgical removal of the affected bone, and
hyperbaric oxygen therapy. Hyperbaric oxygen therapy is a rather new technique that uses a
capsule to release antibiotic that may be placed surgically in the spot or enclave where
osteomyelitis in present. The antibiotics will be releases over a span of months. A severe
infection is difficult to teat. Exogenous osteomyelitis is more common and preventable. It can
occur nosocomial as a consequence of manipulation of the bone for surgeries and with
injections to the joint. A strict sterile technique is important for procedures done to the bones.
Treatment may be successful but Is taxing to the patient.
Joint disease can be inflammatory or non-inflammatory and can be differentiated
between easily. In theory, if no synovial membrane inflammation is present then the disease is
non-inflammatory. The inside of the synovial capsule cannot be directly observed, but if no
signs and symptoms are present is non-inflammatory. A synovial fluid analysis can be done to
also determine inflammation. Inflammatory is a more systemic while non-inflammatory is
localized. Osteoarthritis is one of the degenerative joint diseases and disease of the bone that
results in severe mobility. The occurrence may increase with age and use of assistive devices.

49
The quality of life for the patient may become impaired and patient will eventually require
assistance or placed in a skilled nursing facility. When osteoarthritis occurs, it is inflammation of
the joint that may result in the loss of the articular cartilage and formation of bone spurs. In the
past, the patient most likely had arthritis. Arthritis is joint inflammation. Osteoarthritis is a
degenerative joint disease that is characterized by the process of wear and tear on the joint.
Most people acquire osteoarthritis to some degree and it typically starts in early adulthood and
continues with age. The etiology is unknown, but it I a primary disease which is idiopathic.
Sporting injuries will increase the onset of the disease. During osteoarthritis, the local areas of
damage will occur and result in a loss of cartilage. A new bone will start forming at the joint
margin. Subchondral bones will change and patient will develop mild synovitis and have a
thickening of the joint capsule. The patient may experience muscle pain, pressure, and an
increase in the subchondral bone. This increase will result in the capsule stretching and causing
the ligaments and tendons to be strained and the periosteum will become elevated. Patients
may also experience pain, stiffness, enlargement of the joint, tenderness to touch, mobility
issues, and deformity. With severe osteoarthritis in the knee, the size of the knee will
significantly increase. Inflammatory joint disease is often called arthritis and is different from
osteoarthritis.
Arthritis is inflammatory damage and destruction of synovial membrane, cartilage or
articular cartilage, and has systemic signs of inflammation. When a patient experiences a fever,
the will also experience elevated white blood cell count, malaise, loss of appetite due to an
infectious or non-infectious in origin. If some type of inflammation of joint occurs with systemic
changes, this may be due inflammatory damage secondary to infection.
Rheumatoid arthritis is a separate disorder that is a systemic, inflammatory,
autoimmune disease the results in an autoimmune attack to the self-connective tissues in the
synovial membrane. The patient will have many of the same symptoms as osteoarthritis with a
few differences. The difference between osteoarthritis and rheumatoid arthritis is how the
joints are affected in the hands. Osteoarthritis affects the working joints in the hands such as
the primary, distal, and proximal interphalangeal joints causing swelling and pain. Rheumatoid
arthritis effects all the joints in the hand. A patient with rheumatoid arthritis will have
significant deformity and ulnar deviation. This is a characteristic sing of rheumatoid arthritis.
Osteoarthritis usually does not affect the small bones but is a big joint disease. Lab results will
reveal if rheumatoid factors are present as well as antibodies IgG and IgM. When the synovial
fluid is aspirated, it must be significant for the presence of the inflammatory exudate. However,
if small joints are affected, it is likely rheumatoid arthritis. If big joints are affected, it is likely
osteoarthritis. If there is symmetrical involvement with both hands, it is likely rheumatoid
arthritis. If there is asymmetric involvement, it is osteoarthritis. Historical evaluation for
rheumatoid arthritis includes a list to diagnose with four symptoms present. Morning joint
stiffness that last at least one hour, arthritis in three or ore joint areas, arthritis in the hand
joint, symmetric arthritis, rheumatoid nodules or subcutaneous nodules, are the symptoms that
present in patients with rheumatoid arthritis. The elevation of the Rheumatoid factor can be

50
detected through a blood test. X-rays can show ulnar deviation or ulnar drifts. If four of these
factors are present, then they are used to diagnose rheumatoid arthritis.
Ankylosing spondylitis is an inflammatory joint disease that can cause stiffening and
diffusion of the joints. It is a systemic, autoimmune, inflammatory disease. Inflammation in the
spine or sacroiliac joints occurs causing stiffening and fusion of the joint. The primary sites
affected include sites where ligaments, tendons, and joint capsules are inserted into the bone.
The site may cause enthesis. No known cause is distinguished, but there is association of the
disease with HLA B27 antigen. This disease is one of symptomatology and diagnostic evaluation.
The patient may experience inflammation of the fibrocartilage in the vertebral and sacroiliac
joint. When this occurs, inflammation cells will start infiltrating and destroy or erode
fibrocartilage. The cells will then try to repair the damage, but scar tissue will form and ossify
and calcify resulting in the joints to fuse. The patient will have early symptoms of low back pain,
stiffness, pain decreased mobility, and the lumbar curvature is lost. Patient will have a flat back
due to the fusion.
Gout is a metabolic disorder that results in a impaired uric acid production or excretion
disorder. High levels of uric acid can be found in the blood and other bodily fluids. If the
concentration of uric acid is too high, it will crystallize. The crystallization will result in deposits
in connective tissues such as joints and synovial fluid leading to inflammation. The
inflammation can cause gouty arthritis or gout. Gout is related to purine metabolism. Purine
metabolism refers to the adenine and guanine metabolism. Individuals who have a rapid purine
metabolism synthesize too much purines causing in the purine to start breaking down. The
breakdown could also be due to poor uric acid excretion by the kidneys. The concentration of
uric acid will increase resulting in crystals to deposit. The crystals will deposit in lower
extremities and cause gouty arthritis. The crystals typically deposit in the metatarsal phalangeal
joint or big toe. The crystals that are formed have very sharp edges and may irritate or damage
the joint causing a inflammatory response. Erythema, edema, and tenderness to the touch may
be occur. The patient will have symptoms of deposits of the uric acid crystals in other places
with connective tissues. When the deposits are in the cartilage of the ears it is known as tophis.
The symptoms of Gout do not appear overnight, and the patient will be in a long period of
asymptomatic hyperuricemia. The tophi can deposit in any type of connective tissue such as the
ear cartilage or metatarsal phalangeal joint. The crystals attempt phagocytosis by leucocytes.
Eventually the crystals will be excreted from the phagolysosome and leucocyte will be disturbed
resulting in inflammation.
Fibromyalgia is a disorder that is often misdiagnosed. Patients with this disorder will
present with vague symptoms such as sensitivity to touch. Inflammation will not occur. Fatigue
and sleep disturbances may also occur. There are no objective factors that may confirm the
presence of the disease. Fibromyalgia is a chronic widespread joint and muscle pain. Chronic
fatigue syndrome is often a misdiagnosis of fibromyalgia. Other misdiagnosis include flu like
viral illness. Some patients with HIV or Lyme disease are misdiagnosed with fibromyalgia which

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delays needed treatment. Some medications, such as beta blockers, may cause the symptoms
of fatigue. Other medications like statins may cause muscular tenderness or myalgias. Physical
and emotional trauma can also result in aches and pains. There is no scientific study that clearly
defines the cause or etiology of Fibromyalgia. When a practitioner diagnoses patient with
fibromyalgia a through musculoskeletal examination should be performed. To have a positive
diagnosis practitioner must apply pressure to certain pressure point and that manipulation may
elicit pain. The pain should be symmetrical, and should be present in most of these points.

A brief Overview of Integumentary Disorders

Psoriasis may be viewed as a consequence of the T cell activation, which in turn results in an
attraction to neutrophils and monocytes to the site of the future plaque. Simultaneously, these
growth factors will attack the keratinocytes and create papules or plaques.
Hyperkeratosis is the scaliness and inflammation of the erythema. The neutrophils and
monocytes cause the inflammation growth factor to instruct cells to rapidly divide. An
individual’s immunity type will be dependent upon the t-cells. Sun exposure and skin damage
creates risk for cancers.
Skin cancers. The basal cells, squamous cells and malignant melanoma are three cancers that
are caused by skin damage. The easiest of the three to treat is basal cell. Malignant melanoma
has the most severe consequences. The basal cell is a self-contained cancer and its chances of
metastasizing are low. Squamous cell is in between. Malignant melanoma should be removed
immediately after being found. Basal cell can be treated through ointments. Sunlight creates
ultraviolet radiation which causes the damage. Tanning is a response reduce ultraviolet
radiation. The melanin is oxidized, and the skin gets darker restricting the amount of light that
can go in. When ultraviolet lights go deep into the tissue, it causes DNA damage, inflammation,
and immune damage. Malignant melanoma is caused by melanocytes.
How to describe lesions on the skin:
For any skin cancer or lesion, use the A (asymmetrical), B (border irregularity), C (color
variegation), and D (diameter; >0.6 mm). Another factor that can be used for ‘B' is bleeding. If a
cancerous mole bleeds by itself, it is angiogenesis. It bleeds because it develops a new vessel to
feed itself. This trait is typical of cancers. Immediate removal by a specialist in recommended.
‘E’ can be added to the “A, B, C, D” and examines if the lesion is elevated or evolves over time.
Basal cell is the least dangerous and is characterized an indentation or umbilicated lesion with
no inflammation. A biopsy is used for diagnosis. The lesion will be treated by being cut out or
using an ointment call Aldara. The ointment is antiviral cream that stops the basal cell for
growing. Squamous cell is invasive, and it will go to dermis and lymph nodes. A shallow border
and ulcer bleeding will be present. A difference between basal cell and squamous cell, it that
squamous cell typically bleeds unlike basal cell.

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Actinic Keratosis (AK) is a pre-malignant lesion that includes liver spots or lentigines from sun
damage. Vascular lesions such as angiomas, telangiectasias, and venous lakes are also
considered AK.
Seborrheic Keratosis (SK) is not cancerous. AK has a different appearance that includes a wider
asymmetrical appearance. Liver spots are benign like pigmentation. AK is a risk for progression
to squamous cell carcinoma. Imiquimod cream or Aldara is the antiviral ointment that is used
for treatment.
Xanthelasma is cholesterol or fat deposits over the lids. The clinical significance of this is
cosmetic but also may signify atherosclerotic disease. These cholesterol deposits are
permanent if not surgically removed.

Hematologic Disorders
Hematologic Cancers
Leukemia is a malignant neoplasm of hematopoietic cells. Leukemia involves immature
lymphocytes and their progenitors in bone marrow. Myelocytic or myelogenous involves
pluripotent myeloid stem cells. This includes all the blood cells from the myeloid stem cells. This
characteristic differentiates lymphocytic and myelogenous. The lymphocytic will affect B cells
and T cell natural killer cells. Myelogenous will affect eosinophils, neutrophils, basophils,
platelets and even erythrocytes. Myelocytic leukemia occurs when the multipotent stem cell
produces lymphoid stem cells and neoplastic myeloid stem cells. The lymphoid stem cells may
be normal, but the myeloid stem cells will have neoplastic precursor cells. These will result in
abnormal monocytes or leukocytes. This is related to some type of mutation in which it will
result in an overproduction of abnormal cell. The overproduction of cells results in spending
resources as energy on the production. Other cell types that are not malignant will not keep up
with this production. Normal cell production will decrease because of overproduction of
abnormal myeloid cells. When the mutation occurs in the lymphoid cells, it is lymphocytic
leukemia. The committed precursor cells will be neoplastic because they originate from the
neoplastic lymphoid stem cells. This will result in neoplastic B cells, T cells, or natural killer cells.
Abnormal cell production will increase while the normal cell production will decrease because
the abnormal malignant cells require more energy.
Lymphomas are malignancies that arise from lymphoid tissue cells. They will either be
lymphocytes or histocytes. There are two main types- Hodgkin’s lymphoma and Non-Hodgkin’s
lymphoma. During Hodgkin's lymphoma, malignant B cells will invade lymphatic tissues. In
Non-Hodgkin’s lymphoma, the B cells and T cells will be affected. The presence of Reed
Steinberg cells is a sign of Hodgkin’s lymphoma. Hodgkin's lymphoma usually will come from a
single lymph node and often is a localized disease. It may be treated with radiation. If multiple
nodes are involved chemotherapy and radiation may be used as treatment. The disease may be
presented with lymph node enlargement, the development of a lump in a single lymph node or
group of lymph nodes. The most common concern is the involvement cervical lymph nodes or

53
mediastinal lymph, and sometimes the maxillary and inguinal lymph nodes. Constitutional
symptoms occur once the patient feels sick, tired, experiences night sweats, fevers, chills and
weight loss. Weight loss occurs because of the energy demands of most malignancies. If the
patient drinks alcohol, they lymph node may become painful. This is a unique characteristic of
the disease and cannot be explained. Treatment may involve radiation and chemotherapy. If
the disease is diagnosed early, it is very treatable. This disease typically effects individual in
their twenties. There is a decline in patients who are in their fifties. The disease is more
prevalent in males. There is no known cause of carcinogen for Hodgkin’s lymphoma. There is
some evidence that HIV infection or an acquired immunodeficiency syndrome may increase the
incidence of Hodgkin’s lymphoma. Non-Hodgkin’s lymphoma or neoplastic tumors is composed
of lymphoid cells. The etiology is unknown. It is believed that the presence of the Epstein Barr
virus can affect the incidence and HIV. Non-Hodgkin’s lymphoma malignant transformation can
occur both in T or B cells, while in Hodgkin’s it's only B cells. There is potential for the disease to
spread to various lymphoid tissue through the body. This may affect many vital organs such as
the liver, spleen, and travel through the lymphatic system. The symptoms will depend on the
type of lymphoma. Non-Hodgkin’s includes a variation of different types of lymphomas. The
manifestation of the disease may be slow, fast, or relatively fast. The clinical or natural course
of the disease is approximately five to ten years. The patient may live five to ten years without
treatment even if lymphoma is low-grade.
Myeloma is a disease that presents with abnormal B-cells and malignancy of terminal
differentiated plasma cells. Multiple Myeloma is one of the most common types of plasma cell
disorders. It is relatively rare and makes up one percent of all cancers, but among the disorders
of blood or blood cancers it may increase to 20%. The cause Is unknown, but there is evidence
that points to immune deficit radiation. Pesticides and herbicides may increase chances of
developing the disease. 'Agent Orange' has also been thought to linked to myeloma along with
several other viruses such as HIV. During myeloma, the proliferation of malignant plasma cells
occurs resulting in abnormal cells forming a tumor. Multiple myeloma involves the bones and
bone marrow. It involves the proliferation of marrow plasma cells resulting in bone disorders
such as bone resorption. If the bone resorbs, the bone will be distracted, and fractures will
occur. Hypercalcemia may also occur. Bone pain is one of the most common symptoms that
occurs in individuals with multiple myeloma. The pain is due to the destruction of the bone
which effects the production of other cells. The patient may develop anemia and neutropenia
or agranulocytosis. The patient will also experience typical cancer symptoms such as weight
loss. Diagnostic procedures included blood tests, bone marrow aspiration and examination,
imaging studies, and MRIs. Chemotherapy or a cell transplantation may be appropriate therapy
for patients younger than twenty years old. Relapse may occur to individual with multiple
myeloma; however, treatment may still suppress the disease.

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Hematopoiesis
It is important to know where the cells are coming from. The pluripotent stem cell can go two
different directions- a lymphoid stem cell or myeloid stem cell. After lymphoid cell is produced,
it may transform into a progenitor cell, t-cell progenitor or b-cell progenitor. These cells will
eventually transform into natural killer cells. T-cells will be transformed into a t-cell progenitor
cell. A b-cell will mature into a plasma cell. Unlike lymphoid cells, myeloid stem cells give origin
to many different cell types and to majority of the cells found cells in circulation, point myeloid
stem cell can break down to monocytes. This will result in a monocyte progenitor and then
transform into a mono blast, then a monocyte, and then a granulocyte. Granulocytes can be
transformed into three different type of cells- eosinophils, neutrophils, and basophils cells.
These cells are still considered granulocytes because they contain granules. Granules can have
substances inside that may have toxic properties for the invading organism. Megakaryocytes
will be transferred to the platelets, and the erythrocyte progenitor cell will transform to a
reticulocyte. A reticulocyte is an immature red blood cells that will transform into an
erythrocyte cell. Erythrocytes do not have a nucleus but has an indentation that signifies the
location of a nucleus. White blood cells are also called leukocytes, which is a granulocyte.
Neutrophils, Eosinophils, and Basophils
Neutrophils are the primary pathogen fighting cells and are the first responders to an
invasion. Eosinophils help control allergic responses and fight parasites. They may also evolve
into processes such as asthma. Basophils release heparin, histamine, and other inflammatory
mediators. They may also transform into mast cells when they migrate inside of the tissues. All
three of these types of cells have common features that include the presence of granules.
Granules contain some type of toxic or inflammation mediator counting granules that make
them different. When cells are stained under a microscope, the differentiation is due to the
agranulocytes. These do not contain inclusions that contain granules. Lymphocytes are the
different type of cells. B cells create antibodies, and T cells that control the immune system. B
cells create antibodies and they produce antibodies, and T cells are responsible for cell
mediated immunity. Lymphocytes originate from lymphoid stem cells and are found in the
bone marrow. Lymphocytes constitute approximately 30% of white blood cell counts. Granules
are not present, but agranulocytes are present. B lymphocytes are antibody producing cells that
are involve din humoral mediated immunity. T lymphocytes create cell mediated immunity.
Natural killer cells are lymphocytes that have different receptors. These three types of cells are
distinguished by their surface molecules. Molecules refers to markers that are identified by use
of advanced methods. Monoclonal antibodies are may be used. These markers are clusters of
differentiation that can be grouped into categories that are specific for cells of different origin.
For example, helper T cells may have CD4 markers, a cluster of differentiation marker, and the
effector T cell CD8 marker. CD markers are widely used to identify the cells.
Monocytes make up the largest portion of white blood cells. They are approximately six
percent of white blood cells. This statistic is a median of percentage of monocytes; the number

55
may fluctuate between three and eight percent. Monocytes are the largest and have a ‘U’
shape. They also have a relatively long-life span that is approximately one to three days. This
lifespan is approximately four times longer than the lifespan of a neutrophils cell. Cells may also
survive in the tissues for several months to years. When a monocyte migrates to the tissue, it
becomes a macrophage. These cells have distinct roles such as inflammation roles, antigen
presenting roles. Antigen presenting roles entails the cell digesting an invader. The role of
monocytes and macrophages is important because they are presenting cells, there long survival
rate, and ability to present antigens to T cells. Monocytes have a nucleus with a distinct ‘U’
shape.
Transformation of myeloid stem cells results in emergence of platelets, monocytes and
granulocytes and erythrocytes. The process of transformation of myeloid stem cells involves the
pluripotent stem cell transforming into a committed precursor or colony forming units. Colony
stimulator factors are chemical substances that are affecting bone marrow to produce certain
type of cells. Erythropoietin is the most common factor and is a stimulating factor that will
affect the bone marrow. Erythropoietin may be produced in a synthetic form and administered
to patients with some type of bone marrow suppression, or blood loss secondary to one or the
other factors. Radiation and chemotherapy can suppers the bone marrow production of
erythrocytes.
Other colony-stimulating factors such as thrombopoietin may result in the facilitation of
platelet production. Pluripotent stem cells may transform into lymphoid stem cells. From the
lymphoid stem cells, they may transform into committed precursor cells for T cell progenitor or
B cell progenitor. Both T and B cell progenitor will work through thymus and turn to T and B
cells. These cells will become plasma cells and natural killer cells. White blood cell deficiencies
may result in leucopenia. Leucopenia is a deficiency of leukocytes. Neutropenia refers to
agranulocytosis, which may be present. White blood cell disorders can affect the count of white
blood cells and may affect other factors such as infectious disease, viral disease or even
anemia.
RBC development
Red blood cells contain hemoglobin that's vital for oxygen transport. Hemoglobin
molecules in an adult has two alpha chains and two beta. The term chain refers to polymers or
polypeptides. Each chain is attached to a heme group which is a protein and a heme unit. A
heme unite is an iron atom surrounded by the heme unit. It is vital for the iron atom to connect
to the oxygen for transport and release. The oxygen binds to the heme group or iron. There are
four chains, and each chain has one heme group. In each molecule of hemoglobin, four
molecules of oxygen will be transported. When the blood has consistent low oxygen level, it
signals to kidneys to start producing erythropoietin.
Erythropoietin as Thrombopoietin stimulates bone marrow to produce red blood cells.
The erythropoietin is for red blood cells, and thrombopoietin is for platelets. When the bone
marrow is stimulated it will result in creation of new red blood cells which are initially

56
reticulocytes and then mature red blood cells. In men who are receiving chemotherapy as
cancer treatment, they may become anemic because the chemotherapy can be destructive to
bone marrow. Their kidneys will not be able to respond correctly to the erythropoietin need.
The kidneys do not respond when a decreased blood oxygen need is present. The kidneys will
not produce erythropoietin and the bone marrow is not stimulated. Red blood cell production
is needed to sustain needs for oxygen. A patient will become anemic if bone marrow is not
stimulated enough.
Bone marrow is the site of red blood cell synthesis, and it can be stored there and
released. Immature red blood cells are nucleated. Reticulocytes still have endoplasmic
reticulum, although they lost already their nucleus. Mature red blood cells will have nothing
except hemoglobin. Red blood cells will live three to four months. The cell membranes become
weak due to being squeezed between the tissues in very narrow capillaries. Red blood cells are
not able to repair themselves because they do not have a nucleus. After the damage, the cell
will be out of circulation. Most red blood cells will break in the spleen. A certain type of
leukocytes is found in the spleen that will process the red blood cells and result in the creation
of unconjugated bilirubin.
Unconjugated bilirubin is also produced in the liver, bone marrow, and even lymph
nodes. Unconjugated bilirubin is a toxic form of bilirubin, and it is processed into the
conjugated form that is found in the bile. Men with defective red blood cells will develop
hepatosplenomegaly because there is too much to process in the liver and spleen. Bilirubin
unconjugated will result in jaundice. Jaundice is when the patient turns yellow or green in
extensive cases. The Liver can conjugate the bilirubin by linking it to the glucuronide and is used
to produce bile. An individual will develop jaundice because the liver does not process bilirubin,
and it stay in the blood and accumulates and is deposited in the tissue. The red blood cells are
destroyed outside the spleen in the capillaries. Hemoglobin will be freely floating in the blood
resulting in Hemoglobinemia.

Hemostasis
Hemostasis is a protective mechanism or the consequence of the protective mechanism
of achieving balance. It is also protecting from the loss of blood. Hemostasis occurs by stopping
the blood flow by blood clots. Blood is typically a viscous fluid that flows freely inside vessels
under normal circumstances. When damage to vessels occurs, the vessel will break and become
sealed by a clot. This is a normal mechanism. An abnormal mechanism occurs when there is an
inappropriate clot or insufficient clot. Inappropriate clotting may include hyper-coagulative
states, and insufficient clotting may include hypo-coagulated states. If an excessive amount of
blood is present in the clot, it is hyper-coagulative or inappropriate clotting. If there is too little
blood for a clot, it is a hypo-coagulative or insufficient clotting. For hemostasis to occur, the
transient vessel vasospasm occurs allowing briefly to stop or slow down the blood flow outside
and then form the platelet pug. A clot will form after. Platelets are one of the key factors for

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achieving hemostasis. Platelets are thrombocytes in the blood. Erythrocytes, leukocytes and
platelets are thrombocytes. Platelet formation is facilitated by thrombopoietin which is made in
the liver, kidney, smooth muscle and the bone marrow. When there is not enough platelets,
thrombopoietin is made and signals the bone marrow to produce megakaryocytes.
Megakaryocytes are precursors of the platelets. Megakaryocytes are large formations that
break down to numerous platelets. Platelets are not long lived as red blood cells and live eight
to nine days in circulation. Platelets are stored in the spleen. When a need arises, platelets will
be released. Mediators of hemostasis are chemicals produced by platelets. When injury occurs,
clotting is initiated by reacting with proteins that float in the blood. They also help platelets to
clump or stick together. Clumping is a beneficial process because it facilitates the formation of
the clot and facilitate hemostasis at the end. Mediators of hemostasis will also stimulate wound
healing and facilitate the clumping of the platelets to vessel walls. Vasoconstriction will also
occur.
Coagulation Factors There are numerous coagulation factors. The liver has an important
role besides helping with digestion and being part of GI system. It is involved in the production
of it has an important plasma proteins and synthetization. The liver supply’s the blood with the
coagulation factors. The synthetic function of the liver is to produce clotting factors such as
plasma protein. The Von Willebrand factor is characterized by endothelium. Von Willi brand is a
disease that involves a deficiency of the liver. The plasma proteins or coagulation factors
circulate as inactive procoagulant. This is referred to as coagulation cascade with intrinsic and
extrinsic flow. Factors such as factor 12 may change to factor 12a which may stimulate factor
11 to change to 11a. The result may lead to the formation of fibrin from fibrinogen.
Cyclooxygenase enzymes are the products of the metabolism of arachidonic acid. The result is
the production of the mediator of hemostasis. For example, Celebrex which is a non-steroidal
anti-inflammatory drug that is a cox-2 inhibitor which may reduce the inflammation secondary
to arthritis. It also may result in a reduction of pain secondary to arthritis. When individuals
take Celebrex - cox-1, the thromboxane A2 levels, which is a mediator of hemostasis, may result
in the development of hyper coagulative disorders. These disorders include increased risk
stroke, heart attack, or thrombus of any other kind. The thromboxane A2 results in an increase
the developing of a clot. The prescription of Celebrex is limited and has strict regulations that
include informing the patient about possible side effects and increased risk for stroke and heart
attack. Clotting factors associated with Thromboxane A2 is a result of cox-1 metabolism which
links to the arachidonic acid metabolism.
Plasminogen is a plasma protein that is a pro enzyme in the blood that circulates in
relation to clotting or when coagulation is inactive. When it is converted to an active form, it is
called plasmin. The plasminogen activators can be formed in the endothelial lining of the
vessels, liver and, kidneys. The plasmin will be formed from plasminogen in which plasmin is the
active substance. The plasmin will help to digest the fibrin, and the fibrin will affect clotting
factors such as fibrinogen, factor 5, factor 8, prothrombin, and factor 12. The plasmin will be
inactivated by the plasma inhibitor. The acting of the plasma localized to a certain clot that
should be dissolved. Before the plasminogen is transformed into the plasmin, it needs to be

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activated by the tissue plasminogen activators. These are naturally synthesized substances that
come from different sources including the liver and vascular endothelial lining. The activators
will be released in response to events such as an occlusion of the vein, exercise, and other
factors such as certain vasoactive drugs. These factors are unstable; however, they signal
plasminogen to convert to plasmin. The conversion starts with the fibrin is eaten away and the
clot is dissolved. The tissue plasminogen activator can be natural or synthesized or given as a
medication for a stroke. Heparin and warfarin are acting on prevention of blood clot formation.
The tissue plasminogen activator activates the plasminogen for conversion to the plasmin. The
plasmin in the fibrin in the blood clot that is being digested. TPA helps clot digestion while
heparin and warfarin are merely preventing it. Heparin molecules are basically cofactors that
work on antithrombin.
Antithrombin is the substance that can inactivate thrombin and other clotting factors
such as factor 10. Heparin can be synthesized by body. Warfarin affects the synthesis of the
vitamin K, which is a coagulation factors, that is synthesized by the liver. Heparin can be
digested and cross the GI tract and must be given by injection IV or subcutaneously. TPA will
actively facilitate clot dissolution. Hyper coagulation disorders may be the result of several
factors. When an increase of the number of the platelet occurs, too many platelets are in the
blood causing platelet aggregation. Platelet aggregation refers to the platelets clumping too
much together. This endothelial damage can result in the decrease of production of several
anticlotting factors such as heparin or tissue plasminogen activator or increased procoagulant
factors. Von Willebrand factor is considered part of this type of decrease because it is a
consequence of endothelial damage.
Thrombocytopenia is a decreased number of platelets. A decrease in productions
increases destruction and may result in too many clots forming simultaneously. Impaired
platelet function can occur under normal platelet production circumstances.
Disseminated intravascular coagulation may be examined as a disorder despite the
paradox. It involves hyper coagulability and hypocoagulability which results in too much clotting
or too little clotting will occur simultaneously. Some type of trigger will initiate one of the
pathways in coagulation. It may be intrinsic or extrinsic. The intrinsic pathway can be activated
with extensive endothelial lining damage acquired through injury, infection, virus, immune
disorders, or blood stasis. The extrinsic pathway may be activated when tissue factors become
activated. Common extrinsic pathway activators include obstetrics complications, cancer, and
trauma. Intrinsic pathway activation is typically due to endothelial or cellular injury. Extrinsic
pathway activation is typically due to tissue damage. Thrombin generation will be the result of
both pathways being activated. The thrombin generation may be extensive which may result in
a clotting thrombosis. If the thrombosis has a large amount of vascular fibrin deposited,
ischemia in the tissues will occur along with distraction of the red blood cells. Too much
thrombin leads to the plasminogen involvement. Plasminogen or TPAs attached to plasminogen
will become activated and result in plasmin generation. This will result in blood clot destruction
or fibrinolysis. The products of destruction of the blood clot or fibrin will inhibit thrombin and
platelet aggregation. Bleeding may also occur. Thrombin production will result in platelet
consumption for the clot, but there are not enough platelets to provide clots which will result in

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bleeding. Treatment includes treating underlying disorders. If disseminated intravascular
coagulation occurs, the person may exhibit different signs and symptoms secondary to failure
of the vital organs, such as kidney, heart, lung, or brain. The clots may deposit, or extensive
bleeding may occur. Hemolytic anemia may occur, and patient may have signs of hypoxia.
Primary disease management is very important. If a patient presents with excessive bleeding,
treatment will include replenishing the plasma proteins and correcting the deficiency.
Anticoagulants such as heparin may be considered for treatment.
Red Blood Cells Disorders
Red blood cells are known as erythrocytes. Men have higher content of hemoglobin than
women. On average, men have 14 to 16 and a half grams per decaliter compared to women
who have 12 to 15 grams per decaliter. Hematocrit is the amount of cellular material that
comes out from spinning the blood in the tube in centrifuge. No matter the sediment type, men
will have approximately 40 to 50% hemoglobin and women will have 37 to 47%. Bilirubin can be
measured as byproduct of the hemoglobin breakdown. Red blood cells break down 0 to 1.2
grams per decaliter. This is important in lab work to show liver function or anything else with
hemoglobin and body. If the ratio of normal hemoglobin to normal hematocrit is higher or
lower, it may signify a change in the blood such as dehydration or excessive fluid volume. If the
hemoglobin to hematocrit is higher than 1:3, there are too many blood cells and not enough
water. If it is lower, there is too much water and too little red blood cells.
Mean corpuscular volume (MCV) is the size of the cells. The mean cell hemoglobin
(MCH) and MCHC reflect the color of the cell. The MCHC is more concentrated hemoglobin; it is
more red. It is possible to measure by red blood cell distribution width (RDW). Distribution
width refers to the difference between sizes of cells. If the cell distribution width is narrow, it is
uniform or normal. A wider distribution or increased number will reflect a variety of sizes of
cells. This typically means bleeding and a production of small or immature cells to replenish the
blood loss.
Anemias relates to size or corpuscular volume. If the cells are normal size, but the
patient is still anemic it is due to a low hemoglobin level, and it is normocytic. Macrocytic
refers to the cells being large. Microcytic refers to the cell being small. Microcytic anemia
Macrocytic anemia, Normochromic, and Hypochromic are related to the color or hemoglobin
concentration. Normochromic refers to when the hemoglobin is a normal color. Hyperchromic
refers to when the hemoglobin is not concentrated, or the hemoglobin is pale. An iron
deficiency anemia is characterized by cells that are small. The small size is due to not enough
iron to make the cells normal size. Megaloblastic anemia is when the cells are large.
Megaloblastic anemia is typically a result of a b12 or folic acid deficiency. The large cells are
dysfunctional.
When iron deficiency anemia is present, it is often caused by blood loss. A patient with
Microcytic hypochromic anemia will have an increased RDW due to blood loss but will still have

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normal sized cells. Many new cells will be in circulation that will be relatively small and the
RDW will increase resulting in hypochromic anemia because the new cells are pale.
Megaloblastic anemias are b12 anemia which is also referred to as Pernicious anemia
and folic acid deficiency. Alcoholics are more prone to develop B 12 anemia because of an
impaired absorption of B12. Individuals with impaired GI production of intrinsic factors may
have a b12 deficiency. This can be resolved by intravenous injections of b12 for an acholic in the
acute phase, but for someone who is missing an intrinsic factor it is necessary to absorb b12
from GI tract by intramuscular monthly b12 injections. Folic acid can be corrected by oral
administration of folic acid. Both deficiencies will result in increased cell size and b12 deficiency
that interferes with DNA production and increased size of the cells which are not effective.
Megaloblastic are large cells related to a folic acid deficiency or b12 deficiency. Pernicious
anemia is a b12 deficiency that is secondary to the absence of an intrinsic factor. An intrinsic
factor is necessary for GI absorption. The cells will present the same way for a folic acid or b12
deficiency. Aplastic anemia is a consequence of inability of bone marrow to produce red blood
cells, and is related to bone marrow suppression. Chronic disease anemia is chronic
inflammation and chronic renal failure. Chronic renal failure is the result of decreased
erythropoietin production and decreased stimulation of the bone. This can result in
normochromic anemia because the bone has normal production capacity for producing red
blood cells. However, there is not enough signal to start production of the cells. Iron deficiency
anemia is hyperchromic and microcytic and is characterized by small pale cells.
Hemolytic anemias are membrane disorders. Hereditary Spherocytosis and Acquired
hemolytic anemias may be something like a drug that causes hemolysis and hemolytic disease
of the newborn. Hemolytic disease of the newborn may result in excessive deposits of bilirubin
under the skin. The excessive drug destruction of fetal hemoglobin will result in the newborn
turning yellow. One of the first nursing interventions performed regarding this disorder, was
performed in the 19th century in England. One nurse was believed that fresh air and sunlight is
a benefit to everyone. She would take all the babies, especially the ones who had turned
yellow, and lay them under the sun. The babies be only a benefit to everyone, and she would
take all the babies, especially the ones who turned yellow outside, and lay them under the sun.
It was noticed that the babies under this nurse’s supervision developed better than those in
other hospitals or wards. The babies who had the yellowish tint also lost it. Physicians then
wrote a paper and presented this phenomenon. However, the use of photo therapy was not
widespread until 20th century. Modern technology involves the use of ultraviolet lights in the
nursery to destroy excessive bilirubin.
Hemoglobinopathies, Thalassemia and Sickle -Cell Anemia
Sickle cell anemia may result as a change in the shape. Sickle cell disease is a mutation
in the beta chain of hemoglobin. If hemoglobin is deoxygenated, the beta chain link may clamp
together resulting in a long protein rod. This will make the cell stick and make it stickle. When
the cells become stuck it may cause strokes, retinal infarct, stuck in the eyes, in lungs, and they

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can block the blood flow to bones, avascular necrosis of femoral head. Painful infarcts in the
extremities, fingers and toes, ischemia, pain may also occur due to lack of oxygen supply. Skin
ulcers, atrophy of the spleen, and chronic kidney disease may develop. Blocking of the
capillaries by sick old cells, will result in acute pain infarctions causing damage to most vital
organs. Sickle cells are being destroyed extensively. The patient may develop jaundice as a
result. Individuals who have only alpha chains or have fetal hemoglobin, which has only alpha
chains and gamma chains, are protected from sickle-cell disease. This is due a lack of beta
chains. Beta chains are the only chains that can sickle.
Thalassemia is a defective chain of hemoglobin is due to a defective gene for alpha
chain synthesis or defective gene for beta chain synthesis and depends how many genes are
involved. Fetal hemoglobin does not contain beta chains. This is the reason that alpha
thalassemia will affect both fetal and adult hemoglobin. Beta thalassemia only affects adults.
Individuals of Asian descent may develop alpha thalassemia. Beta thalassemia is more
prominent in individuals of Mediterranean origin such as Greek and Italian. Severity of clinical
manifestations may vary. Alpha thalassemia may result in severe manifestation in newborns
when all the alpha chains are deleted, and only gamma chains are present. Fetal hemoglobin in
newborns may be a severe manifestation. When all the alpha chains are deleted, only gamma
chain chains are present resulting in fetal hemoglobin. This will result in gamma 4 hemoglobin
production. Gamma 4 hemoglobin has a strong affinity to oxygen. The oxygen molecule will be
captured but will never be released into the tissues. This may result in death in utero or shortly
after birth due to the inability to transport oxygen. Beta thalassemia may result in a patient
needing a transfusion or phlebotomy therapy to rid defective hemoglobin. A bone marrow
transplant may also serve as a cure for some patients. The presence of clinical symptoms of
both disorders may vary depending on the number of genes effected and type of anemia.
Treatment may vary due to the manifestation.

Cardiovascular Disorders
The cardiovascular system includes the heart, arteries, and veins with blood. The heart
is a muscular organ. Typically, it is approximately the size of the individual’s fist. It has four
chambers. The cardiovascular system is a closed system. The heart and lungs are connected
with arteries and veins. The left pulmonary and right pulmonary vein is an artery and have
oxygenated blood. Arteries and veins are named based on the direction of blood flow. If the
blood flow is toward the heart, it is a vein. If the blood flow moves away from the heart, it is an
artery. The heart has a muscular structure which is different than a skeletal muscle. The heart
has automaticity and the ability to transfer the electric impulse rapidly between the cells. The
Purkinje fibers allow for a rapid transport of an electric impulse. The heart also has layers. The
muscular structure is one layer. Myocardium is the layer inside the muscular structure.

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Endocardium is the inside lining of the heart and its chambers. Epicardium is the outside lining
of the chambers.
Several diagnostic tests can be performed on the heart. Non-invasive procedures are
becoming more popular. One non-invasive procedure, auscultation, is an older procedure, but
other techniques are relatively new. Cardiac catheterization is an invasive procedure. It involves
inserting a catheter through the vascular system to further evaluate the heart or for
intervention. X-rays having typically are less valuable. Other imaging may include an
Angiocardiography venogram. Blood testing for cardiac enzymes are also important tests used
for diagnostic procedures. A cardiac exam may also be used to determine onset of cardiac
events such as myocardial infarction.
Hypertension is a common disease of the arteries. Hypertension is a chronic disease. It
is a slow developing disease, often called “silent killer” because the patient may not experience
symptoms while developing hypertension. This disease may be related to the development of
cerebral vascular, cardiovascular, arteriosclerotic, and kidney disease. This disease is the leading
cause of hypertensive stroke and heart failure. However, this disease is preventable and
treatable. Primary hypertension has no known cause. It is idiopathic with a gradual onset. It is
also known as essential hypertension. Risk factors for hypertension include smoking, artero
sclerotic disease, obesity, sedentary lifestyle, lack of exercise, and other numerous risk factors.
Heredity and age are also risk factors. Age has influence on hypertension because with age-the
elasticity and ability of the vessels to adapt to higher volume of the blood decreases. This
results in increased blood pressure. Hypertension may be treated by lifestyle changes that
include decreasing sodium chloride or table salt intake. Pharmaceuticals may also be used as
treatment.
Arteriosclerosis and atherosclerosis are diseases of loss of elasticity and thickening or
hardening of artery wall. Both diseases include the development of fibrous plaque that consists
of fatty and lipid materials in the wall of the artery. In atherosclerosis, the vessels affected are
the coronary arteries, cerebral arteries, aorta and peripheral arteries. Atherosclerosis limits
pass capacity of the blood. The arteriosclerotic plaque may rupture causing myocardial
infarction or stroke. Atherosclerosis has two type of risk factors- controllable or non-
controllable factor. Heredity, age, sex and history of diabetes are non-controllable factors.
Diabetes may be modified and result in a lower risk of atherosclerosis development.
Controllable factors include diet, exercise, stress reduction, smoking, and hypertension.
Atherosclerosis is diagnosis by image studies such as an arteriogram and doppler. An increase in
blood pressure may be suggestive of atherosclerosis. If atherosclerosis is becoming advanced,
the patient may experience stable angina or unstable angina. CABG surgery may be needed,
and the occluded arteries will be removed and replaced. Angioplasty is another treatment
option that involves a cardiac cath.
Peripheral vascular disease is a condition that can impair the circulation, quality of life,
and intermediate claudication. It is characterized by muscle cramps, leg pain, and lower calf

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pain during activities such as walking. The pain is typically relieved at rest. It is due to a buildup
of arteriosclerotic plaque in the artery that supplies blood to the legs. Treatment may include a
bypass and angioplasty. Endarterectomy is the cleaning of the affected vessel and may also be
used as treatment. Treatment should happen quickly to avoid occlusion of the vessel occurs.
Tissue loss may occur secondary to necrosis. Amputation may be necessary. When necrosis
occurs, pain is not present. Pain is a positive symptom in this situation and may be indicative
that treatment may be helpful.
An aneurysm is the result of the weakening of the wall of artery and leads to a bulge or
rupture. Aneurysms are asymptomatic. They may be bruit or palpated. An abdominal aortic
aneurysm may be palpated. Aneurysms need to be repaired before rupture. Treatment is
typically successful. If a rupture occurs, treatment cannot be performed due the possibility of a
significant amount of blood loss. If rupture occurs in a hospital or other medical setting, there is
an increased chance of survival compared to in the home.
Coronary artery disease is a consequence of arteriosclerosis and is the single leading
cause of death in the United States. Atherosclerosis will lead to narrowing of arteries that
supply the blood to myocardium. If the atherosclerotic plaque ruptures, it may lead to
inflammatory response, development of a platelet plug, ischemia and infarction. A sudden
decrease of the blood supply to myocardium may lead to infarction, necrosis, and death. The
progressive narrowing of vessels will lead to ischemia of the heart muscle.
A stable angina is a pattern of repeated symptoms such as chest pain when walking for
a certain amount of time or distance. The pain may be relieved by rest or nitroglycerin.
Unstable angina is when the typical intervention does not relieve symptoms (chest
pain). For example, when given two nitroglycerin SL tabs the pain does not cease. This is a
medical emergency and patient should be rushed to hospital or EMS should me called.
Appropriate protocol should be initiated. Occlusion may progress slowly or suddenly secondary
to thrombus or embolus. When the plaque ruptures, the thrombus and platelet plug develop
resulting in an immediate discontinuation of blood supply. A slow progression is not as
dangerous as an immediate, but still needs medical attention. A patient may develop an
accessory vascular system in which the body creates a natural bypass. The development of
plaque may be prevented by lifestyle changes and anti-cholesterol drugs such as statins. Statin
may have side effects such as muscle pain and weakness. Statin may not only prevent the
increase in the size of plaque, but also stabilize existing plaque. In rare cases, Statin may lead to
myocardial infarction due to the drugs stabilizing properties and anti-inflammatory properties.
A myocardial infarction occurs when the blood supply is suddenly decreased or
stopped. Diagnosis is by history, EKG or ECG and angiograms. EKG is an old way of writing; the
correct term in ECG, however, some providers still write EKG. Laboratory work will include
examination of cardiac enzymes such as troponin and CKMB. Troponin is a cardiac specific
enzyme. The CKMB enzyme is non cardiac specific, it may signify other disease such as

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rhabdomyolysis and diseases that result in damage to the skeletal muscles. Treatment will
include revascularization by CABG surgery. A cardiac catheter and angioplasty may be used to
compress existing plaque or for a stent. Angina is treated with vasodilators such as
nitroglycerin. Diet, exercise and reduction of smoking reduce the risk of adverse effects of the
disease.
A thrombus is a clot that sits and does not move in the vessels. An embolus is a clot that
has traveled from another place in the body to the brain or heart. Heparin may be prescribed to
reduce the size of the clot or prevention of a clot. If a patient is under risk, a low weight
Heparin, like Lovenox, with sequential compression devices in lower extremities may be used as
prevention. Rheumatic heart disease is a sequel of streptococcal throat infection. Strep A
testing is done on patients who present with Laryngopharyngitis or Pharyngitis, to eliminate
diagnosis of Streptococcus A. However, when testing is done, there is a change the infection
will not be identified. It is important that Strep A is treated promptly. Strep A has a typical
pharyngeal appearance that can be diagnosed. The development of rheumatic fever may occur.
All layers of the heart, Cardia, Myocardium, and Epicardium may be affected. Valvular
deformities and valvular disease are secondary concerns. Treatment includes prevention,
treatment of streptococcal infection, and treatment of rheumatic fever. Rest during the acute
stage is important for an effective treatment. If valvular damage occurs, a valvuloplasty or
valvular replacement may be utilised for treatment.
Congestive heart failure occurs when the heart fails to pump blood adequately. It
results in an increase of the workload of the heart. The myocardium will slowly thicken, and
symptoms may include gradual increase in dyspnea, tachycardia, tachypnea, and Paroxysmal
Nocturnal Dyspnea or PND. PND is the sudden waking up with shortness of breath in the middle
of the night. secondary to increased workload. Congestive heart failure will also result in neck
vein distension, edema in ankles and lower legs, and pulmonary edema. Different manifestation
of edema may occur.
If the right-side of the heart is not functioning properly, the edema will be peripheral. If
the left-side of the heart is affected, pulmonary edema will occur. Combined right left-side
failure may occur and both peripheral and pulmonary edema will be present. A diagnosis by
history, physical, chest x-ray, and EKG will reveal an increased size of the heart. Decreasing the
workload may reduce vascular volume along with diuretics. A low salt diet, less than two grams,
and fluid restriction should also be implemented. Salt reduction may significantly decrease
vascular volume and workload on the heart. Cardiotonic such as digitalis or digoxin can
strengthen all cardiac muscle and strengthen the contraction. They help the heart to pump
more effectively.
If the heart fails to pump blood adequately, the workload of the heart increases
resulting in the tissue thickening. The myocardium may thicken and result in symptoms to
increase. Symptoms may include a gradual increase in dyspnea. Tachycardia or tachypnea and
Paroxysmal Nocturnal Dyspnea (PND) may also occur. Paroxysmal Nocturnal Dyspnea is

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characterized by a sudden awakening during sleep with shortness of breath. Congestive heart
failure will also result in neck vein distension, edema in ankles and lower legs, pulmonary
edema. Edema may have different presentation whether related to right side heart failure or
left side heart failure. If the right-sided heart is not functioning well, the edema will be
peripheral. If the left-sided heart is not functioning well, the edema will be pulmonary. A
combination of peripheral edema and pulmonary edema may occur if the heart failure has both
left and right sided combination. A diagnosis is made through a medical history, a physical,
chest x-ray and EKG. A chest x-ray will reveal increased size of the heart. Diuretics will be
introduced for treatment. A low salt (low sodium) diet of less than two grams Na and fluid
restriction may also be used as treatment. Diet may also play a significant role in treatment.
Cardiotonic medications such as digitalis or digoxin can strengthen the cardia muscle and
contraction. This may facilitate the heart to pump more effectively.
Cardiomyopathies are disease of the heart muscle. As a result, the heart may become
dilated, enlarged and thick, or flabby. There is no cure and it may certainly lead to myocardial
infarction, congestive heart failure, and death. Carditis is an umbrella term for Pericarditis,
Myocarditis, and Endocarditis. The type depends on the onset of the place. Pericarditis occurs
when the pericardial sac becomes inflamed. This may be a consequence of an infection that
affected the pericardium. The infection typically enters through the respiratory, urinary tract or
a skin and causes inflammation or infection to the heart. Treatment for all types of carditis is
similar. Antibiotics, analgesics, and antipyretics are typically used. A diagnosis is made through
imaging studies and ultrasounds. Antibiotics may resolve the disease. Patients with pericarditis
may have significant chest pain. Positional changes may alleviate the pain of pericarditis. It is
different from pain during the Myocardial infarction: myocardial infarction pain is not
modifiable by positional change or compression of the chest area.
Valvular heart disease may be a consequence of Rheumatic fever as well as
endocarditis. When the endocardial lining is inflamed, deformities of the valves may occur.
Diagnosis is made by an auscultation. Murmurs should be present when the heart valves are
not completely closed or there is a stenosis of the valve. Arrhythmias are abnormal heart
rhythms. However, arrhythmias can be abnormal. Arrhythmias such as ventricular fibrillation
can be deadly. Arrhythmias should be diagnosed and treated with medications or by a
defibrillator. Defibrillators may be implanted to combat life-threatening arrhythmias. Atrial
flutters are characterized by an irregular increase in heart rate. A pattern up to 350 beats per
minute may be observed. A heart block is a regular irregular pattern of interruption in the
conduction system. Atrial fibrillation or flutters are an irregularly irregular pattern in heart
rate. Heart blocks can be classified as first degree, second degree, AV block or a bundle branch
block. Treatments may include medication or implantation of a pacemaker defibrillator.
Rheumatic heart disease is a sequela of streptococcal throat infection. For this reason,
there is concern when Strep A testing done for patients who present with laryngo-pharyngitis
or pharyngitis. Even with the best testing technique, streptococcus A may not be identified. If a

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patient is suspected to have strep clinically, treatment of antibiotics may be prescribed despite
results of testing. Strep A typically has a significant pharyngeal appearance that may be
diagnosed. The sequela of this virus is the development of rheumatic fever. As a consequence,
the valves, layers of the heart, and cardia and epicardium may be affected. Valvular deformities
are the main concern secondary to valvular disease. Treatment may include prevention and
treatment of the streptococcal infection. Rest is the best treatment for rheumatic fever. If
valvular damage occurs, valvular replacement or a valvuloplasty may be used for treatment.
Treatment of the strep infection is key to avoiding rheumatic heart disease and congestive
heart failure.
Cardiomyopathy is a disease of the heart muscle that results in the heart becoming
dilated, enlarged, and thin, or flabby. It may lead to cardio myocardial infarction, congestive
heart failure, or death. Carditis is an umbrella term for pericarditis, myocarditis and
endocarditis. The location of onset determines the type. Pericarditis occurs in the pericardial
sac and may cause constrictive pericarditis due to an infection.

Adult Respiratory Disorders

Respiratory Symptom Evaluation
Auscultation is used to diagnose respiratory diseases by assessing breathing quality and
rates such as labored, tachypnoea, and rapid pace. Rapid respirations may due to
hyperventilation related to respiratory alkaloses. When patients are auscultated, different
sounds and rhonchi may be heard. Rhonchi is rattling sounds due to obstruction. Rale is the
crackle noise that may signify pulmonary congestion. Rale may also signify a chronic condition;
crackle noises are not typical and may be a sign of congestive heart failure. A wheeze has a
musical like tone unlike rale or rhonchi. Chest x-rays are the first step to diagnosis of a
respiratory condition. A sputum culture is an unorthodox diagnostic tool in primary care;
however, it is common in the hospital setting. The culture may be used to diagnose
tuberculosis. Tissue biopsies for bronchoscopy can be done. Arterial blood gases may reveal the
metabolic state and respiratory acidosis or alkalosis. Pulmonary function tests are used to
diagnose restrictive and obstructive diseases. Diseases of upper respiratory tract are common
conditions. In colder regions, diseases of the upper respiratory tract may be more common.
Most respiratory disorders are not life threatening.
Rhinovirus is a common cold virus that can cause an upper respiratory infection. Other
viruses such as Adenovirus or influenza may also cause an infection. Hundreds of different
organisms may also cause infection and makes it hard to develop immunity. Infection occurs
when an organism invades the nasal mucosa resulting in nasal discharge and inflammation. The
mucous production will increase, and the epithelial cell will begin to shed. This is a first line of
defense that increases the vulnerability to a bacterial invasion. The bacterial superimposed
invasions or infections occur when the initial viral infection stars developing. Wet, cold and

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unsanitary conditions may increase risk for infection. The weather does not directly impact the
development of an infection. However, it does directly impact the risk and spread of sickness
because people are in confined spaces closer together and not outside as much during warmer
weather. Treatment will include palliative measures such as rest, fluids, antipyretics, and
analgesics. Antibiotics may be prescribed if a secondary infection occurs. Acute rhinitis can be
contrasted with allergic rhinitis because it does not involve a microorganism infection, but
instead Hay fever. Sinusitis, pharyngitis, and laryngitis has a bacterial origin and may warrant
treatment target toward a specific bacterium. Patients with sinusitis may have facial pain.
Patients with pharyngitis and laryngitis may have a sore throat. Treatment may include
antibiotics. Superimposed infections or sequela of upper respiratory infections may cause life
threatening situation such as Streptococcal A.
Laryngopharyngitis may result in valvular disease of heart. It may become life
threatening. Laryngopharyngitis is not a disease, but the sequela of an infection. Bronchi and
the lungs may be affected by an invasive organism. If not watched closely or treated
immediately, it can manifest into a severe sequela of upper respiratory infection causing life
threatening complications. Disease of bronchi and lungs include asthma and an allergic
reaction. A hypersensitivity reaction will lead to bronchial constriction and spasm resulting in a
difficulty in breathing. When an asthma attack occurs, wheezing and dyspnea will be the result.
Severe episodes may require drastic measure and the treatment. Intervention of asthma will
include removing allergens and bronchodilator treatment. Juvenile asthma can be triggered by
exercise. This is different from adult asthma. Acute bronchitis is most likely a sequela of an
upper respiratory infection. A sequela refers to being able to determine a diagnosis of a viral
disease by a sequence of symptoms such as fever, tightness behind the sternum, sternal,
substernal tightness, and productive cough. A productive yellow greenish sputum may also
occur due to a bacterial infection. Antibiotics should be prescribed. If the diagnosis is acute
bronchitis, it is a viral infection even with the cough and sputum. Palliative measures should be
prescribed instead of antibiotics.
Treatment for upper respiratory infections will include palliative measures such as rest,
increased fluid intake, cough syrups, or Tessalon drops. Cough syrups such as hydrocodone
preparation may lead to addiction and the development of dependence on the medication.
Prescribing Tessalon pearls may be effective and will not create and dependence or opioid
related side effects. If a patient develops a fever, analgesics and antipyretics may be prescribed
for comfort care. Antibiotic should be prescribed to treat secondary superimposed infections if
those occurs.

Influenza is a viral disease that can start as an upper respiratory infection. It is not a
common cold but may have similar symptoms and GI symptoms such as nausea, vomiting, and
diarrhea. Influenza can be caused by three different types of viruses. These viruses are highly
adaptive and constantly mutant. A, B and C types of influenza virus is the most common. Type A

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influenza may have several subtypes and it's the most common type of virus. Influenza can
result in pandemics, epidemics, and global pandemics. The HINI type of influenza or swine flu
started as a pandemic in the United States, Mexico and Canada in 2009. It was characterized by
a dramatic increase in cases and little outcomes of the disease. Type B influenza can also cause
epidemics. Type B is mild and type C is sporadic and typically results in local outbreaks. Type C
has never resulted in a large epidemic. Most people will recover from influenza; however, it
might account for significant number of hospitalizations and even deaths.

If an individual already has an immunocompromised status, preexisting chronic

diseases, or is a child the consequences of the flu may more significant. Death may also be a
result of dehydration or pneumonia from a secondary superimposed pneumonia or flu.
Influenza is a viral disease that is spread by coughing, sneezing, droplet infection and may have
empiric period of 1 to 4 days. The most contagious period is first day after symptoms occur.
Influenza usually lasts approximately 4 to 7 days in adults, and children the infection can be
spread up to 6-7 days from onset of symptoms. Treatment will include palliative measures such
as rest, analgesics and antivirals such as Tamiflu. The average time of decrease of the duration
of the illness is approximately one day with the use of antiviral agents like Tamiflu. For some, a
greater time is needed to recover from the illness. Fluid hydration is also important for
treatment.

Prevention includes hand washing, avoiding crowding spaces, and vaccination. The
effectiveness of the vaccine varies from 60 to 80%. There is also a chance that the vaccine will
not be effective for the certain strain that may be popular during the flu period. The vaccine is a
prediction of which strain will be more prevalent during the current flu season.

Chronic Obstructive Pulmonary Disease is a cluster of disorders that includes asthma,

chronic bronchitis and emphysema. The two major types are chronic bronchitis and
emphysema. These two types have a link to cigarette smoking. They are both difficult to treat,
and improvement is very rare to impossible. If a patient discontinues the behavior, COPD may
occur, but the patient may still maintain the functioning of the of pulmonary system on the
level that it was on a given date. By stopping smoking, the patient can prevent the further
deterioration of the pulmonary system. COPD is irreversible and progressive.

Tissue degeneration will occur along with airway obstruction. Patients will not be able to
work or function independently. Hypoxia and hypocapnia may also occur and result in
respiratory failure. Hypocapnia will result in an irregular pattern of breathing. This is a
consequence of shifting from normal carbon dioxide breathing drive to oxygen related
breathing drive. COPD can lead to Cor Pulmonale, right sided heart failure, and the other rare
diseases. Cigarette smoking, inhalation of chemicals, and pollutants may result in COPD.
Another type of COPD is a familial type and is a alkaline antitrypsin deficiency. This type of

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COPD can be diagnosed by a blood test. This COPD can develop in the early thirties and forties.
Chronic bronchitis and emphysema can be the sources of this disorder. It can be present alone
or together. Diagnostics ay include gathering a history, a physical, chest x-ray, and pulmonary
function tests.

Chronic bronchitis is an obstructive respiratory disorder characterized by inflammation

of the bronchi resulting in a productive cough and excessive mucus production. Acute
bronchitis is related to a viral infection. Chronic bronchitis is an inflammatory response to
smoking or other offending agents like chemical exposure. The inflammation will affect the
mucous glands, resulting in the development of an increased hyperplasia edema mucous
production. Bronchoconstriction cough in a defense against inhaled irritants. When this occurs,
the pulmonary defenses are reduced and consequently the cilia is dying as well. Phagocytosis
will decrease and the chronic bronchitis respiratory infection will occur. The development of
bacterial infections is also common.
Emphysema is an obstructive respiratory disorder that will result in the destruction of
the alveoli or the alveolar walls. This will result in a large permanently inflated alveolus. The
lung tissue will remodel when it grows and will repair if infection inflammation occurs. Enzymes
are involved in this process by influencing or preventing the excessive tissue damage. Smoking
may cause an enzyme deficiency. Smoking initiates inflammation that results in changes in
enzyme levels and structural damages. Emphysema will gradually affect the alveoli causing
them to grow or develop into large irregular pocket. These pockets will have large holes that
results in a loss of oxygen. The alveoli will collapse during expiration, and air will be trapped in
the lungs. The recoil of the lungs in lost in the hyperinflation of the alveoli. The narrowing of the
terminal will lead to distinct shape of the chest. In patient with COPD will open hyperventilate.
They will have a pink appearance to their skin and a shallowing breathing pattern. Patients with
emphysema and chronic bronchitis use accessory muscles to help with the breathing. To breath
more effectively, the patient will develop barrel chest to increase oxygenation. This is a
significant finding during a physical examination.
A VQ mismatch is also a sign of COPD. If the ventilation is larger and the perfusion is in
normal range, it is a VQ mismatch that is typical of COPD. The end stages of COPD are
characterized by the patient losing the reserves of fat resulting in the development of
oxygenation maintenance and a high respiratory breathing rate. The patients may develop
increased hemoglobin and hematocrit to compensate for a fast-respiratory rate. Symptomatic
treatment includes albuterol and mucolytics. Avoidance of exposure to upper respiratory
infection may result in exacerbation of COPD cough suppressants. Individuals with COPD may
need to take mucolytics like Mucinex all year around.
Pneumonia is the inflammation of the bronchioles and the alveoli. It is caused by a
bacterial or viral infection. A viral caused pneumonia will have symptoms such as a non-
productive cough, low-grade fever, and a normal count of blood cells. A bacterial caused

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pneumonia will have symptoms such as a productive cough, high-grade fever, and a left shift in
blood cell count. Bacterial pneumonia or classic pneumonia presents with infiltration. On an x-
ray of a viral pneumonia there will be minimal changes. If the pneumonia is viral, antibiotics
should not be prescribed. If the pneumonia is bacterial, antibiotics may be prescribed to
determine the causative organism. Pneumonia pathophysiology can have a different origin
based on offending agent. For example, aspiration pneumonia occurs the gastric content or
tube feeding formula can reach the lung tissue causing irritation and triggering the
inflammatory response. This will cause an increase in the mucus production resulting in
pneumonia. A feeding tube has a mixture of sugar and protein and serves as an ideal medium
for bacteria growth. If pneumonia develops, the activities of daily living will become more
difficult. The patient will not be able to move or talk normally. Coughing may become disabling
for the patient. Hydration may help the secretion to become easier to expel. Lobular
pneumonia when one or more than one lobe is involved in bronchopneumonia. It is the most
frequent type of pneumonia. Interstitial pneumonia is an atypical type of pneumonia. It occurs
between the alveoli and may be caused by a virus. Nosocomial pneumonia is a hospital related
pneumonia.
Tuberculosis (TB) is a very serious infectious disease. In recent years, the incidence rate
as declined in the United States, however, the rate of TB is increasing worldwide. Populations
typically affected are those who have Acquired Immuno Deficiency Syndrome (AIDS) in
underdeveloped countries. The World Health Organization (WHO) reported that more than two
million people from this disease every year. TB is an opportunistic infection because it may
become active in someone with a weak immune system.
TB is transmitted through infectious aerosol droplets. Many individuals are exposed to
the disease because of a weak immune system. TB is a very old disease and present for
centuries. Nutritional status, drug abuse, and living conditions may also affect who contracts
disease. The offending agent of TB is Mycobacterium Tuberculosis bacillus, which is an aerobic
bacillus. The bacillus can survive in dry secretion or sputum. UV light, heat, alcohol,
formaldehyde can destroy the bacillus. TB may involve the lungs, liver, brain, bones, bone
tissue, and bone marrow. TB pathogenesis has two stages. Primary TB occurs when the bacillus
enters the body and the macrophages surround it resulting in the microbes to become
engulfed. This causes local inflammation. Regardless of inflammation, the bacillus will travel to
the lymph nodes. Type four hypersensitivity reaction will occur. The lymphocytes and
macrophages will attack and form a granuloma. A granuloma is an epithelial nodule that
contains the bacilli that will form into a tuberculum which contains a little ball and a cottage
cheese like substance called caseous necrosis. The immune system will hinder the develop even
with TB exposure. The lesion with and the balls will stay small; only the surrounding fibrous
tissue that will grow. Calcification may also occur creating another barrier.
This growth process of the fibrous tissue and classification is referred to as Ghon’s
complex, and it prevents the bacillus from spreading to surrounding areas causing TB. The
bacilli may remain dormant until the immune system no longer has impact. The TB will enter
the secondary or active phase in which the TB breaks through the Ghon’s complex and spreads
through the lungs into other organs. The patient will develop a cough that progressively

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worsens, hemoptysis, night sweats, fever, chills, anorexia. The constitutional symptoms such as
fatigue nausea, anorexia, and fever will depend on the location that the TB develops. Symptoms
will also depend on the organ affected.
The Mantoux test will be used for diagnosis. A chest x-ray and sputum culture may also
be used in addition. Treatment is typically outpatient but requires a long duration from 6 to 9
months or a year in some cases. Treatment includes a combination of techniques, and this may
result in a resistance to antibiotic or antitubercular medication to develop. Prevention of
transmission mostly affects Health Care providers. Protection includes TB approved mask,
adequate ventilation, and negative pressure rooms.

Renal Disorders

Kidney stones often cause urinary tract obstruction. If the stone is dislodged, it may
travel down the urinary tract to and obstruct the flow. Kidney stones crystals of substance that
typically pass through the urinary system and are excreted. There are certain substances that
may inhibit the growth or excite the growth of these crystals. If the stone is not excreted, it will
stay in the kidney or urinary tract and grow. Kidney stones can be a small as a grain of sand or
as large as the size of a golf ball. The demographics of kidney stones may vary. Urolithiasis is
more common in white male patients. The calculi typical form in the renal pelvis, ureters, and
bladder. A renal stone are not uniform and may be made of a mixture of crystal structures.
There are several types of renal stones. Calcium stones form secondary to different factors.
This type of stone is common and form in the presence of excess calcium intake.
Hyperparathyroidism may also cause calcium stones. It is characterized by the inability of renal
tubules to reabsorb calcium. Chronic bowel disease may result in a loss of fat and steatorrhea.
If fat is lost, the fat may combine with calcium and be absorbed. This will result in the calcium
not binding to oxalate causing stone formation to occur. Steatorrhea may be considered a
precursor of stone formation because of the calcium inability to bind to the oxalate. Treatment
will vary depending on the cause. Phosphate or thiazide diuretics may be administered to
decrease the dietary absorption of calcium. If the stone becomes so large that it cannot be
removed by traditional methods such as increased fluid intake, surgical intervention may be
necessary. If parathyroid dysfunction is present, surgical intervention may be necessary to treat
hyperparathyroidism and decrease the calcium stone formation.
Struvite stones are magnesium ammonium phosphate stones that are caused by
bacteria. If the urinary pH falls below the level of 7.2, the acidity creates and environment that
is nonbeneficial for the bacteria. This creates a narrow pH window for treatment. Unlike
calcium stones, struvite stones are large and may have a soft texture. Patients are also more
susceptive to UTI because of the bacteria that cause the formation of the stones. These stones
are also more common in women than men. Treatment of the UTI may prevent the formation
of the struvite stones. Percutaneous nephron lithotomy may be used as treatment for struvite

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stones as well as other types of stones. Cysteine stones are related to abnormal exertion of
amino acids or cysteine, lysine, and arginine. These types of stones are caused by the abnormal
conditions related to an amino acid excess. Prevention will include the increase of fluid and pH
of urine to create an environment that is not beneficial to the stones. Uric acid stones are large
stones that is caused by an acidic pH environment around 5.5. Common causes may include
rapid and dramas with loss and malignancies. These stones are typically large and may be
dissolved by increasing the urine pH with potassium citrate. When potassium citrate is
introduced, the pH level will increase from a 5.5 to a 6.5 resulting in the stones to dissolve. pH
levels play a significant role in the formation of stones. Stone manifestations cause severe,
colicky pain. Colicky pain refers to pain that fluctuates in intensity. The colic may last to one
hour or ore.
Stone analysis may give clues as to the treatments that should be used. Kidney ureter
bladder x-ray, intravenous Pyelogram, and CT scans are test that may be utilized for the
analysis. Clinical presentation such as colicky pain are also important factors. Imaging such as
KUB compared to IV P and CT scan should be considered. A stone analysis for a uric acid stone
may include decided treatment to increase the pH level to dissolve the stone or removal of the
stone by percutaneous nephrolithotomy or surgery.
A neurogenic bladder is a complicated and complex condition that occurs in types of
neural disorders. These disorders affect the bladder innervation. The bladder innervation
becomes destructed or interrupted. The interruption causes a neurogenic bladder. This
condition may be secondary to brain or spinal cord injury, neurologic system tumors, a brain or
spinal cord infection, dementia, Parkinson disease, spina bifida, stroke, and multiple sclerosis.
Other conditions such as alcoholism, lupus, metal poising, herpes zoster, and medications may
also cause neurogenic bladder. Neurogenic bladder is a condition most commonly found in the
acute setting. Manifestations may include urinary retention and hesitancy. Diagnosis of a
neurogenic bladder will include a case history, physical examination, and urinary diary. Urology
practices may ask the patient to keep a bladder diary, urinalysis, culture sensitivity, cystoscopy,
and imaging procedures such as MRI.
Urinary tract infections (UTI) are one of the most common conditions encountered in primary
care. It is characterized by inflammation of the urinary epithelium. When the epithelium is
attacked by bacteria or other pathogens within the urinary tract, inflammation occurs, and an
infection may develop. A complicated UTI is recurrent and responds vaguely to treatments. An
uncomplicated UTI is sporadic and responds to treatment. Complicated and persistent UTIs are
very similar. Complicated UTIs can be from a lower urinary tract and can travel to the upper
tract resulting in impaired renal function. The duration of treatment depends on the
classification of the UTI. Uncomplicated UTIs occur seldom, and treatment is typically short
because the patient is responsive. Complicated or persistent UTIs will require a longer duration
of treatment. Treatment may last seven to ten das compared to the three-day treatment
regime of an uncomplicated UTI. The dosage of antibiotics will also depend on the nature of the

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UTI. Because of more common sulfur drug allergies, other drugs such as Ciprox may be
considered for treatment. When gather a case history of a UTI, medical personal should focus
on the details. Interstitial cystitis is a debilitation and complicated condition that is often
misdiagnosed as an UTI. There is no known cause for this condition. It is a painful condition that
results from the inflammation of the bladder wall. It often takes four years for diagnosis from
time of the onset of symptoms. This condition most commonly affects people around 30 to 40
years old. Women are ten times more likely to have interstitial cystitis than men.
Treatment for interstitial cystitis is palliative. Pain management and patient education
will be important components of treatment. The disease has no cure but can be managed
through treatment and medication. E. coli is very closely located urinary tract infections. The
risk for contracting E. coli is higher in women than men. E. coli comes from the GI system and a
woman has a shorter urethra causing UTI secondary to E. coli to more common in women.
Treatment in the primary care setting will include ciprofloxacin or Bactrim or Cipro if you
patient is allergic to sulfur drugs. If treatment is ineffective, the infection may be due to a
virulent strain of E. coli. A culture and sensitivity will need to be completed.
Cystitis is inflammation of the bladder. Manifestations such as frequency, dysuria,
urgency, lower abdominal pain, and suprapubic pain may present similar to those of a UTI.
Antimicrobial therapy may help increase fluid intake for both cystitis and UTI. High
concentration of cranberry extract may also be used as treatment provided by a trained
professional. Cranberry extract prevents the attachment of the bacteria to the wall of the
bladder.
Pyelonephritis is an acute infection of ureter, renal pelvis, and renal parenchyma. This
type of infection is commonly cause by Cystitis. It occurs when an obstructive UTI is present
resulting in a reflux of urine. The patient will present with flank pain, fever, chills,
costovertebral tenderness, costovertebral angle, CVA tenderness, and purulent urine. If urine
becomes purulent, further investigation is needed. An uncomplicated UTI will not result in
purulent urine. you better do something to further investigate why this. Chronic Pyelonephritis
is related to a chronic obstructive source or chronic urinary retentions. Treatment will include
antibiotics. Uncomplicated cases may be treated as outpatient, but hospitalization may be
considered if the case if considered complicated.
Glomerulonephritis is an inflammation of the glomerulus. Inflammation may be due to
immunologic abnormalities, drugs, toxins, vascular abnormalities, systemic diseases, or viral
infections. Bilateral inflammation and bilateral disorders that affect the glomeruli may be
sequela of streptococcal infection. This is typically more prevalent in men than women and is
the leading cause of renal failure in the United States. Inflammation and other symptoms such
as congestion and cell proliferation will impair kidney function, the ability to filter, and the
ability to excrete excess water and harmful substances. Glomerulonephritis can be acute or
chronic. It is subdivided or sub diagnosed into nephrotic and nephritic syndromes. A
streptococcal infection may lead to the formation of immune complexes such as antigens and

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antibodies. These immune complexes will circulate in the blood and may be deposited in the
glomerulus. The antibodies will produce and fight against the streptococcal organism, but the
glomerular endothelial cells will cross react with the antibodies. Activations of complement will
occur resulting in recruitment activation of immune cells and mediators. This will result in acute
glomerulus nephritis. Clinical manifestations of acute glomerulonephritis will occur. Hematuria
is a troublesome sign that may be observed. A bloody or brown tinge may be observed. If a cola
or beer color or more blood than bilirubin is observed in the urine, it may be a presentation of
glomerulonephritis. However, on lab work will confirm the results. Proteinuria and low serum
albumin may indicate a loss of protein in the urine. Edema will develop as a result of low serum
albumin due to the permeability. Osmolarity is determined in the blood or serum by the
albumin concentration as well as other solutes. The albumin plays a critical role. As a result of
glomerulonephritis, oliguria will develop. When glomerulonephritis occurs, the kidneys will shut
down and the urine output plays a critical role in measurement. Foley catheters may monitor
urine output. Nephrotic syndrome is manifestation of glomerulonephritis. It occurs when the
antibody antigen lodges in the glomerular membrane and triggers the complement system.
Renal Failure
Post renal failure occurs when something obstructs the outflow of the urine and does not allow
the urine to flow away from the kidneys. BPH may be benign or cancerous. BPH is more
common than prostate cancer and may contribute to the obstruction of urine cause pressure to
build up. This will result in a decrease in rate of the glomerular filtration. Neurogenic bladder
includes bilateral urethral obstruction and bladder outlet obstruction, or anything that
obstructs the urine flow from the bladder. If the urine cannot be evacuated, it will become post
renal failure. Clinical manifestations of acute renal failure include Oliguria, anuria, elevated
BUN, creatinine, hyperkalemia, metabolic acidosis, and hypertension. The volume may overload
resulting in a systemic disorder. Renal failure causes an inability to produce urine resulting the
fluid becoming backed in circulation and hypertension.
Acute renal failure may affect organ systems outside of the renal system. In an acute
renal disorder, function may improve quickly compared to chronic renal failure when
disfunction manifests to all organ systems. The renal reserve will be lowered, and at some
point, the patient will start experiencing renal insufficiency, renal failure, and then end-stage
renal disease. All the stages are described and determined using glomerular filtration rate
determination.
Chronic renal failure is the irreversible loss of renal function. Chronic renal failure can
affect creatinine, urea levels, sodium and water balance, phosphate, calcium, potassium and
acid base balance. Because of sodium and phosphate imbalance, skeletal and bone alteration
will occur resulting in a loss of calcium, cardiopulmonary manifestation, and neural function.
Endocrine reproduction and erythropoietin production will decrease or cease, and hematologic
alterations will occur. Chronic renal failure can affect immunologic, GI, integumentary systems,

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protein, carb, and lipid metabolism is affected. Because of the loss of proteins and lipids, the
liver will try to compensate resulting in hyperlipidemia.
Chronic renal failure is the gradual progression of the disease. Type 1 and Type 2
diabetes is the leading cause of chronic renal failure. It is the sequela of vascular damage and
damage to the endothelial lining. The second leading cause is hypertension and then urine
obstruction. Urolithiasis and Benign Prostate Hyperplasia may block urine flow and result in
postrenal failure that may transform into chronic renal failure. Other renal diseases include
Pyelonephritis, glomerulonephritis, and renal artery stenosis. Renal artery stenosis is due to
prerenal sources of toxic exposure. Other causes of renal disease include sickle-cell disease,
lupus, and smoking. Smoking may cause atherosclerotic changes in blood vessels causing the
vessels to become smaller. This will affect the vessels in the kidneys as well. Chronic ischemia
and necrosis may occur as a result. Age is also a factor that may play a role in chronic renal
failure. Age may affect the GFR and reduce the glomerular filtration rate. The GFR is calculated
by a Cockcroft formula or through another formula. A patient may function well at GFR rate of
50%. GFR will describe the renal insufficiency. Failure occurs when there is a significant loss of
function and the GFR is less than 20% of normal. The patients may still have function, but signs
and symptoms will be present. When the GFR begins to decline, the end-state of renal failure
has started.
When considering treatment involving dialysis or a kidney transplant, there are many
factors that need to be considered. Factors include the patient's comfort, availability of the
donors, availability of the matching kidney, and genetic makeup. A transplant is a complex
procedure and may require lifelong immunosuppressive therapy. Some transplants may
decrease the quality of life for the patient. The decision for a transplant or dialysis is made on a
case by case basis.
Renal insufficiency occurs the GFR is reduced to 25%. The patient will still have mild
clinical symptoms related to mild uremia, BUN, and creatinine. The erythropoietin may be
affected during stress. This is due to the increased blood circulation through the kidneys and
the increase need for filtration. Given a stressful situation, the function of the kidneys will be
decreased. Renal failure with a GFR less than 20% causes BUN and creatinine to continue to
increase. Oliguria urine output is small resulting in metabolic acidosis to begin. This will cause
electrolyte imbalances, hyperkalemia, and hypernatremia, severe anemia, and erythropoietin.
Sub cu shots may be very beneficial for the patient. The uremia may not affect non renal
organs. Renal disorders can be very debilitating and impair the quality of life for the patient.
Renal disorders may result in more complex diseases that effect multiple organs. Diabetes and
hypertension are two precursors of renal disorders, chronic renal failure, and the need for
dialysis.

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Endocrine Disorders

Hormonal Regulation
The endocrine system is responsible for hormone production. Hormones are chemical
messengers that help regulate other systems in the body. The endocrine system is a feedback
system with a negative or positive subtype. When there is dysfunction in any of the endocrine
glands, there is an excessive production of the hormone associated with the gland. This
overproduction may lead to an alteration in the body or an insufficient or inadequate
production of the hormone resulting in other alterations. An altered hormone inactivation or
degradation may also occur. This is characterized by the hormone staying and working too long.
Degradation refers to when the hormone is destroyed too quickly, and no effects occur. Ectopic
hormone release may occur from known endocrine sources such as autonomous production
with no feedback mechanism. For example, a tumor will produce a hormone with
uncontrollable production without any feedback from the body. Target cell failure may also
occur and is most common in type 2 diabetes. This occurs when the receptors decrease in
number of their function is impaired. Antibodies can destroy the receptors and attach to the
receptors and mimic their action although they are not hormones. The receptor may also have
an unusual expression in function, however, that is rare.
The Hypothalamus-Pituitary system is important to understanding may disorders in the
body such as hypo or hyperthyroidism. The hypothalamus can communicate with the anterior
pituitary gland. This results in anterior pituitary gland to release hormones to complete one or
more functions. For example, in the thyroid TRH will be released resulting in the anterior
pituitary gland producing TSH. This catalyzes the thyroid to produce T3 and T4. The
Gonadotrophin releases a hormone that will affect the production of the follicle stimulating
hormone or luteinizing hormone. It is important to know that the anterior pituitary gland is not
the origin of the hormonal messengers. Hormonal messengers originate in the hypothalamus.
In regard to pituitary disorders, the anterior portion of the pituitary gland produces majority of
hormone in comparison to the posterior portion of the gland. The pituitary gland has many
blood vessels and is vascular. It may be vulnerable to ischemia and infarction like the heart. It
can also be traumatized easily by a hemorrhage. Hypopituitarism may be a consequence of a
pituitary infraction related to Sheehan syndrome. Factors such as a hemorrhage, shock, trauma,
head trauma, infections, and tumors may result in significant pressure on the pituitary gland
causing pituitary dysfunction. Sheehan syndrome is a rare syndrome of ischemia related to
maternal bleeding during childbirth. Risk factors include having twins or triplets. The ischemia
or infarction may result in the inability of the pituitary gland to produces hormones. Treatment
include hormone replacement. This may result in Panhypopituitarism resulting in an absence of
production of all hormones in the pituitary gland. Hyperpituitarism is the opposite condition. It
is usually a consequence of a benign tumor resulting in an overproduction of hormones.
Changes in the feedback mechanism may be observed. Hormones that are produced in the

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anterior pituitary gland include the growth hormone. This hormone regulates growth and is
associated with two disorders- hypersecretion of the growth hormone and acromegaly.
Acromegaly occurs when there is an overproduction of the growth hormone during adulthood;
this is not a childhood disease. The disease may slowly progress and may result in death from
cardiac hypertrophy, hypertension, and arthrosclerosis. Diabetes may result as a consequence
of endothelial dysfunction and coronary artery disease may occur due to malignancies.
Giantism is a similar disorder that occurs in children and adolescents. In giantism, the growth
plates are not closed resulting in the child or teen to have a significant growth sprout. In
acromegaly, there is no open growth plate. However, sections of the cartilage that is sensitive
to the growth hormone may grow significantly. These areas include the ears, nose, and other
body parts. Cardiac hypertrophy may also occur. The connective tissue in the ears may
proliferate and the tongue may enlarge. The sebaceous and sweat glands will become overly
active. Skin and body hair may become coarse and bony proliferation, large joint arthropathy,
and periosteal vertebral growth may result from kyphosis. The facial bones, hands, and feed
will grow.
Hypersecretion of prolactin may also occur in the anterior pituitary gland. The
production of prolactin is a consequence of prolactinoma. This is the most common pituitary
tumor and is hormonally active. In a female, prolactin may cause amenorrhea, galactorrhea,
hirsutism and osteopenia. Males do not respond well to a prolactin increase and the
overproduction may result in impaired gonads or hypogonadism. This may result in impaired
testosterone production and erectile dysfunction, a libido decrease, oligospermia, and a
diminished ejaculated volume. These factors may affect quality of life and fertility in male
patients.
Thyroid and Parathyroid Functions
The functions of the thyroid gland are related to thyroid hormone production. If the
thyroid gland is impaired the primary function is altered. If hormones form the pituitary gland
or TSH production is impaired, this is a secondary production impairment. Most thyroid
disorders are related to primary dysfunction. TSH may be use as a diagnostic tool to determine
the type of dysfunction. In the case of hyperthyroidism, TSH levels will be change due to an
excessive production of the thyroid hormone secondary to the dysfunction of the thyroid gland.
In hyperthyroidism, the TSH levels will decrease. In Hypothyroidism, the thyroid hormone
levels will decrease, but the TSH levels will increase. Thyrotoxicosis is the result of an excessive
amount of the thyroid hormone resulting in toxic consequences. Graves’ disease is a significant
disorder that is the most common manifestation of hyperthyroidism. Hyperthyroidism can also
result from nodular thyroid disease resulting in the patient presenting with goiter and
thyrotoxic crisis. It may be very dangerous and may result in numerous metabolic alterations
and life-changing or life-threatening disorders. If a person has some type of hyperthyroidism,
they may have an enlarged thyroid gland. Although goiter is not a definitive diagnosis, if
someone presents with goiter then a diagnostic workup needs to be considered.

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 Hyperthyroidism may result in a non-palpable or mildly palpable thyroid.
Hyperthyroidism is the consequence of the loss of production of thyroid hormone T3 and T4. It
is also a type of sub-acute thyroiditis. Hashimoto’s disease is an autoimmune thyroiditis that
results in the same consequences. Both types will be treated the same, however, once the
function of the thyroid is impaired it cannot be restored. Thyroiditis is usually painless.
Postpartum thyroiditis may resolve. However, approximately 20% of women who have
postpartum thyroiditis will need Thyroid hormone replacement. Postpartum thyroiditis may go
undiagnosed and may occur 3-4 months after delivery. The patient may experience a thyroid
toxic phase in which the levels of the thyroid hormone increases. This phase may go unnoticed
due to consequences of taking care of an infant. Hypothyroid phase is the next phase to occur.
During this phase the patient will become lethargic, sleepy, anxious, or depressed. This phase is
resolved in most women in eighteen months or less. Approximately 1/5 of women will need
thyroid replacement. A myxedema coma is a loss of brain function that occurs secondary to a
long-standing thyroid disease. If hypothyroidism goes undiagnosed, it may result in comatose.
Congenital hypothyroidism may lead to cretinism in children. Early thyroid hormone
replacement may prevent this. Thyroid carcinomas may have life-threatening characteristics
and result in radical thyroidectomy.
The parathyroid hormone (PTH) is produced in one of the four of five parathyroid
glands. Hyperparathyroidism is typically caused by parathyroid adenomas. This can also occur
secondary to chronic disease such as renal failure or vitamin D or calcium deficiency due to a
malabsorptive syndrome. A patient who presents with hyperparathyroidism may also have
hypercalciuria, alkaline urine, hypophosphaturia, and calcium stones.
Hypoparathyroidism will result in low levels of PTH, a decrease in the serum calcium
level, and an increase of the serum phosphate level. This is a consequence of the loss of the
parathyroid in radical thyroidectomy due to the glands being attached and not being able to
implant. Decreased serum calcium levels cause muscle contraction consequences. A patient
with hypocalcemia will also present with Chvostek and trousseau’s symptoms and
laryngospasm may occur. These symptoms are not diagnostic markers. Hypocalcemia will result
in decreased or absent PTH levels causing muscular dysfunction. Hypocalcemia begins when the
threshold for a nerve and muscle excitation occurs. This may be hyperreflexia tonic clonic
convulsion, laryngeal spasm, or asphyxia. Treatment including a calcium gluconate infusion
should be given as soon as possible. Phosphate retention may also be another sign.
Adrenal gland disorders
Adrenal gland disorders may affect one or both part of adrenal glands and
consequences depending on the part that is affected. If the adrenal cortex is affected, Cushing
disease may occur. This disease is caused by an excessive production of anterior pituitary
hormone (ACTH) resulting in excessive amount of glucocorticoids. Excessive levels of cortisol
due to glucocorticoids or other external sources may cause Cushing syndrome. Adrenal tumors
secrete glucocorticoids and pituitary tumors secrete ACTH and cortisol. This may result in

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truncal obesity. Symptoms may include moon face, a buffalo hump, muscle weakness, delayed
growth, acne, striae marks on the abdomen, thighs, belly, and breast, edema, and hypokalemia.
Mood swings and psychosis may also occur by an iatrogenic cause. To diagnosis, the patient’s
cortisol level, ACTH, glucose should be checked as well as a complete blood count chemistry,
imaging studies and biopsy of the glands may be needed. Treatment will depend on the cause.
If the cause of dysfunction is external glucocorticoid related, treatment should be tapered
slowly. If the cause is due to an internal glucocorticoid dysfunction due to a tumor, surgical
intervention may be needed.
Addison disease is an opposite disorder and is caused primarily by adrenal insufficiency
and secondary to adrenal cortical hyper function. Secondary manifestations may include
hypertension, changes in heart rate, arrythmias, and hypoglycemia. The patient may also
experience lethargy, sluggish movement, and may have GI consequences such as anorexia,
nausea and vomiting after eating, and a craving for salt. These consequences are due to a low
cortisol level. To diagnose, a cause history and physical exam should be completed. Cortisol,
ACTH, and glucose levels should be checked as well as imagining studies of both the adrenal
and pituitary glands. Treatment of Addison’s disease will include lifelong hormonal replacement
via corticosteroids.
Diabetes
Diabetes results from the inability to metabolize glucose resulting in hyperglycemia. It
can be classified into Type 1 diabetes, Type 2 diabetes, or gestational diabetes. Gestational
diabetes may resolve or developed into Type 2 diabetes. A glucose test is most commonly used
to diagnosis diabetes. A glucose challenge test involves checking glucose levels after a length of
time. If the patient present with a glucose level of 126 or higher, this may be used for a
diagnosis of diabetes. A1C is glycated hemoglobin; it is not used to diagnosis diabetes but can
be used as a tool to monitor the progression of the disease. Type 1 diabetes is theorized to be
commonly genetic susceptible. However, it is typically triggered by an illness, viral disease, or
autoimmune disorder. It begins with the destruction of beta cells becoming immunologically
mediated. Type 1 diabetes is characterized as hyperglycemia due to the rapid loss of function in
the beta cells. Diabetes is characterized by three P’s: Polydipsia, Polyuria, Polyphagia- no matter
the type. Polyuria is the direct consequence of having too much glucose in the blood. It involves
having an increased osmolarity resulting in intravascular fluid excess and a need to urinate.
Polydipsia is consequence of polyuria, and polyphagia is when the body does not utilize
glucose. Patients with Type 1 diabetes will start losing fat to be broken down as a source of
energy. This will result in ketosis or ketones in the blood or urine. Type 2 diabetes may affect
adults and children. It characterized by the resistance of target cells to insulin or the inability to
accept insulin and glucose. The risk for developing Type 2 diabetes increases with age. Excessive
weight may facilitate the development of Type 2 diabetes as well as genetics and
environmental factors. Metabolic syndrome is a triad of hypertension, hyperglycemia and
hyperlipidemia. A patient with metabolic syndrome will have increased blood pressure. This
syndrome is referred to as pre-diabetes. If the fasting glucose is 116 to 125, it is considered

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metabolic syndrome and puts the patient at risk for developing diabetes. A patient with type 2
diabetes may experience recurrent infections, vision problems, and neuropathy. These
symptoms are a consequence of end organ damage secondary to hyperglycemia. Treatment
will include exercise, weight loss if needed, medication, and insulin. Hypoglycemia may be a
manifestation of diabetes melitus or occur secondary to an overdose of insulin. It should be
treated rapidly. It can be treated by an oral glucose or glucose agents such as orange juices or
an intravenous injection.
Diabetes ketoacidosis (DKA) is a consequence of a diabetes. It occurs when ketone
bodies are excessively accumulated in the Blood. The patient may become acidotic or even
comatose. Introduction to intravenous insulin as well as intravenous fluids should be
administered in a hospital setting and treated as a medical emergency if DKA occurs.
Hyperosmolar hyperglycemic non-ketonic state is another consequence of diabetes. It
most typically occurs with Type 2 diabetes and is characterized by severe dehydration and
potassium deficit. This occurs when the glucose or hyperglycemia is not under control. When a
patient has continuous hyperglycemia, they may develop a polyol pathway resulting in a
sorbitol and fructose increase as well as an increase in the intracellular osmotic pressure. The
pressure will attract water and cause the cells to burst. This can occur in the eyes, nerves, and
red blood cells. Protein kinase C is a kinase enzyme that will be activated by hyperglycemia and
is the hyperosmotic effect that results in damage to the nerves and red bloods cells secondary
to osmosis.
Patients with diabetes may develop microvascular disease, retinopathy, and diabetes
neuropathy. Retinopathy is due to hyperglycemia. Patients with nephropathy will have
albuminuria secondary to glomerular damage and glomerular unit loss. Diabetes nephropathy
is the number one cause of dialysis placement in Western countries. Retinopathy is the leading
cause of blindness in working age adult sin the United States, secondary to diabetes mellitus.
Primary Retinopathy is caused by damage to the blood vessels in the retina causing swelling
and blockages. Secondary Retinopathy occurs when the patient develops new vascular beds
and the vessels try to combat the damage. This may lead to exacerbation of the disease.
Diabetes can also cause damage to the end organs. Macro vascular disease and endothelial
damage results in coronary artery disease. This is the highest mortality cause for patients with
Type 2 diabetes. The longer patients have Type 2 diabetes, the higher the chance of death from
a cardiac disease. Endothelial damage may result in the development of vascular disease such
as coronary artery disease, stroke, and peripheral artery disease. Neuropathies are quite
common and may lead to other negative consequences such as diabetic foot ulcers. They may
also be caused by a B12 deficiency and are characterized by numbness or tingling. Charcot joint
neuropathy should be addressed by medication and frequent physical checks completed by
healthcare providers and patients. If a patient has diabetes mellitus, he or she will be more
susceptible to neuropathy and infection.

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Gastrointestinal Disorders Part 1

Disorders of the Digestive System

One of the most common disorders of the digestive system is gastrointestinal bleeding.
Bleeding can occur the upper or lower tract. Upper portion of the system include the
esophagus, stomach, and duodenum, and the lower portion is anything below the ligament of
the Treitz including the jejunum, ileum, colon, and rectum. The brighter blood indicates
bleeding in a lower portion of the system. A patient with an upper GI bleed may present with
hematemesis. Hematemesis is characterized by profuse bright red blood vomit. Hematochezia
is blood in the stool. Melena in the stool will have a dark tarry appearance. Pepto-Bismol can
often make the stool black and tarry. When taking a history of a patient who complains of
melena, it is important to ask if they have been taking Pepto-Bismol or other bismuth
preparations. Occult bleeding will not be observed in the stool but will be present on an occult
blood test. Occult bleeding may be due to a bleeding malignancy of colon cancer. Occult
bleeding can be a slow upper GI bleed and may even result from dental disorders. Upper and
lower GI bleeds should be considered medical emergencies because of the risk of perforation,
blood loss, and blood loss anemia. However, occult bleeding is not a medical emergency,
however, it may be present in serious conditions such as cancer. In all cases, a lower and upper
endoscopy should be performed for further evaluation. A diagnostic workup that includes CBC,
RDW, and check for hyperchromic and microcytic anemias, anisocytic cells, MCV, and MCHC.
Dysphasia is difficulty swallowing. It can be caused by mechanical obstruction or
functional obstruction. Mechanical obstruction involves a narrowing of the esophagus by some
type of structure or ring such as a Schatzki ring. A Schatzki ring is a ring of connective tissue that
occurs because of gastroesophageal reflux disease. A malignancy or benign tumor may also
cause obstruction and result in dysphasia. A patient may complain of food getting stuck behind
the sternum or chest pains related to food ingestion.
Achalasia is a very concerning disorder characterized by the denervation of the smooth
muscle in the esophagus and lower esophageal sphincter. The esophagus collapses and turns
into a narrow passage or completely closes. During achalasia, the patient may have a built-up
food bolus that is vomited. If the patient complains of an inability to swallow, they may also
have retch. Fluid may even be difficult to swallow. If untreated, the patient may experience
severe nutritional deficiencies. Botox injection may be used as a possible treatment.
Gastroesophageal reflux disorder is a disorder of motility. It occurs when the food bolus
cannot go down into the stomach, but instead comes back up. It is the reflux of chyme form the
stomach to the esophagus. Chyme is an acidic substance or acidic mix. Reflux may cause stricter
rings, damage and inflammation to the esophagus, as well as predispose the patient for
esophageal malignancy. Inflammation to the esophagus is known as esophagitis. Treatment will
include action to reduce acidity as well as recreate lower esophageal sphincter functioning.

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A hiatal hernia occurs when part of the stomach slides into the chest cavity through the
diaphragm. Most patients with EGD will have some degree of hiatal hernia. A paraoesophageal
hernia occurs when the lower esophageal sphincter does not have a diaphragm around it and
becomes loose resulting in acid to come back up. For both, symptoms of gastroesophageal
reflux disorder will present. Treatment may include a Nissen fundoplication if medication does
not work.
Peptic ulcer disease is the breakage or alteration of the mucosal lining in the esophagus
stomach or duodenum. It can be acute or chronic. The patient may have superficial erosions or
deep through ulcers. Ulcers may perforate and bleed causing peritonitis. In severe cases, the
ulcers may also bleed inside causing an acute GI bleed which should be treated as an
emergency. All cases of peptic ulcer disease are related to H pylori. The mucosa of the ulcer is
destroyed causing some bloody discharge. Ulcers are typically approximately two centimeters
in length. If the ulcer is chronic it may exacerbate and perforate. An H pylori infection, NSAID
abuse, cigarette smoking, and alcohol can all cause ulcers.
Duodenal ulcers are most common ones and will be in the duodenum. They have
several layers. The ulcer crater, mucosa, and submucosa is destroyed and may perforate. H
pylori is a very resilient bacteria that lives in acid and produces toxins and enzymes that
promote inflammation, destruction, and ulceration. Hypersecretion of chloric acid and pepsin
may also occur. NSAID and smoking use may promote hypersecretion of acid. An Esophageal
Gastro Duodenoscopy (EGD) can show the location of the ulcer int eh duodenum. If ulcers
appear and then self-heal, connective tissue will appear resulting in a narrowing or obstruction
in the duodenum causing an inability to pass food. The patient may have related bowel
obstruction that may need surgical intervention.
Gastric ulcers will develop in the antral region due to its adjacent location to the acid
secreting mucosa of the body of the stomach. The antrum does not secret acid but is affected
by the acid. H pylori is the cause due to its mucosal permeability to hydrogen ions. Gastric
secretions will be more normal or less normal. An overproduction of gastrin is due to random
acid attack on the stomach mucosa and antrum of the stomach.
Liver disorders
Liver disorders may cause hepatitis, cirrhosis, and portal hypertension. Portal hypertension is
when the blood pressure in the portal vein or venous system increase due to resistance in the
blood flow. The kidneys can be prehepatic, intrahepatic, and post hepatic. Portal hypertension
may cause esophageal varices. Portal veins reach to the stomach, intestines, spleen, and branch
to the liver. If there is an obstruction in the liver, pressure will build up in all the pre liver
portions of the portal system. This will cause esophageal varices. Hemorrhoids may also occur
as well as splenic congestion or splenomegaly. Ascites and hepatic encephalopathy may also
occur due to the inability to dispose of waste products such as ammonia. Varices can occur in
the stomach, in the rectum as hemorrhoids, and in the lower esophagus. They most commonly
occur n the esophagus. They should be treated as a medical emergency, and open and break

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easily. If an esophageal bleed occurs, they patient could bleed out, vomit, or aspirate. An
esophageal bleed or variceal bleed can be stopped by cauterization and banding of the varices.
Banding techniques may also be applied to treat hemorrhoids in the rectum. Hemorrhoidal
bleeding is easier to stop by conventional methods like prednisone suppositories, surge,
banding, and banding. Hemorrhoidal bleeds are typically not as severe as esophageal bleeds. A
bright red blood will signify an esophageal bleed while a coffee ground emesis will indicate a
bleeding ulcer. Melena (black tarry stools) may represent bleeding from any part of the GI
tract. In addition to banding of the bleeding hemorrhoids and varices, treatment may include
prescription of beta blockers to reduce pressure in the portal system. Because of the increased
pressure in venous system, fluids may seep through the veins and collect in the abdominal
cavity causing ascites. Interventions such as paracentesis may be needed to remove extra the
fluid. Treatment for ascites may include diuretic and diuretics such as Aldactone and Lasix. Lasix
may reduce ascites. Hepatic encephalopathy is a related complication that is secondary to the
buildup of ammonia and other waste materials that results in cognitive changes.
Hepatic liver occurs when toxins have built up and ammonia is more abundant in the
blood flowing to the brain. These neurotoxins result in hepatic failure. Ammonia is not recycled
and will affect brain function. The patient may have changes in personality, confusion, memory
loss, unusual behaviors. The patient become comatose or deceased due the ammonia levels.
Treatment includes lactulose and antibiotics.
Viral Hepatitis. Hepatitis A, B, and C are the most common types of viral hepatitis that
affect the liver. Hepatitis A is passed by fecal oral transmission. The virus may be excreted in
feces, bile or serum and passed by the fecal oral route. It is the most common type of hepatitis
and is more prevalent in areas of crowded unsanitary conditions and places of food and water
contamination. Consuming shellfish from a contaminated water sources may cause the virus
and well as other restaurant outbreaks. Treatment includes palliative care and typically does
not require medication or hospitalization. The disease has a high morbidity rate and a low
mortality rate. A patient who has hepatitis A should stay in isolation and their feces should be
isolated and decontaminated. Patients typically recover on their own. Approximately 10% of
people with liver failure may need further intervention for treatment of hepatitis A. Typically
these individuals already have some type of liver condition due to hepatitis C or cirrhosis.
Hepatitis B is transmitted through contact with blood and body fluid. Maternal
transmission may occur when giving birth. A prevention vaccine is available. Treatment includes
a long antiviral treatment, however, there is no cure of 100% effective treatment for hepatitis
B. The transmission of the virus can occur through blood, body fluid, sexual contact, and
contaminated needles. The nationwide rate of hepatitis B is much lower than hepatitis C.
Hepatitis C is another blood-borne disease. The virus can be passed through many
sources, however sexual contact and body fluids are the most prevalent. The virus may also be
passed through a blood transfusion. Approximately 50% to 80% of hepatitis C will result in
chronic hepatitis. Genotype plays a role in determining if the disease will be chronic. Only

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approximately 20% of individual will develop immunity to hepatitis C on their own. Antiviral
preventions and treatment are available. Hepatitis C may lay dormant and accidentally
discovered during routine blood test. When a patient presents with elevated liver enzymes,
further workup will show that patient has Hepatitis C. A patient with hepatitis C may need to
be referred to a hepatology clinic or gastroenterology clinic for further evaluation and
treatment.
Hepatitis D is rare and requires the presence of Hepatitis B for replication. If Hepatitis B
is not present, Hepatitis D will not develop. Hepatitis E is also very rare in the United States but
may be increasing due to an influx in immigration. Hepatitis E is caused by fecal-oral
transmission. Hepatitis G is a newer strand on hepatitis that may be transmitted from parent to
offspring or sexually transmitted. When a hepatitis infection occurs, typically the course
includes an incubation phase. The incubation phase may differ depending on the type of
hepatitis. A Prodromal phase will also occur. This phase occurs before the patient develops
jaundice. The Preicteric phase or development of jaundice will occur next. The last phase will
include a recovery phase. Patients with chronic Hepatitis B or C may not enter the icteric phase
because this phase is mostly association with Hepatitis A. Some patients with types B and C may
be able to recover without drugs. If these patients due not recover, they risk the development
of chronic hepatitis and the deterioration of the liver. Fulminant hepatitis may occur due the
impaired or neurotic hepatocytes. It may also result form acute liver failure due to a worsening
overdose of Tylenol. If a patient presents with hepatic failure and an acetaminophen overdose,
a liver transplant may be required due to the liver’s small chance to recover.
Cirrhosis is the destruction of the liver function and structure. The function of liver will
be lost, and the liver tissue will become nodular, then fibrotic, and then and fibrosis. There will
be less, and less biliary channels and the liver will become more obstructed causing portal
hypertension. This causes the blood to not travel causing fibrosis to contribute to the
development of necrosis. Cirrhosis is a sequela of either hepatitis or alcohol induced hepatitis.
Cirrhosis is not reversible, even patient stops drinking. Other complications such as biliary
obstruction jaundice, ascites, and hepatic encephalopathy may occur secondary to liver failure.
Only cirrhosis patients who have abstained from alcohol or other sub illicit substances for at
least six months are qualified for a needed liver transplant. Alcohol and drugs are taxing on the
liver and damage hepatocytes. After ingestion of alcohol, the liver enzymes will become
elevated. A cirrhotic liver will not have elevated liver enzymes due to damaged hepatocytes.
Primary Biliary cirrhosis is different disease in which the cirrhosis starts in the bile
ducts. This is an autoimmune disorder. Treatment may include medication or weight control.
The cirrhosis is more common than biliary cirrhosis. Post necrosis is consequence of the chronic
disease and is characterized by a loss of blood supply to the liver.

Pancreatic Disorders

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 Pancreatitis is a disorder of the pancreas that has two major causes: alcohol and
gallstone or cholelithiasis. Both causes result in injury to the pancreatic cells and result in duct
leakage will occur of the enzyme into the pancreatic tissue. Self-digestion of the pancreas will
occur and leak into the blood vessels causing damage locally into other organs. Autoimmune
pancreatitis may occur, but it is very uncommon.
Alcohol is a toxic substance to pancreatic cells and duct. If alcohol has an influx into the
pancreatic duct, it will cause destruction in the area. When cholelithiasis occurs, small gall
stones can go upward through the pancreatic duct and cause a blockage resulting in severe
pancreatitis. ERCP procedure may be recommended to remove the duct obstruction and
release inflammation of the pancreas. Other related treatment will include NPO status or an
effort to not encourage the pancreas to produce any digestive enzymes and intravenous
hydration. Counselling may be recommended for patients with extensive history of alcoholism.

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