Past Year Questions: GI

M1/00

1. Vit B12 absoption & transport:

R binder B 12 complex Free vit B12 + IF  IF-B12 complex  bind to IF specific receptor on terminal ileum
B12 transverse membrane  B 12 + transcobalamin II  liver
2. Lipid absorption:
Emulsification by bile salt to increase SA
Colipase displace bile for pancreatic lipase to break down TG into monoglycerides & FA
They are tpt as water sol to brush border for absorption, diffusion into epithelial cells
3. Sites for absorption for folic acid, bile, iron:
Folic acid: proximal jejunum
Iron: duodenum major.. proximal jejunum
Bile: terminal ileum

 Stomach: drugs, alcohol

 Duodenum: Fe and water sol vit
 Jejunum: Folate and fat sol vit
 Ileum: Bile salts and cobalamin
 SI: water, drugs, vit K
4. Protozoan GI infections:
Entamoeba histolytica, Blastocystis hominis, Cryptosporidum parvum, Giardia lamblia
5. Eating disorder: Aneroxia nervosa, bulimia nervosa
6. Protective mechanisms of stomach:
Gastric mucousal barrier: mucus, bicarbonate, tight junction between epithelial cell, impermeable gastric
glandular cell, acid resistant trefoil peptides.
7. Complications of ulcers: hemorrhage, perforation, fistula, peritonitis, gastric ca
8. Anti-peptic ulcers (drugs):
Acid suppression: Antacids (Mg/Al hydroxide)
Antisecretory:
H2 receptor antagonists ( cimetidine, ranitidine) , useful in ZES
proton pump inhibitors (Omeprazole) , selective antimuscarinic (pirenzepine)
mucosal protective agent: sucralfate, bismuth chelate, prostaglandin (msioprostaol, octreotide)
Hpylori eradication
Triple therapy: metronidazole, amoxicillin, omeprazole.
9. Rx of salmonellosis:, chloramphenicol (cheap long course), Cephalosporins, ampicillin (faster course)

M2/00

1. Terms to describe:
a. Vomiting blood: hematemesis
b. Coughing out blood: hemoptysis
2. Diagnosis: Liver cirrhosis
3. 2 sites of porto-systemic anastomosis:
Esophageal plexus at cardioesophageal junction (esophageal varices), paraumbilical veins ( caput medusa),
rectal plexus (hemorrhoids)
4. 4 signs of chronic liver disease:
Hepatic flap, jaundice, ascites, , gynaecomastia
5. Describe the features of the liver in this pt: (assuming end-stage liver cirrhosis)
a. Macroscopic: brown, shrunken, hob-nail appearance (macronodular)
b. Microscopic: ischaemic necrosis & fibrosis obliteration of nodules creates broad areas of cirrhosis
6. 3 coagulation factors produced by liver: clotting factors 2,7,9,10
 7. 2 liver function tests: prothrombin time, Alkaline phosphatase (ALP), Aspartate transaminase (AST), Alanine
transaminase (ALT)

M1/01

A 48 year old female complains of increased volume of urine and frequent dehydration. She is also obese and has a
normal diet. Also complains of diarrhea.

(Endo part)
1. Which type of DM? Give reasons DM II as late onset. Insulin independent. Other risk factors: obesity.
2. Describe the insulin secretion and action in type 2 DM : insulin resistance and relative insulin deficiency.
3. Explain how the volume of urine is increased. Increase glucosuria draws water out
4. What is the significance of microalbuminuria? D glomerulonephropath renal failure albumin filtered
5. 4 complications of DM: glomerulonephropathy, retinopathy, autonomic neuropathy, Peripheral neuropathy
6. What test is used to monitor hyperglycaemic control during drug therapy, and how? HbA1c. glycosylated Hb
poorly controlled diabetics have high levels of glycosylated haemoglobin. This test indirectly indicates the
blood sugar levels of the previous 3-4 months.
Blood is taken by venepuncture (from a vein) and sent to the laboratory where it is tested by haemoglobin
electrophoresis (separation of different types of haemoglobin over a gel) or column chromatography
(separation of different types of haemoglobin over a column). It can be measured at anytime and does not
require a fasting or a post-prandial (after meals) state.
7. 2 types of management for the patient. Insulin injection, diet, exercise

A few years later she developed gallstones.

1. Name the 2 anatomical lobes of the liver Right(caudate, quadrate), left lobe
2. What forms the portal vein.. superior mesenteric vein and spleenic vein….
3. Functions of the gall bladder?
4. Store and concentrate bile, increase alkalinity
5. 4 complications of gallstones:
acute cholangitis, acute pancreatitis, cholecystitis, obstructive jaundice
6. 4 investigations and expected results (excluding ultrasound and X-ray):
Endoscopic Retrograde Cholangio-pancreatography (ERCP): obstruction, may have inflammation upon biopsy
blood test (conjugated/unconjugated bilirubin): increase serum conj bilirubin
urine test (no urobilinogen),
liver function test: serum alkaline phosphatase ( raise when cholestasis)
7. How does it cause jaundice? Obstruction of bile flow, backflow of conj bilirubin to hepatocytes and circulation,
accumulation of bilirubin in peripheral tissue/plasma – jaundice
8. 4 risk factors of developing gallstones: fat fertile female forty
9. Give 2 places of referred pain: right shoulder; right upper quadrant pain, radiating to the back
MCQ:
1. Cholesterol stones are radiopaque: T (50 % cholesterol stone)
2. Majority are asymptomatic: Y
3. Associated with cholestasis: Y
4. Females are more prone to cholecystitis: Y

M2/01

1. Name 1 cause for:

a. Secretory diarrhea: infectious, laxatives
b. Osmotic diarrhea: drugs, lactose intolerance
2. 2 protozoa and 1 helminth that cause diarrhea
Protozoa: Entamoeba histolytica, blastocystis hominis
 Helminth: Trichuris trichuria, Strongyloides stercoralis, enterobius vermicularis
3. 3 lab tests to confirm salmonellosis: typhirapid, Typhidot (EIA dot blot), blood culture, Widal test
4. 4 animal reservoirs of salmonella: pig, dog, cat, birds
5. Mechanism of defecation:
Tension & stretch signals to brain thru pelvic splanchnic nerves, reflex contraction of sigmoid colon, inhibition of
anal sphincter tone, forced expiration & descent of diaphragm & contraction of abd muscles, levator ani
contracts to straighten anorectal angle
6. 2 histological features of
Duodenum: simple columnar, numerous villi broader taller,
jejunum: plica circulares, villi narrow short
ileum: plica circulars, sparest villi narrowest, shortest, peyer’s patches
Major blood supply of jejunum & ileum: Jejunal and ileal branches of Superior Mesenteric Artery

M2/03 viva
1. Role of gastrin: increase parietal cell HCl secretion, gastric motily
2. Explain intestinal phase: fats, CHO, intestinal factor, acid in duodenum and mechanical distension of duodenum
inhibit gastric acid/pepsin secretion/gastric motility
3. Role of vagus in gastric motility: increase
4. Where is cholesterol degraded? Liver
5. What happens when common bile duct is obstructed? Reduced absorption of fats/fat soluble vitamins ADEK +
associated deficiencies, jaundice, cholecystitis, pancreatitis, cholangitis
6. 2 protozoa causing diarrhea: Entamoeba histolytica, Bl. hominis
7. Define jaundice: yellowish discoloration under skin and sclera caused by increase in serum bilirubin
8. 4 sites to check for jaundice: sclera, under tongue, palms, skin
9. 3 types of jaundice + 2 examples each
Pre-hepatic: hemolytic anemia (G6PD def, microangiopathy, sickle cell)
Hepatic: cirrhosis, viral hepatitis, alcoholic liver
Post hepatic: bile duct obstruction, gallstone in ampulla of vater

M1/04
Female patient presents with jaundice and pruritus. She complains of colicky pain at the RUQ of abdomen.
1. 3 blood vessels supplying/draining the liver: portal vein, heptic artery, hepatic veins
2. Structures in relation to pancreas:
Head: 2nd part of duodenum
Back of head of pancreas: superior mesenteric artery/IVC (vein on the right)
3. 5 key physiological roles of liver:
1. Bile formation and secretion
2. Nutrient and vitamin metabolism
3. Reticuloendothelial system (degrade antigen to prevent adverse immunological rxn)
4. Hormone and drug inactivation
5. Systhesis of plasma proteins ( eg. Albumin, clotting factors)
4. Name the anatomical parts of gallbladder & function:
Body – stores bile, contraction to secrete bile
Neck – bile goes out thru here
Fundus – the bottom of body (seen without removing liver.)
Cystic duct
5. 3 causes of post-obstructive jaundice: gallstones, bile duct obstruction, obstruction at ampulla of vater
6. Explain why this patient has jaundice: Bile duct obstruction – backflow of bile to hepatocytes, reduced bilirubin
excretion – accumulation in serum/tissues
7. 2 investigations for this patient: ERCP, ultrasound
8. 2 complications of gallstones: cholecystitis, pancreatitis
 9. Cholagogues: An agent that promotes the flow of bile into the intestine, especially as a result of contraction of
the gallbladder.eg CCK
Choloretics: promoting bile secretion by the liver
Secretin stim releas of HCO3- rich fluid from pancreas
CCK stim rel of pancreatic hormone and contraction of gall bladder.
10. MCQ: (?)
a. 80% of gallstones are radioopaque: T
b. Calcium oxalate is the most common type of gallstone: N
c. Head of pancreas consists most of the part of pancreas: N

Unclassified

1. 3 arterties that supply stomach & areas of supply

a. L gastric art: lesser curvature
b. R gastric art: right portion of lesser curvature
c. Short gastric art: fundus
d. L gastro-omental: L greater curvature
e. R gastro-omental: R greater curvature
2. Relation of 1st pt of duodenum to other organs (list 2)
Neck of pancreas, gallbladder,liver
3. Contents of gastric juice (besides H20): HCl, bicarbonate, pepsin, IF, mucus, Na+, Ca+
4. Name 1 H2 blocker: cimetidine, ranitidine
5. What is ‘black tarry stool’ called? Melena
6. Why is there presence of bloods? Bleeding in stomach or upper GI tract
7. How to confirm the suspicion of bts? Endoscopy
8. 3 risk factors that cause peptic ulcer: H. pylori, stress, NSAIDS, smoking, alcohol,ZES
9. 3 phases of swallowing: oral phase, pharyngeal phase, oesophageal phase
10. Which phase of swallowing will cause respiration to stop? pharyngeal
11. Term for ‘difficulty in swallowing”: dysphagia

M2/03 viva (CVS?)

1. How are triglycerides transported from intestine to liver?

Lipid absorption:
Emulsification by bile salt to increase Surface Area
Colipase displace bile for pancreatic lipase to break down TG into monoglycerides & FA
Fa +monoglyceride + cholesterol = micelles
They are tpt as water sol micelle to brush border for absorption, diffusion into epithelial cells
Long chain fatty acid reesterified to TG
Formation of chylomicron: TG + cholesteryl esters coated with ptn + cholesterol+phospholipid = chylomicrons
Exit epithelial cell To lacteal. Enter blood through thoracic duct
Utilization by adipose and muscle cells (lipoptn lipase) chylomicrons chylomicron remnants + fa +glycerol
enter liver.

2. How is fatty acids transported from liver to cells?

As VLDL(very low density lipoprotein)
TG (from glucose, fa, glycerol) + cholesterol (denovo, degradation of chylomicron remnants) + PPL+apoptn =VLDL
Lipoprotein lipase on endo of blood cap of adipose tissue, muscle and heart
Converst TG in VLDL to fa and glycerol
3. How is cholesterol transported from liver to cell
As Low Density Lipoprotein (LDL) main carrier of cholesterol in plasma
Cell surface has LDL receptors that recognize apo B100 of LDL. Thus LDL is taken up digested by lysosomes to
release free cho
4. Give 2 importance of cholesterol.
Cell membrane integrity, aiding digestion of lipids (precursor of bile acid), formation of hormones(steroids in adrenals,
testes, ovaries)

Past Year Questions: Hemato

M2/00

1. Modes of transmission for malaria: Vector (Anopheles), transplacental, blood transfusion

2. Pathogenesis of relapse of malaria infection: Sporozoites –hypnozoites (dormant, exoerythrocytic) – when
activated produce merozoites
 3. 4 reasons why malaria is difficult to control: cannot kill vector, drug resistance, no vaccine, no prophylaxis for all
subtypes
4. Role of CD4 T-cells in replication of virus and immunosuppression
HIV virus has gp120 ptn while CD 4 has the receptor. The reverse transcriptase MRNA-DNA take over host DNA
replication, produce viral protein.
When it is infected, it will express HIV Gp120 on surface, fuse with uninfected T4 cell and syncytial
4mationlysis
CD4:CD8 ratio decrease. Can’t mediate other T cell dependent immunity.
5. Why difficult to treat low virulence microorganism in HIV infected person?
Low natural immunity. As HIV deplete the natural immunity.
6. Pathogenesis of pyogenic bacteria causing fever: production of toxins (pyrogens) activate macrophages produce
cytokines IL1, alpha TNF, activate AA pathway to secrete PGE that reset thermostat in hypothalamus
7. Why do you need consent to conduct an HIV test on patient? Respect patient’s rights and decision
8. Reservoir in monocyte
9. MCQ: What cells can HIV invade?
a. Macrophages: Y
b. CD8 T-cells: N
c. NK cells: N
d. CD4 T-cel: Y

M1/01

A middle aged man presents with chest pain on his left side, radiating to his left arm and jaw. (CVS questions) A few
years later, the patient develops CML. Bone marrow aspiration was done.
1. List 3 signs and symptoms from the history:
Common: palpitation (anemia), splenomegaly (extramedullary hematopoiesis), fatigue, weight loss
Less common: night sweats, minor bruising.
2. 4 findings expected on bone marrow aspiration:
hypercellular BM, blast < 5%, increased myeloid:erythroid ratio, M increase
myelocyte predom. Megakaryocytes are prominent. Mild fibrosis is often seen in the reticulin stain.
3. 2 causes of CML: Genetics, Radiation, drugs, chemicals
4. A biochemical test was done. Give one of its findings:
low neutrophil alkaline phosphatase
5. List 3 types of management: stem cell transplantation, bone marrow transplant, chemotherapy ( hydroxyurea),
alpha interferon)
6. Name 3 cells that arise from myeloid lineage: Erythrocytes, neutrophils, basophils etc except lymphocytes
7. Name 3 other myeloproliferative disorders: CLL, AML, ALL, polycythemia rubra vera
8. MCQ: in CML:
a. Priaprism: N (seen in chronic anemia)
b. Proerythroblast comes after erythroblast: N
c. The progenitor cells are affected: Y
d. Blood smear will show normocytic normochromic anemia: Y
e. More common in males: N (equal)

A child has high fever and develops petechiae on her lower limbs. Her liver and spleen are also enlarged. Diagnosis is
dengue hemorrhagic fever.
1. Name 2 other viruses that can cause the same symptom: flavivirus(yellow fever) , ebola, lassa virus, hantavirus
2. List 3 other infective causes of hepatosplenomegaly: Leishmaniasis, schistosomiasis, plasmodium (malaria), viral
hepatitis
3. Give animal reservoirs:
a. Filarisis: monkey, cats
 b. Japanese Encephalitis: pigs, sheep, horses, birds
c. Nipah virus: pigs, bats
d. Yersinia pestis: rats
4. Give the vectors
a. Malaria: Anopheles
b. Dengue: Aedes aegypti and albopictus
c. Yellow fever: Haemogogus
5. What is the definition of zoonoses?
Infectious disease transmissible under normal conditions between vertebrate animals and man.
6. How can the patient develop ‘acute shock syndrome’ and death?
Antibody-mediated damage to platelets and blood vessels leading to massive hemorrhage.

30 years later, the girl complained of bone pain. X-ray shows punched-out appearance, and electrophoresis was done.
The biopsy of the bone marrow was done and there was a high amount of plasma cells. She also has a high amount of
protein in her urine, and she later developed renal failure.
1. What is the diagnosis? Multiple myeloma
2. What is the nature of the protein in her urine? Bence Jones proteinuria
How did she develop proteinuria? Renal tubular damage ( monoclonal light chain Ig aka M ptn enter the tubule as
cast renal tubular atrophy) . disrupted GBM and its charge
3. Why protein is not normally filtered in the kidney? Cannot pass through the glomerular filtration membranes
(size, charge, molecular weight)
4. How can her condition lead to renal damage? Refer to 2
5. How would you know when to do a renal biopsy?
To find out cause of GN to give appropriate treatment and managemnt
6. Describe 4 pathological changes in her kidney: Tubular casts, tubular atrophy, degeneration, plasma cell
infiltrate, amyloidosis
7. MCQ: in the normal kidney:
a. ADH can absorb more than 60% of water: N
b. Juxtaglomerular tubules have longer Loop of Henle: T
c. 100% of glucose is reabsorbed in the tubules: T
d. After pH 4.5, there will be no more H+ excreted into the tubules: Y

M2/01

1. 3 features of bone marrow in CML: Hypercellular, >5% blast cells, increased M:E ratio
2. 2 courses of CML:
Triphasic (Chronic accelerated phase blast crisis),
Biphasic (Chronic Blast crisis)
3. 4 cells from myeloid lineage: neutrophil, eosinophil, erythrocyte
4. 3 myeloproliferative disorders, 2 complications:
Polycythemia vera : splenomegaly, AML (progression), abnorm large platelet- bleeding & thrombus ( Stroke, DVT),
myelofibrosis
Essential thrombocytosis : thrombosis, hemorrhage. Emboli, AML, myelofibrosis
Myelofibrosis: splenomegaly, anemia, AML, aplastic crisis, infections, , thrombopenia (hemorrhage)
5. Most common type in children: ALL

M2/02

A woman wanted to travel to Africa, wants to know preventive measures for malaria.
1. Name 1 anti-relapse malaria drug: ? primaquine
2. Prophylaxis: chloroquine
M1/04

History of pregnant lady with anemia, works in soldering factory. Patient complained of fatigue, syncope. Doctor
suspects lead poisoning.
1. 3 screening tests done during antenatal care ToRCHeS
2. Hormone involved in erythropoiesis: Erythropoietin
3. Physiological causes of anemia in pregnancy: increased plasma volume earlier and more than RBC increase
4. What nutritional or mineral deficiency can lead to anemia? Vit B12, folic acid, iron
5. 5 causes of iron deficiency anemia: low dietary iron intake, intestinal malabsorption, bowel resection (sm
intestine), gastrectomy, pregnancy, menstruation, GI bleeding
6. How does anemia affects the fetus? Reduced nutrition, oxygen, low birth weight etc.
7. Why anemia is common in pregnancy : see 3, oso increase consumption of micronutrients necessary for
hematopoeisis
8. 2 bone marrow findings in IDA: complete absence of Fe in marrow (Iron stain – Pearl stain), increase M/E ratio as
E increase. small erythroblasts,
9. What is the normal site of RBC development? Bone marrow
10. Blood cells in peripheral smear given. Write down blood disorders.
a. Target cells: Thalassemia, IDA
b. Fragmented RBCs: microangiopathic hemolytic anemia, burns
c. Low RBC WBC platelets: pancytopenia, aplastic anemia
d. High RBC WBC platelets: polycythemia vera
11. MCQ:
a. Hematocrit is estimation of volume % of RBCs in whole blood obtain by centrifugation Y
b. Schilling test is carried out for vit b12 deficiency Y ( test vit b12 absorption, radioactive vit b12)
c. Coombs test for IDA: N (TIBC, PBS, BM, serum Fe lvl)
d. Atrophic glossitis is one of the clinical features for IDA: Y
12. Why does lead poisoning cause anemia? It inhibit enzymes require for haem syn ( ALA dehydratase, copro
oxidase)
List the types of anemia it causes: Lead inhibit haem synthesis. Hemolytic anemia
13. Routes of lead poisoning based on the trigger given: Inhalation
14. 2 reproductive effects of lead poisoning: premature/still birth, low sperm count
15. 4 clinical features of anemia besides syncope & fatigue: SOB, pallor, peripheral cyanosis, koilonychias, jaundice
(hemolytic)
16. Investigations for lead poisoning: Blood and Urine lead level
17. Prevention from exposure to lead poisoning for the lady: Personal protective Equipment, Ventilation, substitution

Unclassified

1. 3 causes of anemia: leukemia, iron deficiency, sickle cell anemia, aplastic anemia
2. 3 signs of CML: fatigue, night sweats, weight loss, minor bruising
3. Malaria:
a. Stage of growth that causes relapse: Hypnozoites (dormant exoerythrocytic parasites) of P. vivax and ovale
b. Which subtype can cause cerebral malaria: Pl. falciparum
c. 2 drugs used in drug-resistant malaria infection: mefloquine +doxycycline, chloroquine + proguanil
d. 2 ways of how malaria can cause anemia: immune mediated RBC destruction, lysis of RBC during release of
merozoite
4. Describe the molecular defect in thalassemia: absence of synthesis of α or β chains
Molecular defect: deletion of gene ( Alpha ) or mutation of gene (Beta) in globin chain synthesis
5. Why do screening and monitoring of blood group before transfusion? Prevent transfusion reactions
6. A kid is group A positive, give which type of blood? A+ or 0+
7. Besides blood transfusion, name the agent that can prevent:
aplastic anemia: bone marrow transplant
transfusion-related iron accumulation: desferroxamine
splenomegaly: splenectomy