EMQs for

Medical Students
Volume 1
Second Edition

Adam Feather FRCP

Charles H Knowles BChir PhD FRCS (Gen Surg)
Paulo Domizio BSc MBBS FRCPath
Benjamin C T Field MBBS BMedSci MSc MRCP
John S P Lumley MS FRCS
Contents

List of contributors vi

Preface vii

Introduction ix

Glossary xi

Normal values xv

Self-assessment EMQ Papers xviii

Chapter 1 General Pathology 3

Chapter 2 Head and Neck 27

Chapter 3 Neurology and Psychiatry 41

Chapter 4 Cardiovascular and Haematology 75

Chapter 5 Respiratory 107

Chapter 6 General 131

Chapter 7 Radiology 145

Answers 163

Index 278
 G E N E R A L PAT H O L O G Y

1. THEME: PATHOLOGICAL PROCESSES

A Apoptosis
B Atrophy
C Dysplasia
D Embolism
E Fibrosis
F Hyperplasia
G Hypertrophy
H Infarction
I Metaplasia
J Metastasis
K Necrosis
L Thrombosis

For each of the patients listed below choose the most appropriate pathological process
from the above list. Each item may be used once, more than once or not at all.

1. A 45-year-old man presents with ‘acid heartburn’. An endoscopy is performed

at which the lower oesophageal mucosa appears red and velvety. A biopsy
taken from this area shows glandular epithelium. 6
2. A 75-year-old man presents with symptoms of urinary outflow obstruction.
Investigations show an enlarged prostate gland. 6
3. A 21-year-old woman sustains a fractured left femur in a road traffic accident
(RTA). She requires traction and is bed-bound for several weeks. On removal of
the traction, the left leg is weak and the left quadriceps is visibly wasted. 6
4. A 32-year-old woman who is taking the oral contraceptive pill boards a flight
from London to San Francisco. On arrival, her right leg feels uncomfortable.
The following day her right calf is swollen and tender. 6
5. A 40-year-old woman has a cervical biopsy following an abnormal cervical
smear. The biopsy shows lack of maturation throughout the whole thickness of
the epithelium. 6
6. A 65-year-old man with long-standing hypertension develops cardiac failure. A
chest radiograph shows enlargement of the heart and an echocardiogram
shows a thickened left ventricular free wall. 6

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2. THEME: CELLS OF THE IMMUNE SYSTEM

A Cytotoxic T lymphocyte
B Dendritic cell
C Helper T lymphocyte
D Langerhans’ cell
E Macrophage
F Mast cell
G Memory B cell
H Natural killer cell
I Plasma cell
J Stem cell
K Virgin B lymphocyte
L Virgin T lymphocyte

For each of the descriptions below, select the cell type from the above list. Each cell may be
used once, more than once or not at all.

1. An antibody-producing cell with an eccentric nucleus, a ‘clock face’ pattern of

nuclear chromatin and a perinuclear halo. 6
2. An antigen-presenting cell that is important in determining the response to
antigen by virgin T lymphocytes. 6
3. A cell bearing CD3 and CD4 molecules on its surface. 6
4. A phagocytic cell containing lysozyme. 6
5. A cell bearing CD8 that recognises processed antigen in association with class
I major histocompatibility complex (MHC) molecules. 6
6. A type of lymphocyte that bears CD56 on its surface and can attack tumour
cells and virally infected cells without the need for prior sensitisation. 6

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3. THEME: COMPONENTS OF ANTIGENS AND

ANTIBODIES
A Epitope
B Fab fragment
C Fc fragment
D Hapten
E Heavy chain
F HLA
G IgA
H IgE
I IgG
J Light chain
K Superantigen
L Variable region

For each of the descriptions below, choose the component of antigen or antibody from the
above list. Each item may be used once, more than once or not at all.

1. The part of an antigen that binds to an antibody. 6

2. The part of an immunoglobulin molecule that is responsible for antigen
binding. 6
3. An immunoglobulin involved in mast-cell degranulation. 6
4. A molecule that must bind to a carrier protein before it can elicit an immune
response. 6
5. A group of molecules, coded for on chromosome 6, which is responsible for
rejection reactions. 6
6. An antigen that can activate T lymphocytes without being processed by
antigen-presenting cells. 6

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EMQs FOR MEDICAL STUDENTS – VOLUME 1

4. THEME: TECHNIQUES IN MOLECULAR MEDICINE

A DNA fingerprinting
B DNA sequencing
C Hybridisation
D Linkage analysis
E Northern blotting
F Polymerase chain reaction (PCR)
G Southern blotting
H Transfection
I Transformation
J Western blotting

The following are all brief descriptions of common molecular techniques used in medical
research. Please select the technique that best fits each description from the above list.
Each technique may be used once, more than once or not at all.

1. The insertion of a gene or genes into mammalian cells. 6

2. A term used for the in-vitro formation of base pairs between nucleic acids. It is
usually used to probe for the presence of a specific sequence of DNA or RNA. 6
3. A method of separating and detecting proteins using a denaturing sodium
dodecyl sulphate (SDS)/polyacrylamide gel. 6
4. An in-vitro technique designed to isolate and amplify small, specific segments
of DNA between 105 and 108 base pairs from insignificant quantities of
template (less than 1 mg) in a short space of time. 6
5. A method used to investigate the possibility that a gene of interest is close to,
and therefore often inherited with, a known genetic marker. 6

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5. THEME: TYPES OF INFLAMMATION

A Acute suppurative
B Basophil-rich
C Caseating granulomatous
D Chronic
E Eosinophil-rich
F Fibrinous
G Histiocytic
H Non-caseating granulomatous

For each disease listed below, please select the type of inflammation characteristic of the
disease from the above list. Each type may be used once, more than once or not at all.

1. Tuberculosis. 6
2. Helicobacter pylori-associated gastritis. 6
3. Rheumatic pericarditis. 6
4. Sarcoidosis. 6
5. Bacterial meningitis. 6
6. Hookworm infection. 6

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6. THEME: MEDIATORS OF ACUTE INFLAMMATION

A Arachidonic acid
B C3b
C E-selectin
D Factor XII
E Histamine
F Intercellular cell adhesion molecule 1 (ICAM-1)
G Interferon-g
H Interleukin 1 (IL-1)
I Lysozyme
J Plasminogen activator
K Prostaglandin E2
L Superoxide anion

For each of the descriptions below, select the correct inflammatory mediator from the
above list. Each mediator may be used once, more than once or not at all.

1. A substance involved in the opsonisation of bacteria. 6

2. A substance released from mast cells that leads to increased vascular
permeability. 6
3. A molecule important in oxygen-dependent bacterial killing. 6
4. A member of the immunoglobulin gene superfamily expressed on endothelial
cells. 6
5. A multifunctional peptide that induces expression of adhesion molecules on
vascular endothelium and acts as an endogenous pyrogen. 6
6. An enzyme that attacks the cell wall of some bacterial species. 6

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7. THEME: INFECTIOUS DISEASES

A Actinomycosis
B Amoebiasis
C Aspergillosis
D Candidiasis
E Cryptosporidiosis
F Falciparum malaria
G Giardiasis
H Leishmaniasis
I Pneumocystis pneumonia
J Schistosomiasis
K Strongyloidiasis
L Toxoplasmosis

For each of the patients below, select the most likely disease from the above list. Each
disease may be used once, more than once or not at all.

1. A 35-year-old man presents with abdominal pain and bloody diarrhoea 1

month after returning from holiday in India. Colonoscopy shows multiple flask-
shaped ulcers throughout the colon. Biopsy of the ulcerated areas shows
periodic acid–Schiff (PAS-)positive trophozoites with ingested red cells in the
ulcer slough. 6
2. A baby presents soon after birth with jaundice and an enlarged liver. He is also
found to have hydrocephalus and choroidoretinitis. A skull radiograph shows
foci of calcification. 6
3. A 35-year-old woman who is receiving chemotherapy for high-grade
lymphoma develops shortness of breath, accompanied by a dry cough. The
chest radiograph shows bilateral reticulonodular shadowing. Sputum culture is
negative. Transbronchial biopsy shows alveoli filled with a foamy eosinophilic
material and numerous boat-shaped organisms that stain positively with a
silver stain. 6
4. A 48-year-old Egyptian man presents with a 6-month history of haematuria.
Cystoscopy shows a polypoid mass in the bladder. Biopsy of the mass shows
granulomatous chronic inflammation around clusters of parasite ova. 6
5. A 30-year-old English journalist who is working in Africa develops fever and
rigors. On examination, she has hepatosplenomegaly. Examination of a blood
film shows parasitised red blood cells. 6
6. A 32-year-old man with acquired immunodeficiency syndrome (AIDS) presents
with a 2-week history of dysphagia. Endoscopy shows white plaques on the
oesophageal mucosa. Biopsy of the plaques shows fungal hyphae and yeast
forms on the mucosal surface. 6

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8. THEME: BACTERIAL INFECTIONS

A Campylobacter jejuni
B Chlamydia trachomatis
C Clostridium difficile
D Clostridium perfringens
E Escherichia coli
F Haemophilus influenzae
G Listeria monocytogenes
H Neisseria meningitidis
I Salmonella typhi
J Staphylococcus aureus
K Streptococcus pneumoniae
L Streptococcus pyogenes

The patients below have all presented with infections. Select the bacterium which is the
most likely cause from the above list. Each organism may be used once, more than once or
not at all.

1. A 21-year-old medical student presents with a 12-hour history of severe

headache, photophobia and pyrexia. Clinical examination shows a petechial
rash over the trunk. Analysis of the cerebrospinal fluid (CSF) shows numerous
neutrophils and Gram-negative cocci. 6
2. A 32-year-old woman presents with a 2-day history of dysuria and frequency. A
Gram stain of a midstream urine specimen shows neutrophils, erythrocytes and
Gram-negative bacilli. Urine culture shows >105 organisms per ml. The
colonies are lactose-fermenting. 6
3. An 84-year-old man being treated for a chest infection in a care-of-the-elderly
ward develops increasingly severe diarrhoea. Sigmoidoscopy shows white
plaques on the mucosal surface. Faecal analysis isolates a toxin that is
cytopathic in cell culture. 6
4. A 57-year-old vagrant woman presents with a 1-week history of productive
cough, pyrexia and worsening shortness of breath. A chest radiograph shows
consolidation of the left lower lobe. A Gram stain of the sputum shows many
neutrophils and Gram-positive diplococci. Sputum culture shows
a-haemolytic, draughtsman-shaped colonies. 6
5. A 32-year-old man develops a wound infection after a right hemicolectomy for
Crohn`s disease. A Gram stain of the exuded pus shows clusters of Gram-
positive cocci. Culture shows coagulase-positive golden-yellow colonies. 6
6. A 45-year-old woman develops diarrhoea and abdominal pain 2 days after
eating fried chicken in a restaurant. A Gram stain of the faeces shows Gram-
negative, motile, spiral-shaped rods. Faecal culture reveals oxidase-positive
colonies. 6

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9. THEME: PATHOGENIC VIRUSES

A Coxsackievirus
B Cytomegalovirus
C Epstein–Barr virus
D Hepatitis C virus
E Herpes simplex virus type 2
F Herpes zoster virus
G Human papillomavirus
H Measles virus
I Parainfluenza virus
J Parvovirus
K Rhinovirus
L Rotavirus

For each disease listed below, select the virus most likely to cause the disease. Each virus
may be used once, more than once or not at all.

1. Genital warts. 6
2. Infectious mononucleosis. 6
3. Croup. 6
4. Aseptic meningitis. 6
5. Diarrhoea in children. 6
6. Subacute sclerosing panencephalitis. 6

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10. THEME: TYPES OF AMYLOID PROTEIN

A AA amyloid
B AL amyloid
C Atrial natriuretic factor
D Amyloid b protein
E b2-Microglobulin
F Calcitonin
G Islet amyloid polypeptide
H Transthyretin

For each of the diseases below select the type of amyloid protein deposited in each disease
from the above list. Each type may be used once, more than once or not at all.

1. Plasma-cell myeloma. 6
2. Alzheimer’s disease. 6
3. Rheumatoid arthritis. 6
4. Type 2 diabetes mellitus. 6
5. Medullary carcinoma of the thyroid. 6

11. THEME: TYPES OF EPITHELIUM

A Pseudostratified ciliated columnar
B Simple columnar
C Simple cuboidal
D Simple squamous
E Stratified cuboidal
F Stratified squamous, keratinising
G Stratified squamous, non-keratinising
H Transitional-cell

For each of the tissues or organs below, select the type of epithelium found in each from
the above list. Each type may be used once, more than once or not at all.

1. Bladder. 6
2. Ectocervix. 6
3. Trachea. 6
4. Pericardium. 6
5. Skin. 6

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12. THEME: ENVIRONMENTAL CARCINOGENS

A Aflatoxin B1
B Arsenic
C Asbestos
D b-Naphthylamine
E Betel nut
F Cigarette smoke
G Cyclophosphamide
H Ionising radiation
I Nitrosamines
J Polychlorinated biphenyls
K Ultraviolet light
L Vinyl chloride

For each of the tumours below, select the most likely causative carcinogen from the above
list of options. Each agent may be used once, more than once or not at all.

1. Malignant melanoma of the skin. 6

2. Squamous-cell carcinoma of the lung. 6
3. Transitional-cell carcinoma of the bladder. 6
4. Hepatocellular carcinoma. 6
5. Adenocarcinoma of the stomach. 6
6. Papillary carcinoma of the thyroid. 6

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 ANSWERS TO CHAPTER
– GENERAL PATHOLOGY 1
1. PATHOLOGICAL PROCESSES
1. I – Metaplasia
Metaplasia is a change in cell type from one fully differentiated form to another fully
differentiated form. It is usually a protective response to chronic irritation or cell
damage, the new cell type being more able to withstand the irritating agent than the
original. A common cause of ‘acid heartburn’ is gastro-oesophageal reflux, during
which gastric acid refluxes from the stomach into the lower oesophagus. The
oesophagus is normally lined by stratified squamous epithelium. This type of
epithelium cannot easily withstand the damage caused by gastric acid and so meta-
plasia occurs to gastric-type glandular epithelium, which is better able to bear the
damage. Endoscopically, the metaplastic mucosa has a red, velvety appearance, in
contrast to the smooth, white appearance of normal oesophageal epithelium. This
condition is known as ‘Barrett’s oesophagus’. In common with many other metaplastic
conditions, Barrett’s oesophagus is associated with an increased risk of malignancy.

2. F – Hyperplasia
Hyperplasia is an increase in the number of cells in a given cell population. In contrast,
hypertrophy is an increase in the size of cells without an increase in number.
Hyperplasia is usually hormonally driven, while hypertrophy occurs in response to an
increased workload. Prostatic enlargement in men is common with increasing age. The
growth is hormonally driven and involves an increase in cell number rather than cell
size. The process is therefore hyperplasia rather than hypertrophy.

3. B – Atrophy
Atrophy is a decrease in the size of cells, tissues or organs, often leading to a loss of
function. Lack of use of striated muscles, which often occurs in patients who are bed-
bound, leads to shrinkage in the size of myocytes and to loss of muscle bulk. This is
known as ‘disuse atrophy’.

4. L – Thrombosis
Thrombosis is the formation of an intravascular mass from the constituents of blood in
a flowing circulation. Factors that predispose to the development of thrombosis include
prolonged immobility, as occurs during long-distance flights, and the oral contra-
ceptive pill. Susceptible patients on transatlantic flights can develop thrombosis in
deep calf veins, which manifests as a swollen painful calf.

5. C – Dysplasia
The term ‘dysplasia’ literally means abnormal growth, but it is most often used to
describe failure of normal maturation of an epithelium, with partial expression of a
neoplastic phenotype. In a cervical biopsy this is recognised as large pleomorphic
nuclei above the basal layer. This condition is known as ‘cervical intraepithelial
neoplasia’ (CIN) and is graded 1–3 according to the severity of the abnormality.
Dysplasia is a premalignant condition.

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6. G – Hypertrophy
As described above, hypertrophy is an increase in the size of cells without an increase
in number and usually occurs in response to an increased workload. In patients with
hypertension, the heart has to pump against increased vascular resistance and its
workload is therefore increased. The consequent increase in size of the cardiac
myocytes leads to left ventricular hypertrophy and enlargement of the heart.

2. CELLS OF THE IMMUNE SYSTEM

1. I – Plasma cell
Memory B cells and plasma cells are both fully differentiated B lymphocytes. Memory
B cells maintain memory of the encounter with the antigen and become activated if the
antigen is encountered again, while plasma cells produce and secrete antibody to a
specific antigen. Plasma cells have a single, eccentrically placed nucleus, in which the
chromatin is peripherally aggregated at the nuclear membrane, giving a ‘clock face’
appearance. They also have a perinuclear halo, the site of the Golgi apparatus, and
basophilic cytoplasm, indicating abundant RNA secretion.

2. B – Dendritic cell
Dendritic cells and macrophages are both antigen-presenting cells. Dendritic cells are
so-named because of their irregular shape and numerous dendritic processes.
Dendritic cells play an important role in establishing the first-time response to an
antigen by ‘virgin’ T lymphocytes and, like other antigen-presenting cells, express high
surface levels of class II major histocompatibility complex (MHC) molecules, which
augment antigen presentation.

3. C – Helper T lymphocyte
The CD4 molecule is a transmembrane glycoprotein found on the surface of both
macrophages and helper T lymphocytes, although the concentration is considerably
lower in macrophages. This molecule interacts with class II MHC molecules on
antigen-presenting cells and increases the affinity of binding. The CD3 complex, on the
other hand, is expressed only in T cells and is an absolute requirement for T-cell
function. It acts as a signal transducer for the T-cell receptor to initiate T-cell activation.

4. E – Macrophage
Macrophages act not only as antigen-presenting cells but also as phagocytes and are
therefore important in bacterial killing. Lysozyme is an enzyme that attacks the
bacterial cell wall (see answer 6, Theme: Mediators of acute inflammation, page 171)
and is found within lysosomes in macrophage cytoplasm.

5. A – Cytotoxic T lymphocyte
T lymphocytes that express the CD8 molecule are called cytotoxic T cells. Like CD4,
the CD8 molecule is also a transmembrane protein. Its function is to bind with class I
MHC molecules on cells, thereby stabilising T-cell interactions with cells presenting
antigen through the class I MHC molecule.

6. H – Natural killer cell

Natural killer (NK) cells are cells that resemble lymphocytes morphologically but
which represent a separate lineage from B lymphocytes and T lymphocytes. NK cells

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carry two distinct surface molecules, CD16 and CD56, though the function of these is
unknown. NK cells can kill target cells such as tumour cells and virally infected cells
without previous known sensitisation to the target, in contrast to cytotoxic T cells,
which can also kill target cells but require prior exposure.

3. COMPONENTS OF ANTIGENS AND ANTIBODIES

1. A – Epitope
An antigen is the structure that generates a response by the immune system. An
antibody is a glycoprotein that recognises an intact antigen. The precise part of the
antigen bound by antibody is called the ‘epitope’. This region of the antigen determines
which antibody will bind and so is also referred to as an ‘antigenic determinant’.

2. B – Fab fragment
Treatment of an immunoglobulin molecule with the proteolytic enzyme papain cleaves
it into three fragments. Two of the fragments are identical and each contains an intact
light chain and part of one heavy chain. These fragments can bind to antigen and so are
known as the ‘Fab’ (fragment antigen binding) fragments. The third fragment is
composed of part of both heavy chains. It cannot bind to antigen but is easily crys-
tallised and so is called the ‘Fc’ (fragment crystallisable) fragment. It is the site of
important functions such as complement activation and adherence to specific
receptors on the surface of neutrophils and macrophages.

3. H – IgE
Immunoglobulin E (IgE) is present at extremely low levels in the serum of normal indi-
viduals but is increased in individuals who are atopic or in patients with allergies and
type I (immediate) hypersensitivity. IgE is also raised in response to parasitic infections.
The main effector function of IgE is to bind to mast cells through Fc receptors on the
surface of the mast cell and to activate them. Activation causes mast-cell degranulation,
which results in potent localised, and occasionally generalised, vascular effects.

4. D – Hapten
Some molecules are too small to act as antigens themselves. Such molecules, known as
‘haptens’, can only elicit an immune response when bound to carrier proteins. In the
resulting hapten–carrier complex, the hapten acts as an epitope. The antibodies formed
against this complex can react specifically in solution with the free hapten (eg in sensi-
tivity reactions to certain drugs).

5. F – HLA
The MHC is a collection of genes that code for proteins involved in immune functions
such as recognition of antigen by T lymphocytes. The human MHC system is also called
the ‘human leucocyte antigen’ or ‘HLA’ system and is coded for on chromosome 6,
where there are six loci, three for class I antigens (A, B and C) and three for class II
antigens (DP, DQ and DR). Class I molecules are expressed on virtually all nucleated
cells, whereas class II molecules are found only on antigen-presenting cells and B
lymphocytes. HLA molecules are the dominant group of antigens governing transplant
rejection reactions.

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6. K – Superantigen
A few antigens can bind to MHC class II proteins without first being processed by
antigen-presenting cells. These are known as ‘superantigens’. They are implicated in
several disorders, including rabies, acquired immunodeficiency syndrome (AIDS), and
acute T-lymphocyte responses to certain bacterial exotoxins such as those of
Staphylococcus aureus, which are responsible for toxic shock syndrome.

4. TECHNIQUES IN MOLECULAR MEDICINE

1. H – Transfection
Transfection is a method of putting genes into mammalian cells. The term arose
because the transfer of genes is similar to viral infection. In contrast, bacterial cells are
said to be ‘transformed’ because in a classic experiment non-pathogenic bacteria were
made pathogenic by adding a ‘transforming principle’. Both cell types spontaneously
pick up DNA, but efficiency is very low. Selection and screening techniques allow
‘stable’ transfectants to be detected.

2. C – Hybridisation
Hybridisation is the formation of base pairs between nucleic acids. The term was origi-
nally restricted to the formation of hybrid double-stranded molecules, as in a northern
blot, where DNA/RNA hybrids are formed. Typically, a mixture of nucleic acids is
resolved on a gel, blotted onto nitrocellulose, and the blot is hybridised with a labelled
(easily detectable) piece of DNA or RNA – the ‘probe’. The probe sticks to its comple-
mentary strand, the blot is then washed to remove unbound and non-specifically
bound probe, and the remaining probe is then detected (usually by using radioactive
labelling and autoradiography). A modification of the technique can be used in situ to
detect the presence of mRNA in tissues.

3. J – Western blotting
‘Blotting’ is a descriptive term for the transfer of molecules out of a gel and onto a filter
membrane by a wicking action, although the term is now used for electro- or vacuum
transfers. In the original description of blotting, Dr Edwin Southern developed the tech-
nique to make the gel-resolved nucleic acid DNA more accessible to subsequent
manipulation, such as identification by hybridisation – ‘Southern blotting’. Northern
and western blotting followed the original nomenclature (perhaps not very helpfully).
In western blotting, proteins are separated on a gel, blotted, and then probed with anti-
bodies to detect the specific protein of interest. Northern blotting is the similar sepa-
ration and blotting of RNA.

4. F – Polymerase chain reaction

The polymerase chain reaction (PCR) is still a relatively new technique that has revolu-
tionised many aspects of molecular biology. It amplifies DNA to produce adequate
amounts for subsequent use. In principle, two synthetic oligonucleotide primers are
designed, which are typically 20–25 nucleotides long, and flank the DNA segment to
be amplified. These primers, orientated 5’ to 3’, are hybridised to opposite strands of
the target sequence and extended using DNA polymerase until the region between the
two primers is completely replicated. Initial hybridisation of the two oligonucleotides
requires heat denaturation of the double-stranded DNA template. The temperature is
then lowered to an optimum at which primers anneal to their complementary

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sequences. Finally, polymerase elongation, again requiring an optimal temperature,

completes the synthesis, which effectively results in doubling the concentration of the
target DNA segment. This cycle is repeated 25–35 times using commercially available
thermal cyclers.

5. D – Linkage analysis
If the only information available about a gene is the phenotype that it produces (eg a
disease or characteristic), the gene can be demonstrated to lie near to a chromosomal
region containing an established marker (usually a restriction-length polymorphism or
another gene whose genomic position is known), that therefore tends to be inherited
with it. The region of interest can then be examined for the presence of a candidate
gene causing the disorder or characteristic in question and the exact mutation can then
identified by other techniques such as direct DNA sequencing.

5. TYPES OF INFLAMMATION
1. C – Caseating granulomatous
Tuberculosis is the archetypal granulomatous disease. The granulomas are composed
of histiocytes, a Langhans-type multinucleate giant cell and a peripheral rim of
lymphocytes. Typically there is central caseating necrosis. The terms ‘caseating’ or
‘caseous’ are used when the necrosis appears soft and ‘cheesy’ macroscopically and
structureless histologically.

2. D – Chronic
Helicobacter pylori causes a chronic gastritis with numerous lymphocytes and plasma
cells in the lamina propria. Often there are also numerous lymphoid follicles.
Neutrophils are commonly seen within surface and gland epithelium, in which case
the term ‘active chronic gastritis’ is used, but they are never the predominant T cell as
they would be in acute gastritis.

3. F – Fibrinous
Fibrinous pericarditis is the most common pathological type of pericarditis. Common
causes include acute myocardial infarction, uraemia, rheumatic fever and systemic
lupus erythematosus (SLE). In fibrinous pericarditis the surface is dry with a fine
granular roughening. At autopsy, the strands of fibrin on the surfaces of the parietal and
visceral pericardium pull apart like two pieces of buttered bread, giving rise to the term
‘bread and butter’ pericarditis. A pericardial friction rub is the most striking clinical
feature. The development of a pericardial effusion can obliterate the friction rub by
separating the two layers of pericardium.

4. H – Non-caseating granulomatous
Like tuberculosis, sarcoidosis is a granulomatous multisystem disease but, in contrast
to tuberculosis, the granulomas are not caseating. This feature can be helpful in
distinguishing pulmonary tuberculosis from pulmonary sarcoid in lung biopsies, but
cannot be completely relied upon because tuberculosis occasionally causes non-
caseating granulomas.

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5. A – Acute suppurative
In bacterial meningitis, the subarachnoid space contains a creamy, purulent acute
inflammatory exudate that is rich in neutrophils. The cerebrospinal fluid (CSF), which
circulates in the subarachnoid space, is therefore turbid and shows numerous
neutrophils on microscopic examination. This contrasts with viral meningitis, in which
the CSF contains scattered lymphocytes but no neutrophils.

6. E – Eosinophil-rich
Eosinophils play an important role in defence against parasitic infestation. Tissue and
blood eosinophilia is often seen in such infections. Hookworm larvae penetrate
human skin and pass in the bloodstream to the lungs, where they can cause an
eosinophilic pneumonia. From the lungs the larvae ascend through the bronchi into
the pharynx and are then swallowed, ending up in the small intestine, where they
mature into adult worms. The adults ‘suck’ blood from the small-intestinal mucosa,
causing an iron-deficiency anaemia.

6. MEDIATORS OF ACUTE INFLAMMATION

1. B – C3b
Opsonisation is one of the steps involved in the phagocytosis of bacteria by
macrophages and neutrophils. Bacteria coated with certain substances are ingested
more readily. The factors that coat bacteria are called ‘opsonins’ (from the Greek
opson, ‘ready for eating’) and the process is known as ‘opsonisation’. There are two
main opsonins: immunoglobulin (IgG) and the C3b component of complement. There
are receptors for both these opsonins on the cell surface of phagocytic cells.
Opsonised fragments attach to the phagocytic cell and are internalised to become
phagosomes. Lysosomes fuse with the phagosome and release proteolytic enzymes
that kill the bacteria.

2. E – Histamine
Histamine is a vasoactive amine that is stored in and released from mast cells,
basophils and platelets. It causes vasodilation and increases the permeability of
venules. The action of histamine on vessels is mediated via H1 receptors, while some of
its other actions, such as bronchoconstriction, are effected by H2 receptors. Factors that
stimulate histamine release include physical injury from heat, mechanical trauma or
radiation, and chemical agents, such as immunoglobulins, bee-sting venom, C3a and
C5a, and interleukin 1 (IL-1). Anti-H1 antihistamines only inhibit the immediate phase
of the vascular response to injury, meaning that histamine is only important during this
early phase.

3. L – Superoxide anion
After an invading bacterium has been phagocytosed, its killing involves oxygen-
dependent and oxygen-independent mechanisms. The oxygen-dependent mechanism
is associated with a burst of oxidative activity known as the ‘respiratory burst’. This
essentially results in the stepwise reduction of molecular oxygen into an oxygen-free
radical, the superoxide anion, and then to hydrogen peroxide. Phagocytes cannot kill
ingested organisms in the absence of the respiratory burst and without production of
the superoxide anion. Indeed, lack of one of the enzymes involved in this process,
nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, leads to chronic

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granulomatous disease of childhood, an inherited disease in which neutrophils are able

to ingest bacteria but cannot kill them.

4. F – Intercellular cell adhesion molecule 1 (ICAM-1)

The immunoglobulin gene superfamily is a group of intercellular adhesion molecules
so named because each contains several domains resembling the structure of
immunoglobulins. Three such molecules have been identified: intercellular cell
adhesion molecules 1 and 2 (ICAM-1 and ICAM-2) and vascular cell adhesion
molecule (VCAM-1). ICAM-1 is expressed at low levels normally but its expression is
increased in acute inflammation by stimulants such as IL-1. Leucocytes bind to ICAM-
1 through ligands on their surface known as ‘integrins’.

5. H – Interleukin 1 (IL-1)
IL-1 is a potent regulator of both local inflammatory events and a number of systemic
ones. Many of its activities are similar to those of tumour necrosis factor alpha (TNFa).
The synthesis of IL-1 is stimulated by other cytokines and by various microbial
products, such as bacterial endotoxin. Locally, it upregulates expression of ICAM-1,
increasing leucocyte adhesion, it stimulates release of histamine and stimulates
macrophages to produce chemokines. Systemically, IL-1 acts as an endogenous
pyrogen (ie it produces fever), induces glucocorticoid synthesis and stimulates the
release of prostaglandins and acute-phase proteins.

6. I – Lysozyme
Lysozyme is a low-molecular-weight cationic enzyme that attacks the mucopeptide
cell walls of some bacterial species, particularly Gram-positive cocci. It is found in
lysosomes and is one of the oxygen-independent mechanisms of bacterial killing.

7. INFECTIOUS DISEASES
1. B – Amoebiasis
Infection with Entamoeba histolytica causes amoebiasis. Both this and schistosomiasis
can lead to colonic ulceration, but in schistosomiasis the ulcers are not typically flask-
shaped. The finding of periodic acid–Schiff (PAS-)positive trophozoites with ingested
red cells is diagnostic of amoebiasis.

2. L – Toxoplasmosis
Congenital toxoplasmosis is caused by maternal infection with Toxoplasma gondii in
the first trimester. In normal adults, this parasite causes subclinical infection or mild
lymphadenopathy, but in infants, who have not developed cell-mediated immunity,
infection leads to severe abnormalities. There is widespread necrosis of the brain,
liver, heart, lungs and retina. Calcification can occur in foci of long-standing necrosis
in the brain.

3. I – Pneumocystis pneumonia
Pneumocystis carinii is an ubiquitous organism that does not cause disease in normal
individuals but causes a severe pneumonia in immunosuppressed patients, including
those on chemotherapy. The organism cannot be grown in culture, so diagnosis requires
cytological or histological identification. Useful cytological preparations include
bronchial washings or lavage. Transbronchial biopsy shows foamy eosinophilic material

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in the alveolar spaces. On both cytology and histology the organism is seen as a boat-
shaped or cup-shaped structure on silver staining.

4. J – Schistosomiasis
Infection with Schistosoma haematobium is endemic in parts of the Middle East and
Africa. Biopsy of the infected bladder shows parasite ova surrounded by granulo-
matous inflammation and numerous eosinophils. Healing by fibrosis leads to ureteric
obstruction, with consequent hydronephrosis and chronic pyelonephritis. There is
also an association between urinary schistosomiasis and squamous-cell carcinoma of
the bladder.

5. F – Falciparum malaria
Malaria is caused by four species of Plasmodium parasites and is transmitted by the
female Anopheles mosquito. Falciparum malaria is caused by Plasmodium falciparum
and is the most common type. The signs, symptoms and pathological features of
malaria are related to the sequelae of various aspects of the parasite’s life cycle in man.
It is diagnosed by finding ring trophozoites inside red cells on a blood smear.

6. D – Candidiasis
The finding of fungal hyphae in this patient’s biopsy is diagnostic of fungal
oesophagitis. The differential diagnosis lies between aspergillosis, caused by
Aspergillus species, and candidiasis caused by Candida species, usually Candida
albicans. The fact that yeast forms were also present rules out Aspergillus as this is not a
yeast-forming fungus. In addition, the endoscopic appearance of white plaques on the
mucosal surface is typical of candidiasis. This disease is common in immunosup-
pressed patients such as those with AIDS.

8. BACTERIAL INFECTIONS
1. H – Neisseria meningitidis
This patient has bacterial meningitis. The two most likely causes from the list are
Neisseria meningitidis (meningococcus) and Streptococcus pneumoniae (pneumo-
coccus). The petechial rash is characteristic of meningococcal septicaemia. This is
confirmed by finding Gram-negative cocci on CSF examination.

2. E – Escherichia coli
The patient’s symptoms and findings on urinalysis are typical of urinary tract infection.
Escherichia coli is the cause of 60–90% of urinary tract infections. This organism is a
normal commensal of the large intestine and in women enters the urinary tract by
direct spread up the urethra from the perineum. E. coli is a Gram-negative, lactose-
fermenting bacillus

3. C – Clostridium difficile
This patient has a complication of antibiotic therapy, namely pseudomembranous
colitis. The finding of white plaques on the large-bowel mucosa is characteristic of this
disease. The causative organism is a toxigenic strain of Clostridium difficile, an
anaerobic Gram-positive bacillus. C. difficile produces two toxins: toxin A is an entero-
toxin that is responsible for the gastrointestinal symptoms; toxin B is a cytotoxin that
has a cytopathic effect in cell cultures.

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4. K – Streptococcus pneumoniae
This patient is suffering from lobar pneumonia. Vagrants and alcoholics who have poor
social and medical care are particularly prone to this type of pneumonia. The causative
organism in approximately 90% of cases is Streptococcus pneumoniae. These occur as
Gram-positive diplococci, which show alpha-haemolysis on blood agar. The colonies
are typically described as draughtsman-shaped on account of their sunken centre.

5. J – Staphylococcus aureus
Wound infection is an important cause of postoperative sepsis. The most common
cause is Staphylococcus aureus, but other possible organisms include Streptococcus
pyogenes, particularly when there is associated cellulitis, and Escherichia coli when the
wound follows abdominal surgery. In this patient, Gram stain of the pus from the
wound shows Gram-positive cocci, ruling out E. coli. S. aureus and S. pneumoniae are
both Gram-positive cocci, but the finding of coagulase-positive organisms is diagnostic
of S. aureus.

6. A – Campylobacter jejuni
Campylobacter species, particularly Campylobacter jejuni, are now recognised as a
major cause of diarrhoeal disease in the UK. Common sources of infection are poultry,
meat and milk. C. jejuni is a Gram-negative curved or spiral-shaped rod. It is a flagellate
organism and therefore highly motile. This feature distinguishes it from enteropatho-
genic strains of E. coli, which are also Gram-negative rods but are non-flagellate.

9. PATHOGENIC VIRUSES
1. G – Human papillomavirus
Warts are benign tumours of squamous epithelium and are known as ‘squamous-cell
papillomas’. They arise not only in keratinised squamous epithelium, such as the skin,
but also in non-keratinised squamous epithelium such as that lining the ectocervix. All
warts are caused by human papillomavirus (HPV), a DNA virus belonging to the papo-
vavirus family. There are many serotypes of HPV. Genital warts are sexually transmitted
and are caused by HPV types 6 and 11. Other serotypes, notably 16, 18 and 31 have
been implicated in the development of high-grade cervical intraepithelial neoplasia
and invasive cervical carcinoma.

2. C – Epstein–Barr virus
Infectious mononucleosis is a multisystem disorder caused by Epstein–Barr virus (EBV).
This is a DNA virus belonging to the herpesvirus family. Diagnosis of infectious
mononucleosis is made by finding heterophil antibodies to sheep erythrocytes in the
patient’s serum. As well as causing infectious mononucleosis, EBV has a strong associ-
ation with certain human malignancies, particularly Burkitt’s lymphoma and nasopha-
ryngeal carcinoma.

3. I – Parainfluenza virus
Croup or acute laryngotracheobronchitis, is most commonly associated with parain-
fluenza virus type 1. This is an RNA virus belonging to the Paramyxovirus family. Croup is
seen mainly in infants and young children, and the symptoms include hoarseness, cough
and inspiratory stridor. As well as croup, parainfluenza viruses are associated with bron-
chiolitis and pneumonia in young children and with the ‘common cold’ in adults.

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4. A – Coxsackievirus
In ‘aseptic’ meningitis, the CSF contains lymphocytes rather than neutrophils and CSF
culture is negative. Aseptic meningitis is usually due to viruses of the Enterovirus group,
of which coxsackievirus is a member. Enteroviruses are RNA viruses that belong to the
picornavirus family. Other enteroviruses that cause aseptic meningitis include
echovirus and poliovirus.

5. L – Rotavirus
Viruses are an important cause of acute diarrhoea, particularly in children. In the devel-
oping world, viral gastroenteritis is a major cause of infant mortality but the condition is
less severe in the UK. A common cause of viral gastroenteritis is rotavirus, an RNA virus
that belongs to the Reovirus family. Other causes include adenovirus and astrovirus.

6. H – Measles virus
Subacute sclerosing panencephalitis is a rare, severe, progressive neurological disease
that occurs in children and young adults. It presents with personality change and intel-
lectual impairment, followed by convulsions and myoclonic movements, and even-
tually leads to coma and death. It is caused by persistent infection with defective
measles virus following a primary measles infection several years previously. Measles is
an RNA virus that belongs to the Paramyxovirus family.

10. TYPES OF AMYLOID PROTEIN

1. B – AL amyloid
Amyloid deposited in this disease is often systemic in distribution and is of the AL type.
The malignant plasma cells produce abnormal amounts of monoclonal
immunoglobulin, either the whole molecule or just the light chains, usually of one
type. These light chains are referred to as Bence Jones protein and are found in the
serum and urine of patients with plasma-cell myeloma and other monoclonal B-cell
proliferations. Around 5–15% of patients with plasma-cell myeloma who have free
light chains develop clinical amyloidosis.

2. D – Amyloid b protein
Amyloid beta protein (Ab) is a 4000-dalton peptide that constitutes the core of cerebral
plaques found in Alzheimer’s disease as well as the amyloid deposited in the walls of
cerebral blood vessels in patients with this disease. The Ab protein is derived from a
much larger transmembrane glycoprotein called ‘amyloid precursor protein’ (APP), the
function of which is unknown.

3. A – AA amyloid
The amyloid deposits in this condition are systemic in distribution and are composed of
AA protein. This is derived from serum amyloid A (SAA), an acute-phase protein synthe-
sised by the liver in a number of chronic inflammatory conditions such as rheumatoid
arthritis, tuberculosis, chronic osteomyelitis, bronchiectasis and inflammatory bowel
disease. Nowadays, rheumatoid arthritis is the most commonly associated condition.
Amyloidosis occurs in about 3% of patients with rheumatoid arthritis and is clinically
significant in about half of those affected.

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4. G – Islet amyloid polypeptide

Islet amyloid polypeptide (IAPP), also known as ‘amylin’, is a 37-amino-acid peptide
that is normally produced by the b-cells of the islets of Langerhans and is co-secreted
with insulin. In patients with type 2 diabetes mellitus, this protein accumulates in the
sinusoidal space outside the b-cells, in close contact with their cell membranes. It is
not known whether deposition of IAPP actually contributes to the pathogenesis of the
disease or if it is a consequence of disordered b-cell function.

5. F – Calcitonin
Medullary carcinoma of the thyroid is one of the endocrine tumours in which localised
deposits of amyloid can be found in the stroma, other examples being phaeochromo-
cytoma and islet-cell tumours of the pancreas. The amyloid in medullary carcinoma is
derived from the peptide hormone calcitonin, which is secreted by the tumour cells.

11. TYPES OF EPITHELIUM

1. H – Transitional-cell
Transitional-cell epithelium is a special form of stratified epithelium that is only found
in the urinary tract and so is also called ‘urothelium’. It is specialised to withstand the
toxicity of urine and to accommodate a high degree of stretching. It has an appearance
intermediate between that of stratified cuboidal epithelium and stratified squamous
epithelium, hence ‘transitional’.

2. G – Stratified squamous, non-keratinising

Stratified squamous epithelium is usually several layers thick and matures progressively
from the basal layer, which has cuboidal-shaped cells, through to the surface layer,
where the cells are flattened. When the maturing cells reach the surface, they degen-
erate and eventually slough off. Ectocervical epithelium can withstand moderate
abrasion because of its thickness but is not keratinised as it does not normally need to
withstand desiccation.

3. A – Pseudostratified ciliated columnar

The trachea is lined by pseudostratified ciliated columnar epithelium, also known as
‘respiratory epithelium’. This is actually a true simple epithelium because all the cells
rest on the basement membrane, but the nuclei of the cells are at different levels, giving
a false impression of stratification. The luminal surface of the cells bears cilia, the
function of which is to propel surface films of mucus or fluid in a consistent direction
over the epithelial surface.

4. D – Simple squamous
Simple squamous epithelium consists of a single layer of flattened cells and is found
lining surfaces involved in the transport of gases, namely the alveoli, and fluids (ie
lymphatics and blood vessels). It also lines the serous body cavities, such as the peri-
cardium, pleura and peritoneum, where it is known as ‘mesothelium’. Mesothelium
permits the passage of a small amount of fluid into and out of the cavities as required.

5. F – Stratified squamous, keratinising

Like the cervix, the skin is lined by stratified squamous epithelium. Unlike the cervix,
however, the skin is keratinised as it must be able to withstand desiccation.

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12. ENVIRONMENTAL CARCINOGENS

1. K – Ultraviolet light
The ultraviolet (UV) portion of the solar spectrum can be divided into three wave-
length ranges: UVA (320–400 nm), UVB (280–320 nm) and UVC (200–280 nm). Of
these, UVB is believed to be responsible for the induction of cutaneous neoplasms,
including malignant melanoma, squamous-cell carcinoma and basal-cell carcinoma.
The carcinogenicity of UVB is attributed to its formation of pyrimidine dimers in DNA.
This type of damage is repaired by the nucleotide excision repair pathway. With
excessive sun exposure, this pathway is overwhelmed, and so some damaged DNA
remains unrepaired. This leads to transcriptional errors and subsequent development
of malignancy.

2. F – Cigarette smoke
Cigarette smoke contains a number of carcinogens, including polycyclic aromatic
hydrocarbons, which are among the most potent carcinogens known. They are acti-
vated by mixed-function oxidases to form epoxides, which are more water soluble and
more reactive than the parent compound. Epoxides bind to DNA, causing mutations,
and also to macromolecules in the cytoplasm of target cells.

3. D – b-Naphthylamine
Beta-naphthylamine has been responsible in the past for an increased incidence of
bladder cancer in workers in the aniline dye and rubber industries. By itself, b-naph-
thylamine is not carcinogenic, but after absorption it is hydroxylated in the liver to an
active form before being detoxified by conjugation with glucuronic acid. This non-toxic
compound is excreted by the kidney and concentrated in the bladder. The human bladder
mucosa contains the enzyme b-glucuronidase, which cleaves the non-toxic substance
and in so doing releases the carcinogenic molecule.

4. A – Aflatoxin B1
Aflatoxin B1 is a naturally occurring carcinogen that is produced by some strains of
Aspergillus flavus that thrive on improperly stored grains and peanuts. A strong corre-
lation has been found between the dietary level of this toxin and the incidence of hepa-
tocellular carcinoma in certain parts of Africa and the Far East. It appears that synergy
exists between aflatoxin and chronic hepatitis B virus infection. Aflatoxins produce a
point mutation at codon 249 of the TP53 gene, leading to production of an abnormal
gene product.

5. I – Nitrosamines
Like b-naphthylamine, nitrosamines require metabolic activation to form a carcino-
genic agent. In the course of this activation, alkylating agents are produced that bind to
guanine in DNA, thereby enhancing malignant transformation. Nitrosamines are
formed in the gastrointestinal tract from the reaction of nitrostable amines and nitrites.
Nitrites are present in large amounts in pickled, salted and smoked foods, and the inci-
dence of gastric carcinoma is high in countries such as Japan, where there is a high
dietary intake of these foods. In addition, nitrites can be formed in the stomach from
nitrates (found in food preservatives) by the action of bacteria.

6. H – Ionising radiation
There is an increased risk of carcinoma of the thyroid in people who have had
ionising radiation to the neck, particularly in childhood. This ionising radiation can

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be therapeutic, such as treatment for head and neck tumours, or environmental, such
as the nuclear explosions at Hiroshima and Nagasaki or the nuclear accident at
Chernobyl. The mechanisms by which ionising radiation induces malignancy are
unclear. Irradiation leads to the generation of free radicals and these active chemical
species might react with elements of the target-cell genome.

13. VIRAL AND MICROBIAL CARCINOGENS

1. G – Human papillomavirus
Human papillomaviruses (HPV) have been implicated in the genesis of several malig-
nancies, particularly squamous-cell carcinoma of the cervix and anogenital region.
Approximately 85% of squamous-cell carcinomas of the cervix contain DNA
sequences of HPV, most commonly types 16 and 18. Studies have shown that the E6
and E7 proteins of HPV disable two important tumour-suppressor proteins that regulate
the cell cycle, thereby initiating the carcinogenetic process. Additional somatic muta-
tions, caused by co-factors such as smoking, co-existing microbial infections or
hormonal changes then complete the malignant transformation.

2. D – Helicobacter pylori
Primary gastric lymphoma is a low-grade B-cell lymphoma that is strongly associated
with Helicobacter pylori infection. It arises in mucosa-associated lymphoid tissue
(MALT), and so is also known as ‘MALToma’. Unlike small-intestinal mucosa, the
normal gastric mucosa lacks MALT and acquires it only as a result of chronic infection,
such as with H. pylori. Initially, this MALT is a polyclonal B-cell proliferation, but with
continued infection, a monoclonal population emerges that is recognisable as a low-
grade B-cell lymphoma. Even at this stage, eradication of H. pylori with antibiotics can
result in regression of the tumour as the stimulus for MALT production is removed.
Eventually, however, the tumour becomes H. pylori-independent and behaves like a
typical lymphoma.

3. F – Human herpesvirus type 8

Kaposi’s sarcoma is a vascular tumour that is common in patients with AIDS but is rare
in the rest of the population. The association with human herpesvirus type 8 (HHV-8) is
now firmly established, although the precise role the virus plays in the pathogenesis of
the tumour is unclear. DNA of HHV-8 is found both in tumour cells and in circulating
B lymphocytes of affected patients. It is thought that these, together with human
immunodeficiency virus (HIV-)infected T lymphocytes, produce a variety of cytokines
and growth factors that stimulate proliferation of mesenchymal cells, followed even-
tually by neoplastic transformation.

4. E – Hepatitis B virus
The evidence linking hepatitis B virus (HBV) with the development of hepatocellular
carcinoma is compelling, yet the mechanism of action remains unclear. HBV DNA is
integrated into the hepatocyte genome but does not encode any oncoprotein and is not
associated with a known proto-oncogene. It is likely therefore that the effect of HBV is
indirect and might be multifactorial. Possible factors include liver-cell damage and
accompanying regenerative hyperplasia, secretion of a protein that disrupts normal
growth control of infected liver cells, and disabling of a tumour-suppressor gene that
controls the cell cycle.

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