GIT – 2018

• At the L2 vertebral level, a CT scan of acute pancreatitis usually shows structures in the upper abdomen.

• Present at L2:

  • Duodenum (2nd and 3rd parts)

  • Spleen (lies in the left hypochondrium, extending down to this level)

  • Abdominal aorta (retroperitoneal, anterior to vertebral column)

  • Liver (especially its inferior surface and right lobe extend to this level)

• Sigmoid colon, however, is a pelvic structure, typically found at the level of L4–S1, far below L2.

• Thus, it will not appear in an axial CT slice at the L2 level in pancreatitis.

Incorrect answer explanations:

• Duodenum → The head of the pancreas is surrounded by the duodenum at this level.

• Spleen → Close to the pancreatic tail, visible at L2.

• Abdominal aorta → Major retroperitoneal vessel, present at L2.

• Liver → Inferior margin is still visible around L2.

The esophagus is lined by non-keratinized stratified squamous epithelium (keratinized in some parts in people with a tougher diet). Its primary role is protection against mechanical trauma from food boluses.

It is not absorptive like the intestine, and not secretory like the stomach glands. Mucus secretion in the esophagus is done by submucosal esophageal glands, not by the epithelial cells themselves.

Answer breakdown:

• Absorptive only → Wrong (esophagus does not absorb).

• Protective and absorptive → Wrong (no absorption).

• Protective and secretory → Wrong (secretion comes from glands, not epithelium).

• Secretory only → Wrong.

• Protective only → Correct.

• Urine is composed mostly of water, which acts as the solvent for metabolic waste products such as urea, creatinine, and electrolytes.

• Typically, urine is about 95% water and 5% solutes.

• This high water content allows the kidneys to maintain fluid and electrolyte balance in the body.

Incorrect Options:

• 99% ❌ – Overestimates water content; urine always contains solutes.

• 80% ❌ – Underestimates water content; would make urine unusually concentrated.

• 85% ❌ – Slightly low; normal urine is more dilute.

• 75% ❌ – Far below normal water content; not physiologically typical.

• The subhepatic recess is the space between the right lobe of the liver and the right kidney (and sometimes the duodenum).

• It is clinically significant because fluid, pus, or blood can accumulate here in peritonitis or trauma.

• Other peritoneal recesses are located in different regions of the abdominal cavity.

Incorrect answer explanations:

• Paracolic gutters are between colon and root of mesentery → Wrong; paracolic gutters lie lateral to the ascending and descending colon, not between colon and mesenteric root.

• Paramesenteric recesses are between colon and abdominal wall → Incorrect; paramesenteric recesses are near the mesentery, not between colon and wall.

• Paraduodenal recess is the largest duodenal recess → False; the superior or inferior duodenal recesses are smaller, paraduodenal recesses are variable in size.

• Superior duodenal recess lies to the left of the third part of the duodenum → Wrong; the superior duodenal recess is typically above the duodenojejunal junction, not to the left of the 3rd part.

• The coronary ligaments (superior and inferior) are peritoneal reflections that connect the liver to the diaphragm.

• The inferior coronary ligament specifically attaches the diaphragmatic surface of the liver to the diaphragm, helping stabilize the liver in the subphrenic region.

• These ligaments also contribute to forming the bare area of the liver.

Incorrect answer explanations:

• Falciform ligament → Connects the anterior abdominal wall to the liver, not the diaphragm.

• Hepatoduodenal ligament → Part of the lesser omentum, connects liver to duodenum, contains portal triad.

• Hepatogastric ligament → Also part of the lesser omentum, connects liver to stomach.

• Lesser omentum → General term for the hepatogastric and hepatoduodenal ligaments, not a direct liver–diaphragm connection.

• In gluconeogenesis, pyruvate is first converted into oxaloacetate (OAA) inside the mitochondria by the enzyme pyruvate carboxylase (requires biotin and ATP).

• OAA is then converted into PEP by PEP carboxykinase.

• Thus, the initiating step is catalyzed by pyruvate carboxylase, making it the correct answer.

Incorrect answer explanations:

• Malate dehydrogenase → Converts oxaloacetate to malate for transport across mitochondrial membranes, but does not catalyze the first step.

• Glucose-6-phosphatase → Final step of gluconeogenesis, converting glucose-6-phosphate into free glucose.

• Pyruvate kinase → Catalyzes PEP → pyruvate in glycolysis (opposite direction, not gluconeogenesis).

• Phosphoglucoisomerase → Converts glucose-6-phosphate ↔ fructose-6-phosphate, part of glycolysis/gluconeogenesis middle steps, not the first.

• Pyloric glands are located in the antrum of the stomach.

• Their main functions:

  • Mucous-secreting cells → produce mucus to protect the gastric epithelium and neutralize acid.

  • G cells (gastrin-secreting cells) → secrete gastrin, which stimulates parietal cells in the fundus/body to release HCl.

• This combination protects the pyloric mucosa and regulates gastric secretion.

Incorrect answer explanations:

• Parietal cells and chief cells → Found mainly in the gastric (fundic/body) glands, not pyloric glands.

• Chief cells only → Secrete pepsinogen, but these are not typical in the pyloric region.

• Parietal cells only → Acid-secreting cells, mostly in the fundus/body, sparse in pylorus.

• Gastrin secreting cells only → Present, but pyloric glands also have abundant mucous cells, so this option is incomplete.

• Insulin promotes fatty acid synthesis rather than breakdown.

• It activates acetyl CoA carboxylase (ACC) by dephosphorylation (via protein phosphatase action).

• ACC converts acetyl CoA → malonyl CoA, the committed step in fatty acid synthesis.

• Malonyl CoA also inhibits carnitine palmitoyltransferase I (CPT-I), thereby reducing fatty acid oxidation.

• This ensures energy is stored as fat when insulin levels are high.

Incorrect answer explanations:

• Increase in the release of fatty acids from adipose tissues → Opposite effect; insulin inhibits lipolysis, preventing fatty acid release.

• Decreases the transport and metabolism of glucose into adipocytes → Wrong; insulin increases glucose uptake (via GLUT-4) and metabolism in adipose tissue.

• Activates the intracellular lipase → Incorrect; insulin inhibits hormone-sensitive lipase, reducing triglyceride breakdown.

• Decreased expression of the gene for lipoprotein lipase → Wrong; insulin increases lipoprotein lipase activity, promoting triglyceride storage in adipose tissue.

• The reticuloendothelial system (RES) — mainly macrophages in the spleen, liver (Kupffer cells), and bone marrow — is responsible for degrading senescent RBCs.

• Hemoglobin from destroyed RBCs is broken down:

  • Heme → biliverdin → bilirubin (processed by the liver).

  • Iron is recycled for new hemoglobin synthesis.

  • Globin chains are degraded into amino acids.

• This system prevents toxic accumulation of free hemoglobin in circulation.

Incorrect answer explanations:

• Paneth cells → Specialized intestinal epithelial cells that secrete antimicrobial peptides, unrelated to RBC destruction.

• Hepatocytes → Involved in bilirubin conjugation and excretion, but they don’t directly degrade hemoglobin.

• Lymphocytes → Involved in immune responses, not RBC breakdown.

• Stellate cells → Found in the liver, primarily store vitamin A and contribute to fibrosis, not hemoglobin degradation.

• Erythrocytes lack mitochondria and rely heavily on the pentose phosphate pathway (HMP shunt) to generate NADPH.

• NADPH maintains glutathione in its reduced form (GSH).

• Glutathione peroxidase (a selenium-containing enzyme) uses GSH to detoxify hydrogen peroxide and lipid peroxides, preventing oxidative damage to hemoglobin and the RBC membrane.

• This mechanism is vital — deficiency of G6PD (which produces NADPH) makes RBCs vulnerable to hemolysis under oxidative stress.

Incorrect answer explanations:

• NADPH and superoxide dismutase → Superoxide dismutase converts superoxide → hydrogen peroxide, but in RBCs, the key protective system is glutathione peroxidase with NADPH.

• Superoxide dismutase and glutathione peroxidase → Both enzymes protect against oxidative damage, but without NADPH, glutathione peroxidase cannot function (GSH wouldn’t be regenerated).

• Hydrogen peroxide and glutathione peroxidase → H₂O₂ is harmful, not protective; this pair doesn’t serve as protection.

• NADPH and hydrogen peroxide → Hydrogen peroxide damages RBCs; NADPH alone cannot neutralize it.

• In the electron transport chain (ETC) of mitochondria:

  • Complex I (NADH dehydrogenase) pumps protons from the matrix to the intermembrane space.

  • Complex III (cytochrome bc1 complex) also pumps protons.

  • Complex IV (cytochrome c oxidase) pumps protons while reducing oxygen to water.

• Together, these generate the proton gradient used by Complex V (ATP synthase) to produce ATP.

• Complex II (succinate dehydrogenase) does not pump protons — it only transfers electrons from FADH₂ to ubiquinone.

Incorrect answer explanations:

• Complexes II, III, and IV → Wrong, because Complex II is not a proton pump.

• Complexes I, II, and V → Wrong, Complex II doesn’t pump protons, and Complex V uses the gradient rather than pumping protons out.

• Complexes I, II, and IV → Wrong, same reason: Complex II is not a proton pump.

• Complexes II, IV, and V → Wrong, because both Complex II and V are not proton pumps.

• Pelvic splanchnic nerves are parasympathetic fibers arising from S2–S4.

• They supply the hindgut (distal 1/3 of transverse colon to rectum) and pelvic organs (e.g., bladder, rectum, reproductive organs).

• They are crucial in regulating bladder emptying and relaxing the internal urethral sphincter.

• They do not supply the midgut (duodenum to proximal 2/3 of transverse colon), which is innervated by the vagus nerve.

Incorrect answer explanations:

• Control opening and closing of the internal urethral sphincter → True, they mediate parasympathetic control of bladder function.

• Arise from S2, S3, and S4 nerve roots of the sacral plexus → True, this is their exact origin.

• Innervates rectum and pelvic organs → True, major function of these nerves.

• Regulate the emptying of the urinary bladder → True, parasympathetic control promotes bladder contraction.

• The superior mesenteric artery (SMA) arises from the abdominal aorta just below the celiac trunk.

• As it courses downward, it passes anterior to the 3rd part (horizontal part) of the duodenum and then enters the root of the mesentery.

• This relationship is clinically important because compression of the duodenum between the SMA and the aorta can cause superior mesenteric artery syndrome (intestinal obstruction).

Incorrect answer explanations:

• Splenic vein → Lies posterior to the pancreas, not related to SMA crossing above the mesentery.

• Pyloric part of stomach → Located more superiorly; not directly crossed by SMA.

• Body of pancreas → SMA runs posterior to the pancreas, not anterior.

• Neck of pancreas → Lies over the portal vein formation; SMA does not pass anterior to it.

• Bile salts are amphipathic molecules (having both hydrophilic and hydrophobic ends).

• Their detergent-like action emulsifies large fat globules into smaller micelles.

• This increases the surface area for pancreatic lipase to act, aiding efficient digestion and absorption of dietary fats and fat-soluble vitamins.

Incorrect answer explanations:

• Acts as an agglutinator → Wrong; bile salts do not clump molecules together.

• Changes the conformation of fatty acids → Incorrect; they don’t alter fatty acid structure, only their dispersion.

• Causes lipid molecules to coalesce → Opposite effect; bile salts prevent coalescence by emulsifying fats.

• Mixes lipids with carbohydrates → False; bile salts only act on fats, not on carbohydrates.

• Proteins are synthesized by ribosomes according to the genetic code.

• Each of the 20 standard amino acids has specific codons in mRNA that are recognized by corresponding tRNAs.

• Citrulline and arginine are important in metabolism (urea cycle, nitric oxide synthesis), but citrulline has no codon in the genetic code, and arginine is coded but citrulline is not directly incorporated into proteins.

• Instead, citrulline is an intermediate, and arginine is incorporated via codons but here the question refers to why both aren’t standard universally incorporated amino acids → the key point is lack of codons for citrulline.

Incorrect answer explanations:

• Are acidic in nature → False; citrulline and arginine are not acidic; arginine is basic.

• Trapped inside mitochondria → Wrong; both can move across mitochondrial membranes.

• Are heavy amino acids → Incorrect; molecular weight doesn’t determine incorporation into proteins.

• Cannot enter the cell → False; both can be transported into cells.

• The hepatic sinusoids are specialized capillaries in the liver.

• They are lined by fenestrated endothelial cells without a basement membrane, allowing plasma to pass freely into the space of Disse, where it directly contacts hepatocytes.

• This structural adaptation facilitates efficient exchange of nutrients, metabolites, and waste between blood and liver cells.

Incorrect answer explanations:

• Is continuous without junctions → Wrong; sinusoidal endothelium has fenestrations, not continuous endothelium.

• Has a basement membrane → False; absence of a basement membrane is key to free exchange.

• Collagen fibers surround the endothelial cells → Incorrect; collagen is not normally present around sinusoids unless in fibrosis.

• Has non-fenestrated capillaries → Wrong; hepatic sinusoids are fenestrated, not continuous.

• Antacids are alkaline substances (e.g., magnesium hydroxide, aluminum hydroxide, calcium carbonate) that neutralize gastric acid immediately, giving quick relief from gastric irritation, heartburn, and dyspepsia.

• They act faster than other classes of acid-suppressing drugs (like H2 blockers or PPIs) though their effect is short-lived.

Incorrect answer explanations:

• Aspirin → An NSAID that worsens gastric irritation by inhibiting prostaglandins and damaging the gastric mucosa.

• Lemon juice → Acidic; increases irritation instead of relieving it.

• Milk → May give temporary soothing effect, but proteins and calcium later stimulate gastrin → increases acid secretion.

• Alcohol → Damages gastric mucosa and worsens irritation.

• Protein turnover is the continuous process of protein synthesis and degradation in the body.

• In adults, the normal daily protein turnover is about 300–400 grams per day.

• Despite this large turnover, the net protein balance in healthy adults remains nearly zero, since synthesis and breakdown are closely matched.

Incorrect answer explanations:

• 200–500 g/day → Too wide of a range; not the standard reference value.

• 700 g/day → Too high; not seen under normal conditions, may occur in extreme hypermetabolic states.

• 100–200 g/day → Too low; underestimates the normal turnover.

• 200–300 g/day → Slightly below the normal range; does not fully represent average adult turnover.

• Normal bowel sounds are produced by movement of air and fluid during peristalsis.

• They are typically heard at a frequency of about 5–30 times per minute.

• Incorrect answer explanations:

  • 10–20 seconds → Slightly broad but not the standard clinical description; normal is more specifically 15–20 seconds.

  • 1–3 minutes → Too infrequent; this would indicate hypoactive or reduced bowel sounds.

  • 1–5 seconds → Too frequent; suggests hyperactive bowel sounds, as in diarrhea or early obstruction.

  • 5–10 seconds → Also more frequent than normal; again associated with hyperperistalsis, not the normal rate.

    This corresponds to roughly one sound every 15–20 seconds, which is considered normal in a healthy individual.

• The spermatic cord passes through the inguinal canal and contains structures that travel to and from the testis.

• Its main constituents include:

  • Ductus deferens

  • Testicular artery

  • Pampiniform plexus of veins

  • Cremasteric artery

  • Artery to the ductus deferens

  • Genital branch of the genitofemoral nerve

  • Autonomic nerves (testicular plexus)

  • Lymphatics

• The ilioinguinal nerve does pass through the inguinal canal but runs outside the spermatic cord, accompanying it, not inside it.

Why other options are correct constituents

• Pampiniform plexus of testicular veins → part of venous drainage inside spermatic cord.

• Ductus deferens → a key structure within the cord.

• Testicular nerve (autonomic fibers) → travels with testicular vessels inside the cord.

• Cremasteric arteries → branch of inferior epigastric artery inside the cord.

• The cremasteric reflex is elicited by stroking the medial thigh → this stimulates the femoral branch of the genitofemoral nerve and the ilioinguinal nerve (sensory).

• The motor response (cremaster muscle contraction → testis elevation) is mediated by the genital branch of the genitofemoral nerve.

• The genitofemoral nerve arises from L1–L2 nerve roots.

• Therefore, the reflex is innervated by fibers from L1–L2.

Why other options are wrong

• Above L1 → Too high; nerves above L1 (like T12) don’t contribute to this reflex.

• Between L2 and L3 → The reflex doesn’t involve L3.

• L1–L3 → Incorrect; L3 isn’t part of the reflex arc.

• Below L2 → Too low; reflex fibers don’t come from below L2.

• Contraction in smooth muscle begins when calcium binds calmodulin → activates MLCK → phosphorylates myosin light chains → cross-bridge cycling occurs.

• Relaxation requires removal of phosphate groups from myosin.

• Myosin light-chain phosphatase performs this dephosphorylation → stops cross-bridge formation → contraction ends.

Why other options are wrong

• Active MLCK calcium–calmodulin chain complex → activates contraction, not relaxation.

• Calcium–calmodulin complex → triggers MLCK activation → promotes contraction.

• Myosin light-chain phosphorylase → not an enzyme involved in smooth muscle physiology (distractor).

• Myosin light-chain kinase (MLCK) → initiates contraction, not responsible for relaxation.

The primary case refers to the very first individual who develops or introduces a communicable disease into a population. This person becomes the source from which subsequent infections (secondary and tertiary cases) arise. Identifying the primary case is important in epidemiology because it helps in understanding the origin of an outbreak and controlling further spread.

Incorrect options

• Secondary case → This is a person who acquires the infection from the primary case (or another infected person). It is not the initial case but rather part of the chain of transmission.

• Tertiary case → A person infected by a secondary case; it represents a further step in the chain of spread, not the origin.

• Index case → This is the first case detected or reported to health authorities, which may or may not be the true first case (primary case).

• None of these → Incorrect because the correct epidemiological term does exist, and it is “primary case.”

• Hemoglobin – contains heme (iron in Fe²⁺ form) that binds oxygen.

• Myoglobin – similar to hemoglobin, stores oxygen in muscles, also contains heme with iron.

• Cytochromes – electron carriers in the ETC, each contains a heme group with iron that undergoes Fe²⁺ ↔ Fe³⁺ transitions.

• Transferrin – a plasma glycoprotein that transports iron in blood by binding Fe³⁺.

• Collagen – a structural protein of connective tissue. It contains hydroxyproline and hydroxylysine, but no iron.

Incorrect options:

• Transferrin → transports iron (so contains it bound).

• Hemoglobin → iron essential for O₂ transport.

• Cytochrome → iron in heme for electron transport.

• Myoglobin → iron in heme for O₂ storage.

• The HMP shunt (Pentose Phosphate Pathway) occurs in the cytosol and has two phases:

  1. Oxidative phase → produces NADPH and ribulose-5-phosphate.

  2. Non-oxidative phase → interconverts sugars (ribose-5-phosphate for nucleotide synthesis).

• The main end product is NADPH, which is essential for:

  • Fatty acid and cholesterol synthesis

  • Maintaining reduced glutathione (protection against oxidative stress)

  • Cytochrome P450 system

Incorrect options:

• ATP: Not produced here; glycolysis and oxidative phosphorylation handle ATP generation.

• FADH: Produced in the TCA cycle (e.g., by succinate dehydrogenase), not in HMP shunt.

• ADP: Not an end product of this pathway.

• H₂O: Not a direct product of HMP shunt.

✅ Key point: HMP shunt is mainly for NADPH + Ribose-5-phosphate, not energy.

• The duodenum has Brunner’s glands located in the submucosa.

• These glands secrete alkaline mucus (rich in bicarbonate) that protects the mucosa and helps neutralize the acidic gastric chyme entering from the stomach.

• These are unique because most GI glands are located in the mucosa, not the submucosa.

Incorrect options:

• Stomach: Has gastric glands in the mucosa (fundic, pyloric), but no submucosal glands.

• Ileum: Has Peyer’s patches (lymphoid tissue) in the submucosa, not secretory glands.

• Colon: Contains mucosal crypts of Lieberkühn, but no submucosal glands.

• Cecum: Also has crypts of Lieberkühn, but lacks submucosal glands.

✅ Key memory tip: Only the duodenum among the small intestine has submucosal (Brunner’s) glands.

Lipoproteins have different roles depending on their density and content:

• LDL (Low Density Lipoprotein):

  • Main role = transport cholesterol from the liver to peripheral tissues for membrane synthesis, steroid hormone production, etc.

  • This is why LDL is often called “bad cholesterol”—because excess LDL leads to cholesterol deposition in vessel walls → atherosclerosis.

Incorrect options:

• Very low density lipoprotein (VLDL): Transports endogenous triglycerides from the liver to adipose and muscle tissue, not mainly cholesterol.

• Intermediate density lipoprotein (IDL): Transitional particle between VLDL and LDL, carries triglycerides and cholesterol but not the main cholesterol transporter.

• Chylomicrons: Carry dietary triglycerides (exogenous fat) from the intestines to peripheral tissues.

• High density lipoprotein (HDL): Performs reverse cholesterol transport—collects cholesterol from peripheral tissues and brings it back to the liver. Known as “good cholesterol.”

👉 A quick memory tip: “LDL = Lays Down Lipids” in tissues, while “HDL = Hauls lipids back to the Liver.”

The gallbladder histology has some distinctive features:

• Epithelium: Simple columnar with folds (not villi), which increase surface area.

• Lamina propria: Lies just beneath the epithelium.

• Muscular layer: A thin, irregularly arranged smooth muscle layer oriented in different directions (mainly oblique/diagonal).

• No muscularis mucosa and no true submucosa: This is a classic hallmark of the gallbladder wall.

• Perimuscular connective tissue: A layer of dense connective tissue containing blood vessels, lymphatics, and nerves.

Therefore, the incorrect statement is “Nerves and blood vessels in submucosa”, because the gallbladder does not have a submucosa. Instead, vessels and nerves are found in the perimuscular connective tissue.

Incorrect options:

• Thin smooth muscle oriented diagonally → Correct feature; gallbladder muscle fibers are irregular, not in neat layers.

• Epithelium with folds → True; folds of columnar epithelium are present, especially when the gallbladder is empty.

• No muscularis mucosa and submucosa → Correct statement; both are absent.

• Perimuscular dense connective tissue → True; this layer contains vessels and nerves instead of a submucosa.

The L1 vertebra (transpyloric plane) is a very important anatomical landmark. Several abdominal structures lie at this level:

• Duodenum (specifically the 1st part) lies at L1.

• Fundus of the gallbladder is located at the transpyloric plane (L1) in the midclavicular line.

• Neck of the pancreas also lies at L1.

• Pylorus of the stomach lies at the transpyloric plane, thus at L1.

However, the sigmoid colon is not located at this level — it lies much lower, in the pelvic cavity.

Incorrect options:

• Duodenum → The 1st part of the duodenum crosses the transpyloric plane (L1).

• Fundus of the gallbladder → Lies at L1, in line with the transpyloric plane.

• Neck of the pancreas → Found at L1, anterior to the portal vein formation.

• Pylorus of the stomach → Classically lies at L1.

The sigmoid colon is the only structure listed not associated with the L1 vertebral level.

Brunner’s glands are specialized mucus-secreting glands found specifically in the submucosa of the duodenum. Their main role is to secrete alkaline mucus rich in bicarbonate. This helps to:

• Neutralize gastric acid entering from the stomach.

• Provide an optimal pH for pancreatic enzymes to function.

• Protect the duodenal lining from damage.

Thus, their presence is a hallmark feature distinguishing the duodenum from other parts of the GI tract histologically.

Incorrect options:

• Colon → Contains crypts of Lieberkühn but no Brunner’s glands.

• Esophagus → Has esophageal glands, but these are mucus glands in the submucosa, not Brunner’s glands.

• Antrum of the stomach → Contains gastric glands, not Brunner’s glands.

• Ileum → Has Peyer’s patches (lymphoid aggregates) in the submucosa, not Brunner’s glands.

• Fundus of the stomach → Contains fundic glands (parietal, chief, mucous cells), but no Brunner’s glands.

In one turn of the Krebs cycle (citric acid cycle), one acetyl-CoA molecule (2 carbons) enters and combines with oxaloacetate (4 carbons) to form citrate (6 carbons). During the cycle:

• Isocitrate → α-ketoglutarate: catalyzed by isocitrate dehydrogenase, 1 CO₂ released.

• α-ketoglutarate → succinyl-CoA: catalyzed by α-ketoglutarate dehydrogenase, 1 CO₂ released.

Thus, 2 molecules of CO₂ are produced per cycle.

Incorrect options:

• 8 → Far too high. Total 6 CO₂ are released from the complete oxidation of one glucose (through 2 acetyl-CoA in the cycle), but not in a single turn.

• 4 → This is the number of CO₂ produced per glucose in the Krebs cycle (since glucose yields 2 acetyl-CoA, 2 turns = 4 CO₂).

• 0 → False, because decarboxylation reactions clearly occur.

• 1 → Incorrect, as there are two separate decarboxylation steps.

The body (fundus) of the stomach contains fundic glands, which are classified as simple branched tubular glands. They extend from the gastric pits down into the lamina propria and contain a mixture of specialized cells:

• Parietal cells (secreting HCl and intrinsic factor),

• Chief cells (producing pepsinogen),

• Mucous neck cells (secreting protective mucus),

• Enteroendocrine cells (hormones like gastrin, somatostatin).

The branching allows for different secretory regions within a single gland to serve the stomach’s digestive role.

Incorrect options:

• Simple coiled tubular → Found in sweat glands, not in the stomach.

• Simple unbranched alveolar → Rare, but an example is embryonic stage glands; not stomach.

• Simple straight tubular → Seen in the intestines (crypts of Lieberkühn).

• Tubuloalveolar → Found in salivary glands and mammary glands, not in gastric mucosa.

Normal bowel sounds are due to the movement of gas and fluid in the intestines during peristalsis.

• They are usually heard at a frequency of about 5–30 per minute.

In this case, the boy’s peristaltic waves are heard every 3 seconds, which equals about 20 sounds per minute or more. This is faster than usual, consistent with hyperactive bowel sounds.

Such exaggerated activity is commonly seen in diarrhea, gastroenteritis, early intestinal obstruction, or laxative use, where intestinal motility is increased.

Incorrect options:

• None of these → Incorrect because “hyperactive” accurately describes the condition.

• Polarised → Not a term used in clinical classification of gut sounds.

• Hypoactive → Means reduced frequency and intensity of bowel sounds (e.g., in ileus, peritonitis). This is opposite to what’s described.

• Absent → Means no bowel sounds are heard, usually in severe ileus or peritonitis, which is not the case here.

Misoprostol is a synthetic analogue of prostaglandin E₁ (PGE₁).

• Prostaglandins normally stimulate mucus and bicarbonate secretion and increase mucosal blood flow in the stomach, protecting it from acid.

• NSAIDs cause peptic ulcers mainly because they inhibit cyclooxygenase (COX), reducing prostaglandin synthesis.

• By replacing this lost prostaglandin activity, misoprostol prevents and helps heal NSAID-induced gastric ulcers.

It is often used prophylactically in patients who require long-term NSAID therapy.

Incorrect options:

• Vulvovaginitis → Misoprostol has no role; treatment depends on cause (fungal, bacterial, etc.).

• Aphthous mouth ulcers → These are usually self-limiting; topical corticosteroids or analgesics are used, not misoprostol.

• Alcoholic hematemesis → Most often due to esophageal varices or gastric erosions in alcoholics. Management involves endoscopic intervention, not misoprostol.

• Henoch-Schönlein purpura → An IgA-mediated small vessel vasculitis, treated with supportive care or steroids. Misoprostol is not relevant.

Starvation progresses in distinct stages as the body shifts its energy sources:

• First stage (early fasting): The body uses glycogen stores in the liver for glucose. These are depleted within about 24 hours.

• Second stage (prolonged fasting): The body shifts to fat metabolism. Fatty acids are used directly by tissues, and the liver converts them into ketone bodies, which can fuel the brain and muscles. This “protein-sparing” phase conserves muscle tissue.

• Third stage (end stage of starvation): Once fat stores are nearly exhausted, the body begins breaking down muscle proteins for gluconeogenesis, providing amino acids for glucose production to sustain essential tissues (like red blood cells that cannot use ketones). This stage is destructive, leading to severe muscle wasting and eventually death.

So, depletion of muscle tissue best describes the third stage.

Incorrect options:

• Metabolism of fatty acids into ketone bodies → This characterizes the second stage, not the third.

• Depletion of the glycogen stores → Occurs early (first 24 hours), not third stage.

• None of these → Incorrect because one option clearly fits.

• Exhaustion of the contents of digestive tract → This is irrelevant to starvation stages; digestion stops soon after fasting begins.

• Bile canaliculi (Correct) → These are tiny channels formed between adjacent hepatocytes inside the liver. They collect bile at the microscopic level and drain into intrahepatic bile ducts. Since they lie within the liver tissue, they are part of the intrahepatic biliary system, not the extrahepatic one.

• Cystic duct → Connects the gallbladder to the common bile duct. This is an extrahepatic structure.

• Bifurcation of the left and right hepatic ducts → This occurs just outside the liver, forming the common hepatic duct. Therefore, it belongs to the extrahepatic system.

• Common bile duct → Major extrahepatic duct that carries bile to the duodenum.

• Gallbladder → Storage organ for bile, entirely extrahepatic

• Trypsinogen (Correct)

  • Secreted by the pancreas as an inactive precursor.

  • Activated in the duodenum by enterokinase (enteropeptidase) into trypsin, which then activates other pancreatic zymogens (chymotrypsinogen, procarboxypeptidases, etc.).

  • This is a key proteolytic enzyme of pancreatic secretion.

• Sucrase

  • A brush-border enzyme of the small intestine.

  • Breaks down sucrose into glucose + fructose.

  • Not secreted by the pancreas.

• Maltase

  • Also a brush-border enzyme of the small intestine.

  • Breaks down maltose into glucose.

  • Not a pancreatic enzyme.

• Pepsinogen

  • Secreted by gastric chief cells in the stomach.

  • Activated to pepsin in acidic conditions.

  • Not pancreatic in origin.

• Salivary amylase

  • Secreted by salivary glands in the mouth.

  • Begins starch digestion in the oral cavity.

  • Not secreted by the pancreas (though pancreas secretes pancreatic amylase).

Cholesterol synthesis pathway:

• First step (Correct – Cytosol):

  • Two molecules of acetyl-CoA condense to form acetoacetyl-CoA, then combine with another acetyl-CoA to produce HMG-CoA (3-hydroxy-3-methylglutaryl-CoA).

  • These initial reactions occur in the cytosol.

• Next step (Smooth endoplasmic reticulum):

  • HMG-CoA is reduced by HMG-CoA reductase (rate-limiting enzyme) to mevalonate.

  • This enzyme is bound to the membrane of the smooth ER.

Now evaluating the options:

• Golgi bodies → Important in protein modification and sorting, not cholesterol synthesis.

• Smooth endoplasmic reticulum → Involved in later steps of cholesterol synthesis, but not the first step.

• Cytosol (Correct) → Site of the very first condensation reactions forming HMG-CoA.

• Mitochondrion → Mitochondrial HMG-CoA is used for ketone body synthesis, not cholesterol.

• Rough endoplasmic reticulum → Involved in protein synthesis, not lipid biosynthesis.

• Gastroduodenal artery (Correct)

  • A branch of the common hepatic artery (from the celiac trunk).

  • It runs posterior to the first part of the duodenum.

  • A posterior duodenal ulcer can erode into it, causing severe upper GI hemorrhage (massive hematemesis or melena).

• Superior pancreaticoduodenal artery

  • Branch of the gastroduodenal artery.

  • Supplies the head of pancreas and duodenum but is not the vessel classically involved in posterior duodenal ulcer bleeding.

• Inferior pancreaticoduodenal artery

  • Branch of the superior mesenteric artery (SMA).

  • Supplies lower pancreas and duodenum, but not the site most commonly affected by ulcer erosion.

• Superior mesenteric artery

  • Major midgut artery, not directly endangered by duodenal ulcers.

• Left gastric artery

  • Branch of celiac trunk.

  • Supplies the stomach and lower esophagus. It is more commonly involved in gastric ulcers, not duodenal ones.

• Lesser omentum

  • Extends from the liver (specifically the porta hepatis, fissure for ligamentum venosum, and fissure for ligamentum teres) → to the lesser curvature of the stomach and the proximal duodenum.

  • It is divided into two parts:

    • Hepatogastric ligament → connects liver to stomach.

    • Hepatoduodenal ligament → connects liver to duodenum, enclosing the portal triad (portal vein, hepatic artery proper, common bile duct).

Now let’s consider the options:

• Gallbladder → Lies beneath the liver, not a point of attachment for the lesser omentum.

• Pancreas → Retroperitoneal organ, related to the posterior abdominal wall, not directly connected by the lesser omentum.

• Ovaries → Located in the pelvis, completely unrelated to the omentum.

• Liver (Correct) → The origin of the lesser omentum.

• Spleen → Connected to the stomach by the gastrosplenic ligament, not the lesser omentum.

• Omeprazole (Correct)

  • A proton pump inhibitor (PPI).

  • Irreversibly inhibits the H⁺/K⁺ ATPase in parietal cells.

  • This is the final step in acid secretion, so inhibition is profound and long-lasting.

  • PPIs are the most effective drugs for suppressing gastric acid secretion and are widely used in peptic ulcer disease, GERD, and Zollinger–Ellison syndrome.

• Ranitidine

  • An H₂ receptor antagonist.

  • It reduces acid secretion by blocking histamine stimulation of parietal cells.

  • Effective, but weaker compared to PPIs.

• Misoprostol

  • A prostaglandin E₁ analog.

  • Inhibits acid secretion modestly while promoting mucus and bicarbonate secretion.

  • Mainly used for NSAID-induced ulcer prevention, not as potent as PPIs.

• Atropine

  • A muscarinic receptor antagonist.

  • Can reduce acid secretion by blocking vagal stimulation, but has widespread side effects and is not used clinically for this purpose.

• Bismuth subsalicylate

  • A mucosal protectant with antimicrobial activity (against H. pylori).

  • It does not significantly suppress acid secretion.

• Chylomicrons (Correct)

  • Formed in the intestine after a meal.

  • They carry dietary triglycerides (mainly) and some cholesterol to peripheral tissues.

  • Because they are rich in triglycerides and very low in protein, they have the lowest density of all lipoproteins.

• Very low-density lipoproteins (VLDL)

  • Synthesized in the liver.

  • They carry endogenous triglycerides, but less than chylomicrons.

  • Denser than chylomicrons, but less dense than LDL and HDL.

• Intermediate-density lipoproteins (IDL)

  • Formed as a VLDL remnant after triglyceride removal.

  • Contains fewer triglycerides and more cholesterol than VLDL.

  • Denser than VLDL.

• Low-density lipoproteins (LDL)

  • Cholesterol-rich lipoproteins derived from IDL.

  • Their main role is to deliver cholesterol to tissues.

  • Far denser than VLDL and chylomicrons.

• High-density lipoproteins (HDL)

  • Protein-rich lipoproteins.

  • They are involved in reverse cholesterol transport (bringing cholesterol back to the liver).

  • Because they have the highest protein content, they are the most dense.

Anterior relation of spleen:

• The stomach lies directly anterior to the spleen, specifically its fundus, separated by the gastrosplenic ligament (which contains short gastric and left gastroepiploic vessels).

Other relations (not anterior):

• Left colic flexure → lies inferior to the spleen.

• Diaphragm → lies posterior and lateral to the spleen, separating it from the pleura, lung, and ribs.

• Left kidney → lies posterior and medial to the spleen.

• Tail of the pancreas → lies medial to the spleen, within the splenorenal ligament.

Choledochoduodenostomy is a surgical procedure in which the common bile duct (CBD) is directly anastomosed to the second part of the duodenum.

• This allows bile to drain directly into the intestinal lumen, bypassing an obstruction at the distal bile duct or sphincter of Oddi.

• It is typically indicated for recurrent choledocholithiasis or benign/malignant strictures of the distal CBD.

Now let’s consider the options:

• The duct of Santorini → This is the accessory pancreatic duct, which drains into the duodenum separately. It is not involved in bile drainage.

• Common bile duct (Correct) → Main extrahepatic bile duct, carrying bile from liver and gallbladder to duodenum. This is the duct used in choledochoduodenostomy.

• The duct of Wirsung → This is the main pancreatic duct, carrying pancreatic juice. Not used in this procedure.

• Left hepatic duct → Drains bile from the left lobe of the liver, but higher up in the biliary tree; not directly connected to the duodenum.

• Right hepatic duct → Same reasoning as left hepatic duct; not part of this surgical anastomosis.

✅ In summary: In choledochoduodenostomy, the common bile duct is surgically joined to the duodenum.

The quadrate lobe is part of the anatomical (not functional) left lobe of the liver. Its boundaries are:

• Anteriorly → Inferior border (anterior margin) of the liver

• Posteriorly → Porta hepatis

• Right → Fossa for the gallbladder

• Left → Fossa for the umbilical vein (ligamentum teres)

So the quadrate lobe is framed like a small rectangle on the inferior surface.

Now, the ligamentum venosum is associated with the caudate lobe, which is on the posterior-superior surface of the liver, between the inferior vena cava and the ligamentum venosum. It does not form a boundary of the quadrate lobe.

✔ Boundaries of quadrate lobe = porta hepatis, fossa for gallbladder, fossa for umbilical vein, anterior margin.
✘ Not a boundary = ligamentum venosum → related to the caudate lobe instead.

The esophagus is supplied segmentally:

• Cervical part → supplied by the inferior thyroid artery (branch of the thyrocervical trunk).

• Thoracic part → supplied by branches from the thoracic aorta and sometimes bronchial arteries.

• Abdominal part → supplied by the left gastric artery (branch of the celiac trunk) and the left inferior phrenic artery.

Now let’s review the options:

• Suprarenal artery → supplies the adrenal glands, not the esophagus.

• Left iliac artery → supplies the pelvic and lower limb regions, far from the esophagus.

• Inferior thyroid artery → correct for the cervical esophagus, not the abdominal segment.

• Left gastric artery (Correct) → arises from the celiac trunk, gives esophageal branches that supply the abdominal esophagus.

• Thoracic aorta → supplies the thoracic portion of the esophagus, not the abdominal.

Therefore, the left gastric artery provides the main arterial supply to the abdominal esophagus

When analyzing this, recall the embryological division of gut blood supply:

• Celiac trunk → foregut (esophagus to proximal duodenum, plus pancreas up to the superior head).

• Superior mesenteric artery (SMA) → midgut (distal duodenum to proximal 2/3 of transverse colon, including appendix, uncinate process, and inferior head of pancreas).

So, the key is to differentiate between foregut vs midgut vascular territories.

Explanation

• Uncinate process
  Part of the pancreas derived from the ventral bud (midgut territory). It is supplied by branches of the SMA, specifically the inferior pancreaticoduodenal artery.

• Appendix
  A midgut structure supplied by the appendicular artery, which comes from the ileocolic artery, a branch of the SMA.

• Duodenum
  The duodenum is divided: the proximal part (up to the major papilla) is foregut → celiac supply; the distal part (beyond the major papilla) is midgut → SMA supply. So part of the duodenum is indeed supplied by the SMA (via the inferior pancreaticoduodenal artery).

• Inferior region of the head of pancreas
  Supplied by the SMA (via the inferior pancreaticoduodenal artery).

• Superior region of the head of pancreas (Correct)
  This portion is supplied by the celiac trunk, specifically the gastroduodenal artery (from the common hepatic), which gives rise to the superior pancreaticoduodenal arteries. It does not fall under SMA supply.

Thus, the superior region of the head of the pancreas is not supplied by the SMA.

There are two isoenzymes of HMG-CoA synthase in humans, and their location determines their function:

• Mitochondrial HMG-CoA synthase → involved in ketone body synthesis (important during fasting).

• Cytosolic HMG-CoA synthase → involved in the mevalonate pathway, which is the first step in cholesterol synthesis.

Now, looking at the options:

• Triacylglycerols (TAGs)
  These are synthesized from glycerol-3-phosphate and fatty acyl-CoA in the cytosol/ER, but not via HMG-CoA synthase.

• Pyruvate
  Pyruvate is generated mainly through glycolysis. HMG-CoA synthase has no role in pyruvate metabolism.

• Ketone bodies
  True for the mitochondrial isoform of HMG-CoA synthase, but the question specifically asks about the cytosolic enzyme.

• Glycerol
  Produced from glycolysis (via dihydroxyacetone phosphate) or from dietary sources. Not linked to HMG-CoA synthase.

• Cholesterol (Correct)
  The cytosolic HMG-CoA synthase converts acetyl-CoA to HMG-CoA, which is then reduced by HMG-CoA reductase (the rate-limiting step) to mevalonate, a precursor of cholesterol.

Thus, in the cytosol, HMG-CoA synthase participates in cholesterol synthesis, while its mitochondrial counterpart is used in ketone body synthesis.

• Correct option: Albumin
  Albumin is synthesized exclusively by the liver. It is the most abundant plasma protein and has crucial roles: maintaining plasma oncotic pressure and transporting substances such as fatty acids, bilirubin, calcium, hormones, and drugs. Its synthesis is a marker of liver function; low albumin levels are seen in chronic liver disease and malnutrition.

• Incorrect option: Myosin
  Myosin is a motor protein found in muscle cells, responsible for contraction. It is not synthesized exclusively by the liver; instead, it’s produced by muscle cells themselves.

• Incorrect option: Keratin
  Keratin is a structural protein found in skin, hair, and nails. It is synthesized by keratinocytes, not the liver.

• Incorrect option: Gamma globulin
  Gamma globulins refer mainly to immunoglobulins (antibodies), which are produced by plasma cells (differentiated B lymphocytes), not by the liver.

• Incorrect option: Hemoglobin
  Hemoglobin is synthesized in developing red blood cells in the bone marrow, not in the liver.

Thus, the only protein in this list synthesized exclusively by the liver is Albumin.

Von Gierke disease (Glycogen storage disease type I) is caused by a deficiency of glucose-6-phosphatase (or sometimes its transporter). This enzyme is located in the endoplasmic reticulum of the liver and kidney. Its role is to convert glucose-6-phosphate → free glucose + Pi, the last step of both glycogenolysis and gluconeogenesis.

If this enzyme is deficient:

• Glucose-6-phosphate cannot be converted into free glucose.

• This leads to severe fasting hypoglycemia.

• Excess G6P is shunted into glycolysis and the HMP shunt, causing lactic acidosis, hyperuricemia, and hyperlipidemia.

• The liver and kidney enlarge due to glycogen accumulation (hepatomegaly, renomegaly).

Now let’s examine why the other options are incorrect:

• 6-Phosphogluconate dehydrogenase (6PGD)
  An enzyme of the HMP shunt, not related to glycogen storage. Deficiency does not cause von Gierke disease.

• Phosphofructokinase (PFK)
  A key regulatory enzyme of glycolysis, not involved in glycogenolysis or gluconeogenesis. Its deficiency leads to glycogen storage disease type VII (Tarui disease), not von Gierke.

• 6-phosphogluconolactonase (PGLS)
  Also part of the HMP shunt, not relevant here.

• Glucose-6-phosphate dehydrogenase (G6PD)
  This is the rate-limiting enzyme of the HMP shunt. Its deficiency leads to hemolytic anemia due to lack of NADPH, but not glycogen accumulation or hypoglycemia.

Therefore, the enzyme deficient in von Gierke disease is Glucose-6-phosphatase.

The hexose monophosphate (HMP) shunt, also called the pentose phosphate pathway (PPP), has two phases:

• Oxidative phase (irreversible, generates NADPH and ribulose-5-phosphate)

• Non-oxidative phase (reversible, interconverts sugars like ribose-5-phosphate)

The rate-limiting enzyme of the oxidative phase is Glucose 6-phosphate dehydrogenase (G6PD).

• Correct option: Glucose 6-phosphate dehydrogenase (G6PD)
  This enzyme catalyzes the first reaction of the oxidative phase, converting glucose-6-phosphate into 6-phosphogluconolactone, producing NADPH in the process. Because it’s the initial, committed step, it’s heavily regulated by the cell’s NADP⁺/NADPH ratio. A deficiency of G6PD leads to reduced NADPH, which makes red blood cells more vulnerable to oxidative stress, causing hemolysis.

• Incorrect option: 6-phosphogluconolactonase (PGLS)
  This enzyme hydrolyzes 6-phosphogluconolactone to 6-phosphogluconate. It is part of the oxidative phase but is not rate-limiting and is not tightly regulated.

• Incorrect option: 6-Phosphogluconate dehydrogenase (6PGD)
  This enzyme catalyzes the oxidative decarboxylation of 6-phosphogluconate to ribulose-5-phosphate with NADPH production. Important, but not the rate-limiting step.

• Incorrect option: Ribose-5-phosphate isomerase (RPI)
  This belongs to the non-oxidative phase, interconverting ribulose-5-phosphate and ribose-5-phosphate. It is not rate-limiting.

• Incorrect option: Phosphofructokinase (PFK)
  This enzyme is the rate-limiting step of glycolysis, not the HMP shunt.

Thus, the rate-limiting enzyme of the oxidative phase of the HMP shunt is G6PD.

The appendix receives its blood supply through the appendicular artery, which is a branch of the ileocolic artery. Let’s analyze why this is correct and why the other options are not:

• Correct option: Ileocolic artery
  The ileocolic artery is a branch of the superior mesenteric artery (SMA). It runs towards the terminal ileum, cecum, and appendix. From it arises the appendicular artery, which passes behind the terminal ileum to reach the appendix, providing its sole arterial supply. This is clinically important because thrombosis or blockage of this artery can cause appendicular ischemia, contributing to appendicitis.

• Incorrect option: Left colic artery
  This arises from the inferior mesenteric artery (IMA) and supplies the descending colon and left colic flexure. It has no connection to the appendix, which belongs to the midgut territory, not the hindgut.

• Incorrect option: Middle colic artery
  A branch of the SMA that supplies the transverse colon. It does not extend far enough to supply the appendix.

• Incorrect option: Sigmoid artery
  A branch of the IMA, it supplies the sigmoid colon. Again, it is part of the hindgut, not the midgut where the appendix resides.

• Incorrect option: Right colic artery
  A branch of the SMA that supplies the ascending colon. While it is close in territory, it does not directly give rise to the appendicular artery.

Hence, the ileocolic artery is the correct answer because it directly provides the branch (appendicular artery) that supplies the appendix.

Von Gierke’s disease (Glycogen Storage Disease Type I) is caused by a deficiency of the enzyme glucose-6-phosphatase, which is crucial for the final step of both glycogenolysis and gluconeogenesis. Without this enzyme:

• Glucose-6-phosphate cannot be converted to free glucose, so glucose cannot be released into the bloodstream.

• As a result, blood glucose levels remain abnormally low, especially during fasting.

This leads to severe fasting hypoglycemia, and to compensate, the body activates other metabolic pathways that cause various metabolic imbalances.

Key Features of von Gierke’s Disease:

✅ Hypoglycemia – due to failure to release glucose
✅ Hyperuricemia – from impaired glucose metabolism and increased nucleotide turnover
✅ Hyperlactatemia – due to excess glycolytic flux and lactic acid buildup
✅ Hyperlipidemia – from increased fat mobilization and liver triglyceride synthesis

❌ Hyperglycemia is not a feature — it’s the opposite of what happens in von Gierke’s disease. Therefore, it is the correct answer to the question asking what is not true.

Non-compliance refers to a situation where a patient does not follow the medical advice or prescribed treatment regimen provided by their healthcare provider. This can include:

• Not taking medications as prescribed

• Skipping follow-up appointments

• Ignoring dietary or lifestyle recommendations

• Failing to complete a course of therapy

This term has historically been used in clinical settings to describe non-adherence, but it carries a somewhat judgmental tone, implying blame on the patient.

📝 Today, many healthcare professionals prefer the term “non-adherence”, or even better, “concordance”, which emphasizes shared decision-making and mutual agreement between the patient and provider.

Why the Other Options Are Incorrect:

• Discordance: ❌ Refers to a lack of agreement or harmony, often between the patient and healthcare provider, but it’s not the standard term for failing to follow treatment.

• Compliance: ❌ This is the desired behavior—following medical advice or treatment, not the failure to do so.

• Concordance: ❌ This is a modern, more respectful approach focusing on collaborative decision-making, not a term for treatment refusal.

• None of these: ❌ Incorrect because “non-compliance” is the recognized traditional term for what the question describes.

Glycogenin is a self-glucosylating protein that plays a critical role in the initiation of glycogen synthesis.

Here’s how it works:

• Glycogen synthase, the enzyme responsible for adding glucose units to a growing glycogen chain, cannot begin the process from scratch.

• Glycogenin solves this by attaching glucose residues to a specific tyrosine residue on itself.

• Once about 8 glucose units are added, glycogen synthase can then elongate the chain.

• Glycogenin remains covalently attached to the core of the glycogen molecule.

Without glycogenin, de novo glycogen synthesis would not occur.

Why the Other Options Are Incorrect:

• Gloverin: ❌ An antimicrobial protein found in insects; not involved in glycogen metabolism.

• Dystrophin: ❌ A muscle protein that connects the cytoskeleton of muscle cells to the extracellular matrix; not related to glycogen.

• Globulin: ❌ A class of blood proteins (like immunoglobulins); not involved in glycogen synthesis.

• Albumin: ❌ The most abundant plasma protein, responsible for maintaining oncotic pressure and transporting molecules—unrelated to glycogen.

The space of Disse (perisinusoidal space) is the narrow space between hepatocytes and liver sinusoidal endothelial cells. It plays a key role in exchange of substances between blood and hepatocytes.

Structures present in the space of Disse:

• Blood plasma (but not RBCs)

• Hepatic stellate cells (Ito cells) → vitamin A storage, fibrosis

• Microvilli of hepatocytes (increase surface area)

• It lies adjacent to liver sinusoidal endothelial cells (which form the boundary)

Structure NOT present in the space of Disse:

• ❌ Kupffer cells → these are macrophages located within the sinusoidal lumen, not in the space of Disse

Why the other options are incorrect:

• ❌ None of these → incorrect because Kupffer cells are not present

• ❌ Blood plasma → present for metabolic exchange

• ❌ Hepatic stellate cells → classic resident cells of the space of Disse

• ❌ Liver sinusoidal endothelial cells → form the boundary adjacent to the space

The portal vein is a vital vessel that transports nutrient-rich, deoxygenated blood from the gastrointestinal tract and spleen to the liver for metabolism, detoxification, and storage.

It is typically formed posterior to the neck of the pancreas by the union of:

• The superior mesenteric vein (SMV) — drains blood from the small intestine, cecum, ascending colon, and transverse colon

• The splenic vein — drains blood from the spleen, pancreas, and part of the stomach

🧠 This anatomical convergence occurs around the level of L2 vertebra, and the inferior mesenteric vein (IMV) usually drains into the splenic vein before this union.

Why the Other Options Are Incorrect:

• The inferior mesenteric vein and the splenic vein: ❌ While the IMV typically drains into the splenic vein, this union does not directly form the portal vein.

• The splenic vein and the inferior pancreaticoduodenal vein: ❌ The inferior pancreaticoduodenal vein is a tributary of the SMV, not a major partner in forming the portal vein.

• The superior mesenteric vein and the inferior mesenteric vein: ❌ These don’t directly unite to form the portal vein.

• The inferior mesenteric vein and the inferior pancreaticoduodenal vein: ❌ Neither of these alone or together form the portal vein; both are tributaries of larger veins.

The portal vein is a key vessel in the portal venous system, which carries nutrient-rich, deoxygenated blood from the gastrointestinal tract and associated organs to the liver for processing.

It is formed by the union of the superior mesenteric vein and splenic vein behind the neck of the pancreas.

The portal vein drains:

• The entire alimentary canal (from lower esophagus to upper anal canal)

• Spleen (via the splenic vein)

• Pancreas

• Gall bladder

These organs are involved in digestion, absorption, or blood cell turnover, and the blood from them is filtered and detoxified in the liver.

❌ Kidney is not drained by the portal vein.

• It is drained by the renal veins, which drain directly into the inferior vena cava (IVC).

• The kidneys are not involved in digestion but rather in filtration, electrolyte balance, and excretion.

Why the Other Options Are Correct (i.e., are drained by the portal vein):

• Gall bladder: ✔️ Drained via cystic veins, which connect to portal venous branches.

• Pancreas: ✔️ Venous drainage enters the splenic vein or superior mesenteric vein, both of which contribute to the portal vein.

• Spleen: ✔️ Drains into the splenic vein, a direct tributary of the portal vein.

• Abdominal part of the alimentary canal (except the anus): ✔️ All parts from lower esophagus to upper anal canal drain into the portal system.

Somatostatin is a powerful inhibitory hormone secreted by D cells found in the stomach, intestine, and pancreas. Its primary function is to suppress the secretion of several other hormones, making it a key regulatory brake in the digestive system.

One of its main targets is the G cell, which secretes gastrin—a hormone that:

• Stimulates parietal cells to secrete hydrochloric acid (HCl)

• Promotes gastric motility

• Enhances growth of the gastric mucosa

By inhibiting G cells, somatostatin:

• Reduces gastrin release

• Indirectly decreases acid secretion

• Helps protect the mucosa from excess acidity

Why the Other Options Are Incorrect:

• Endocrine cells: ❌ This is too broad—somatostatin may inhibit several endocrine cell types, but the question seeks the most specific, known target in the context of gastric regulation.

• Chief cells: ❌ These secrete pepsinogen. Somatostatin doesn’t directly target them; their activity is more influenced by gastrin and vagal stimulation.

• PP cells (Pancreatic polypeptide cells): ❌ Found in the pancreas, not the stomach. Somatostatin can inhibit them, but G cells are the primary gastric target.

• Mucosal epithelial cells: ❌ These form a protective barrier, not primarily hormone-secreting cells. They’re not a direct target of somatostatin

In the Krebs cycle (citric acid cycle), the conversion of fumarate to malate is catalyzed by the enzyme fumarase (fumarate hydratase).

This reaction is a hydration reaction, meaning it adds water (H₂O) across the double bond of fumarate to form L-malate.

Fumarate+H2O→MalateFumarate+H2​O→Malate

• No ATP or electron carriers (like NAD⁺ or FAD) are required for this step.

• It is a simple addition of water, preparing malate for the next step—oxidation to oxaloacetate by malate dehydrogenase.

Why the Other Options Are Incorrect:

• ATP: ❌ Not required in this step. The Krebs cycle only involves substrate-level phosphorylation at one point (succinyl-CoA to succinate).

• NADPH₂: ❌ Not involved in the Krebs cycle; NADH, not NADPH, is produced in the cycle, but not in this step.

• O₂ (oxygen): ❌ Oxygen is the final electron acceptor in the electron transport chain, but it is not directly involved in any Krebs cycle reactions.

• FADH₂: ❌ Produced (not consumed) in another step of the cycle—succinate to fumarate (by succinate dehydrogenase). It is not needed for fumarate to malate conversion.

The enzyme phosphoglycerate kinase is involved in both glycolysis and gluconeogenesis, making it bidirectional and functionally reversible.

In glycolysis, it catalyzes:

1,3-bisphosphoglycerate+ADP→3-phosphoglycerate+ATP1,3-bisphosphoglycerate+ADP→3-phosphoglycerate+ATP

— this is an ATP-generating step (substrate-level phosphorylation).

In gluconeogenesis, the same reaction proceeds in reverse:

3-phosphoglycerate+ATP→1,3-bisphosphoglycerate+ADP3-phosphoglycerate+ATP→1,3-bisphosphoglycerate+ADP

— this is an ATP-consuming step.

Phosphoglycerate kinase is one of the enzymes that catalyze reversible steps, unlike the irreversible, regulated enzymes in glycolysis (like hexokinase, phosphofructokinase-1, and pyruvate kinase), which are bypassed in gluconeogenesis.

Why the Other Options Are Incorrect:

• Phosphofructokinase-2 (PFK-2): ❌ Not part of the main glycolytic pathway; regulates fructose 2,6-bisphosphate, which controls PFK-1 activity. It’s not shared between glycolysis and gluconeogenesis.

• Phosphofructokinase-1 (PFK-1): ❌ A key irreversible enzyme of glycolysis; it’s bypassed in gluconeogenesis by fructose-1,6-bisphosphatase.

• Pyruvate kinase: ❌ Also irreversible and specific to glycolysis. In gluconeogenesis, its action is bypassed by pyruvate carboxylase and PEP carboxykinase.

• Hexokinase: ❌ Irreversible enzyme that phosphorylates glucose in glycolysis. In gluconeogenesis, it’s bypassed by glucose-6-phosphatase.

Trypsin is the main enzyme responsible for protein digestion in the duodenum.

Here’s how it works:

• Trypsinogen, the inactive zymogen form of trypsin, is secreted by the pancreas.

• In the duodenum, it is activated by the enzyme enteropeptidase (also called enterokinase), which converts it to active trypsin.

• Trypsin then digests proteins by cleaving peptide bonds, especially those next to lysine and arginine residues.

• It also activates other pancreatic proteases (like chymotrypsinogen and procarboxypeptidase), making it essential for full protein digestion.

Why the Other Options Are Incorrect:

• Lipase: ❌ Digests fats (lipids), not proteins. Active in the duodenum but unrelated to protein digestion.

• Pepsin: ❌ Active in the stomach, not the duodenum. It begins protein digestion but is inactivated by the alkaline pH in the duodenum.

• Amylase: ❌ Breaks down carbohydrates (starch) into sugars, not proteins.

• None of them: ❌ Incorrect—trypsin definitely digests proteins in the duodenum.

The citric acid cycle (Krebs cycle or TCA cycle) occurs in the mitochondrial matrix and is a central hub of aerobic metabolism. While the cycle itself directly produces very little ATP, its main function is to generate reduced coenzymes that feed into the electron transport chain (ETC) for ATP production.

For each acetyl-CoA that enters the cycle, the following are produced:

• 3 NADH → Each yields ~3 ATP → 9 ATP

• 1 FADH₂ → Yields ~2 ATP → 2 ATP

• 1 GTP (substrate-level phosphorylation) → Equivalent to 1 ATP

🔸 Total = 7.5 + 1.5 + 1 = 12 ATP per acetyl-CoA

Since each glucose yields 2 acetyl-CoA molecules, the total yield per glucose from the TCA cycle is 24 ATP — but the question specifically asked per cycle turn (per acetyl-CoA).

Parietal cells (also called oxyntic cells) are large, round to pyramidal cells found mainly in the gastric glands of the fundus and body of the stomach. They perform two key functions:

• Secretion of hydrochloric acid (HCl): Aids in protein digestion and creates a sterile acidic environment.

• Secretion of intrinsic factor: Essential for vitamin B12 absorption in the ileum.

Under the microscope, parietal cells have a characteristic “fried-egg” appearance due to:

• A large, round, centrally placed nucleus (like the yolk),

• A pale, eosinophilic cytoplasm (the egg white), which is due to their abundant mitochondria and intracellular canaliculi used for acid secretion.

They stand out clearly in H&E-stained sections of the gastric mucosa.

Why the Other Options Are Incorrect:

• Enteroendocrine cells: These are small, hormone-secreting cells found scattered in the base of gastric and intestinal glands. They have granules at the base and are often difficult to see without special stains. They do not have a “fried-egg” appearance.

• Zymogenic cells (chief cells): Found in the deeper part of gastric glands, they produce pepsinogen and have a basophilic, granular cytoplasm due to rough ER—not pale, and not fried-egg–like.

• Mucous neck cells: Located in the neck of gastric glands, they secrete mucus and are irregular in shape with basophilic cytoplasm—not resembling a fried egg histologically.

• Stem cells: These reside in the neck region of gastric glands and are small with a high nucleus-to-cytoplasm ratio. Their appearance is dense and compact, not pale and not egg-like.

Pancreatic juice plays a crucial role in digestive function, and its composition is tailored to both:

• Neutralize the acidic gastric contents (chyme)

• Provide the optimal pH environment for pancreatic enzymes to function in the duodenum

The predominant ion in pancreatic juice is bicarbonate (HCO₃⁻). It is secreted by the ductal cells of the pancreas in response to the hormone secretin, which is released when acidic chyme enters the small intestine.

The high concentration of bicarbonate in pancreatic secretions serves to:

• Raise the pH of the intestinal contents

• Protect the duodenal mucosa from gastric acid

• Activate and optimize the function of digestive enzymes like pancreatic amylase, lipase, and proteases

Why the Other Options Are Incorrect:

• Hydrogen ion (H⁺): ❌ This would acidify the environment, which is the opposite of what pancreatic juice does.

• Fluoride ion (F⁻): ❌ Not physiologically significant in pancreatic juice composition.

• Potassium ion (K⁺): ❌ Present in very low concentrations and not a major component.

• Chloride ion (Cl⁻): ❌ Present, but inversely related to bicarbonate concentration—as HCO₃⁻ increases, Cl⁻ decreases in pancreatic secretions.

The liver is a multifunctional organ with major roles in metabolism, detoxification, storage, synthesis, and digestion-related processes. However, oxygenation of blood is not one of its functions.

Here’s a breakdown:

✅ Bile production and secretion:
The liver continuously produces bile, which is essential for emulsifying fats in the small intestine and aiding in fat absorption.

✅ Storage of glycogen, vitamins, and minerals:
The liver stores glycogen (a glucose polymer), fat-soluble vitamins (A, D, E, K), vitamin B12, iron, and copper for later use.

✅ Detoxification of chemicals:
One of the liver’s most vital roles is to detoxify drugs, alcohol, hormones, and metabolic waste products via enzymes like those in the cytochrome P450 system.

✅ Metabolism of fats, proteins, and carbohydrates:
The liver metabolizes amino acids, fatty acids, and glucose, playing a central role in gluconeogenesis, lipogenesis, urea cycle, and protein synthesis.

❌ Oxygenation of blood:
This function is performed by the lungs, not the liver. Oxygenation refers to the exchange of gases in the alveoli, where blood releases carbon dioxide and picks up oxygen—a process completely unrelated to hepatic function.

In epidemiology, the index case is the first case that comes to the attention of health authorities or investigators, prompting an outbreak investigation.

• The index case may not necessarily be the first person infected, but it is the first identified and reported case that sets the investigation in motion.

• Identifying the index case helps establish time, place, and person distribution and is crucial in constructing the epidemic curve and tracing contacts.

Why the Other Options Are Incorrect:

• Secondary case: Refers to individuals who become infected from contact with the index case or other primary cases. These cases help measure transmission.

• Crucial case: ❌ Not a recognized epidemiological term.

• Primary case: Refers to the actual first person to become infected in a population, which may or may not be the index case. The primary case could go undetected if asymptomatic or misdiagnosed.

• Tertiary case: Refers to those infected by secondary cases, i.e., the third level in the chain of transmission. This term is rarely used in outbreak descriptions.

Cholesterol biosynthesis is a multi-step process that occurs mainly in the liver and involves the conversion of acetyl-CoA into cholesterol through a complex series of enzymatic reactions.

The major regulatory (rate-limiting) enzyme in this pathway is 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoA reductase). This enzyme catalyzes the conversion of HMG-CoA to mevalonate, a crucial early step in cholesterol synthesis.

• Regulation: HMG-CoA reductase is highly regulated via:

  • Feedback inhibition by cholesterol

  • Hormonal control (e.g., insulin upregulates it, glucagon downregulates it)

  • Pharmacologic inhibition by statins, which are competitive inhibitors of this enzyme

Why the Other Options Are Incorrect:

• Mevalonate kinase: While it acts after HMG-CoA reductase in the pathway (phosphorylating mevalonate), it is not rate-limiting or a major regulatory point.

• Acetyl-CoA acetyltransferase: Involved in the very early step of forming acetoacetyl-CoA from acetyl-CoA, but not a regulatory enzyme in cholesterol biosynthesis.

• HMG-CoA synthase: Catalyzes the formation of HMG-CoA from acetoacetyl-CoA and acetyl-CoA, but this step is not regulated and occurs prior to the rate-limiting step.

• Farnesyl-PP (pyrophosphate) synthase: Functions later in the pathway during the synthesis of isoprenoids and cholesterol intermediates; it’s important, but not rate-limiting.

Extrapyramidal side effects (EPSEs) are drug-induced movement disorders that include dystonia, akathisia, parkinsonism, and tardive dyskinesia. These occur due to dopamine D2 receptor blockade in the nigrostriatal pathway of the brain, which is essential for regulating motor activity.

Metoclopramide is a dopamine D2 receptor antagonist primarily used as an antiemetic and prokinetic agent. While effective for nausea, vomiting, and gastroparesis, it crosses the blood-brain barrier and can block D2 receptors in the basal ganglia, leading to extrapyramidal symptoms, especially with prolonged use or high doses.

Why the Other Options Are Incorrect:

• Benztropine: ❌ Not a cause—actually used to treat extrapyramidal symptoms. It’s an anticholinergic agent that restores dopamine-acetylcholine balance in the basal ganglia.

• Benzodiazepine: ❌ These are GABA-A receptor agonists, used for anxiety, seizures, and muscle relaxation. They do not block dopamine receptors and don’t cause EPSEs.

• Clozapine: ❌ An atypical antipsychotic with very low affinity for D2 receptors. It is least likely among antipsychotics to cause extrapyramidal symptoms. It may cause agranulocytosis and sedation, but not EPSEs.

• Procyclidine: ❌ Like benztropine, it is an anticholinergic drug used to manage or prevent extrapyramidal side effects caused by antipsychotic medications.

The caudate lobe of the liver is often referred to as the “autonomous zone” because of its distinct blood supply and venous drainage, which set it apart from the rest of the liver.

Here’s why it earns that title:

• It receives blood from both the right and left branches of the portal vein and hepatic artery, allowing it to function independently of either lobe.

• It has its own direct drainage into the inferior vena cava (IVC) via small hepatic veins, not through the main hepatic veins shared by the other lobes.

• This autonomy means that in cases of portal vein thrombosis, cirrhosis, or lobar atrophy, the caudate lobe often enlarges compensatorily and remains functional.

Why the Other Options Are Incorrect:

• Right lobe: While large and functionally significant, it is not autonomous—its blood supply and venous drainage are typical and dependent on common hepatic vasculature.

• Left lobe: Also shares the common portal and hepatic circulation; it does not function independently.

• Quadrate lobe: An anatomically defined area near the gallbladder and left lobe, with no autonomous supply; considered part of the functional left lobe.

• None of these: ❌ Incorrect, because the caudate lobe is the correct answer.

Bile is produced by hepatocytes and first collected in bile canaliculi, which are tiny channels formed by grooves in adjacent hepatocyte membranes. From there, bile must enter progressively larger channels until it eventually reaches the common hepatic duct and beyond.

The first structure to receive bile from the bile canaliculi is the Canal of Hering.

• The Canals of Hering are short, narrow passages that serve as a transitional zone between the bile canaliculi and the intrahepatic bile ductules.

• They contain both hepatocytes and cholangiocytes (bile duct epithelial cells) and are also thought to be a niche for hepatic progenitor cells.

Why the Other Options Are Incorrect:

• Duct of Wirsung: This is the main pancreatic duct, which joins the common bile duct before entering the duodenum. It has no role in bile flow from hepatocytes.

• Cystic duct: Connects the gallbladder to the common bile duct, allowing storage and release of bile, but it is well downstream of the canaliculi.

• Ductules: Also called intralobular bile ductules, they receive bile after it passes through the Canals of Hering.

• Common hepatic duct: A large extrahepatic duct formed by the union of the right and left hepatic ducts; bile passes through this much later in the drainage sequence.

Pancreatic secretion is a vital component of digestion, as the pancreas releases digestive enzymes (like lipases, proteases, and amylase) and bicarbonate-rich fluid into the duodenum to help break down food components.

Among the key regulators of pancreatic secretion, two main hormones are secreted by the small intestine:

1. Cholecystokinin (CCK) – Released by I cells in the duodenum and jejunum in response to fats and partially digested proteins.

   • Primary action: Stimulates the acinar cells of the pancreas to secrete enzyme-rich pancreatic juice, essential for digestion.

   • Also causes gallbladder contraction and relaxation of the sphincter of Oddi.

2. Secretin – Released by S cells in response to acidic chyme (low pH) from the stomach.

   • Primary action: Stimulates ductal cells of the pancreas to secrete bicarbonate-rich fluid, neutralizing stomach acid.

Why the Other Options Are Incorrect:

• Hydrochloric acid (HCl): While it triggers secretin release, it does not directly stimulate pancreatic enzyme secretion. Its main role is in protein denaturation and pepsin activation in the stomach.

• Histamine: Primarily acts on parietal cells in the stomach to increase acid secretion via H₂ receptors. It has no direct role in pancreatic secretion.

• Acetylcholine (ACh): A parasympathetic neurotransmitter that can augment pancreatic secretion, but it is not the primary regulator. It works synergistically with CCK but doesn’t initiate enzyme release in response to chyme.

• Secretin: Important for bicarbonate secretion, not digestive enzyme secretion.