GIT – 2022

🔎 Step 1: Glycolysis and Energy Regulation

• Glycolysis breaks down glucose to pyruvate, producing ATP.

• Several enzymes are key regulatory points, often called rate-limiting steps:

  1. Hexokinase / Glucokinase: Glucose → Glucose-6-phosphate

  2. Phosphofructokinase-1 (PFK-1): Fructose-6-phosphate → Fructose-1,6-bisphosphate

  3. Pyruvate kinase: Phosphoenolpyruvate → Pyruvate

• Regulation depends on energy status:

  • High ATP → inhibits glycolysis

  • Low ATP / high AMP → activates glycolysis

✅ Correct Answer: Phosphofructokinase (PFK-1)

• PFK-1 is the rate-limiting enzyme of glycolysis.

• Activated by low ATP / high AMP, ensuring glycolysis proceeds when the cell needs energy.

• Inhibited by high ATP and citrate.

❌ Why the Other Options Are Incorrect

• Isomerase (phosphoglucose isomerase) → Catalyzes a reversible step; not rate-limiting; not regulated by ATP.

• Pyruvate kinase → Final step enzyme; regulated by fructose-1,6-bisphosphate (feed-forward) and ATP, but PFK-1 is the main energy-sensing enzyme.

• Hexokinase → Catalyzes first step; inhibited by its product (G6P), not directly by ATP levels.

• Glucokinase → Liver isoform; not sensitive to ATP; regulated by glucose levels and glucokinase regulatory protein.

🔎 Step 1: Recall the Chemiosmotic Theory

• Proposed by Peter Mitchell, the chemiosmotic theory explains how ATP is generated in mitochondria during oxidative phosphorylation.

• Key points:

  • Electron transport through Complexes I–IV of the electron transport chain (ETC) pumps protons (H⁺) from the mitochondrial matrix into the intermembrane space.

  • This creates a proton gradient (electrochemical potential).

  • Protons flow back into the matrix via ATP synthase, driving the synthesis of ATP from ADP + Pi.

✅ Correct Answer: Proton gradient

• The proton-motive force across the inner mitochondrial membrane is the central concept of chemiosmosis.

• Without the proton gradient, ATP synthase cannot generate ATP, regardless of the presence of electrons.

❌ Why the Other Options Are Incorrect

• Glycolysis → Generates ATP via substrate-level phosphorylation, not chemiosmosis.

• Beta-oxidation → Produces NADH and FADH2, which feed electrons into the ETC, but does not directly generate ATP via chemiosmosis.

• NADH+ transport → NADH donates electrons, but ATP is not generated simply by NADH transfer; it’s the proton gradient that drives ATP synthesis.

• Ca⁺ concentration → Calcium ions are not involved in ATP generation via chemiosmosis.

🔎 Step 1: Recall the Electron Transport Chain (ETC)

• The ETC is a series of protein complexes in the inner mitochondrial membrane that transfer electrons from reduced cofactors (NADH, FADH2) to oxygen, generating a proton gradient for ATP synthesis.

• Key complexes:

  1. Complex I: NADH–coenzyme Q reductase → accepts electrons from NADH

  2. Complex II: Succinate–coenzyme Q reductase → accepts electrons from FADH2

  3. Complex III: Coenzyme Q–cytochrome c reductase

  4. Complex IV: Cytochrome c oxidase → transfers electrons to O2

✅ Correct Answer: NADH–coenzyme Q reductase

• This is Complex I of the ETC.

• Function:

  • Accepts a pair of electrons from NADH

  • Transfers them to coenzyme Q (ubiquinone)

  • Pumps protons into the intermembrane space to help generate the proton gradient

❌ Why the Other Options Are Incorrect

• Cytochrome c oxidase (Complex IV) → Accepts electrons from cytochrome c, reduces O2 to water; does not directly accept electrons from NADH.

• Succinate–coenzyme Q reductase (Complex II) → Accepts electrons from FADH2 (from succinate), not NADH.

• Coenzyme Q–cytochrome c reductase (Complex III) → Accepts electrons from reduced coenzyme Q, not directly from NADH.

🔎 Step 1: Interpreting the Clinical Picture

• Patient: 40-year-old man

• Symptoms: Fever (102°F), abdominal pain, diarrhea, pale skin

• Laboratory finding: Elevated liver enzymes

This presentation suggests hepatocellular injury likely due to infectious hepatitis or another acute liver insult.

🔎 Step 2: Liver Enzymes

Key liver enzymes and their significance:

• Alanine aminotransferase (ALT) → Found predominantly in hepatocytes; highly specific for liver injury.

• Aspartate aminotransferase (AST) → Found in liver, heart, muscle, kidney, RBCs; less liver-specific.

• Lactate dehydrogenase (LDH) → Found in many tissues; elevated in hemolysis, tissue injury.

• Creatine kinase (CK) → Muscle enzyme; not specific for liver.

• Glutamate kinase → Not a standard liver function test; likely a distractor.

✅ Correct Answer: Alanine aminotransferase (ALT)

• ALT is the most specific marker of hepatocellular damage.

• In hepatitis (viral, bacterial, or toxic), ALT rises markedly, often more than AST.

• Other clinical clues (fever, abdominal pain, diarrhea, pale skin) support an infectious process affecting the liver.

❌ Why the Other Options Are Incorrect

• Lactate carboxylase → Likely intended as lactate dehydrogenase (LDH); nonspecific, elevated in many tissues.

• Glutamate kinase → Not a standard liver enzyme.

• Creatinine kinase (CK) → Muscle-specific; not liver-specific.

• Aspartate dehydrogenase → Likely intended as AST; less liver-specific than ALT.

🔎 Step 1: Understanding Gluconeogenesis vs Glycolysis

• Glycolysis: Breakdown of glucose to pyruvate; certain steps are irreversible.

• Gluconeogenesis: Synthesis of glucose from non-carbohydrate precursors; bypasses irreversible glycolytic steps using specific enzymes.

Key irreversible glycolytic steps and their gluconeogenic bypasses:

Other steps are reversible and shared between glycolysis and gluconeogenesis.

✅ Correct Answer: Conversion of pyruvate to phosphoenolpyruvate

• This reaction is unique to gluconeogenesis and bypasses the irreversible glycolytic step catalyzed by pyruvate kinase.

• It occurs via two enzymes:

  1. Pyruvate carboxylase: Pyruvate → Oxaloacetate (OAA)

  2. PEP carboxykinase: OAA → Phosphoenolpyruvate (PEP)

• This step does not occur in glycolysis, which goes in the opposite direction (PEP → pyruvate).

❌ Why the Other Options Are Incorrect

• Fructose-6-phosphate → Fructose-1,6-bisphosphate → Glycolysis step, not unique to gluconeogenesis.

• Dihydroxyacetone → Glyceraldehyde-3-phosphate → Reversible; occurs in both glycolysis and gluconeogenesis.

• Fumarate → Malate → Part of TCA cycle, not a gluconeogenic-specific reaction.

• Glucose → Glucose-6-phosphate → Glycolysis step, not unique to gluconeogenesis.

🔎 Step 1: Background

The gastrointestinal (GI) tract exhibits different patterns of electrical and motor activity depending on whether the person is fed or fasting:

• Fed state:

  • Segmentation → mixes food and enhances absorption

  • Peristalsis → moves chyme along the gut

• Fasting state:

  • The stomach and small intestine are mostly empty, but the gut is not silent.

  • It exhibits a cyclical pattern of electrical and motor activity called the migratory motor complex (MMC).

  • MMC clears residual food, secretions, and bacteria from the stomach and small intestine.

✅ Correct Answer: Migratory motility complex

• MMC occurs every 90–120 minutes during fasting.

• It has three phases:

  1. Quiescent period (minimal contractions)

  2. Intermittent contractions

  3. Intense, regular contractions sweeping from the stomach to the ileum

❌ Why the Other Options Are Incorrect

• Segmentation → Occurs during the fed state to mix chyme and enhance absorption.

• Peristalsis → Continuous, but the strong peristaltic waves are primarily postprandial (after eating).

• Slow wave complex / Basic electrical rhythm → These are the electrical oscillations of the smooth muscle (pacemaker activity), but on their own they do not constitute a motor pattern that sweeps contents.

🔎 Step 1: Understanding Sugar Absorption

• Monosaccharides absorbed in the small intestine include glucose, galactose, and fructose.

• Their transport mechanisms differ:

  • Glucose and galactose: Active transport via SGLT1 (sodium-dependent)

  • Fructose: Facilitated diffusion via GLUT5

• Once inside the enterocyte, all three sugars can exit the basolateral membrane via GLUT2 into the blood.

✅ Correct Answer: GLUT5

• GLUT5 is a facilitated diffusion transporter specific for fructose, located on the apical membrane of enterocytes.

• Fructose uptake does not require sodium or active transport.

❌ Why the Other Options Are Incorrect

• GLUT4 → Insulin-dependent glucose transporter in muscle and adipose tissue, not intestinal epithelium.

• SGLT1 → Sodium-dependent transporter for glucose and galactose, not fructose.

• SGLT2 → Sodium-dependent glucose transporter in the renal proximal tubule, not intestine.

• GLUT2 → Basolateral transporter in enterocytes; transports glucose, galactose, and fructose out of the cell, not into the cell from the lumen.

🔎 Step 1: Role of Hepcidin

• Hepcidin is a peptide hormone produced by the liver.

• It is the key regulator of systemic iron homeostasis.

• Mechanism:

  • Hepcidin binds to ferroportin, the iron-export protein on enterocytes, macrophages, and hepatocytes.

  • This causes internalization and degradation of ferroportin, blocking iron release into the blood.

  • Result: Decreased dietary iron absorption and reduced iron mobilization from stores.

✅ Correct Answer: Iron

• By preventing iron absorption, hepcidin prevents iron overload in the blood.

• Hepcidin levels increase in inflammation, infection, and high iron stores.

❌ Why the Other Options Are Incorrect

• Vitamin B12 → Absorbed via intrinsic factor in the ileum; hepcidin has no role.

• Folate → Absorbed in the jejunum; not regulated by hepcidin.

• Magnesium → Absorbed passively in small intestine; not affected by hepcidin.

• Copper → Absorbed in the small intestine; regulated by other transporters, not hepcidin.

🔎 Step 1: Regulation of Gastric Acid Secretion

Parietal cells secrete HCl under stimulation from:

• Histamine (H2 receptors) → ↑ cAMP → ↑ H⁺ secretion

• Acetylcholine (M3 receptors) → ↑ intracellular Ca²⁺ → ↑ H⁺ secretion

• Gastrin (CCK-B receptors) → ↑ intracellular Ca²⁺ → ↑ H⁺ secretion

Inhibitors of acid secretion act either directly on parietal cells or indirectly via other pathways.

✅ Correct Answer: Prostaglandin E

• Prostaglandin E (PGE2) acts directly on parietal cells to inhibit adenylate cyclase, decreasing cAMP, which reduces H⁺ secretion.

• It also stimulates mucus and bicarbonate secretion, protecting the gastric mucosa.

❌ Why the Other Options Are Incorrect

• Histamine → Strong stimulant via H2 receptors; increases acid secretion.

• Acetylcholine → Stimulates parietal cells via M3 receptors; increases acid.

• Gastrin → Stimulates parietal cells directly and indirectly (via histamine release).

• Epinephrine → Mainly acts on blood vessels; has minimal direct effect on parietal cells for acid secretion.

🔎 Step 1: Understanding Gastric Acid Secretion

Gastric acid (HCl) secretion from parietal cells is controlled by three main stimulatory pathways:

1. Histamine (H2 receptors) → Activates adenylate cyclase → ↑ cAMP → stimulates H⁺/K⁺ ATPase

2. Acetylcholine (M3 muscarinic receptors) → Via vagus nerve → ↑ intracellular Ca²⁺ → stimulates H⁺/K⁺ ATPase

3. Gastrin (CCK-B receptors) → ↑ intracellular Ca²⁺ → stimulates H⁺/K⁺ ATPase

Importantly, maximal acid secretion occurs when all three pathways act together. Individually, each pathway produces less than the maximal response.

✅ Correct Answer: Cholinergic receptor stimulation

• Stimulation of cholinergic (M3) receptors mimics vagal stimulation, which:

  • Directly stimulates parietal cells

  • Indirectly stimulates G cells to release gastrin

  • Enhances histamine release from enterochromaffin-like cells

• This combined effect produces maximum gastric acid secretion.

❌ Why the Other Options Are Incorrect

• H2 receptor stimulation → Increases acid via cAMP, but alone produces less than maximal secretion.

• Neurogenic stimulation → General nerve activity is less specific; maximal effect requires targeted cholinergic pathways.

• Inhibition of acetylcholine release → Decreases acid secretion, not increase.

• Na/K ATPase pump stimulation → Parietal cells require H⁺/K⁺ ATPase for acid secretion; stimulating Na/K pump alone is insufficient for maximal HCl output.

🔎 Step 1: Recall the physiology of gastrin

• Source: G cells in the antrum of the stomach.

• Main actions: Stimulates gastric acid (HCl) secretion from parietal cells, and promotes gastric mucosal growth and motility.

• Regulation:

  • Stimulated by: products of protein digestion (especially peptides and amino acids), gastric distension, vagal stimulation (via GRP – gastrin-releasing peptide).

  • Inhibited by: low pH (acid), somatostatin, secretin, GIP, VIP.

✅ Correct Answer: Products of protein digestion

• Peptides and amino acids are the strongest natural stimuli for gastrin release because they signal the stomach that food (protein) has arrived and more acid is needed for digestion.

❌ Why the Other Options Are Incorrect

• Low pH of gastric juice → Inhibits gastrin release (negative feedback to prevent excessive acidity).

• Vasoactive intestinal peptide (VIP) → Inhibits gastric acid secretion; it promotes intestinal secretion instead.

• Somatostatin → Potent inhibitor of gastrin secretion.

• Gastric inhibitory peptide (GIP) → Inhibits gastric acid secretion; stimulates insulin release.

🔎 Step 1: General role of parasympathetic system

• The parasympathetic nervous system (PNS) is the “rest and digest” system.

• In the gastrointestinal tract, its stimulation (via vagus nerve and pelvic splanchnics) generally:

  • Increases motility (smooth muscle contraction, peristalsis).

  • Relaxes sphincters (to allow food passage).

  • Increases glandular secretion (saliva, gastric, pancreatic, intestinal).

✅ Correct Answer: Increase in motility and tone

• Parasympathetic stimulation enhances peristalsis and increases tone of the gut wall, promoting movement of food.

❌ Why the Other Options Are Incorrect

• Increase in absorption of nutrients → Absorption is not directly under parasympathetic control; it depends on digestive/transport processes.

• Inhibition of secretion from the stomach → Opposite is true; PNS stimulates gastric secretion (via vagus).

• Inhibition of intestinal secretions → Wrong, because PNS actually stimulates intestinal secretions.

• Contraction of sphincters → Parasympathetic stimulation causes sphincter relaxation, not contraction.

🔎 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.

🔎 Step 1: Background

The pancreas develops from two buds arising from the endodermal foregut:

• Dorsal pancreatic bud → Appears first, gives rise to the majority of the pancreas.

• Ventral pancreatic bud → Later rotates dorsally, fuses with the dorsal bud, and contributes to specific parts.

✅ Derivatives of the Dorsal Pancreatic Bud

• Neck

• Body

• Tail

• Most of the head (upper part)

✅ Derivatives of the Ventral Pancreatic Bud

• Lower part of the head

• Uncinate process

• Major contribution to the main pancreatic duct (duct of Wirsung)

❌ Correct Answer (Incorrect Option): Entire main pancreatic duct

• The main pancreatic duct is formed mostly from the ventral duct and only partly from the distal portion of the dorsal duct.

• So, saying the dorsal bud gives rise to the “entire” main pancreatic duct is incorrect.

🔎 Step 1: Understanding the Question

The hepatic bud (also called the liver diverticulum) develops from the endoderm of the foregut. The key is to remember which structures in the liver come from endoderm (the hepatic bud itself) and which come from mesoderm.

✅ Correct Answer: Parenchyma of liver

• The parenchyma of the liver (hepatocytes and bile duct epithelium) develops from the endodermal cells of the hepatic bud.

• These endodermal cells proliferate into the septum transversum mesenchyme and form the bulk of the functional tissue of the liver.

❌ Why the Other Options Are Incorrect

• Hepatic sinusoids → Derived from the vitelline veins and umbilical veins, i.e., mesodermal in origin.

• Hemopoietic cells → Derived from mesoderm of the septum transversum, not from the hepatic bud.

• Stroma of liver (connective tissue framework) → Mesodermal origin.

• Kupffer cells (specialized macrophages) → Derived from mesoderm (monocyte lineage), not from the endodermal hepatic bud.

🔎 Step 1: Understanding the Question

We’re looking at a histological section with these features:

• Compound tubulo-acinar serous gland

• Secretory units made of pyramidal serous cells

• Pale, low cuboidal epithelial cells present inside acini

• Scattered spherical clusters within the tissue

These clues together are pointing toward one very specific organ.

✅ Correct Answer: Pancreas

The pancreas is a compound tubulo-acinar gland made entirely of serous acini, where pyramidal serous cells produce digestive enzymes. A unique hallmark is the presence of centroacinar cells, which are pale, low cuboidal cells seen within the acini — these are not found in salivary glands. Additionally, the pancreas contains islets of Langerhans, which appear as scattered spherical clusters and represent the endocrine component. No other gland combines these three features.

❌ Why the Other Options Are Incorrect

The submandibular gland is a mixed gland, containing both mucous and serous acini, with serous demilunes but no centroacinar cells or islets.

The sublingual gland is predominantly mucous, with some serous demilunes, but again, lacks centroacinar cells and islets.

The parotid gland is entirely serous, similar in some ways to the pancreas, but it does not have centroacinar cells or endocrine islets.

The duodenum is not a gland of this type at all; it shows villi and Brunner’s glands in the submucosa, not acinar structures with endocrine cell clusters.

Step 1: Recall what hypertrophic/ectopic pancreatic tissue is

Ectopic or heterotopic pancreas refers to pancreatic tissue located outside its normal anatomical position, without a direct connection to the pancreas itself.

Key points:

• It may contain acini, ducts, and islet cells, like the normal pancreas.

• Commonly detected in areas of the gastrointestinal tract during surgery or autopsy.

• It can sometimes lead to obstruction, bleeding, or inflammation if it becomes hypertrophic or symptomatic.

Embryological basis:

• During gut development, pancreatic tissue can abnormally migrate or persist in remnants of the foregut or midgut.

• Sites where this occurs often reflect areas embryologically or anatomically close to the developing pancreas.

Step 2: Analyze each option

• Anal canal ❌

  • Ectopic pancreatic tissue is extremely rare here. The anal canal develops from the hindgut/ectoderm, far from the pancreas’s embryologic origin.

• Jejunum ❌ (less common)

  • While small intestine can occasionally harbor ectopic pancreas, the proximal small intestine (duodenum) is more common than jejunum. Among the options, Meckel’s diverticulum is more classical.

• Rectum ❌

  • Rectum arises from the hindgut and is an unusual site for pancreatic heterotopia.

• Mouth ❌

  • No pancreatic tissue develops in the oral cavity; this is ectoderm-derived.

• Meckel’s diverticulum ✅

  • Correct.

  • Meckel’s diverticulum is a remnant of the vitelline (omphalomesenteric) duct.

  • It can contain ectopic gastric or pancreatic tissue, sometimes hypertrophic.

  • This is clinically significant because it can cause ulceration, bleeding, or obstruction.

  • Embryologically, the midgut origin of Meckel’s diverticulum is near the pancreatic bud, which explains the possibility of ectopic pancreatic tissue.

Step 3: Correct Answer

Meckel’s diverticulum

Step 1: Recall the types of splanchnic nerves

Splanchnic nerves are visceral nerves that carry autonomic fibers to abdominal and pelvic organs.

1. Thoracic, lumbar, and sacral splanchnic nerves

   • Mostly sympathetic

   • Carry preganglionic sympathetic fibers to prevertebral ganglia

   • Originate from sympathetic trunks

2. Pelvic splanchnic nerves (S2–S4)

   • Unique among splanchnic nerves

   • Preganglionic parasympathetic fibers

   • Arise from ventral primary rami of S2–S4

   • Contribute to the inferior hypogastric (pelvic) plexus

   • Provide parasympathetic innervation to pelvic organs and distal colon (sigmoid, rectum)

Key distinction:

• All other splanchnic nerves are sympathetic, whereas pelvic splanchnic nerves are parasympathetic.

Step 2: Analyze each option

• Derived from ventral primary rami of L2, L3, L4 ❌

  • These are lumbar splanchnic nerves, sympathetic.

• Provide postganglionic sympathetic innervation to the cecum ❌

  • Cecum receives sympathetic postganglionic fibers via thoracic/lumbar splanchnic nerves, not pelvic splanchnics.

• Convey preganglionic parasympathetic fibers to the inferior hypogastric plexus ✅

  • Correct. This is the unique feature of pelvic splanchnic nerves.

• Derived from the sympathetic trunks ❌

  • True for other splanchnic nerves, not pelvic splanchnic nerves.

• Convey postganglionic parasympathetic innervation to the ascending colon ❌

  • Pelvic splanchnics supply distal colon (sigmoid, rectum), not ascending colon.

Step 3: Correct Answer

Convey preganglionic parasympathetic fibers to the inferior hypogastric plexus

Step 1: Recall the anatomy and pathophysiology

Caput medusae is the appearance of dilated veins radiating from the umbilicus, seen in portal hypertension.

• The portal vein carries blood from the GI tract and spleen to the liver.

• In portal hypertension, blood finds collateral pathways to bypass the liver.

• One important portal-systemic collateral pathway involves:

  • Para-umbilical veins (small veins in the ligamentum teres of the liver, connecting the portal vein to the superficial epigastric veins of the anterior abdominal wall).

Key principle:

• When para-umbilical veins dilate, they cause tortuous veins around the umbilicus—caput medusae.

Step 2: Analyze each option

• Para-umbilical vein ✅

  • Correct. Direct connection between portal vein and superficial abdominal veins; dilation produces caput medusae.

• Splenic vein ❌

  • Part of portal system, but does not directly cause visible abdominal wall veins.

• Pancreatic vein ❌

  • Tributary of portal system; not involved in abdominal wall collaterals.

• Cystic vein ❌

  • Drains gallbladder; not involved in caput medusae.

• Proper hepatic vein ❌

  • Drains liver into inferior vena cava; not part of portal-systemic collateral pathway.

Step 3: Correct Answer

Para-umbilical vein

Step 1: Recall abdominal wall fossae

The anterior abdominal wall has peritoneal fossae (depressions) in the inguinal region, important for hernias:

1. Lateral inguinal fossa

   • Lateral to the inferior epigastric vessels.

   • Site of indirect inguinal hernias (congenital, through deep inguinal ring).

2. Medial inguinal fossa (Hesselbach’s triangle)

   • Medial to inferior epigastric vessels, bounded by:

     • Lateral: inferior epigastric vessels

     • Medial: lateral border of rectus abdominis

     • Inferior: inguinal ligament

   • Site of direct inguinal hernias (acquired, due to weakness in the posterior wall).

3. Supravesical fossa

   • Between median and medial umbilical folds.

   • Site of supravesical hernias.

4. Iliac fossa

   • Region overlying iliacus; not related to inguinal hernias.

5. Ischiorectal fossa

   • Perineal fossa around anal canal; unrelated to inguinal hernias.

Step 2: Analyze each option

• Lateral inguinal fossa ❌

  • Site of indirect hernias, not direct hernias.

• Medial inguinal fossa ✅

  • Correct. Site of direct inguinal hernias, through Hesselbach’s triangle.

• Supravesical fossa ❌

  • Can develop supravesical hernias, not inguinal.

• Iliac fossa ❌

  • Not a hernia site.

• Ischiorectal fossa ❌

  • Perineal region, unrelated.

Step 3: Correct Answer

Medial inguinal fossa

Step 1: Recall the anatomy of the inguinal region

• The inguinal ligament is formed by the inferior border of the external oblique aponeurosis, running from anterior superior iliac spine (ASIS) to pubic tubercle.

• There are several associated structures:

  • Reflected inguinal ligament – arises from the lateral part of the inguinal ligament, curves medially and upward, inserting into the linea alba.

• Key principle:

  • The reflected inguinal ligament is formed by fibers of the contralateral external oblique aponeurosis.

  • It reinforces the anterior wall of the inguinal canal medially and helps prevent hernias.

Step 2: Analyze each option

• Transversus abdominis ❌

  • Contributes to conjoint tendon, not the reflected ligament.

• Rectus abdominis ❌

  • Vertical midline muscle, does not contribute aponeurotic fibers to the reflected ligament.

• External abdominal oblique ✅

  • Correct. The contralateral external oblique aponeurosis contributes fibers to the reflected inguinal ligament.

• Internal abdominal oblique ❌

  • Forms conjoint tendon with transversus abdominis, not reflected ligament.

• Pyramidalis ❌

  • Small triangular muscle, anterior to rectus abdominis; not involved.

Step 3: Correct Answer

External abdominal oblique

Step 1: Recall the reflex involved

• The reflex described is the cremasteric reflex.

• Afferent limb: sensory fibers from genital branch of the femoral branch of the genitofemoral nerve and femoral branch of the genitofemoral/ilioinguinal nerves, triggered by stroking the medial thigh.

• Efferent limb: motor fibers to the cremaster muscle, causing elevation of the testis.

Key principle:

• The cremaster muscle is a thin muscle that arises from lower fibers of the internal oblique and some fibers of the transversus abdominis, forming a sling around the spermatic cord.

• Contraction of the cremaster pulls the testis upward into the scrotum.

Step 2: Analyze each option

• Rectus abdominis ❌

  • Vertical abdominal wall muscle; does not elevate the testis.

• Transversus abdominis ❌

  • Contributes fibers to cremaster but not the main contracting muscle responsible for the reflex.

• Pyramidalis ❌

  • Small muscle anterior to rectus, not involved in testicular movement.

• External oblique ❌

  • Contributes to spermatic cord formation via external spermatic fascia, but not responsible for reflex contraction.

• Cremaster ✅

  • The primary muscle responsible for the cremasteric reflex.

  • Contraction elevates the testis in response to medial thigh stimulation.

Step 3: Correct Answer

Cremaster

Step 1: Recall rectus abdominis anatomy

• Rectus abdominis is a paired, long, vertical muscle of the anterior abdominal wall.

• Originates from the pubic crest and symphysis and inserts into the xiphoid process and costal cartilages of ribs 5–7.

• Function: flexes the vertebral column, compresses abdominal contents, stabilizes pelvis.

Innervation:

• Innervated by the thoracoabdominal nerves, which are the anterior rami of T7–T11, and the subcostal nerve (T12).

• These nerves run between internal oblique and transversus abdominis, then enter rectus sheath to innervate rectus abdominis.

Key principle:

• Rectus abdominis receives segmental motor innervation from T7–T12, sometimes including T5–T12 depending on the source.

• Clinically, textbooks often mention T5–T12 as the range.

Step 2: Analyze each option

• T5 to T12 ✅

  • Correct. Matches classic description of thoracoabdominal and subcostal nerves innervating rectus abdominis.

• T3 to T7 ❌

  • Too high; nerves above T5 mainly supply pectoral region, upper thorax, or upper abdominal wall muscles above umbilicus, not the whole rectus.

• T2 to T7 ❌

  • T2–T4 supply intercostal muscles and upper chest; T5–T7 may contribute to upper rectus, but lower rectus is not covered.

• T3 to T11 ❌

  • Lower T12 (subcostal nerve) is missing, so incomplete for full rectus coverage.

• T1 to T5 ❌

  • T1–T5 mostly innervates upper thoracic muscles; does not reach the rectus abdominis.

Step 3: Correct Answer

T5 to T12

Step 1: Recall lymphatic drainage of the stomach

The stomach has a rich network of lymph nodes that run along its arterial supply:

1. Superior (lesser curvature) gastric nodes – along left and right gastric arteries.

2. Inferior (greater curvature) gastric nodes – along left and right gastroepiploic arteries (also called gastro-omental arteries).

3. Short gastric nodes – along the short gastric arteries supplying the fundus.

4. Pyloric nodes – along gastroduodenal artery, near pylorus.

5. Pancreatico-duodenal nodes – along pancreaticoduodenal arteries.

6. Pancreatico-splenic nodes – along the splenic artery, often near the tail of pancreas and fundus.

Key principle:

• Lymph nodes are named based on the artery they accompany.

• The short gastric arteries and left gastro-omental artery run along the fundus and greater curvature, so the corresponding lymph nodes are often called pancreatico-splenic nodes.

Step 2: Analyze each option

• Pyloric ❌

  • Along gastroduodenal artery, drains the distal stomach (pylorus).

• Inferior gastric ❌

  • Along right and left gastroepiploic arteries, mainly the greater curvature, not the short gastric arteries.

• Superior gastric ❌

  • Along left and right gastric arteries, lesser curvature.

• Pancreatico-duodenal ❌

  • Along pancreaticoduodenal arteries, near duodenum.

• Pancreatico-splenic ✅

  • Located along short gastric and left gastro-omental (gastroepiploic) arteries, near fundus and upper greater curvature.

  • Correct answer.

Step 3: Correct Answer

Pancreatico-splenic

Step 1: Recall gastric lymphatic drainage

The stomach has a rich lymphatic network that drains along its major arterial branches.

Main gastric lymph nodes:

1. Gastric (lesser curvature) nodes – along left and right gastric arteries

   • Receive lymph from the lesser curvature and parts of the body and fundus.

2. Gastroepiploic (greater curvature) nodes – along left and right gastroepiploic arteries

   • Receive lymph from the greater curvature.

3. Pyloric nodes – around the pylorus and along gastroduodenal artery

   • Drain the pylorus and distal stomach.

4. Celiac nodes – receive lymph from all gastric and pancreatic nodes, eventually draining into the thoracic duct.

Key principle:

• When the report says “enlarged gastric nodes”, it usually refers to nodes along the lesser curvature (proximal to celiac nodes).

• These nodes primarily drain the superior 2/3 of the stomach (body and fundus), especially along the lesser curvature.

Step 2: Analyze each option

• Superior 2/3rd of stomach ✅

  • Correct. Lymph from the body and fundus, especially along the lesser curvature, drains into the gastric nodes.

• Right 2/3rd of inferior 1/3rd of stomach ❌

  • This is the distal stomach/pyloric region, which drains mainly into pyloric nodes, not gastric nodes.

• Pylorus of stomach ❌

  • Drains into pyloric nodes, not directly into gastric nodes.

• Middle part of esophagus ❌

  • Drains into mediastinal nodes, unrelated to gastric nodes.

• Left 1/3rd of greater curvature ❌

  • Drains into gastroepiploic/short gastric nodes, not the gastric nodes along the lesser curvature.

Step 3: Correct Answer

Superior 2/3rd of stomach

Step 1: Recall stomach anatomy

The stomach has several main regions:

• Cardia – surrounds the esophageal opening.

• Fundus – the dome-shaped upper portion, usually filled with gas.

• Body – the central, largest portion of the stomach.

• Pyloric part – distal portion leading to the duodenum, divided into pyloric antrum and pyloric canal.

• Lesser curvature – the concave right border of the stomach.

Key principle:

• The incisura angularis is a small notch along the lesser curvature, near the junction of the body and pyloric part.

• It is more prominent when the stomach is empty and serves as a landmark separating the body from the pyloric region.

Step 2: Analyze each option

• Cardia and fundus ❌

  • These are proximal parts; the incisura angularis is distal, closer to the pylorus.

• Cardia and pyloric part of stomach ❌

  • Cardia is at the proximal end, pylorus is at the distal end. They are not adjacent.

• Body and pyloric part of stomach ✅

  • Correct. The incisura angularis lies along the lesser curvature, marking the transition from the body to the pyloric part.

• Fundus and pyloric part of stomach ❌

  • Fundus is proximal, pylorus is distal; they are far apart.

• Cardia and body ❌

  • The junction between cardia and body is higher up, near the gastroesophageal junction, not marked by the incisura angularis.

Step 3: Correct Answer

Body and pyloric part of stomach

Step 1: Recall the anatomy of the conjoint tendon

• The conjoint tendon (also called falx inguinalis) is a fusion of aponeurotic fibers from two abdominal muscles.

• It reinforces the posterior wall of the inguinal canal, particularly the medial part, which is prone to direct inguinal hernias.

• Its main role is to resist herniation.

Key principle:

• The tendon is formed by the lower fibers of the internal oblique and the transversus abdominis muscles.

• It inserts into the pubic crest and pectineal line, strengthening the inguinal floor.

Step 2: Analyze each option

• External oblique and internal oblique ❌

  • The external oblique aponeurosis forms the anterior wall of the inguinal canal, not the conjoint tendon.

• Internal oblique and transversus abdominis ✅

  • Correct. Both contribute aponeurotic fibers that fuse to form the conjoint tendon, reinforcing the posterior wall of the inguinal canal.

• External oblique and transversus abdominis ❌

  • External oblique does not contribute to the conjoint tendon.

• Internal oblique and rectus abdominis ❌

  • Rectus abdominis fibers do not fuse with internal oblique to form this tendon.

• External oblique and rectus abdominis ❌

  • Neither structure contributes to the conjoint tendon.

Step 3: Correct Answer

Internal oblique and transversus abdominis

Step 1: Recall the anatomy of the 2nd part of the duodenum

• The second part of the duodenum (descending part) is where many ducts from the liver and pancreas empty.

• Key structures:

  • Major duodenal papilla – receives the common bile duct and the main pancreatic duct (sometimes called the duct of Wirsung) via the Ampulla of Vater.

  • Minor duodenal papilla – receives the accessory pancreatic duct (duct of Santorini).

Key principle:

• The cystic duct, which drains the gallbladder, does not open directly into the duodenum. It joins the common hepatic duct to form the common bile duct, which then enters the duodenum.

Step 2: Analyze each option

• Ampulla of Vater – ✅ Forms the dilated opening of the common bile duct and main pancreatic duct into the duodenum. Opens in 2nd part of duodenum.

• Pancreatic duct – ✅ Main pancreatic duct drains into the duodenum through the Ampulla of Vater.

• Cystic duct – ❌ Drains the gallbladder into the common bile duct. Does not open directly into the duodenum. ✅ Correct answer

• Bile duct (common bile duct) – ✅ Opens into the major duodenal papilla in the 2nd part of the duodenum.

• Accessory pancreatic duct – ✅ Opens into the minor duodenal papilla in the 2nd part of the duodenum.

Step 3: Correct Answer

Cystic duct

Step 1: Recall pancreas anatomy

The pancreas has five main parts:

• Head – lies in the curve of the duodenum, mostly retroperitoneal.

• Uncinate process – a hook-like extension of the head, retroperitoneal.

• Neck – short segment between head and body, retroperitoneal.

• Body – crosses midline, posterior to the stomach, retroperitoneal.

• Tail – extends toward the spleen, enveloped by the splenorenal ligament, making it intraperitoneal.

Key principle:

• Most of the pancreas is retroperitoneal, meaning it lies behind the peritoneum.

• Only the tail of the pancreas is suspended in the peritoneal cavity by the splenorenal ligament, making it intraperitoneal.

Step 2: Analyze each option

• Head – Retroperitoneal, nestled in duodenal curve.

• Uncinate process – Part of the head, retroperitoneal.

• Neck – Retroperitoneal, anterior to the superior mesenteric vessels.

• Body – Retroperitoneal, posterior to the stomach.

• Tail – Intraperitoneal, enclosed in the splenorenal ligament, reaching the spleen.

Step 3: Correct Answer

Tail

Step 1: Recall anatomical relationships

• Ribs 9–11 are lower thoracic ribs, curving around the lateral abdomen.

• Posteriorly and laterally, these ribs protect underlying organs.

• We are specifically asked about the left side, which narrows our focus.

Step 2: Analyze each option

 Gall bladder ❌

• Located under the liver, in the right upper quadrant.

• Trauma on the left side rarely affects the gall bladder.

 Pancreas ❌

• Located retroperitoneally, mostly behind the stomach, extending from the right (head) to left (tail near spleen).

• While the tail of the pancreas is on the left, it is well protected by other structures, making it less directly vulnerable to rib trauma.

 Appendix ❌

• Located in the right lower quadrant.

• Trauma to the left ribs is unlikely to affect it.

 Kidney ⚠️

• Left kidney is retroperitoneal, roughly between T12–L3 vertebrae, partially protected by ribs 11–12.

• It can be injured by blunt trauma to the left flank, but the lower ribs protect it partially, and it is posterior, not lateral.

 Spleen ✅

• Located in the left upper quadrant, beneath ribs 9–11.

• It is relatively unprotected laterally by the rib cage, making it most vulnerable to blunt trauma from left-sided rib injuries.

• Spleen rupture is the most common solid organ injury in blunt abdominal trauma on the left.

Step 3: Correct Answer

✅ Spleen

Step 1: Understand the liver’s blood flow

The liver has two main blood supplies:

1. Hepatic artery → supplies oxygen-rich blood from the systemic circulation.

2. Portal vein → supplies nutrient-rich blood from the gastrointestinal tract.

Inside the liver:

• Blood from both the hepatic artery and portal vein flows through sinusoids, where it is filtered and metabolized by hepatocytes.

• After processing, blood collects in central veins, which merge to form hepatic veins, and finally drain into the inferior vena cava (IVC).

Bile vs blood:

• Bile, produced by hepatocytes, exits via the bile canaliculi → bile ducts → hepatic duct.

• Blood and bile flow in opposite directions.

Step 2: Analyze each option

 Cystic duct ❌

• Carries bile from the gallbladder to the common bile duct.

• Does not carry blood, so not the answer.

 Hepatic vein ✅

• Receives filtered blood from the liver sinusoids via central veins.

• Drains into the inferior vena cava.

• This is the correct answer.

 Hepatic portal vein ❌

• Brings unfiltered, nutrient-rich blood from the gut to the liver.

• Blood enters the liver here, it does not exit.

 Hepatic duct ❌

• Carries bile from liver to common bile duct.

• Not a blood vessel.

 Hepatic artery ❌

• Brings oxygenated blood to the liver.

• Blood enters, it does not exit.

Step 3: Correct Answer

✅ Hepatic vein

Step 1: Recall the portal vein anatomy

The portal vein carries nutrient-rich blood from most of the gastrointestinal tract and spleen to the liver. Its main tributaries are:

• Left gastric vein → drains the lesser curvature of the stomach

• Splenic vein → drains spleen, part of the stomach, pancreas

• Superior mesenteric vein → drains small intestine, cecum, ascending colon, part of transverse colon

• Inferior mesenteric vein → drains descending colon, sigmoid colon, rectum (usually joins the splenic vein before forming portal vein)

• Pancreatic veins → drain pancreas (part of portal circulation)

Key principle: The portal vein drains gut, spleen, and pancreas, but systemic veins from other organs may bypass it.

Step 2: Analyze each option

 Left gastric vein ✅

• Drains the stomach directly into the portal vein.

• This is a tributary → NOT the answer

 Cystic vein ❌

• Drains the gallbladder.

• Some small veins from the gallbladder drain directly into the liver (via hepatic sinusoids) rather than joining the portal vein.

• Therefore, the cystic vein is not typically considered a tributary of the portal vein. ✅ This is likely the correct answer.

 Superior pancreaticoduodenal vein ✅

• Drains pancreas and duodenum.

• Drains into the portal vein or its tributaries.

• This is a portal tributary, so not the answer.

 Superior mesenteric vein ✅

• Major tributary of the portal vein, drains small intestine and part of colon.

Splenic vein ✅

• Joins superior mesenteric vein to form the portal vein.

Step 3: Identify the correct answer

✅ Cystic vein – it drains the gallbladder and usually enters hepatic veins directly, not the portal vein.

Step 1: Understand the structure being observed

During a colonoscopy, the physician examines the colon—the large intestine. To answer this question, we need to recall the histological and anatomical features of the colon.

Step 2: Analyze each option

 Crypts of Lieberkuhn ✅

• These are intestinal glands present in both the small and large intestine.

• They are deep invaginations of the mucosa and secrete mucus, water, and electrolytes.

• Characteristic of the colon, so this is correct as a feature.

 Glands in the mucosa ✅

• The colon contains numerous tubular glands (these are basically the Crypts of Lieberkuhn).

• These glands are located in the mucosa, the innermost layer of the colon.

• This is true for the colon, so this is a correct feature.

 Few villi ❌ (the trick option)

• Villi are finger-like projections primarily found in the small intestine (duodenum, jejunum, ileum).

• The colon does not have villi; instead, it has a flat surface with deep crypts.

• Saying the colon has “few villi” is misleading. The colon lacks villi, making this not a characteristic feature.

 Teniae coli ✅

• These are longitudinal bands of smooth muscle visible on the colon’s outer layer (muscularis externa).

• They are unique to the colon and help in its motility.

• This is a true feature, so it’s correct.

 Numerous goblet cells ✅

• Goblet cells are abundant in the colon and secrete mucus to lubricate the fecal matter.

• This is a classic histological feature of the colon.

Step 3: Identify the correct answer

The option that is not a characteristic feature of the colon is:

✅ Few villi

During embryological development, the midgut normally herniates into the umbilical cord around the 6th week of gestation and returns to the abdominal cavity by the 10th–12th week. Failure of this return leads to an omphalocele. Let’s break it down:

Key features of Omphalocele:

• Midline abdominal wall defect at the base of the umbilical cord.

• Herniation of abdominal contents (intestine, sometimes liver) covered by a membrane composed of peritoneum and amnion.

• Often associated with other congenital anomalies (cardiac, chromosomal).

• Caused by failure of physiological herniation to return to the abdominal cavity.

Why the other options are incorrect:

• Retrocolic hernia → Abnormal herniation of intestines behind the colon; not related to failure of physiological midgut return.

• Megacolon → Abnormal dilation of the colon, often due to Hirschsprung disease; unrelated to embryological herniation.

• Persistence of vitelline duct → Leads to Meckel’s diverticulum or fistulas, but does not cause omphalocele.

• Gastroschisis → Lateral abdominal wall defect with herniation of intestines not covered by a membrane; caused by vascular disruption, not failure of physiological herniation.

This patient presents with chronic diarrhea, abdominal pain, and characteristic colonoscopic and histologic findings, which point toward Crohn’s disease, a type of inflammatory bowel disease (IBD). Let’s break it down:

Key clinical and pathological features:

1. Skip lesions – Some segments of the bowel are affected while others are spared. This is classic for Crohn’s disease.

2. Transmural inflammation – Leads to deep linear fissures and fistula formation.

3. Aphthous ulcers – Small, superficial ulcers in early disease, often seen in the colon and terminal ileum.

4. Creeping fat – Mesenteric fat wraps around the bowel wall, characteristic of Crohn’s.

5. Non-caseating granulomas – Seen on biopsy, differentiating it from ulcerative colitis.

6. Lamina propria cryptitis – Inflammatory cells infiltrate the mucosa.

Why the other options are incorrect:

• Celiac disease → Primarily affects the small intestine (duodenum/jejunum), not colon; villous atrophy is hallmark.

• Ulcerative colitis → Continuous inflammation starting from the rectum; no skip lesions, no transmural involvement, no granulomas.

• Whipple disease → Systemic disease; causes malabsorption with foamy macrophages in lamina propria; typically PAS-positive.

• Lactose intolerance → Functional disorder; no inflammation, ulcers, or granulomas.

Meckel’s diverticulum is a congenital anomaly resulting from persistence of the vitelline (omphalomesenteric) duct. It has several characteristic features, often remembered by the “rule of 2s”:

• Present in ~2% of the population

• Located about 2 feet from the ileocecal valve

• Usually 2 inches in length

• Can contain ectopic gastric or pancreatic tissue

• Often called ileal diverticulum

Key point about location:

• Meckel’s diverticulum forms on the antimesenteric border of the ileum, not the mesenteric side.

• This is important clinically because it helps differentiate it from other ileal diverticula.

Why the other options are correct:

• Present in 2% of the population → Classic epidemiologic fact (“rule of 2s”).

• Can function as ectopic pancreatic tissue → True; can also contain gastric mucosa.

• Due to persistent vitelline duct → Pathogenesis of Meckel’s diverticulum.

• Also called ileal diverticulum → Alternate name, accurate description.

In epidemiology:

• Primary case → The first case that introduces the disease into a population. This is the original source from which other cases may arise.

• Index case → The first case identified or reported to health authorities. (May or may not be the primary case.)

• Secondary case → A person who gets infected from the primary case.

• Tertiary case → A person infected from a secondary case.

• Quaternary case → Not a standard classification; “quaternary prevention” exists in public health, but not “quaternary case.”

So, the “first case that brings infection into a population” is the primary case.

Why the other options are wrong

Quaternary ❌ → Term relates to prevention, not case classification.
Secondary ❌ → Infected by the primary case, not the first.
Index ❌ → First identified/reported case, but not necessarily the first infected.
Tertiary ❌ → Infected by a secondary case.
Primary ✅ → First case that introduces the disease into the population.

The porta hepatis is the transverse fissure on the visceral surface of the liver where important structures enter or leave the liver.

Contents of porta hepatis include:

• Right and left hepatic ducts (bile outflow).

• Right and left branches of the hepatic artery proper.

• Right and left branches of the portal vein.

• Lymphatic vessels.

• Autonomic nerves.

Not included:

• Hepatic veins – they drain blood from the liver into the inferior vena cava, and they do not pass through the porta hepatis. Instead, they open directly into the IVC on the posterior surface of the liver.

Why the other options are correct contents

• Right hepatic duct ✅ (content) → bile drainage from right lobe.

• Left hepatic duct ✅ (content) → bile drainage from left lobe.

• Hepatic portal vein ✅ (content) → brings nutrient-rich blood from GI tract.

• Hepatic lymphatic vessels ✅ (content) → drain lymph from liver.

• Hepatic vein ❌ (NOT a content) → drains blood into IVC, not via porta hepatis.

• The appendix is a midgut derivative.

• Visceral pain from midgut structures is referred to dermatomes supplied by T10.

• That’s why early appendicitis typically causes vague pain around the umbilicus (T10 dermatome).

• As inflammation progresses and irritates the parietal peritoneum, pain shifts to the right lower quadrant (McBurney’s point) with localized somatic innervation.

Why the other options are wrong

T8 ❌

• Upper part of abdomen (epigastrium, foregut pain).

T7 ❌

• Also upper abdomen, foregut related.

T9 ❌

• Above the umbilicus, still foregut-midgut transitional.

T6 ❌

• Supplies epigastrium (xiphoid region), not umbilical.

T10 ✅

• Correct — umbilical dermatome, pain referred here in early appendicitis.

Spontaneous bacterial peritonitis (SBP) is a life-threatening infection in patients with cirrhosis and ascites. Primary prophylaxis aims to prevent the first episode of SBP in high-risk patients.

Key Risk Factors for Primary Prophylaxis:

• Advanced liver disease: Child-Pugh score ≥ 9 plus serum bilirubin > 3 mg/dL

• Low ascitic fluid protein: < 1.5 g/dL, which increases susceptibility to infection

• Other lab derangements like elevated creatinine or hyponatremia indicate severity, but the main criterion for primary prophylaxis is high Child-Pugh score with low ascitic protein.

So, patients with Child-Pugh score > 9 are routinely considered for primary prophylaxis even before the first episode of SBP.

Why the other options are incorrect:

• Bilirubin < 2.5 mg/dL → Lower bilirubin indicates less severe liver disease; primary prophylaxis is not indicated.

• Ascites fluid protein > 1.5 g/L → Higher protein is protective; prophylaxis is not needed.

• Creatinine > 1.2 mg/dL → Indicates renal involvement, but is not the primary trigger for prophylaxis.

• Serum Na > 130 mg/L → Mild hyponatremia isn’t an indication for prophylaxis.

The transversus abdominis muscle takes origin from:

• Lateral one-third of the inguinal ligament,

• Inner lip of the iliac crest,

• Thoracolumbar fascia,

• Inner surfaces of costal cartilages of ribs 7–12.

It inserts into the linea alba and contributes to the conjoint tendon (with internal oblique) near the pubic crest.

Why the other options are wrong

Medial head of rectus abdominis ❌

• Rectus abdominis arises from the pubic symphysis and pubic crest, not inguinal ligament.

Cremaster muscle ❌

• Derived from internal oblique fibers, but specifically from the middle portion of the inguinal ligament, not the lateral one-third directly.

External oblique ❌

• Originates from the external surfaces of ribs 5–12, not the inguinal ligament.

Lateral head of rectus abdominis ❌

• Rectus abdominis has no “lateral head” separate origin at the inguinal ligament.

Transverse abdominis ✅

• Correct — one of its origins is the lateral one-third of the inguinal ligament.

• Vibrio cholerae is a waterborne pathogen that thrives in brackish water and estuaries.

• Natural reservoirs include marine organisms such as plankton and shellfish (especially oysters, clams, mussels).

• Humans are the main hosts where the disease manifests, but the bacteria can persist in aquatic environments and biofilms, particularly associated with shellfish.

• Outbreaks are often linked to consumption of raw or undercooked seafood contaminated with V. cholerae.

Why the other options are wrong

Shellfish ✅

• Correct — established reservoir and transmission source.

Chicken ❌

• Important reservoir for Salmonella and Campylobacter, not cholera.

Unknown ❌

• The reservoir is known: aquatic environments and shellfish.

Reptile ❌

• Reptiles are carriers of Salmonella, not Vibrio cholerae.

Hospital ❌

• Nosocomial transmission is not typical for cholera; spread is fecal-oral, not hospital reservoir.

Meckel’s diverticulum (the “rule of 2s”):

• True diverticulum of the ileum.

• Located on the anti-mesenteric border of the ileum, about 2 feet from the ileocecal valve.

• Present in ~2% of the population.

• Can contain ectopic gastric or pancreatic tissue → may cause ulceration and bleeding.

• Caused by persistence of the vitelline (omphalomesenteric) duct.

Why the other options are correct (not odd)

• It can function as ectopic pancreatic tissue ✅ → True, may also contain gastric tissue.

• It is also called ileal diverticulum ✅ → Correct name.

• It is present in 2% of the population ✅ → Matches the “rule of 2s.”

• It is due to a persistent vitelline duct ✅ → Correct embryological cause.

• It forms on mesenteric side ❌ → Wrong; it is on the anti-mesenteric side.

Vitamin B6 exists in several forms:

• Pyridoxine (alcohol form)

• Pyridoxal (aldehyde form)

• Pyridoxamine (amine form)

All of these are precursors that must be converted into the biologically active coenzyme:

👉 Pyridoxal 5-phosphate (PLP)

Functions of PLP:

• Coenzyme for transamination, decarboxylation, and glycogen phosphorylase reactions.

• Involved in synthesis of neurotransmitters (dopamine, serotonin, GABA), heme, niacin (from tryptophan).

Clinical correlation:

• Deficiency → irritability, seizures, neuropathy, anemia (sideroblastic), and pellagra-like symptoms.

• Can be caused by isoniazid (which inactivates PLP).

Why the other options are wrong

NAD ❌

• Derived from niacin (vitamin B3), not B6.

Pyridoxal 5-phosphate ✅

• Correct — the active coenzyme form of B6.

Pyridoxine ❌

• One of the dietary forms, but must be phosphorylated to PLP to be active.

FMN ❌

• Flavin mononucleotide, derived from riboflavin (vitamin B2), not B6.

Pyridoxamine ❌

• Another form of B6, but inactive until converted to PLP.

The gastrointestinal tract has contributions from different embryonic layers:

• Endoderm → gives rise to the epithelial lining of the gut and its glands (e.g., liver, pancreas).

• Mesoderm (splanchnic layer of lateral plate mesoderm) → forms the connective tissue, blood vessels, and smooth muscle layers of the gut, including the muscularis externa.

• Ectoderm → contributes only at the ends of the gut (oral cavity epithelium, anal canal below pectinate line).

• Neural crest cells → migrate into the gut wall to form the enteric nervous system (Auerbach’s and Meissner’s plexuses), but they do not form the muscle itself.

• Neural tube → forms the central nervous system, not gut layers.

Thus, the muscularis externa is derived from splanchnic mesoderm.

Why the other options are wrong

Endoderm ❌ → forms epithelium and glands, not muscle.
Ectoderm ❌ → forms oral/anal lining, not gut muscle.
Neural crest cells ❌ → form enteric ganglia, not smooth muscle.
Neural tube ❌ → forms CNS, unrelated to gut wall.

• The gallbladder receives its sympathetic innervation from the celiac plexus, which carries fibers from T7–T9 spinal segments (sometimes up to T10).

• Pain fibers travel back along these sympathetic pathways to the spinal cord.

• Because of dermatomal overlap, the pain is referred to:

  • Right hypochondrium / epigastrium (T7–T9 dermatomes).

  • Right infrascapular region — because the dorsal roots at T7–T9 also supply sensation to this cutaneous area.

• Irritation of the diaphragm by an inflamed gallbladder can also cause shoulder pain (referred via C3–C5 phrenic nerve), but the specific “right infrascapular region” points to T7–T9.

Why the other options are wrong

C3–C5 ❌

• Phrenic nerve → referred pain to shoulder, not infrascapular region.

T12–L2 ❌

• Innervate lower abdominal and pelvic organs, not gallbladder.

T11–L1 ❌

• Supply structures like kidney, ureter, lower gut. Not the gallbladder.

T7–T9 ✅

• Correct. Sympathetic innervation to gallbladder → referred pain to right infrascapular region.

L1–S2 ❌

• Innervates pelvis and lower limbs. Not gallbladder.

During inflammation, different chemical mediators are responsible for the cardinal signs:

• Redness & heat → Histamine, prostaglandins, nitric oxide (vasodilation).

• Swelling → Histamine, leukotrienes (increased vascular permeability).

• Pain → Bradykinin and prostaglandins sensitize nerve endings, lowering their threshold and causing the sensation of pain.

• Loss of function → Results from pain and tissue damage.

So the chemicals most directly responsible for pain are bradykinin (kinin system) and prostaglandins (especially PGE₂).

Why the other options are wrong

Interleukins and tumor necrosis factor ❌

• These are cytokines important in fever, leukocyte activation, and systemic inflammation. They do not directly cause pain.

Bradykinin and prostaglandins ✅

• Correct — both are pain mediators in inflammation.

Histamine and serotonin ❌

• Mediate vasodilation and vascular permeability (redness, swelling), but not direct pain.

Nitric oxide and leukotrienes ❌

• NO: vasodilation.

• Leukotrienes: increased vascular permeability, chemotaxis.

• Not primary pain mediators.

Acetylcholine and dopamine ❌

• Neurotransmitters but not classical inflammatory pain mediators.

The rectus abdominis muscle:

• Origin → pubic crest, pubic symphysis, pubic tubercle.

• Insertion →

  • Costal cartilages of the 5th, 6th, and 7th ribs.

  • Xiphoid process of the sternum.

So, its rib-level insertion corresponds to V–VII (5th–7th).

Why the other options are wrong

VIII–X ❌

• These costal cartilages are related more to the transversus abdominis and internal oblique insertions, not rectus abdominis.

V–VII ✅

• Correct — rectus abdominis inserts into the costal cartilages of ribs 5, 6, 7, plus the xiphoid.

VII–IX ❌

• Too low; rectus abdominis doesn’t extend to 8th and 9th costal cartilages.

V–XI ❌

• Includes ribs too low (10th–11th), unrelated to rectus abdominis.

V–IX ❌

• Again too low; only 5th–7th are correct.

The omental foramen (foramen of Winslow) is the communication between the greater sac and the lesser sac (omental bursa) of the peritoneal cavity. Its boundaries are very important surgically (e.g., Pringle’s maneuver).

• Anterior boundary → Hepatoduodenal ligament, which contains the portal triad (portal vein, hepatic artery proper, bile duct).

• Posterior boundary → Peritoneum covering the inferior vena cava.

• Superior boundary → Caudate lobe of liver.

• Inferior boundary → First part of duodenum.

Thus, the posterior boundary is specifically the peritoneum overlying the IVC.

Why the other options are wrong

Peritoneum of duodenum ❌

• Forms the inferior boundary, not posterior.

Peritoneum of hepatoduodenal ligament ❌

• Forms the anterior boundary.

Peritoneum of inferior vena cava ✅

• Correct. Posterior boundary is the peritoneum covering the IVC.

Hepatic portal vein ❌

• Lies inside the anterior boundary (within hepatoduodenal ligament), not posterior.

Peritoneum of liver ❌

• Liver forms the superior boundary (caudate lobe), not posterior.

The muscle described has the following features:

• Small and triangular in shape.

• Lies within the rectus sheath, in front of the lower part of rectus abdominis.

• Attachments → arises from the pubic symphysis and pubic crest, inserts into the linea alba.

• Action → tenses the linea alba.

• Variation → frequently absent (present in about 80% of people).

These features match perfectly with the pyramidalis muscle.

Why the other options are wrong

External oblique ❌

• Large flat muscle of abdominal wall, not small/triangular. Lies superficially, not within rectus sheath.

Psoas ❌

• A posterior abdominal wall muscle, related to lumbar vertebrae, not in rectus sheath.

Internal oblique ❌

• A broad abdominal muscle between external oblique and transversus abdominis. Not triangular and not confined to rectus sheath.

Transversalis fascia ❌

• Not a muscle, but a fascial layer deep to transversus abdominis.

Pyramidalis ✅

• Small triangular muscle in rectus sheath, tenses linea alba, sometimes absent. Correct answer.

The gallbladder has four anatomical parts: fundus, body, infundibulum (Hartmann’s pouch), and neck.

• Hartmann’s pouch (also called the infundibulum) is a small outpouching of the gallbladder wall that lies between the neck of the gallbladder and the cystic duct.

• It is clinically significant because gallstones often lodge here, potentially leading to biliary obstruction or cholecystitis.

Why the other options are wrong

Major duodenal papilla ❌

• Opening of the hepatopancreatic ampulla (ampulla of Vater) into the duodenum. Not related to gallbladder neck.

Hartmann’s pouch ✅

• Correct. Outpouching located between the neck and cystic duct.

Body of stomach ❌

• Unrelated to the biliary tract.

Common hepatic duct ❌

• Formed by the union of the right and left hepatic ducts, not located at the gallbladder neck.

Fundus ❌

• Rounded distal end of gallbladder, far from the cystic duct.

The descending colon and the rectum have similar general wall structure (mucosa, submucosa, muscularis externa, serosa/adventitia), but there are some key histological differences:

• Descending colon → Muscularis externa has three longitudinal bands called the teniae coli. These bands cause sacculations of the colon (haustra).

• Rectum → The teniae coli spread out to form a continuous, smooth outer longitudinal layer of muscularis externa. This is the main distinguishing feature.

So, histologically, the rectum is identified by its uniform muscularis externa, while the colon has the characteristic teniae coli.

Why the other options are wrong

It lacks Peyer’s patches ❌

• True for both colon and rectum. Peyer’s patches are characteristic of the ileum, not of colon/rectum.

It has a comparatively smooth muscularis externa ✅

• Correct. The rectum differs from the colon in that its muscularis externa forms a smooth continuous layer instead of teniae coli.

It has no submucosa ❌

• Both colon and rectum have a submucosa.

It is completely covered by adventitia ❌

• Rectum is partly covered by serosa (peritoneum) in its upper third, and by adventitia in the lower two-thirds. Not “completely” adventitia.

It has no muscularis mucosa ❌

• Rectum does have a muscularis mucosa, just like the colon.

Vitamin B₁₂ (cobalamin) absorption is a multistep process:

1. In the stomach → B₁₂ is released from dietary proteins by gastric acid and pepsin.

   • It first binds to haptocorrin (R-protein) secreted in saliva.

2. In the duodenum → Pancreatic proteases degrade haptocorrin, releasing B₁₂.

   • Now B₁₂ binds to intrinsic factor (IF), which is secreted by parietal cells of the stomach.

3. In the terminal ileum → The B₁₂–intrinsic factor complex binds to specific receptors (cubilin receptors) on ileal enterocytes and is absorbed.

4. In circulation → B₁₂ binds to transcobalamin II for transport to tissues.

Thus, although the stomach and duodenum prepare B₁₂ for absorption, the actual absorption occurs in the ileum.

Why the other options are wrong

Stomach ❌

• B₁₂ is released from food here and binds to haptocorrin, but it is not absorbed in the stomach.

Duodenum ❌

• B₁₂ is transferred from haptocorrin to intrinsic factor here, but absorption does not happen yet.

Ileum ✅

• Site of actual absorption of the B₁₂–intrinsic factor complex. Correct answer.

Jejunum ❌

• Absorbs most nutrients, but not vitamin B₁₂.

Colon ❌

• Involved in water and electrolyte absorption; does not absorb B₁₂.

The coronary ligament is a peritoneal reflection that attaches the superior surface of the liver to the inferior surface of the diaphragm.

• It consists of an anterior and posterior layer of peritoneum that meet at the margins of the bare area of the liver.

• Its lateral extremities form the right and left triangular ligaments.

• Function: helps anchor the liver to the diaphragm, stabilizing it in the upper abdominal cavity.

Why the other options are wrong

First part of duodenum ❌

• Connected to the liver by the hepatoduodenal ligament (part of the lesser omentum), not the coronary ligament.

Pancreas ❌

• Lies posterior to the stomach, with no direct ligamentous attachment to the liver.

Left suprarenal gland ❌

• Related to the left kidney, not attached to the liver by the coronary ligament.

Transverse colon ❌

• Connected via the gastrocolic ligament and transverse mesocolon, not via coronary ligament.

Diaphragm ✅

• Correct. The coronary ligament secures the liver to the diaphragm, leaving the “bare area” of the liver.

The hepatic artery proper is a continuation of the common hepatic artery after it gives off the gastroduodenal artery.

• It ascends toward the liver within the hepatoduodenal ligament, which is part of the lesser omentum.

• The hepatoduodenal ligament contains the portal triad:

  • Hepatic artery proper (left side)

  • Portal vein (posterior)

  • Common bile duct (right side)

This ligament connects the liver to the first part of the duodenum and serves as a key landmark in hepatobiliary surgery (e.g., Pringle’s maneuver, where the ligament is clamped to control hepatic bleeding).

Why the other options are wrong

Splenorenal ligament ❌

• Connects spleen to left kidney.

• Contains splenic vessels, tail of pancreas — not hepatic artery proper.

Hepatophrenic ligament ❌

• Connects liver to diaphragm.

• Does not transmit hepatic artery proper.

Hepatoduodenal ligament ✅

• Correct answer. Part of the lesser omentum, contains the portal triad including the hepatic artery proper.

Hepatogastric ligament ❌

• Connects liver to lesser curvature of stomach.

• Contains left and right gastric arteries, not hepatic artery proper.

Gastrosplenic ligament ❌

• Connects stomach to spleen.

• Contains short gastric and left gastro-omental arteries.

Marasmus is a form of severe protein-energy malnutrition that results from deficiency of calories overall (protein + carbohydrates + fats), but calorie deficiency is greater than protein deficiency.

• It usually occurs in children under 1 year of age who are weaned too early or fed on very dilute food.

• Clinical features:

  • Severe wasting of muscles and subcutaneous fat (“skin and bones” appearance).

  • Growth retardation.

  • No edema (because total protein deficiency is not as severe as in kwashiorkor).

  • Anemia and micronutrient deficiencies are common.

Why the other options are wrong

Too much edema ❌

• Seen in kwashiorkor, due to severe protein deficiency → hypoalbuminemia → edema. Not in marasmus.

Malnutrition but no anemia ❌

• Marasmus does cause anemia due to generalized malnutrition.

Lack of protein more than calorie ❌

• That is kwashiorkor, not marasmus.

Lack of calorie more than protein ✅

• Correct. This is the defining feature of marasmus.

Excessive body weight ❌

• Opposite of marasmus, which causes severe wasting and low body weight.

The space of Disse is the perisinusoidal space located between the fenestrated endothelium of hepatic sinusoids and the hepatocytes.

• It is important for exchange of plasma and metabolites between blood and hepatocytes.

• It contains hepatic stellate cells (Ito cells), which:

  • Store vitamin A in lipid droplets under normal conditions.

  • Transform into myofibroblast-like cells during liver injury → produce collagen → responsible for fibrosis in cirrhosis.

Why the other options are wrong

Cholangiocytes ❌

• Epithelial cells lining bile ducts and canaliculi.

• Located in the portal triad, not in the space of Disse.

Kupffer cells ❌

• Specialized macrophages lining the sinusoidal lumen (inside the sinusoidal endothelium).

• Not within the space of Disse.

Hepatic veins ❌

• Large vessels that collect blood from central veins.

• Far downstream, not part of sinusoidal microanatomy.

Endothelial cells ❌

• Line the sinusoidal lumen.

• The space of Disse lies beneath the endothelial lining, so these cells are not inside the space itself.

Hepatic stellate cells ✅

• Reside within the space of Disse.

• Key for vitamin A storage and fibrosis developmen

The lesser sac (omental bursa) is the peritoneal space posterior to the stomach and lesser omentum.

• Boundaries of the lesser sac in transverse section:

  • Anterior → Stomach, lesser omentum, gastrocolic ligament.

  • Posterior → Pancreas, left kidney, left adrenal.

  • Right → Omental (epiploic) foramen (communication with greater sac).

  • Left → Splenorenal ligament and gastrosplenic ligament, both attaching the spleen to the posterior abdominal wall/stomach.

Thus, the left boundary is formed by the splenorenal ligament.

Why the other options are wrong

Omental foramen ❌

• Defines the right boundary (communication with greater sac).

Splenorenal ligament ✅

• Forms the left boundary along with the gastrosplenic ligament. Correct answer.

Lesser omentum ❌

• Forms the anterior boundary, not the left.

Liver ❌

• Specifically, the caudate lobe of liver helps form the superior boundary, not the left.

Left kidney ❌

• Lies posterior to the lesser sac, not forming its left boundary.

The rectus abdominis muscle is one of the main anterior abdominal wall muscles. It extends from the pubic symphysis/pubic crest to the xiphoid process and costal cartilages of ribs 5–7.

• Nerve supply → segmental innervation by the anterior rami of the lower six thoracic spinal nerves (T7–T12).

• This includes the subcostal nerve (T12) as the lowest contributor.

• Function: flexes the trunk, compresses abdominal viscera, stabilizes pelvis during walking.

Why the other options are wrong

Lowest thoracic ❌

• Refers to the subcostal nerve (T12).

• This does contribute, but not alone — the rectus abdominis requires the entire range T7–T12.

Cervical plexus ❌

• Supplies neck muscles (e.g., sternocleidomastoid, infrahyoids), not abdominal wall.

Lower six thoracic ✅

• Correct answer: segmental innervation from T7–T12.

Upper six thoracic ❌

• T1–T6 supply chest wall and intercostal spaces, not the rectus abdominis.

Ilioinguinal ❌

• Supplies skin of groin and part of inguinal canal, not rectus abdominis.

When we fast, the body must maintain blood glucose to supply glucose-dependent tissues (especially brain and red blood cells). The sources change depending on the duration of fasting:

• Early fasting (first 12–18 hours) → Blood glucose is mainly maintained by hepatic glycogenolysis (breakdown of stored glycogen to glucose).

• Later fasting (>18–24 hours) → Glycogen stores become depleted, so the body switches to hepatic gluconeogenesis (using substrates like lactate, glycerol, and amino acids).

• Fatty acid oxidation → Provides energy (ATP, NADH, acetyl-CoA) for gluconeogenesis but does not yield glucose.

• Ketogenesis → Becomes important after ~2–3 days of fasting to supply the brain with ketone bodies, sparing muscle protein breakdown.

• Glycolysis → Consumes glucose, it doesn’t generate it.

Thus, in the early stages of fasting, the steady level of glucose is maintained by hepatic glycogenolysis.

Why the other options are wrong

Hepatic glycogenolysis ✅

• Correct: major source of glucose during first hours of fasting.

Hepatic fatty acid oxidation ❌

• Provides energy for gluconeogenesis but does not directly supply glucose.

Hepatic ketogenesis ❌

• Becomes significant only after 2–3 days of fasting, not in early fasting.

Hepatic glycolysis ❌

• Uses glucose rather than producing it.

Hepatic gluconeogenesis ❌

• Important in prolonged fasting (after glycogen depletion), not the early stage.

The patient has:

• Epigastric pain relieved by meals and antacids → This is classically duodenal ulcer pain (in contrast, gastric ulcer pain typically worsens with meals).

• Gastric analysis: Increased basal and active acid secretion → This indicates gastric hypersecretion, strongly linked with excessive gastrin activity.

Gastrin is secreted by G cells of the stomach antrum and proximal duodenum. It is the key hormone that:

• Stimulates HCl secretion from parietal cells (direct effect and indirect effect via histamine release from enterochromaffin-like cells).

• Promotes gastric mucosal growth.

• Increases gastric motility.

Excess gastrin (e.g., Zollinger–Ellison syndrome) → massive gastric acid hypersecretion → recurrent peptic ulcers.

Why the other options are wrong

Vasoactive intestinal peptide (VIP) ❌

• Inhibits gastric acid secretion.

• Stimulates intestinal secretion of water and electrolytes.

• Seen in VIPoma → watery diarrhea, hypokalemia, achlorhydria (WDHA syndrome).

Secretin ❌

• Secreted by S cells of duodenum in response to acid.

• Stimulates pancreatic bicarbonate secretion.

• Inhibits gastric acid secretion.

Gastrin ✅

• The only hormone listed that increases gastric acid secretion.

Somatostatin ❌

• Secreted by D cells.

• A universal inhibitor — suppresses gastrin release, histamine release, and parietal cell acid secretion.

Enterogastrone ❌

• General term for duodenal hormones (like CCK, GIP, secretin) that inhibit gastric secretion and motility.

Ascites can develop due to several mechanisms, including increased hydrostatic pressure, decreased oncotic pressure, increased capillary permeability, or lymphatic obstruction.

Key Point:

• Hydrostatic-pressure–driven ascites occurs when portal hypertension develops, as in cirrhosis.

• In cirrhosis, fibrosis and nodular regeneration obstruct portal blood flow → increased hydrostatic pressure in the portal venous system → fluid transudation into the peritoneal cavity.

Why the other options are incorrect:

• Neoplasm → Can cause ascites, but usually via peritoneal metastasis → increased vascular permeability, not hydrostatic pressure alone.

• Nephrotic syndrome → Ascites is due to low plasma oncotic pressure from hypoalbuminemia, not hydrostatic pressure.

• Constrictive pericarditis → Causes ascites, but mechanism is elevated systemic venous pressure; usually affects right-sided pressures more than portal hydrostatics.

• Infection (e.g., tuberculosis, bacterial peritonitis) → Causes exudative ascites through inflammation and increased permeability, not pure hydrostatic pressure.