Medicine & Paediatrics

Viva Solve
by Seinfeld Medicos

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 Paediatrics viva 3
Medicine Viva (Hafiz sir on ECG Board) 25
Medicine Viva (Shyamol sir on ECG Board) 38
Medicine Viva (Hafiz sir on X-ray Board) 43
Medicine Viva (Shyamol sir on X-ray Board) 51

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 Paediatrics Viva
(Iffat Ara madam & Sayeeda Anwar madam)

Picture

TOF
-Findings (cyanosed tongue, congested eyes, clubbing- it was a picture of TOF)
-Congenital heart diseases:
Based on presence/absence of cyanosis: name some cyanotic and noncyanotic heart disease
Cyanotic CHD
Tetralogy of fallot (TOF)
Transposition of great vessels
Total anomalous pulmonary venous return
Persistent Truncus arteriosus
Tricuspid atresia
Ebstein anomaly
Acyanotic CHD
With left to right shunt
VSD (ventricular septal defect)
ASD
PDA (patent ductus arteriosus)

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 Without shunt
Coarctation of aorta
Pulmonary stenosis
Aortic stenosis
-commonest congenital heart disease (VSD) , common cyanotic heart disease (TOF)
-ki niye present Kore (hypercyanotic spell), hole ki korte hoi (squatting/ knee elbow position),
keno ....(squatting causes increased resistance in peripheral systemic blood vessels. This
raises left ventricular pressure above that of right ventricle which decreases right-to-left
shunt across the VSD. Blood thus flows through the stenosed pulmonary infundibulum. This
ultimately improves pulmonary circulation, better oxygenation and relieves the child from
dyspnoea and episodes of cyanotic spells.)
-components of TOF (Pulmonary stenosis, right ventricular outflow obstruction, Right
ventricular hypertrophy, Ventricular septal defect (VSD), Overriding or aorta )
-causes of peripheral cyanosis ( Exposure to severe cold, frostbite, ,
Heart failure, Shock and peripheral circulatory failure, Deep vein thrombosis,
Cryoglobulinaemia)
-sites for seeing cyanosis (central-tongue, mucous membrane of mouth; peripheral- lip,
fingernail, toe nail)
-complications
Hyper cyanotic spells
Severe polycythemia (hypoxia ->erythropoietin ->increased RBC production)
Cerebral abscess
Stroke/Cerebral thromboembolism
Infective endocarditis
Delayed growth and development
Delayed puberty
Others
o Hyperuricemia and gout
o Iron deficiency anemia (increased rbc production depletion of iron store)
o Coagulopathy (due to hyperviscocity from polycythemia)

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Hereditary hemolytic anemia
-diagnosis?
-complications?

o thinning of bones
o pathological fracture
o spinal cord compression
due to iron overload and iron deposition in organs (due to hemolysis in thalassemia)
o heart: arrythmia
o liver: CLD
o pancreas: DM
o thyroid gland: hypothyroidism
o parathyroid gland: hypoparathyroidism
o pituitary gland: GH deficiency

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 o allergic reaction
o transmission of infectious agents
o TRALI (transfusion related acute lung injury)
o TACO (transfusion associated circulatory overload)
o Acute hemolytic reaction
-What type of disease is it?- autosomal recessive
-Mongoloid facies. Show me the malar prominence. Dx? What type of disease is it?
Thalassemia major or minor? (major)
-thalassemic face er feature chobi te dekhao, ki type thalassemia (beta thalassemia major),
beta thalassemia ki type disease, defect kishe hoy (beta globin chain), ei baby te r ki
finding pabe (jaundice, splenomegaly), complications , how to confirm dx (Hb electrophoresis)
-what other findings?-jaundice, splenomegaly
-Thalassemia , clinical sign? Dx, inv? (CBC e PBF, Iron profile, Hb electrophoresis), Kon kon
Hb thake? (HbA, HbA2, HbF, HbE, HbS, hbC, HbD Punjab) Bd te extra kon Hb thakte pare?
(Hb E trait)
-Thalassemia,sign,pathology (absence or decreased beta chain production),Confirmatory test,
complications
-thalassemic face, c/f, confirmatory test, ki pabo test e? (shows markedly reduced or
absent HbA and raised HbF & HbA2), Fetal hb normally kokhn present thake (newborn)

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Severe anemia.
-Causes of anemia in children.Thalassemia vs IDA dff korba kivabe pbf diye ( hbe na dui tai
microcytic), confirmatory test for thalassemia (Hb electrophoresis), Anemia bacchader
kothay dekhi? (palm, sole, generalized skin)

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Breast feeding
-Breast feeding, components (positioning & attachment)
-good attachment er point bolo

o Baby
o More areola seen above than below
-recommendations for breastfeeding
early initiation of breast feeding (w/n 1st hour of birth)
exclusive breast feeding for 1st 6 months (180 days) of life
proper complementary feeding from 6 months of age with continuation of breast feeding
up to 2 years of age
-EBF ki (Exclusive breast feeding means an infant receives only breast milk from his/her
mother or a wet nurse or expressed breast milk, no other liquids or solids are given, not even a
drop of water except ORS, drops or syrups containing vitamins, minerals, supplements or
medicines )

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NS
-Ki ki findings dekhte pacco picture e (puffy face, periorbital swelling, pedal edema)
-What is NS (Characterized by:
Massive proteinuria (>3.5 g/24 hours or >1 gm/m2/24 hours)
Hypoalbuminemia (<2.5 gm/dL)
Generalized edema
Hyperlipidemia (>200 mg/dL)
-NS vs AGN (boi theke pore nio..)
-C/F of NS
-Investigations ki diba
-components of NS? important investigation done in ward? (heat coagulation test) name
another common renal disease (AGN, PCKD, AKI, CKD)
-Agn, ns opd te kmne alada korbo? (H/O skin infection, hematuria, AGN pt is hypertensive)

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Baggy pant -> Severe muscle wasting.
-SAM criteria (for children>6 months=> MUAC<115mm, z score<-3, bipedal edema present;
for children<6 months=>visible wasting, z score<-3, bipedal edema present)
-What complications may baby get?

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down syndrome
-pic e ki ki finding ache (protuded tongue, simian crease, depressed nasal bridge, medial
epicantic fold, upslanting of eyes)
-Down ki dhoroner disease : chromosomal bolo ...not genetic .ki hoi (there is an extra copy of
chromosome 21)
-Down er baccha er ki problem hoi
o Severe mental retardation (IQ 25-50)
o Early onset Alzheimer disease (at 40 y)
o Heart disease (endocardial cushion defects) these are the major cause of death
o Increased risk of leukemia
o Duodenal atresia
o Increased risk of umbilical hernia
o Increased gap b/n 1st and 2nd toe

-hematological ekta disease bolo hematooncological ekta disease bolo (IDA, Thalassemia;
Leukemia, lymphoma)

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HSP
-s/s
-diascopy test ki? Kothay kori?

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X-ray

Hydropneumothorax
-explanation (X-ray chest PA view showing:

costophrenic and cardiophrenic

angles
-why?

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Miliary TB
-Classify tb (primary, secondary; pulmonary, extra-pulmonary). Location of primary lesion
(Primary complex/ Ghon complex- including granuloma with hilar lymphadenopathy) and its
definition (Infection of a previously uninfected individual. It is a self limiting febrile illness.
Clinical disease occurs only if there is hypersensitivity reaction or progressive infection)
-bacchader ar ki type tb hoi? (tell the extra-pulmonary TBs- intestine, bone, brain, meninges,
skin, spine, lymph node, pleura)
-kivabe hoy (hematogenous spread/ dissemination)
-Dx ki, R kothay pai emn mottling (kerosene poisoning, histoplasmosis, sarcoidosis,
pneumoconiosis) Ki korbo na? (gastric lavage is contraindicated as it is associated with
aspiration of kerosene into the lungs) Wash ar koi dibo na? (absolute-corrosive poisoning,
relative- convulsion, coma, volatile poison, upper GIT disease, pt with marked hypothermia &
hemorrhage diathesis)

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-radiological dx? (miliary mottling/TB) any other Cause? Other types of tb? What will you
find in tb meningitis?(fever, headache, meningism, vomiting, focal neurological sign)
Csf findings? (straw colour, spider erb like clot, lymphocyte upto 500/cm3, protein increased,
glucose decreased, ZN stain- AFB present)
-how to prevent in childhood (BCG vaccination),If BCG wasn't given just after birth-when to
give? (after completion of 6 weeks, with pentavalent vaccine), organ affected by tb (every
organ except TSC- thyroid, smooth muscle, cardiac muscle),csf findings of pyogenic
meningitis (colour cloudy, clot present, neutrophil 300-2000, protein increased, glucose
decreased)
-Complications (
Pulmonary

Non pulmonary

creates an extrapulmonary extrapleural abscess on the chest wall)

Laryngitis

o Enteritis (GIT TB)

o Anorectal disease

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right sided upper lobe pneumonic consolidation
-findings? (You are given a pen to point at the findings) radiological dx? (consolidation)
auscultation findings? (breath sound bronchial, vocal resonance increased, pleural rub present
in case of pleurisy) other types of breath sounds? (vesicular-normal, vesicular with prolonged
expiration COPD, asthma; bronchial- collapse, cavitation, consolidation, fibrosis) Which found
where? causes of consolidation? organisms causing pneumonia? (Abid Mollah- page 88), EPI
vaccine available for prevention of pneumonia? which one?(PCV) EPI vaccine against
TB?(BCG) What other manifestation can that organism cause? (Pneumococcus/
Streptococcus pneumoniae, meningitis) how will you confirm? (CSF examination, culture)
-Ki feature niye ashbe baccha. (fever, cough, respiratory distress, chest pain, unable to feed
& drink)
-causes and organism names,EPI vaccines,konta ki disease prevent kore,dose(see EPI chart)
-chest findings of it (inspection- tachypnea, restricted movement of the affected side;
palpation- trachea centrally placed, chest expansibility reduced, vocal fremitus- increased;
percussion- woody dull; auscultation- breath sound- bronchial, vocal resonance- increased,
pleural rub maybe present, crepitation present in resolution stage), Clinical dx (pneumonia)
-Cz, ki ki findings, complications, meningitis bolar por LP needle er use (diagnostic-

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 meningitis, encephalitis, SAH, GBS; therapeutic- spinal anesthesia, intrathecal drug
administration), meningitis er organisms (Neonatal- E. coli, Gr. B Streptococci, L.
monocytogenes; Beyond neonatal period- H. influenza, Strep. Pneumonia, N. meningitides), CSF
finding
-Air bronchogram dekhao, Baccader pneumonia er koketa organism er name bolo,EPI te
kono vaccine ase ki aitar jonno

Right sided pleural effusion,

-auscultation finding (breath sound- diminished/ absent, vocal resonance- diminished)
-Ki ki organism responsible? (parapneumonic effusion-Abid Mollah- page 88; Tubercular- MTB),
EPI vaccine ache kina? (PCV, BCG)
-further investigation (Pleural fluid aspiration study, MT, GeneXpert, CBC e ESR, blood C/S)
-confirmation of dx (aspiration)

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-Pleural fluid examination parameters: (physical, biochemical, cytological, microbiological)
-Confirm korba : aspiration kore; Jodi pus ase taile : empyema thoracis

Rickets.
-Show the findings. (widening, cupping & fraying of metaphysis, wide gap between epiphysis &
metaphysic, osteopenia)
-Source of vitamin D (endogenous synthesis in skin- major source; foods rich in vit D e.g. egg
yolk, cod liver oil, butter, any fat rich diet, milk & milk products)

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Instrument
Bone marrow aspiration needle (Abid Mollah, page 318)
-use , site, use of adjustable guard
-parts, indications. where it is introduced?

ORS and cholera saline

-use, difference
-cholera saline: eta ki? indications. ORS: eta ki? indications
-cholera saline uses, ors uses, rehydration in some dehydration

LP needle, (Abid Mollah, page 316)

-pick up the instrument needed for this procedure?
-site/ level of introduction, CSF findings of pyogenic meningitis
-Lumbar puncture needle site? Other site if L3/L4 not possible? (cisternal puncture)
-Pyogenic Meningitis r CSF findings, neonate e head e ki paba? (bulging of anterior
fontanelle)
-indication & contraindications
-pyogenic meningitis er findings
-uses
-cause of meningitis, kader intra thecal medicine deya hoy (methotrexate (MTX), liposomal
cytarabine, and thiotepa)
-LP needle, ki kori. Kon kon disease e CSF study kori

AMBU bag (Abid Mollah- page 318)

-Ekta baby resp distress niye asche, saturation koto hole take O2 dite hbe? (90%) Er age
ki korbe (CPR with AMBU),
-instrument ta dekhao (ambu bag), parts (AMBU bag proper, mouth piece/ mask, oxygen
connector, oxygen reservoir, pop-up valve)
-AMBU bag- parts, function of pop-up valve
-parts, functions
-define PNA (Peri natal asphyxia a clinical condition resulting from impairment of gas exchange
in the fetus leading to hypoxia, hypercarbia, acidosis)

Growth & Development

-def of growth & development (Growth refers to physical maturation and signifies an increase
in size of the body parts and various organs. Development refers to acquisition & maturation of
skills, behavious and values on the part of the growing child)
-developmental milestone 1 year (Abid Mollah, page 14)
-Domain of development (8-Motor-gross & fine, vision, hearing, speech, social, emotional, self-
help/ emotional, cognitive)
Nutritional disorder
-WHO classification of PEM (MAM, SAM)
-common konta (PEM), who classification, SAM criteria in >6month, <6 month hole amra wt for
ht na bole ki boli (weight for length), SAM er baby der ki ki micronutrient deya hoy (vitamin
A, Multivitamin, Folic acid, Zinc, Copper, Elemental iron )
-IYCF
-PEM,WHO criteria of SAM
GIT & HBPS
-Common gastrointestinal disease in children. (acute watery diarrhea)

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-Severe dehydration signs (lethargy, sunken eyes, unable to drink, skin pinch goes back very
slowly) rehydration plan (cholera saline; age <12 months; age >12 months:100ml/kg)
-Hepatitis is children, how will you investigate. (liver function tests, viral screening &
markers) What are the causes? Any role of consanguinity? (hereditary hemolytic anemia pt
needs repeated transfusion from which he might receive blood borne hepatitis virus)
-4 day Fever with jaundice cause (acute viral hepatitis)
-Acute Viral Hepatitis. Inv ki dibo? Viral markers
Hematology
IDA
-Scenario
-Common causes of IDA in children (hookworm infestation, dietary deficiency, malabsorption)
-What is pica? (appetite for non-food substance persistently for 1 month)
-One investigation to confirm your dx- serum iron profile
-IDA scenario ( details)
-PBF e ki Paba IDA te? (microcytosis, hypochromia with aniso-poikilocytosis) Thalassemia te
ki paba? (same)

Thalassemia
-features, inv, Kon anemiay pbf e ki paba

Leukemia
-kon ta beshi common pediatric age group e (ALL)..confirm korba kibabe..(Bone marrow
examination) BM korar jnne ekhane kono instrument ache? Dekhao (paedi er instruments
gulo valovabe dekhe jaiyo)

ALL
-scenario,BM needle parts
-Ki investigation korba (CBC with PBF, Bone marrow examination)
-Investigation e lagbe emn ekta instrument tulo(BM needle) Use
-ALL, investigations, BM biopsy needle er parts.

Renal
-common childhood diseases in the kidney (AGN, NS, PCKD)
-Common renal diseases in children, Nephrotic syndrome Ki , bedside investigation for
confirmation of diagnosis (heat coagulation test)
-Hypersensitivity type in ARF (type II-antibody deposition) and AGN (type III- antigen-
antibody complex deposition). AGN prior infection (beta hemolytic strep skin infection)
-AGN, UTI, NS normal question
Endocrine
-Congenital hypothyroidism, one investigation (Serum TSH), findings in x-ray (Skeletal
survery: delayed skeletal development in relation with age, epiphyseal dysgenesis, Abid Mollah,
page 251)
-common endocrine disease in children (
Congenital hypothyroidism

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-features of hypothyroidism

Prolonged jaundice (persists beyond 2 weeks)

tongue

-common congenital endocrine anomaly in children, Congenital hypothyroidism er C/F bolo

Neurology
-Common diseases in children (meningitis, neonatal convulsion, poliomyelitis, GBS, ATM,
Autism). meningitis dx korte kon instrument ta lage? (LP needle) Kon level e dei
-Pyogenic meningitis er CSF findings
-Tx ki diba (parenteral antibiotic: Ceftriaxone+ vancomycin; if meningococcus- penicillin G;
pseudomonas- ceftazidime; Listeria- ampicillin)
-common neurological disease of children,
-meningitis tb diye hote pare? (yup)
-name a pathological condition with fever (febrile convulsion, meningitis, cerebral malaria, viral
encephalitis, brain abscess) Criteria of febrile convulsion (characteristic clinical features and
absence of any evidence of meningitis clinically or in CSF profile ....ei qs vvi.Abid Mollah, page
235) -How to differ from meningitis (clinically:absence of signs of meningitis- neck rigidity,
, bulging anterior fontanelle; investigation-csf examination )
Connective tissue diseases?
-JIA vs Rheumatic fever differences (Abid Mollah, page 140)
-JIA r feature
-Name some connective tissue disease in Children (ARF, JIA, septic/tubercular, reactive)
type 2 hypersensitivity (ARF) and type 3 hypersensitivity (AGN) disease in children
-SLE er feature (11 features- malar rash, discoid rash rash, photosensitive rash, oral ulcer,
arthritis, serositis, renal disorder, neurological disorder, hematological disorder,immunological,
ANA),
-RA er feature (
Articular

o Ulnar deviation of fingers

o Z deformity of thumb
o Swan neck deformity
o Boutonniere deformity (button hole deformity)

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-acute rheumatic fever kemne hoy (Type II hypersensitivity), diagnostic criteria ta bolo
(revised Jones criteria)
Dermatological diseases
-flaky paint dermatosis location? (leg, thigh, buttock, back) in which type do we get this?
(Kwashiorkor)
-skin disease of children common ki ki ase (scabies, eczema)
-complication of scabies (secondary bacterial infection- PSGN, ARF; secondary eczematization,
urticaria)
-Scabies er clinical feature?

Linear/curvilinear papule
Reddish
Caused by the mite

Intense
More at night

-Site of lesions
n body except face (in neonate, face as well)

-Causative organism? (Sarcoptes scabiei hominis)

Poisoning
-Name some common poisoning (kerosene, OPC, cosmetics, medicine, detergent, soap, shampoo)
-What procedure is contraindicated in kerosene poisoning, (gastric lavage, as it may cause
aspiration pneumonia)
-can OPC poisoning occur in children (yes), C/F of OPC poisoning (muscarinic-all secretions
increased, nicotinic- muscle cramp, pupil constricted), which ones are muscarinic, Mx. of OPC
poisoning (atropinization, Abid Mollah, page 274)
-Kerosene poisoning e Gastric lavage kno dei nah
-Tx of kerosene poisoning (only supportive, oxygen inhalation; Abid Mollah, page 273)
-Kerosene poisoning, Rx R kothay gastric lavage contraindicated?
-Kerosene poisoning e ki treatment dba?
Neonatology
-term baby (after 37 completed wks), preterm baby (born before 37 weeks), post term
(beyond 2 weeks of edd), LBW baby (wt<2500gm) def
-Neonate ?(<=28 days) Neonatal problem ki ki? (LBW, perinatal asphyxia, neonatal sepsis,
neonatal jaundice)
-Preterm baby with perinatal asphyxia
-PNA er scenario, ei baccha take help korar jnne tmi kon instrument use korba seta nao..show

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 the parts.. Function of pop up valve, nicher opening e kon ta diye ki jay. (AMBO bag)
-preterm baby with perinatal asphyxia, clinical features (no respiration, no cry, absent or
weak respiratory efforts, gasping respiration with long pauses in between respiration,
convulsion due to HIE, bradycardia, muscular hypotonia),how to evaluate(APGAR score),APGAR
elaboration (appearance, pulse, grimace, activity & muscle tone, respiration), & interpretation
(>=8 is better).Which one is used here?(AMBU Bag)....show the parts of it.Function
of pop up valve (to release extra air pressure)
-ki ki prbm hbe ei babyr/complications of preterm baby(early-hypothermia, hypoglycemia,
RDS, apnoea, hemorrhage, feding difficulty, physiological jaundice exaggeration, anemia of
prematurity, PDA; late- metabolic bone disease, retinopathy of prematurity, delayed growth &
development, CP)
-cause of neonatal sepsis (risk factors: prematurity, LBW, fetal distress, PROM, prolonged
labour, PNA, poor cord care)
-Neonatal sepsis: Name the organisms (EONS- group B strep., E coli, H influenza; LONS-
Staph aureus, Klebsiella, Pseudomonas, Candida)
Infectious diseases
-Mosquito-borne diseases ki ki ache? (dengue, chikungunya, malaria) Bd te common ki ki
-what is EPI? (expanded programme on immunization) what are the vaccine preventable
diseases? (EPI+ rabies, rota virus, covid-19, influenza) Measles ki diye hoy? (measles virus)
-Epi vaccine Time of administration of bcg vaccine (<14 days, >42 days)
-name some infectious diseases (covid- , dengue virus name (dengue virus), vector borne
(Aedes aegypti), how it causes disease ( )
-Infectious disease -baby der ki ki hoy (scabies, meningitis, tonsillitis, pneumonia, dysentery,
TB, Typhoid kon route e hoy? (faeco-oral), Ki diye hoy (Salmonella typhi,
S paratyphi) Dengue kivabe transmit hoy (vector borne- Aedes aegypti, Aedes albopictus)
Aedes diye hoy arekta disease nam bolo (Chikungunya, zika, yellow)
-Common infectious dss in bd?
-Infectious diseases - Name common ones - prevention of each of them - TB vaccination
Short case
MUAC
-don't forget to ask permission from mother
-Process, finding
-muac tape and interpretation
-ki paiso, kno bolla, yellow hole ki, red hole ki
-classify SAM according to WHO

General Examination
-NS findings, which test to perform, how to confirm (don t say renal biopsy)
-periorbital oedema, leg oedema
-HHA

Plotting weight for age:

-obese (as it is more than 95 th percentile) Ei baby k dekhe obesityr cause ber koro, finding -
buffalo hump, moon face, striae, dx - cushing syndrome, most common cause of cushing -
(steroid toxicity), babuder kivabe hoy (by treating nephrotic syndrome baby with steroid)
-Pt was obese and madam asked the cause of obesity ...I said Cushing syndrome...madam asked
why...I said due to steroid toxicity in case of NS...madam asked to describe the face and
neck...I said moon face ,buffalo hump,acanthiosis nigricans(neck finding ta khub sunte chaise)
-inspection- describe steroid toxicity features, why happened? Steroid toxicity? What's name

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 of the syndrome? Cushing
-Weight for age, weight for height diye Ki bujha jay
-interpretetion,height for age hole ki hoto
-causes of Underweight, C/F of Vitamin A deficiency

Abdomen palpation:
-hepatosplenomegaly. Cause
-Inspect and palpate abdomen :( ascitis chilo) (superficial and deep palpation korar porei thamay
diche.. Then tell ur findings, cause of huge ascitis in this children..)
-timely shb dekha jay na.ki dekho nai?chele hle ki extra dekhba
-huge splenomegaly
-weight for height e ki boli, wt for age e ki boli, who criteria for sam
-Palpate the abdomen, findings, ki ki dekhoni, liver palpable na? Kivabe bujhla na, splenomegaly er
cause ki ki, ei bacchar ki dekhba r thalassemia hole face dekhe bolo
-Inspection and palpation of abdomen...time was too short ...no need to measure liver and
spleen...there was hepatospleenomegaly and madam asked the causes
-Inspect n palpate abd (huge ascites)
-Causes of hepatosplenomegaly in children... HHA--- ma er kac theke ki hx niba, r ki ki examine
krte chao, Face kmn, Thalassemic facies er criteria
-case hepatosplenomegaly) Relevant- anemia, jaundice, bony tenderness
-hepatosplenomegaly = congenital hemolytic anaemia ...ei case e momgoloid face word ta bolo na
keo....amnei feature gula bolbo )
-splenomegaly chilo, Cz, thalassemia er confirmatory investigation, Leukemia er confirmatory
investigation

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 Medicine Viva
(Hafiz sir on ECG Board)

ECG/ Cardiology
AF:
-r-r wave dekhao, keno irregular bolla, dekhao, fibrilatory wave dekhay bolte ble je egula ki??
-CF (
Palpitation
Breathlessness
Fatigue
Lightheadedness
In old age may be asymptomatic
o Stroke
Examination

o Pulse irregularly irregular

o Pul
o Murmur of MS present (if that is the cause)
-kon dhoroner pulse paoa jai (irregularly irregular),kno, what is pulsus deficit (when heart
rate is >10 beats greater than pulse rate), pulsus deficit dekhla pordin aro bere gece ,
prognosis vlo naki kharap (kharap)
-S/S, complications
thromboembolism
o stroke
o limb ischemia
o mesenteric ischemia
o MI
Heart
o Ventricular Tachycardia
o Ventricular Fibrillation
o Heart failure
-rate control drug (beta blocker, digoxin, verapamil, amiodarone), b blocker kno young patient
k dibo na (sinus bradycardia and greater than first degree heart block, uncompensated heart
failure, asthma, and sick sinus syndrome) (??)
-cause,(tell according to Davidson- coronary artery disease including acute MI, valvular heart
disease especially rheumatic mitral valve disease, HTN, sinoatrial disease, hyperthyroidism,
alcohol, cardiomyopathy, congenital heart disease, chest infection, pulmonary embolism,
pericardial disease, idiopathic/ lone atrial fibrillation)
-cause of sinus tachycardia (anxiety, fever, anaemia, heart failure, thryotoxicosis,
pheochromocytoma, beta agonists)
-thyrotoxicosis a AF chara r ki pawa jay ( high volume pounding pulse)
-management (
Paroxysmal atrial fibrillation
o
o If symptoms cause trouble: beta blockers are 1st line drugs (class II)
Persistent atrial fibrillation
o Rhythm control
cardioversion

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 o Rate control
Drugs

catheter ablation
o Thromboprophylaxis
Warfarin
Oral direct anticoagulant such as

thromboprophylaxis: start 4 weeks before, and continue for 3 months after

cardioversion

Acute ST elevation anteroseptal MI:

-Findings (st elevation in v1,2,3,4, T inversion, pathological Q)
-Presentation of this patient (
Symptom:
Chest pain
o Central
o Sudden onset
o Heavy, constricting
o Radiating to neck, arm, jaw, epigastrium
o Associated with:
Nausea
Vomiting
Breathlessness
Feeling of impending death
o Persisting for >20 mins
o Not relieved by rest/nitrate
o Severe
Sign:
General examination
o Pallor
o Sweating
o Tachycardia
Parasympathetic/vagal sign
o Vomiting
o Bradycardia
Sign of impaired myocardial function
o Decreased SBP, increased DBP, narrow pulse pressure
o If associated ALVF
Cold periphery
Lung crepitation
-Management in upazilla (ECG, high flow oxygen, loading dose of aspirin(300mg) & clopidogrel
(300mg), morphin, injectable antiemetic, sublingual GTN, refer to CCU)
-Immediate Mx steps (same as above, then PCI within 6 hours, streptokinase within 12 hours,
LMWH)

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-Would you discharge this patient home after immediate Mx ( No- I said monitoring is
needed for acute complications like arrhythmia, Cardiogenic shock, acute HF, re-attack--
sir accepted)
-Definitive Mx in higher center (PCI)/ -Mx in CCU level
-if PCI unavailable, what to do (Thrombolysis)
-Pharmacological agents used in thrombolysis (streptokinase)
-Why primary PCI is preferred? (minimal myocardial damage, no chance of anaphylaxis)
-How Morphine is introduced (relieves pain, prevents air hunger)
-Premanagement of PCI (ECG, high flow oxygen, loading dose of aspirin(300mg) & clopidogrel
(300mg), morphin, injectable antiemetic, sublingual GTN, refer to CCU)
-Which MI is most dangerous? (anterior MI, bcz it can cause cardiac arrhythmia and sudden
cardiac death)
-Non ST elevated but you think it's MI what will you do next?(supportive mx including
LMWH)
-Acute keno bolla (tall T- hyperacute; ST elevation- acute; Q wave- old); ST elevated na , but
severe chest pain,tahole Ki MI hote pare, kivabe bujhba (Troponin I), Tokhon oi MI ke Ki
bola hoy (NSTEMI)
-what do leads v1, v2, v3 indicate? (v1, v2->right ventricle; v3, v4-> septal; v5, v6-> left
ventricle) What leads are they? (chest lead)
-if a MI pt would come to you at upazilla level how would you manage?

LVH with strain

-Causes(systemic HTN, aortic stenosis, coarctatin of aorta, hypertrophic cardiomyopathy, VSD)
-Precordium finding (apex beat is heaving, shifted)
-Cause of heaving (HTN, AS) and thrusting apex beat (MR, AR)
-Complications (myocardial ischemia, MI, ALVF, CCF)
-Why strain?(due to increased muscle mass,the oxygen demand is not met and ischemia ensues)
-Cause of LVH

CHB:
-C/F
i. Asymptomatic
ii. Bradycardia
iii. High volume pulse
iv. Wide pulse pressure
v. Cannon wave in neck
vi. Variable intensity of 1st heart sound
-What is the heart rate? (around 40)
-Cause
i. Acute myocardial infarction
ii. Drugs: beta blocker
iii. Cardiomyopathy
iv. Myocarditis

vi. Idiopathic fibrosis

vii. Collagen disease (SLE, RA)
-Treatment. (Temporary pacemaker followed by Permanent pacemaker)
-Tmr frnd er CHB, hatte giye unconscious hoye pore gelo, tumi ki korbe (Stokes Adams
syndrome. I will give CPR)
-CHB more common in anteroseptal or in inferior MI? (inferior MI) which one is more

27
 dangerous? (anteroseptal MI)
-Tell some causes of sinus bradycardia (
Physiological causes
o Rest
o Sleep

Pathological
o MI
o Sick sinus syndrome
o Hypothermia
o Hypothyroidism
o Raised ICP (cushing reflex)
o Drugs (beta blocker, digoxin, verapamil)
-tell one neurological cause (raised ICP/ cushing reflex), tell one hepatobiliary cause
(obstructive/ cholestatic jaundice)
-Mechanism of bradycardia in raised ICP, what is this reflex called (cushing reflex)
-Causes of Severe chest pain (acute MI, unstable angina, pulmonary embolism, aortic
dissection, tension pneumothorax)
-LVF feature (cardinal features of ALVF- pulsus alternans, bilateral basal crepitation, gallop
rhytm; others- dyspnea, orthopnea, PND, cool periphery)

GIT+HBPS
Stomach
-20 (PUD,
Chronic pancreatitis) Which PUD most likely here? (Gastric ulcer- as pain occurs after intake
of food, so patient avoids food and lose weight). Cause? (NSAID, H. Pylori). Treatment of H.
Pylori? Triple drug therapy. What antibiotics are used? 2 among 4 (metro, clarithro,
amoxicillin, tetracyclin), plus PPI. If tr what then?
Quadruple. Name one drug of QDT -salicylate, sucralfate. Name some non GIT
causes where triple drug therapy/H. Pylori eradication therapy is indicated
Megaloblastic anemia, but they wan deficiency/Refractory Iron

-60 years er patient er long history of taking PPI ache, epigastric pain ache, endoscopy
kore ulcerative lesion paoya gelo,DX Ki (PUD) , confirm hoba kivabe (
For diagnosis of ulcer
o Upper GIT endoscopy with biopsy from the ulcer to exclude malignancy
For diagnosis of H pylori infection
o Non invasive method
Urea breath test (with radioactive Carbon)
Fecal antigen test
Serology
o Invasive
Histology
Culture and sensitivity
Rapid urease test)
-clinical examination kore Ki Ki findings pabo. (
Anemia present
Malnourished
Wasting seen

28
 Epigastric tenderness
In perforation, signs of peritonitis and shock present
-Long term Triple therapy er antibiotics khaoyar pore diarrhoea keno hoy (Antibiotic
associated diarrhea), pathogenesis ki (caused by alterations in the composition and function of
the intestinal flora)
-PUD er 3 ta cause bolo (
H. pylori infection
NSAID
Smoking
Alcoholism
Stress
Burn
Shock
Gastrin producing tumor: Zollinger Ellison syndrome
-triple therapy dilam, ppi dilam onek din khaise, 60 yrs age, ekhn amra endoscopy kre
ulcer pelam pet e, ki cz hote pare? (ulcerative carcinomatous growth) ei patient e anemia ki
karone hote pare? (bleeding-> anemia;due to IF deficiency)
-A 65 y/o male patient with history of asthenia, lump in epigatrium. Dx? (Ca stomach; triad
of ca stomach- AAA=> anemia, asthenia, age>40yrs)
-What other relevant findings you will get? (Supraclavicular lymph node enlargement),
what's the name? (Virchow's gland), ki paba GE e ( supraclavicular LN )

Hepatitis
-Patient on anti-tb drug came to you with jaundice after 4 days of starting treatment of
TB. Is it due to drug or due to viral hepatitis? (History: prodromal, examination: tender
hepatomegaly, investigation: viral marker, serum ALT will be very high. IF these are present
then it is due to viral cause. If not, then most probably due to drug toxicitity.)
-a person came to you with HBsAg +ve. Now he wants to go to Saudi Arabia and tells you
to make him negative. What will you do? (Counsel that it is a chronic process, may resolve
spontaneously or may remain chronic. At first will do a HBcAb and see if IgG or IgM present.
If IgM present then tell patient to wait for at least 6 months while the virus may resolve
spontaneously. If IgG is positive it means chronic hepatitis. Then according to symptoms and
serum ALT level, I will decide when to give anti-viral therapy. I will also check HBeAg and HBV
DNA to check viral load. Considering everything, I give him antiviral and then he may become
HBsAg -ve and go to KSA. In the meantime I will counsel him about contact, needle sharing and
sexual intercourse.)
-Acute hepatitis er complication? (

r disease, cirrhosis (Hep B, C)

)

CLD
-20 yr old patient with CLD, What are the causes?
alpha 1 antitrypsin deficiency, alcoholism)
-Young patient with jaundice... Cz wilson's disease. wilson disease er pathophysiology (excess
copper is accumulated in the body),kon kon organ e Cu joma hoi (liver, brain, cornea), K-F
ring,chokher kothay hoi(Sclero corneal junction) ,cornea r kon membrane e hoi(Descemet

29
 membrane)
-Young age CLD cause? -Findings of wilsons disease? Eye finding?(K-F ring present in cornea)
Can ceruloplasmin be normal in wilson? (usually low, can be normal) In which area of brain
does it affect? (Basal ganglia) Tell 2 neurological manifestation of it (chorea, athetosis,
rigidity, bradykinesia)
-Haemochromatosis: patient dkhso? CF (Joint pain, Abdominal pain, Fatigue, Weakness,
Diabetes, Loss of sex drive, Impotence, Heart failure) pathology (Hereditary hemochromatosis
(HH) encompasses several inherited disorders of iron homeostasis characterized by increased
gastrointestinal iron absorption and tissue iron deposition due to low expression of hepcidin, an
iron regulatory hormone)
-A jaundiced patient presented with altered sleep rhythm and violent behavior. Dx-
Hepatic Encephalopathy. Investigation to confirm Hepatic encephalopathy (EEG). EEG
findings of hepatic encephalopathy (high-amplitude low-frequency delta waves and triphasic
waves), waves in EEG (alpha, beta, gamma, delta, theta)

Pancreas
-Features of chronic pancreatitis (features of malabsorption & features of DM)
-Management of chonic pancreatitis pain (NSAIDs, opioids, pregabalin, TCA low dose, oral
pancreatic enzyme supplement, celiac plexus neurolysis, total pancreatectomy)
-DM type (1, 2, 3/others) & mechanism
-Is Chronic pancreatitis type 1 or type 2 DM?
-How to correct hyperglycemia in C. pancreatitis? (insulin)
-What to do if patient doesn't want to take insulin? (convince him, even he has to put insulin
in water to keep it cool)
-Management of type 1 dm, including the regimens (insulin)
-DKA management (
it is a medical emergency

Catheterize patient to monitor urine output

o 0.1 U/kg/hr insulin IV

o Expected rate of fall of glucose: 3-6 mmol/L
o When blood glucose <14 mmol/L: add 10% DA + continue insulin infusion
o This will promote insulin entry in cell and promote metabolism
o Switch patient to his/her regular SC Insulin only when pt is stable biochemically, and able
to eat and drink normally
eplacement
o 0.9% NaCl (normal saline)
o Na >155 mmol/L: 0.445% NaCl (half strength normal saline)
Correct electrolyte imbalance
o Potassium:

ney ok), give K supplement (KCl 40 mmol/L)

o Bicarbonate: usually not needed

o When stable/refractory to treatment, refer to endocrinologist

o Investigate the precipitating factors
o Prevention of future episodes by appropriate measures

-30 y old lady with DM& recurrent abdominal pain diagnosis (DKA) ,r ki ki features, what

30
are the micronutrients (Fe, Zn, Folic acid) features of Zn deficiency (acrodermatitis
enteropathica, growth retardation in infants, anorexia & diarrhea, hair loss, impaired night
vision related to altered vitamin A metabolism, infertility)

Renal
CKD
-3 commonest causes of CKD (DM, HTN, Chronic GN)
-Features
Symptom:
Incidental dx: raised urea and creatinine
Presence of risk factor: DM, HTN
Early symptom: nocturia
Tiredness (anemia)
Breathlessness (pulmonary edema an fluid overload)
Non specific features
o Anorexia, nausea, vomiting
o Headache
o Pruritus
o Hiccup

Sign:
General examination
o Yellow color of body
o Anemia
o Nail: brown line seen in nails
o Easy bruising
o Scratch marks all over body
CVS examination
o Pulsus paradoxus
o Pericardial rub
Respiratory examination
o Increased respiratory rate

Examination of CNS
o Absent reflex
o Anesthesia
o Parasthesia
o Restless legs (itching inside leg)
-PCKD te brain e ki somossa hoi (Berry aneurysm) / APCKD theke Neuro te jabe? Ki niye
jabe? (Sub arachnoid hemorrhage) Keno? (rupture berry aneurysm)
-How to control HTN in CKD pt? (ACEi/ARB, as it reduce proteinuria & slow the progression
of CKD)
-cause of ckd

-Cause of systemic hypertension (Primary/ Essential (95%)- no apparent cause; Secondary-

alcohol, obesity, pregnancy, renal (AGN, renal artery stenosis, PCKD), endocrine

-Name of some glomerulonephritis (AGN, RPGN, FSGN, Anti-GBM disease)

31
-Hematuria cz
S (stone), T (tumor, trauma, cyst), I (Infection, inflammation)
Pre renal
o Bleeding disorder
o Renal infarction (I)
o Vasculitis (I)

o Renal tumor (T)

o Renal TB (I)
o Cysts (T)
o Glomerulonephritis (I)
o Interstitial nephritis (I)
o Pyelonephritis (I)
o Vasculitis (I)
o SLE (I)
o Renal Stone (S)
o Trauma (T)

o Ureter: Stone, Tumor, Infection, Trauma

o Bladder: Stone, Tumor, Infection (cystitis)
o Prostate: BPH, Tumor
o Urethra: Inflammation/infection (urethritis), trauma
**cause of painful hematuria: UTI, Stone ; others are painless
Hematology
-A patient presented with anemia, mention other findings in GE to help understand etiology
(koilonychia- IDA; jaundice- hemolytic anemia; glossitis, cheilosis etc-- Fe/B12/folic acid def;
tingling of legs dx: Megaloblastic anemia due to B12 def)
-Findings of vit B12 deficiency in brain (I said optic atrophy, sir accepted but also wanted
to hear about dementia), (Subacute Combined degeneration- spinal cord)
-Cause of megaloblastosis without macrocytosis (i told post splenectomy, they nodded)
-1 cause of macrocytosis without megalobastosis (CLD, Hypothyroidism, Alcoholism,
Hemorrhage, Hemolysis, )
-60 yrs patient came with koilonychia. What could be cause? What are the causes of IDA
in this patient? (blood loss, nutritional deficiencies, medications, cancer therapies and poor
absorption. Long-term use of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) can
cause significant bleeding from the digestive tract)

Thalessimia
-CF (severe anemia, jaundice, splenomegaly)
-gene defect (point mutation), mutation ki type (nonsense), inv ki korbo? (CBC, PBF, Hb
electrophoresis, Serum iron profile)
-Complications (transfusion reactions, transmission of diseases- HBV, HCV, malaria, HIV; iron
overload, others- RBC allosensitization, HLA allosensitization, GVH disease)
-Does this patient need to consult endocrinologist? ( pancreas , adrenal gland iron deposit
hye diabetes, addison hote pare ajnne). Gonad a ki hote pare? (hae)
-long time hereditary hemolytic anaemia now presents with paraparesis cause? (due to
paravertebral extramedullary hematopoiesis causing spinal cord compression)

HbE

32
-what is the pathology in Hb E disease? (Point Mutation) Protein/ Amino acid Name? (At
position 26 there is a change in the amino acid, from glutamic acid to lysine)
-Single genetic test to detect the pathology of Hb E disease (Beta globin gene (HBB)
sequencing)
-is it curable? (No)

Leukemia
-CF (anemia, fever, bleeding manifestation, bony tenderness, hepato-splenomegaly,
lymphadenopathy)
-CML ar genetic basis (reciprocal translocation) Ki gene exchange hoy? (Philodelphia
chromosome) Philodelphia pele prognosis kmn hoy? (more favourable) Ar ki ki genetic change
thakte pare?

Multiple myeloma: full details

-dx criteria
2 of the following 3:
Skeletal lesion (lytic lesion)
Bone marrow plasma cell >30%
Serum and urinary paraprotein),
-Complications
C- Hypercalcaemia
R-Renal failure
P- paraplegia due to fracture
V- hyperviscocity
-neurology te jete pare? (yes) ki niye jabe? (paraplegia) cervical myopathy (there is no such
term) ar myelopathy (Cervical myelopathy is a form of myelopathy that involves compression
of the spinal cord in the cervical spine. It is a complication of Multiple myeloma) konta ki..
Psychiatry
Dementia
-Definition (according to Davidson) (Dementia is a clinical syndrome characterised by a loss of
previously acquired intellectual function in the absence of impairment of arousal)
-Dementia and memory loss
-Causes of dementia
Vascular: diffuse small vessel disease
Inherited: Alzheimer
Neoplastic: Secondary tumor to CNS
Traumatic: chronic subdural hematoma
Metabolic: alcoholism, B1, B12 deficiency
Hydrocephalus: normal pressure hydrocephalus
Inflammatory: Multiple sclerosis
Infective: HIV, syphilis
Prion disease: Creutzfeldt-Jakob disease
-worldwide commonest cause (I said Alzheimer's), latest treatment of Alzheimer
(Aducanumab)
-Reversible cause of dementia
Neoplastic: Secondary tumor to CNS
T raumatic: chronic subdural hematoma
Metabolic: alcoholism, B1, B12 deficiency
Infective: HIV, syphilis

33
 Prion disease: Creutzfeldt-Jakob disease )

Major depressive disorder

-Features
Psychological
o Depressed mood
o Reduced self esteem
o Pessimism
o Guilt
o Loss of interest
o Loss of enjoyment (anhedonia)
o Suicidal thinking
Somatic
o Reduced appetite
o Weight change
o Disturbed sleep
o Fatigue
o Loss of libido
o Bowel disturbance
o Motor retardation/slowing of activity )
-Anti depressant drug: names (TCA- imipramine, amitriptyline; SSRI- citalopram, sertraline,
fluxetine; SNRI- vanlafaxine; MAOi- selegiline; Novel- Mirtazapine, Bupropion), common side
effect (TCA- anti muscarinic, postural hypotension, reflex tachycardia; SSRI- sexual
dysfunction, serotonin syndrome)

-Define Hallucination ( Sensory perceptions occurring without external stimuli )

illusion (Illusions are misperception of real stimuli )
delusion (A delusion is a false belief (not related to religion/cultural belief which is held in
conviction (firmly believed despite evidence to the contrary )
-Neurosis types
Anxiety neurosis.
Depressive neurosis.
Obsessive-compulsive neurosis.
Somatization, formerly known as hysterical neurosis.
Post-traumatic stress disorder, also known as war or combat neurosis.
Compensation neurosi
-Anxiety neurosis type (GAD, panic, phobic, OCD)
-psychosis (Psychosis is a major personality disorder marked by mental and emotional
disruptions), neurosis (Neurosis refers to a mild mental disorder characterised by physical and
mental disturbance), somatoform disorder (somatic symptoms, but no underlying medical/
surgical cause found )
Poisoning
-Ki ki poisoning dekheso ward e? (OPC, Benzodiazepine, Datura, Snake venom, Paracetamol,
Household poisoning: Harpic, Kerosene poisoning)
-OPC poisoning: features, mechanism (AChEi-> increase ACh conc at synapse-> increased Ach
activity-> muscarinic, nicotinic effects)
-Snake venom poisoning: effects/ features, ki ki toxicity hoy? (Neurotoxin, Myotoxin, acute
renal failure, hematological abnormality) Myotoxicity te ki features paba? (Muscle weakness,
Respiratory failure, Black urine (myoglobinuria), Renal failure)

34
-BDZ poisoning: features
o CNS: confusion, slurred speech, sedation, coma
o CVS: bradycardia, hypotension
o Respiratory: respiratory depression
o Muscle: reduced muscle tone
o Temperature: hypothermia
o Eyes: diplopia, nystagmus (but pupil size normal)
lethal dose (40-50 tablets), antidote (flunazenil)
-Diseases caused by alcoholism? (alcoholic fatty liver disease, PUD, chronic pancreatitis,
xephalopathy) Complications of alcoholism?
-Paracetamol poisoning: antidote (N acetyl cystein-NAC)
-Herpic poisoning (corrosive poisoning- gastric lavage contraindicated; management supportive)
Immunological
-Tell me some Immunological diseases (autoimmune+immunodeficiency+allergy) and
autoimmune disease

-Name autoimmune disease that involve single organs? (celiac disease, Graves disease,
Hashimoto thyroiditis, type I diabetes mellitus, and Addison disease)
-Neurological ekta jetay sondha bela haat obosh hoye ashe (myasthenia gravis),
pathogenesis (autoantibody acts as competitive blocker at nicotinic receptor)
-Type 1 DM associated autoimmune disease? (autoimmune thyroid disease (ATD), celiac
disease (CD), autoimmune gastritis (AIG), pernicious anemia (PA) and vitiligo)
-Pathophysiology of Type 1 DM (autoimmune destruction of pancreatic beta cell)
Genetics
-Name some Genetic disease
AD-

sclerosis

AR-

35
 metabolism

XLD-
Vitamin D resistant rickets

XLR-

-nyhan syndrome (HGPRT deficiency gout)

lport syndrome
-Difference between genetic and congenital disease? (genetic diseases are those where
there is a lesion/ abnormality present in gene. Congenital disease is a disease which is present
from birth that can be due to genetic or non-genetic causes)
-Types of genetic disease? (genomic, chromocomal, gene)
-Gene sequencing? (In the mid-1970s, a scientist called Fred Sanger pioneered a DNA
precise order and nucleotide
type (thymine, cytosine, adenine and guanine) in a molecule of DNA). Examples of diseases
diagnosed (parina)
-some purely genetic disease names (AD, AR, XLD, XLR)
-types of genetic diseases.name some choromsomal diseases (aneuploidy-trisomy 21, 18, 13,
Klin - 3N, 4N ). defect kontay ki hoy?example (gene defect
(point, frameshift, triplet repeat), chomosomal (invertion, deletion, translocation), genome
(number alteration- aneuploidy, polyploidy))
-Genetic disease r congenital disease er dif, example
-Common genetic dss ki ki? HbE te point mutation kontar sthe konta hoy? (single point
. At position 26 there is a change in the amino acid, from glutamic acid
to lysine)
-Hematological genetic disease er nam bolo ekta (Thalassemia), eta ki dhoroner genetic
disease (AR)
Electrolytes
-A patient with diarrhoea, now presents with oliguria. Dx: AKI Mx:which fluid will you use?
Why? (NORMAL SALINE. AKI is causing hyperkalemia, so I'll choose a fluid that doesn't
contain potassium; Cholera saline will aggravate the situation as it contains K +)
-3 cause of hypokalemia (diarrhea, vomiting, diuretics), 2 features (

- may lead to polyuria and polydipsia)

-Hyponatraemia: causes (diarrhea, vomiting, excessive sweating, SIADH, CCF, cirrhosis of

liver, NS, CKD), deficit kivabe count kore? (Total Na+ deficit= 0.6 x (weight in kg) x (desired

36
 Na actual Na) Why 0.6?? (Normal Total Body Water= fraction water x weight in Kg. fraction
water: Child: 0.6 for both male & female child. Adult: 0.6 for males, 0.5 for females. Elderly:
0.5 for males, 0.45 for females)
Geriatrics
-Common geriatric problems/ old age diseases (geriatric giants- immobility, instability (falls),
incontinence, intellectual impairment, and iatrogenic complications)
-Cause of fall in geriatric age group

o Cataract
o Glaucoma

-Old age pt chronic diarrhoea niye aslo 2 ta cz bolo (colon cancer, malabsorption)
Miscellaneous
-Tumor markers with diseases (CA 15-3, CEA, HER-2, ER, PR, PSA, CA 19-9, CA 125) (ward e ja
dekhecho)
-Scenario: 65 year old man with severe temporal headache, High ESR, dx? (Temoral
arteritis) Rx options-- I said glucocorticoids but sir wanted to hear sth else in addition
(prednisolone?) Complication if untreated-- visual loss, name of this condition (amaurosis
fugax), which vessel (central retinal artery and posterior ciliary arteries of eye)
-Name some cutaneous manifestation of malignancy anywhere in the body. (Paraneoplastic
dermatoses- Acanthosis nigricans, the sign of Leser-Trélat, tripe palm, acquired ichthyosis,
and palmoplantar keratoderma; infiltration of skin by malignant cells)

37
 Medicine Viva
(Shyamol sir on ECG Board)

ECG/ Cardiology
AF
-Most common cause konta? (MS) auscultation finding in MS? (loud 1st heart sound, low
pitched localized, rough, rumbling mid diastolic murmur best heard in the mitral area in left
lateral position with breath hold in expiration with presystolic accentuation) most common
complication? (thromboembolism/ stroke) Stroke how? (thromboembolism) Which type of
stroke in this case? (ischemic) How to prevent stroke? (thromboprophylaxis- warfarin,
apixaban, rivaroxaban, dabigtran)
-complication
-Thromboembolism theke ki hote pare? (stroke, limb ischemia, mesenteric ischemia, MI )
Ki drug diba?
-thromboprofylaxis (onekjon eikhane vul kore heparin bole felse , amio.please say warfarin)
warfarin dile ki monitoring kori(INR- international normalized ratio, to monitor coagulopathy),
AF theke HF hote pare ki na ? (haa, V-fib develop kore)

Acute ST elevation anteroseptal MI

-Findings
-Bedside findings (central constricting chest pain, radiating to neck, jaw, arm; fear of
impending death, sweating, vomiting, tachycardia, low BP)
-characteristic pain of MI. How u differentiate MI & angina? (rest & GTN relieves angina,
not MI)
-Do we check bilateral basal crep. in MI? (yes, to see if ALVF has developed)
-Heart sound in MI. (pan systolic murmur due to mitral regurgitation)
-causes of ST elevation other than MI (left ventricular hypertrophy, pericarditis,
ventricular-paced rhythms, hypothermia, hyperkalemia and other electrolyte imbalances, and
left ventricular aneurysm)
-difference between MI and pericarditis clinically (the pain associated with pericarditis is
usually positional in nature the patient states the pain worsens when lying down,taking a deep
breath, or coughing. Leaning forward while sitting may alleviate the pain associated with
pericarditis. Other signs and symptoms of pericarditis are low-grade fever, dyspnea,
tachypnea, and malaise. A pericardial friction rub with a superficial scratchy or squeaking
quality may be auscultated and is a good indication that the patient has pericarditis)
-ST elevation in MI patient still after 4 months cause (ventricular aneurysm)
-Anteroseptal MI (ST elevation in v1, v2, v3, v4), why not inferior (as ST elevation spared II,
II, aVF), when will you call it ex. anterior? (if ST elevation present in v1-6, I, aVL)
-acute/chronic? (ST elevation- acute; pathological Q present- chronic)
-blood supply of anteroseptal region (LAD- left anterior descending artery, branch of left
coronary artery)
-Rx of MI
-how old is your father? IHD ache kina? ki disease ache?(DM) tar ki MI howar risk ache
kina? risk factors of MI (modifiable- sedentary lifestyle, DM, HTN; non-modifiable- age, sex,
personality type)

38
LVH with strain
-kno bolla (S in v1+ R in v6 >35mm; strain as T inversion present in v5, v6) MI er T inversion er
sathe kivabe alada korba (here, asymmetric T wave present), bilateral basal creps hole ki
hobe (pulmonary edema due to ALVF), ekta drug ki diba (ACEi/ ARB- to prevent cardiac
remodelling)
-RVH hole ecg changes? (deep S in lead I, tall R in lead III- denoting right axis deviation; tall
R in v1, v2 with T inversion- denoting RVH), RVH features (left parasternal heave, epigastric
pulsation), causes (cor pulmonale, pulmonary hypertension, pulmonary stenosis, TOF, ASD, VSD,
TR, Eisenmenger syndrome), PHTN kivabe hy (Pulmonary arterial hypertension; Left sided
heart dsease- MS, AS, ALVF; lung disease- COPD, pulmonary fibrosis, obstructive sleep
apnoea; Pulmonary embolism; sarcoidosis, polycythemia vera) , PHTN er precordium findings
(palpable P2, left parasternl heave- if RVH present), Causes, TR er murmur (high pitched,
holosystolic murmur it is best heard at the left lower sternal border and it radiates to the
right lower sternal border), features (pulsating neck vein, ascites, leg edema)

VF
-Amak VF diyei pura board sesh korsen

Pericarditis
-pericarditis bollo sir but munna sir bolsen oikhane pericarditis er ecg nai Kono. Question:
mi r pericarditis er ecg findings er difference (ST elevation konta te kmn- convexity upwards
for MI, concavity upwards for pericarditis; Q wave present in MI, not in pericarditis; reciprocal
ST segment change- only in MI) Pericarditis er auscultation findings (pericardial friction rub
present)
GIT+HBPS
-causes of epigastric pain (PUD, Cholecystitis, Pancreatitis, inferior MI, DKA), pt with pain in
upper right side of the abdomen and liver palpable, what are the d/d?(Acute viral
hepatitis, Liver abscess, CCF, Chronic constrictive pericarditis, ) differentiate
between pain of pud (epigastric, burning, radiates to back, meal related, wakes the pt &
relieved by antacids), acute pancreatitis (high epigastric, severe, felt front to back,
immediately after eating, relieved by leaning/ sitting forward), acute cholecystitis (rt upper
quadrant, severe, colicky over long time period, radiates to right shoulder, accompanied by
nausea), 1 cause of acute pancreatitis only ("hepatobiliary disease" - gallstone) 1
biochemical investigation and one imaging (serum amylase/lipase + USG- i said ct scan first
but sir said its not available everywhere), findings in USG (evidence of pancreatic swelling,
gallstone, biliary obstruction or pseudocyst may be found), management of acute pancreatitis
Establish the diagnosis + assess disease severity by doing necessary investigations

o Manage severe case in HDU/ICU

o Analgesics: opioid analgesic
o Treat hypovolemia and shock: IV saline and crystalloid
o Heparin to prevent DVT
Treatment of complication
o O2 therapy if hypoxic
o Correct hyperglycemia
o Correct hypocalcemia
o Paralytic ileus: NG aspiration
o Ventilator support if SIRS develops
o Necrotizing pancreatitis: necrosectomy operation

39
 o Pseudocyst: cyst-gastrostomy operation
Treatment of the underlying cause
o If cholangitis and jaundice present during attack of AP: urgent ERCP to treat
choledocholithiasis
o If these are not present, laparoscopic cholecystectomy should be done after the acute
pancreatitis has resolved )
enteral feeding or parenteral feeding (parenteral), advantage and disadv of enteral
feeding here (disavantage- intestinal obstruction, perforation, peritonitis)
-Classification of jaundice (prehepatic, hepatic, posthepatic), triad of HHA (anemia, jaundice,
splenomegaly), does any liver enzyme increase in Hemolytic jaundice (LDH increase, AST
mildly elevated), can hemolytic jaundice cause obstructive jaundice? (??)
-vomiting of blood ke clinically ki bole (hematemesis).blood er color kemon hobe (coffee
ground colour).. Cause ki...(ruptured esophageal varices, bleeding PUD, Mallory weiss
syndrome, anti coagulant therapy, esophagitis, stomach cancer) Portal Htn kake bole.. Ekta
esophageal varices er pt ar PUD er pt abdomen check kore kivabe dff korbo
(spleenomegaly,epigastric tenderness)..
-2 jn pt eki sathe ward e ashlo hematemesis niye,ki ki dd mathay rakhba?kontar jnno kon
cause thakte pare?hx, c/f kontar jnno ki thakbe? investigation ki ki korte hobe?
-Diarrhoea +vomiting ward a kivabe manage korba?

Hepatitis
-Jaundice -types, hemolytic jaundice cause (congenital hemolytic anemia, Rh incompatibility,
congenital hyperbilirubinemia (Gilbert, Criggler Najjar, Dubun Johnson, Rotor), name virus
causing hepatitis (Hepatotrophic- Hepatitis A,B,C,D,E; Non-hepatotropic-CMV, EBV, HSV,
yellow fever virus), HAV,HBV,HEV -which one cause chronic hepatitis? (HBV) Which one
never turn to chronic? (HEV) Any vaccine against which virus? (HBV) Newly married couple,
husband HBsAg+ve Now how to evaluate wife? (HBsAg screening; if negative, immunize) Wife
wants baby, how u will proceed? (first immunize wife, then allow for baby)

Pancreas
-steatorrhea ki , er feature ( pale , bulky , frothy , foul smelling , floats on pan ) Say some
condition where steatorrhea found ( Ami chronic pancreatitis bolchilam ) then pain of
chronic pancreatitis ( dull aching pain radiate to back ) exocrine (Serum Lipase, Serum
Amylase) and endocrine (RBS) function er test of pancreas , inv of chronic pancreatitis
( x ray to see calcification , then usg , then say mrcp )
Renal
-Dysuria (discomfort or burning during micturition), diff. between complicated and
uncomplicated UTI, name of the condition of UTI (Uncomplicated UTI infection in a
healthy, non-pregnant, pre-menopausal female patient with anatomically and functionally normal
urinary tract. Complicated UTI infection associated with factors increasing colonization and
decreasing efficacy of therapy. e.g. UTI in male & in females with risk factors) in a newlywed
woman,use of cranberry juice in UTI (Cranberry juice has often been the go-to for
preventing UTIs because it contains proanthocyanidins which inhibit bacteria from sticking to
the walls of the bladder. . Diff. between NS and AGN. Two symptoms
and one sign. Findings in urin RME (NS- massive proteinuria+++, hyaline cast, granular cast;
AGN- hematuria, RBC, RBC cast). Causes of AGN (Streptococcal skin infection).
-Burning during micturition er clinical term ki (dysuria)... Cause ki ki (UTI- cystitis, urethritis,
ureteritis, prostatitis, pyelonephritis)... Common organism (E coli, Proteus, Staph aureus,
Klebsiella). Treatment (plenty of water intake, cystitis- nitrofurantoin, trimethprim;

40
 pregnancy- cefalexin, pyelonephritis- cefalexin, ciprofloxacin; epididymoorchitis-
ciprpofloxacin; acute prostatitis- trimethoprim) Side effects of co trimoxazol (like
sulfonamide toxicity)
-uti te ki symp paba,predisposing factor ki,2 ta test ki ki diba,
-bony feature of ckd k ki bole ( reanal osteodystrophy : x ray findiings : marginal
sclerosis na ki Jani bollo jiboneo Suni nai )

Hematology
Lymphoma
-lymphomar nam suncho? Types (Hodgkin & Non-Hodgkin Lymphoma), HL r NHL kemne alada
korba clinically (In Hodgkin lymphoma, central, contiguous lymphadenopathy; itching; systemic
features: B symptoms- fever, weakness, drenching sweat, weight loss>10% body weight, Pel
Ebstein fever- these are present. These are absent in NHL) , mukhe ki dekhi (Among the
intraoral findings, the most frequent are ulcerations, pain, swelling, and tooth mobility, while
the extraoral findings include facial asymmetry and cervical, submandibular, and submental
lymphadenopath), kon lymphoma te paoa jay (Hodgkin), B symptom ki (Fever, weakness,
drenching sweating- all these are collectively called B symptoms), -
(Period of pyrexia followed by apyrexia and repeatation of the cycle)
Poisoning
-OPC (atropine, pralidoxime) benzodiazepen (flumazenil) paracetamol (N acetyl cystein)
poisoning er antidote
-Atropinization...kivabe bujhba?
4DFluT

-OPC poisoning, c/f, pt er chest auscultate kore ki paba? (crepitation) Antidote ki,
Atropinization sign
-what happens due to too much paracetamol ingestion? (acute liver necrosis/ failure) Name
antidotes
-name some benzodiazepines. (diazepam, oxazepam, midazolam, clonazepam, lorzepam) What is
the dose of poisoning? (40-50 tablets) Antidote name? (flumazenil)
Genetics
-Name some multifactorial disease. (lung cancer, DM, HTN, ischemic heart disease) Name
some pure genetic disease (AD, AR, XLD, XLR). Which gene is altered in Hemophilia? (factor
VIII gene on x chromosome)
-Turnur symdrome scenario, features (short stature, broad chest, widely spaced nipples, low
hair line, low set ear, fish mouth, high arched palate, webbing of neck, steak gonads),
karyotype (45, XO)

Electrolytes
-Normal level of serum Potassium (3.5-5 mmol/L) Hypokalemia er cause. HTN er ekta pt er
Hypokalemia hocche but eta kono drug/ diuretics neyar jonno na.cause ki? (Primary

disease, malignant hypertension) Conn's disease kivabe hocche?? (Conn syndrome is most

41
 often caused by an adrenal tumor, such as aldosterone-producing adenomas. Commonly, these
tumors are benign but in rare cases, they can be malignant)
-Hyponatrimia scenario,causes, SIADH er features (euvolemia, mild hyponatremia, no
evidence of cardiac, renal or hepatic disease potentially associated with hyponatremia), causes

o Anticonvulsant
o Antipsychotic
o Antidepressant
o Cytotoxic drugs
o OHA

treatment (water restriction, withdrawl of the drug responsible, Demeclocycline), tolvaptan

kivabe kaj kore (selective vasopressin V2 receptor antagonist), Pancoast tumor (tumour at
apex of the lung) and syndrome ki (Superior pulmonary sulcus tumors or Pancoast tumors arise
from the apical pleuro-pulmonary groove located superior to the first rib. When these tumors
involve the surrounding structures such as the brachial plexus, cervical paravertebral
sympathetic nervous system, and stellate ganglion, they cause a group of signs and symptoms
that are collectively called Pancoast syndrome. This is characterized by ipsilateral shoulder
and arm pain, paresthesias, paresis and atrophy of the thenar muscles of the hand, and
Horners syndrome (ptosis, miosis, and anhidrosis))

42
 Medicine Viva
(Hafiz sir on X-ray Board)

X-ray
Pneumothorax
-why do you think it is a pneumothorax?
i. Increased translucency in left lung
ii. Absence of broncho-vascular marking
iii. Trachea and mediastinum shifted to right side
iv. Collapsed lung margin can be seen
x ray dekhe ki tumi bujhba ki karone pneumothorax holo ei pt er? (if visible bony lesion
present, then traumatic/ penetrating chest injury. If characteristic TB lesion is present on
opposite lung, it may be due to tuberculosis. If mediastnum is shifted, diaphragm depressed
and rib cage is expanded, it is tension pneumothorax) causes of pneumothorax (spontaneous:
by etiology: primary:COPD, abscess, TB; secondary: on the background of lung disease. By
communication: closed, open, tension;; Traumatic: iatrogenic, injury). ei x ray k aro specific
vabe bolte hole dx ki bolba?(tension pneumothorax) why? types?
-tension pneumothorax presentation
-Etai jodi trachea ta shifted thakto tahole ki boltam (tension pneumothorax)
-Ekta patient asche onkdin dhore cough sathe sputum, breathlessness ache, examination
kore bilateral crepitation paila..whats ur clinical impression? (Bronchiectasis) Brochiectasis
er ekta patient ashole hothat kore renal impairment hye AKI hye gelo..whats the cause?
(Amyloidosis) common causes of secondary amyloidosis (chronic inflammation e.g. RA & chronic
infection e.g. TB)
-Why tension? Ekhane kno tension bolba? Kivabe hoiche x ray te dekhao (Rupture of
emphysematous bullae on left side) collapse lung margin dekhao
-Does it need immediate management? (yes, via needle thoracostomy) Causes of
pneumothorax in a senile patient. (1.rupture of emphysematous bulla 2.copd 3.trauma 4.tb)

Hydropneumothorax
-Collapse lung margin dekhao Auscultation r percussion er findings kon jayga te ki paba? (in
hydrothorax region, percussion note stony dull and breath sound absent/ diminished, vocal
resonance diminished) (in pneumothorax region, percussion note hyperresonant and breath
sound absent/ diminished)
-Kivabe bujhla xray te dekhao. (definite air fluid level) Eta ber korte koyta futo korte hbe?
(ekta. Water seal drainage) Bilateral basal creps - causes? (Bilateral bronchiectasis,
Pulmonary oedema (commonly due to acute LVF), DPLD)
-auscultation upore ki paba niche ki,alada korba kemne (percussion), cause (iatrogenic,
bronchopleural fistula, trauma, rupture of lung abscess, esophageal rupture, erosion by
bronchial carcinoma, PTB), iatrogenic kemne hoy (during aspiration of pleural fluid)

Pleural effusion.
-Why pleural effusion? (trachea normal/ shifted to opposite side- when massive pleural
effusion) Why not collapse? (in collapse, trachea is shifted to same side) Types of collapse
( 1.compression collapse due to pleural effusion 2. Absorption collapse due to bronchial
obstruction) Causes of repeated pleural effusion in 60 yrs old pt. Why? (Bronchial CA)

43
 what inv? (Pleural biopsy)

Consolidation,
-findings (partly homogenous, partly non-homogenous opacity with definite air bronchogram,
trachea & mediastinum centrally placed), causes/dds (Consolidation, Bronchial carcinoma, TB),,
investigation ( AFB and
malignant cells.)
-Rt sided consolidation,air bronchogram keno hy (gas-filled bronchi surrounded by alveoli
filled with fluid, pus or other material), Eta resolution hole auscultation e ki pabo (fine
crepitation), Cavitary lesion er x ray kmn hy (well defined cavity with visible air fluid level
inside),Tb active na latent x ray te ki dekhe bujhba (CXR appears normal and sputum is
negative for AFB in latent TB. Active TB has abnormal x ray findings)
-right sided upper lobe pneumonic consolidation. Findings in the x-ray,clinical dx
(Pneumonia), findings in ESR (high), other confirmatory tests , next step of management
(sputum & blood for c/s, then start empirical antibiotic, later antibiotic according to c/s)
-Rt sided upper lung consolidation- radiological dx? causes of consolidation? presentation of
pneumonia pt? (high grade fever with chils & rigor, cough, pleuritic chest pain, breathlessness,
hemoptysis) Description of fever in pneumonia? (high grade fever with chills & rigor)
organisms causing pneumonia?

o Streptococcus pneumonia
o Mycoplasma pneumonia
o Legionella pneumophila
o Haemophilus influenzae
o Staphylococcus aureus

o Influenza
o Para influenza
o SARS CoV (CoVid-19)
o MERS CoV
-Consolidation er auscultation finding? (breath sound bronchial, vocal resonance increased,
pleural rub, crepitation present in resolution stage)
-Pneumonia, Investigations

Mitral stenosis :
-a patient of mitral stenosis came with 3 month of fever : how to evaluate this ( sir clue
disilo , infective endocarditis ,er feature dekhbo-
Fever
Unuaul tiredness
Night sweat
Weight loss
Signs of valve dysfunction
Signs and symptoms of heart failure
Classic signs (due to formation of microthrombi on damaged valve and embolism)
o Sub-conjunctival hemorrhage
o Roth spots (hemorrhage in retinal vessels)
o Splinter hemorrhage (under finger/toenail)
o Osler nodes (painful tendr swelling at fingertips)
o Janeway lesions

44
 Digital clubbing may be present
IE e eye e ki paba ( Roth spot ) urine rme te ki paba ( hematuria )..test to confirm : blood
culture and eco ( eco pore bolo ) Blood culture er criteria gula from dukes
Typical organism in 2 cultures
Persistent positive blood culture in samples taken >12 hours apart
3 or more positive culture in samples taken over >1 hour apart )
management : antibiotic er name Soho sunte chai (
Antimicrobial therapy
o Empirical therapy
Sub acute:

Acute

Prothetic valve endocarditis

-600 mg twice daily

o After identification of organism: specific antimicrobial according to organism
Continue for 2 weeks )
-Indication of surgery in Mitral stenosis .....( if the mitral valve is severely calcified, if there
is moderate to severe mitral regurgitation coexists with MS, if mitral valvuloplasty is not
available or the patient has unfavorable valve morphology, and if there is left atrial thrombus
that persists despite anticoagulation)

Endocrinology
-name some endocrine diseases m,
Hyperthyroidism, DM).complications of DM (Microvascular- retinopathy, nephropathy,
neuropathy, foot disease. Macrovascular- MI, stroke, TIA, intermittent claudication)
-endocrine ki ki disease ward e dekhcho,over phn e konta diagnosis kora jay
(hypothyroidism/ myxoedema- harseness of voice present)
-Hypothyroidism features (wt gain, cold intolerance, somnolence, dry skin, dry hair,
menorrhagia, constipation, depression, hoarseness of voice, face- loss of lateral eyebrow,
purplish ips, periorbital puffiness, bradyvardia, hypertension, non pitting edema, delayed
relaxation of ankle jerk), 80 yr pt with IHD lavothyroxine dose (patients with ischemic heart
disease cannot tolerate full replacement doses of thyroxine as it precipitates angina
symptoms)
-25 yrs old man. Profuse sweating and anxiety. (Hyperthyroidism)
-type 1 DM er main defect (autoimmune destruction of beta cell-> absolute insulin deficiency)
r type 2 DM er main defect..(insulin insensitivity in peripheral tissues) Ekjon elderly patient
aschen DM niye kon ekta OHA dbo ( metformin) metformin kivabe kaj kore (The mechanism
of action of metformin has not been precisely
because it lowers insulin levels, its main effects are on fasting glucose and are
insulin-independent. Metformin reduces hepatic glucose production, may also increase insulin-
mediated glucose uptake, and has effects on gut glucose uptake and utilization)
-Hypoglycemia kon organ first e affect korbe? (brain/ nervous system) Dekhso kokhno
hypoglycemia r pt? ki ki findings thake? (Neurogenic- sweating, hunger, palpitation, sweating,
increased heart rate, increased systolic blood pressure; Neuroglycopenic- confusion, tiredness,
drowsiness, disorientation) pulse kmn thake? (increased/ tachycardia) DM er r ki ki

45
 complications ache? (microvascular, macrovascular)
-young girl presents with weight loss, what is the reason? (Thyrotoxicosis, DM, anorexia
nervosa) GE findings of thyrotoxicosis pt? (tachycardia, HTN)

Rheumatology
-In which gender are joint diseases more common (females) one joint disease common in
males(AS) Difference bw ankylosis spondylitis and spondylosis (Inflammation of the joint
and fixation of the joint)
-degenerative r infective arthritis er difference
-RA. Other causes of symmetrical arthritis (OA, SLE, viral arthritis), Dx criteria of RA,
Drugs (NSAID, Glucocorticoid, DMARD, Biologics), Why does it need immediate mx (it causes
permanent damage and deformity of joint), Follow up of Mtx therapy (full blood count and
renal and liver function tests repeated every 1 2 weeks until therapy stabilised, thereafter
patients should be monitored every 2 3 months), what systemic disease can cause
splenomegaly (SLE, sarcoidosis)
-name the hand joints (carpo-metacarpal, metacarpo-phalangeal, PIP, DIP), name a distal
(Psoriatic arthritis) and proximal phalanges disease (RA), RA diagnostic criteria (European
League Against Rheumatism/American College of Rheumatology 2010 Criteria)
-SLE criteria (
1. Malar rash (facial rash sparing the nasolabial fold)
2. Discoid rash (if rash on scalp: alopecia there)
3. Photosensitive rash (rash on exposure to sunlight)
4. Oral ulcer
5. Arthritis (2/more peripheral joint)
6. Serositis (pleuritis, pleural effusion, pericarditis, peritoneal effusion, peritonitis)
7. Renal disorder (proteinuria, RBC/granular/tubular cast)
8. Neurological disorder (seizure, psychosis)
9. Hematological disorder (reduced RBC/WBC/platelet or in combination)
10. Immunological (Anti DNA antibody, anti smith antibody, anti phospholipid antibody +ve_
11. Anti nuclear antibody +ve
Any 4 out of these 11 present: SLE present) ,
male/ female besi hoy? (female) Ki problem hoy female a? (alopecia, photosensitivity,
recurrent abortion), Tokhn ki test korbo? (antiphospholipid antibody)
-Monoarthritis cz (

ve arthritis ),
ki ki test korbo dd exclude korte (

o Gram staining
o C/S
o Polarized light microscopy (to see crystal in gout/pseudogout)

ut, reactive arthritis

46
 ), ki ki findings pabo

Neurology
-neurology OPD te patient most commonly ki symptoms niye ashe (headache) type of
headache..
Primary headache syndromes
Migraine (with or without aura)
Tension-type headache
Trigeminal autonomic cephalalgia (including cluster headache)
Primary stabbing/coughing/exertional/sex-related headache
Thunderclap headache
New daily persistent headache syndrome
Secondary causes of headache
Medication overuse headache (chronic daily headache)
Intracranial bleeding (subdural haematoma, subarachnoid or intracerebral haemorrhage)
Raised intracranial pressure (brain tumour, idiopathic intracranial hypertension)
Infection (meningitis, encephalitis, brain abscess)
Inflammatory disease (temporal arteritis, other vasculitis, arthritis)
Referred pain from other structures (orbit, temporomandibular joint, neck) Kon ta beshi
kharap primary naki secondary (secondary)
-Headache,define, type, konta clinically important.(secondary) secondary headache sign
symptoms (according to cause; meningitis- fever, meningism, rash, false localizing sign, signs of
raised ICP; SAH- 20% isolated headache only, nausea, vomiting, reduced consciousness, false
localizing signs, III nerve palsies; Temporal arteritis- age >55 yrs, jaw pain on chewing, visual
symptoms, tender temporal arteries, elevated ESR & CRP)

-stroke (Stroke maybe defined as sudden development of focal neurological deficit due to non-
traumatic vascular cause lasting for more than 24 hours )
seizure(A seizure can be defined as the occurrence of signs and/or symptoms due to abnormal,
excessive or synchronous neuronal activity in the brain) definitions
-define stroke. key words gulor details. konta keno bola hocche tai. ekhane 24 hours
theke TIA te gese.2 tar difference ki? risk factors of stroke (boi e kivabe lekha ache
sevabe bolo
Fixed risk factors
Age
Gender (male > female except at extremes of age)
Race (Afro-Caribbean > Asian > European)
Previous vascular event: Myocardial infarction, Stroke, Peripheral vascular disease
Heredity
Sickle cell disease
High fibrinogen
Modifiable risk factors
Blood pressure
Cigarette smoking
Hyperlipidaemia
Diabetes mellitus
Heart disease: Atrial fibrillation, Congestive cardiac failure, Infective endocarditis
Excessive alcohol intake

47
 Oestrogen-containing drugs: Oral contraceptive pill, Hormone replacement therapy
Polycythaemia)
-Pregnant mother with convulsions..ki drug diba? (Lamotrigine, Levetiracetum) Lactating
mother with convulsions ..kon drug diba? (carbamazepine, valproate, phenytoin, Phenobarbital,
gabapentin)

-What is a peripheral nerve, are anterior horn cells also peripheral nerves? (yes) what is
it's disease called (PMA-Progressive muscular atrophy/ MND- motor neuron disease), causes?
What type of disease is GBS? (demyelinating) S&S
(Symptom/History:
History of upper resp tract infection/gastro-enteritis 1-3 week ago
Pain/parasthesia/tingling in distal part of limbs
Weakness/paralysis in lower limbs
Ascending paralysis, eventually involving upper limb
Face involved
Diaphragm involved (respiratory paralysis in 20% of cases)
Autonomic dysfunction
o Postural hypotension
o Tachycardia
Bowel bladder: not involved
Sign (flaccid paraplegia + absent jerk)
Muscle tone: diminished
Jerk: diminished
Planter response: absent
Sensory involvement usually absent )
definitive MX? (IVIG, Plasmapheresis (plasma exchange) )
Why do you do CSF in GBS? (
o Albumino-cytologic dissociation: high albumin, but normal lymphocyte count
o Albumin/csf protein count is normal in 1st 10 days (albumin seen only when the inflammation
reaches the spinal cord, not seen at 1st when inflammation is limited to peripheral nerve)
Why is protein high? (The increase in CSF protein is thought to reflect the widespread
inflammation of the nerve roots)
-MS bolte neurology ward e ki bujhai ( multiple sclerosis ).. what is it (purely demyelinating
disease of CNS) name other few demyelinating disease (AIDP and CIDP ) Treatment of
both ...(AIDP- IVIG, Plasmapheresis; CIDP- IVIG, corticosteroid, azathioprine,
cyclophosphamide, ciclosporin, and methotrexate) Why steroid is indicated in cidp and
contraindicated in aidp ...(corticosteroids inhibit the recruitment of scavengers, which are
helpful for the nerve regeneration, resulting in the delay of clinical improvement in GBS)
Environmental medicine
-ongoing environmental change (global warming, earthquake, wild fire), ki ki disease hoy
-environmental hazards e flooding hole kon disease hobe? (diarrhoea, dysentery), dif..
-Global warming er health hazards/ Disease caused by global warming (mosquito borne
diseases e.g. malaria, dengue
-recent environmental hazards - say also earthquake, wild fire in USA, Haiti etc - just
Google)
Nutrition
-nutritional disorder names/ Common nutritional disorder (PEM, IDA, Xerophthalmia,
Nutritional rickets, scurvy)
-when does a Beriberi patient go to a cardiologist? (wet beriberi- heart failure)

48
-Iron deficiency anemia er investigations (CBC with PBF, Serum iron profile) and PBF ki pabo?
(microcytosis, hypochromia with anisopoikilocytosis)
-Vit B-12 deficiency neurological disease? (SACD spinal cord, peripheral neuropathy, optic
atrophy, dementia) why combined? (degeneration of the posterior and lateral columns of the
spinal cord) Pain pathway (there are two major ascending pathways for pain: a direct lateral
spinothalamic pathway and an indirect medial spinoreticulothalamic pathway)
-osteomalacia (features of vitamin D deficiency in adults), Vit D source (endogenous,
exogenous- oily fish such as salmon, sardines, herring and mackerel, red meat, liver, egg yolks,
fortified foods such as some fat spreads and breakfast cereals)
-complications of obesity? (HTN, CHD- angina, MI; stroke, type 2 DM, osteoarthritis)
Critical illness
Good medical practice
-Bronchial asthma pt having ICS, SABA and propanolol. Good prescription? (No, B blocker
should be avoided)
Adolescent, Transition medicine
Infectious disease
-endemic diseases of bd (cholera, dengue fever, malaria, Japanese encephalitis, yellow fever,
and poliomyelitis) and Nepal
-tests for covid? (
-PCR, to detect viral RNA

o CT-Chest/HRCT: bilateral, basal, peripheral ground glass opacity + multiple area of

consolidation
o Chest x ray: bilateral consolidation

o CBC: lymphopenia, leukopenia, low platelet

o CRP, procalcitonin: to indicate sepsis/secondary infection
o Blood culture: secondary bacterial infection
o LFT, RFT, ABG: to see effect of dss
o D dimer: to see sepsis/DIC
o Exclude: malaria, TB and other endemic diseases)
-Infectious disease ki ki ache? (dengue, chikungunya, herpes zoster, rhabies, enteric fever,
leprosy, TB, ricketsial fever, malaria, kala azar, hookworm) Typhoid er complication (

o Ulceration
o Perforation
o Hemorrhage

o Meningitis

o Myocarditis

o Nephritis

o Osteomyelitis

o Persistent carrier state in gallbladder )

R ekta systemic disease er name bolo sob jaygay affect kore? (sarcoidosis)
-How many times a patient can have dengue - (4 serotypes, ans 4 and subsequents are more

49
 dangerous) Cytokine storm present in - (dengue, covid)
-STD names (syphilis, gonorrhea, HIV, genital herpes, chronic viral hepatitis, chanchroid)
-scabis er complications (

Bacterial skin infection

Post streptococcal glomerulonephritis
Acute rheumatic fever

)
Miscellaneous/
-Don't say RA as an example of type 3 hypersensitivity reaction

50
 Medicine Viva
(Shyamol sir on X-ray Board)

X-ray
Pneumothorax
-why tension? Ki features niye ashbe? (cyanosis, rapid feeble pulse, hypotension, sweaty cold
periphery) Immediately ki korba? (needle thoracostomy- insertion of wide bore needle at 2nd
intercostals space along the mid clavicular line) Er pore ki r kichu korte Chao? (water seal
drainage)
-what type is it? Open/closed/tension? (Tension, as the trachea was shifted) > what may
be the underlying risk factors (TB, emphysemia, COPD, ruptured bulla) > what may be the
most alarming sign (hypotension, tachycardia, rapid thready pulse, pulsas paradoxus) >
what immediate management will you do (puncture at 2nd intercostal space with wide bore
needle)
-Mx of tension pneumothorax
-Respiratory failure ki (when pulmonary gas exchange fails to maintain normal arterial oxygen
and carbon di oxide levels )
features , investigation (ABG), kotha theke blood neya hoy (radial, femoral, brachial artery)
-causes of sudden severe breathlessness (tension pneumothorax, ALVF)
-Examination finding of it. C/f & treatment, why shock occurs? (The rise in pressure
reduces the amount of blood returning from the body to the heart because the blood cannot
force its way into the chest and back to the heart. As a result, the heart has less blood to
pump to the body, resulting in shock)
-How shock develops in tension pneumothorax?
-ki dhoroner injury (spontaneous rupture), koi hoy (subpleural bleb)
-Pneumothorax e ki hypotension hoite pare?
-Tension pneumothorax er mechanism (air can enter, but cannot leave, increasing intrapleural
pressure causing tension pneumothorax). Complications (respiratory failure, shock, recurrence,
cardiac arrest)
-why Pneumothorax? Definitive signs on chest examination (percussion note hyperresonant
and breath sound diminished). OPEN (Communication between the lung and pleural space
persists (bronchopleural fistula). Intrapleural pressure and atmospheric pressure are equal
throughout the respiratory cycle, which prevents re-expansion of the collapsed lung.
Hydropneumothorax develops. Infection is common and empyema develops. Physical
examination shows features of hydropneumothorax), Close pneumothorax (Communication
between the lung and pleural space is sealed off. Intrapleural pressure, atmospheric pressure.
Trapped air is slowly reabsorbed, lung re-expands in 2 to 4 weeks ) er mechanism. Ki diba tx.
water seal drainage dekhco kina? Kon level e insertion dey? (4, 5, 6 intercostal space)
Boundary of safety Triangle (anterior border of latissimus dorsi, the lateral border of the
pectoralis major, a line superior to the horizontal level of the nipple and an apex below the
axilla). Pneumonia er classification.(CAP, nosocomial, in immunocompromised; broncho, lobar)
Causative organisms of CAP. Chest findings in case of pneumonia . Pneumonia er Patient
valo hoye gece, 2months por aslo foul smelling sputum with fever, Ki dx? (Lung abscess,
bronchiectasis) Lung abscess er Tx ki? (

o IV broad spectrum covering both aerobic and anaerobic: Co-amoxiclav + metronidazole

51
 for 4-6 weeks
o Modification of antibiotic upon report of culture and sensitivity
o Once stable pt may be switched to an oral agent
ffect, percutaneous aspiration )
Chest physiotherapy er nam ta ki? (percussion (clapping), vibration, deep breathing, and
huffing or coughing, postural drainage) Other complications of Pneumonia (

o Para pneumonic effusion

o Empyema
o Suppurative pneumonia/lung abscess
o Pneumothorax
o Retention of sputum in major bronchi may cause lobar collapse
o ARDS

o Ectopic abscess formation

o DVT and PE
o Inflammation in other organ

encephalitis
o Organ failure

o Arrhythmia
o Pyrexia (drug hypersensitivity)

Hydropneumothorax
-Percussion auscultation findings

Pleural effusion.
-(describe),50 y old man chest pain ,no fever ,hemoptysis diagnosis ki (bronchial ca),
physical sign, classify bronchongenic carcinoma (small cell, non small cell- adeno, squamous,
large), investigation (CBC, sputum for malignant cell, CT/ USG guided FNAC of lymph node,
bronchial brushing for malignant cell)
-Scenario of parapneumic effusion - complications of parapneumonic effusion (empyema
thoracis, ARDS)-confirmation of empyema thoracis dx (aspiration reveals frank pus) -
Physical Examination findings of Empyema ( clubbing, pyrexia, toxicity) - Percussion note
difference between empyema and pleural effusion (empyema te dull+tender bolsi, pleural
eff non tender, sir accept korsen) - Rx of empyema thoracis
(According to cause:
1. Non-tuberculous:
Drainage of pus.
Antibiotic for 2 to 6 weeks. I/V co-amoxiclav or cefuroxime plus metronidazole.Antibiotic
may be needed according to C/S.
If the pus is thick or loculated: surgical intervention may be needed.

52
 2. Tuberculous empyema:
Wide bore needle aspiration or intercostal tube drainage.
Antitubercular therapy.
Sometimes surgical ablation of pleura),
what are the surgical options ((1) removal of the empyema space (decortication with or
without lung resection) and (2) obliteration of the pleural space with muscle flaps or omentum
flaps, or by thoracoplasty)
-cause,clinical differentiation, treatment
-50 y old man chest pain ,no fever ,hemoptysis diagnosis ki, physical sign,classify
bronchongenic carcinoma, investigation, cause ki ki ase, pleural fluid study te ki ki dekhba
(appearance, biochemical, cytology, ADA), outdoor e asthma patient ke ki ki drug diba name
bolo (high flow oxygen, nebuliation, normal saline, inj Hydrocortisone, Salbutamol inhaler,
Beclomethasone inhaler, Tab Montelukast),asthma r complications bolo (constant fatigue,
frequent leave from work or school due to constant asthma flare-ups, pneumonia, increased
mucus production, thickening and narrowing of bronchial tubes which can become permanent
leading to respiratory failure, respiratory failure, severe chest pain.)
-cause, inv, ADA kiser jnno dekhba (TB), BA vs COPD, BA bronchodilator dile reverse
korbe bolte ki bujho (FEV1 >15% or 200ml uncrease after short acting beta agonist therapy),
Lung a r ki genetic disease hote pare (Emphysema/ Cystic fibrosis, Primary ciliary dyskinesia,
drome)
-Ei patient er 2 month coughing r hemoptysis with no fever er history thakle dx Ki hobe? R
Ki Ki investigation kore confirm korba? Lung carcinoma er types , small cell carcinoma er
paraneoplastic features Ki ki (
o Endocrine
SIADH secretion of excess/abnormal ADH hyponatremia
Secretion of ectopic cortisol cushing
Secretion of PTH related protein Hypercalcemia
Secretion of serotonin Carcinoid syndrome
Secretion of abnormal sex hormone gynecomastia
o Neurological
Polyneuropathy (peripheral nerve) & myelopathy (spinal cord)
Lambert eaton myasthenic syndrome
o Other

Hypertrophic pulmonary osteoarthropathy

SIADH mane Ki (Syndrome of Inappropriate ADH hormone secretion) , kon hormone er jonno
hoy (ADH/ vasopressin), kon electrolyte abnormality hoy (mild hyponatremia), kivabe manage
korba (Demeclocycline, Tolvaptan) Critical care unit e kon kon disease er treatment deya
hoy (
Acute kidney injury.
Acute liver failure.
Acute respiratory failure.
ARDS.
Cardiogenic shock.
Cerebral edema.
Congenital metabolic disorder.

53
 Drug overdose
severe pneumonia kivabe bujhba, CURB65
-anti tb drug, side effect

Consolidation
-inv, treatment, DM er karone pneumonia hote pare ki? (immunocompromised-> pneumonia)

-some causes of acute severe breathlessness (ALVF, tension pneumothorax, acute

exacerbation of COPD, acute severe asthma), cardiac and extracardiac causes, cardinal
features of acute left ventricular failure (pulsus alternans, gallop rhytm, bilateral basal
crepitation), management of acute left ventricular failure (propped up position, high flow
oxygen, sublingual GTN, loop diuretic, ACEi/ARB, morphin/ opioid, antiemetic)
-Bronchial asthma at OPD
-abscess er cause bolo (aspiration pneumonia, hematogenous spread, complication of
anesthesia, alcoholic or comatose pt), ki C/F paba lung abscess e (rapid deterioration in
general health, marked weight loss, clubbing, consolidation, pleural friction, rub, amphoric
breath sound) ,treatment ki diba
-Severe chest pain ,cause ki ? (MI, ALVF, pericarditis, myocarditis, endocarditis, aortic
dissection; esophagitis, tension pneumothorax, pleuritic chest pain)
Endocrinology
-A patient presented with polyuria and polydypsia. What are your differentials? (Ami DI,
DM, psychogenic polydypsia bolsilam. Pore sir ra clue diye hypercalcemia and hypokalemia
ber kore anlen) - How to differentiate between DM and DI from urine examination (urine
specific gravity is high in DM, low in DI)
-patient had PPH 6 months ago, now she has amenorrhea, lactional failure and
hyponatremia. Dx? (Panhypopituitarism). Why? (Due to pituitary apoplexy following PPH).
What is this syndrome called? (Sheehan s syndrome)
-DM definition, drug ki ki diba name bolo sob (Insulin, OHA- sulphonylurea & meglitinides,
metformin, alpha glucosidase inhibitors, thiazolidinediones, DPP-4 inhibitors, GLP-1 receptor
agonists, SGLT2 inhibitors), akta patient er pancreas ny mone koro diabetic drug konta
diba (metformin, alpha glucosidase inhibitors, thiazolidinediones, SGLT2 inhibitors),
-oral hypoglycemic agent er naam
-Diabetes patient er hypoglycemia hoise ki ki symptoms paba, r ki ki acute condition hote
pare dm patient er (hyperglycemic hyperosmolar state, DKA)
-Hypothyroid: scenario,diagnosis (T3, T4 decreased; TSH level increased; anti TPO, anti TG),
treatment (Thyroid hormone replacement- levothyroxine, liothyronine)
-features of hypothyroidism
-A scenario of Addison disease(cachectic+hyperpigmentation+ postural hypotension). Most
common cause in BD: (TB). Electrolyte findings: hyponatremia, hyperkalemia. K+ 9.5 what
will you do? Sir shobgula shunte chay details. Renal function jotokkhn intact thakbe
diuretics dibo, renal failure hole then dialysis. R diuretics dile hypovolemia hbe so NS
dite hbe sathe. Resin er kotha boilo na
Rheumatology
-RA (symmetrical, PIP), PsA (DIP), OA - lunate) wrist er kon kon joint
involve kore-- Shyamol sir nijer haat baray pencil diye dekhate bolsen - Diff between PsA
and OA from hand examination (PsA e te nail pitting, onycholysis thake. OA te heberden's
(DIP), bouchard's nodules (PIP) thake. Sir accept korsen)
-Gout: Scenario, what type of crystal (mono sodium urate crystal )
acute management of gout (

54
 o 1st choice: colchicine
o Oral NSAID
o Oral prednisolone
o Intra articular steroid
o Biologic: Canakinumab
o In severe case: joint aspiration )
-Name some connective tissue disease that may affect the uvea and sclera (ankylosing
spondylitis, rheumatoid arthritis, seronegative spondyloarthorpathies)
-SLE er criteriar puro 10 ta point bolte bolsilen
-Ankylosing spondylitis er scenerio, c/f (
low back pain
stiffness
other feature of seronegative arthritis
examination
- restricted spine movement ( mainly lumber)
- obliteration lumber lordosis
schober test --- negative & feature of extra articular manifestation),
kon gender predominant (male), kon marker dekha hoi (HLA B27 gene),
extra articular features
(C---- conjunctivitis
P---- prostatitis
U---- Ant. uveitis
C---- conduction defect
A---- aortic regurgitation
M---- mitral regurgitation
Puter---- pulmonary fibrosis in upper lobe), AR e ki pulse pabo (Wate Hammer pulse/
collapsing pulse), chest findings (apex beat shifted, thrusting apex beat, early diastolic
murmur, Austin Flint murmur), kon murmur paoa jai? (early diastolic murmur, Austin Flint
murmur) SI joint involvement ase kivabe bujhbo? (X ray of Sacro iliac joint : irregularity,
marginal sclerosis, later on fusion at S.I joint from below to upward)
-Monoarthritis causes, Acute gout scenerio,confirmation (by identification of monosodium
urate crystals in synovial fluid of the affected joint), crystal er naam (monosodium urate),
drugs for it (
Treatment of acute attack
o 1st choice: colchicine
o Oral NSAID
o Oral prednisolone
o Intra articular steroid
o Biologic: Canakinumab
o In severe case: joint aspiration
Prophylaxis to prevent future attack (for those with <1 acute attack in 12 month/tophi/joint
erosion)
o Xanthine oxidase inhibitor: Allopurinol, Febuxostat (the latter is metabolized in liver,
can be given to pt with renal failure)
o Others: Probenecid (lower serum uric acid level), pegloticase )
difference btw gout and septic arthritis (by synovial fluid analysis:demonstrating monosodium
urate crystal (MSU) for gout by a polarized microscope and bacteria by Gram staining or culture
in the case of septic arthritis)
Neurology

55
-Causes of hemiplegia
Stroke
Transient ischemic attack
Trauma to brain
Subdural hematoma
Brain tumor
Inflammation: multiple sclerosis
Infection
o Meningitis
o Encephalitis
o Brain abscess
o TB
o Syphilis
-Stroke and icsol, how to differentiate bedside (stroke presents with acute onset
hemiparesis. Features of convulsion may be present. ICSOL mainly presents with gradual onset
focal neurological deficit. Convulsion is a late feature) , one finding to confirm raised ICP
(papilloedema in ophthalmoscopy)
-Difference between stroke and brain tumor (stroke acute onset tumor chronic,tumor e
raised icp,vomiting thake)
-Kon level e katle quadriplegia (C4 and above), paraplegia hbe (C5 and below)
-LMN lesion er nam bolo (acute poliomyelitis, progressive muscular atrophy, GBS) * Facial
nerve palsy examination korte patient k kivbe approach korba?
examine)
-meningitis, org (

Bacterial
Neonate: Group B Streptococci (S. agalactiae), E Coli, Proteus, Listeria
Pre school: H. influenzae, N meningitidis, Streptococcus pneumoniae, M tuberculosis
Adult: N meningitidis, Strep pneumonia, Listeria, M tuberculosis
Viral
Enterovirus (echo, coxsackie, polio)
Mumps
HSV
Influenza
VZV
EBV
Protozoal
Cysticercosis
Amoeba
Fungal
Cryptococcus
Candida
Histoplasma

Malignant: Breast, lung cancer; leukemia, lymphoma

Inflammatory
Sarcoidosis
SLE
drugs ki dei (according to cause: Antibiotic/ anti TB, steroid), raised ICP features (headache,
vomiting, papilledema, -increased

56
 systolic pressure/wide pulse pressure, bradycardia, and respiratory irregularity )
lumber puncture contraindicated kothay (raised ICP), ki hobe korle (herniation), ei effect er
nam ki (??)
-Meningitis e r causative organism according to Age, Pyogenic Meningitis er CSF findings ki
(cloudy/ purulent in colour, clot present, neutrophil 300-2000/cm3, protein increased, glucose
reduced, Gram staining bacteria present) Treatment of Pyogenic meningitis (IV antibiotic,
steroid) GBS er CSF study te ki paba? Jinish ter specific nam ace...(Albumino-cytologic
dissociation)

Nutrition
-Vitamin D deficiency te ki hoy (osteomalacia), diff btn osteoporosis & osteomalacia
-Nutritional anemia causes (IDA, megaloblastic anemia), B12 defi ki type anemia
(megaloblastic), neurological ki finding
-Vitamin D deficiency te ki hoy,diff btn osteoporosis & osteomalacia ,
-Fat soluble vitamin ki ki ase (vit A, D, E, K),Vitamin er A,D deficiency te ki hoy, (A-
xerophthalmia; D- osteomalacia in adults & rickets in children)
-Osteomalacia & osteoporosis er difference bolo (osteomalacia- demineralization of bone due
to vit D deficiency presenting with weakness of the muscles and fragile bones. Osteoporosis-
reduction of bone mineral density due to deficiency of calcium & phosphorus, endocrine
disorder, alcohol presenting as curving of the back and risk of fractures)
-nutritional deficiency, water solublr vitamin (vit B & C), B1 deficiency types (beriberi,
wet beriberi
clinical feature (generalized edema due to biventricular heart failure with pulmonary
congestion)
-Name Vit- D deficiency disorder in adult? (osteomalacia) * Difference between
Osteoporosis & Osteomalacia
Infectious diseases
-Kala Azar er nam shunso? Ki diye hoy? (Leishmania donovani) Kothay Pawa jay?
(Mymensingh, Tangail, Gazipur) * Tmr bari koi? Tmr Division e ekta endemic disease er nam
bolo... (Malaria) * Malaria ki diye hoy? (Plasmodium) Types? (

o Uncomplicated falciparum malaria (UM)

o Severe falciparum malaria (SM)

* Malaria hoile brain e kono prblm hoy? (cerebral malaria) * ki treatment diba? (
o Management of the coma
Maintain airway, breathing, circulation

Exclude other cause: hypoglycemia, meningitis, encephalitis (RBS, Lumbar puncture and
CT scan)
o If there is convulsion, PR diazepam
o Management of malaria (treated as Severe Falciparum malaria or SM)

-kala azar, parasite , ki diye choray (Phlebotomous argentypes- sand fly), amader desher kon
elakay beshi, ward a ki test Kore (ICT for kala azar/ rapid dipstick rk39 test),

57
 national guide line er diagnostic criteria (History of fever for more than 2 weeks Residing/
traveling in endemic areas Any one of the following symptoms and signs: Splenomegaly
Weight loss Anemia ), treatment (

o Drug of choice: LAMb (single dose: 10 mg/Kg in 10% DA, over 3-4 h)
o Alternative drug: Miltefosine (75 mg, 2x daily, for 28 days)
o Combination: LAMb+Milt/LAMb+Paromo/Milte+Paromo

o Amp B D.O.C
o SSG
Other supportive treatment should be given as needed ).
-patient with 10 days fever 104 degree, on examination you found pulse was not as high as
expected, and there was splenomegaly. Dx? (Enteric fever). Investigation? (Blood culture,
widal test, urinary and stool culture) Treatment: Ceftriaxone, Azithromycin,

-Step-ladder fever er cause (Typhoid fever), Typhoid er complications

-Travellers' diarrhoea caused by- Enterotoxigenic E. coli, -
-Define dysentery (bloody diarrhea), define diarrhea (frequent passage of loose stool)
Amoebic dysentery vs bacillary dysentery (guide page 420), Name of organism (Shigella,
EHEC), Type of Shigella (Shigella sonnei (the most common species in the United States)
Shigella flexneri. Shigella boydii. Shigella dysenteriae)
-ei season e fever body ache niye aslo cz- dengue, Cz of death of dengue (Dengue shock,
fulminant hepatitis, encephalitis and acute respiratory distress syndrome), DSS er symptoms
(DF +- DHF + shock (rapid thready pulse, low SBP and high DBP, cold clammy skin) )

-Scabies r organism (Sarcoptes scabiei) , treatment (

Drugs used:

5% permethrin: durg of choice

Malathion
Lindane
Benzyl benzoate

Ivermectin
Antihistamine )
kivbe dei (Application of topical scabicide such as 5% permethrin:

-12 hours

-Features of Scabies (burrow, furrow- Shyamol sir) Rx of Scabies

-STDs, gonorrhea organism (Neisseria gonorrhoeae), gm +/- (gram negative), cell er vetore
na baire thake (vetore), complication of urethral discharge in male (

-orchitis

58
and female

Infertility
Ectopic pregnancy )
treatment

Uncomplicated infection
Ceftriaxone 500 mg IM + Azithromycin 1g orally /
Ciprofloxacin 500 mg orally /
Cefixime 400 mg
Pregnant and lactating woman
Ceftriaxone 500 mg IM + Azithromycin 1g orally /
Spectinomycin 2g IM
Longer course may be needed for complicated infection

-3 causes of STD with the name of their organisms ((Gonorrhea- Neisseria gonorrrhoeae;
Syphilis- Treponema pallidum; AIDS- HIV)
Miscellaneous/
-Vaginal discharge er Ekta Nam ache, ki??(leucorrhea) Er cz ki? Koyekta pathological cz
bolo,moniliasis, trichomoniasis r bacterial vaginosis ke ki clinically differentiate krte
parba?
-Post menopausal ladyr health hazards (osteoporosis, stroke, weight gain, UTI, urinary
incontinence, depression)
-A newly married girl, came with per vaginal discharge (leucorrhoea), causes (bacterial-
Gardenella, fungal- candida, protozoal- trichomonas vaginalis), kon organism e kon osudh dibe,
gardenellar discharge kemon (curd like)
- niye asche eta k ki bole (leukorrhea), ki ki qstn ask korba (foul smell,
itching, passage of blood, pain)
-Psoriasis ki? (Psoriasis is a chronic inflammatory hyperproliferative skin disease characterized
by erythematous, scaly patches affecting the extensor surfaces, scalp, nails with a relapsing
and remitting course)
Sites (extensor surface of elbow, knee, wrist, limb,scalp, hairline, cleft and flexures), guttate
psoriasis er Nam shunso? Ki eta?(This is most common in children and adolescents and is
often the initial presentation. It may present shortly after a streptococcal throat infection and
evolves rapidly. Individual lesions are droplet-shaped, small (usually less than 1 cm in diameter),
erythematous, scaly and numerous. An episode of guttate psoriasis may clear spontaneously or
with topical treatment within a few months, but UVB phototherapy is often required and is
highly effective. Guttate psoriasis often heralds the onset of plaque psoriasis in adulthood)
Ki treatment dba?
-Psoriasis er typical Patch describe koro (
Raised, well demarcated erythematous plaque
Silver scale
Itching occurs
bleeding point from the scale when it is scraped/scratched (Auspitz sign) )
-name some medical diseases you can diagnose by ophthalmoscopy (papilledema = raised
ICP, hypertensive and diabetic retinopathy)
-Colicky pain koi hoi ? (biliary colic, nephrolithiasis, small bowel obstruction) Cholecystitis r
pain describe krn .( right upper abdominal pain, pain in the right shoulder. Often gallbladder

59
 attacks (biliary colic) precede acute cholecystitis. The pain lasts longer in cholecystitis than in
a typical gallbladder attack)
-multiple myeloma (Multiple myeloma is a cancer of plasma cells. It's called multiple myeloma as
the cancer often affects several areas of the body, such as the spine, skull, pelvis and ribs. The
abnormal plasma cells produce abnormal antibodies, which can cause kidney problems and overly
thick blood. The plasma cells can also form a mass in the bone marrow or soft tissue. When one
tumor is present, it is called a plasmacytoma; more than one is called multiple myeloma. Multiple
myeloma is diagnosed based on blood or urine tests finding abnormal antibodies (Bence Jones
protein), bone marrow biopsy finding cancerous plasma cells, and medical imaging finding bone
lesions. Another common finding is high blood calcium levels.)

60