GIT- PATHOLOGY

Gastroesophageal reflux disease (GERD) occurs when gastric contents (acid, bile, enzymes) reflux upward into the esophagus due to incompetence of the lower esophageal sphincter (LES). This leads to symptoms like heartburn, regurgitation, and sometimes chronic cough or laryngitis. Chronic GERD can cause complications such as esophagitis, Barrett’s esophagus, and strictures.

Incorrect Options

❌ The esophagus shows a bird beak sign on X-ray
The “bird beak” sign is seen in achalasia cardia, where there is failure of LES relaxation and proximal esophageal dilation—not GERD.

❌ Contents from the esophagus move down into the stomach
That is normal physiology of swallowing, not reflux disease.

❌ The stomach undergoes intestinal dysplasia
Intestinal metaplasia can occur in the esophagus (Barrett’s esophagus) due to chronic reflux, not in the stomach because of GERD.

❌ The stomach shrinks
There is no shrinking of the stomach in GERD. Gastric size is not directly altered by reflux disease.

In liver failure or liver injury, serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) rise due to hepatocellular damage. ALT is more specific to the liver, while AST is also present in cardiac and skeletal muscle. Thus, a predominant rise in ALT is more characteristic of liver injury/failure.

Incorrect Options

❌ Estrogen
Estrogen is a hormone, not an enzyme. While estrogen metabolism is impaired in liver disease (leading to signs like spider angiomas or gynecomastia), it is not measured as an enzyme marker.

❌ Histamine aminotransferase
This enzyme is not a clinically relevant marker for liver function and is not routinely measured in liver disease.

❌ Aspartate hydroxylase
This enzyme is not recognized as a standard biochemical marker of liver injury. (Possibly a confusion with AST, aspartate aminotransferase, which does increase, but ALT is more specific.)

❌ Enterokinase
Enterokinase is a duodenal enzyme that activates trypsinogen; it has no diagnostic role in liver function.

✅ Gliadin peptides
Celiac disease is an autoimmune-mediated enteropathy triggered by gluten ingestion. The toxic component is gliadin, a peptide found in wheat, barley, and rye. In genetically susceptible individuals (HLA-DQ2/DQ8), gliadin peptides stimulate an abnormal immune response, leading to villous atrophy, crypt hyperplasia, and malabsorption.

Incorrect Options

❌ Intussusception
This is a mechanical obstruction where a segment of bowel telescopes into another. It is not related to the immune mechanism of celiac disease.

❌ Aldolase B deficiency
This causes hereditary fructose intolerance, a metabolic disorder due to impaired fructose metabolism, not gluten sensitivity.

❌ Tropheryma whippelii
This bacterium causes Whipple disease, another malabsorption disorder, but it is distinct from celiac disease.

❌ Tumor
Certain gastrointestinal tumors can develop as complications of long-standing celiac disease (e.g., enteropathy-associated T-cell lymphoma), but tumors are not the cause of celiac disease.

✅ Broad-based ulcers
Ulcerative colitis (UC) is an inflammatory bowel disease limited to the mucosa and submucosa of the colon, starting at the rectum and extending proximally in a continuous manner. UC typically shows broad-based, shallow ulcers with overlying pseudopolyps.

Incorrect Options

❌ Creeping fat
This is characteristic of Crohn’s disease, where mesenteric fat wraps around the bowel due to transmural inflammation. It is not seen in UC.

❌ Skip lesions
Crohn’s disease has patchy involvement with “skip areas” of normal mucosa between diseased segments. UC, in contrast, is continuous without skip lesions.

❌ Cobblestone mucosa
This classic appearance is seen in Crohn’s disease, caused by deep, linear ulcers and edematous mucosa. UC mucosa is more friable and ulcerated, not cobblestoned.

❌ Fissures
Deep fissuring ulcers that extend into the bowel wall are a feature of Crohn’s disease (transmural inflammation), not UC, which is superficial.

✅ Whipple disease
Whipple disease is caused by the bacterium Tropheryma whipplei, which invades the small intestine mucosa. It leads to malabsorption due to infiltration of the lamina propria with PAS-positive foamy macrophages. Clinically, patients present with diarrhea, steatorrhea, weight loss, arthralgia, and sometimes neurologic or cardiac manifestations.

Incorrect Options

❌ Hirschsprung disease
This is a congenital absence of ganglion cells in the distal colon due to failure of neural crest cell migration. It is not infectious and does not involve pathogen invasion of the small intestine.

❌ Chronic gastritis
Usually caused by Helicobacter pylori infection, but this bacterium invades the stomach, not the small intestine.

❌ Oral candidiasis
Caused by Candida albicans, but it affects the oral cavity (mouth, tongue, pharynx), not the small intestine.

❌ Celiac disease
This is an autoimmune reaction to gluten (gliadin component) leading to villous atrophy in the small intestine. It is not caused by a pathogen but by an immune-mediated response.

✅ Diabetes mellitus
Hyperlipidemia is a common metabolic complication of diabetes mellitus. Insulin deficiency (in type 1) or insulin resistance (in type 2) leads to increased lipolysis, elevated free fatty acids, and overproduction of VLDL and triglycerides in the liver. Impaired insulin action also reduces lipoprotein lipase activity, worsening lipid accumulation in the blood.

Incorrect Options

❌ Tropical sprue
This condition causes malabsorption in the small intestine, leading to nutrient deficiencies (like folate and B12), not hyperlipidemia. Lipid absorption is impaired, so lipid levels are usually low.

❌ Celiac disease
Similar to tropical sprue, celiac disease is a malabsorption disorder. Damage to the intestinal villi reduces fat absorption, leading to steatorrhea and hypolipidemia, not hyperlipidemia.

❌ Duodenal atresia
This congenital anomaly involves obstruction of the duodenum, preventing passage of food. It causes vomiting, dehydration, and nutritional deficiency, but not hyperlipidemia.

❌ Abetalipoproteinemia
This rare genetic disorder involves absence of apolipoprotein B, impairing formation of chylomicrons and VLDL. Patients cannot properly absorb dietary fats, resulting in hypolipidemia (very low triglycerides and cholesterol), not hyperlipidemia.

✅ Jaundice
Portal hypertension leads to increased pressure in the portal venous system, producing complications such as varices, ascites, and splenomegaly. Jaundice, however, is not a direct complication of portal hypertension. Instead, jaundice occurs due to impaired bilirubin metabolism (e.g., hepatocellular failure or bile duct obstruction). While liver disease can cause both jaundice and portal hypertension, they are separate processes.

Incorrect Options

❌ Caput medusae
This is the appearance of distended, tortuous veins radiating from the umbilicus due to portosystemic shunting. It is a classical sign of portal hypertension.

❌ Esophageal varices
These dilated veins at the gastroesophageal junction are a direct result of portosystemic collateral formation. They are a major, life-threatening complication of portal hypertension.

❌ Ascites
Ascites (fluid accumulation in the peritoneal cavity) occurs due to increased hydrostatic pressure in portal circulation, hypoalbuminemia, and secondary hyperaldosteronism.

❌ Congestive splenomegaly
Increased portal venous pressure leads to congestion of the spleen, causing splenomegaly, another hallmark feature of portal hypertension.

✅ T-cell lymphoma
Celiac disease is an autoimmune disorder triggered by gluten ingestion, leading to chronic inflammation of the small intestinal mucosa. Prolonged, uncontrolled inflammation and mucosal damage increase the risk of enteropathy-associated T-cell lymphoma (EATL), a rare but serious complication. Patients with poorly controlled or refractory celiac disease are particularly at risk.

Incorrect Options

❌ B-cell neoplasia
While B-cell lymphomas are common in the general population, they are not the classical neoplastic complication of celiac disease. The strong link is specifically with T-cell lymphoma, not B-cell origin cancers.

❌ Diabetes insipidus
This condition results from deficiency of ADH (central) or renal resistance to ADH (nephrogenic). It is unrelated to the autoimmune intestinal pathology of celiac disease.

❌ Hepatosplenomegaly
Although some celiac patients may develop mild hepatomegaly due to associated autoimmune liver disease, hepatosplenomegaly is not a recognized common complication. It is seen more in hematologic malignancies or storage disorders.

❌ Central pontine myelinolysis
This neurological disorder is usually linked to rapid correction of hyponatremia, not to celiac disease. There is no direct pathophysiological connection between gluten sensitivity and this demyelination syndrome.

Physiologic jaundice in newborns arises because the liver’s bilirubin-processing machinery is not yet fully mature. The enzyme responsible for conjugating bilirubin is temporarily underactive, leading to a buildup of unconjugated bilirubin. This condition is common, usually harmless, and resolves as the enzyme system matures.

• ❌ Low glucose consumption – no link to bilirubin.

• ❌ Absence of gut bacteria – only influences enterohepatic circulation, not the root cause.

• ❌ Transiently low glycuronyl hydroxylase activity – not a real enzyme here.

• ❌ Absence of UGT – complete absence = severe disease (Crigler–Najjar), not physiologic jaundice.

• Crigler–Najjar syndrome → rare genetic disorder caused by deficiency or complete absence of UDP-glucuronyl transferase, the enzyme needed for bilirubin conjugation in the liver.

• Result = severe unconjugated hyperbilirubinemia → kernicterus in newborns.

• It is pathological, unlike physiologic jaundice.

Why the others are wrong

• Annular pancreas ❌ → congenital anomaly causing duodenal obstruction, not bilirubin metabolism defect.

• Physiologic jaundice of the newborn ❌ → common, due to immature enzyme system, but not pathologic (self-limiting).

• Dubin–Johnson syndrome ❌ → problem with conjugated bilirubin excretion, so it causes conjugated hyperbilirubinemia.

• Biliary tract obstruction ❌ → leads to conjugated hyperbilirubinemia (post-hepatic jaundice).

Clinical Pearl

👉 Pathological unconjugated bilirubin in neonates = Crigler–Najjar
👉 Physiological unconjugated bilirubin = transient, due to immature liver enzyme.

Step 1: Interpreting the symptoms

• Dark urine → excess conjugated bilirubin being excreted in urine.

• Clay-colored stools → lack of stercobilin in stool due to obstructed bile flow.

• Jaundice (scleral icterus, yellow skin) → bilirubin buildup in blood.

👉 These findings are classic for obstructive (post-hepatic) jaundice.

Step 2: Cholelithiasis as the cause

• Gallstones (especially when they obstruct the common bile duct) block bile flow.

• This leads to conjugated hyperbilirubinemia, dark urine, pale stools, and jaundice.

Why the other options are wrong

• Hemochromatosis ❌ → Iron overload; causes bronze skin, diabetes, cirrhosis, but not clay-colored stools/dark urine.

• Ischemic colitis ❌ → Ischemia of colon → abdominal pain, bloody diarrhea, not obstructive jaundice.

• Acute pancreatitis ❌ → Can sometimes compress bile duct, but typical presentation is severe epigastric pain radiating to the back, not isolated clay-colored stools.

• Reye syndrome ❌ → Acute liver failure and encephalopathy in children after aspirin; does not present with gallstone-like obstructive jaundice.

Clinical Pearl

• Obstructive jaundice triad = dark urine + clay stools + jaundice.

• Common causes = gallstones, pancreatic head carcinoma, biliary strictures.

• Familial hypercholesterolemia (FH) is due to a mutation most often in the LDL receptor gene (also sometimes ApoB or PCSK9 genes).

• This results in impaired LDL clearance from the blood → very high LDL cholesterol levels.

• Clinical features: tendon xanthomas, xanthelasma, premature atherosclerosis, increased risk of early myocardial infarction.

👉 Inheritance is autosomal dominant — meaning just one defective allele is enough to cause the disorder.

Why the other options are wrong

• Autosomal recessive ❌ → would require two defective alleles, but FH typically manifests with one (heterozygotes).

• X-linked recessive ❌ → FH is not linked to the X chromosome.

• Mitochondrial disease ❌ → mitochondrial inheritance involves maternal transmission, not the case here.

Clinical Pearl

• Heterozygous FH → cholesterol ~300 mg/dL, premature CAD by age 30–40.

• Homozygous FH → cholesterol ~700+ mg/dL, severe CAD in childhood/adolescence.

• Chronic gastritis = long-standing inflammation of the gastric mucosa.

• The most common cause worldwide is Helicobacter pylori infection.

• It colonizes the stomach (especially the antrum), producing urease, which neutralizes gastric acid and damages mucosa → chronic inflammation.

Why the other options are wrong

• Staphylococcus saprophyticus ❌ → common cause of urinary tract infections, not gastritis.

• Vibrio cholerae ❌ → causes acute watery diarrhea (cholera), not chronic gastritis.

• Escherichia coli ❌ → causes diarrheal diseases, UTIs, sepsis, not chronic gastritis.

• Clostridium difficile ❌ → causes pseudomembranous colitis after antibiotics, not chronic gastritis.

Clinical Pearl

• Chronic H. pylori infection increases risk of:

  • Peptic ulcer disease

  • Gastric adenocarcinoma

  • MALT lymphoma

• Lysosomal storage diseases (LSDs) are a group of inherited metabolic disorders.

• They are caused by deficiency or malfunction of specific lysosomal enzymes → failure to degrade certain macromolecules.

• This leads to accumulation of undegraded substrates within lysosomes → cellular dysfunction, organ damage.

Why the other options are wrong

• Increased enzyme concentration ❌ → Wrong, the issue is deficiency or non-functional enzymes, not excess.

• Decreased lysosome production ❌ → Lysosomes themselves are normal in number; the problem is inside them (enzyme defect).

• Increased lysosome production ❌ → Not true, cells don’t overproduce lysosomes in LSDs.

• Increased product degradation ❌ → Opposite of reality; there is decreased degradation of substrates.

Classic Examples

• Gaucher disease → deficiency of glucocerebrosidase.

• Tay–Sachs disease → deficiency of hexosaminidase A.

• Niemann–Pick disease → deficiency of sphingomyelinase.

Clinical Pearl

👉 Lysosomal storage diseases = “Trash collection system works, but the shredders (enzymes) are broken.”

Step 1: Helicobacter pylori and its role

• H. pylori is a gram-negative bacterium that colonizes the stomach.

• It causes chronic gastritis and peptic ulcer disease, but long-term infection can progress to malignancy.

Step 2: Cancer associations

• MALT lymphoma (low-grade B-cell lymphoma of the stomach) ✅

  • Strongly linked to chronic H. pylori infection.

  • Eradication of H. pylori with antibiotics can lead to regression of early MALT lymphoma.

• Gastric adenocarcinoma is also associated with chronic H. pylori infection (not listed among the options here).

Step 3: Why the other options are wrong

• Gallbladder cancer ❌ → Related to gallstones, chronic cholecystitis, not H. pylori.

• Cervical carcinoma ❌ → Caused by high-risk HPV, not H. pylori.

• Bladder carcinoma ❌ → Linked to smoking, schistosomiasis (squamous cell type), chemical exposure.

• Pancreatic carcinoma ❌ → Risk factors include smoking, chronic pancreatitis, diabetes, but not directly H. pylori.

Clinical Pearl

👉 H. pylori = Ulcers → Gastric adenocarcinoma → Gastric MALT lymphoma

Step 1: Principle of the UBT

• H. pylori produces urease enzyme, which breaks down urea into ammonia + CO₂.

• In the urea breath test, the patient ingests urea labeled with either ¹³C or ¹⁴C.

• If H. pylori is present, urease will generate labeled CO₂, which is detected in the patient’s breath.
  👉 This makes it a highly sensitive and specific non-invasive test.

Step 2: Why the other options are wrong

• Stool antigen test ❌

  • Good, non-invasive, and used for diagnosis & follow-up, but slightly less accurate than UBT.

• Urine culture ❌

  • H. pylori does not infect urinary tract; irrelevant.

• Radioactive iodine ❌

  • Not related to H. pylori detection; used in thyroid disorders.

• None of these ❌

  • Incorrect, because UBT is a valid, highly accurate test.

Clinical pearl

• Gold standard (invasive): gastric biopsy with histology, rapid urease test, or culture.

• Most accurate non-invasive test: Urea breath test.

Step 1: What is Barrett’s esophagus?

• A premalignant condition caused by chronic gastroesophageal reflux disease (GERD).

• It involves metaplasia: normal stratified squamous epithelium of the lower esophagus is replaced by intestinal-type columnar epithelium with goblet cells.

Step 2: Morphological features

• Endoscopically: tongues or patches of red, velvety mucosa extending upward from the gastroesophageal junction. ✅

• Histology: columnar epithelium with mucous (goblet) vacuoles.

Step 3: Why the other options are wrong

• Cuboidal esophageal epithelium ❌

  • Wrong; it’s columnar with goblet cells, not cuboidal.

• None of them ❌

  • Incorrect, because “velvety red patches” is correct.

• No mucous vacuoles ❌

  • Wrong; Barrett’s has goblet cells with mucous vacuoles.

• One type of mucosa with no alternates ❌

  • Wrong; it specifically shows metaplasia, meaning one epithelium is replaced by another.

Clinical pearl

• Barrett’s esophagus is a precursor lesion for esophageal adenocarcinoma.

• Surveillance endoscopy is important.

Step 1: Helicobacter pylori and cancer

• Helicobacter pylori is a gram-negative spiral bacterium that colonizes the stomach.

• It causes chronic gastritis and peptic ulcer disease.

• Long-standing infection leads to intestinal metaplasia, dysplasia, and increased risk of gastric adenocarcinoma and MALT lymphoma.
  👉 This makes H. pylori the key factor linking peptic ulcer disease and cancer.

Step 2: Why the other options are wrong

• Gastritis ❌

  • Chronic gastritis predisposes to cancer, but it is usually caused by H. pylori in this context. It’s a step, not the primary answer here.

• Dumping syndrome ❌

  • A complication after gastric surgery; not related to carcinogenesis.

• Duodenal compression ❌

  • Mechanical problem, no link to cancer development.

• None of them ❌

  • Incorrect, since H. pylori is strongly associated with gastric cancer.

Quick clinical pearl

• H. pylori = Ulcer + Cancer risk (adenocarcinoma, MALT lymphoma).

• Treat with eradication therapy (triple or quadruple regimen).

Step 1: Common causes of acute pancreatitis

• The two most important and common causes are:

  1. Gallstones (obstructing the pancreatic duct)

  2. Alcohol abuse (toxic effect on acinar cells, increases secretion, alters duct flow)

Together, they account for ~70–80% of cases.

Step 2: Why the other options are wrong

• Alcohol and liver injury ❌

  • Alcohol alone can cause pancreatitis, but “liver injury” is not a direct cause.

• Obesity and gallstones ❌

  • Obesity is a risk factor for gallstones, but not an independent direct cause of pancreatitis.

• Colectomy and liver injury ❌

  • Neither colectomy (colon removal) nor liver injury cause acute pancreatitis directly.

• All of them ❌

  • Incorrect, since not every listed pair is a cause.

Clinical pearl

• Remember the mnemonic: “I GET SMASHED” for causes of pancreatitis:

  • Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion sting, Hypercalcemia/hypertriglyceridemia, ERCP, Drugs.

• But in practice, alcohol and gallstones are by far the most frequent.

Step 1: Understanding hepatitis B markers

• HBsAg (surface antigen): present in active infection.

• Anti-HBs (surface antibody): indicates immunity to HBV.

• This immunity can come from:

  1. Recovery after past infection

  2. Successful vaccination

👉 So, the presence of anti-HBs = protection against hepatitis B.

Step 2: Why the other options are wrong

• Past infection only ❌

  • Wrong, because anti-HBs can also come from vaccination, not just infection.

• None of them ❌

  • Incorrect, because anti-HBs has clear diagnostic meaning (immunity).

• No vaccination to hepatitis B ❌

  • Opposite of correct: if anti-HBs is present, vaccination may well have occurred.

• No successful recovery from infection ❌

  • Wrong: recovery from infection does produce anti-HBs.

Clinical pearl

• Anti-HBs alone positive → Vaccination

• Anti-HBs + Anti-HBc positive → Past infection & recovery

Step 1: What is celiac disease?

• An autoimmune disorder triggered by gluten (gliadin peptide).

• Causes villous atrophy in the small intestine, leading to malabsorption.

• Classic features: chronic diarrhea, bloating, weight loss, anemia, chronic fatigue.

Step 2: Why the correct option is “Colectomy”

• Celiac disease is managed with a lifelong gluten-free diet, not surgery.

• Colectomy (surgical removal of colon) is not a treatment and not associated with this disease.

• Surgery may be done for complications of IBD (Crohn’s, ulcerative colitis) — not celiac disease.

Step 3: Why the other options are correct (associated)

• Chronic fatigue ✅ → due to iron-deficiency anemia from malabsorption.

• Chronic diarrhea ✅ → classic GI symptom.

• Malabsorption ✅ → hallmark of celiac disease (due to villous atrophy).

• Bloating ✅ → common due to fermentation of undigested nutrients.

Quick memory aid

👉 Celiac disease = Malabsorption + Gluten trigger + Lifelong diet therapy
👉 Surgery = NOT a part of management

Step 1: What is Gastroparesis?

• Gastroparesis = delayed gastric emptying without mechanical obstruction.

• Caused by impaired motility of the stomach (often due to autonomic neuropathy in diabetes, vagus nerve injury, or idiopathic).

• Symptoms: nausea, vomiting, bloating, early satiety, fluctuating glucose levels in diabetics.
  👉 This is the classic condition of impaired GI motility.

Step 2: Why the other options are wrong

• Celiac disease ❌

  • Autoimmune reaction to gluten → villous atrophy and malabsorption. Not primarily a motility disorder.

• Inflammatory bowel disease (IBD) ❌

  • Crohn’s/Ulcerative colitis → chronic inflammation, ulcers, strictures. Pathology is inflammation, not motility defect.

• Dumping syndrome ❌

  • Rapid emptying of stomach contents into small intestine after gastric surgery. This is too rapid emptying, not impaired/delayed motility.

• None of these ❌

  • Incorrect, because Gastroparesis is the correct option.

Clinical pearl

• Gastroparesis = delayed motility.

• Dumping syndrome = excessively rapid transit.

Step 1: What is Achalasia?

• Achalasia is an esophageal motility disorder.

• The lower esophageal sphincter (LES) fails to relax due to loss of inhibitory ganglion cells (Auerbach’s/myenteric plexus).

• Leads to:

  • Functional obstruction at LES

  • Progressive dysphagia (solids & liquids)

  • “Bird-beak” appearance on barium swallow.

Step 2: Why the other options are wrong

• Ulcerative colitis ❌ → Affects colon/rectum; no LES involvement.

• Duodenal atresia ❌ → Congenital obstruction of duodenum; not related to LES.

• Crohn disease ❌ → Can affect any part of GIT but does not cause LES defect.

• Hirschsprung disease ❌ → Congenital absence of ganglion cells in colon/rectum → failure of relaxation in anal sphincter, not LES.

Clinical pearl

👉 Both Achalasia and Hirschsprung disease involve loss of ganglion cells → defective relaxation.

• Achalasia = LES

• Hirschsprung = Anal sphincter

Step 1: Peptic ulcer basics

• Peptic ulcers are breaks in the mucosa of the stomach or duodenum caused by acid and pepsin injury.

• Complications occur if ulcers erode deeply into surrounding tissues.

Step 2: Most common complication = Hemorrhage

• Hemorrhage is the most frequent complication, occurring in about 15–20% of patients with peptic ulcer disease.

• Mechanism: ulcer erodes into a blood vessel (e.g., gastroduodenal artery).

• Clinical signs: hematemesis (vomiting blood), melena (black stools), or anemia.

Step 3: Why the other options are wrong

• Perforation ❌

  • Serious complication but less common (~5–10%).

  • Causes peritonitis and acute abdomen.

• Diverticulum ❌

  • Not a complication of peptic ulcers; this is an outpouching of the gut wall (different pathology).

• Obstruction ❌

  • Results from chronic scarring/edema at the pylorus but is rare compared to bleeding.

• Gastric cancer ❌

  • Malignant transformation risk is associated with chronic gastric ulcers, but still far less common than bleeding.

Quick clinical pearl

👉 “Bleed first, perforate later” — hemorrhage is the most common, perforation is the most dangerous.

Step 1: About Hepatitis A virus (HAV)

• HAV is a non-enveloped, single-stranded, positive-sense RNA virus.

• It belongs to the Picornaviridae family, genus Hepatovirus.

• Transmission: fecal–oral route (contaminated food/water).

• It causes acute, self-limiting hepatitis with no chronic carrier state.

Step 2: Why the other options are wrong

• Coronaviruses ❌

  • Enveloped, +ssRNA, large genome. Cause SARS, MERS, COVID-19 — not hepatitis.

• Retroviruses ❌

  • +ssRNA viruses with reverse transcriptase (e.g., HIV). Not HAV.

• Reoviruses ❌

  • Double-stranded RNA viruses, e.g., Rotavirus (gastroenteritis). Not hepatitis.

• Flaviviruses ❌

  • Enveloped, +ssRNA. Includes Hepatitis C virus, Dengue, Yellow fever. Not HAV.

Quick Memory Aid

👉 “A is for Acute and A is for a tiny Picornavirus” (HAV is small, unlike the big enveloped flaviviruses and coronaviruses).

Step 1: What is celiac disease?

• Celiac disease is an autoimmune disorder triggered by ingestion of gluten (a protein in wheat, barley, rye).

• It causes immune-mediated damage to the small intestinal mucosa, particularly villous atrophy in the proximal small intestine.

• The only effective treatment is lifelong avoidance of gluten.

Step 2: Why the correct option is right

• Patients have to avoid gluten containing diet throughout the life ✅

  • True statement. Even small amounts of gluten can cause mucosal damage and symptoms to return.

  • Lifelong dietary restriction is essential for recovery of mucosa and prevention of complications (e.g., malabsorption, lymphoma).

Step 3: Why the other options are wrong

• Removal of lactose-containing products… ❌

  • Lactose intolerance may occur secondarily due to mucosal damage, but removing lactose alone does not treat celiac disease.

• Intestinal infection by anaerobes… ❌

  • Pathogenesis is autoimmune, not infectious. Triggered by gluten peptides (gliadin) in genetically predisposed individuals (HLA-DQ2/DQ8).

• Gluten is a carbohydrate ❌

  • Gluten is a protein, specifically a mixture of gliadins and glutenins.

• Lamina propria… foamy macrophages ❌

  • That describes Whipple’s disease (caused by Tropheryma whipplei), not celiac disease.

Quick memory aid

👉 Celiac = gluten protein sensitivity → lifelong gluten-free diet.
👉 Whipple’s = foamy macrophages in lamina propria.

• 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.

• 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.

• 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.

Correct Answer: Gastric acid reflux into the esophagus damages the mucosa ✅

Why this is correct:

• In GERD, gastric acid (and sometimes bile) refluxes into the distal esophagus.

• The normal squamous epithelium of the esophagus is not adapted to withstand acid → mucosal injury, inflammation, and ulceration → heartburn, regurgitation, dysphagia.

• With chronic exposure, the squamous epithelium is replaced by intestinal-type columnar epithelium with goblet cells (Barrett esophagus), as in this patient.

Why the Others Are Incorrect

• Gastric acid aids in neutralizing bile salts ❌ – Incorrect; bile salts may worsen mucosal injury, acid does not neutralize them.

• Gastric acid stimulates peristalsis ❌ – Acid secretion mainly aids digestion, not peristalsis.

• Gastric acid secretion is decreased in GERD ❌ – GERD is due to acid reflux, not decreased secretion.

• Gastric acid helps activate pepsinogen in the esophagus ❌ – True in the stomach, but in the esophagus this leads to additional mucosal injury, not a protective or normal mechanism.

Correct Answer: Chronic acid exposure resulting in intestinal metaplasia ✅

Why this is correct:

• Long-standing GERD causes Barrett esophagus: replacement of normal non-keratinized stratified squamous epithelium of the distal esophagus with non-ciliated columnar epithelium containing goblet cells (intestinal metaplasia). This is an adaptive change to chronic acid injury and carries a risk for dysplasia/adenocarcinoma.

Why the others are incorrect

• Chronic irritation leading to squamous metaplasia ❌ – Squamous metaplasia is the opposite direction (e.g., in bronchi of smokers). Here it’s squamous → columnar (intestinal).

• Conversion of columnar epithelium to squamous epithelium ❌ – Reverse of Barrett changes.

• Degeneration of esophageal squamous epithelium ❌ – Nonspecific injury term; doesn’t explain goblet cell–containing columnar replacement.

• Increased proliferation of esophageal squamous cells ❌ – Would thicken squamous mucosa, not produce intestinal-type columnar cells.

Correct Answer: Tonic contraction of the lower esophageal sphincter ✅

Why this is correct:

• The lower esophageal sphincter (LES) maintains a baseline tonic pressure higher than gastric pressure, which prevents gastric contents from refluxing into the esophagus. Brief transient LES relaxations (e.g., after meals) allow belching, but impaired LES tone predisposes to GERD and, over time, Barrett esophagus (as in this case).

Why the others are incorrect

• Contraction of the upper esophageal sphincter ❌ – Prevents air entry and reflux into the pharynx, not gastric-to-esophageal reflux.

• Increased production of bicarbonate by the stomach ❌ – Gastric bicarbonate is minimal and does not prevent reflux; protection is primarily via LES tone and esophageal clearance.

• Peristaltic movements of the esophagus ❌ – Help clear refluxed acid (secondary peristalsis) but do not prevent it.

• Secretion of protective mucus by the esophagus ❌ – Provides some mucosal protection, but doesn’t stop reflux from occurring.

Correct Answer: Obesity ✅

• Non-alcoholic fatty liver disease (NAFLD) is strongly associated with metabolic syndrome, and obesity is the primary risk factor.

• Mechanism:

  • Insulin resistance → ↑ lipolysis in adipose tissue → ↑ free fatty acid delivery to liver

  • Hepatic fat accumulation → steatosis → possible progression to non-alcoholic steatohepatitis (NASH) → fibrosis/cirrhosis.

Why the Others Are Incorrect

• Excessive alcohol consumption ❌ – That defines alcoholic fatty liver disease, not NAFLD.

• Viral hepatitis ❌ – Can cause chronic liver disease, but not NAFLD.

• Hemochromatosis ❌ – Iron overload disorder; separate etiology.

• Autoimmune liver disease ❌ – Causes autoimmune hepatitis, not fatty change due to metabolic risk.

Correct Answer: Alcohol abuse ✅

• In adults, the most common cause of chronic pancreatitis is long-term alcohol abuse.

• Alcohol causes:

  • Increased protein concentration in pancreatic secretions → plugs and ductal obstruction

  • Direct toxic effect on acinar cells

  • Repeated acute injury → chronic inflammation, fibrosis, and acinar loss

Why the Others Are Incorrect

• Gallstones ❌ – Leading cause of acute pancreatitis, not chronic.

• Cystic fibrosis ❌ – Major cause of chronic pancreatitis in children/young patients, not adults.

• Hyperlipidemia ❌ – Can precipitate acute pancreatitis, not the main cause of chronic disease.

• Autoimmune disorders ❌ – Cause autoimmune pancreatitis, but this is rare compared to alcohol.

Correct Answer: Direct hepatocyte damage by acetaldehyde, a toxic alcohol metabolite ✅

• In the early stages of alcoholic liver disease (fatty liver, alcoholic hepatitis), the key mechanism is the toxic effect of acetaldehyde, the primary metabolite of ethanol (via alcohol dehydrogenase).

• Acetaldehyde:

  • Binds to proteins → impairs function

  • Damages cell membranes

  • Promotes inflammation

  • Interferes with mitochondrial function → impaired fatty acid oxidation → hepatic steatosis

Why the Others Are Incorrect

• Increased oxidative stress leading to lipid peroxidation ❌ – Important in progression (alcoholic hepatitis, cirrhosis), but not the earliest step.

• Deposition of amyloid proteins ❌ – Seen in amyloidosis, not alcoholic liver disease.

• Iron overload ❌ – Characteristic of hemochromatosis, not alcohol-induced disease.

• Activation of stellate cells causing fibrosis ❌ – Central to cirrhosis (late stage), not early fatty liver changes.

Correct Answer: Enterotoxigenic E. coli (ETEC) ✅

• ETEC is the most common cause of traveler’s diarrhea, especially in people visiting developing countries.

• It produces heat-labile (LT) and heat-stable (ST) enterotoxins, which ↑ cAMP or cGMP → stimulate chloride and water secretion → watery diarrhea.

• Transmission: contaminated food and water.

Why the Others Are Incorrect

• EIEC ❌ – Invades colonic mucosa → dysentery-like illness (bloody diarrhea, fever), not classic traveler’s watery diarrhea.

• EPEC ❌ – Causes diarrhea in infants (especially in developing countries), not usually traveler’s diarrhea.

• EHEC (O157:H7) ❌ – Causes bloody diarrhea and can progress to HUS; not the main cause of traveler’s diarrhea.

• EAggEC ❌ – Causes persistent diarrhea in children and HIV patients; less commonly linked to traveler’s diarrhea.

Correct Answer: Hepatitis A virus ✅

• Key clues in the stem:

  • Teenager with acute onset of right upper quadrant pain, nausea, and dark urine → acute viral hepatitis.

  • Distaste for cigarettes → classic prodromal feature of acute hepatitis A.

  • History of travel to interior Sindh + cousin with same illness → suggests fecal–oral transmission, outbreak pattern.

• All these point strongly toward Hepatitis A (HAV).

Why the Others Are Incorrect

• Hepatitis B ❌ – Spread via blood/sexual/perinatal transmission, not typically by food/water outbreaks. Chronicity more common in young.

• Hepatitis C ❌ – Mainly via blood (IV drug use, transfusions), tends to be chronic, not outbreak-related.

• Hepatitis D ❌ – Needs HBV coinfection, not seen as isolated outbreak.

• Hepatitis E ❌ – Also fecal–oral and causes outbreaks, especially in Asia. But more severe in pregnant women; here, classic HAV clues (adolescents, travel, smoking aversion) fit better.

Correct Answer: No symptoms ✅

• Portal vein thrombosis (PVT) often develops silently.

• Many patients are asymptomatic, with the condition discovered incidentally on imaging.

• Symptoms, if present, usually come from portal hypertension (splenomegaly, varices, ascites), but these tend to develop later.

Why the Others Are Incorrect

• Ascites ❌ – Can occur in portal hypertension, but it is not the most common initial feature of PVT.

• Esophageal varices ❌ – May develop, but again usually after chronic portal hypertension, not in most early cases.

• Hepatomegaly ❌ – Not a hallmark; liver size is often preserved.

• Splenomegaly ❌ – Common in portal hypertension, but many patients with PVT are diagnosed before symptoms develop.

Correct Answer: Superior vena cava thrombosis ✅

• Circulatory disorders of the liver arise from impaired inflow (portal vein, hepatic artery) or outflow (hepatic veins, IVC).

• Superior vena cava (SVC) drains the head, neck, and upper extremities — it has no direct role in hepatic circulation.

• Thus, SVC thrombosis does not significantly affect liver circulation.

Why the Others Are Relevant

• Inferior vena cava thrombosis ❌ – Impedes hepatic venous outflow → hepatic congestion.

• Hepatic artery thrombosis ❌ – Cuts off arterial supply → ischemia/necrosis of liver.

• Hepatic vein thrombosis ❌ – Budd–Chiari syndrome; causes hepatic congestion and infarction.

• Portal vein thrombosis ❌ – Blocks main inflow to liver → portal hypertension, reduced perfusion.

Correct Answer: Autoimmune hepatitis ✅

• Key clues:

  • Fatigue + jaundice → suggests liver dysfunction.

  • Markedly raised AST & ALT → hepatocellular injury pattern.

  • High-titer ANA (antinuclear antibody) → autoimmune marker.

  • Positive anti–smooth muscle antibody → classic for autoimmune hepatitis.

  • (Antimitochondrial antibody is more typical for primary biliary cholangitis, but overlap can exist. In this case, the overall antibody pattern + high transaminases fits autoimmune hepatitis best.)

Why the Others Are Incorrect

• Hepatocellular carcinoma ❌ – Would show liver mass, raised AFP, often with cirrhosis background, not autoimmune antibodies.

• Cholestasis ❌ – Would show raised ALP & GGT rather than AST/ALT, plus pruritus and pale stools.

• Congenital abnormality ❌ – Typically presents earlier in life and not with autoimmune markers.

• Adenoma ❌ – Benign tumor linked with OCP use, not autoimmune antibodies or high transaminases.

Correct Answer: Urea breath test ✅

• Urea breath test detects active H. pylori infection.

• Principle: patient ingests urea labeled with ¹³C or ¹⁴C → H. pylori urease splits it → labeled CO₂ measured in breath.

• It’s non-invasive, highly sensitive and specific, and distinguishes active infection from past exposure.

• Thus, it’s widely used to confirm diagnosis and to check eradication.

Why the Others Are Incorrect

• Bacterial DNA detection by PCR in gastric biopsy ❌ – Very sensitive, but not standard due to cost, complexity, and variability.

• Fecal bacteria detection ❌ – Stool antigen tests are useful, but less accurate than urea breath test for confirmation.

• Rapid urease test ❌ – Invasive (requires endoscopy) and while good, its accuracy can be reduced by recent antibiotics/PPIs.

• Serologic test for antibodies ❌ – Cannot distinguish past exposure from current infection, so not reliable for confirmation.

Correct Answer: Volvulus ✅

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

• This leads to both luminal obstruction (food/stool/air can’t pass) and compromised blood supply (ischemia, infarction) very early in its course.

• Clinical presentation: abdominal pain, distension, vomiting, rapid progression to ischemia and necrosis.

Why the Others Are Incorrect

• Infarction ❌ – This is the end result of compromised blood supply, but obstruction is not necessarily an early feature.

• Intussusception ❌ – Causes obstruction and can compromise blood supply later if untreated, but vascular compromise is usually not immediate.

• Strictures ❌ – Cause obstruction, but vascular compromise is rare.

• Tumors ❌ – Can obstruct the lumen, but blood supply compromise is typically not seen early.

Correct Answer: Metaplastic gastric epithelium ✅

• Acute gastritis shows transient, reversible changes:

  • Edema and vascular congestion in lamina propria

  • Neutrophilic infiltrates (sometimes a few lymphocytes/plasma cells too)

  • Foveolar cell hyperplasia due to irritation/regeneration

• Metaplasia, however, is a chronic adaptive change (e.g., intestinal metaplasia in chronic gastritis) — not a feature of acute gastritis.

Why the Others Are Incorrect

• Few lymphocytes and plasma cells ❌ – May be present, though neutrophils dominate.

• Foveolar cell hyperplasia ❌ – Common in acute injury/regeneration.

• Moderate edema in lamina propria ❌ – Typical of acute gastritis.

• Slight vascular congestion ❌ – A hallmark of acute inflammation.

Correct Answer: Fibrosis and acinar cell loss ✅

• In chronic pancreatitis, the defining feature is progressive, irreversible fibrosis with acinar cell loss and distortion of pancreatic architecture.

• This scarring process is what separates it morphologically from acute forms.

Why the Others Are Incorrect

• Focal areas of fat necrosis ❌ – Seen in acute pancreatitis, due to lipase release digesting peripancreatic fat.

• Interstitial edema ❌ – Also typical of acute pancreatitis, an early feature.

• Mild inflammation ❌ – Present in both, but not a defining feature of chronic disease.

• Necrosis of acinar and ductal tissue ❌ – Seen in acute necrotizing pancreatitis, not chronic.

Correct Answer: Duct-centric mixed inflammatory cell infiltrate, and increased plasma cell ✅

• Autoimmune pancreatitis is a form of chronic pancreatitis caused by an immune-mediated process.

• Key microscopic findings:

  • Periductal (duct-centric) lymphoplasmacytic infiltrates

  • Abundant IgG4-positive plasma cells

  • Associated fibrosis (often storiform pattern)

• This distinguishes it from other forms of pancreatitis.

Why the Others Are Incorrect

• Dilated ducts with eosinophilic ductal concretions with increased neutrophils ❌ – This describes chronic obstructive pancreatitis (e.g., stone-related), not autoimmune.

• Extensive fibrosis and atrophy ❌ – Seen in end-stage chronic pancreatitis, not specific for autoimmune type.

• Extensive hemorrhage within the substance of the gland ❌ – Describes acute hemorrhagic pancreatitis, not autoimmune.

• Necrosis of acinar and ductal tissues ❌ – Seen in acute necrotizing pancreatitis, not autoimmune.

Correct Answer: Esophageal atresia ✅

Clues in the question:

• Polyhydramnios in pregnancy → fetus cannot swallow amniotic fluid.

• Vomits all feedings immediately → esophagus not continuous with stomach.

• Respiratory difficulty + fever → aspiration pneumonia due to reflux of secretions/feeds into the lungs (common with TEF – tracheoesophageal fistula).

• No stomach bubble on X-ray → classic for esophageal atresia without distal tracheoesophageal fistula (if there were a fistula to the distal esophagus, air would enter the stomach → stomach bubble seen).

Why the Others Are Incorrect

• Achalasia ❌ – A motility disorder with failure of LES relaxation; presents in young adults with dysphagia, not in neonates with polyhydramnios and absent stomach bubble.

• Diaphragmatic hernia ❌ – Causes bowel loops in thorax, mediastinal shift, small lungs; but here lungs and heart are normal, no stomach bubble instead.

• Hiatal hernia ❌ – Stomach herniates into thorax; would show a gastric bubble in chest, not absence of stomach bubble.

• Pyloric stenosis ❌ – Presents at 2–6 weeks of age with projectile nonbilious vomiting and visible peristalsis, but stomach bubble is present and polyhydramnios is not a feature.

🔎 Step 1: Clinical background

A tracheoesophageal fistula (TEF) is a congenital anomaly where there’s an abnormal connection between the trachea and esophagus.

• Common presentation in neonates: excessive salivation, coughing, choking, cyanosis during feeding, aspiration, and vomiting.

• Often associated with polyhydramnios in utero (because the fetus cannot swallow amniotic fluid properly).

✅ Correct Answer: Esophageal atresia with distal TEF

• This is the most common type (~85–90% of cases).

• In this type, the upper esophagus ends in a blind pouch, while the lower esophagus connects abnormally to the trachea.

• Clinical findings:

  • Infant chokes and coughs with feeds (milk enters the trachea via the distal fistula).

  • Stomach and intestines still contain air (since the trachea communicates with the distal esophagus).

❌ Why the Other Options Are Incorrect

• Esophageal atresia with proximal TEF → Very rare; air cannot reach the stomach, so abdomen is scaphoid.

• Esophageal atresia with double TEF → Extremely rare; both proximal and distal ends communicate with trachea.

• Pure esophageal atresia → Both ends blind; no fistula. Stomach is gasless.

• Isolated TEF (H-type) → Esophagus intact but abnormal connection to trachea. Less common; presents later with recurrent aspiration and pneumonia rather than neonatal distress.

🔎 Step 1: Clinical Clues

• Age: 1-day-old newborn

• Symptom: Bilious vomiting (means obstruction is distal to the ampulla of Vater)

• History: Polyhydramnios in pregnancy → suggests GI obstruction in utero (fetus can’t swallow amniotic fluid properly).

• X-ray: “Double bubble” sign = dilated stomach + dilated proximal duodenum with no distal gas.

✅ Correct Answer: Duodenal atresia

• Caused by failure of recanalization of the duodenum during embryogenesis.

• Presents with:

  • Bilious vomiting within first day of life

  • Polyhydramnios (because fetus can’t absorb swallowed amniotic fluid)

  • Double bubble sign on X-ray (classic finding).

❌ Why the Other Options Are Incorrect

• Midgut volvulus → Can also cause bilious vomiting, but X-ray usually shows a “bird-beak” obstruction or abnormal gas patterns, not the classic double bubble.

• Pyloric stenosis → Causes non-bilious projectile vomiting at 2–6 weeks of age, not on day 1.

• Imperforate anus → Causes failure to pass meconium and abdominal distension, but not a double bubble appearance.

• Esophageal atresia → Causes excessive drooling, choking, and inability to swallow; not bilious vomiting or double bubble.

🔎 Step 1: Understanding the Clinical Clue

• A newborn failing to pass meconium within the first 24 hours is a red flag.

• Normally, most infants pass meconium in the first 12–24 hours. Delay suggests an obstructive or motility disorder of the distal bowel.

✅ Correct Answer: Hirschsprung disease

• Hirschsprung disease (congenital aganglionic megacolon) is caused by the failure of neural crest cells to migrate into the distal colon → absence of ganglion cells (Auerbach and Meissner plexuses).

• This leads to lack of peristalsis in the affected segment → functional obstruction.

• Classic presentation: failure to pass meconium within 24–48 hours, abdominal distension, bilious vomiting.

❌ Why the Other Options Are Incorrect

• Intestinal malrotation → Presents with volvulus, bilious vomiting, abdominal distension, but not classically with failure to pass meconium.

• Tracheoesophageal fistula → Manifests with excessive salivation, choking, coughing, and cyanosis during feeds, not delayed meconium passage.

• Esophageal atresia → Causes inability to swallow, drooling, and aspiration, but meconium passage is unaffected.

• Duodenal atresia → Presents with bilious vomiting and the “double bubble sign” on X-ray, but infants can still usually pass meconium since obstruction is proximal.

• Crohn’s disease is characterized by skip lesions → patchy, discontinuous areas of inflammation separated by normal mucosa.

• In contrast, ulcerative colitis (UC) always has continuous inflammation, beginning in the rectum and extending proximally.

• This discontinuous nature is one of the strongest histologic and endoscopic clues for Crohn’s disease.

Why the Other Options Are Wrong ❌

Pseudopolyps

• Seen more commonly in ulcerative colitis, not Crohn’s.

• They result from regeneration of inflamed mucosa.

Exclusiveness of rectum

• UC always involves rectum (proctitis → pancolitis).

• Crohn’s often spares rectum or may be patchy there.

Mucosal atrophy

• Seen in ulcerative colitis due to chronic mucosal damage.

• Crohn’s involves transmural inflammation, not just mucosal atrophy.

Inflammation

• Both UC and Crohn’s involve inflammation — this finding does not distinguish between them.

Decrease in lysosomal degradation

• Lysosomal storage diseases (LSDs) are a group of inherited metabolic disorders caused by deficiencies of specific lysosomal enzymes.

• Because of these enzyme defects, lysosomes cannot degrade complex substrates such as sphingolipids, glycosaminoglycans, or glycoproteins.

• This leads to accumulation of undigested molecules inside lysosomes, producing cellular and tissue damage.

• Examples:

  • Tay–Sachs disease → deficiency of hexosaminidase A → accumulation of GM2 ganglioside.

  • Gaucher disease → deficiency of glucocerebrosidase → accumulation of glucocerebroside.

  • Pompe disease → deficiency of acid maltase → glycogen accumulation in lysosomes.

So the key underlying mechanism is a decrease (deficiency) in lysosomal degradation.

Why the Other Options Are Wrong ❌

Increase in peroxisomes

• Peroxisomes handle fatty acid oxidation (especially very-long chain fatty acids), not degradation of carbohydrates or sphingolipids.

• Peroxisomal disorders (e.g., Zellweger syndrome) are separate from lysosomal storage diseases.

Deficiency of carboxypolypeptidase

• This enzyme is a pancreatic exopeptidase involved in protein digestion in the gut.

• It has nothing to do with lysosomal degradation or storage disorders.

Increase in carboxypolypeptidase

• Even if levels increased, it wouldn’t affect lysosomal function.

• Again, irrelevant to the pathology of LSDs.

Increase in lysosomal degradation

• This would reduce buildup, not cause storage diseases.

• LSDs happen due to failure of degradation, not excessive degradation.

Increased ALP, GT and SGPT

• In biliary obstruction (cholestasis), the characteristic liver function test pattern is:

  • ↑ Alkaline phosphatase (ALP) → marker of cholestasis/biliary obstruction.

  • ↑ γ-Glutamyl transferase (GGT/GT) → rises with ALP in biliary obstruction, confirming hepatobiliary origin.

  • Mild ↑ in transaminases (ALT/SGPT, AST/SGOT) → usually less pronounced than ALP and GGT.

• This pattern (high ALP + high GGT) helps differentiate cholestasis from isolated bone disease (where ALP rises but GGT does not).

Why the Other Options Are Wrong ❌

Increased ALT and CK-BB

• ALT does rise in hepatocellular damage, but CK-BB is a marker of brain tissue damage, not relevant here.

Increased ALP and SGPT

• Partially correct, but GGT is also a classic cholestasis marker and is missing here.

Decreased ALT and CK-MB

• ALT doesn’t decrease; it increases with hepatocellular injury.

• CK-MB is a marker of cardiac muscle injury (MI), not liver.

Decreased alkaline phosphatase and SGOT

• Wrong — ALP rises, not decreases, in biliary obstruction.

• Pancreatic acinar cells secrete inactive zymogens (trypsinogen, chymotrypsinogen, procarboxypeptidase, etc.).

• Normally, trypsinogen is activated to trypsin by enterokinase (brush border enzyme in duodenum).

• Once formed, trypsin activates all other pancreatic zymogens.

• If trypsin were to get prematurely activated inside the pancreas, it would cause autodigestion → acute pancreatitis.

• To prevent this, pancreas secretes trypsin inhibitor proteins that block trypsin activity until it reaches the duodenum.

Why the Other Options Are Wrong ❌

Enterokinase

• Enzyme in duodenal mucosa that activates trypsinogen → trypsin.

• Its inhibition is not the protective mechanism inside the pancreas.

Lipoprotein lipase

• Involved in triglyceride metabolism (breaks down circulating lipoproteins).

• Not related to pancreatic enzyme activation.

Pepsinogen

• Secreted by gastric chief cells, activated to pepsin by stomach acid.

• No role in pancreatic secretion.

Phospholipase

• A pancreatic enzyme that requires trypsin activation.

• But the critical regulatory point is trypsin itself, not phospholipase.