GIT – 2023

• Esophagus ❌ – Only transports food; no role in fat digestion.

• Stomach ❌ – Gastric lipase does a little fat breakdown, but minimal (~10–15%).

• Colon ❌ – No digestion; mainly water and electrolyte absorption.

• Small intestine ✅ – The primary site:

  • Pancreatic lipase hydrolyzes triglycerides → monoglycerides + free fatty acids.

  • Bile salts emulsify fat → form micelles → facilitate absorption.

  • Occurs mainly in the duodenum and jejunum.

• Helicobacter pylori infection → chronic gastritis → prolonged stimulation of gastric mucosa and lymphoid tissue.

• This chronic antigenic stimulation can lead to:

  • Peptic ulcer disease (gastric & duodenal ulcers)

  • Gastric adenocarcinoma

  • Gastric MALT lymphoma (mucosa-associated lymphoid tissue lymphoma) → low-grade B-cell lymphoma.

• Interestingly, early H. pylori–associated MALT lymphomas may regress with eradication therapy.

Why the others are wrong

• Acute lymphoblastic leukemia ❌ – Hematologic malignancy, not linked to H. pylori.

• Aplastic anemia ❌ – Bone marrow failure, unrelated.

• Giardiasis ❌ – Caused by Giardia lamblia, not related to H. pylori.

• MALT lymphoma ✅ – Strong, well-established association.

• Ulcerative colitis ❌ – Idiopathic IBD, not linked to H. pylori.

• The gold standard for confirming Helicobacter pylori infection is gastric biopsy obtained during endoscopy, followed by:

  • Histopathology (direct visualization of organisms + inflammation),

  • Rapid urease test (CLO test), or

  • Culture/PCR for H. pylori.

• It allows direct confirmation of the bacteria in the stomach lining.

Why the others are wrong

• Breath test ❌ – Urea breath test is highly accurate, non-invasive, and often first-line clinically, but it’s not the gold standard.

• CBC ❌ – May show anemia, but nonspecific.

• Gastric biopsy ✅ – Direct evidence, definitive.

• Stool culture ❌ – Not routinely used; stool antigen test is good, but culture is difficult and not standard.

• Urinalysis ❌ – No role in H. pylori diagnosis.

Case recap

• Biopsy was from the cardiac region of the stomach.

• Each region (cardiac, fundic, pyloric) has a characteristic pit-to-gland ratio.

Histological feature of cardiac region

• The gastric pits in the cardia are deeper compared to the fundus/body.

• The glands are relatively shorter, composed mostly of mucous cells.

• Thus, in the cardia, pits are deeper.

✅ Correct Answer

Pits are deeper

Why the others are wrong

• Pits occupy 1/3 of mucosa ❌ – That’s the fundic/body region.

• Glands occupy 2/3 of mucosa ❌ – Also typical of fundic/body region.

• Pit and gland ratio is equal ❌ – Not in the cardia; this fits more with pyloric region.

• Pits are deeper ✅ – Correct for cardiac region.

• Pits are shallow ❌ – That describes the fundic region.

Case recap

• Biopsy was taken from the cardiac region of the stomach.

• Cardiac glands are located near the gastroesophageal junction.

Histology of cardiac glands

• Cell types present:

  • Mucous cells → secrete mucus for protection at GE junction.

  • Enteroendocrine cells → scattered, secrete hormones.

  • Stem cells → for regeneration.

  • Mucous neck cells → can be present in small numbers.

• Cell types absent:

  • Chief cells → normally in the fundus and body, secrete pepsinogen.

  • Parietal cells → also predominantly in fundus/body, much fewer in cardia.

Thus, the cardiac glands are essentially devoid of chief cells.

✅ Correct Answer

Chief

Why the others are wrong

• Enteroendocrine ❌ – Present in all gastric regions, including cardia.

• Parietal ❌ – Abundant in fundus/body, rare in cardia but not completely absent.

• Stem ❌ – Present for epithelial renewal.

• Mucous neck ❌ – Present, help in mucus secretion.

• Chief ✅ – Absent in cardiac glands.

Case link

• On upper GI endoscopy, the structure examined = stomach (cardiac region biopsy, gastric ulcer).

• The epithelium of the stomach (fundus, body, cardia, antrum) is lined by simple columnar cells, whose main job is to secrete mucus and protect the gastric mucosa from autodigestion.

• These are called surface mucous cells.

✅ Correct Answer

Surface mucus

Why not the others

• Enterocytes ❌ – Absorptive cells of small intestine, not stomach.

• Mucous neck cells ❌ – Found in gastric glands, secrete mucus, but not forming the surface lining.

• Paneth cells ❌ – Found at the base of small intestinal crypts (antimicrobial function).

• Parietal cells ❌ – Secrete HCl and intrinsic factor, located deeper in glands, not the epithelial surface lining.

• Surface mucous cells ✅ – Line the gastric surface & pits, secrete alkaline mucus for protection.

• Smoking is a well-established lifestyle factor that:

  • Stimulates gastric acid secretion.

  • Impairs mucosal blood flow and healing.

  • Increases risk of peptic ulcer disease and delays ulcer healing.

• In someone with elevated gastric acid output + gastric ulcer, smoking is highly relevant.

Other options:

• Regular exercise ❌ – Generally protective for health, no link with acid hypersecretion.

• Vegan diet ❌ – Not directly linked to excess gastric acid production.

• Adequate sleep ❌ – Restorative, not a risk factor.

• Low-stress job ❌ – Stress can sometimes worsen ulcers, but a low-stress job reduces risk.

• Since she already underwent endoscopy for her ulcer, the next step is to test biopsy samples for H. pylori.

  • Options include rapid urease test (CLO test), histology, or PCR on biopsy tissue.

• This is the most direct and confirmatory method when endoscopy is already being done.

Other options:

• Hydrogen breath test ❌ – Used for carbohydrate malabsorption (like lactose intolerance), not H. pylori.

• Complete blood count (CBC) ❌ – Can show anemia but not specific for H. pylori.

• Stool culture ❌ – Not practical; stool antigen test is used, but culture is rarely done.

• Urinalysis ❌ – No role in H. pylori diagnosis.

• Zollinger–Ellison Syndrome (ZES) is caused by a gastrinoma (gastrin-secreting tumor, usually in pancreas or duodenum).

• Gastrin → strongly stimulates parietal cells → massive gastric acid hypersecretion.

• Clinical features:

  • Recurrent, intractable ulcers (often multiple).

  • Abdominal pain, heartburn, diarrhea, malabsorption.

  • Elevated basal and maximal acid output on gastric secretion analysis.

• This fits best with the patient’s markedly elevated gastric acid output + ulcer symptoms.

Why the others are wrong

• Celiac disease ❌ – Malabsorption with diarrhea, weight loss, not acid hypersecretion.

• Gallstones ❌ – RUQ colicky pain, not linked to gastric acid output.

• IBS ❌ – Functional bowel disorder, normal acid secretion.

• Pancreatic cancer ❌ – Causes weight loss, jaundice, pain radiating to back, not high gastric acid.

• Zollinger–Ellison Syndrome ✅ – Directly causes excess acid secretion + ulcer disease.

• The most important physiological driver of elevated gastric acid secretion is hormonal regulation, especially gastrin.

• In gastric ulcer disease:

  • H. pylori infection reduces somatostatin → leads to unchecked gastrin secretion → ↑ parietal cell stimulation → excess HCl output.

  • Other hormones like histamine (from ECL cells) and acetylcholine (vagal stimulation) amplify the effect, but gastrin dysregulation is the key hormonal factor.

Why the others are less likely

• Dietary habits ❌ – Can aggravate symptoms but don’t directly cause persistently elevated gastric acid output.

• GERD ❌ – A consequence of acid reflux, not the cause of increased secretion.

• Medication use ❌ – NSAIDs cause ulcers, but via mucosal damage, not by directly raising gastric acid output.

• Stress ❌ – Can modestly increase acid, but not to the level of markedly elevated output described here.

• Hormonal changes ✅ – Most direct explanation: hypergastrinemia driving acid hypersecretion.

Case clues

• Student already has low self-esteem, feels “not as talented or smart.”

• Teacher praises her for exceptional effort on a tough project.

• As a result → she feels more confident and motivated.

✅ Correct Answer

It would boost her self-esteem

Explanation

• Positive reinforcement (teacher’s praise) strengthens the student’s sense of competence and value.

• This leads to:

  • Improved self-confidence.

  • Higher motivation to continue performing well.

  • A positive cycle of achievement and self-belief.

Why the others are wrong

• Lower her self-esteem further ❌ – Praise increases confidence, not decreases it.

• Make her less self-conscious ❌ – She might still be self-aware, but the main effect is confidence, not just reduced self-consciousness.

• Make her more self-conscious ❌ – That would be criticism, not praise.

• Have no effect ❌ – The scenario clearly shows she becomes more motivated and confident.

Case breakdown

• The student already has:

  • Physiological needs met → food, shelter.

  • Safety needs met → stable living situation.

  • Love and belongingness met → close friends, supportive family.

• He is actively pursuing extracurricular activities and personal growth → indicates striving for higher-level fulfillment.

In Maslow’s hierarchy of needs:

1. Physiological needs

2. Safety needs

3. Love and belongingness

4. Self-esteem (confidence, recognition, achievement)

5. Self-actualization (realizing personal potential, growth, creativity)

The description (personal growth, maximizing potential) best fits self-actualization.

✅ Correct Answer

Self-actualization

Why not the others

• Physiological needs ❌ – Already satisfied (food, shelter).

• Love and belongingness needs ❌ – Already fulfilled with friends & family.

• Safety needs ❌ – Already stable.

• Self-esteem needs ❌ – Extracurriculars may boost esteem, but the key phrase “personal growth opportunities” points higher → self-actualization.

Case summary

• Pregnant (8 months) woman.

• Symptoms: Jaundice (yellow skin & sclera), fever, vomiting.

• Labs:

  • Very high ALT (1236) & AST (900) → hepatocellular injury pattern.

  • High bilirubin (total 11.4, direct 9.7).

  • Mildly raised ALP (432) & GGT (155) → some cholestasis, but not predominant.

Stepwise reasoning

• Acute hepatitis → fits best because:

  • Very high ALT/AST (in thousands, hepatocellular pattern).

  • Direct hyperbilirubinemia.

  • Symptoms: jaundice + fever + vomiting.

• Acute cholecystitis ❌ – Would show RUQ pain, fever, raised ALP/GGT much higher than ALT/AST.

• Malaria ❌ – Can cause jaundice, but would expect anemia, splenomegaly, parasites on smear.

• Hepatic abscess ❌ – Fever + RUQ pain, not such marked transaminase elevation.

• Sepsis ❌ – Can cause cholestatic jaundice, but not massive hepatocellular injury like here.

• Fatty liver (NAFLD/NASH) can be suspected on ultrasound, CT, MRI, or Fibroscan, but none of these can reliably stage the degree of inflammation and fibrosis.

• The gold standard for diagnosis, grading inflammation, and staging fibrosis = liver biopsy.

  • Provides histological detail → distinguishes simple steatosis from steatohepatitis (NASH).

  • Assesses degree of fibrosis and cirrhosis.

Why the others are wrong

• CT scan abdomen ❌ – Can show fatty infiltration, but not inflammation/fibrosis accurately.

• Fibroscan liver ❌ – Non-invasive tool for fibrosis, useful for follow-up, but not gold standard.

• Ultrasound abdomen ❌ – Detects fatty changes but cannot assess severity of inflammation/fibrosis.

• Liver function tests ❌ – Show enzyme elevations but are nonspecific; cannot stage fibrosis.

• Liver biopsy ✅ – Definitive and gold standard.

• In highly endemic areas (like Pakistan), Hepatitis A virus (HAV) infection usually occurs in early childhood.

• Most infections in children are asymptomatic or very mild, often going unnoticed.

• As a result, by adulthood, the majority of the population has already developed immunity.

• Severe or fulminant hepatitis is rare in these settings.

Why the others are wrong

• Carriers ❌ – HAV does not have a carrier state (unlike HBV, HCV).

• Fulminant ❌ – Rare complication, not the usual presentation.

• Asymptomatic ✅ – Correct, especially in children of endemic regions.

• Immuno-compromised ❌ – Not a defining feature of endemic HAV cases.

• Symptomatic ❌ – Symptomatic disease is more common in non-endemic areas and in adults, not in endemic childhood cases.

• Epidemic → An unusual occurrence of disease in a community with an excess number of cases or rapid spread within a short period. Example: sudden outbreak of measles in a school.

• Pandemic → An epidemic that spreads across countries or continents, affecting a very large population (e.g., COVID-19).

• Endemic → A disease that is constantly present at a predictable level in a community (e.g., malaria in parts of Africa).

• Sporadic → A disease that occurs occasionally and irregularly (e.g., tetanus).

• Zoonotic symptomatic ❌ – Refers to diseases transmitted from animals to humans (like rabies), not about outbreak patterns.

• Vaccines available:

  • Hepatitis A → Inactivated or live-attenuated vaccine, highly effective.

  • Hepatitis B → Recombinant HBsAg vaccine, part of EPI schedule.

• No vaccines currently available for:

  • Hepatitis C → High variability of virus, no approved vaccine yet.

  • Hepatitis D → Prevented indirectly by Hepatitis B vaccination (since HDV requires HBV for replication).

  • Hepatitis E → A vaccine exists in China but not widely available globally.

Why other options are wrong

• Hepatitis C ❌ – No vaccine.

• Hepatitis B ❌ – Yes, but the question asks plural “vaccines available,” so A + B is more complete.

• Hepatitis B and D ❌ – HBV vaccine protects against HDV indirectly, but no direct HDV vaccine.

• Hepatitis A ❌ – True, but incomplete since HBV also has a vaccine.

• Mainstay of treatment for acute watery diarrhea in children = Oral Rehydration Therapy (ORT).

• WHO/UNICEF recommend low-osmolarity ORS (75 mmol/L Na⁺, total osmolarity 245 mOsm/L).

  • Reduces stool output.

  • Decreases vomiting.

  • Lowers need for IV fluids.

Other options:

• Oral antibiotics ❌ – Not indicated in viral watery diarrhea; reserved for dysentery (bloody stools, suspected bacterial infection).

• ORS (old formula) ❌ – Effective, but low-osmolar ORS is now the standard of care.

• Intravenous fluid ❌ – Reserved for severe dehydration or if ORS cannot be tolerated.

• Lactose-free formula ❌ – Used in persistent post-infectious diarrhea with lactose intolerance, not in this case.

• According to the National Nutrition Survey (Pakistan), the most common micronutrient deficiency is iron deficiency, presenting as iron deficiency anemia.

• It is highly prevalent among women of reproductive age and children, mainly due to:

  • Poor dietary intake of iron-rich foods.

  • High rates of infections/parasites.

  • Maternal malnutrition.

Other deficiencies are also significant but less common than iron:

• Zinc deficiency diarrhea ❌ – Prevalent, but not the leading micronutrient deficiency.

• Vitamin A deficiency blindness ❌ – Public health problem, but not the most common.

• Vitamin D deficiency rickets ❌ – Common in children, but still less than iron deficiency.

• Vitamin B12 deficiency anemia ❌ – Seen in strict vegetarians or malabsorption, but not as prevalent as iron deficiency.

• The process described is reducing water activity (aᵥ), which microorganisms need for growth.

• Methods: sun drying, salting, sugaring, alcohol addition → all lower available free water.

• This makes the environment unfavorable for microbial growth, preserving the food.

Other options:

• Fermentation ❌ – Uses controlled microbial growth to produce acids/alcohol that preserve food, not lowering water activity directly.

• Modified atmosphere ❌ – Changing gases (e.g., high CO₂, low O₂) in packaging, not about water removal.

• Preservatives ❌ – Chemical agents (e.g., nitrates, benzoates), not water-binding.

• Dehydration ✅ – Correct → lowering water activity via drying/salt/sugar.

• Asepsis ❌ – Preventing contamination by sterilization/sealing, not water activity reduction.

• Best overall method to diagnose intestinal parasites (protozoa + helminths) = direct microscopic examination of stool.

• The stool sample is examined in saline (for motility of trophozoites) and in iodine (to highlight cysts, eggs, larvae).

• This allows detection of:

  • Protozoa (e.g., Entamoeba histolytica, Giardia lamblia).

  • Helminths (e.g., Ascaris, Trichuris, Hookworm eggs).

Why the others are wrong

• Stool culture ❌ – Used for bacteria (e.g., Salmonella, Shigella), not routine parasites.

• Perianal swab ❌ – Not sensitive for most parasites; specific tests are better.

• Microscopy of stool in saline and iodine ✅ – Gold standard screening for intestinal parasites.

• Buffy coat of blood ❌ – Used for blood parasites (e.g., malaria, filaria), not intestinal.

• Scotch tape method ❌ – Special method for Enterobius vermicularis (pinworm), but not for general intestinal parasites.

• Portal vein thrombosis (PVT) = obstruction of portal venous blood flow into the liver.

• Many patients are asymptomatic and diagnosed incidentally on imaging.

• When symptoms do occur, they are due to portal hypertension and its complications:

  • Esophageal varices → GI bleeding.

  • Splenomegaly → congestion.

  • Ascites → fluid accumulation.

  • Hepatomegaly → sometimes due to congestion, but not always.

But the key point is:

• Most patients remain asymptomatic until complications develop.

Why the others are wrong

• Esophageal varices ❌ – A complication, but not seen in most early patients.

• No symptoms ✅ – Most common presentation.

• Hepatomegaly ❌ – Can occur, but not the usual finding.

• Splenomegaly ❌ – Common later, not in the majority at first.

• Ascites ❌ – Usually occurs in advanced cases, not the initial or most common.

The liver’s blood supply and drainage involve:

• Hepatic artery → arterial inflow (oxygenated blood).

• Portal vein → venous inflow (nutrient-rich blood from GIT).

• Hepatic veins → venous outflow from liver → IVC.

• Inferior vena cava (IVC) → directly receives hepatic vein drainage.

So thrombosis in any of these (hepatic artery, portal vein, hepatic vein, IVC) → can impair liver circulation.

• Portal vein thrombosis → portal hypertension, impaired inflow.

• Hepatic vein thrombosis → Budd–Chiari syndrome, obstructed outflow.

• Hepatic artery thrombosis → ischemic necrosis of liver (esp. after transplant).

• Inferior vena cava thrombosis → blocks hepatic venous outflow.

• Superior vena cava thrombosis ❌ – Drains the upper body (head, neck, upper limbs), not related to liver circulation.

• Fundic gland polyps:

  • Most common gastric polyps in Western countries.

  • Associated with PPI use → due to hypergastrinemia and glandular hyperplasia.

  • Can also be seen in familial adenomatous polyposis (FAP) → here they involve APC/β-catenin pathway mutations.

  • Sporadic forms also show APC pathway alterations.

  • Usually asymptomatic and discovered incidentally.

• Hyperplastic polyps:

  • Associated with chronic gastritis and H. pylori infection.

  • Tend to be smaller (<1 cm), not typically multiple in fundus.

  • Rarely >3 cm.

Why the others are wrong

• The majority of hyperplastic polyps are 3 cm in size ❌ – Most hyperplastic polyps are small (<1 cm).

• These polyps are highly associated with H. pylori infections ❌ – That’s hyperplastic polyps, not fundic gland polyps.

• Alteration of APC β-catenin pathway are seen in both sporadic and syndromic fundic gland polyps ✅ – Correct.

• These polyps are not associated with the use of proton pump inhibitors ❌ – Actually, they are strongly associated with long-term PPI use.

• These polyps are always associated with nausea, vomiting, and abdominal pain ❌ – Usually asymptomatic, discovered incidentally.

• Diffuse gastric carcinoma:

  • Composed of signet ring cells → mucin pushes nucleus to periphery.

  • Infiltrates stomach wall → linitis plastica (“leather bottle stomach”).

  • Associated with E-cadherin (CDH1) loss, not presence.

• Intestinal type carcinoma:

  • Gland-forming, often related to H. pylori, chronic gastritis, nitrosamines.

  • Typically grows as an exophytic mass and penetrates gastric wall.

• Prognostic indicator: Most important is tumor stage (depth of invasion and lymph node status), not just depth alone.

• Genetics: Intestinal type often linked to APC mutations, diffuse type to CDH1 mutations (E-cadherin loss), not CDKN2A.

Why others are wrong

• Most commonly affected gene is CDKN2A ❌ – That’s linked to pancreatic carcinoma, not gastric diffuse type.

• The diffuse infiltrative pattern carcinomas are mostly composed of signet ring cells ✅ – Correct.

• The intestinal type carcinomas mostly penetrate the gastric wall ❌ – They form glandular masses, not diffuse infiltration.

• The most powerful prognostic indicator is tumor depth of invasion only in gastric cancers ❌ – Prognosis depends on stage = depth + nodal status + metastasis.

• There is presence of E-cadherin in these cells ❌ – It is loss of E-cadherin that is characteristic.

• Biliary atresia = progressive fibro-obliterative disease of the extrahepatic biliary tree → bile flow blocked → conjugated hyperbilirubinemia, cholestasis, cirrhosis.

• First-line treatment: Kasai portoenterostomy (hepatoportoenterostomy).

  • Surgeon removes the obliterated bile ducts and connects a loop of jejunum directly to the liver hilum → allows bile drainage.

  • Best performed before 2 months of age for optimal survival.

• Liver transplant may eventually be required, but it is usually considered if Kasai fails or at a later stage.

Why the others are wrong

• Steroids ❌ – Sometimes given post-Kasai to reduce inflammation, not first-line therapy.

• Kasai portoenterostomy ✅ – First and immediate surgical treatment.

• Rifampicin ❌ – Used for intractable pruritus in cholestasis, not definitive treatment.

• Liver transplant ❌ – Done later if Kasai fails or advanced cirrhosis occurs.

• Ursodeoxycholic acid ❌ – Improves bile flow in cholestatic disorders, but not curative for biliary atresia.

Normal serum bilirubin: <1 mg/dl.

Jaundice (yellowish discoloration of skin, sclera, mucous membranes) becomes clinically apparent when serum bilirubin rises above ~2–2.5 mg/dl.

Below this threshold, mild hyperbilirubinemia may exist but won’t be visible to the naked eye.

Higher levels (like 4–7 mg/dl) indicate more severe jaundice, but the visibility threshold is ~2–2.5 mg/dl.

Why the others are wrong

• 4–4.5 mg/dl ❌ – Too high, jaundice is already visible earlier.

• 2–2.5 mg/dl ✅ – Correct threshold for visible jaundice.

• 3–3.5 mg/dl ❌ – Still jaundiced, but not the “appearance point.”

• 6–7.5 mg/dl ❌ – Severe jaundice, but jaundice begins earlier.

Case clues

• Middle-aged woman → common demographic for autoimmune liver disease.

• Acute fatigue + jaundice → hepatocellular injury.

• Very high AST & ALT → hepatocellular pattern of injury.

• Antinuclear antibody (ANA) positive → autoimmune process.

• Smooth muscle antibody (SMA) positive → classic for autoimmune hepatitis.

• Anti-mitochondrial antibody (AMA) positive → usually seen in primary biliary cholangitis (PBC), but the key here is the hepatocellular pattern (very high transaminases), not cholestatic pattern.

✅ Correct Answer

Autoimmune hepatitis

Why not the others

• Hepatocellular carcinoma ❌ – Would not present with high autoantibodies; usually arises in cirrhosis.

• Cholestasis ❌ – Would show elevated ALP and GGT, not markedly high AST/ALT.

• Autoimmune hepatitis ✅ – Fits ANA and SMA positivity with hepatocellular injury.

• Adenoma ❌ – Benign hepatic tumor, no link to autoantibodies.

• Congenital abnormality ❌ – Presents earlier, not acute middle-age onset.

• There is no single gold-standard test for Helicobacter pylori. Diagnosis is usually confirmed by combining invasive and non-invasive tests.

• The urea breath test is considered one of the most accurate and practical tests:

  • Patient ingests urea labeled with C¹³ or C¹⁴.

  • If H. pylori urease is present, it splits urea → CO₂ + NH₃.

  • Labeled CO₂ is detected in exhaled breath.

  • High sensitivity & specificity, and useful for confirming eradication after treatment.

Why the others are less accurate alone

• Serologic test for antibodies ❌ – Cannot distinguish past from current infection.

• Rapid urease test (CLO test) ❌ – Reliable, but invasive (requires biopsy) and may give false negatives if patient on PPI/antibiotics.

• Bacterial DNA detection by PCR ❌ – Very sensitive, but not widely available or practical for routine use.

• Fecal antigen test ❌ – Also accurate and non-invasive, but slightly less specific than the urea breath test.

• Volvulus = twisting of a loop of intestine around its mesenteric attachment.

  • This causes lumen obstruction (→ abdominal distension, pain, constipation).

  • The twist also compromises the mesenteric blood vessels, leading to ischemia, hemorrhage, and gangrene if untreated.

Why the others are wrong

• Stricture ❌ – Causes obstruction, but blood supply usually preserved unless secondary ischemia develops.

• Intussusception ❌ – Can cause both obstruction and ischemia, but classic teaching for simultaneous obstruction + vascular compromise points most directly to volvulus.

• Tumor ❌ – Causes obstruction, but blood supply isn’t directly compromised.

• Polyp ❌ – May obstruct locally but does not compromise blood flow.

• Acute gastritis = transient inflammation of gastric mucosa, usually due to alcohol, NSAIDs, stress, H. pylori, etc.

• Microscopic features include:

  • Edema in lamina propria ✅

  • Vascular congestion ✅

  • Foveolar cell hyperplasia (proliferation of surface mucous cells in response to injury) ✅

  • Scattered neutrophils, lymphocytes, plasma cells (mild inflammatory infiltrate) ✅

• Metaplastic gastric epithelium ❌ → This is a feature of chronic gastritis, especially intestinal metaplasia, not acute.

Why others are correct for acute gastritis

• Moderate edema in lamina propria → Yes, acute change.

• Foveolar cell hyperplasia → Common compensatory finding.

• Slight vascular congestion → Early acute change.

• Few lymphocytes and plasma cells → Mild inflammation possible.

Acute pancreatitis = sudden onset inflammation with reversible damage.

• Morphology: interstitial edema, fat necrosis, hemorrhage, necrosis of acinar/ductal cells, neutrophilic infiltrates.

Chronic pancreatitis = irreversible damage due to long-standing inflammation.

• Morphology:

  • Extensive fibrosis replacing normal parenchyma.

  • Acinar cell loss (atrophy).

  • Dilated or distorted ducts with protein plugs.

  • Variable chronic inflammatory infiltrates.

Thus, fibrosis and acinar cell loss is the key morphological feature distinguishing chronic from acute pancreatitis.

Why others are wrong

• Interstitial edema ❌ – Acute pancreatitis.

• Focal areas of fat necrosis ❌ – Acute pancreatitis.

• Mild inflammation ❌ – Nonspecific, seen in both but not diagnostic.

• Fibrosis and acinar cell loss ✅ – Hallmark of chronic pancreatitis.

• Necrosis of acinar and ductal tissue ❌ – Acute necrotizing pancreatitis.

• Autoimmune pancreatitis (AIP) is a unique form of chronic pancreatitis.

• Microscopic hallmarks:

  • Lymphoplasmacytic sclerosing pancreatitis → ducts show mixed inflammatory infiltrates (mainly lymphocytes + plasma cells).

  • Storiform fibrosis around ducts.

  • Obliterative venulitis (inflammation of small veins).

  • Often associated with IgG4-positive plasma cells.

• This combination distinguishes autoimmune pancreatitis from other forms.

Why the others are wrong

• Dilated ducts with eosinophilic concretions + neutrophils ❌ – Seen in chronic calculous pancreatitis.

• Necrosis of acinar, ductal, and islets ❌ – Seen in acute necrotizing pancreatitis.

• Extensive fibrosis + residual islets/ducts with chronic exudate ❌ – Describes advanced chronic pancreatitis, not specifically autoimmune type.

• Extensive hemorrhage with neutrophils ❌ – Classic for acute hemorrhagic pancreatitis.

• Duct-centric mixed inflammatory infiltrate with venulitis + plasma cells ✅ – Hallmark of autoimmune pancreatitis.

Case clues

• Polyhydramnios in pregnancy → fetus unable to swallow amniotic fluid → suggests upper GI obstruction.

• Infant vomits all feedings → food cannot reach the stomach.

• Fever + respiratory difficulty → aspiration of secretions.

• X-ray: no stomach bubble → stomach not filling with swallowed air/food.

• Normal heart & lungs, no infiltrates → rules out primary respiratory disease.

All of this points strongly to esophageal atresia.

✅ Correct Answer

Esophageal atresia

Why not the others

• Pyloric stenosis ❌ – Projectile non-bilious vomiting, but stomach bubble would be visible on X-ray; develops later, not immediately at birth.

• Achalasia ❌ – Failure of LES relaxation in older patients, not neonates.

• Hiatal hernia ❌ – Stomach herniates into thorax, but stomach bubble still visible.

• Esophageal atresia ✅ – No connection to stomach → no stomach bubble, polyhydramnios, aspiration risk.

• Diaphragmatic hernia ❌ – Gas-filled bowel loops in thorax + lung hypoplasia, not seen here.

Case clues

• Recurrent epigastric pain → points to pancreas or upper GI pathology.

• Progressive weight loss + foul-smelling diarrhea (steatorrhea) → fat malabsorption due to loss of pancreatic enzymes.

• Anemia → malabsorption and chronic disease.

• Constant, intractable abdominal pain → advanced disease.

• X-ray: multiple areas of calcification in mid-abdomen → pathognomonic for chronic pancreatitis.

✅ Correct Answer

Chronic pancreatitis

Why not the others

• Crohn’s disease ❌ – Causes diarrhea and weight loss, but not pancreatic calcifications on imaging.

• Celiac disease ❌ – Malabsorption with anemia and diarrhea, but small bowel biopsy shows villous atrophy, not abdominal calcifications.

• Chronic cholecystitis ❌ – RUQ pain after fatty meals, but no calcifications scattered in pancreas.

• Acute pancreatitis ❌ – Sudden severe pain, ↑ amylase/lipase, but no long-term calcifications or chronic malabsorption.

Case clues

• Alcoholic male → classic risk factor for pancreatitis (along with gallstones).

• Severe constant epigastric pain radiating to the back → hallmark of pancreatitis.

• Fever + steatorrhea (fat malabsorption) → pancreatic enzyme insufficiency.

• Discoloration around the flank (Grey Turner’s sign) and umbilicus (Cullen’s sign) → retroperitoneal hemorrhage, strongly linked to hemorrhagic pancreatitis.

• Labs: elevated serum amylase and lipase → diagnostic of acute pancreatitis.

✅ Correct Answer

Acute pancreatitis

Why not the others

• Acute appendicitis ❌ – Pain starts periumbilical → migrates to right lower quadrant, not radiating to back.

• Acute cholangitis ❌ – Presents with Charcot’s triad (fever, jaundice, RUQ pain), not back-radiating epigastric pain.

• Acute cholecystitis ❌ – RUQ pain radiating to right shoulder, Murphy’s sign positive, not epigastric pain to back.

• Acute pancreatitis ✅ – Fits clinical and lab picture.

• Acute diverticulitis ❌ – Left lower quadrant pain, fever, not epigastric or elevated pancreatic enzymes.

• Chronic gastritis:

  • The most common cause worldwide is infection with Helicobacter pylori.

  • H. pylori colonizes the gastric mucosa (especially antrum), producing urease which neutralizes stomach acid.

  • This causes chronic inflammation, mucosal atrophy, and eventually intestinal metaplasia.

• Cancer risk:

  • Chronic H. pylori infection is strongly associated with gastric adenocarcinoma and MALT lymphoma.

Why the others are wrong

• Staph. aureus ❌ – Causes food poisoning (pre-formed enterotoxin), not chronic gastritis.

• E. coli ❌ – Causes diarrhea, UTIs, sepsis; not chronic gastritis.

• Rotavirus ❌ – Viral gastroenteritis in children, self-limiting.

• Enterococci ❌ – Cause endocarditis, UTIs; not linked to chronic gastritis.

• H. pylori ✅ – Correct → chronic gastritis and gastric cancer.

• Acute Liver Failure (ALF) has different leading causes depending on geography:

  • Western countries (US/Europe): Most common = Acetaminophen (paracetamol) overdose.

  • Asia & developing regions: Most common = Acute viral hepatitis, especially Hepatitis B virus (HBV).

• Other less common causes include:

  • Drugs & toxins (e.g., isoniazid, halothane, poisonous mushrooms).

  • Autoimmune hepatitis – rare cause.

Why the others are wrong

• Acetaminophen overdose ❌ – #1 in the West, not in Asia.

• Acute Hepatitis B ✅ – #1 cause of ALF in Asia.

• Drugs ❌ – Important but not the leading cause in Asia.

• Toxins ❌ – Can cause fulminant liver failure, but uncommon.

• Autoimmune hepatitis ❌ – Rare overall.

• Dubin–Johnson syndrome is a rare inherited disorder of bilirubin metabolism.

• Cause: mutation in the MRP2 (multidrug resistance-associated protein 2) gene → impaired transport of conjugated bilirubin from hepatocytes into bile canaliculi.

• Leads to conjugated hyperbilirubinemia (but usually benign).

• Histology: liver shows black pigmentation due to deposition of polymerized epinephrine metabolites.

• Inheritance pattern = autosomal recessive.

Why the others are wrong

• X-linked recessive ❌ – Not related to sex chromosomes.

• Mitochondrial ❌ – Passed only maternally, not the case here.

• Autosomal recessive ✅ – Correct.

• Autosomal dominant ❌ – Some liver enzyme disorders follow this, but not Dubin–Johnson.

• Y-linked ❌ – Impossible, only affects males via Y chromosome.

• Unconjugated (indirect) bilirubin increases when there is excess production of bilirubin beyond the liver’s ability to conjugate it, or when hepatocyte uptake/conjugation is impaired.

• In hemolytic anemia:

  • Accelerated breakdown of RBCs → ↑ heme breakdown → ↑ bilirubin load.

  • Liver conjugation capacity is overwhelmed → predominant unconjugated hyperbilirubinemia.

Why the others are wrong

• Gallstones ❌ – Cause post-hepatic (obstructive) jaundice → conjugated hyperbilirubinemia.

• Primary biliary cirrhosis ❌ – Intrahepatic cholestasis → mainly conjugated hyperbilirubinemia.

• Pancreatic cancer ❌ – Obstructs common bile duct → conjugated hyperbilirubinemia.

• Hemolytic anemia ✅ – Causes unconjugated hyperbilirubinemia.

• Drug-induced hepatitis ❌ – Causes hepatocellular damage, leading to mixed or conjugated hyperbilirubinemia.

• Cyanide binds to the Fe³⁺ of cytochrome a₃ in Complex IV (cytochrome oxidase) of the electron transport chain.

• This blocks the transfer of electrons to oxygen, the final electron acceptor.

• As a result:

  • The entire ETC halts.

  • No proton gradient is generated.

  • Oxidative phosphorylation stops → no ATP formed.

  • Cells undergo histotoxic hypoxia → oxygen is present in blood, but tissues cannot use it.

Why the others are wrong

• Complex I ❌ – Inhibited by rotenone, barbiturates (not cyanide).

• Carbonic anhydrase ❌ – Enzyme in RBCs/kidney for CO₂ transport, unrelated.

• Cytochrome oxidase (Complex IV) ✅ – Target of cyanide poisoning.

• ATP synthase ❌ – Inhibited by oligomycin, not cyanide.

• Complex II ❌ – Inhibited by malonate, not cyanide.

• The HMP pathway (Hexose Monophosphate Shunt / Pentose Phosphate Pathway) produces NADPH + H⁺.

• NADPH is critical for maintaining reduced glutathione (GSH) in red blood cells by regenerating it from its oxidized form (GSSG) through glutathione reductase.

• Reduced glutathione protects RBCs from oxidative damage by neutralizing hydrogen peroxide and free radicals.

• Without NADPH (e.g., in G6PD deficiency), RBCs are prone to oxidative stress → hemolysis, Heinz bodies, jaundice.

Why the others are wrong

• Hemoglobin ❌ – Oxygen transport protein, not directly maintained by NADPH.

• Heme ❌ – Requires NADPH for synthesis, but the protective antioxidant role in RBCs is via glutathione.

• LDL ❌ – Lipoprotein for cholesterol transport, unrelated here.

• Glutathione ✅ – Directly depends on NADPH to stay reduced and protect RBCs.

• Bilirubin ❌ – Product of heme breakdown, not linked to NADPH protection.

• Gluconeogenesis = making glucose from non-carbohydrate precursors (important during fasting).

• Best precursors:

  • Lactate (Cori cycle).

  • Glucogenic amino acids (esp. alanine).

  • Glycerol → comes from hydrolysis of triglycerides in adipose tissue → converted into dihydroxyacetone phosphate (DHAP) → enters gluconeogenic pathway.

Now the options:

• Fructose ❌ – Already a monosaccharide that can be converted to intermediates of glycolysis, not the main gluconeogenic precursor.

• Glucose ❌ – End-product of gluconeogenesis, not its precursor.

• Galactose ❌ – Can enter glycolysis via Leloir pathway, not a major gluconeogenic precursor.

• Mannol (Mannose) ❌ – Can be converted to fructose-6-phosphate, but again, not the classic gluconeogenic substrate.

• Glycerol ✅ – Major substrate from fat breakdown, classic gluconeogenesis precursor.

• Kernicterus = bilirubin encephalopathy in neonates.

• In newborns, the blood-brain barrier is immature, and albumin-binding capacity is limited.

• When unconjugated (indirect) bilirubin levels rise excessively → bilirubin crosses into the basal ganglia and brainstem nuclei.

• Being lipid-soluble, unconjugated bilirubin deposits in brain tissue → neurotoxicity → poor feeding, high-pitched cry, lethargy, seizures, apnea.

• Direct (conjugated) bilirubin is water-soluble and does not cross the blood-brain barrier, so it does not cause kernicterus.

Why the others are wrong

• Direct bilirubin in the brain ❌ – Water-soluble, cannot cross BBB.

• Total bilirubin in brain and liver ❌ – Misleading; the toxic part is indirect bilirubin in brain.

• Indirect bilirubin in the liver ❌ – The problem is not liver deposition but CNS deposition.

• Direct bilirubin in the liver ❌ – Seen in obstructive jaundice, not kernicterus.

• PKU is caused by deficiency of phenylalanine hydroxylase (or its cofactor tetrahydrobiopterin).

• Leads to ↑ phenylalanine and accumulation of its toxic metabolites (phenylpyruvate, phenylacetate, phenyllactate).

• These cause CNS damage, seizures, mental retardation, and mousy odor of urine.

• Lack of tyrosine formation also reduces melanin → hypopigmentation (fair skin, hair, eyes).

Other options:

• Alkaptonuria (AKU) ❌ – Due to homogentisate oxidase deficiency, causes dark urine on standing, ochronosis, arthritis.

• Albinism ❌ – Pure defect in melanin synthesis (tyrosinase deficiency), no seizures or mousy odor.

• Hawkinsiuria ❌ – Rare tyrosine metabolism disorder, not linked with mousy odor.

• Tyrosinemia ❌ – Liver/kidney failure, cabbage-like odor, not mousy odor.

• Oxidative phosphorylation takes place in the mitochondrial inner membrane.

• It couples the electron transport chain (ETC) with ATP synthesis via ATP synthase.

• Final outcomes:

  • ATP → produced as protons flow back through ATP synthase.

  • H₂O → produced when oxygen acts as the final electron acceptor and combines with H⁺ and electrons.

Now check the options:

• NADH ❌ – It is consumed (oxidized) in ETC, not formed.

• Oxygen ❌ – It is consumed as the final electron acceptor, not formed.

• ADP ❌ – Substrate that gets phosphorylated, not a product.

• Pyruvate ❌ – Product of glycolysis, enters TCA, not made by oxidative phosphorylation.

• ATP + H₂O ✅ – End products of oxidative phosphorylation.

• Erythrocytes (RBCs) lack mitochondria.

• That means they cannot perform the TCA cycle or oxidative phosphorylation, so pyruvate cannot be fully oxidized to CO₂.

• Instead, RBCs rely only on anaerobic glycolysis (Embden–Meyerhof pathway, EMP) for ATP.

• In this pathway, pyruvate is converted to lactate by lactate dehydrogenase (LDH).

• This regenerates NAD⁺, allowing glycolysis to continue.

Now check the options:

• Lactate ✅ – Correct product in RBCs.

• CO₂ ❌ – Requires mitochondria (via TCA cycle), which RBCs don’t have.

• Ethanol ❌ – Produced in yeast, not humans.

• Hemoglobin ❌ – A protein, not a product of glycolysis.

• Bilirubin ❌ – Produced from heme breakdown, unrelated to pyruvate metabolism.

• During fasting, blood glucose levels must be maintained for glucose-dependent tissues (like the brain and RBCs).

• The liver is the primary organ responsible for regulating glucose during fasting:

  • In short-term fasting (up to ~12 hrs) → liver maintains glucose via glycogenolysis (breakdown of glycogen).

  • In prolonged fasting (>12–24 hrs) → glycogen stores are depleted → liver produces glucose through gluconeogenesis (from lactate, glycerol, and amino acids).

• Other tissues:

  • Smooth muscle ❌ – Consumes glucose but does not release it into blood (no glucose-6-phosphatase).

  • Brain ❌ – Only consumes glucose (and ketones later), cannot regulate blood glucose.

  • Bone ❌ – No role in glucose homeostasis.

  • Red blood cells ❌ – Rely only on glycolysis for energy, cannot regulate blood glucose.

• Massive obesity + dyspnea → strongly suggests Obesity Hypoventilation Syndrome (OHS), also known as Pickwickian syndrome.

• In OHS:

  • Excess body weight restricts diaphragm and chest wall movement.

  • This leads to alveolar hypoventilation → patient cannot blow off CO₂ effectively.

  • Result = hypercapnia (↑ CO₂ retention).

• Acid–base status:

  • ↑ CO₂ combines with water → carbonic acid → dissociates into H⁺ and HCO₃⁻.

  • This lowers pH → respiratory acidosis.

  • Kidneys try to compensate by retaining more bicarbonate (↑ HCO₃⁻), but the primary defect is CO₂ retention.

Why not the others

• Decreased HCO₃⁻ retention ❌ – That’s metabolic acidosis (like DKA), but here the problem is hypoventilation, not ketoacids.

• Decreased CO₂ retention ❌ – Seen in hyperventilation (respiratory alkalosis).

• O₂ retention changes ❌ – Not the key metabolic shift; hypoxemia can occur, but it’s not the defining acid–base change.

• In the electron transport chain (ETC), electrons are passed from NADH and FADH₂ through a series of complexes (I–IV).

• At Complex IV (cytochrome c oxidase), the electrons are finally transferred to molecular oxygen (O₂).

• Oxygen combines with electrons and protons (H⁺) to form water.

• Without oxygen, the ETC cannot operate, oxidative phosphorylation halts, and ATP production collapses → that’s why oxygen is called the final electron acceptor.

Why the others are wrong

• Carbon dioxide ❌ – It’s a product of the Krebs cycle, not the final electron acceptor.

• FADH₂ ❌ – It donates electrons to the ETC at Complex II, not the final acceptor.

• Hydrogen ❌ – Protons are used in chemiosmosis, but not the final acceptor.

• NADH ❌ – Donates electrons at Complex I, not the final acceptor.

• Oxygen ✅ – Correct → accepts electrons at the end of the chain to form water.

What the patient has

The triad of dermatitis (photosensitive, hyperpigmented/scaly rash around exposed areas), glossitis (beefy red tongue), and generalized weakness in someone eating mostly maize points strongly to pellagra — niacin (vitamin B3) deficiency. Lab confirmation of low niacin supports the clinical diagnosis.

Why maize (corn) causes pellagra

• Niacin (nicotinic acid / nicotinamide) can be obtained directly from diet or synthesized de novo from the essential amino acid tryptophan in the body.

• Maize-based diets are problematic two ways:

  • Maize is low in tryptophan, so there’s reduced substrate for endogenous niacin synthesis.

  • In untreated maize, some niacin is bound and not bioavailable unless the corn is processed (e.g., nixtamalization — treatment with alkali, used in traditional Mesoamerican preparation).

• The net result in populations relying primarily on unprocessed maize and little animal protein: insufficient niacin → pellagra.

Biochemical detail (concise)

• Conversion: tryptophan → niacin (NAD⁺ precursor) requires cofactors (e.g., vitamin B6). Insufficient tryptophan reduces niacin production and therefore NAD⁺/NADP⁺ pools needed for many metabolic reactions — explaining the systemic manifestations.

Why the other options are less likely or incorrect

• Genetic defect in tryptophan absorption (Hartnup disease)

  • Hartnup causes pellagra-like features due to impaired neutral amino acid (including tryptophan) absorption and increased urinary loss. It is genetic and typically presents earlier in life with episodic photosensitive rash and ataxia; history here (longstanding maize diet, adult onset) makes dietary deficiency far more likely.

• Excessive diversion of tryptophan into serotonin synthesis (carcinoid syndrome)

  • Carcinoid tumors can shunt tryptophan to serotonin and cause pellagra, but that is uncommon and would usually have other features (flushing, diarrhea, bronchospasm). No such features are described here.

• Increased urinary excretion of niacin due to renal tubular disorder

  • Renal losses of niacin are not a typical or common cause of pellagra; the history points to deficient intake/substrate rather than renal wasting.

• Reduced intestinal bacterial production of niacin due to antibiotics

  • Gut flora can contribute some niacin, but antibiotic suppression causing frank pellagra is rare and would be less likely than the strong dietary explanation given (maize diet with little animal protein).

Clinical takeaways

• In a patient with pellagra features and a maize-based diet, the primary cause is dietary niacin deficiency due to lack of tryptophan and low bioavailability of niacin in corn.

• Management: niacin (nicotinamide) supplementation, improve dietary protein intake, and address any cofactors (e.g., vitamin B6). Educate about processing maize (nixtamalization) or dietary diversification.

• Hepatic bile (freshly secreted from liver): watery, isotonic with plasma.

• Gallbladder bile: concentrated because the gallbladder mucosa actively absorbs water, sodium, chloride, and bicarbonate, while relatively retaining bile salts, bilirubin, cholesterol, and lecithin.

So compared with hepatic bile:

• Sodium ions → ↓ (absorbed actively).

• Bilirubin → ↑ concentration.

• Cholesterol → ↑ concentration.

• Lecithin → ↑ concentration.

• Bile salts → ↑ concentration.

This concentration process makes gallbladder bile thicker and more effective for fat digestion.

Why the others are wrong

• Bilirubin ❌ – More concentrated in gallbladder bile.

• Cholesterol ❌ – More concentrated, can predispose to gallstones.

• Lecithin ❌ – More concentrated in gallbladder bile.

• Bile salts ❌ – More concentrated.

• Sodium ions ✅ – Reduced, because actively absorbed during bile concentration.

The pancreas produces many proteolytic enzymes (trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidases). To avoid autodigestion, these enzymes are secreted in inactive zymogen form.

But the most critical safeguard is:

• Pancreatic acinar cells secrete a trypsin inhibitor (pancreatic secretory trypsin inhibitor, PSTI).

• This prevents premature activation of trypsinogen → trypsin inside the pancreas.

• If trypsin were to activate early, it would trigger a cascade activating all proteases, leading to acute pancreatitis.

Why the other options are wrong

• Storage of enzymes in zymogen granules in acinar cells ❌ – True mechanism, but not the enzyme preventing activation.

• Inflammatory blockage of pancreatic duct ❌ – That’s a complication, not a protective mechanism.

• Absence of enterokinase in the intestinal epithelium ❌ – Wrong, enterokinase is present in duodenal brush border and is needed to activate trypsinogen.

• Secretion of trypsin inhibitor by acinar cells ✅ – Correct protective mechanism.

• Decreased secretion of sodium bicarbonate in ducts ❌ – Leads to acidity and damage, not protection.

• During the fasting state, the GI tract shows a special motor pattern called the migrating motor complex (MMC).

• MMC = waves of strong, sequential contractions that start in the stomach, move through the small intestine, and fade in the ileum.

• This “housekeeping wave” clears residual food, mucus, and bacteria between meals.

• Motilin, secreted from the M cells of the small intestine, is the key hormone that initiates MMC.

Why the others are wrong

• Gastrin ❌ – Secreted in fed state, stimulates acid secretion and gastric motility, not MMC.

• VIP (Vasoactive Intestinal Peptide) ❌ – Relaxes smooth muscle, increases intestinal secretions, not MMC.

• Secretin ❌ – Stimulates bicarbonate secretion from pancreas in response to acid, not MMC.

• Somatostatin ❌ – Inhibitory hormone, suppresses GI activity, not initiator of MMC.

• Enterokinase (also called enteropeptidase) is a brush-border enzyme in the duodenum.

• Its job: convert trypsinogen → trypsin.

• Trypsin is the master protease that activates all other pancreatic proteases (chymotrypsinogen, proelastase, procarboxypeptidases).

• Without enterokinase → no trypsin → almost no activation of pancreatic proteases → severe impairment of protein digestion.

Why the others are wrong

• Ptyalin (salivary amylase) ❌ – Carbohydrate digestion, not protein.

• Enterokinase ✅ – Essential for protein digestion via trypsin activation.

• Pancreatic amylase ❌ – Starch digestion, not protein.

• Chymotrypsin ❌ – Important protease, but even if chymotrypsin is absent, trypsin and others can still partly digest proteins.

• Aminopeptidase ❌ – Helps in final brush-border digestion of peptides, but not as critical as enterokinase.

• The gastric mucosa produces several important substances:

  • HCO₃⁻ → protects mucosa from acid.

  • Pepsin → protein digestion, but other proteases in intestine can compensate.

  • Intrinsic factor → essential for vitamin B₁₂ absorption in the ileum.

  • Mucin → protects epithelium from acid/enzymes.

  • Somatostatin → inhibitory hormone, regulates acid secretion.

• If the gastric mucosa atrophies, loss of intrinsic factor has the most serious long-term consequence → leading to vitamin B₁₂ deficiency → pernicious anemia (megaloblastic anemia + neurological deficits due to demyelination).

• The other losses (pepsin, mucin, HCO₃⁻, somatostatin) are significant but can be partly compensated by pancreatic enzymes or other regulatory mechanisms.

Why the others are less severe

• HCO₃⁻ ❌ – Loss increases mucosal injury risk but not systemic long-term deficiency.

• Pepsin ❌ – Protein digestion can still occur via pancreatic proteases.

• Intrinsic factor ✅ – Essential, no alternative source; deficiency leads to irreversible B₁₂ malabsorption.

• Mucin ❌ – Loss predisposes to ulceration, but not systemic deficiency.

• Somatostatin ❌ – Loss causes excess acid secretion but not long-term deficiency effects like B₁₂ deficiency.

Saliva is unique among GI secretions:

• It is hypotonic because ductal cells reabsorb more Na⁺ and Cl⁻ than they secrete K⁺ and HCO₃⁻.

• It contains high HCO₃⁻ (important for neutralizing oral acids).

• Its secretion depends heavily on vagal parasympathetic stimulation, so it drops sharply after vagotomy.

• Pancreatic juice ❌

  • Rich in HCO₃⁻, but it is isotonic (not hypotonic).

  • Also regulated mainly by secretin, not vagus.

• Bile ❌

  • Isotonic, not hypotonic. HCO₃⁻ content is modest.

• Gastric juice ❌

  • Mainly HCl (parietal cells), not rich in HCO₃⁻, and hypertonic/isotonic depending on secretion.

• Succus entericus (intestinal juice) ❌

  • Isotonic with plasma, not hypotonic.

Since the recorded basic electrical rhythm is 8 per minute, this matches the slow wave frequency of the ileum.

• Stomach ❌ – Too slow (3/min).

• Duodenum ❌ – Too fast (12/min).

• Jejunum ❌ – Slightly faster (~10–11/min).

• Ileum ✅ – Matches the given rate (~8/min).

• Esophagus ❌ – No regular BER.

The defecation reflex has multiple coordinated phases:

• Filling phase → Rectum gradually fills with feces, wall distends.

• RAIR (Rectoanal inhibitory reflex) → Distension of the rectum causes reflex relaxation of the internal anal sphincter (involuntary, mediated by myenteric plexus). This allows stool to enter the anal canal and gives the conscious urge to defecate.

• Parasympathetic phase → Pelvic splanchnic nerves enhance rectal contraction and further internal sphincter relaxation.

• Inhibition phase → Voluntary relaxation of the external anal sphincter (somatic control via pudendal nerve).

• Efferent phase → Final motor output leading to coordinated defecation.

Thus, the first key step where internal sphincter relaxes and urge is felt = RAIR.

Why others are wrong

• Efferent phase ❌ – Refers to motor output, not initial sphincter relaxation.

• Filling phase ❌ – Rectum distends but internal sphincter hasn’t relaxed yet.

• Inhibition phase ❌ – Voluntary relaxation of external sphincter, comes later.

• Parasympathetic phase ❌ – Strengthens rectal contraction after RAIR, not the initial trigger.

• Pancreatic lipase is the primary enzyme for hydrolyzing dietary triglycerides into monoglycerides and free fatty acids.

• These products, along with bile salts, are essential for micelle formation, which allows lipids to be transported across the unstirred water layer to the intestinal epithelium.

If pancreatic lipase is severely deficient:

• Triglycerides cannot be properly broken down.

• Micelles cannot form efficiently, because their building blocks (monoglycerides and fatty acids) are missing.

• This leads to fat malabsorption and steatorrhea.

Why the other options are wrong

• Upregulation of gastric lipase activity ❌ – Gastric lipase does contribute a little, but it cannot compensate enough for pancreatic lipase deficiency.

• Enhanced synthesis of bile salts ❌ – Bile salt synthesis is a hepatic function, not regulated by pancreatic lipase deficiency.

• Reduced formation of micelles ✅ – Correct → micelles need lipase products.

• Decreased production of cholecystokinin ❌ – Fat in the duodenum actually increases CCK secretion, not decreases.

• Increased absorption of dietary triglycerides ❌ – Opposite happens → malabsorption.

• Zollinger–Ellison syndrome = gastrinoma (gastrin-secreting tumor, usually in pancreas or duodenum).

• Gastrin’s normal role:

  • Stimulates parietal cells directly → ↑ HCl secretion.

  • Stimulates chief cells → ↑ pepsinogen release.

  • Increases gastric mucosal growth.

• In Zollinger–Ellison:

  • Uncontrolled excess gastrin → massive hypersecretion of gastric acid (hyperchlorhydria).

  • This leads to peptic ulcers, diarrhea, and steatorrhea (due to inactivation of pancreatic lipase by low pH).

Now the other options:

• Decreased release of pepsinogen ❌ – Gastrin increases pepsinogen, not decreases.

• Enhanced secretion of somatostatin ❌ – Somatostatin inhibits gastrin, but here the tumor bypasses normal control.

• Hyperchlorhydria (Excessive HCl production) ✅ – Correct.

• Hypochlorhydria (Reduced HCl production) ❌ – Opposite of what happens.

• Reduced synthesis of intrinsic factor ❌ – Intrinsic factor secretion from parietal cells is preserved, often increased along with HCl.

• G cells in the pyloric antrum secrete gastrin, which stimulates parietal cells (HCl secretion) and gastric motility.

• Regulation of gastrin secretion:

  Stimulants (increase gastrin release):

  • Gastric distension → via local reflexes.

  • Vagal stimulation → via gastrin-releasing peptide (GRP).

  • Peptides and amino acids in food.

  • Alkaline pH (removes inhibitory effect of acid).

  Inhibitors (decrease gastrin release):

  • Increased acidity (low pH < 3) → negative feedback, directly inhibits G cells.

  • Somatostatin from D cells (triggered by acid).

• Therefore, increased acidity in the antrum is the main factor that inhibits gastrin secretion.

Why the other options are wrong

• Distension of stomach ❌ – Stimulates gastrin release via vagovagal reflex.

• Increased acidity ✅ – Inhibits gastrin (correct).

• Alkaline pH ❌ – Promotes gastrin secretion.

• Activation of vagal efferent ❌ – Stimulates gastrin via GRP.

• Epinephrine release ❌ – Not the primary regulator of G cell activity.

• Alpha-amylase (ptyalin) is the enzyme in saliva that begins starch digestion.

• All major salivary glands contribute, but in different proportions:

  • Parotid gland → purely serous secretion, richest source of alpha-amylase → secretes the highest concentration and maximum amount.

  • Submandibular gland → mixed serous and mucous, contributes a moderate amount of amylase.

  • Sublingual gland → mainly mucous, only small amounts of amylase.

  • Minor salivary glands (labial, buccal, palatine, lingual) → mostly mucous, negligible amylase.

So, the parotid gland is the main contributor of salivary amylase for starch digestion.

Why others are wrong

• Buccal glands ❌ – Minor glands, mucous secretion, little to no amylase.

• Submandibular glands ❌ – Mixed, some amylase but not as much as parotid.

• Parotid glands ✅ – Purely serous, secrete maximum amylase.

• Labial glands ❌ – Minor, mucous, negligible amylase.

• Sublingual glands ❌ – Mostly mucous, very little amylase.

Swallowing (deglutition) occurs in stages:

1. Voluntary (oral preparatory + oral propulsive stage) → Food is chewed, mixed with saliva, and pushed back by the tongue into the oropharynx. Respiration continues normally.

2. Pharyngeal stage → Involuntary reflex once the bolus reaches the pharynx.

   • The nasopharynx closes (soft palate elevates).

   • The larynx elevates and the epiglottis closes over the glottis.

   • The upper esophageal sphincter relaxes.

   • Respiration is temporarily inhibited to prevent aspiration → this is called the deglutition apnea.

3. Esophageal stage → Peristaltic waves propel the bolus down to the stomach; respiration resumes.

Why others are wrong

• Postprandial stage ❌ – No such standard stage in swallowing classification.

• Esophageal stage ❌ – Bolus moves by peristalsis, breathing is not inhibited.

• Voluntary stage ❌ – Mouth to oropharynx, still breathing normally.

• Oral propulsive stage ❌ – Tongue pushes bolus back, respiration continues.

• Gastric emptying is regulated by both mechanical factors (distension, pyloric tone) and chemical factors (nutrient composition of chyme).

• Among macronutrients:

  • Carbohydrates (starch, lactose) → empty the fastest.

  • Proteins / amino acids → slower than carbs, but faster than fats.

  • Fats (fatty acids) → empty the slowest.

• Why? Fatty acids in the duodenum trigger the release of cholecystokinin (CCK) and also stimulate the enterogastric reflex, both of which strongly inhibit gastric emptying to allow more time for digestion and absorption.

Why the others are not correct

• Starch ❌ – Carbohydrate, empties relatively fast.

• Lactose ❌ – Also a carbohydrate, similar to starch in terms of emptying speed.

• Amino acids ❌ – Slow down emptying, but not as much as fats.

• Proteins ❌ – Same as above, slower than carbs but faster than fats.

• The brush border of the small intestine contains disaccharidases that finish carbohydrate digestion.

• Key linkages:

  • Maltase → breaks α-1,4 glycosidic bonds in maltose.

  • Sucrase → breaks sucrose into glucose + fructose.

  • Lactase → breaks lactose into glucose + galactose.

  • Glucoamylase → acts on α-1,4 bonds of oligosaccharides (similar to maltase).

  • Isomaltase → the only enzyme that cleaves α-1,6 glycosidic linkages, the branch points in starch/glycogen.

So the brush border enzyme specifically responsible for breaking α-1,6 bonds is isomaltase.

• In the small intestine, different monosaccharides use different transporters:

  • Glucose & Galactose → absorbed via SGLT-1 (sodium-dependent active transport).

  • Fructose → absorbed via GLUT-5 (facilitated diffusion across the apical/brush border membrane).

  • Once inside the enterocyte, all three sugars exit into the blood via GLUT-2 on the basolateral membrane.

Now the other options:

• GLUT-2 ❌ – Important for moving all monosaccharides (glucose, galactose, fructose) from enterocyte → blood, not for apical fructose entry.

• GLUT-1 ❌ – Basal transporter in many tissues (RBCs, blood-brain barrier).

• GLUT-4 ❌ – Insulin-sensitive transporter in skeletal muscle and adipose tissue.

• GLUT-3 ❌ – High-affinity glucose transporter in neurons.

• The right and left hepatic ducts drain bile from the respective lobes of the liver.

• They join to form the common hepatic duct.

• The cystic duct (from the gallbladder) then joins the common hepatic duct → together they form the common bile duct.

• The common bile duct later unites with the main pancreatic duct at the hepatopancreatic ampulla (ampulla of Vater), which opens into the second part of the duodenum at the major duodenal papilla.

Now the other options:

• Cystic duct and right hepatic duct ❌ – Right hepatic duct first joins left hepatic duct to form common hepatic duct.

• Cystic duct and pancreatic duct ❌ – Pancreatic duct only joins later at ampulla of Vater.

• Left hepatic duct and right hepatic duct ❌ – They form the common hepatic duct, not the common bile duct.

• Common hepatic and pancreatic duct ❌ – That union forms the hepatopancreatic ampulla, not the common bile duct.

✅ Correct Answer

Omphalocele is usually a right-sided abdominal wall defect without a covering membrane.

That statement is false because it actually describes gastroschisis, not omphalocele.

• Omphalocele → midline defect at umbilical ring, covered by amnion + peritoneum, due to failure of midgut return, often linked with chromosomal anomalies and neural tube defects.

• Gastroschisis → right-sided, no covering membrane, less often associated with anomalies.

• The septum transversum (mesoderm) contributes to Kupffer cells, hematopoietic cells, and connective tissue of liver.

• The biliary system (intrahepatic and extrahepatic ducts, gallbladder, cystic duct) develops from the endodermal hepatic diverticulum, not from the septum transversum.

The primary intestinal loop arises during midgut development and has two limbs:

• Cranial limb → forms the distal duodenum, jejunum, ileum.

• Caudal limb → forms the cecum, vermiform appendix, ascending colon, and proximal two-thirds of the transverse colon.

The rectum, however, does not come from the midgut at all. It is a hindgut derivative. The hindgut gives rise to the distal third of transverse colon, descending colon, sigmoid colon, rectum, and upper anal canal.

So, while cecum, appendix, ascending colon, and proximal 2/3 of transverse colon are correctly from the caudal limb of the midgut, the rectum is not.

• It’s a duct within the lobule of the pancreas, not in the connective tissue septa (so not interlobular).

• Lumen is small to moderate, lined by simple cuboidal epithelium.

• This exactly matches an intralobular duct (which includes intercalated ducts feeding into it).

Checking options again:

• Intralobular duct ✅ – Correct → small ducts found inside lobules, lined by cuboidal cells.

• Interlobular duct ❌ – Bigger ducts, found in connective tissue septa between lobules.

• Blood vessel ❌ – Would show endothelial lining and RBCs, not ductal epithelium.

• Collecting duct ❌ – Kidney structure, not pancreas.

• Acini ❌ – Clusters of secretory cells, not ducts.

HistoQuarterly: PANCREAS

• C is pointing to small, darkly stained clusters of secretory cells with narrow lumina in the center.

• These are the functional exocrine units of the pancreas that produce digestive enzymes.

Checking options:

• Acini ✅ – Correct → exocrine secretory units of the pancreas.

• Intercalated duct ❌ – Much smaller lumen lined by cuboidal epithelium, not clusters of secretory cells.

• Striated duct ❌ – Absent in the pancreas (only in salivary glands).

• Follicle ❌ – Refers to thyroid follicles (colloid-filled), not in pancreas.

• Blood vessel ❌ – Would have endothelial lining and possibly RBCs, not secretory cells.

HistoQuarterly: PANCREAS

• It has a fairly wide lumen compared to intercalated ducts.

• It is located in connective tissue between lobules.

• The lining looks cuboidal/columnar, not like acini.

• This matches an interlobular duct.

Checking options:

• Acini ❌ – Small, darkly stained secretory clusters, no large lumen like this.

• Interlobular duct ✅ – Correct: larger duct in connective tissue septa between lobules.

• Follicles ❌ – Seen in thyroid gland (spherical colloid-filled), not pancreas.

• Trabeculae ❌ – Connective tissue septa, not a duct with lumen.

• Blood vessels ❌ – Would have red blood cells in lumen and endothelial lining, not this appearance.

HistoQuarterly: PANCREAS

• A is pointing to a very small duct with a narrow lumen lined by low cuboidal epithelium, located directly next to the secretory acini.

• This appearance is characteristic of an intercalated duct, the first part of the duct system in the pancreas.

• Intercalated ducts collect secretions from acini and drain into larger intralobular ducts.

Now, why not the others?

• Striated duct ❌ – Found in salivary glands, not in the pancreas (pancreas lacks striated ducts).

• Intralobular duct ❌ – General term for ducts inside lobules, but here the specific type is the intercalated duct.

• Interlobular duct ❌ – Larger ducts located between lobules, with wider lumen, not the tiny duct shown.

• Collecting duct ❌ – A structure of the kidney, not the pancreas.

HistoQuarterly: PANCREAS

Observations from the labeled image:

• We can see acini (clusters of secretory cells).

• Multiple ducts are visible: intercalated ducts, intralobular ducts, interlobular ducts.

• Prominent blood vessels nearby.

• The arrangement is very typical of an exocrine gland with ductal system.

Among the given options:

• Pituitary gland ❌ – Shows anterior/posterior lobes with endocrine cells, not ducts.

• Adrenal gland ❌ – Shows cortex (zona glomerulosa, fasciculata, reticularis) and medulla, no ducts.

• Thyroid gland ❌ – Has follicles filled with colloid, not acini + ducts like this.

• Pancreas ✅ – Characterized by exocrine acini + duct system (intercalated, intralobular, interlobular) and scattered endocrine islets (not clearly labeled here).

• Parathyroid gland ❌ – Has chief and oxyphil cells, no duct system.

HistoQuarterly: PANCREAS