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Causology is the lock

History is key
Medicine ward is locked door

History & causology


For block posting ,
3rd to 5th year and
post graduate student
Dr . Shahidullah shamol
FCPS (medicine )
FEVER –history taking
Cough –history taking
FEVER –Causology
Cough –causology
FEVER
duration(for how many days) <7 days –viral / > 7 enteric fever

low grade or high grade—high –dengue /enteric . Low --TB

onset (chill or rigor )—malaria , UTI , pneumonia ,cholangitis

how long fever persist –continued –enteric fever /dengue

how subsided with sweating / spontaneously/ with medication

when the fever comes and subsided (at evening or subsided at


night/ no specific pattern )—evening rise TB
character (continued—enteric fever / intermittent—most fever )

highest recorded temperature—if patient measure the temp


Now systemic query
cough present or not
running nose, sore throat , malaise --viral
chest pain –chest pain and short duration fever indicate pneumonia
contact with Tb patient/ history of taking previous anti-tb drug
travelling to hilly area –malaria / patient residence ---endemic zone of
kala-azar –mymensingh
night sweat and weight loss and anorexia(TB)
if wt loss then how many kg lost in last few months
head ache ,photophobia , convulsion , unconsciousness –meningitis
,encephalitis
jaundice –viral hepatitis , liver abscess,malaria and leptospira
if female / elderly male
Ho UTI ---burning sensation of micturation /during voiding/urgency
/frequency
When u will not get any clue to cause of fever extra history?
abdominal pain (TB/ liver abscess)
joint pain , rash (connective tissue)
bowel habit alteration (TB)
lymphoma –itching , pelbestin fever ()
Iv drug user / dental caries / know valve disease (infective
endocarditis)
any bleeding manifestation –epistaxsis , gumbleeding , bruise
,purpura ,
Just memorize this history..use every where u got fever to describe it like this ,
or better than this
Example:
Presenting complains started 2 month ago when the patient developed fever
which initially was low grade intermittent subsequently turned in to high grade
(or which was high grade and continued in nature1). The temperature raised
mostly at the evening and used to persist 4 to 6 hrs and subsided with
sweating with or (without) medication (or without sweating spontaneously or
after medication ). Highest recorded temperature was 1040F (or the fever was
not documented).this febrile period was accompanied with anorexia, nausea,
malaise, drenching night sweating (only mention if patient tells u). The patient
did not complain any cough, chest pain, bowel disturbance , abdominal pain
,joint, rash, any bleeding manifestation, urinary problem like frequency or
burning sensation during voiding .(if present then elaborate each complained
next line e.g. Cough -- ).he lost 10 kg weight during the course of illness . The
patient had not any contact with known TB patient or no history of taking ant
TB drug previously. He didn’t travel hilly area or border area recently. Personal
history (important --- IV drug user history)
COUGH
Duration –how long? acute < 3wks
episodic / intermittent, --asthma or other illness or persistent ==ILD
dry or productive (dry ---ILD,drug, productive –COPD,TB , brochiectasis )
if productive the following history of sputum should be taken
Amount –scanty / moderate / profuse
color –whitish / yellowish
nature –mucoid , purulent , forthy / serous
smell—foul-smelling (lung abscess / brochiectasis )
diurnal variation present or not (for asthma more at early morning
/night )
seasonal variation present or not
relation with posture –changing posture increase sputum production
(brochiectasis ))
triggering factor –pollen cold air , exposure to dander—asthma
does the cough hamper sleep
HO atopy or allergy –asthma
family history asthma
occupation history –animal contact ,asthma, ILD—stone
crashing , ship breaking
is it associate with fever or not –pneumonia , TB , lung
abscess
chest pain or not –peumonia , ca bronchus
breathlessness or not –heart failure , bronchial asthma
Swelling of body –heart failure
drug history --ACE
personal history –smoker
haemoptysis or coughing out of blood
if present then
fresh or clotted blood
mixed with sputum
amount (mild / massive / profuse )
how many episode
need any hospitalization
HO atopy or allery
family history asthma
occupation history –animal contact ,asthma, ILD—stone crashing
, ship breaking
is it associate with fever or not –pneumonia , TB , lung abscess
chest pain or not –peumonia , ca bronchus
breathlessness or not –heart failure , bronchial asthma
drug history --ACE
personal history –smoker
Just memorize this history ..use every where u got cough to describe it like this
, or better than this
The patient also developed episodic / intermittent cough for same duration or
last 1 months .which initially was dry and later turn into productive ( or the
patient developed episodic productive cough for same duration or for last 1
month) containing………scanty (in case mucoid )/ moderate / profuse(use in
case of purulent ) ………whitish (in case mucoid )/ yellowish (use in case of
purulent )………mucoid / purulent /mucopurulant / frothy sputum which more
marked or aggravated at night/ early morning, exposure to cold / more in
winter and exposure to trigger factor like pollen , dander (or having no diurnal
variation or seasonal variation or any specific triggering factor ). (If case is
brochiectasis then add—sputum production is increased with change of
posture more at left lateral position). He has no history coughing out of blood
(or patient also give history several episodes of coughing out moderate/
profuse/ scanty clotted blood that mixed with sputum or fresh blood). The
cough was not associated with fever, chest pain, breathlessness (if present then
elaborate each complained in next line --). The patient has no history of contact
with TB patient,
Personal History: smoker or not
Occupation: contact with animal,
Stone crashing / ship breaking (ILD)
Past history TB (bronchiectasis ), atopy
Family history of asthma
In case of dry cough
Patient also developed episodic or intermittent dry cough for last 1
month without specific diurnal or seasonal variation or triggering
factors and no history of coughing out of blood
in case of persistent cough
Usually in ILD –dry and persistent cough (associated with exertion
breathlessness )
Can present in COPD(more common ) / bronchial asthma in acute
exaggeration –(usually productive)
eg.—patient has history of episodic productive cough for l5 year but for
last 1 month it become persistent
ABC OF FEVR
What is the normal temperature ?
Normal temperature is 370 C or 98.40 F
Site where temperature seen?
in oral cavity-- under surface of the tongue
in the axilla & in rectum or internal ear
Where core temperature is seen?
in rectum or the external auditory meatus
What is the difference of temperature in different site?
temperature in mouth is 0.5°C or 1 0 F higher than the axilla
temperature in rectum is 0.5°C or 1 0 F higher than the mouth
When temp is highest n lowest? What Is the diurnal variation of temp?
body temperature is lowest in the morning and reaches a peak between 6 pm and 10 pm
this diurnal difference is not more than 0.50 C
What do you mean by fever?
Fever is an elevation of body temperature that exceeds the normal daily variation and occurs in
conjunction with an increase in the hypothalamic set point (e.g., from 37°C to 39°C).
What do you mean by hyperthermia ?
Hyperthermia is characterized by an uncontrolled increase in body temperature that exceeds the
body's ability to lose heat. The setting of the hypothalamic thermoregulatory center is
unchanged
What is hyperpyrexia?
when body temperature increases hyperpyrexia defined as above 41.6°C
causes
cerebral malaria
garm negative septicaemia
heat stroke
malignant hyperthermia-drug
 anaesthetic agents [e.g. halothane] or
 muscle relaxants [e.g. suxamethonium]),
 the neuroleptic malignant syndrome (a reaction to antipsychotic medication)
intracranial haemorrhage or head injury
Deference between hyperthermia and fever
FEVER HYPERTHERMIA
causes /pathology Involve pyrogenic Failure in thermoregulatory
cytokines homeostasis
Change in hypothalamic set point occur remain unchanged
temp Rarely exceed 41 0 C Can exceed 41 0 C
Complications rare common
Diurnal variation present Absence
Classify fever with definition and example?
Type of fever
 Continued
 Remittent
 Intermittent -
o a.Quotidian
o b.Tetrtian
o C.Quartan
1. Continued fever : When fever does not fluctuate more than about 1` C (1.5' F) during 24
hours but never touches the base line is called continued fever.
 Causes :-
I. I .Typhoid fever
II. 2- Millar,y tuberculosis
III. Lobar pneumonia
2. Remmittent fever
 When daily fluctuations exceed 20C called remittent fever.
 Causes
I. Amoebic liver abscess
II. Lung abscess
III. Collection of pus in the tissues
3. Intermittent fever
When the fever is present only, for several hours during the day it is called intermittent-
fever.
a) Quotidian:
When a paroxysm of intermittent fever occurs daily. the type is quotidian.
Cause - Kala-azar (double quotidian)
b) Tertian
When fever comes on alternate days, it is tertian.
Causes: P. Vivax and P .Ovale Malaria.
C) Quartan
When there is Two days interval between two consecutive attacks. Then it is call quartan.
Cause- P. Malariae infection.

Pel-Ebstein fever
A specific kind of fever associated with Hodgkin's lymphoma, being high temp for one week
and low temp for the next week and so on
Stepladder pattern
Typhoid fever may show a specific fever pattern, with a slow stepwise increase and a high
plateau
PUO?
PUO is defined as a temperature persistently above 38.0 °C for more than 3
weeks, without diagnosis despite initial investigation
during 3 days of inpatient care or
after more than two outpatient visits
Causes of PUO : MIC
Malignancy----
 Heamatological malignancy :lymphoma, leukamia, myeloma
 Solid tumour : renal,liver,colon carcinoma
Infection-------Abscess, infective endocarditis , TB
Connective tissue disease—SLE , vasculitis , adult still
a patient with three days fever more than 7 day fever
viral fever enteric fever
malaria Malaria
UTI pneumonia
pneumonia TB (>2week)
kala-azar (>2week)
liver absecess
fever with unconsciousness
 cerebral malaria
 encephalitis
 meningo-encephalitis
What is hypothermia ?
Hypothermia is defined as a temperature of less than 35°C.
Usually measure in core temperature
 Prolong water immersion
 exposure to cold weather (elderly immobile patients)
 severe hypothyroidism/maxedema coma
 drug overdosage
 alcohol intoxication
 stroke or head injury
What is Fictitious fever? Clue of Fictitious fever ?
Fictitious fever is produced artificially by the patient or an attendant
A—appearancc—Patient looks well
B— Bizarre temperature chart with temperatures >41°C
C— No correlation between temperature and pulse rate
D--- absence of diurnal variation
E— ESR and C-reactive protein is normal
F—fall of temp—No sweating during when temp fall or subsided
g—X
H— Evidence of self-harm ,injection
I—independent observer--Temperature is normal when taken by an independent supervised
FEVR WITH CAUSOLOGY
First few slide only for MBBS
fever with unconsciousness fever with convulsion
for MBBS student answer (1,2,3) if want 1. Cerebral Malaria
more (5,6) 2. viral encephalitis
infection 3. meningoencephalitis
1. Cerebral Malaria 4. Dengue (only post graduate )
2. viral encephalitis 5. cerebral abscess
3. meningoencephalitis
4. Dengue (only post graduate )*
5. cerebral abscess
6. septicemia
non-infectious
1. heat stroke
2. pontine haemorrhage
3. malignant hyperpyerexia / drug
* in dengue actually patient become
unconscious when fever subside so it is
better to omit
fever jaundice fever jaundice & unconsciousness
for MBBS student (1 ,2,3,4, 5,6) 1. cerebral malaria
1. acute viral hepatitis 2. fulminative hepatic failure
2. leptospirosis 3. dengue
3. cerebral malaria 4. leptospirosis
4. liver abscess 5. septicemia
5. cholangitis
6. septicemia
7. Dengue
8. yellow fever (nt in bangladesh)
9. drug reaction
10.herediatary haemolytic anaemia
with fever due to any causes
fever jaundice f fever jaundice &
unconsciousness
for MBBS student (1 ,2,3,4, 5,6) 1. cerebral malaria
1. acute viral hepatitis 2. fulminative hepatic failure
2. leptospirosis 3. dengue
3. cerebral malaria 4. leptospirosis
4. liver abscess 5. septicemia
5. cholangitis
6. septicemia
7. Dengue
8. yellow fever (nt in bangladesh)
9. drug reaction
10.herediatary haemolytic anaemia
with fever due to any causes
fever with rash –white color only for MBBS
infection connective tissue
bacteria virus SLE
MERIT—Less RP of D MCH dermato-myositis
M --- R-- Rubella vasculitis
--meningococcal inf. P—parvo-virus B—19 PAN
E—enteric fever of henoch scholein
R—rickettsia D--dengue purpura
I—infective M-- Measles adult still
endocarditis C—chikungunya
T-TSS --Chickenpox (varicella)
le–leptospirosis H—HIV
--Lyme disease ---viral haemorrhagic fever
S-Syphilis,
S -scarlet fever
blood drug
acute leukaemia & aplastic anaem ia drug rash
causes fever with rash according to day of
appearance ?
very sick person must take double eggs
1st day -> varicella (chicken pox )
second day  scarlet fever
third day  pox (small pox)
fourth day measles , rubella /german measles
fifth day typhus/ rickettsia
six day  dengue
seven day enteric fever
fever with purpuric rash
infection blood
bacteria 1. acute leukaemia
1. meningococcal infection 2. aplastic anaemia
2. leptospirosis connective tissue
3. Rickettsia 1. SLE
virus 2. vasculitis
1. dengue a. PAN
2. viral haemorrhagic fever b. henoch scholein purpura
Drug
1. Fever with Rash with arthritis white color for MBBS
viral (duration is less than 6 connective tissue other
wk) 1. psoriasis 1. Sarcoidosis
1. chikungynia 2. SLE 2. Rheumatic fever
2. parvovirus 3. vasculitis
3. HBV 4. systemic sclerosis
4. HIV 5. Dermatomyositis
5. Rubella 6. Adult still
Fever with relative bradycardia Fever with relative tachycardia
in this condition increase pulse rate increase pulse rate more than 10 /
less than 10 / min for per degree F min for per degree F increase of
increase of temperature – temperature is called relative
example : tachycardia
1. viral fever --dengue Example :
2. first week of enteric fever 1. acute rheumatic fever
other 2. polyarteritis nodosa
1. pyogenic meningitis
2. leptospirosis
3. brucellosis
fever with hepatopleno megaly with spleno megaly
thrombocytopenia
In CBMC In CBMC
In—infection In—infection
1. Kala-azar 1. Kala-azar
2. chronic Malaria with hypersplenism 2. chronic Malaria
3. AIDS 3. Disseminated TB
C--Congestion 4. AIDS
1. CLD with hypersplenism 5. Infective endocarditis
B—blood C--Congestion
1. lymphoma 1. CLD with SBP
2. CML with blast crisis B—blood
3. Acute leukaimia 1. lymphoma
M—malignancy 2. CML with blast crisis
1. hepatoma on the top of CLD 3. Acute leukaimia
C— connective tissue M—malignancy
1. SLE 1. hepatoma on the top of CLD
2. Felty C— connective tissue
1. SLE
2. Felty
3. adult still
on
fever for 14 day with drowsy / fever with neurological sign
unconsciousness
1. enteric fever –coma vigil cerebral abscess
2. tuberculous meningitis tuberculoma / tb meningitis
encephalitis
3. meningococcal meningitis meningoencephalitis
4. rickettsia infective endocarditis
Toxoplasma (HIV)
5. Addison
Vasculitis /SLE
6. septicemia
7. fever with electrolytes
imbalance
fever with shock to remember fever with carditis/ heart failure
AIDS
A--Algid malaria MISS RIVER pr (MR. VIRSSEL )
I--infective endocarditis R--Rhematic fever
D--Dengu sock syndrome I--infective endocarditis
S--staph. Toxic shock syndrome V--viral myocarditis
S--septicemia due to E—complicated enteric fever
pneumonia R—Ricketts ia
UTI Mi—miningococcal
skin infection /cellulitis S--SLE
meningococcal infection S—Septicaemia
pelvic infection L—leptospirosis
obstetrical
septic abortion
retained dead fetus /
amionictic fluid embolism
fever with renal failure fever with haematuria
infection infection
SR. MILU DR. MILU
S-- septicaemia D-- dengue
R-- Rickettsia R-- renal TB
M-- Malaria M-- Malaria
I-- infective edocarditis I-- infective edocarditis
L-- leptospirosis L-- leptospirosis
U--UTI/ pyelonephriti s U--UTI/ pyelonephriti s
Hantavirus heamatological
septicaemia due to acute leukaemia
pneumonia connective tissue
UTI SLE
skin infection /cellulitis Vasculitis –
meningococcal infection MP ,
pelvic infection henoch scholein purpura
obstetrical Renal cell carcinoma
blood
TTP
HUS
connective tissue
fever with bleeding fever with thrombocytopenia / coagulopahty
to remember MD eat VADKA (rassian wine) to remember MD eat VADKA (rassian wine)
M—severe malaria M—severe malaria
D—Dengue haemorrhagic fev er D—Dengue haemorrhagic fev er
V—viral haemorrhagic fever V—viral haemorrhagic fever
A—acute leukemia A—acute leukemia
D—DIC / septicaemia D—DIC / septicaemia
k—kala—azar k—kala—azar
A__Aplastic anaemia A__Aplastic anaemia
leptospirosis leptospirosis
meningococcal septicaemia
TTP
fever with respiratory distress fever with brady cardia
MP from RASSIA enteric fever
M—severe malaria viral fever (dengue)
P—pneumonia brucellosis
R—rheumatic fever psittacosis
A—ARDS weils disease
S—septicaemia
S—SARI/SARS
I—infective endocarditis
A—Aspiration pneumonia
fever with volume over load
fever with subcutaneous abscess fever with pain full nodule
1. meliodosis Lisst—B
2. histoplasmosis L-- type II lepra reacation
3. myceotoma I-- IBD
4. TB S--Sarcoidos
fever with eschar S --SLE
Rickettsia T-- primary TB
anthrax B-- Bechet diseases
M—mycoplasma
P--Poly-arteritis nodusa
S—strepto coccuss
fever with haematomesiss and fever with red eye
melena
dengue 1. leptospirossi
leptospirosis 2. dengue
Rickettsia 3. sarcoidosis
Malaria
4. RA
Kala-azar
leukaemia 5. type II lepra reaction
aplastic anaimia
COUGH
Cough is a characteristic sound caused by a forced expulsion against
an initially closed glottis.
1. Acute cough ---lasting less than 3 weeks.
chronic cough-- lasting more than 8 weeks
origin of cough
respiratory causes
1. pharynx,
2. larynx,
3. trachea and
4. bronchi
5. parenchyma
other than respiratory
1. cardiac heart-failure
2. GIT—GERD
3. Drug
respiratory causes : non respiratory causes
Pharynx 1. heart failure
Post-nasal drip 2. GIT—GERD
Larynx 3. Drug--ACE
Laryngitis 4. neurological disorder
Trachea
Tracheitis
Bronchi
1. Bronchitis (acute)
2. COPD/ chronic bronchitis
3. Asthma
4. Eosinophilic bronchitis
5. Bronchial carcinoma
Lung-parenchyma
1. Tuberculosis
2. Pneumonia
3. Bronchiectasis
4. Pulmonary oedema
5. Interstitial lung disease (ILD)
dry cough –cough without production of productive cough
sputum cough with sputum
1. asthma / cough variant asthma 1. TB
2. GERD 2. pneumonia (initially dry later productive)
3. ILD 3. bronchiectasis
4. Drug—ACE inhibitor 4. chronic bronchitis / COPD
5. Eosinophilic bronchitis 5. Lung abscess
6. bovine cough due to –vocal cord palsy /
neuromuscular weakness

name some causes of chronic cough cough with normal X—ray and chest
Chronic cough > 8 weeks examination
1. Tuberculosis 1. post nasal drip
2. Bronchiectasis 2. GERD
3. Lung tumour 3. drug
4. Interstitial lung disease 4. cough variant asthma
5. chronic bronchitis /copd 5. endo-bronchial TB or carcinoma
6. Asthma 6. pharyngitis and laryngitis
7. GERD 7. Postviral bronchial hyperreactivity
8. drug
8. Cigarette smoking
‘Red flag’ symptoms associated with common
cough?  cough more at night –ashtma
WBC--HF  cough at early morning  chronic bronchitis
W--Weight loss  cough with increase production of sputum
B--Breathlessness with change posture  bronchiectasis
C--Chest pain  cough with foulsmelling sputum –lung abscess
H--Haemoptysis and bronchiectasis , empyema
F--Fever
Name different type of sputum with example?
Type Appearance Cause
Serous Clear, watery ,Frothy, pink Acute pulmonary oedema
Mucoid Clear ,White, viscid Chronic bronchitis/ COPD
Asthma
Purulent Yellow (live neutrophils) Acute bronchopulmonary infection
Green (dead neutrophils) Longer-standing infection
Pneumonia
Bronchiectasis
Lung abscess
Rusty Rusty red Pneumococcal pneumonia
Causology is the lock
History is key
Medicine ward is locked door

DYSPNEA

History & causology


For block posting ,
CHEST PAIN 3rd to 5th year and
post graduate student
Dr . Shahidullah shamol
FCPS (medicine )

ABDOMINAL
PAIN
Breathlessness
1. duration how long
1. onset –sudden / insidiously (sudden –pulmonary edema ,
pulmonary embolism)
2. progression-- progressive or static(progressive --HF/COPD)
3. in exertional or rest (at rest indicate stage IV/severe dyspnea )
1. aggravating factor
a. exertion
b. climbing stair
c. walking
d. exposure to pollen /dust / cold weather
1. relieve by
a. taking rest (heart failure )
b. inhaler / medication (asthma /copd )
c. nitroglycerin spray(heart failure )
1. duration how long
1. onset –sudden / insidiously (sudden –pulmonary edema ,
pulmonary embolism)
2. progression-- progressive or static(progressive --HF/COPD)
3. in exertional or rest (at rest indicate stage IV/severe dyspnea )
1. aggravating factor
a. exertion
b. climbing stair
c. walking
d. exposure to pollen /dust / cold weather
1. relieve by
a. taking rest (heart failure )
b. inhaler / medication (asthma /copd )
c. nitroglycerin spray(heart failure )
1. in case of asthma should take following history
a. night disturbance
b. frequency of use inhaler
c. any exacerbation needed to hospitalization
d. history of atopy : skin disease (dermatitis )/ allergic rhinitis

1. association history
a. cough with or without productive sputum
b. chest pain present or not
c. joint pain / rash , any connective tissue disease ---ILD

1. smoker or not –COPD


exertional breathlessness / heart failure
Just memorize this history..use every where u got breathlessness (heart failure) to
describe it like this , or better than this
The presenting complains started one year ago when the patient insidiously
developed exertional breathlessness which was progressive. Initially
breathlessness appeared during climbing stair (if the patient resides in city) or
after walking near about half mile on the level ground and relieved by taking rest
(or nitroglycerine spray –if patient tell u). But for the last 15 days it increased in
severity. Now he feels breathlessness during walking around house, going to
bathroom or simple work like dressing or undressing himself and sometimes even
in rest. Patient also give history breathlessness in lying position (orthopnea) and
feeling better in sitting position or lying on 2 or 3 pillow under head . He had no
history of sudden severe breathlessness that woke him immediately after sleep
(PND). This breathlessness had no diurnal variation (or initially breathlessness had
no diurnal variation but now a days it more marked at night) or triggering factor
like exposure to cold, dust, pollen. He had no history of chest pain, cough, and
fever along with breathlessness. (If symptoms are present then elaborate)
bronchial asthma / copd
Just memorize this history..use every where u got breathless
(asthma )to describe it like this , or better than this
The presenting complains started one year ago when the
patient developed episodic or intermittent breathlessness (or
patient also developed episodic / intermittent breathlessness
for last one year) .initially it was mild to moderate in severity ,
triggered or aggravated by exposure to pollen , dust , dander,
cold wind and relieved by taking inhaler( or medication ) . The
symptoms are more marked at night or early morning and also
in winter season. For the last 15 days the breathlessness
become so severe that he can’t speech a whole sentence in
single breath. It also hampers his sleep .Now it become
refractory or not relieved after taking inhaler. He had no
history of breathlessness in lying position.
Define Dyspnoea (breathlessness) ?
Dyspnoea (breathlessness) is undue awareness of breathing.
causes
Acute dyspnoea Chronic exertional dyspnoea
cardiac
Acute pulmonary oedema/ALVF 1. Chronic heart failure
2. Myocardial ischaemia (angina equivalent)
3. Constrictive pericarditis
4. Pericardial effusion
lung
air way air way
Acute severe asthma 1. Chronic asthma
Acute exacerbation of COPD 2. COPD
Inhaled foreign body ( children) 3. Bronchial carcinoma
Laryngeal oedema (e.g. anaphylaxis
pleura pleura
1. Pneumothorax Large pleural effusion
parenchyma parenchyma
Pneumonia 1. ILD
ARDS a. sarcoidosis,
Lobar collapse b. fibrosing alveolitis,
c. extrinsic allergic alveolitis,
d. pneumoconiosis
2. Lymphatic carcinomatosis
pulmonary vessel pulmonary vessel
Acute Pulmonary embolus 1. Chronic pulmonary thromboembolism
2. Primary pulmonary hypertension
Chest wall Chest wall
XX 1. Kyphoscoliosis
1. flail chest / chest injury fracture 2. Ankylosing spondylitis
other other
Metabolic acidosis 1. Severe anaemia
1. diabetic ketoacidosis, 2. Obesity
2. uraemia Neurological
3. lactic acidosis, , Neuropathies
4. salicylates, ethylene glycol poisoning Muscular dystrophies
neurological / acute neuropathy
1. Myasthenia gravis
breathlessness with chest pain breathlessness with clear chest
1. acute MI with LVF 1. metabolic acidosis
2. acute pulmonary embolism a. diabetic ketoacidosis,
3. spontaneous pneumothorax b. uraemia
4. pneumonia 2. pulmonary embolism
5. pericarditis and myocarditis 3. neurological causes
6. aortic –dissection and aortic aneurysm a. GBS
7. trauma rib-fracture b. Myasthenia gravis
8. malignancy 4. anaemia
9. Anaemia 5. psychogenic
10. psychogenic 6. obesity
11. heart failure due to 7. laryngeal edema
a. IHD if question is X—ray normal
b. Aortic stenosis all + bronchial asthma
c. HOCOM
post operative breathlessness breathless with shock
1. acute pulmonary embolism 1. acute LVF with MI
2. acute LVF 2. acute pulmonary emboliss
3. aspiration pneumonia 3. tension pneumothorax
4. ARDS 4. cardiac temponad
5. metabolic acidosis 5. pneumonia
6. pneumothorax (positive pressure
ventilation )
Breathlessness: modes of onset/ duration and progression
Minutes Hours to days
Pulmonary thromboembolism Pneumonia
Pneumothorax Asthma
Acute left ventricular failure Exacerbation of COPD
Asthma
Inhaled foreign body

Weeks to months / all chronic Months to years / chronic


exertional cause exertional cause
Anaemia COPD
Pleural effusion Pulmonary fibrosis/ ILD
Respiratory neuromuscular disorders Pulmonary tuberculosis
Heart failure
New York Heart Association (NYHA) functional classification
Class I No limitation during ordinary activity
Class II Slight limitation during ordinary activity
Class III Marked limitation of normal activities
without Symptoms at rest
Class IV Unable to undertake physical activity without
symptoms; symptoms may be present at rest
only for remember easily
Class I No limitation --ordinary activity
Class II Slight limitation--- ordinary activity
Class III Marked limitation-- ordinary activity
+ symptom on rest
no
Class IV unable ordinary or (any physical ) activity
+ symptom on rest
yes
(MRC =Medical Research Council)--original
Grade Degree of breathlessness related to activities
0 No breathlessness, except with strenuous exercise
1 Breathlessness when hurrying on the level or walking up a slight hill
2 Walks slower than contemporaries on level ground Because of
breathlessness or has to stop for breath when walking at own pace
3 Stops for breath after walking about 100 m or after a few minutes on
level ground
4 Too breathless to leave the house, or breathless when
dressing or undressing
(MRC =Medical Research Council)—modified to remember
Grade Degree of breathlessness related to
activities
0 breathlessness on strenuous exercise
1 breathlessness on walking hurrying or
walking up a slight hill
2 for breathlessness Walks slower or
stop for breath
3 breathlessness on walking about 100 m or after a few
minutes
4 breathlessness on dressing or undressing or
Abdominal
Pain
S- Site 1. epigastric pain—PUD, acute pancreatitis
 upper / lower abdomen 2. lower abdominal pain UTI , PID
 localized /diffuse 3. loin pain –pyelonephritis, renal stone
4. right iliac fossa  appendicitis
5. right upper abdomen –liver abscess and
acute choecystitis
1. diffuse pain –peritonitis
O--onset 1. sudden –acute abdomen
 sudden 2. insidious / gradual –chronic pain
 insidious 3. intermittent –PUD, chronic pancreatitis
 intermittent / episodic / recurrent
 continuous / persistent / constant
 progressively increasing

C--character 1. burning is pud


 burning , 2. spasmodic / colicky /cramping –obstruction
 dull, ,stone
 spasmodic / cramping
 colic
R--radiation –present or not 1. back –pancreatitis
 back 2. right shoulder –acute cholecystitis
 shoulder 3. left shoulder –splenic infarction
 loin to groin 4. loin to goin –uteric stone
A--associated 1. vomiting –pud , acute abdomen
 vomiting , fever , 2. fever ---infective causes /
 diarrhea or constipation 3. diarrhea / alteration of bowel habit  TB ,
 or alteration of bowel habit IBS,malignancy
4. diarrhea --IBD
T-Timing and Duration when it comes and how long it persist
E-exacerbating relieving factor exacerbation factor
factors empty stomach –pud
 alcohol , Alcohol/ after fatty meal ---chronic pancreatitis
 empty stomach , after meal after meal pancreatitis , ischaemic pain , IBD
 relieving factor relieving factor
o food , antacid or after food/ antacid ---PUD
o medication , bending forward –acute pancreatic
o bending forward vomiting ---PUD/ GERD
S--Severity and intensity --mild to moderate or severe
Example of abdominal pain :

According to the statement of the patient she was reasonable well


1 month back then she suddenly / gradually (insidiously )
developed upper abdominal pain (or diffuse abdominal pain
).Which is mild to moderate in intensity, burning /colic / dull in
nature (or character ) having no radiation (or radiate towards the
back) .each attack persist several hours . The pain is aggravated by
food / more in empty stomach and relieved by food / antacid /
drugs like ranitidine, omeprazole (only mention if patient can tell
the name) / bending forward / knee-elbow position / pressing the
abdomen with pillow ( or the pain has no specific aggravating or
reliving factors ) . The pain was not associated fever/ vomiting /
diarrhea or bloody diarrhea / alteration of bowel habit (or
Patient’s bowel habit is normal.)
recurrent upper abdominal pain Recurrent lower abdominal pain :
from gastro intestinal GIT
1. PUD 1. IBD
2. GERD 2. IBS
pancrease 3. Ca-colon
1. Acute /chronic pancreatitis 4. sub-acute obstruction
billiary system a. TB
1. cholecystitis b. lymphoma
2. choledocholithiasis 5. Recurrent appendicitis
kidney 6. Diverticulitis
1. renal colic 7. ischaemic colitis
2. chronic pyelonephritis 8. vasculitis
less common RENAL
1. CA stomach / pancrease 1. renal colic
referred pain 2. UTI
1. angina in case of female :
PID
other extra intestinal causes
1. see below Salphingitis
2. MBBS ONLY TELL THE BLACK
dysmenorrhoea
endometriosis
abdominal pain with normal USG, colonoscopy , CT , endoscopy
GIT
IBS
non ulcer dyspepsia
ischaemic colitis
vasculitis
Non—GIT
L—locomotors O-Oral medication
vertebral compression Corticosteroids
abdominal muscle stain Azathioprine
M—metabolic R—Retroperitoneal/ REFERED
DM/ DKA MI / IHD
Addison Aortic aneurysm
Acute intermittent porphyria S
Hypercalcaemia Sickle-cell disease & Haemolytic anaemia
hyperparathyroid T—Toxic
N—Neurological Lead
Spinal cord lesions Alcohol
Tabes dorsalis angina or inferion ischemia
Radiculopathy/ PLID
Herpes Zoster
post herpetic neuralgia
abdominal pain with abdominal pain with bleeding
diarrhea
1. IBS 1. IBD
2. IBD 2. ischaemic colitis
3. intestinal TB 3. diverticulitis
4. chronic pancreatitis 4. radiation enteritis
5. lymphoma 5. Ca rectum
6. giardiasis 6. bloody diarrhea
7. Addison 7. bloody dysentery
8. CA colon (enteromebea histolica )
9. ischeamic colitis 8. Rectal ulcer
10.radiation enteritis
CHSET
PAIN
S- Site
1. central / peripheral  Central –MI/angina
2. right /left sided (if peripheral )  peripheral pain --pneumonia
O--onset  sudden --MI
1. sudden  insidious – Angina
2. insidious  after exercise or walking – Angina
3. after exercise or walking  rest pain =MI
4. intermittent / episodic / recurrent
5. continuous / persistent / constant
6. progressively increasing
C--character  chocking , compressing , tightening --
1. chocking , compressing , tightening MI
2. sharp , stabbing  sharp , stabbing--pneumonia
3. tearing  tearing ----aortic dissection
 burning –GERD
R--radiation –present or not in MI
jaw ,neck ,shoulder ,inner surface of left
arm and forearm
A--associated  sweating , vomiting, cold clammy
1. sweating , vomiting , skin--MI
2. fever ,  fever , cough ---pneumonia
3. palpitation  palpitation –heart causes
4. breathlessness  breathlessness---cardiac causes
5. GIT symptoms  GIT symptoms --GERD
T-Timing and Duration how long persist
E-exacerbating relieving factor : E-exacerbating factors
E-exacerbating factors  after exertion , after heavy meal—
1. after exertion , ischamia
2. after heavy meal  deep inspiration , movement and
3. inspiration , cough –acute pericarditis / pleural
4. movement and cough pain
relieving factor relieving
1. rest , after taking nitrate  rest , after taking nitrate—angina
s-Severity and intensity --mild to moderate / severe
cardiac or central chest pain
Patient also developed (suddenly / gradually )central chest pain
(left sided ) which is chocking / tightening in nature , mild to
moderate in intensity sometimes radiated to inner left arm and
forearm . The pain is exacerbated by exertion and relieved by taking
rest and sublingual nitrate. The pain has no association with
respiration, sweating, nausea, vomiting, fever, palpitation and
breathlessness, cough.
peripheral chest pain /non-cardiac test pain
Patient also developed right sided chest pain which is stabbing in
nature, mild to moderate in intensity having no radiation but
exacerbated by movement, Deep inspiration ,cough and relieved by
taking oral medication. it is associated with high grade intermittent
fever and episodic dry cough . The pain has no association with
palpitation and breathlessness
central chest pain peripheral chest pain
Cardiac Lungs
heart parenchyma
1. Myocardial ischaemia(angina) 1. Pneumonia
2. MI 2. Malignancy
3. Pericarditis 3. Tuberculosis
4. Myocarditis 4. Connective tissue disorders
5. Mitral valve prolapse pleura
Aortic 1. Pneumothorax
1. Aortic dissection vessel
2. Aortic aneurysm 1. Pulmonary infarct
Massive pulmonary embolus Musculoskeletal--MORIC
Non-cardiac : Skeletal
Oesophageal 1. O--Osteoarthritis
1. Oesophagitis 2. R--Rib fracture/injury
2. Oesophageal spasm 3. C--Costochondritis (Tietze’ssyndrome)
Mediastinal muscle
1. Tracheitis 1. I--Intercostal muscle injury
2. Malignancy 2. M--Epidemic myalgia
Anxiety/emotional (Bornholm disease)
Neurological
1. P--Prolapsed intervertebral disc
2. H--Herpes zoster
3. O--Thoracic outlet syndrome
Difference between MI and angina
SOCRATES MI angina
site Retrosternal SAME
onset very rapid and sudden gradual
Character Constricting, heavy,Tight, SAME
squeezing, choking
Radiation Jaw/neck/shoulder/arm SMAE
Associated features Sweating, nausea, Breathlessness
vomiting,
breathlessness,
feeling of impending
death
(angor animi )
Timing 2–10 minutes Prolonged
Exacerbating/ spontaneous. Precipitated by exertion
relieving factors Not relieved by rest and/or emotion , cold,
or nitrates windy
Rest
Quick response to nitrates
Severity very severe Mild to moderate
compare chest pain
Angina Myocardial Aortic dissection Pericardial pain Oesophageal pain pleural pain
infarction
site Retrosternal / Retrosternal Interscapular Retrosternal left- Retrosternal or peripheral
sided epigastric
onset gradual over 1–2 Rapid Very sudden Gradual, postural gradual gradual /slow
minutes change may sudden if (spasm
suddenly )
aggravate
Character Constricting, Constricting, Tearing or Sharp, ‘stabbing’ Gripping, tight or Sharp, ‘stabbing’
heavy heavy ripping, pleuritic burning pleuritic
Radiation Jaw/neck/ Jaw/neck/ Back, between Left shoulder or Often to back, non radiation
shoulder/arm shoulder/arm shoulders back sometimes to
arms
Associated breathlessness Sweating, Sweating, Flu-like Heartburn, acid fever ,cough
features nausea, vomiting, syncope,focal prodrome, reflux
breathlessness, neurological breathlessness,
feeling of signs, loss of fever
impending death pulse
Timing 2–10 minutes Prolonged Prolonged variable duration Nighttime variable
common,
variable duration
Exacerbating Precipitated by spontaneous. Spontaneous Pleuritic Lying flat some cough , deep
exertion and/ or Sitting up/lying foods may trigger inspiration
emotion , cold, down may affect
windy intensity
relieving factors Rest Not relieved by No manoeuvres NSAIDs may help Not relieved by NASIDs
Quick response rest relieve pain rest; nitrates
to nitrates or nitrates sometimes
relieve
Severity Mild to moderate Usually severe Very severe Can be severe Usually mild mild to moderate
Haemoptysis ?
Coughing up blood is called Haemoptysis .
cause according to anatomy
Bronchial disease Parenchymal disease
1. A--Acute bronchitis* MALT
2. B—Bronchiectasis 1. Tuberculosis
3. C- Carcinoma (bronchial CA / 2. Suppurative pneumonia
adenoma) 3. Lung abscess
Lung vascular disease 4. Mycetoma
1. Pulmonary infarction* 5. Actinomycosis
2. Goodpasture’s syndrome 6. hydatid disease
3. vasculitis Cardiovascular disease
a. Polyarteritis nodosa 1. Acute left ventricular failure /pulmonary
b. wegner granulomatosis edema
4. Arteriovenous malformation 2. Mitral stenosis
Blood disorders Iatrogenic
Blood dyscrasias 1. biopsy
1. Leukaemia
2. Haemophilia
3. Anticoagulants
haemoptysis with normal chest XRY massive haemoptysis /frank
? haemoptysis
Bronchial disease to ABC--MT
1. A--Acute bronchitis* A--lung abscess
2. B—Dry Bronchiectasis B--Bronchiectasis
3. C- Carcinoma (endobronchial C—cancer—bronchial carcinoma
tumour/ TB ) M--intracavitary mycetoma
Lung vascular disease T—tuberculosis
1. Pulmonary infarction* recurrent haemoptysis
2. Goodpasture’s syndrome Bronchial disease
3. vasculitis Bronchiectasis
a. Polyarteritis nodosa Carcinoma (bronchial CA / adenoma)
b. wegner granulomatosis Parenchymal disease
4. Arteriovenous malformation Lung vascular disease
Blood dyscrasias Blood dyscrasias
1. Haemophilia
2. Anticoagulants
Causology is the lock
History is key
Medicine ward is locked door

Jaundice
History & causology
For block posting ,
3rd to 5th year and
post graduate student
Dr . Shahidullah shamol
FCPS (medicine )
Dr shamol /history
duration
which part involved in first sclera  urine and the whole body
sequence
HO- viral prodome anorexia , nausea , vomiting , joint pain , malaise
fever simple fever + prodome  viral hepatitis
fever with chill and rigor  cholangitis
fever + jaundice  viral hepatitis ,leptospirosis ,
malaria , liver abscess , cholangitis
the jaundice progressive , progressive malignancy (Ca-pancreas )
static , fluctuating static  viral hepatitis
fluctuating—stone
recurrent –stone / Wilson/ haemolytic anaemia
stool pale or not obstructive jaundice
itching / dark color urine

Dr shamol /history
Ho bleeding obstructive jaundice—due to ViT –K
manifestation deficiency
(epistaxis , purpura,
gumbleeding )
abdominal pain viral hepatitis /stone

HO for etiology HO Alcohol, IV drug , Blood transfusion ,


saving in salon extramarital sexual
exposure , tattoos –B virus
water and sanitation –for A and E virus
Dr shamol /history drug History –anti-TB drug
Family history  other siblings –wilson
and haemolytic anaemia
Ho recurrent blood transfusion + anaemia
–thalasemia
travel history to abroad
unconsciousness encephalopathy

stigmata of CLD  immunization


 loss body hair decrease saving frequency ,
edema , ascites , loss of libido

Bowel habit if constipation chance of encephalopathy


steatorrhoea –in case of obstructive jaundice

Dr shamol /history
A=Anorexia , ALCOHOL
B=Bleeding manifestation , blood transfusion

C=Color of stool (pale)/ urine (dark )


D=Drugs (herbal drug), drinking water and sanitation

E= Exposure –extramarital sexual exposure


F=Fever
G=GIT—nausea , vomiting , abdominal pain
H=Ho—previous jaundice , family HO , HO of consanguinity
I=Itching , IV drug
J=Joint pain

L=Loss of body hair , libido --CLD


Dr shamol /history
If viral hepatitis: If viral

hepatitis:

Dr shamol /history
If viral hepatitis:
According to the statement of the patient he was reasonable well one
month back. Then he noticed yellow coloration of sclera, skin and urine
which was associated with (preceded by) anorexia/ loss of appetite,
nausea, malaise, joint pain. This yellow coloration was progressively
increasing and not associated with fever, abdominal pain, itching, pale
color stool and any bleeding manifestation.(((( if patient complained
pain then write this line ---The patient also complained right upper
abdominal pain Which was mild to moderate in intensity dull aching
in nature (or character ) having no radiation. The pain had no specific
aggravating or reliving factors.)))) .he used to save in the salon but
unaware of using disposable razor. The patient had no history loss
consciousness, pubic or axilary hair loss ,blood transfusion. His bladder
and bowel habit is normal and libido is intact Dr shamol /history
He is non-alcoholic, non smoker, no history of IV drug abuse
He has two brothers and three sisters. None of his siblings are suffering
this type of disease. His parent has not consanguinity.
He drinks arsenic free tube-well water and use sanitary latrine
obstructive jaundice

Dr shamol /history
If obstructive jaundice:
According to the statement of the patient he was reasonable well one
month back. Then he noticed yellow coloration of sclera, skin and urine
which was progressively increasing. This yellow coloration was
associated with generalized itching and pale stool. The patient also
complained right upper abdominal pain which was mild to moderate in
intensity, colicky in nature (or character) having no radiation. The pain
had no specific aggravating or reliving factors. He had no history of
nausea, vomiting, malaise, joint pain, fever and any bleeding
manifestation. He used to save in the salon but unaware of using
disposable razor. The patient had no history loss consciousness,
alteration of behavior, blood transfusion. His appetite, bladder and
bowel habit is normal and libido is intact.
He is non-alcoholic, non smoker, no history of IV drug abuse . no HO
history extra-marital sexual exposure Dr shamol /history
He has two brothers and three sisters. None of his siblings are suffering
this type of disease. His parent has not consanguinity.
Classify jaundice?
Prehepatic or Haemolytic jaundice
Hepatocellular
Post Hepatic or Obstructive jaundice
haemolytic jaundice hepatocellular jaundice
 Haemolysis.—thalassamia  Acute viral hepatitis,
, autoimmune haemolytic  Alcoholic,
anaemia  Autoimmune,
 Falciparam malaria  Drug-induced—anti-
 Gilbert's disease. tubercular drugs
 Dubin-Johnson syndrome.  Cirrhosis
Dr shamol /history
 Rotor syndrome
Post Hepatic or Obstructive jaundice
Intrahepatic Extrahepatic
1. Primary biliary cirrhosis 1. Carcinoma
2. Primary sclerosing cholangitis a. Ampullary
3. Alcohol b. Pancreatic
4. Drugs c. Bile duct(cholangiocarcinoma)
5. Hepatic infiltrations d. Liver metastases
a. lymphoma, 2. Choledocholithiasis
b. granuloma, 3. Parasitic infection (worm )
c. amyloid, 4. Traumatic biliary strictures
d. metastases 5. Chronic pancreatitis
6. Cystic fibrosis
7. Severe bacterial infections
8. Pregnancy Dr shamol /history
9. Inherited cholestatic liverdisease,
e.g. benignrecurrent intrahepatic
cholestasis
10.Chronic right heart failure
causes of recurrent jaundice cause of prolong Jaundice not for MBBS
CONGENITAL CONGENITAL
1. Gilbert 1. Gilbert
2. Wilson 2. Wilson
HEAMATOLOGICAL HEAMATOLOGICAL
1. hameolytic anaemia 1. hameolytic anaemia
a. thalassaemia a. thalassaemia
b. auto-immune-haemolytic anemia HEPATIC
HEPATIC 1. Auto-immune hepatitis
1. Auto-immune hepatitis 2. Alcoholic hepatitis
2. primary sclerosis cholangitis 3. chronic active hepatitis / cirrhosis
3. CLD / chronic active hepatitis 4. Carcinoma of liver primary or 2ndary
billiary duct and pancrease billiary duct and pancrease
1. choledocolithiasis 1. primary sclerosis cholangitis
2. recurrent cholangitis 2. Primary billiary cirrhosis
3. choledochal cyst 3. Extraheaptic billiary obstruction
4. recurrent pancreatitis a) choledochal cyst / helminthes
b) cholangiocarcinoma
Dr shamol /history c) stricture
d) impacted gall stone
1. carcinoma of head of pancrease
common causes biliary causes
bile duct A. intraluminal obstruction
a) choledocholithiasis 1. cholangiocarcinoma
b) cholangitis 2. impacted stone in bile duct
c) Choledochal cyst 3. Primary biliary cirrhosis
liver 4. Primary sclerosing cholangitis
a) viral hepatitis B. Extra luminal obstruction
b) hepatocellular carcinoma / 1. in porta-hepatis by lymphoma
hepatoma on the top of CLD 2. Carcinoma of head of
c) liver abscess pancreases
other than hepato-biliary C. liver causes
a) pancreatitis 1. decompnesated CLD
b) lymphoma with protahepatic 2. hepatocellular carcinoma a
obstruction Fluctuating
uncommon 1. Choledocholithiasis
Dr shamol /history
a) PSC 2. Stricture
b) SBP with CLD 3. Choledochal cyst
4. Primary sclerosing cholangitis
5. Pancreatitis
abdominal mass and jaundice lymphadenopathy with jaundice
billiary and pancreases liver
1. Carcinoma 1. autoimmune hepatitis
a. Of head pancreases malignancy
b. Cholangiocarcinoma 1. haematological
2. Pancreatitis (cyst) a. lukaemia (ALL, CLL)
3. Choledochal cyst b. Lymphoma
hepatic 2. other
1. hepatolcellular carcinoma a. disseminated malignancy
with /out CLD infection
2. secondaries in the liver 1. disseminated TB
3. liver abscess 2. infectious mononucleosis
other than hepato-billiary
1. lymphoma Dr shamol /history
jaundice with hepatomegaly jaundice with
hepatosplenomegaly
1. viral hepatitis hepatic
2. cirrhosis 1. Decompensate CLD with portal
a. haemochromatosis hypertension
b. Alcoholic 2. Hepatoma on the Top of CLD
3. Carcinoma hematological
a. HCC with / out—CLD 1. hameolytic anaemia
b. secondary’s in the liver 2. lymphoma
4. infection 3. CLL
a. liverabscess infective
b. disseminated TB 1. disseminated TB
(granulomatous hepatitis ) 2. Kala-azar

Dr shamol /history
fever with jaundice jaundice with fatigue
hepatic 1. Auto-immuno hepatitis
1. viral hepatitis 2. PBS
2. liver abscess 3. psc
3. cholangitis jaundice with arthritis
infective 1. Viral hepatitis
acute : Mbbs only white
Color 2. autoimmune hepatitis
1. malaria 3. haemochromatosis
2. leptospirosis 4. lymphoma
3. septicaemia 5. PBC
4. dengue 6. SLE and vasculitis
chronic 7. Drug reaction
1. Kala-azar and 8. haemolytic anaemia with
2. disseminated TB pseudo gout
others
Dr shamol /history
1. lymphoma
jaundice with pregnancy
not related with pregnancy
1. viral hepatitis
2. drug
3. cirrhosis
4. auto-immuno hepatitis
5. Wilson
related with pregnancy
1. intrahepatic cholestatic of pregnancy
2. acute fatty liver of pregnancy
3. HELLP
Dr shamol /history
Causology is the lock
History is key
Medicine ward is locked door

Edema
History & causology
For block posting ,
3rd to 5th year and
post graduate student
Dr . Shahidullah shamol
FCPS (medicine )
1. type of swell generalized  CLD , NS, CCF
generalized or localized
localized –>if only ascites ---CLD, intestinal TB, lymphoma, intra-
abdominal Malignancy with metastases to peritonium
if only pedal edema  mal-absorption , drug –NSAID, Ca
channel blocker , malnutrition ,early NS , Heart failure

1. if generalized  first periorbital region then generalized - ns/ AGN


which part  first lower limb then generalized CCF
first involved  first abdomen then generalized  CLD

DR SHAMOL /EDEMA
now take history for etiology

if your diagnosis is regarding renal origin

onset sudden –AGN ,


insidious or gradual ---NS
urinary oligouria –scanty , dark color / coacola color
output urine in case of AGN
Normal volume &frothy– in NS but in later
stage may be scanty.
HO etiology history skin infection , itching , boil
for AGN sore throat and ear infection or
any other infections prior to onset of this
swelling
DR SHAMOL /EDEMA
NS: history for DM--polyuria and polydipsia
etiology SLE/ connective tissue diseases/ vasculitis :
/secondary joint swelling and pain ,rash(purpura, malar
causes rash ), oral ulcer , alopecia
Drug history  taking pain killer (NSAID ),
anti-hypertensive drug –captopril (ACE
inhibitor),herbal drug , pencillamine gold (not
use now day so don’t tell first )
History of jaundice (HBV,HCV)
History of infection –Malaria
History malignancy –lymphoma –fever +
lymphadenopathy (nodular swelling )

DR SHAMOL /EDEMA
complication HTN encephalopathy  head ache and blurring
of AGN vision, convulsion and unconsciousness
LVF orthropnea , sudden severe dyspnea

Complication Recurrent infection –fever


of NS Thrombo-embolism (loin pain –renal vein
thrombosis )

in case nephrotic previous HO edema (relapse )—how many


syndrome treatment times and what was the treatment
history likes
Drug history (steroid /how many times )
History renal biopsy
to exclude CCF  breathlessness present or not
DR SHAMOL /EDEMA
If the if breathlessness present then exertional or rest
patient
orhtropnea –( dyspnea in lying posture)
have CCF
paroxysmal nocturnal dysnpnea - sudden severe
Take breasthlessness that awake him from sleep
following cough / frothy sputum with /without heamoptysis
HO
palpitation
chest pain
anaemic heart failure –Ho –chronic blood loss
fatigue , weakness , dizziness
child hood joint pain –rheumatic diseases
alcohol –alcoholic heart disease
if female –recent pregnancy to exclude post partum
DCM DR SHAMOL /EDEMA
HO jaundice present now or previously

if jaundice detailed history of jaundice (see jaundice


present now topic)
take important history like 
viral prodrome -- , anorexia / loss of
appetite , vomiting, nausea
itching + pale color stool –obstructive
jaundice
HO hepatic loss of body hair , decrease frequency of
insufficiency saving , decrease libido, amenorrhoea
HO jaundice present now or previously
DR SHAMOL /EDEMA
HO haematemesis vomiting out of blood
complication melena black tarry offensive and sticky stool that stained
reddish after washing ( rupture esophageal varices) ,
fever and abdominal pain(SBP),
Recent and past HO alter level of consciousness , alter
behavior and alteration of sleep pattern(encephalopathy
urine output (hepato renal )
Bowel moves per day (as constipation is risk for hepatic
encephalopathy)
etiology : previous HO jaundice (viral hepatitis)
H/O transfusion of blood and blood product (HBV)
shaving in salon & using of disposable blade or not (HBV)
abdominal surgery previously (biliary cirrhosis)
autoimmune disease , arthritis ,women (autoimmune
hepatitis)
DR SHAMOL /EDEMA
personal history Alcoholic. IV drug user, multiple extra
marital sexual exposure family history
HO recurrent jaundice in other siblings
(willson)
patient’s partner is suffering from
jaundice or not
immunization HO immunized against HBV or not
special attention HO of recurrent jaundice
if the patient is young
other family member (siblings )
then take HO to exclude
the Wilson dementia –poor school performance /
academic performance
neurological feature –involuntary
DR SHAMOL /EDEMA movement (tremor , chorea)
if patient have fever and abdominal pain night sweat ,
ascites take this HO weight loss
to exclude TB and remember that fever and abdominal can occur
lymphoma also in CLD with HCC
in all case following history of rare cause
bowel history alteration bowel habit –intra-abdominal
malignancy
chronic diarrhea or mal-absroption
drug history NSAID , calcium channel blower , OCP
hypothyroidism Weight gain, cold intolerance, constipation,
fatigue and lethargy, menorrhgia.
Aspiration of if yes
fluid than color DR SHAMOL /EDEMA
red—malignancy
straw –TB , serous /clear - CLD
turbid –bacterial infection
DR SHAMOL /EDEMA
NS
key point –insidiously
According to the statement of the patient, he was reasonable well 25 days ago
then He Insidiously developed generalized body swelling .initially he noticed
swelling or puffiness at face specially around the eye lids then it involved
both legs and subsequently it become generalized. At the beginning of the
swelling urine output was normal and frothy but for the last 5 days he noticed
reduction in both urinary volume and frequency.
There is no history of sore throat or skin infection prior to this illness .He
denies ( or he does not give) any history of fever ,chest pain, breathlessness ,
palpitation , joint pain and swelling , skin rash , alteration bowel habit ( in
form of loose motion ) , vomiting out of blood and passes of black tarry stool
during the course of illness(only mention if edema is associated with ascites) .
He also denied any recent or past history of jaundice and similar type of
swelling .
DR SHAMOL /EDEMA
The patient has no HO HTN and diabetic. The patient has no history taking
pain killer and anti hypertensive drug. After admission in hospital he getting
some injectable and oral drug but name of which he could not be mentioned
AGN
key point –suddenly
According to the statement of the patient, he was reasonable well 5
days ago then He suddenly developed generalized body swelling
.initially he noticed swelling or puffiness at face specially around
the eye lids then it involved both legs and subsequently it become
generalized . He also developed scanty micturation (or voiding) and
high color urine for same duration. There is a history of sore throat
(or skin infection) 2 wks prior to this illness. The patient also
complaint of mild head ache and blurring of vision for the last few
days (mention if only pt told u – as feature severe hypertension )
.He denies ( or he does not give) any history of fever ,chest pain,
breathlessness , palpitation , joint pain and swelling , skin rash ,
convulsion, unconsciousness ,alteration bowel habit ( in form of
loose motion ) , vomiting out of blood and passes of black tarry
stool (only mention if edema is associated with ascites) during the
courses of illness. He also denied any recent or past history of
jaundice and similar type of swelling previously DR SHAMOL /EDEMA
CLD/ ascites
According to the statement of patient he was relatively well 6 months ago then
he gradually developed generalized swelling of whole body which first noticed at
abdomen subsequently become generalized
He denies (or he does not give) any history of fever, abdominal pain, night
sweats, chest pain, breathlessness, palpitation, alternation bowel habit and
passage of mucus with or without blood.
The patient had history of jaundice 4 yrs ago which subsided spontaneously (only
tell if pt give the history) The patient used to shave in salon and was unaware
about using of disposable blade every time .but He denies any history of
transfusion of blood and blood product, abdominal surgery, vomiting out of
blood and Passage black tarry tool, bleeding manifestation from other side of
body, unconsciousness and alteration of sleep pattern.
His urinary output is normal and bowel moves once daily. For the last few
months he noticed that he gradually losing his body and pubic hair and
decreased frequency of saving and loss of libido. He also gave history aspiration
of fluid from his abdomen twice after admission in medicine unit and color of the
fluid was clear
PERSONAL HISTORY DR SHAMOL /EDEMA
The patient is Non smoker, Non alcoholic. And have no history IV drug user. The
patient had history multiple extra marital sexual exposure
CLD

ASCITES

CCF DR SHAMOL /EDEMA


Ascites with TB or malignancy
key : ascites plus History of ---fever , weight loss with ( +/- ) diarrhea or abdominal pain
According to the statement of patient he was relatively well 6 months ago then he gradually
developed swelling of whole body which first noticed at abdomen subsequently become
generalized .
This swelling was associated with fever. Which was low grade intermittent in nature The
temperature raised mostly at the evening and used to persist 4 to 6 hrs and subsided with
sweating with or (without) medication. Highest recorded temperature was 1010F.
He denies any recent and past history of jaundice, abdominal pain (if present then
elaborate it), chest pain, palpitation, joint pain and swelling, skin rash, alternation bowel
habit (in form of loose motion) and passage of mucus with or without blood (if give history
of diarrhea –then elaborate it also),He also denies vomiting out of blood and black tarry
stool, bleeding manifestation from other side of body during the courses of illness. He also
denies axillary and pubic hair loss and his saving frequency is normal .his urinary output is
normal .But he complained of fatigue and anorexia to all kinds of food,
He loses 10 kg weight during the course of illness. He had no history of contact with TB
patient. He also gave history aspiration of fluid from his abdomen twice after admission in
medicine unit and which was straw in color
PERSONAL HISTORY DR SHAMOL /EDEMA
The patient is Non smoker, Non alcoholic. And have no history IV drug user. The patient had
not history of extra marital sexual exposure
CCF-- Key point – breathlessness plus edema
First take history breathlessness ---see under dyspnea / breathlessness
the patient also give history of generalized body swelling for 2moths .initially
he noticed swelling in both leg then it involved abdomen and subsequently it
become generalized. The patient also developed episodic productive cough
for same duration containing scanty frothy sputum having no diurnal variation
or seasonal variation and no history of coughing out of blood.
His bowel & bladder habit is normal.
He denies any recent and past history of jaundice, chest pain (if present then
elaborate it ), palpitation, fever , night sweat and weight loss , joint pain and
swelling, skin rash, vomiting out of blood and black tarry stool, bleeding
manifestation from other side of body during the courses of illness. He also
denies axillary and pubic hair loss and his saving frequency is normal .But he
complained of fatigue and anorexia to all kinds of food. He had no history of
contact with TB patient
PERSONAL HISTORY DR SHAMOL /EDEMA
The patient is Non smoker, Non alcoholic. And have no history IV drug user.
The patient had not history extra marital sexual exposure
Nephritic syndrome Nephrotic syndrome
Haematuria (red or brown urine) massive Overt proteinuria usually >3.5
Oedema g/24 hrs Oedema
Oliguria Hypoalbuminaemia < 30 g/L
Hypertension hypercholesterolemia
difference between nephrotic syndrome and AGN
AGN nephrotic syndrome
onset sudden insidious
HO sore throat not so
skin infection in adult HO 2ndary cause e.g. DM
urine color red / dark /cocacola color frothy , smoky
HTN present absent
edema mild to moderate massive
oligouria present may present at late stage
urine RME RBC and RBC cast no RBC or RBC cast
protein uria + to ++ protein uria ++++
DR SHAMOL /EDEMA
AGN—causes NS—causes
1st say primary causes
1. post streptococcal glomerulonephritis 1st say 1 and 2 if want more than 3,4,5
if sir want to more than say FM3
1. connective tissue disease M—minimal change (in child )
a. SLE M—membranous GN (in adult )
M—mesangio-capillary GN
2. vasculitis
F—Focal and segmental glomerulosclerosing
3. Henoch scholein purpura I—IgA nephropathy
other infection secondary causes CID
other bacterial infection C—collagen disease –SLE , RA
1. infective endocarditis C—Carcinoma –bronchial , non-Hodgkin
2. meningo coccal infection lymphoma
3. pneumococcal infection I—infection
4. plasmodium malarae 1. HBV,HCV, HIV
5. viral hepatitis 2. plasmodium malarae
3. secondary syphilis
4. leprosy (type II lepra reaction )
5. bacterial endocarditis
DR SHAMOL /EDEMA D—DM
D—drug –pencillamine , captopril (ACE), gold,
NSAID
Abnormal accumulation fluid in interstitial space is called oedema.
Unilateral Bilateral
1. Lymphoedema 1. Heart failure
a. filariasis 2. cirrhosis
b. lymphatic obstruction due 3. Hypoproteinaemia
to a. nephrotic syndrome,
malignancy , b. kwashiorkor / mal-nutrion
radiation , c. mal-absorption
surgery 4. Chronic venous insufficiency
2. Deep vein thrombosis 5. Inferior vena caval obstruction
3. cellulites 6. Drugs, e.g. NSAIDs, nifedipine,
4. Chronic venous insufficiency amlodipine, fludrocortisones
5. Immobility, e.g. hemiplegia 7. Thiamine (vitamin B1) deficiency
(wet beriberi)
8. Milroy’s disease (unexplained
DR SHAMOL /EDEMA lymphoedema which appears at
puberty; more common in females)
define oedema
oedema is an abnormal accumulation of fluid in the interstitium or in one or
more cavities of the body
classification with example
according to distribution
 generalized and localized
according to depress on pressure
 pitting and nonpitting edema
generalized edema localized
 heart causes –CCF lymphatic obstruction/ lymphoedema
 liver causes –CLD  Filariasis
 renal cause -- nephrotic Venous causes
syndrome  Deep venous thrombosis or chronic
 other causes venous insufficiency
o mal absorption / Inflammatory causes.
malnutrition Allergic causes
o protein-losing enteropathy  Angio-oedema (the face, lips and
o pregnancy mouth )
DR SHAMOL /EDEMA
o drug
What do u mean by pitting edema ? name some causes of non pitting edema ?
the oedema that leaves an indentation after pressure on the affected area is called
'pitting' oedema,
non pitting edema
lymphatic obstruction/ lymphoedema
 Infection: filariasis,
 Malignancy
 Radiation injury
 Congenital abnormality
myxoedema in hypothyroidism
pitting edema ---rest causes r pitting edema (eg heart , liver , kidney causes )
in which malnutrition edema occur ? name some drug causes edema
Kwashiorkor
drug causes edema
 calcium channel blocker –Amlodipine , NSAID, steroid , OCP
name two endocrine disease where we get edema
 Conn
 hypothyroidism
if a diabetic patient come with edema what may be causes
o nephrotic syndrome DR SHAMOL /EDEMA
o due to loss of vasomotor tone
what is the mechanism of edema
there several causes –
 ↓colloid osmotic (or oncotic) pressure due to hypoalbuminea ---(eg. Renal , git )
 Increase hydrostatic pressure (heart failure)
 Increase capillary permeability (inflammatory causes )
 Secondary hyperaldosteronism (mainly in heart failure )
 Lymphatic obstruction
Where we see edema?
over the shin of tibia just above the medial maleolus …. Press with both thumb over
both leg for 10/ 15 sec ..during pressing you should look at patients face to pain
in case bed ridden patient
ask the patient to sit down see over sacrum or
zygomatic arch of face (tell only if ask where we see also)
mechanism of edema in different disease
heart failure due to increase hydrostatic pressure
Secondary hyperaldosteronism
nephrotic syndrome decrease colloid osmotic (or oncotic) pressure due to
hypoalbuminea
CLD portal hypertension
decrease colloid osmotic (or oncotic) pressure due to
hypoalbuminea DR SHAMOL /EDEMA
How will differentiate different type of edema?
heart failure HO
 Respiratory distress or breathlessness. orthopnea
 HO heart disease
 Edema first appear at dependent part (leg)
examination :
tachycardia
JVP raised
tender hepatomegaly
investigation :
ECG , ECHO , CXR—feature of heart failure
unrine RME—normal
nephrotic syndrome HO
edema first appear at face
HO of renal disease ---frothy urine . oliguria
no HO breathlessness
examination :normal ( HTN—if AGN)
investigation
urinary –protienuria (massive )
DR SHAMOL /EDEMA
24 hr total urinary protein
serum albumin –decrease
 How will differentiate different type of edema?
CLD HO
 history jaundice , Alcohol , risk factor for HBV (sexual
exposure )
 swell first appear at abdomen / ascites
examination
 feature of hepatic insufficiency –hepatic faces ,
gynaecomastia , spider navi, loss body hair , engorged
vein , splenomegaly , testicular atrophy
investigation
 viral marker (HBS ag) (anti-HCV)
 USG
 liver function test –Albumin , AG ratio
 endoscopy to see varices
tell one bed side test that can help u to diagnosis of cuases of edema
heat coagulation test --- nephrotic syndrome
DR SHAMOL /EDEMA
what is lymphedema and why it is non pitting and causes ?
Normally, small amount of albumin filtered through the capillaries is absorbed
through lymphatics. In lym¬phatic obstruction, water and solutes are reabsorbed
into the capillaries, but the protein remains. Fibrosis occurs in the interstitial space
and the area becomes hard or thick. Non pitting on pressing .
causes of lymphoedema is due to lymphatic obstruction such as
 Infection: filariasis,
 Malignancy
 Radiation injury
 Congenital abnormality—turner , yellow nail syndrome
what investigation you will do in patient with edema ?
urine RME
24 hr total urinary protein
S.creatinine
RBS
ECG
CXR
ECHO
DR SHAMOL /EDEMA
USG of whole abdomen
s.Albumin , A/G ration
What are the causes of unilateral leg swell?
 Deep venous thrombosis.
 cellulitis.
 Lymphoedema---filariasis
 Ruptured Baker's cyst.
How will differentiate DVT and cellulitis ?
DVT cellulitis
less erythemous , non toxic , more erythemous , pt toxic , fever ,
less rise of temperature high rise of local temperature
tenderness along the distribution of deep diffuse
venous system
infective foci absent present
leg swelling entire leg swelling localized swelling
calf swelling > 3 cm than opposite limb < 3 cm than opposite limb
collateral superficial present absent
vein
investigation CBC –normal CBC—leucocytosis
color dopplor --- + color dopplor --- negative
risk factor present immobilization DM
surgery ,pregnancy DR SHAMOL /EDEMA
malignancy ,ocp
What are thrombophlebitis and phlebothrombosis ?
Thrombophlebitis (superficial vein thrombosis): inflammation involving
superficial veins (after intravenous fluid or injection . Pain, Increased local
temperature ,prominent superficial vein
Phlebothromhosis (DVT): thrombosis in deep veins is non-inflammatory in
nature. Present with unilateral swell
investigation of unilateral leg swelling
 CBC—
o eosinophil may be high in filariasis,
o leucocytosis---cellulitis
 Blood film to see microfilaria (usually at night)
 Compliment fixation test (CFT) or ICT for filaria.
 Lymphoscintigraphy
 FOR DVT
o D-dimer
o Doppler USG of lower limb vessels
DR SHAMOL /EDEMA
What are thrombophlebitis and phlebothrombosis ?
Thrombophlebitis (superficial vein thrombosis): inflammation involving
superficial veins (after intravenous fluid or injection . Pain, Increased
local temperature ,prominent superficial vein
Phlebothromhosis (DVT): thrombosis in deep veins is non-inflammatory
in nature. Present with unilateral swell
investigation of unilateral leg swelling
 CBC—
o eosinophil may be high in filariasis,
o leucocytosis---cellulitis
 Blood film to see microfilaria (usually at night)
 Compliment fixation test (CFT) or ICT for filaria.
 Lymphoscintigraphy
 FOR DVT
o D-dimer
o Doppler USG of lower limb vessels
DR SHAMOL /EDEMA
grading definition
"Absent Absent or unilateral
"
Grade + Both feet / ankles
Mild:
Grade Both feet, plus 00+= no pitting edema
++ lower legs, 1+= mild pitting edema , 2 mm
Modera hands or lower depression that disappears rapidly
te: arms 2+= moderate pitting edema ,4 mm
Grade Generalised depression that disappears in 10-15
+++ bilateral pitting second
Severe edema, 3+= moderately severs pitting edema
including both ,6 mm depression that may last more
feet,legs, arms and
than 1 minute
face 4+= severe pitting edema 8mm
DR SHAMOL /EDEMA depression that can last more than 2
minutes
Causology is the lock
History is key
Medicine ward is locked door

Jaundice
History & causology
For block posting ,
3rd to 5th year and
post graduate student
Dr . Shahidullah shamol
FCPS (medicine )
Dr shamol /history
duration
which part involved in first sclera  urine and the whole body
sequence
HO- viral prodome anorexia , nausea , vomiting , joint pain , malaise
fever simple fever + prodome  viral hepatitis
fever with chill and rigor  cholangitis
fever + jaundice  viral hepatitis ,leptospirosis ,
malaria , liver abscess , cholangitis
the jaundice progressive , progressive malignancy (Ca-pancreas )
static , fluctuating static  viral hepatitis
fluctuating—stone
recurrent –stone / Wilson/ haemolytic anaemia
stool pale or not obstructive jaundice
itching / dark color urine

Dr shamol /history
Ho bleeding obstructive jaundice—due to ViT –K
manifestation deficiency
(epistaxis , purpura,
gumbleeding )
abdominal pain viral hepatitis /stone

HO for etiology HO Alcohol, IV drug , Blood transfusion ,


saving in salon extramarital sexual
exposure , tattoos –B virus
water and sanitation –for A and E virus
Dr shamol /history drug History –anti-TB drug
Family history  other siblings –wilson
and haemolytic anaemia
Ho recurrent blood transfusion + anaemia
–thalasemia
travel history to abroad
unconsciousness encephalopathy

stigmata of CLD  immunization


 loss body hair decrease saving frequency ,
edema , ascites , loss of libido

Bowel habit if constipation chance of encephalopathy


steatorrhoea –in case of obstructive jaundice

Dr shamol /history
A=Anorexia , ALCOHOL
B=Bleeding manifestation , blood transfusion

C=Color of stool (pale)/ urine (dark )


D=Drugs (herbal drug), drinking water and sanitation

E= Exposure –extramarital sexual exposure


F=Fever
G=GIT—nausea , vomiting , abdominal pain
H=Ho—previous jaundice , family HO , HO of consanguinity
I=Itching , IV drug
J=Joint pain

L=Loss of body hair , libido --CLD


Dr shamol /history
If viral hepatitis: If viral

hepatitis:

Dr shamol /history
If viral hepatitis:
According to the statement of the patient he was reasonable well one
month back. Then he noticed yellow coloration of sclera, skin and urine
which was associated with (preceded by) anorexia/ loss of appetite,
nausea, malaise, joint pain. This yellow coloration was progressively
increasing and not associated with fever, abdominal pain, itching, pale
color stool and any bleeding manifestation.(((( if patient complained
pain then write this line ---The patient also complained right upper
abdominal pain Which was mild to moderate in intensity dull aching
in nature (or character ) having no radiation. The pain had no specific
aggravating or reliving factors.)))) .he used to save in the salon but
unaware of using disposable razor. The patient had no history loss
consciousness, pubic or axilary hair loss ,blood transfusion. His bladder
and bowel habit is normal and libido is intact Dr shamol /history
He is non-alcoholic, non smoker, no history of IV drug abuse
He has two brothers and three sisters. None of his siblings are suffering
this type of disease. His parent has not consanguinity.
He drinks arsenic free tube-well water and use sanitary latrine
obstructive jaundice

Dr shamol /history
If obstructive jaundice:
According to the statement of the patient he was reasonable well one
month back. Then he noticed yellow coloration of sclera, skin and urine
which was progressively increasing. This yellow coloration was
associated with generalized itching and pale stool. The patient also
complained right upper abdominal pain which was mild to moderate in
intensity, colicky in nature (or character) having no radiation. The pain
had no specific aggravating or reliving factors. He had no history of
nausea, vomiting, malaise, joint pain, fever and any bleeding
manifestation. He used to save in the salon but unaware of using
disposable razor. The patient had no history loss consciousness,
alteration of behavior, blood transfusion. His appetite, bladder and
bowel habit is normal and libido is intact.
He is non-alcoholic, non smoker, no history of IV drug abuse . no HO
history extra-marital sexual exposure Dr shamol /history
He has two brothers and three sisters. None of his siblings are suffering
this type of disease. His parent has not consanguinity.
Classify jaundice?
Prehepatic or Haemolytic jaundice
Hepatocellular
Post Hepatic or Obstructive jaundice
haemolytic jaundice hepatocellular jaundice
 Haemolysis.—thalassamia  Acute viral hepatitis,
, autoimmune haemolytic  Alcoholic,
anaemia  Autoimmune,
 Falciparam malaria  Drug-induced—anti-
 Gilbert's disease. tubercular drugs
 Dubin-Johnson syndrome.  Cirrhosis
Dr shamol /history
 Rotor syndrome
Post Hepatic or Obstructive jaundice
Intrahepatic Extrahepatic
1. Primary biliary cirrhosis 1. Carcinoma
2. Primary sclerosing cholangitis a. Ampullary
3. Alcohol b. Pancreatic
4. Drugs c. Bile duct(cholangiocarcinoma)
5. Hepatic infiltrations d. Liver metastases
a. lymphoma, 2. Choledocholithiasis
b. granuloma, 3. Parasitic infection (worm )
c. amyloid, 4. Traumatic biliary strictures
d. metastases 5. Chronic pancreatitis
6. Cystic fibrosis
7. Severe bacterial infections
8. Pregnancy Dr shamol /history
9. Inherited cholestatic liverdisease,
e.g. benignrecurrent intrahepatic
cholestasis
10.Chronic right heart failure
causes of recurrent jaundice cause of prolong Jaundice not for MBBS
CONGENITAL CONGENITAL
1. Gilbert 1. Gilbert
2. Wilson 2. Wilson
HEAMATOLOGICAL HEAMATOLOGICAL
1. hameolytic anaemia 1. hameolytic anaemia
a. thalassaemia a. thalassaemia
b. auto-immune-haemolytic anemia HEPATIC
HEPATIC 1. Auto-immune hepatitis
1. Auto-immune hepatitis 2. Alcoholic hepatitis
2. primary sclerosis cholangitis 3. chronic active hepatitis / cirrhosis
3. CLD / chronic active hepatitis 4. Carcinoma of liver primary or 2ndary
billiary duct and pancrease billiary duct and pancrease
1. choledocolithiasis 1. primary sclerosis cholangitis
2. recurrent cholangitis 2. Primary billiary cirrhosis
3. choledochal cyst 3. Extraheaptic billiary obstruction
4. recurrent pancreatitis a) choledochal cyst / helminthes
b) cholangiocarcinoma
Dr shamol /history c) stricture
d) impacted gall stone
1. carcinoma of head of pancrease
common causes biliary causes
bile duct A. intraluminal obstruction
a) choledocholithiasis 1. cholangiocarcinoma
b) cholangitis 2. impacted stone in bile duct
c) Choledochal cyst 3. Primary biliary cirrhosis
liver 4. Primary sclerosing cholangitis
a) viral hepatitis B. Extra luminal obstruction
b) hepatocellular carcinoma / 1. in porta-hepatis by lymphoma
hepatoma on the top of CLD 2. Carcinoma of head of
c) liver abscess pancreases
other than hepato-biliary C. liver causes
a) pancreatitis 1. decompnesated CLD
b) lymphoma with protahepatic 2. hepatocellular carcinoma a
obstruction Fluctuating
uncommon 1. Choledocholithiasis
Dr shamol /history
a) PSC 2. Stricture
b) SBP with CLD 3. Choledochal cyst
4. Primary sclerosing cholangitis
5. Pancreatitis
abdominal mass and jaundice lymphadenopathy with jaundice
billiary and pancreases liver
1. Carcinoma 1. autoimmune hepatitis
a. Of head pancreases malignancy
b. Cholangiocarcinoma 1. haematological
2. Pancreatitis (cyst) a. lukaemia (ALL, CLL)
3. Choledochal cyst b. Lymphoma
hepatic 2. other
1. hepatolcellular carcinoma a. disseminated malignancy
with /out CLD infection
2. secondaries in the liver 1. disseminated TB
3. liver abscess 2. infectious mononucleosis
other than hepato-billiary
1. lymphoma Dr shamol /history
jaundice with hepatomegaly jaundice with
hepatosplenomegaly
1. viral hepatitis hepatic
2. cirrhosis 1. Decompensate CLD with portal
a. haemochromatosis hypertension
b. Alcoholic 2. Hepatoma on the Top of CLD
3. Carcinoma hematological
a. HCC with / out—CLD 1. hameolytic anaemia
b. secondary’s in the liver 2. lymphoma
4. infection 3. CLL
a. liverabscess infective
b. disseminated TB 1. disseminated TB
(granulomatous hepatitis ) 2. Kala-azar

Dr shamol /history
fever with jaundice jaundice with fatigue
hepatic 1. Auto-immuno hepatitis
1. viral hepatitis 2. PBS
2. liver abscess 3. psc
3. cholangitis jaundice with arthritis
infective 1. Viral hepatitis
acute : Mbbs only white
Color 2. autoimmune hepatitis
1. malaria 3. haemochromatosis
2. leptospirosis 4. lymphoma
3. septicaemia 5. PBC
4. dengue 6. SLE and vasculitis
chronic 7. Drug reaction
1. Kala-azar and 8. haemolytic anaemia with
2. disseminated TB pseudo gout
others
Dr shamol /history
1. lymphoma
jaundice with pregnancy
not related with pregnancy
1. viral hepatitis
2. drug
3. cirrhosis
4. auto-immuno hepatitis
5. Wilson
related with pregnancy
1. intrahepatic cholestatic of pregnancy
2. acute fatty liver of pregnancy
3. HELLP

Dr shamol /history
Causology is the lock
History is key
Medicine ward is locked door

ANAEMIA
History & causology
For block posting ,
3rd to 5th year and
post graduate student
Dr . Shahidullah shamol
FCPS (medicine )
Anaemia leukaemia , aplastic
Anaemia + fever= anaemia , kala-azar ,
lymphoma
Anaemia + bleeding = aplastic anaemia +
leukemia
naemia +HTN / nausea = CKD
Anaemia + edema = CKD ,anaemic heart
failure , malnutrition
Anaemia + organomegaly = thalassaemia ,
lymphoma , leukaemia ,
Kala-azar
AAnaemia + neurological = B12
feature +
Symptoms due  weakness, fatigue , palpitation ,
to anaemia  dizziness
 breathlessness / oedema
HO blood loss  acute or chronic
/bleeding o epistaxsis, gumbleeding , haemoptysis
maninifestation ,haematomesis , melena ,bloody diarrhea ,
 chronic hemorrhoid, menorrhagia
skin rash  purpuric rash –if present following HO
 non-itchy ,painless /painful , palpable , variable
size and shape
fever fever , weight loss , night sweat –TB ,lymphoma
fever , bleeding manifestation, toxic --leukemia
HO for etiology
Iron deficiency  HO abdominal pain , dyspepsia
anaemia  alteration of bowel habit / melena –ca colon
 drug steroid and NSAID
vitB12  dietary HO –vegan
 malabsorption 
 neurological feature tingling and numbness
parasthesia ,limb weakness
 visual disturbance (optic atrophy ), loss of
memory –dementia
 HO surgery , gastrectomy , ileal surgery, IBD
 chronic pancreatitis –recurrent upper
abdominal pain , diarrhea
 prolong use of PPI and
 pernicious anaemia --vitiligo / other
autoimmune disease –thyroid and DM
if suspect aplastic past ho jaundice/ viral hepatitis –
anaemia
drug history –cytotoxic , anti-convulsant,
anti-thyroid
radiotherapy –
exposure to –OPC, DDT, benzene
occupation  farmer , dye industry ,
radiotherapy department
for anemia of  CRF—anorexia , nausea , HTN, edema ,
chronic diseases DM
 joint pain and rash connective tissue
disease
 edema + breathlessness ---HF
in all cases  sanitary latrine , blood transfusion , bone
marrow aspiration
Prototype
history

Causology
viva
question
According to the statement of the patient he was reasonable well 2
months back. Then He insidiously developed fatigue or generalized
weakness .But now it becomes so severe that He feels difficulties
during doing ordinary daily activities like, shopping, climbing stair. This
weakness was associated with occasional dizziness and palpitation
especially after exertion.
He denies any history of fever, recurrent upper abdominal pain,
anorexia, and nausea, alteration of bowel habit, jaundice, cough, chest
pain, and breathlessness, joint pain, rash and leg edema. Patient also
denies any episode of acute and chronic blood loss in form of vomiting
and coughing out of blood, Nasal or gum bleeding, passes of fresh per
rectal blood or black tarry stool.(if present then mention it )
His bowel and bladder habit is normal and having no neurological
symptoms like, burning, tingling, numbness, visual and memory
disturbance.
With this complains He visited several physicians treated with
oral medication that transiently improved his symptoms .so
He admitted in MMCH for better management. Here 2 unit of
whole blood was transfused (tell if given) and endoscopy,
colonoscopy and bone marrow examination was done
(mention only if patient tell),
Drug history reveals patient is occasional user of anti-ulcer
drug but no history taking pain killer drug
None of his family member suffered from similarly type of
disease
He is non-alcoholic, non-smoker, Uses sanitary latrine and
drink arsenic free tube well water
Morphological
Microcytic, TISA
hypochromic T— Thalassaemia
(MCV<76 fl) I— Iron deficiency
S— Sederoblastic anaemia
A--- Anaemia of chronic disease (in some
case)
Macrocytic 1.Megaloblastic: vitamin B12 or folate
MCV>95 fl deficiency
2.Non-megaloblastic: alcohol, liver disease,
Myelodysplasia, hypothyroid
, *first tell 1 & if want to more then tell 2
Normocytic C-(Chronic)-Anemia of chronic disease
anemia ABC CRF,
connective tissue disease
A--(Aplastic )--Aplastic aneamia
B—(Blood)--Anemia due to acute blood loss
etiological classification
due to blood loss acute haemorrhage
increased haemolysis Haemolysis
Hypersplenism
Decreased or 1. Lack of iron, vitamin B12 or
ineffective marrow folate
production 2. Hypoplasia/myelodysplasia
3. Invasion by malignant cells
4. Renal failure
5. Anaemia of chronic disease
in general --J—jaundice S—Splenomegaly , O—no organomegaly -H--
hepatomegaly L—Lymphadenopathy
common causes anaemia / simple haemolytic anemia
anaemia 1. Auto-immune anaemia--JSH
1. iron deficiency anaemia--O 2. thalassaemia --JSH
2. megaloblastic anaemia –O,S
3. aplastic anaemia--O
4. malabostion --O
5. multiple myeloma--O
haematological malignancy chronic diseases
lympho proliferative disease- 1. connective tissue disease
1. acute leukaemia--- JSHL a. RA, SLE --SHL
2. CLL--- JSHL 2. CRF--O
3. lymphoma-- JSHL 3. CLD--JSH
myloproliferative disease 4. endocrine
1. mylofibrosis--S a. hypothyroid--O
2. CMI-- SH b. hypopituitism --O
3. multiple myeloma--o c. Addison’s --O
4. waldenstrom macrogolbinaemia--SH
causes of anemia with --J—jaundice S—Splenomegaly , O—no
organomegaly -H--hepatomegaly L—Lymphadenopathy
common causes anaemia 1. iron deficiency anaemia--O
/ 2. megaloblastic anaemia –O,S
simple anaemia 3. aplastic anaemia--O
4. malabostion –O
5. multiple myeloma--O
haematological lympho proliferative disease-
malignancy 1. acute leukaemia--- JSHL
2. CLL--- JSHL
3. lymphoma-- JSHL
myloproliferative disease
1. mylofibrosis--S
2. CMI—SH
3. multiple myeloma--o
4. waldenstrom macrogolbinaemia--SH
1. mylodysplastic syndrome—S
GO NEXT SLIDE
causes of anemia with --J—jaundice S—Splenomegaly , O—no
organomegaly -H--hepatomegaly L—Lymphadenopathy
infection 1. Kala-azar--JSH
2. chronic malaria—JSH
3. disseminated TB—JSHL
haemolytic 1. Auto-immune anaemia—JSH
anemia 2. thalassaemia --JSH
chronic 1. connective tissue disease
diseases a. RA, SLE --SHL
2. CRF--O
3. CLD--JSH
4. endocrine
a. hypothyroid--O
b. hypopituitism –O
c. Addison’s --O
Malignancy -O
anemia with edema
here edema may be due to underlying oedema may result of
causes it self Likes: complication like heart failure
abdominal causes due to severe anaemia of any
1. Malabsorption causes
2. CRF 1. iron deficiency anaemia
3. CLD 2. aplastic anaemia
connective tissue disease 3. megaloblastic anaemia
1. SLE 4. thalassamia
2. RA 5. heamatological malignancy
endocrine 6. combined deficiency
1. hypothyroid
infection
1. Kala-azar
haematological
1. Multiple myeloma (nephrotic
syndrome)
2. lymphoma (nephrotic syndrome)
aneamia with ascites
here ascites may be due to ascites may result of complication
underlying causes it self likes: like heart failure due to severe
1. malabsorption anaemia of any causes
2. organ failure 1. iron deficiency anaemia
a. CLD 2. aplastic anaemia
b. CRF/ CKD 3. megaloblastic anaemia
3. infection 4. thalassamia
a. abdominal TB 5. heamatological malignancy
b. HIV 6. combined deficiency
4. malignancy
a. lymphoma
b. intra-abdominal malignancy
5. endocrine disease
a. hypothyroid disease
6. connective tissue
a. SLE.RA
b. Adult still disease
causes of refractory anemia
common causes hematological other causes where ongoing loss or
1. aplastic anemia replacement therapy is inadequate :
2. myelodysplastic syndrome 1. iron deficiency anemia due to
3. sideroblastic anemia Malabsorption with oral iron
4. myelofibrosis replacement
5. thalassamia major 2. ongoing loss –bleeding
heamatological malignancy 3. any malignancy
1. lymphoma 4. anemia due to hypersplenism
2. CLL
3. CML
4. Multiple myeloma
other than heamatological
1. CKD
Connective tissue disease
1. SLE
2. RA
anaemia with high ESR striking pallor
infection this striking pallor may be
1. kala-azar 1. due to anaemia or
2. disseminated TB 2. other than anaemia
connective tissue diseases in case of severe anaemia
1. SLE 1. Aplastic anaemia
2. RA 2. Iron deficiency anaemia
malignancy 3. multiple myeloma
1. Multiple myeloma 4. thalassaemia major
2. lymphoma 5. myelodysplastic syndrome
3. leukaemia other than anaemia
4. other malignancy Endocrine
heamatological 1. Hypothyroidism
1. aplastic anaemia 2. hypopituitarism
2. myelodysplastic syndrome shock
3. myelobfibrosis
any causes of anemia causes high ESR
Q. Define Anaemia.
Anaemia is a clinical condition characterized by both qualitative
and quantitative decrease in Hb below the normal level irrespective
to age and sex of a person.
Q. Where we look anemia?
 Lower palpebral conjunctiva.
 Dorsal surface of tongue.(tongue is smooth and loss of papilla )
 Palm and sole of feet.
 Whole body
Then what is your finding : tell with adjective such pt is mildly
/moderately / severely anemic
Classify anaemia
Etiological Central cause Marrow failure  aplastic
anaemia, anemia of chronic
disease
Peripheral cause  blood loss, heamolysis
Morphological Microcytic (MCV<76 fl)
hypochromic anaemia to remember TISA
T— Thalassaemia
I— Iron deficiency
S— Sederoblastic anaemia
A-- Anaemia of chronic disease (in
some case )
Macrocytic anaemia MCV>95 fl
to remember---MND
M--Megaloblastic: vitamin B12 or folate
deficiency
N--Non-megaloblastic: alcohol, liver
disease,hypothyroid
D--(dysplastic)--Myelodysplasia,
Normocytic to remember ABC
normochromic A--Aplastic aneamia
anaemia B--Anemia due to acute blood loss
C--Anemia of chronic disease
–CRF, connective tissue disease
what is the normal Hb level ?
male: 13-18 gm/dl
Female: 11.5-16.5 gm/dl
Q. In which condition Hb level is 100% and ESR `0’?
Ans. Polycythaemia
what r causes of iron deficiency anemia?
In both male & In female- Other-
female Pregnancy malabsorbtion
PUD Menorrheagia Coeliac disease
Hook worm
Carcinoma stomach
Drug- NSAID
haemorrhoid
What are investigation of iron deficiency , thalassemia ,Megaloblastic anemia?
Iron deficiency thalassemia megaloblastic
blood blood blood
TC, DC, Hb%, ESR TC, DC, Hb%, ESR Hb%
PBF- Microcytic hypochromic PBF- Microcytic hypochromic PBF- macrocytic RBC
anaemia anaemia Bone marrow- megaloblast
Iron profile: reticulocyte ↑ Vitamin B₁₂ level or red cell
Serum ferritin ↓ S.bilirubin folate level
Total iron binding capacity ↑ Iron profile: To see cause:
To find etiology: Serum ferritin ↑  Schilling test
Upper GI endoscopy Total iron binding capacity ↓  Enodoscopy to see
Colonoscopy To comfirm diagnosis: atrophic gastritis
barium follow through Heamoglobin  Anti-parietal cell
Stool for ova of helminthes electrophorosis antibody
single test to dx single test to dx single test to dx
Serum ferritin ↓ Heamoglobin Bone marrow- megaloblast
electrophorosis S. Vitamin B₁₂ level
What is the clinical feature of iron? thalassemia, megaloblastic?
iron thalassemia megaloblastic
HO of blood loss family history HO etiology
dietary HO --vegan
gastric/ intestine
operation
pernicious anemia
malabsorption
eye :anemia face eye :anemia
tongue: smooth pale and  heamolytic face tongue : glossitis
loss of papillae eye neurological
Mouth: glossitis, angular  anemia Eye: optic atrophy
stomatitis  jaundice Loss of memory :
nail : koilonychia abdomen dementia
 hepato-splenomegaly sensory : Sensation loss
in gloves and stocking
pattern ,
loss of vibration and
Investigation of anemia ?
iron thalassaemia anemia of chr. Dis
CBC Hb ↓ Hb ↓ Hb ↓
PBF microcytic microcytic normocytic
hypochromic hypochromic normochromic
reticulocyte N ↑ N
bone marrow iron ↓ ↑ ↑
s.feritin ↓ ↑ ↑
S.iron ↓ ↑ n/
TIBC ↑ ↓ ↓
Transferrin ↓
saturation
Soluble transferrin ↑ N/ N /↓
receptor
Hb electrophorosis not done confirm diagnosis not done
for etiology Upper GI genetic study S.creatinine
endoscopy
Colonoscopy
Stool for ova of
Q. What are the PBF findings in iron deficiency anaemia?
Ans. Microcytic hypochromic anaemia, anisocytosis, pencil cell, target cell,
nucleated RBC.
How will you differentiate PBF of iron deficiency anaemia and
Thalassaemia.?
Iron deficiency anaemia Thalassaemia
Few target cell Plenty of target cell
No features of heamolysis Features of heamolysis present
eg. Fragment cell, Pencil cell
What are the PBF findings of Vitamin B₁₂ and Folic acid deficiency?
Ans. Pancytopenia with Macrocytosis with hypersegmented neutrophil.
Megaloblast & Howel-jolly body may present.
Q. Bone marrow findings of Vitamin B₁₂ deficiency?
Ans. Megaloblastic change in erythoid series .
Q. what are the other causes of macrocytosis?
Ans.
Alcohol
Liver disease
Hyperlipidaemia
Name the sites of iron and Vitamin B₁₂ absorption.?
Iron absorbed in jejunam.
Vitamin B₁₂ absorbed in ileum

Q. What are the causes of megaloblastic anaemia?


Deficiency of Vitamin B₁₂ and Folic acid.
Q. Vitamin B₁₂ and Folic acid deficiency- which one is more common? Why?
Ans. Folic acid deficiency is more common than vitamin B12 deficiency.
Point Vitamin B₁₂ Folic acid
Store 3years 3 months
Sources Animal plant
Effect of cooking Not destroyed Destroyed during cooking
Q. in which anaemia causes neurological manifestation ?
Megaloblastic anaemia due to Vitamin B₁₂ deficiency
Q. Name causes of Vitamin B₁₂ and Folic acid deficiency
causes of Vitamin B₁₂ and Folic acid deficiency:
Vitamin B₁₂ Folic acid
 Diet: vegan diet:
 Stomach: Increased demand,
o pernicious anaemia, poor intake of vegetables
o partial/ total gastrectomy Intestine: malabsorption, coeliac
 Intestinal: malabsorption disease
o tropical sprue, Drug: phenytoin, MTX
o coeliac disease, Other
o crohn’s haemolysis,
Q. How Vitamin B₁₂ absorbed in GIT?
Ans. Vitamin B₁₂+food stomach acid causes release of Vitamin B₁₂ from food
 Vitamin B₁₂ + intrinsic factor(secrete from parietal cell)  absorption at
terminal ileum.
What is pernicious anaemia?
It is an autoimmune disease in which antibody is formed against parietal cell
(which secrete intrinsic factor)
Q. Tell me the one investigation to diagnose iron deficiency anaemia.
Ans. Serum Ferritin
Q. Mention the treatment of iron deficiency anaemia
Ans. Tab. Ferus Sulphate (200mg), tds, for 3-6 months.
how will follow uP / how will understand that anemia is improved?
Follow up:
 Hb will increase 1gm/dl in every 7-10 days.
 Reticulocyte count will increase after 1 week
What are the indications of blood transfusion in anaemia?
 Angina
 Heart failure
 Evidence of cerebral hypoxia.
What are the complications of oral iron therapy?
Dyspepsia, Altered bowl habit.
What is the indication of Parenteral iron therapy?
Malabsorption.
severe anaemia
. Infusion of 1 unit of blood causes how much increase in Hb level?
Infusion of 1bag blood causes 1gm/dl increment of Hb level.
name iron therapy ?
oral parental
 Ferrous sulphate 200 mg times old preparation
(195 mg of elemental iron per day) iron dextran
 ferrous gluco-nate 300 mg twice iron sucrose
daily (70 mg of elemental iron) new preparations
iron isomaltose and
iron carboxymaltose
what is the treatment of Vitamin B₁₂ deficiency anaemia?
Vitamin B₁₂ supplementation:
Inj. Hydroxycobalamine 1000 µgm , 1 ampule, I.M. every 2 day for 5 days.
Maintenance: 1 amp, I.M. 3 monthly for lifelong.
What is the treatment of folic acid deficiency?
Tab. Folic acid 5 mg, (1+0+0) for 3 weeks, than lifelong
What is the importance of folic acid in pregnancy?
Deficiency of folic acid during pregnancy causes neural tube defect in fetus.
To prevent neural tube defect in fetus, when folic acid supplementation
should be started ?
Folic acid supplementation should be started before conception, because,
In witch conditions folic acid is used prophylactically?
Haemolytic anaemia
Pregnancy
With MTX therapy
Q. If a patient with Vitamin B₁₂ deficiency is given folic acid without giving
Vitamin B₁₂, what will happen
Ans. It will cause subacute combined degeneration of spinal cord.
Q. . What are the neurological feature of subacute combined degeneration of
spinal cord?
Ans. Jerks absent but planter extensor .
Q. what is the daily requirement of Vitamin B₁₂?
Ans. 1µgm/ day
what are the sources of Vitamin B₁₂?
Animal source.
What are the causes of anaemia of chronic disease?
Renal failure
Connective tissue disease
Q. What are the PBF findings of anaemia of chronic disease?
Q. what is the mechanism of anaemia of chronic disease
Ans. IL₆ suppresses the bone marrow.
Q. What biochemical abnormality occurs in heamolytic anaemia?
Ans. Mnemonic: BDR- Head- quarter
B- ↑billirubin
D- ↑LDH
R-↑Reticulocyte
Head-↓heptoglobin
Quarter-↑urobillinogen
how will calculate parental needed iron is
iron = (15—measured Hb ) X Wt in kg X2. 3 +
requirement. 500mg (for storage )
given in 3 dose every alternate day in 500
DA
xenofer –100mg /5ml
Causology is the lock
History is key
Medicine ward is locked door

ARTHRITIS
History & causology
For block posting ,
3rd to 5th year and
post graduate student
Dr . Shahidullah shamol
FCPS (medicine )
1. duration of pain acute /chronic
< 6 wks –viral and > 6 wk inflammatory
arthritis
1. onset insidious –inflammatory
sudden –gout , trauma
sub acute –septic
1. joint number mono arthritis –1
2. single or oligoarhtritis –(2 to 4)seronegative (AKS,)
multiple poly arthritis – 5 or more RA, SLE

1. Sequence of which joint first affect ---sequencly mention


arthritis their name –such first – first ankle joint then
knee and then hand joint
1. symmetrical symmetrical –RA/ SLE
involvement asymmetric --seronegative
1. intensity severe
mild to moderate
1. nature inflammatory—pain is more on rest/
inactivates and decrease during
activities
non-inflammatory - pain is more on
activites and less on rest
1. Swelling and timing of stiffness –early morning or after
stiffness inactivities
how long persist  more or less than
one hour
1. functional Can patient hold glass , dressing himself
capability Can go toilet without help of other
1. any deformity flexor deformity of knee
or Deformed hand
extra-articular sign
face hair  alopecia --
red painful eye –RA, reactive arthitis
malar rash-discoid rash
oral ulcer --SLE
photosensitivities
dry mouth , eye –sjogren syndrome
hand HO raynuad –change of color of finger tips exposure to
cold
skin rash present or not –if present painful or painless , ichy
or non itchy ,scale or not
rash –SLE—face , any where of body
Gottron's papules—over knuckle ----dermatomyositis
heliotrope rash—peri- orbital --dermatomyositis
skin lesion /psoriasis –pt himself or his family member
abdomen HO bloody diarrhea , abdominal pain -
IBD
HO UTI , urethral discharge ,diarrhea 1
month before pain 
Bad obstetrical abortion ,stillbirth , death fetus ---SLE with
history anti-phospholipid syndrome
CNS convulsion / headache
/ unconsciousness –in SLE
tightening of skin of systemic sclerosis
hand
dysphasia
microstomia
difficulty in standing dermatomyositis and polymyositis
from squatting
position and rash
1. HO low back pain –more on rest and less in
seronegative activities --inflammatory
arthritis that
stiffness --inflammatory
means HO restricted spine move / unable to bending and
back pain looking forward , question mark posture --AK
pain radiate below knee , unilateral or bilateral -
-PLID
neurological sign  bladder , bowel
saddle anaesthesia –Conus or cauda equine
&weakness of limb
1. neuropathy tingling and numbness parasthesia
1. complication cough , fever , breathlessness
intra-articular injection-- steroid injection
History
of
RA
According to statement of the patient she was reasonable well 6 months back then she
insidiously developed pain and swelling of multiples joints. At first it symmetrically
involved small joints of both hands subsequently / gradually involved both wrists,
right elbow, left shoulder, both ankles and right knee joint. This pain increases after
prolong inactivity or in rest and decrease during activities. The pain was more marked
after awakening at morning and sometime this pain awaken her form sleep. This pain is
accompanied / associated with morning stiffness which persists more than one hour.
The patient have no history of oral ulcer, hair loss, red eyes, dry mouth, skin rash,
photo sensitivity , tighten of skin over hand . She also denied any color change of (or
pale coloration of finger) her figure in to exposure to cold. She has no recent and
previous HO skin disease of herself or her family member. His bowel and bladder habit
is normal. This episode of illness was not preceded by any urethral discharge, diarrhea
or burning sensation during voiding. Initially patient can do her daily activities like
dressing, combing hair, holding glass but now the pain is so severe that she has to
depend on others for for these daily activities. The patient has no HO of low back pain,
cough, breathlessness, fever, unconsciousness or behavior (CNS Involvement), difficulty
in standing from standing position. She had no bad obstetrical history .None of his
family member suffering from these types of diseases. She took several types of pain
killer and intra-articular injections which give her partially relieved not completely
History
of
SLE
According to statement of the patient he was reasonable well 6 months
back then he insidiously developed pain and swelling of multiples joints.
At first it involved left ankle joint subsequently / gradually involved
right knee, right elbow, left shoulder. This pain increases after prolong
inactivity or at rest and decrease during activities. The pain was more
marked after awakening at morning and sometime this pain awaken him
form sleep. He gives history of chronic low back pain and stiffness which
more marked in rest and relieved after activities. He gave a history of
watery diarrhea (or burning sensation during voiding) 1 month before
these attack which resolve spontaneously. He has no recent and
previous HO skin disease of himself or his family member. His bowel and
bladder habit is normal. He also denied any color change of (or pale
coloration of finger) her figure in exposure to cold. The patient have no
history of oral ulcer, hair loss, red eyes, dry mouth, skin rash, photo
sensitivity , tighten of skin over hand . Patient has no HO of cough,
breathlessness, fever, unconsciousness, difficulty in standing from
standing position.
History of
Ankylosing
spondyilitis
According to statement of the patient she was reasonable well 6 months back
then she insidiously developed pain and swelling of multiples joints (if arthralgia
–omit swelling ). at first it symmetrically involved small joints of both hands
subsequently / gradually involved both wrists, right elbow, left shoulder, both
ankles and right knee joint. This pain increases after prolong inactivity or in rest
and decrease during activities. This pain is accompanied / associated with
morning stiffness which persists more than one hour. The patient also gives HO
multiple recurrent painful oral ulcer, hair loss, non itchy painless skin rash over
face and photosensitivity. She has no history of red eyes, dry mouth; tighten of
skin over her hand & face. She also noticed that her fingers becomes pale
followed by reddish in exposure to cold. The patient has no HO of low back pain,
cough, breathlessness, dry mouth, fever, unconsciousness ,behavior abnormality
, swelling of leg, difficulty in standing from standing position. She had HO of two
spontaneous abortion and one IUD but is menstrual cycle is normal in flow and
duration. His bowel and bladder habit is normal. This episode of illness was not
preceded by any urethral discharge, diarrhea or burning sensation during
voiding. She has no recent and previous HO skin disease of herself or her family
member. She took several types of pain killer which give her partially relieved
not completely abolish this pain and swelling.
Arthralgia: only pain in the joint
Arthritis: Pain & swelling of joint.
Monoarthritis (single joint involvement)
Oligoarthritis involvement of 2–4 joints
Polyarthritis involvement of ≥5 joints
Stiffness Stiffness is the inability to move the joints after a period
of rest. It may be due to mechanical dysfunction, local
inflammation of a joint or a combination of both

Site of joint Distal interphalangeal Osteoarthritis,


involvement psoriatic arthritis
Metacarpophalangeal, Rheumatoid arthritis,
PIP systemic lupus erythematosus
First metatarsal phalangeal Gout
asymmetrical lower limb seronegative arthritis
joint
spine ankylosing spondylitis
What is difference between mechanical and inflammatory pain
point mechanical inflammatory
Onset Acute insideires
Exercise ↑pain ↓pain
Rest ↓pain ↑pain
Morning stiffness Absent Present

Systemic feature (-) (+)

Swell/warm joint (-) (+)

ESR Normal Raised


Only
for
MBBS
student
monoarthritis Oligo-arthritis
to Remember SGPT-- HOM RAPE--
S— Septic arthritis* Seronegative spondyloarthritis
G— gout R--Reactive arthritis
P— pseudogout A--Ankylosing spondylitis
T— Trauma: ( haemarthrosis) / P--Psoriatic arthritis
Foreign body E--Enteropathic arthritis
H—Haemophilia (/clotting
abnormality )
O—Oteoarthritis
M— Monoarticular presentation
of oligo- or polyarthritis
deforming arthitis migratory arthritis
1. RA 1. rheumatic fever
2. OA 2. gonocoocal
3. tropheous gout 3. lyme
4. psoriasis 4. SLE
5. Ankylosing spondylitis

arthritis with raynaud arthritis with diarrhea


1. To Remember MRCS--3 WHIST
2. M--MCTD 1. W--whipple diseases
3. R--RA 2. H--HIV
4. C--Cryoglobin 3. I--IBD
5. S--systemic sclerosis 4. S--scleroderma
6. S--SLE 5. T—TB
7. S--Sjogren when sir ask the question first u tell IBD
when sir ask the question first u tell and 2nd scleroderma then rest
systemic sclerosis 2nd SLE then rest
Only for postgraduate
student
Acute mono arthritis
monoarthritis of previously healthy mono arthritis of damage /abnormal
joint joint
to Remember SGPT-- HOME to remember
S— Septic arthritis* F—SHAPE
G— gout F—fibro-cartilaginous damage
P— pseudogout S—Septic arthritis
T— Trauma: ( haemarthrosis) / S—secondary osteoarthritis
Foreign body H—Haemoarthrosis
H—Haemophilia (/clotting A— avascular necrosis/ Subchondral
abnormality ) collapse or fracture
O—Oteoarthritis P—Pseudogout in osteoarthritis
M— Monoarticular presentation of E—exaggeration of
oligo- or polyarthritis underlyingdiseases
 Reactive, psoriatic
 other seronegative spondarthritis
 Rheumatoid arthritis
 Juvenile idiopathic arthritis
E--- Erythema nodosum
chronic monoarthritis Oligo-arthritis
FAST POEMS RAPE--JiOE
F— Foreign body (e.g. plant thorn) Seronegative spondyloarthritis
A— Amyloidosis R--Reactive arthritis
S— Chronic sarcoidosis A--Ankylosing spondylitis
T— tuberculosis, fungi P--Psoriatic arthritis
P— Pigmented villonodular E--Enteropathic arthritis
synovitis Erythema nodosum
O— osteoarthitis Juvenile idiopathic arthritis
E— Enteropathic arthritis ( Crohn's) Oligoarticular presentation of
M— Monoarticular presentation of polyarthritis
oligo-/polyarticular disease Infection,
Rheumatoid arthritis Infective endocarditis
Seronegative spondarthritis Neisseria
Juvenile idiopathic arthritis Mycobacteria
S-- Synovial sarcoma
Poly-arthritis Detail
Common Rare
1. Rheumatoid arthritis 1. Systemic sclerosis
2. Viral arthritis 2. polymyositis
3. Osteoarthritis 3. Hypertrophic osteoarthropathy
4. Psoriatic arthritis 4. Haemochromatosis (Small and
5. Ankylosing spondylitis large join)
6. enteropathic arthritis 5. Acromegaly (Mainly large
7. SLE joints and spine)
uncommon
1. Juvenile idiopathic arthritis
2. Chronic gout
3. Chronic sarcoidosis (Symmetrical,
small and large joints)
4. Polymyalgia rheumatica
bone pain without fracture recurrent fracture
To remember 2 MOP + CKD to remember MOP
1. M— M—
a. Malignancy 1. Metastasis malignancy
i. primary tumor O—
ii.metastatic tumor (breast 1. osteomalacia
, lung , prostate )
b. Multiple myeloma 2. OsteOporosis
2. O-- P—
a. osteomalacia 1. paget disease
b. osteomyelitis 2. parathyoroid --
c. osteonecrosis Hyperparathyroidism
3. P—
a. Paget disease
b. Parathyoroid --
Hyperparathyroidism
4. CKD
name the causes viral arthritis Arthritis of small joint of
if duration is less than 6 wk Hand?
Viral 1. Viral
MRCP--BIH 2. RA
M--mumps 3. SLE
R—Rebulla, (L) 4. Psoriatic
C—chickungynia / chicken pox 5. nodal osteoarthritis
P—parvo-virus –B--19 6. systemic sclerosis
B—HBV<HCV
I— infectious mononucleosis
(L)
H—HIV
joint pain with oral ulcer joint pain with leg ulcer
1. SLE 1. RA
2. reactive arthritis 2. Ankylosing spondylitis
3. rieter s 3. systemic sclerosis
4. enteropathic arthritis 4. enteropathic arthritis
5. Bechet disease 5. vasculitis
6. Vasculitis 6. HIV
7. drug reaction 7. TB
joint pain with red eye arthritis with nodule
1. RA RA
2. sarcoidosis CREST of SS
3. AKS osteoarhitis
4. reactive Gout
5. rieters Rheumatic fever
6. IBD
7. Vasculitis
joint pain renal failure joint pain + exertional dyspnea
musculoskeletal musculoskeletal
1. SLE 1. RA
2. systemic sclerosis 2. systemic sclerosis
3. Vasculitis 3. Dermatomyositis
4. NSAID + RA 4. polymyositis
infiltrative 5. SLE
1. sarcoidosis 6. MCTD
2. amyloidosis 7. Vasculitis
infection 8. Ankylosing spondylitis
1. infective endocarditis infiltrative
1. Sarcoidosis
Digital gangrene and arthritis arthritis with jaundice
1. SLE 1. viral hepatitis (HBV,HCV)
2. Systemic sclerosis 2. Auto—immune hepatitis
3. Vasculitis—primary and 3. PBC(primary biliary cirrhosis )
secondary 4. haemochromatosis
4. anti—phospholipid syndrome 5. Sarcoidosis
JOINT PAIN AND SEROSITIS joint pain and splenomegaly +/- fever
(PLEURAL EFFUSION AND ASCITES)
connective tissue disease connective Tissue disease
1. SLE 1. SLE
2. RA 2. RA with felty
3. vasculitis 3. Adult still
4. adult still infection :
5. MCDT 1. TB
6. adult still 2. infective endocarditis
7. in children JIA 3. HIV
infection blood
1. TB 1. lymphoma
haematology : 2. leukaemia
1. Lymphoma 3. hemolytic anaemia with secondary
2. leukaemia haemochromatosis
other
1. amyloidosis
2. sarcoidosis
arthritis with fever with
connective tissue disease 1. SLE
2. RA
3. Sjogren
4. sarcoidosis
5. Adult still
infection 1. HIV
2. TB
1. Viral fever
if duration is less than < 6 wk
MRCP--BIH
M--mumps
R—Rubella,
C—chickungynia / chicken pox
P—parvo-virus –B--19
B—HBV<HCV
I— infectious mononucleosis
H—HIV
Blood 1. Lymphoma
2. ALL (child)
Drug :
Causes of proximal muscle pain or weakness ? MI-DIE
M—Metabolic D--- Drugs/toxins
Myophosphorylase deficiency Alcohol &Cocaine
Hypokalaemia Fibrates & Statins
Osteomalacia Penicillamine &Zidovudine
I –Inflammatory I—infection
Polymyositis Viral (HIV, cytomegalovirus, rubella,
Dermatomyositis Epstein–Barr, echo)
Inclusion body myositis Parasitic (cysticercosis, toxoplasmosis)
Polymyalgia rheumatica Bacterial (Clostridium perfringens,
staphylococci, tuberculosis,
Mycoplasma”)
E –Endocrine
Hypothyroidism
Hyperthyroidism
Cushing’s syndrome
Addison’s disease
arthritis with raynaud arthritis with diarrhea
1. To Remember MRCS--3 WHIST
2. M--MCTD 1. W--whipple diseases
3. R--RA 2. H--HIV
4. C--Cryoglobin 3. I--IBD
5. S--systemic sclerosis 4. S--scleroderma
6. S--SLE 5. T—TB
7. S--Sjogren when sir ask the question first u tell IBD and 2nd scleroderma
when sir ask the question first u tell systemic then rest
sclerosis 2nd SLE then rest
60 yr older generalized body ache Back pain
MP—MOFEJ to remember MINO/ MINS
— Metastatic bone disease 1. M-Mechanical
multiple myeloma 2. I-Inflammatory
P— Paget’s disease a. Ankylosing spondylitis
Polymyalgia rheumatica b. Psoriasis
M— Myositis c. Spondyloarthritis
O— Osteomalacia& Osteoarthritis 3. N-Neoplastic
F— Fibromyalgia a. Malignancy
E—endocrine (PAT) b. Infection
P—primary hyperparathyroidism 4. O-Other (structure itself)/S-Spine
A—Addison a. Prolapsed disc
T—hypothyroidism b. Spinal stenosis& Paget’s disease
J--- Joint hypermobility (omit it older age ) c. Fracture & lumbar spondylosis
neck
M—Mechanical N—neoplastic
Postural Metastases
Whiplash injury Myeloma
Disc prolapsed Lymphoma
Cervical spondylosis • Intra thecal tumours
M—Metabolic O—others
Osteoporosis Fibromyalgia
Osteomalacia Torticollis
Paget’s disease R—referred Pain
I—Inflammtory Cervical lymph nodes
Infections Teeth
Spondylitis Pharynx
Juvenile idiopathic arthritis Angina pectoris
RA Aortic aneurysm
Polymyalgia rheumatica Pancoast tumour
Diaphragm
thicken skin
musculoskeletal endocrine
1. systemic sclerosis 1. DM
2. morphea 2. Hypothyroid
3. scleroedema 3. Acromegaly
4. eosinophilic fasciitis infection
Metabolic 1. leprosy
1. amylodosis Drug (bleomycine , venylchloride )
2. porphyuria cutena tarda
Causology is the lock
History is key
Medicine ward is locked door

WEAKNESS
History & causology
For block posting ,
3rd to 5th year and
post graduate student
Dr . Shahidullah shamol
FCPS (medicine )
weakness It may occur due to muscle weakness –myopathy

Neurological causes  GBS and peripheral


neuropathy
Spinal cord lesion cord compression , ATM(acute
transverse myelitis )

Neuromuscular junction  myasthenia

Stroke –hemiparesis
age Duchene and backer child hood
limb girdle adult
onset sudden onset –stroke
sub acute--ATM
gradual –Myopathy ,neuropathy
static or static –stroke
progressive progressive –myopathy and neuropathy
duration intermittent –myasthenia and
hypokalaemic periodic paralysis
diurnal variation –myasthenia occur at the
end of day
if Intermittent or How frequent / interval between attack
episodic How long persist
How recovery occur
Involvement of Which group of in neuropathy--distal group
the limb muscle involve  in myopahty –proxymal group
sequence – which (symptoms )--- Lower limb 1.Standing from sitting
limb involves first the way patient proximal position
(upper or lower / describe their 2.Climbing upward stair
right or left) and weakness Lower Limb 1.Shoe comes out of feet
which limb distal Spontaneously (foot drop)
involve next. 2.Climbing downward stair
which part of Upper limb 1.Raise the hand above
limb involve proximal shoulder
Proximal or distal a)Combing hair
b)Dressing / undressing
Upper limb Buttoning , writing ,hold a
distal glass
Eating and unlocking key ,
functional status now the patient is
bed ridden
chair bound
have to depend on others for daily
activities
involvement of Dysphagia (difficulty in swallowing )
other muscle of the Dysarthia (difficulty in articulation )
body Dysphonia (difficulty in phonation )
brainstem or bulbar Diplopia (double vision)
muscle involvement Dyspnea (breathless ness )
respiratory muscle Dropping eye lids (ptosis)
involvement Drooling of saliva
to remember 6 D Nasal regurgitation / chocking / nasal voice
sphincter or Bowel bladder–in form of retention or
bladder incontinence
involvement bowel—fecal in continence
if ur case is neuropathy
1. Sensory feature negative symptoms
 Numbness ,heaviness
positive symptoms
 tingling , cramp
 burning sensation , parasthesia
1. Feature of dorsal column lesion Pt state that when she walk , she feel that she
is walking on cobble
1. Autonomic involvement  Increases or decreases sweating ,
 Dry mouth / eye
 Erectile Dysfunction
 Diarrhea and gastroparesis
 Dizziness or fall (due to postural
hypotension)
Feature of inflammatory myopathy  Fever
(polymyositis /dermatomyositis )  Rash
 Joint pain
 Muscle pain
 Muscle pain after exercise then weakness –
HO periodic paralysis thus the weakness
 occur after taking carbohydrate food ,
exercise
 short lasting (4 to 24 hr)
 recurrent
 family history
muscle wasting and muscle wasting
twitching of muscle neuropathy –early
myopahty --late
wasting / spontaneous twitching
MND
History of higher psychic specially incase of stroke
function –dementia , speech
Family HO hereditary neuropathy
hereditary spastic paraparesis
Alcoholic
Drug and toxin OPC / herbal drug ,steroid / statin
exposure to toxin  arsenic tubewel water, lead
IQ/ academic in case of child (Duchene and backer)
performance
In case of GBS Ho diarrhea , fever and vaccination ,1-3 week
Take preceding HO before of development of this symptoms
take history in case cervical 
spondylosis neck pain with /without radiate to upper
limb
in case lumber 
back pain with or without radiate to lower
limb
H/ O radicular pan
 severe electrical shock like , lancating pain
confine to specific dermatome , increase on
straining coughing
history of trauma
history of fever, TB (pott)
weight loss, night
sweat ,
History of malignancy such
in case female –breast lump
in case of male –
 bronchial carcinoma - cough ,
smoker , haemoptysis
 prostate  increase frequency and
urgency , hesitancy
in both
 lymphoma , leukemia
 multiple myeloma  old age ,
generalized body ache
if the patient is Face –Cushing , hypothyroid , thyrotoxic ,
myopathy Feature of hypo thyroid ---weight gain , cold
exclude endocrine intolerance , husky and croaky voice ,
causes constipation
Cushing Hyperthyroid---wt loss, heat intolerance,
hypothyroid diarrhea, increase appetite. Palpitation ,
Addison sweating
Hyperthyroid Addison –wasting , fever , diarrhea , vomiting
,pigmentation ,
 First sure its neuropathy or myopathy or cord compression
 First describe the pattern of weakness from first to present and
what functional status is
 Now history of muscle ---brainstem, bladder and bowel, cerebellar
,
 Any sensory complained specially if neurology
 Then go for etiology
NEUROPATHY
According to the statement of the patient she was reasonable well 6 months back then she
gradually developed weakness of both lower limbs which was progressive in nature .
Initially the weakness started from right lower limb then subsequently involved the left
lower limb and then both upper limbs. At first she noticed that her Shoe comes out of her
feet Spontaneously (foot drop) and she felt difficulty in walking specially Climbing
downward stair( be-care full people from village may not opportunity to climbing stair so
not use this term for them ) and she also felt difficulty in fine activities like Buttoning ,
writing ,holding a glass ,Eating , unlocking key , opening mouth of bottle. For the last one
month she become bed ridden / chair bound and has to depend on others for day to day
activities. She also complained pain and needles sensation / numbness and parasthesia in
all limbs in glove and stocking pattern. She also noticed gradual wasting of his distal part
of limb. She has no history of double vision, difficulty in swallowing, breathlessness. Her
bowel and bladder habit is normal .Patient has no complained regarding increased or
decreased sweating, dry mouth, palpitation, diarrhea (autonomic neuropathy, include
erectile dysfunction—incase male). She has no history of rash, muscle and joint pain or
oral ulcer. She has no history of diabetic or kidney disease
She is non smoker, non-alcoholic, no significant drug history and NO history exposure to
OPC (if patient is male and farmer—the patient is cultivators has exposure to OPC). Use
arsenic free drinking water
None of her family members suffering from this type of illness.
MYOPATHY
According to the statement of the patient she was reasonable well 6 months back
then she gradually developed weakness of both lower limbs and this weakness
was progressively increasing. Initially the weakness started from right lower limb
then subsequently involved the left lower limb and then both upper limbs. At first
she noticed difficulty from standing from sitting posing / squatting position and
climbing upstairs. Subsequently she developed difficulty in raising the hand above
shoulder, combing hair, Dressing / undressing herself. For the last one month she
become bed ridden / chair bound and has to depend on others for her daily
activities. This weakness not related with exertion (metabolic & mitrochrondial ),
muscle pain, no diurnal variation and she has no history of double vision, difficulty
in swallowing, breathlessness. Her bowel and bladder habit is normal. She also
noticed gradual wasting of his proximal part of limb .She denies any fever, joint
pain, rash, sensory complains like parasthesia, numbness. The patient has no
history of weight gain or weight loss, cold or heat intolerance, palpitation,
polyuria or polydipsia.
She is non smoker, non-alcoholic, no significant drug history and NO history
exposure to OPC (if patient is male and farmer—the patient is cultivators has
exposure to OPC). Use arsenic free drinking water.
None of her family members suffering from this type of illness.
COMPRESSIVE
MYELOPATHY
According to the statement of the patient he was reasonable well 6 months back then he
developed Low back pain which was dull and aching is nature mild to moderate in severity
aggravated during movement, coughing and straining and relieved by rest or lying down
.sometime the pain radiate along the buttock up to below knee like lancating or electrical
shock. He also complained parasthesia (only mention if patient tell u about pain and
sensory). Two months later he gradually developed weakness of both lower limbs and this
weakness was progressively increasing. Initially it started from right lower limb then
subsequently involved the left lower limb (then both upper limbs –only mention if patient
have quadriparesis ). Earlier part of weakness He was able to walk with some difficulties. For
the last one month he become bed ridden / chair bound and has to depend on others for day
to day activities like going toilet .He also noticed numbness/ loss of sensation that extend
from feet with upper limit just below the costal margin . At last he developed bladder
involvement in form of acute retention that relieved by catheterization. He also becomes
constipated. This weakness has no diurnal variation .He denies any blurring of vision ,double
vision, difficulty in swallowing, breathlessness, muscle pain ,rash ,fever ,cough out of blood
and night sweat and weight loss during the course of illness .
he is non smoker, non-alcoholic, no significant drug history and having no past history of
urinary frequency urgency and hesitancy(Ca prostate ),coughing out of blood (Ca bronchus),
generalized body ache (multiple myeloma) trauma NO history exposure to OPC (if patient is
male and farmer—the patient is cultivators has exposure to OPC) or other Toxin . Use arsenic
free drinking water.
None of her family members suffering from this type of illness.(hereditary paraparesis )
TRANSVERSE MYELITIS
According to the statement of the patient he was reasonable well 1months
back then he suddenly developed weakness of both lower limbs and this
weakness was progressive for few hours then it become static .for this
weakness he become bed ridden / chair bound and has to depend on others
for day to day activities like going toilet .He also noticed band like tightness
around the chest associated with numbness / loss of sensation that extend
from feet with upper limit just below the costal margin. Simultaneously HE
develops bladder and bowel involvement in form of retention that was
relieved by catheterization. There was a history of fever (or diarrhea) 2 wks
prior to this illness. This weakness has no diurnal variation .He denies any
blurring of vision ,double vision, difficulty in swallowing, breathlessness,
muscle pain ,rash ,fever and night sweat and weight loss during the course of
illness.
he is non smoker, non-alcoholic, no significant drug history and having no past
history of urinary frequency urgency and hesitancy(Ca prostate ),coughing out
of blood (Ca bronchus), generalized body ache (multiple myeloma) , trauma
,NO history exposure to OPC (if patient is male and farmer—the patient is
cultivators has exposure to OPC) or other Toxin . Use arsenic free drinking
water. None of her family members suffering from this type of
illness.(hereditary paraparesis )
STROKE
ischaemic stroke
According to the statement of the patient or patient attendant, he was reasonable
well 2 days ago. At mid noon of that day he was working/doing daily activities in his
house suddenly he noticed weakness right side of his body. The weakness was
progressive and few hrs later he was totally unable to move right side of his body. He
also noticed that his mouth is deviated toward the left side and food accumulate in
right check with dribbling of saliva from right side. This episode was not associated
with headache, vomiting, fever and convulsion. The patient was fully conscious
/Drowsy. Initially patient has difficulty in Swallowing especially liquid food and slurred
speech (only mention if pt give such HO) subsequently both improved. The patient
denies any visual disturbance like blurring of vision, &double of vision, vertigo,
difficulty in speech, any bowel and bladder disturbance during or after these
episodes. The patient also denies presence chronic daily morning headache with
nausea (ICSOL) with focal neurological sign ,joint pain rash (vaculities) ,recent and
previous history of head injury
. The patient is hypertensive for 5 years with irregular medication and for last few
months he was abstinence from anti-hypertensive drugs. He is non diabeticug history
History of irregularly taking anti-HTN drug s Betanol for last 2 year. Also give history
of using OCP (in case of female)
History of past illness
The patient had no previous history of similar type attack (MS , recurrent stroke ), TB and
malignancy .. exertional chest pain , palpitation and valvular heart disease
Drug history
History of irregularly taking anti-HTN drug s Betanol for last 2 year. Also give history of using
OCP (in case of female)
PERSONAL HISTORY
The patient is smoker and taking 10 stick / per day for last 45 years, non alcoholic and no
history of IV drug user and addiction.
Family history
Both of father and mother was hypertensive and used died from acute attack of stroke and
rest of the family members healthy and enjoining sound health
Menstrual and obstetrical history
If female no bad obstetrical history
haemorrhagic stroke
According to the statement of the patient or patient attended, he was reasonable well 2 days
ago. At mid noon of that day he was working/doing daily activities in his house suddenly he
complaint of severe headache and vomiting followed by inability to move right side of the
body. The headache was spontaneous onset, continuous and associated with vomiting for
several time and the vomiting was non projectile and contained semi digest food particle.
causology
spastic paraparesis –common (MBB) S
compressive myelopathy non compressive
to remember 3 TIME Congenital
T--Trauma 1. Hereditary spastic paraplegia
T—Tuberculosi/ POtt 2. Fried reich ataxia (if pt is child)
T—TUMOR inflammatory
Metastatic carcinoma 1. acute Transverse myelitis
e.g. breast, prostate, bronchus Vascular
Neural tumor 1. Anterior spinal artery thrombosis
i. meningioma, Metabolic
ii. neurofibroma, 1. Vitamin B12 deficiency
iii. ependymoma a. SCD
hematological Infection :
i. lymphoma, 1. Tabes dorsalis
Degenerative
ii. leukaemia
1. Motor neuron disease
I--Intervertebral disc prolapse 2. Syringomyelia
M—multiple Myeloma (only mention if quadriparesis—here
E--Epidural abscess upper limb is lower motor and lower limb is upper
motor type lesion )
ONLY FOR ‘4T + MD ( At least remember this 6 )
T--Trauma
T—Tuberculosi/ POtt
T—TUMOR
T-- Transverse myelitis
M—MND (MND—Lateral sclerosis)
D—degenerative DISC disease eg. -- Intervertebral disc prolapse
SPASTIC PARAPARESIS –detail (post graduate )
compressive myelopathy non compressive
extradural Vertebral 80% to remember 3 TIME Congenital
T--Trauma 1. Hereditary spastic paraplegia
T—Tuberculosi/ POtt 2. Fried reich ataxia
T—TUMOR inflammatory
Metastatic carcinoma 1. acute Transverse myelitis
e.g. breast, prostate, bronchus 2. spinal MS
I--Intervertebral disc prolapse 3. SLE with anti-phospholipid syndrome
M--Myeloma Vascular
E--Epidural abscess 1. Anterior spinal artery thrombosis
intradural, 2. Spinal AVM
extramedullary(Meninges) 15% Metabolic
1. Tumours e.g. 1. Vitamin B12 deficiency
a. Neural tumor a. SCD
i. meningioma, Infection :
ii. neurofibroma, 1. Tabes dorsalis
iii. ependymoma, Degenerative
b. metastasis tumor 1. Motor neuron disease
c. hematological 2. Syringomyelia
i. Lymphoma, & leukaemia (only mention if quadriparesis—here
2. Epidural abscess upper limb is lower motor and lower limb is
intramedullary (Spinal cord) 5% upper motor type lesion )
1. Neural Tumours
a. glioma,
b. ependymoma,
2. Metastasis
flaccid paraparesis
peripheral nerve spinal cord
1. GBS 1. any spinal cord lesion with spinal
2. motor neuropathy due to any cause shock
a. CMT 2. Tabes dorsalis
b. CIDP 3. MND(progressive muscle atrophy )
3. Acute intermittent porphyria 4. Fried reich ataxia
4. chronic lead poisoning electrolyte
5. OPC 1. hypokalaemia with periodic paralysis
6. hereditary motor neuropathy neuromuscular junction
7. leprosy 1. myasthenia graves
8. diabetic amyotrophy (usually muscle –
unilateral ) 1. any form of myopathy
for MBBS
G-MAIL. COM COM--
G- GBS any causes of motor neuropathy
M- MND CMT
A- Acute intermittent porphyria CIDP
I-Inherited-- hereditary motor PLUS
neuropathy hypokalaemia (never forget to tell this)
L- chronic lead poisoning
central causes of paraparesis Acute paraparesis
To remember –MASHIC A—peripheral
M- parasagital meningioma 1. spinal cord /spastic
A— thrombosis of unpaired a)compression
ant.cerebral artery 1. Trauma
S- thrombosis of superior sagital 2. TB / potts
sinus 3. Prolapsed intervertbral DISC
H- Hydrocephalus b)noncompressive
I— multiple cerebral infarction I)Vascular
C-- cerebral palsy 1. Anterior spinal artery thrombosis
2. Spinal AVM
II)inflammatory :
1. acute transverse myelitis
2.flaccid
1. GBS
2. Acute intermittent porphyria
3. lead poisoning / toxin (alcohol)
B)Central causes
1. thrombosis of superior sagital sinus
2. thrombosis of unpaired ant.cerebral
artery
3. bullet injury to para sagital region
Causes Progressive paraparesis
Spinal cord peripheral neuropathy
compressive 1. CIDP
1. TB / potts 2. CMT
2. Tumours e.g. 3. MMN—multifocal motor neuropathy
a. Neural tumor 4. Diabetic amyotrophy
i. meningioma, 5. TOXIC –arsenic , chronic lead
ii. neurofibroma, myopathy
iii.ependymoma, hereditary (LMF…BD)
b. metastasis tumor L— Limb girdle
c. hematological M— Myotonic dystrophy
i. Lymphoma, & leukaemia F— Facioscapulohumeral(FSH)
non-compressive B— Becker
Congenital D— Duchenne
1. Hereditary spastic paraplegia ENDOCRINE –O--CAT
2. Fried reich ataxia O-- Osteomalacia
Metabolic C— Cushing’s & Conn’s syndrome
a. Vitamin B12 deficiency --SCD A—Acromegaly & Addison’s disease
Infection : T— Hyper & Hypothyroidism
1. Tabes dorsalis
Degenerative
1. Motor neuron disease
2. Syringomyelia (if quadriparesis)
central causes
1. parasagital meningioma
causes of recurrent or episodic weakness spastic paraparesis with normal
(para or quadriparesis) sensory level
brain 1. MND
1. MS 2. Hereditary spastic paraparesis
2. TIA OF BRAIN STEAM 3. Bilateral stroke (quadriparesis)
muscle –periodic paralysis 4. paraneoplastic
1. Channelopathies 5. early intramedullary tumor
a. Paramyotonia congenita (Na) (late sensory loss)
b. Hyperkalaemic periodic paralysis (Na) 1. central causes of paraparesis
c. hypokalaemic periodic paralysis PSA---IN---CMH
(Na+Ca) P—parasagital meningioma
d. Myotonia congenital Thomsen’s S—thrombosis of superior sagital sinus
disease (Ca) A---thrombosis of unpaired ant.cerebral
2. thyrotoxic periodic paralysis artery
3. metabolic myopahty C—cerebral palsy
NEUROMUSCULAR JUNCTION : M—multiple cerebral infarction
1. Myasthenia graves H—Hydrocephalus
2. Eaton lambert syndrome
Recurrent Hypokalaemia (diuretic /laxative )
quadriparesis with dysphagia Flaccid paraparesis with sensory loss
GMB Poly neuropathy
G— 1. DM
1. GBS 2. Deficiency
M— 3. leprosy
1. MND 4. Toxic
2. Myasthenia graves 5. paraneoplastic
3. Multiple sclerosis 6. ureamia
B— CIDP
1. bilateral stroke hereditary motor sensory neuropathy
2. brain stem stroke
Thyroid disorder
muscle weakness –due to
myopathy
dysphagia due to ---Retrosternal
compression
flaccid paraparesis with normal sensory intact
any cause of pure motor neuropathy G-MAIL. COM
or G mail.com G- GBS
PGT –IN -CLD M- MND
P-- porphyria A- Acute intermittent porphyria
G-- GBS I-Inherited-- hereditary motor neuropathy
T--Toxic L- chronic lead poisoning
C—CMT C
L—LEPROSY any causes of motor neuropathy
D—DM—amyotrophy CMT
spinal cord lesion with spinal shock CIDP
O—OPC or T OXIN
M— other causes muscle weak ness
hypokalaemia (never forget to tell this)
D—DM—amyotrophy

Flaccid paraparesis with normal jerk and sensory dissociated sensory loss
1. MYOPATHY 1. syringomyelia (quadriparesis)
2. HYPOKALAEMIA 2. Ant.spinal artery
3. MYASTHENIA thrombosis(quadriparesis)
4. RECOVERY STAGE OF SPINAL STROKE 3. brownsquard syndrome (unilateral
weakness )
unilateral leg weakness / wasting unilateral wasting of upper limb
brain brain
1. stoke / monoplegia 1. stoke / monoplegia
2. CP—cerebral palsy 2. CP—cerebral palsy
ant. Horn cell of spinal cord ant.horn cell of spinal cord
1. MND 1. MND
2. Poliomyelitis 2. Poliomyelitis
3. DM—Amyotrophy Roots / radiculopathy
Roots / radiculopathy 1. Cervical disc prolapse
1. PLID/lumber disc prolapse 2. Spondylitis
2. Spondylitis 3. Malignancy
3. Malignancy plexus / plexopathy (bronchial pleux)
plexus / plexopathy (lumber plexus) 1. Malignancy
1. Malignancy 2. Vasculitis
2. Vasculitis 3. haematoma
3. haematoma peripheral nerve
peripheral nerve 1. leprosy
1. leprosy
causes of proximal muscle weakness
HIDE--DMP
H—hereditary (LMF…BD) ENDOCRINE & METABOLIC
L— Limb girdle ENDOCRINE –O…CAT
M— Myotonic dystrophy O-- Osteomalacia
F— Facioscapulohumeral(FSH) C— Cushing’s & Conn’s syndrome
B— Becker A—Acromegaly & Addison’s disease
D— Duchenne T— Hyperthyroidism & Hypothyroidism
I-INFLAMATORY (PID) METABOLIC
P--Polymyositis Mitochondrial myopathy
I--Inclusion body myositis( distal effects) electrolytes
D--Dermatomyositis Hypokalaemia
D-DRUG & TOXIC Hypercalcaemia
Drug-–ABCD—CVS (disseminated bony metastases)
A—Amiodarone, other causes of muscle weakness
B-- Beta-blockers, D-
C—Chloroquine DM
D—Diuretic , Zidovudin , M-
C—Ciclosporin, Corticosteroid -Myasthenia graves
V—Vincristine, P--
S-- Statins Paraneoplastic
toxin — • Carcinomatousneuromyopathy
Alcohol (chronic and acute syndromes) Periodic paralysis
Amphetamines/cocaine/ heroin
Vitamin E
Organophosphates
Snake venom
common casues of peripheral neuropathy for MBBS
VITAMIN—D I---INFLAMMATORY
V—VITAMIN deficiency (B1, B6,B12) 1. GBS--Guillain–Barré syndrome
I—INFECTIVE --Leprosy 2. CIDP--Chronic inflammatory
T—TOXIC-- MALA demyelinating
m- mercury, A—Alcohol, L- lead A-- polyradiculoneuropathy
arsenic 3. Vasculitis
A—AUTO-IMMUNE and HERIDARY / a. polyarteritis nodosa,
genetic b. Wegener’s granulomatosis
1. Charcot–Marie–Tooth disease c. rheumatoid arthritis, SLE
(CMT) N—NEOPLASTIC
M—METABOLIC & ENDOCRINE 1. infiltration
1. Diabetes 2. lymphoma
2. Renal failure/ Uraemia 3. multiple myeloma (paraprotien )
3. Hypothyroid 4. paraneoplastic (bronchial Ca)
4. porphyria D—DRUG
5. Sarcoidosis
causes of neuropathy for post graduates
VITAMIN—D A—AUTO-IMMUNE and HERIDARY /
V—VITAMIN genetic
1. Thiamin 1. Charcot–Marie–Tooth disease
2. Pyridoxine (CMT)
3. Vitamin B12 2. Hereditary neuropathy with liability
4. Vitamin E to pressure palsies (HNPP)
I—INFECTIVE--BALL 3. Hereditary sensory ± autonomic
1. B- Brucellosis neuropathies (HSN, HSAN)
2. A- AIDS/HIV 4. Familial amyloid polyneuropathy
3. L--Leprosy 5. Hereditary neuralgic amyotrophy
4. L--Lyme M—METABOLIC & ENDOCRINE
T—TOXIC 1. Diabetes
MALTA 2. Hypothyroid
m- mercury, A—Alcohol, L- lead,
T—thalidomide, A-- arsenic 3. Acromegaly
1. Alcohol 4. Renal failure
2. organophosphates,
3. lead, arsenic, mercury, solvents 5. Porphyria
4. Nitrous oxide (recreational use) 6. Sarcoidosis
causes of neuropathy for post graduates (CONTINUE)
I---INFLAMMATORY D—DRUG
1. GBS--Guillain–Barré syndrome CASTING MP Vote D(the ) MP
2. CIDP--Chronic inflammatory C— cisplatin
demyelinating A—Amiodarone/ Albendazole
polyradiculoneuropathy S—Statin
3. Vasculitis T— thalidomide
a. polyarteritis nodosa, I—isoniazid
b. Wegener’s granulomatosis N—nitroforuntin
c. rheumatoid arthritis, SLE G—Gold
4. Paraneoplastic (antibody-mediated) VOTE— vincristine
N—NEOPLASTIC D-- dapsone
1. infiltration M— metronidazole,
2. lymphoma P- Phenytoin
3. multiple myeloma (paraprotien ) in Davidson 22
4. paraneoplastic (bronchial Ca) 1. Amiodarone
2. Antibiotics
a. dapsone, isoniazid,metronidazole,
ethambutol
3. Antiretrovirals
4. Chemotherapy
a. cisplatin, vincristine,thalidomide
5. Phenytoin
Others Amyloidosis
Critical illness polyneuropathy/myopathy
acute neuropathy Multifocal neuropathy (mononeuritis
multiplex)
ABCD—PGT VDRL__MASHI
A— Alcohol V— Vasculitis
B—Vasculitis (PAN) D— Diabetes mellitus
C—Cryoglobinaemia R—RA
D—DM L— leprosy, Lyme disease/ LYMPHOMA
P— porphyria …….x…….x…….
G—GBS M—Malignancy
T—Toxic A—Amyloidosis
1. organophosphates, S— Sarcoidosis
2. lead, HI-- HIV
3. arsenic,
4. mercury

Pes Cavus nerve thickening


PH of CSF NACLAS
C—CMT N—neurofibroma
S—Spinocerebellar Ataxia A—Acromegaly
F—Friedriech Ataxia C—CIDP
P—Peripheral neuropathy L—Leprosy
H—Herediatery motor neuropathy A— Amyloidosis
S-- Sarcoidosis
motor neuropathy sensory neuropathy
PGT –IN -CLD LUCS—BD
P-- porphyria L—Leprosy
G-- GBS U—uraemia
T--Toxic C—carcinoma
C—CMT S—syphilis
L—LEPROSY B—B12
D—DM D—DM
painfull neuropathy joint pain with peripheral peripheral and Autonomic
neuropathy neuropathy
ABCD P-VAT 1. SLE GDP BASA
A—Alcohol 2. RA G— GBS
B—B12 3. Sjogren D— Diabetes
C—carcinoma 4. Vasculitis---PAN , wG P— porphyria
D—Diabetes 5. paraneoplastic B—Butulism
P—Porphyria 6. uraemia A—amyloidosis
V—Vasculitis 7. Sarcoidosis S—Sjogren
A—Arsenic 8. Amyloidosis A—AIDS
T—Thalidamide 9. Drug

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