GIT – 2021

Glutathione peroxidase

• Hydrogen peroxide (H₂O₂) is a reactive oxygen species (ROS) that can cause free radical damage.

• It is detoxified mainly by glutathione peroxidase, an enzyme that uses reduced glutathione (GSH) as a cofactor:

2 GSH+H2O2    ⟶    GSSG+2H2O2 \, GSH + H₂O₂ \;\; \longrightarrow \;\; GSSG + 2 H₂O2GSH+H2​O2​⟶GSSG+2H2​O

• This is a major antioxidant defense system inside cells.

Why the Other Options Are Wrong ❌

Glutathione oxidase

• No such enzyme in ROS defense. The enzyme is glutathione peroxidase, not oxidase.

Vitamin D

• Important for calcium/phosphate metabolism, not an antioxidant defense against free radicals.

Glutathione dismutase

• Doesn’t exist. Likely a distractor option.

Superoxide peroxidase

• Not a standard enzyme. The enzyme is superoxide dismutase (SOD), which converts superoxide radicals (O₂⁻•) into H₂O₂.

• But the question is about removing H₂O₂, so the correct answer is glutathione peroxidase.

Superoxide dismutase (SOD)

• Protects against superoxide radicals by converting them into H₂O₂, but then H₂O₂ itself must be removed by catalase or glutathione peroxidase.

• Cori’s disease (Glycogen Storage Disease type III) is caused by a deficiency of the debranching enzyme (α-1,6-glucosidase).

• Without this enzyme, glycogen breakdown is incomplete → abnormal glycogen with short outer chains accumulates.

• Clinical features: hepatomegaly, fasting hypoglycemia, muscle weakness, and growth retardation.

• Milder than Von Gierke’s disease (GSD type I), because gluconeogenesis is intact.

Why the Other Options Are Wrong ❌

Glycogen lyase (glycogen phosphorylase)

• Deficiency causes McArdle’s disease (GSD type V) with exercise-induced muscle cramps.

Glycogen synthase

• Deficiency would impair glycogen synthesis, not breakdown.

• Not related to Cori’s disease.

Pyruvate kinase

• Deficiency causes hemolytic anemia, not a glycogen storage disease.

Branching enzyme

• Deficiency causes Andersen’s disease (GSD type IV) with abnormal glycogen structure and liver cirrhosis.

HMG CoA reductase

• The rate-limiting and regulatory step in endogenous cholesterol synthesis is catalyzed by HMG CoA reductase.

• Reaction:

  HMG-CoA  ⟶  MevalonateHMG\text{-}CoA \; \longrightarrow \; MevalonateHMG-CoA⟶Mevalonate

• This enzyme is tightly regulated by:

  • Feedback inhibition (by cholesterol and bile salts).

  • Hormonal control → Insulin ↑ activity, Glucagon ↓ activity.

  • Drug inhibition → Statins (competitive inhibitors of HMG CoA reductase).

Why the Other Options Are Wrong ❌

Glucose-6-phosphatase

• Enzyme of gluconeogenesis/glycogenolysis.

• Not involved in cholesterol synthesis.

Glycogen synthase

• Enzyme of glycogen synthesis.

• No role in cholesterol metabolism.

HMG CoA synthase

• Catalyzes formation of HMG CoA.

• Important step but not regulatory — the regulation happens at HMG CoA reductase.

Mevalonate

• Product of HMG CoA reductase action.

• Not an enzyme, so not the regulatory step.

Tryptophan

• Niacin (Vitamin B3) can be synthesized in the body from the essential amino acid tryptophan.

• Approximately 60 mg of tryptophan can yield 1 mg of niacin equivalent (NE), provided vitamin B6 is available as a cofactor.

• This is why diets deficient in tryptophan (like maize-based diets) can lead to pellagra (dermatitis, diarrhea, dementia, and if untreated, death).

Why the Other Options Are Wrong ❌

Adenine

• A purine base found in nucleotides (ATP, DNA, RNA).

• Not related to niacin synthesis.

Tyrosine

• Precursor for catecholamines (dopamine, norepinephrine, epinephrine), thyroid hormones, and melanin.

• Not for niacin.

Methionine

• Sulfur-containing amino acid, important for methyl group transfers (via S-adenosyl methionine).

• Not a niacin precursor.

Phenylalanine

• Precursor of tyrosine → catecholamines, melanin.

• No role in niacin synthesis.

• Free energy change (ΔG) of a reaction can be expressed in terms of redox potential (E₀′), especially in biological oxidation-reduction (redox) reactions.

• The relationship is given by the Nernst equation:

ΔG∘=−nFΔE∘\Delta G^\circ = -n F \Delta E^\circΔG∘=−nFΔE∘

where:

• n = number of electrons transferred

• F = Faraday’s constant

• ΔE° = change in redox potential

Thus, the energetics of electron transfer (like in the electron transport chain) are directly linked to ΔG.

Why the Other Options Are Wrong ❌

Exergonic reaction

• Means ΔG is negative (energy-releasing), but it is a type of reaction, not how free energy is expressed.

Reduction

• A chemical process of gaining electrons.

• Not a unit or expression of free energy.

Endergonic reaction

• Means ΔG is positive (energy-requiring), again a type of reaction, not the expression of free energy.

Oxidation

• Loss of electrons, but again a chemical process, not a way to express ΔG.

• In the electron transport chain (ETC), located in the inner mitochondrial membrane, the main function is to establish a proton gradient.

• As electrons pass through Complexes I, III, and IV, protons (H⁺) are pumped from the mitochondrial matrix into the intermembrane space.

• This creates an electrochemical proton gradient (proton motive force) across the inner mitochondrial membrane.

• The return flow of protons through ATP synthase (Complex V) drives the phosphorylation of ADP to ATP.

Why the other options are incorrect

O₂ ❌

• Oxygen is the final electron acceptor in Complex IV, reduced to water, but it does not cross into the intermembrane space.

CO₂ ❌

• Produced mainly in the TCA cycle within the matrix, but it is not part of the ETC proton pumping mechanism.

Mg²⁺ ❌

• Important as a cofactor for ATP-utilizing enzymes but not pumped in the ETC.

Ca²⁺ ❌

• Transported into mitochondria for signaling and metabolism regulation, but not by the ETC complexes.

• The electron transport chain (ETC) occurs in the inner mitochondrial membrane.

• Electrons move sequentially through complexes I–IV, ultimately reducing oxygen to water.

• The final step occurs in Complex IV (cytochrome c oxidase), which contains cytochromes a and a3 along with copper ions.

• Here, electrons are transferred from cytochrome c → cytochrome a → cytochrome a3 → oxygen.

• Oxygen is the final electron acceptor, combining with electrons and protons to form H₂O.

Why the other options are incorrect

NAD ❌

• NADH donates electrons to Complex I, but it is not directly involved in reducing oxygen.

Ubiquinone (CoQ) ❌

• A mobile electron carrier between Complex I/II and Complex III, not the final step.

FMN ❌

• Flavin mononucleotide is a prosthetic group in Complex I; it transfers electrons from NADH but does not interact with oxygen directly.

Cytochrome Q ❌

• Another name for ubiquinone (CoQ), which is not the terminal complex.

• FMN (Flavin mononucleotide) is a coenzyme derived from riboflavin (vitamin B2).

• In the body, riboflavin is phosphorylated by riboflavin kinase to form FMN.

• FMN can be further converted to FAD (flavin adenine dinucleotide) by addition of AMP.

• Both FMN and FAD serve as important cofactors in oxidation–reduction reactions (e.g., in complex I and II of the electron transport chain).

Why the other options are incorrect

Vitamin B12 (Cobalamin) ❌

• Functions in methyl group transfers and odd-chain fatty acid metabolism, not FMN formation.

Thiamine (Vitamin B1) ❌

• Forms thiamine pyrophosphate (TPP), a coenzyme in decarboxylation reactions, not FMN.

Pyridoxine (Vitamin B6) ❌

• Forms pyridoxal phosphate (PLP), a coenzyme for transamination and amino acid metabolism, not FMN.

Niacin (Vitamin B3) ❌

• Forms NAD⁺ and NADP⁺, coenzymes in redox reactions, not FMN.

UDP-glucuronosyltransferase (UGT) is the key enzyme in the process of glucuronidation, a phase II biotransformation reaction. It catalyzes the transfer of glucuronic acid from UDP-glucuronic acid to substrates (like bilirubin, drugs, hormones, toxins), making them more water-soluble for excretion in bile or urine.

• UGT is an ER-membrane–bound enzyme (specifically, in the smooth endoplasmic reticulum).

• That’s why hepatocytes with well-developed SER are the primary site for detoxification reactions.

Why the Other Options Are Wrong

Golgi apparatus ❌

• The Golgi modifies, sorts, and packages proteins and lipids.

• It is not the main site for glucuronidation.

Mitochondria ❌

• Mitochondria handle oxidative phosphorylation, TCA cycle, fatty acid oxidation.

• They do not play a role in glucuronidation.

Cytosol ❌

• Some phase II enzymes (e.g., glutathione-S-transferase) are cytosolic, but UGT is specifically ER-bound, not cytosolic.

Nucleolus ❌

• The nucleolus is involved in ribosomal RNA synthesis and ribosome assembly.

• No detoxification enzymes are located here.

• The spermatic cord is a male anatomical structure that passes through the inguinal canal and contains structures related to the testis.

• Its main contents include:

  • Vas deferens

  • Testicular artery (from abdominal aorta)

  • Pampiniform plexus of veins (thermoregulation of testes)

  • Cremasteric artery (branch of inferior epigastric artery)

  • Lymphatic vessels, autonomic nerves, and genital branch of genitofemoral nerve.

• Ovaries are female gonads and have their own suspensory ligament with ovarian vessels — they are not part of the spermatic cord.

Why the Other Options Are Correct ✅ (part of spermatic cord)

• Pampiniform plexus → venous network around testicular artery.

• Testicular artery → supplies testis.

• Vas deferens → carries sperm from epididymis to ejaculatory duct.

• Cremasteric artery → supplies cremaster muscle and coverings of cord.

Common hepatic duct and cystic duct

• The biliary tree is formed as follows:

  • Right hepatic duct + Left hepatic duct → join to form the common hepatic duct.

  • Common hepatic duct + Cystic duct → join to form the common bile duct (CBD).

  • The common bile duct then joins the pancreatic duct at the hepatopancreatic ampulla (ampulla of Vater) before opening into the 2nd part of the duodenum.

Thus, the common hepatic duct and cystic duct together form the common bile duct.

Why the Other Options Are Wrong ❌

Common hepatic duct and pancreatic duct

• Wrong — the pancreatic duct joins later, at the ampulla, not at the point of CBD formation.

Left hepatic duct and cystic duct

• Left hepatic duct first joins with right hepatic duct → common hepatic duct.

• It doesn’t directly join cystic duct.

Cystic duct and pancreatic duct

• No direct anatomical connection.

Right hepatic duct and left hepatic duct

• These form the common hepatic duct, not the bile duct.

• Secretin is released from S cells of the duodenal mucosa in response to acidic chyme entering from the stomach.

• Its main action is to stimulate the pancreatic ductal cells to secrete bicarbonate-rich fluid.

• This neutralizes gastric acid, creating an optimal pH (~7–8) for pancreatic enzyme activity in the small intestine.

Why the Other Options Are Wrong ❌

Cholecystokinin (CCK)

• Released by I cells in duodenum/jejunum.

• Stimulates pancreatic enzyme secretion and gallbladder contraction, not bicarbonate secretion.

Trypsinogen

• Inactive zymogen secreted by pancreas, converted to trypsin in the duodenum.

• Involved in protein digestion, not bicarbonate release.

Gastric inhibitory peptide (GIP)

• Secreted by K cells.

• Stimulates insulin secretion in response to glucose and fat.

• No role in bicarbonate secretion.

Somatostatin

• Universal inhibitory hormone (secreted by D cells).

• Inhibits gastric acid, pancreatic secretions, and many hormones.

• Does not stimulate bicarbonate.

• The incubation period is the time interval between entry of a pathogen into the body and the appearance of the first symptoms or signs of disease.

• During this period, the person is infected and the pathogen may be multiplying, but there are no clinical symptoms yet.

• Example:

  • Influenza → incubation ~1–4 days

  • Hepatitis B → incubation ~1–6 months

Why the Other Options Are Wrong ❌

Latency period

• Refers to a phase when the pathogen remains in the body without causing symptoms and without being infectious (e.g., herpes virus latent in neurons).

• Different from incubation, where the pathogen is actively replicating before symptoms.

Infectious period

• The time when the infected person can transmit the disease to others.

• May overlap with incubation (e.g., measles, COVID-19) but is not the same definition.

Growth period

• Not a standard epidemiological term in this context.

Lysogenic period

• Refers to bacteriophage infection cycles (virus DNA integrates into bacterial genome).

• Not relevant for human infectious disease timing.

Biological vector transmission

• When a mosquito bites and transmits a pathogen (like Plasmodium in malaria or arboviruses in dengue, Zika, etc.), the pathogen undergoes part of its life cycle or multiplication inside the mosquito before being passed to humans.

• This is called biological vector transmission.

• The vector (mosquito) is essential for transmission, not just a passive carrier.

Why the Other Options Are Wrong ❌

Direct vector transmission

• Not a standard epidemiological term.

Vehicle transmission

• Refers to inanimate objects (food, water, air, fomites) acting as carriers, not living organisms like mosquitoes.

Scalar transmission

• Not a recognized mode of transmission. (Probably a distractor).

Indirect vector transmission

• Sometimes used loosely, but the precise and correct term when the pathogen develops or multiplies inside the vector is biological vector transmission.

I cells

• Cholecystokinin (CCK) is secreted by I cells located in the mucosa of the duodenum and jejunum.

• Stimuli for release: presence of fatty acids, amino acids, and partially digested proteins in the small intestine.

• Functions of CCK:

  • Stimulates gallbladder contraction → bile release.

  • Stimulates pancreatic enzyme secretion.

  • Relaxes sphincter of Oddi.

  • Slows gastric emptying to allow digestion.

Why the Other Options Are Wrong ❌

Ito cells

• Stellate cells of the liver, store vitamin A and play a role in fibrosis.

• Not related to gut hormone secretion.

S cells

• Found in the duodenum.

• Secrete secretin, which stimulates pancreatic bicarbonate secretion.

K cells

• Found in the duodenum/jejunum.

• Secrete GIP (glucose-dependent insulinotropic peptide).

G cells

• Found in the gastric antrum.

• Secrete gastrin, which stimulates gastric acid secretion.

• In the gastrointestinal tract, the parasympathetic nervous system stimulates motility and secretion.

• The primary neurotransmitter here is acetylcholine (ACh), which acts on muscarinic receptors in smooth muscle and glands.

• Effects:

  • ↑ Peristalsis

  • ↑ Secretion of digestive enzymes and mucus

  • Relaxation of sphincters (indirectly via inhibitory neurons)

Thus, acetylcholine is the major neurotransmitter that stimulates GI activity.

Why the Other Options Are Wrong ❌

Epinephrine

• Sympathetic neurotransmitter.

• Inhibits GI motility and secretion (causes relaxation of gut smooth muscle).

Norepinephrine

• Another sympathetic neurotransmitter.

• Reduces gut activity by inhibiting peristalsis and constricting sphincters.

Glutamate

• Excitatory neurotransmitter in the CNS.

• Not a major player in peripheral GI motility regulation.

Dopamine

• In the GI tract, dopamine generally inhibits motility by reducing acetylcholine release from enteric neurons.

• Excess dopamine can cause constipation.

• The appendix is a blind-ended tube attached to the cecum.

• Its position is highly variable, but the most common location is retrocecal (behind the cecum), seen in about 65% of individuals.

• Other less common positions:

  • Pelvic (~30%)

  • Subcecal

  • Pre-ileal

  • Post-ileal

Why the Other Options Are Wrong ❌

Behind ileum (post-ileal)

• Possible but rare (<5%).

• Not the most common site.

Epigastric region

• Not anatomically correct — appendix is always in the right lower quadrant (RLQ), not upper abdomen.

Behind stomach

• Impossible, stomach is in the upper abdomen (LUQ). Appendix is always attached to cecum in RLQ.

Lateral to the sigmoid colon

• Wrong, sigmoid colon lies in the left lower quadrant, while appendix is in the right lower quadrant.

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

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

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

Why the Other Options Are Wrong ❌

Pseudopolyps

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

• They result from regeneration of inflamed mucosa.

Exclusiveness of rectum

• UC always involves rectum (proctitis → pancolitis).

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

Mucosal atrophy

• Seen in ulcerative colitis due to chronic mucosal damage.

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

Inflammation

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

• The space of Disse is the perisinusoidal space between the endothelium of sinusoids and the hepatocytes.

• It allows exchange of nutrients, plasma, and metabolites between blood and hepatocytes.

• It contains stellate (Ito) cells which store vitamin A and can transform into myofibroblasts in fibrosis.

• Kupffer cells, however, are not in the space of Disse. They are specialized macrophages located within the sinusoidal lumen, attached to the endothelial lining.

Why the Other Options Are True ✅

• It lies between hepatocytes → Yes, hepatocyte microvilli project into the space of Disse.

• It lies in peri-sinusoidal space → Correct, that’s exactly its definition.

• It contains stellate cells → Yes, Ito cells are present here and are crucial in liver fibrosis.

• It is lined by endothelial cells → Yes, fenestrated sinusoidal endothelial cells line one side of the space of Disse.

Decrease in lysosomal degradation

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

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

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

• Examples:

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

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

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

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

Why the Other Options Are Wrong ❌

Increase in peroxisomes

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

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

Deficiency of carboxypolypeptidase

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

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

Increase in carboxypolypeptidase

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

• Again, irrelevant to the pathology of LSDs.

Increase in lysosomal degradation

• This would reduce buildup, not cause storage diseases.

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

Increased ALP, GT and SGPT

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

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

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

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

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

Why the Other Options Are Wrong ❌

Increased ALT and CK-BB

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

Increased ALP and SGPT

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

Decreased ALT and CK-MB

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

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

Decreased alkaline phosphatase and SGOT

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

• The duodenum is the only part of the GI tract that has both villi (for absorption) and submucosal glands (Brunner’s glands).

• Villi → finger-like projections of mucosa that increase surface area for absorption.

• Brunner’s glands (in submucosa) → secrete alkaline mucus + bicarbonate, which neutralizes acidic chyme from the stomach and optimizes pH for pancreatic enzymes.

Why the Other Options Are Wrong ❌

Ileum

• Has villi (shorter compared to jejunum), but no submucosal glands.

• Instead, it has Peyer’s patches (lymphoid aggregates).

Stomach

• Has gastric pits and glands, but no villi and no submucosal glands.

Jejunum

• Has tall villi and prominent plicae circulares, but no submucosal glands.

Large intestine

• No villi (only crypts of Lieberkühn).

• Submucosa lacks Brunner’s glands.

The stomach is characterized by longitudinal mucosal folds known as rugae, which allow for expansion during food intake. Its lamina propria contains numerous gastric glands (fundic, cardiac, or pyloric depending on region), responsible for secretion of acid, enzymes, and mucus.

Unlike the duodenum, the stomach lacks submucosal glands (Brunner’s glands) — a key distinguishing feature.

Why Others Are Incorrect:
❌ Duodenum – Has Brunner’s glands in the submucosa for alkaline mucus secretion.
❌ Jejunum – No glands in lamina propria; has long villi and prominent plicae circulares.
❌ Ileum – Contains Peyer’s patches (lymphoid aggregates), not glands.
❌ Large intestine – Has crypts of Lieberkühn but no villi or rugae; mucosa is smooth.

• Normally, during development (6th week), the midgut undergoes physiological herniation into the umbilical cord because the abdominal cavity is too small.

• By the 10th week, the gut returns to the abdominal cavity after completing a 270° counterclockwise rotation.

• If this return fails, the bowel remains herniated and covered by peritoneum and amnion, forming an omphalocele.

Why the Other Options Are Wrong ❌

Persistence of vitelline duct

• Leads to Meckel’s diverticulum.

• Not due to failure of gut return.

Retrocolic hernia

• An internal hernia due to abnormal rotation of the gut, not failure of return.

Gastroschisis

• Congenital defect where bowel herniates through the abdominal wall (usually right of umbilicus).

• Here, the bowel is not covered by peritoneum.

• Cause: abdominal wall closure defect, not failed return of physiological hernia.

Megacolon (Hirschsprung disease)

• Due to failure of migration of neural crest cells, leading to absence of enteric ganglia.

• Not related to herniation or return of the gut.

• The midgut loop has a cranial limb and a caudal limb:

  • Cranial limb → develops into most of the small intestine (distal duodenum, jejunum, and upper ileum).

  • Caudal limb → develops into lower ileum, cecum, appendix, ascending colon, and proximal 2/3 of transverse colon.

• The duodenum (proximal parts) develops mainly from the foregut (upper half) and cranial limb of midgut loop (distal half), not from the caudal limb.

Thus, among the options, duodenum does not arise from the caudal end.

Why the Other Options Are Wrong ❌

Cecum

• Develops from the caudal limb of the intestinal loop.

Lower part of ileum

• Also from the caudal limb.

Appendix

• Outgrowth of the cecum → caudal limb derivative.

Ascending colon

• Direct derivative of the caudal limb.

Mucus and bicarbonate

• Brunner’s glands are specialized submucosal glands found in the duodenum (especially proximal part).

• They secrete alkaline mucus rich in bicarbonate, which has two important roles:

  1. Protects duodenal mucosa from acidic chyme coming from the stomach.

  2. Optimizes pH for pancreatic enzyme activity in the small intestine.

Why the Other Options Are Wrong ❌

Enzymes

• Digestive enzymes are secreted mainly by the pancreas and intestinal mucosal cells, not Brunner’s glands.

Catecholamines

• These are neurotransmitters (epinephrine, norepinephrine), secreted by adrenal medulla, not duodenal glands.

Cholecystokinin (CCK)

• Hormone secreted by I cells in the duodenum/jejunum mucosa.

• Stimulates gallbladder contraction and pancreatic secretion, but not produced by Brunner’s glands.

NaCl

• Chloride secretion occurs in intestinal crypts (crypts of Lieberkühn), not in Brunner’s glands.

• The exocrine pancreas is made up of compound acinar glands.

• Each acinus is formed of pyramidal serous cells that secrete enzyme-rich pancreatic juice (amylase, lipase, proteases, nucleases).

• These are serous secreting units, not mucous.

• Their secretion is alkaline (due to bicarbonate from ductal cells), helping neutralize gastric acid and digest macromolecules.

Why the Other Options Are Wrong ❌

Mucous secreting units

• Seen in salivary glands like sublingual gland, not in pancreas.

• Pancreatic acini don’t produce mucous.

Seromucous

• Mixed acini (serous + mucous) occur in submandibular salivary gland, not in pancreas.

Insulin-secreting

• Done by beta cells of islets of Langerhans (endocrine pancreas), not acini.

Glucagon-secreting

• Done by alpha cells of islets of Langerhans (endocrine pancreas), not acini.

• Research consistently shows that the quality of communication and trust between doctor and patient is the major determinant of compliance (adherence) to treatment.

• If the patient feels understood, respected, and involved in decision-making, they are far more likely to follow the prescribed regimen — even if cost, access, or side effects are not ideal.

• This is why counseling, empathy, and shared decision-making are central to improving adherence.

Why the Other Options Are Wrong ❌

Cost effectiveness

• Important factor, but not the major determinant. Some patients still comply even with higher cost if they trust the doctor and understand the necessity.

Access of medications

• Access influences compliance, but even when access is easy, poor communication or lack of trust leads to non-compliance.

Benefits/drawbacks of medications

• Patients do consider side effects and benefits, but if the doctor–patient bond is strong, many are willing to tolerate drawbacks.

Regimen of medications

• Simpler regimens help, but adherence still depends more on the relationship and counseling provided by the physician.

Inferior pancreaticoduodenal vein

• The portal vein is formed by the union of the splenic vein and the superior mesenteric vein (SMV), and it also receives tributaries like the left gastric vein and superior pancreaticoduodenal vein directly.

• However, the inferior pancreaticoduodenal vein drains into the superior mesenteric vein, not directly into the portal vein.

Why the Other Options Are Wrong ❌

Splenic vein

• Direct tributary → joins SMV to form portal vein.

Superior mesenteric vein

• Direct tributary → unites with splenic vein to form portal vein.

Left gastric vein

• Direct tributary → drains into portal vein.

• Clinically important because it forms a portosystemic anastomosis with esophageal veins (→ esophageal varices in portal hypertension).

Superior pancreaticoduodenal vein

• Drains directly into the portal vein (sometimes via gastroduodenal vein).

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

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

• Once formed, trypsin activates all other pancreatic zymogens.

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

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

Why the Other Options Are Wrong ❌

Enterokinase

• Enzyme in duodenal mucosa that activates trypsinogen → trypsin.

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

Lipoprotein lipase

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

• Not related to pancreatic enzyme activation.

Pepsinogen

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

• No role in pancreatic secretion.

Phospholipase

• A pancreatic enzyme that requires trypsin activation.

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

• G cells are specialized enteroendocrine cells that secrete gastrin.

• They are located mainly in the gastric antrum (the distal part of the stomach, just before the pylorus).

• Gastrin stimulates:

  • Parietal cells → HCl secretion

  • Chief cells → pepsinogen secretion

  • Mucosal growth

Why the Other Options Are Wrong ❌

Pylorus of stomach

• Careful: “pylorus” refers to the opening into the duodenum. The G cells are concentrated in the antrum, not specifically at the pyloric sphincter region.

Fundus of stomach

• Contains parietal cells (acid, intrinsic factor) and chief cells (pepsinogen).

• Not the main site of gastrin secretion.

Duodenal mucosa

• Contains I cells (cholecystokinin), S cells (secretin), and some G cells in small numbers, but not the primary source of gastrin.

Body of stomach

• Rich in parietal and chief cells, not G cells.

• Parietal cells (in the gastric glands of fundus and body) secrete hydrochloric acid and, importantly, intrinsic factor (IF).

• Autoimmune destruction of parietal cells → loss of intrinsic factor → impaired absorption of vitamin B₁₂ in the terminal ileum.

• This leads to pernicious anemia, a type of megaloblastic anemia seen with malabsorption.

Why the Other Options Are Wrong ❌

Chief cells

• Secrete pepsinogen (inactive precursor of pepsin).

• Not related to intrinsic factor or B₁₂ absorption.

Mucous neck cells

• Secrete protective mucus.

• Destruction won’t cause vitamin B₁₂ deficiency.

Vitamin D

• Its deficiency leads to rickets/osteomalacia, not megaloblastic anemia.

Enteroendocrine cells

• Secrete hormones (gastrin, somatostatin, etc.).

• No role in intrinsic factor production or B₁₂ absorption.

• The patient has malabsorption + midline neck swelling (goiter, due to hypothyroidism) + megaloblastic anemia (↑ MCV).

• This points toward autoimmune thyroid disease coexisting with pernicious anemia (both are autoimmune and often cluster together).

• Pernicious anemia occurs due to autoimmune destruction of gastric parietal cells or antibodies directly against intrinsic factor (IF).

• IF is required for vitamin B₁₂ absorption in the terminal ileum.

• Lack of IF → vitamin B₁₂ deficiency → megaloblastic anemia (↑ MCV, hypersegmented neutrophils, neurologic symptoms possible).

Why the Other Options Are Wrong ❌

Anti-nuclear antibodies

• Seen in autoimmune disorders like SLE.

• Not directly causing vitamin B₁₂ malabsorption.

Gliadin

• Autoantigen in celiac disease → causes malabsorption and sometimes anemia (iron deficiency > B₁₂).

• But here, the classical finding is antibodies against intrinsic factor, not gliadin.

Vitamin D

• Deficiency causes rickets/osteomalacia, not megaloblastic anemia.

Chief cells

• Chief cells secrete pepsinogen, not intrinsic factor.

• Destroying chief cells won’t lead to B₁₂ deficiency.

• Chronic pancreatitis leads to destruction of pancreatic tissue and a deficiency of pancreatic enzymes (lipase, amylase, proteases).

• This impairs the breakdown of fats, proteins, and carbohydrates within the intestinal lumen before they can be absorbed.

• Therefore, the problem is mainly with intraluminal digestion.

• Clinically, this results in steatorrhea (fat malabsorption) and malnutrition.

Why the Other Options Are Wrong ❌

Lymphatic absorption

• Refers to absorption of digested fats as chylomicrons into lacteals.

• This process is intact; the problem is that fats aren’t digested in the first place due to lack of pancreatic lipase.

Terminal digestion

• Refers to the action of brush-border enzymes (disaccharidases, peptidases) breaking down nutrients into absorbable monomers.

• This step is normal in chronic pancreatitis.

Absorption in blood through capillaries

• Once nutrients are digested, they can be absorbed normally.

• The problem here is lack of digestion, not absorption.

Transepithelial transport

• Transport of nutrients across enterocytes is unaffected.

• Again, the limiting step is enzyme deficiency in the lumen.

• The main pancreatic duct (duct of Wirsung) carries digestive secretions from the pancreas.

• It typically joins with the common bile duct to form the hepatopancreatic ampulla (ampulla of Vater).

• This opens into the medial wall of the second part of the duodenum at the major duodenal papilla.

• This area is clinically very important because a tumor in the head of the pancreas can compress the duct, leading to obstructive jaundice.

Why the Other Options Are Wrong ❌

Second and third part of duodenum

• Wrong, because the duct opens specifically into the second part only (major duodenal papilla).

First part of duodenum

• The bulb of the duodenum (near pylorus) has no pancreatic duct opening.

Third part of duodenum

• Crosses behind the superior mesenteric vessels, but no duct opening occurs here.

Third and fourth part of duodenum

• Same reason — neither part has openings for pancreatic or bile ducts.

Short gastric arteries are a branch of splenic artery

• The stomach is mainly supplied by branches of the celiac trunk:

  • Left gastric artery → supplies lesser curvature (along with right gastric).

  • Right gastric artery → usually from proper hepatic artery (not a direct celiac branch).

  • Right gastroepiploic artery → branch of gastroduodenal artery (from common hepatic).

  • Left gastroepiploic artery → branch of splenic artery.

  • Short gastric arteries → also branches of splenic artery, supplying the fundus.

Why the Other Options Are Wrong ❌

Gastroepiploic artery supplies the lesser curvature of stomach

• Wrong, the gastroepiploic (gastro-omental) arteries supply the greater curvature, not the lesser.

Right gastroepiploic artery is a direct branch of celiac trunk

• Wrong, it is a branch of the gastroduodenal artery (which itself comes from common hepatic artery → celiac trunk).

Right gastric artery is a direct branch of celiac trunk

• Wrong, it usually arises from the proper hepatic artery (sometimes common hepatic), not directly from the celiac trunk.

Stomach is generally supplied by superior mesenteric artery

• Wrong, SMA supplies the midgut (jejunum, ileum, cecum, ascending colon, transverse colon), not the stomach.

• Stomach is supplied by the celiac trunk.

Reasoning:

• Chronic diarrhea + abdominal pain → suggests inflammatory bowel disease.

• Aphthous ulcers + deep linear fissures → classic for Crohn’s disease.

• Distribution: ascending & transverse colon affected, rectum spared, and skip lesions → again points toward Crohn’s (UC usually starts in rectum and is continuous).

• Fat creeping over mucosa → “creeping fat” is a hallmark of Crohn’s due to transmural inflammation.

• Histology: cryptitis + non-caseating granulomas → strongly supports Crohn’s (granulomas are diagnostic when present).

Why the Other Options Are Wrong ❌

Whipple disease

• Caused by Tropheryma whipplei.

• Presents with malabsorption, weight loss, arthritis, and PAS-positive macrophages in lamina propria.

• Does not show skip lesions, creeping fat, or granulomas typical of Crohn’s.

Ulcerative colitis

• Continuous lesion starting in rectum and extending proximally.

• No skip lesions.

• No creeping fat.

• Histology shows crypt abscesses but no granulomas.

Lactose intolerance

• Functional malabsorption due to lactase deficiency.

• Presents with bloating, diarrhea after dairy intake, but no ulcers, fissures, or granulomas.

Celiac disease

• Gluten-sensitive enteropathy.

• Involves small intestine (especially duodenum), not colon.

• Histology shows villous atrophy and lymphocytic infiltration, not granulomas.

• In malabsorption syndromes (like celiac disease, tropical sprue, pancreatic insufficiency), the hallmark clinical feature is chronic diarrhea, often steatorrhea (bulky, greasy, foul-smelling stools).

• It reflects the inability of the intestine to absorb nutrients, fat, and water properly.

• Other findings such as weight loss, anemia, and deficiencies can occur, but the most frequent and consistent manifestation is chronic diarrhea.

Why the Other Options Are Wrong ❌

Acute gastroenteritis

• This is an infectious condition, usually viral or bacterial, and not a feature of malabsorption.

Hemoptysis

• Coughing up blood from the respiratory tract, unrelated to GI malabsorption.

Iron deficiency

• Can occur in malabsorption (especially in celiac disease due to duodenal involvement), but it is a secondary feature, not the most frequent manifestation.

Hematemesis

• Vomiting blood, usually due to upper GI bleed (ulcer, varices).

• Not associated with malabsorption.

• The posterior abdominal wall muscles are mainly:

  • Psoas major

  • Psoas minor

  • Iliacus

  • Quadratus lumborum

• These muscles form the posterior abdominal wall and are related to structures like the lumbar plexus, kidneys, and diaphragm.

Pectineus, on the other hand:

• Is not part of the posterior abdominal wall.

• It is a muscle of the anterior thigh (adductor compartment).

• It flexes and adducts the hip, supplied mainly by the femoral nerve (sometimes obturator nerve too).

Thus, Pectineus is the odd one out.

Why the Other Options Are Wrong ❌

Psoas minor

• Lies on the anterior surface of psoas major.

• A weak flexor of the lumbar spine.

• Contributes to the posterior abdominal wall.

Quadratus lumborum

• Extends between iliac crest and 12th rib.

• Helps in lateral flexion of vertebral column and fixing the 12th rib during respiration.

• Definitely part of posterior abdominal wall.

Psoas major

• Large muscle arising from lumbar vertebrae, forming part of posterior abdominal wall.

• Combines with iliacus to form iliopsoas → strong hip flexor.

Iliacus

• Fills iliac fossa, joins psoas major → iliopsoas.

• Lies against posterior abdominal wall.

The junction between lateral 1/3rd and medial 2/3rd on the line joining ASIS and umbilicus

• McBurney’s point is a surface anatomical landmark used in diagnosing acute appendicitis.

• It is located at the point one-third the distance from the anterior superior iliac spine (ASIS) to the umbilicus.

• Tenderness here is a classical sign of appendiceal inflammation.

Why the Other Options Are Wrong ❌

The junction between lateral 2/3rd and medial 1/3rd on the line joining AIIS and umbilicus

• Wrong landmark.

• Uses AIIS (anterior inferior iliac spine) instead of ASIS (the correct bony landmark).

• Also wrong ratio.

The junction between lateral 1/3rd and medial 2/3rd on the line joining AIIS and umbilicus

• Again uses AIIS instead of ASIS. Incorrect.

The junction between lateral 2/3rd and medial 1/3rd on the line joining ASIS and umbilicus

• This is a common confusion.

• But the correct ratio is lateral 1/3rd and medial 2/3rd, not the other way around.

The junction between lateral 1/2nd and medial 2/2nd on the line joining AIIS and umbilicus

• Not a standard anatomical description.

• Also uses AIIS, which is incorrect.

• The most common complication of peptic ulcer disease is hemorrhage (bleeding).

• This can occur when the ulcer erodes into a blood vessel, most often the gastroduodenal artery (in posterior duodenal ulcers).

• Clinically, bleeding presents as hematemesis (vomiting blood) or melena (black, tarry stools).

Why the Other Options Are Wrong ❌

Perforation

• A serious complication but less common than bleeding.

• More frequent with anterior duodenal ulcers, leading to peritonitis and free air under the diaphragm.

Jaundice

• Not a direct complication of peptic ulcer disease.

• Can occur if there is obstruction of the bile duct, but it’s rare and indirect.

Obstruction

• Can result from chronic scarring and narrowing of the pyloric channel.

• Presents with persistent vomiting, abdominal distension, and succussion splash.

• Again, less common than bleeding.

Adenocarcinoma

• Associated with chronic gastric ulcers (especially in the lesser curvature).

• But this is a rare complication compared to bleeding.

Duodenal bulb (first part of the duodenum)

• The most common site of peptic ulcer is the duodenal bulb (first part of duodenum, just beyond the pylorus).

• Over 70–80% of all peptic ulcers are duodenal, and among those, the anterior wall of the duodenal bulb is the most frequent site.

• Gastric ulcers are less common, and when present, are most often in the lesser curvature near the antrum.

Why the Other Options Are Wrong ❌

Antrum of stomach

• Gastric ulcers can occur here, but duodenal ulcers are far more common overall.

• So this is not the most common site.

3rd part of duodenum

• Rare site for ulcers.

• Ulcers here raise suspicion for Zollinger–Ellison syndrome (gastrinoma with excessive acid).

Jejunum

• Ulcers are very rare here.

• If present, also usually due to Zollinger–Ellison syndrome.

Postbulbar duodenum

• This means ulcers beyond the duodenal bulb (second part of the duodenum).

• Less common than bulb ulcers.

Water deprivation test

• A young woman with polyuria and polydipsia but no glucose in urine rules out diabetes mellitus.

• The next suspicion is diabetes insipidus (DI) or primary polydipsia.

• The water deprivation test is the gold standard for differentiating between:

  • Central DI (lack of ADH)

  • Nephrogenic DI (kidneys unresponsive to ADH)

  • Primary polydipsia (psychogenic/excessive water intake)

This test works by restricting water and observing changes in urine osmolality. After that, desmopressin (synthetic ADH) is given to differentiate central from nephrogenic DI.

Why the Other Options Are Wrong ❌

Serum osmolality

• Useful, but by itself not diagnostic.

• Can support the suspicion (low urine osmolality with high serum osmolality in DI), but the confirmatory test is water deprivation.

Fasting blood glucose

• Appropriate if diabetes mellitus was suspected.

• But urine dipstick is negative for glucose, and the patient has no weight loss. DM is unlikely here.

Brain MRI

• Helpful later if central DI is confirmed (to look for pituitary or hypothalamic lesions).

• Not the immediate next step in workup.

Urine electrolytes

• Can provide supportive information but won’t distinguish between central DI, nephrogenic DI, or primary polydipsia.

• Not the test of choice in this diagnostic sequence.

Hartmann’s pouch

• At the junction of the neck of the gallbladder and cystic duct, there is sometimes a small outpouching called Hartmann’s pouch.

• It is a common site where gallstones can lodge, leading to obstruction of the cystic duct → causing acute cholecystitis.

• Important surgically because gallstones in this pouch can make dissection during cholecystectomy more difficult.

Why the Other Options Are Wrong ❌

Rathke’s pouch

• An embryological structure in the roof of the mouth.

• Gives rise to the anterior pituitary gland.

• Unrelated to the gallbladder.

Cystic pouch

• Not an anatomical term. Sometimes students confuse it with cystic duct, but no such pouch exists.

Hepatorenal pouch (of Morison)

• A peritoneal recess between the liver and right kidney.

• Fluid can collect here in conditions like ascites or trauma.

• Not related to gallbladder neck.

Pharyngeal pouch

• Outpouchings of the foregut during embryological development that form structures of the head and neck (e.g., tonsils, thymus, parathyroid).

• Nothing to do with gallbladder.

Lower ⅓ has smooth muscles only

The muscularis externa of the esophagus is unique because it transitions from voluntary to involuntary control:

• Upper ⅓ → Skeletal muscle only (voluntary, helps in initiation of swallowing).

• Middle ⅓ → Mixed skeletal and smooth muscle (transition zone).

• Lower ⅓ → Smooth muscle only (involuntary, controlled by autonomic nervous system).

This arrangement allows swallowing to begin voluntarily and then continue involuntarily as the bolus moves toward the stomach.

Why the Other Options Are Wrong ❌

Lower ⅓ has skeletal and smooth muscles

• Wrong. The lower third is purely smooth muscle, no skeletal component.

Middle ⅓ has smooth muscles only

• Wrong. The middle third is mixed skeletal and smooth muscle.

Lower ⅓ has skeletal muscles only

• Wrong. Skeletal muscle is only in the upper third, not in the lower.

Upper ⅓ has smooth muscles only

• Wrong. The upper third is entirely skeletal muscle, not smooth.

• The liver has a dual blood supply:

  • Portal vein (~75%) → brings nutrient-rich, but deoxygenated blood from the gastrointestinal tract and spleen.

  • Hepatic artery (~25%) → brings oxygenated blood from the systemic circulation (via the celiac trunk → common hepatic artery → proper hepatic artery).

Even though the portal vein supplies the majority of the blood volume, the oxygen requirement of the liver is mainly met by the hepatic artery.

Why the Other Options Are Wrong ❌

Hepatic vein

• Drains blood out of the liver into the inferior vena cava.

• Does not supply the liver with oxygenated blood.

Inferior mesenteric vein

• Drains blood from the hindgut (descending colon, sigmoid, rectum).

• Joins the splenic vein → portal vein, bringing nutrient-rich blood to the liver.

• Not a direct oxygen source.

Superior mesenteric vein

• Drains blood from midgut structures (small intestine, ascending and transverse colon).

• Also joins the splenic vein to form the portal vein.

• Again, nutrient-rich but deoxygenated blood.

Portal vein

• Brings nutrient-rich blood from GI tract and spleen.

• Supplies about 75% of liver blood flow, but it is not oxygenated blood.

Pylorus part of stomach

• The gastric mucosa varies in different parts of the stomach.

• Pyloric region is particularly known for its deep gastric pits that extend down into the mucosa.

• These pits occupy almost two-thirds of the mucosal thickness, and the glands (mostly mucous glands) open into them.

• Functionally, the pylorus secretes mucus and gastrin, protecting the duodenum from acidic gastric contents.

Why the Other Options Are Wrong ❌

Fundus

• Contains fundic (oxyntic) glands, with shallow pits compared to pylorus.

• Pits occupy only about one-fourth of the mucosal thickness.

Antrum

• Sometimes used synonymously with pylorus, but technically it refers to the pyloric antrum, which also has deep pits.

• If antrum is treated separately from pylorus in the options, the term “pylorus” is the more accurate choice.

Anal canal

• Lined by stratified squamous epithelium below the pectinate line, not gastric mucosa.

• No gastric pits present here.

Cardiac part of stomach

• Has cardiac glands with short pits and coiled glands.

• Pits are not nearly as deep as in the pyloric region.

• Parietal cells (oxyntic cells) are large, round or pyramidal cells found mainly in the neck/isthmus region of gastric glands.

• They are described as having a “fried egg” appearance:

  • Central, round, prominent nucleus (the yolk).

  • Clear or eosinophilic cytoplasm (the egg white).

• These cells secrete hydrochloric acid (HCl) and intrinsic factor (essential for vitamin B₁₂ absorption).

Why the Other Options Are Wrong ❌

Goblet cells

• Found in the intestines and respiratory tract, not in the gastric glands.

• Function: secrete mucus.

• They have a goblet (cup)-like appearance, not a fried egg look.

Enteroendocrine cells

• Scattered throughout the gastric glands (especially base).

• Secrete hormones (e.g., gastrin, somatostatin, histamine).

• They are small, basal, and not recognizable as “fried egg” cells on light microscopy.

Chief cells

• Located in the base of gastric glands.

• Basophilic cytoplasm due to abundant rough ER.

• Secrete pepsinogen (precursor of pepsin).

• Do not have the fried egg morphology.

Mucous neck cells

• Located in the neck of gastric glands.

• Secrete mucus that protects against acid.

• Appear irregular, with pale cytoplasm, not the classic fried egg shape.

It increases surface area by about 3 fold

Plicae circulares (valves of Kerckring) are large folds of the mucosa and submucosa in the small intestine (especially prominent in the jejunum). Their main function is to increase surface area for absorption.

• They increase surface area by approximately 3 times compared to a smooth, unfolded mucosa.

• On top of this, villi add about 10-fold, and microvilli add about 20-fold → giving a total of ~600-fold increase in absorptive surface.

Why the Other Options Are Wrong ❌

It consists of only mucosa

• Wrong, because plicae circulares are formed by both mucosa and submucosa.

• Simple mucosal folds (without submucosa) would be called villi, not plicae.

It increases surface area by about 10 fold

• This is the role of villi, not plicae circulares.

It only contains submucosa

• Wrong, because the mucosa is also part of the fold.

• Plicae circulares are permanent folds of mucosa + submucosa, not just submucosa.

Glisson’s capsule

The classical hepatic lobule is a histological unit of the liver, typically represented as a hexagon. Its key components are:

• Central vein → in the center.

• Portal triads → at the corners (containing portal vein branch, hepatic artery branch, bile duct).

• Sinusoidal capillaries → radiating between portal triads and central vein.

• Endothelium → lining the sinusoids.

But Glisson’s capsule is the connective tissue capsule that surrounds the entire liver externally, not part of the microscopic architecture of the classical lobule.
Therefore, it cannot be visualized within a single lobule structure.

Why the Other Options Are Wrong ❌

Sinusoidal capillaries

• Present between portal triad and central vein.

• Allow exchange of blood between hepatocytes and circulation.

• Clearly visible in histological sections.

Central vein

• Located in the middle of the lobule.

• Collects blood after it passes through sinusoids and drains into hepatic veins.

• Always part of the classical lobule diagram.

Portal triad

• Found at the periphery (corners) of the lobule.

• Includes a branch of the hepatic artery, portal vein, and bile duct.

• Essential landmark of lobular organization.

Endothelium

• Lines sinusoidal capillaries.

• Includes fenestrated endothelial cells and Kupffer cells.

• Integral to the microscopic view of the lobule.

The urea breath test is considered the best non-invasive test to determine whether Helicobacter pylori infection persists after treatment.

• H. pylori produces the enzyme urease, which breaks down orally administered urea into carbon dioxide and ammonia.

• If the labeled urea (C¹³ or C¹⁴) is broken down, the labeled CO₂ appears in the patient’s breath, confirming the presence of live bacteria.

• This test is highly sensitive and specific, and importantly, it can distinguish between active and past infection (unlike serology).

Why the Other Options Are Wrong ❌

Endoscopy and biopsy

• Very accurate and allows direct visualization plus histology.

• However, it is invasive, more expensive, and not ideal for routine follow-up after treatment.

• Reserved for patients with alarming symptoms or suspected complications (like gastric cancer or ulcer bleeding).

Culture

• Definitive for diagnosis and antibiotic sensitivity.

• But it is time-consuming, technically difficult, and not routinely used for post-treatment testing.

• Mainly used in cases of antibiotic resistance or research.

Antigen test

• Stool antigen test is reliable, non-invasive, and widely used.

• It is good for follow-up, but sensitivity can sometimes be lower compared to the urea breath test.

• Slightly less accurate in post-treatment testing.

PCR

• Detects bacterial DNA with high sensitivity.

• But it cannot reliably differentiate between live bacteria and dead bacteria, meaning it may give a false-positive after successful treatment.

• Therefore, not the best choice for determining residual infection.

The inferior mesenteric artery (IMA) supplies the hindgut, which extends from the left one-third of the transverse colon all the way down to the upper part of the anal canal (above the anal valves). This includes:

• Left third of transverse colon

• Descending colon

• Sigmoid colon

• Rectum (upper part)

However, the anal canal below the anal valves (pectinate line) is derived embryologically from the ectoderm (proctodeum) and is supplied by the inferior rectal artery (branch of the internal pudendal artery, which comes from the internal iliac artery).
Thus, it is not supplied by the IMA.

Why the Other Options Are Wrong ❌

Descending colon + sigmoid

1. • Both of these are hindgut derivatives.

   • They are directly supplied by branches of the IMA:

     • Left colic artery → descending colon

     • Sigmoid arteries → sigmoid colon

   • ✅ Wrong because these are supplied by IMA.

     Sigmoid + rectum

     • Both lie in the hindgut region.

     • Supplied by:

       • Sigmoid arteries (from IMA) → sigmoid

       • Superior rectal artery (from IMA) → rectum

     • ✅ Wrong because both are within IMA supply.

       Left one third of transverse colon + rectum

       • Left one third of transverse colon: hindgut → supplied by IMA (via left colic artery).

       • Rectum (upper part): supplied by superior rectal artery (branch of IMA).

       • ✅ Wrong because these are supplied by IMA.

         Transverse colon + sigmoid

         • Trick option. Entire transverse colon is not supplied by IMA.

         • Right two-thirds = midgut → supplied by SMA (middle colic artery).

         • Left one-third = hindgut → supplied by IMA (left colic artery).

         • Since this option says “transverse colon” without specifying part, it includes the majority (right two-thirds) which is not supplied by IMA.

         • However, the question asks for which part is not supplied at all by IMA. The transverse colon has partial IMA supply, so this is not the best answer.

• In suspected malabsorption syndromes, the investigation of choice to evaluate the small intestine is a Barium follow through.

• In this test, the patient swallows barium, and serial X-rays are taken at timed intervals as the contrast passes through the small bowel.

• It helps detect:

  • Mucosal pattern changes

  • Dilated loops

  • Transit time abnormalities

  • Diseases like celiac disease, Crohn’s disease, and other malabsorption disorders

Why the other options are wrong

• Barium enema ❌ → Used for large bowel (colon) evaluation, not small bowel.

• Abdominal X-ray ❌ → Can show obstruction, perforation, or gas patterns but not detailed small bowel mucosa.

• Barium swallow test ❌ → Used to study the esophagus.

• Barium meal ❌ → Studies stomach and duodenum only, not the rest of the small intestine.

• Duodenal ulcers most commonly occur in the first part of the duodenum.

• An ulcer on the posterior wall of the first part is particularly dangerous because it may erode into the gastroduodenal artery, which lies just posterior to the duodenum.

• Erosion can cause massive upper gastrointestinal bleeding, presenting as hematemesis (vomiting blood) or melena.

Why the other options are incorrect

Right gastric artery ❌

• Runs along the lesser curvature of the stomach; not related to the posterior duodenal wall.

Middle colic artery ❌

• Branch of the superior mesenteric artery, supplies transverse colon; unrelated to duodenal ulcer bleeding.

Pancreaticoduodenal artery ❌

• Branches do supply the duodenum and pancreas, but the posterior duodenal wall ulcer classically erodes the gastroduodenal artery, not these smaller vessels.

Left gastric artery ❌

• Supplies the lesser curvature of the stomach and lower esophagus; not directly related to duodenal ulcer bleeding.

Why Kupffer Cells Are Not Seen at 40x:

1. Size Limitation at 40x Magnification:
   • The portal triad, sinusoids, central vein, and hepatocytes are all macroscopic structures or clearly organized cellular arrangements that remain visible at 40x magnification.
   • Kupffer cells, however, are individual macrophages lining the sinusoids and require higher magnification (100x-400x) to be clearly distinguished.
2. Functional vs. Structural Visibility:
   • Kupffer cells are part of the liver’s immune surveillance system rather than its structural framework.
   • At 40x, they appear as indistinct cells within the sinusoidal lining and cannot be reliably identified without higher resolution.

Why Other Structures Are Visible at 40x:

1. Portal triad – Clearly seen as a triangular region containing the hepatic artery, portal vein, and bile duct.
2. Sinusoids – Appear as thin, blood-filled channels between hepatocyte cords.
3. Central vein – A larger vessel at the center of liver lobules, easily identifiable.
4. Hepatocytes – The primary liver cells form distinct plates and are clearly visible due to their size and arrangement.

• The cremaster muscle is a thin layer of skeletal muscle associated with the spermatic cord and testes.

• It arises as extensions of the internal oblique muscle fibers and fascia.

• Function: contracts to elevate the testes, regulating temperature for spermatogenesis (cremasteric reflex).

• Innervation: genital branch of the genitofemoral nerve (L1–L2).

Why the other options are incorrect

Transversalis fascia ❌

• Gives rise to the internal spermatic fascia, not the cremaster muscle.

External oblique ❌

• Its aponeurosis forms the external spermatic fascia, not the cremaster muscle.

Internal spermatic fascia ❌

• Derived from the transversalis fascia; a covering, not a muscle.

External spermatic fascia ❌

• Derived from the aponeurosis of the external oblique, not muscle fibers.

• In skeletal muscle, contraction is regulated by troponin, which binds calcium and exposes actin’s binding sites for myosin.

• Smooth muscle lacks troponin. Instead, it uses the calmodulin system:

  1. Calcium ions enter the cytoplasm (from SR and extracellular space).

  2. Calcium binds to calmodulin (a calcium-binding protein).

  3. The Ca²⁺–calmodulin complex activates myosin light chain kinase (MLCK).

  4. MLCK phosphorylates myosin light chains → allows myosin to bind actin → contraction occurs.

Thus, calmodulin is the calcium-binding regulatory protein in smooth muscle.

Why the other options are incorrect

Sequesterin ❌

• Found in sarcoplasmic reticulum (helps calcium storage), but not the main calcium-binding protein for contraction in smooth muscle.

MLCK ❌

• Enzyme that phosphorylates myosin, but it requires activation by Ca²⁺–calmodulin; not the direct calcium-binding protein.

Myosin ❌

• Motor protein responsible for contraction, but not the calcium sensor.

Actin ❌

• Thin filament; interacts with myosin during contraction but does not regulate calcium binding.

The esophagus is a muscular tube that transports food from the pharynx to the stomach. Its inner lining is composed of non-keratinized stratified squamous epithelium, which serves primarily a protective function.

Key Reasons:

1. Mechanical Protection – The stratified squamous epithelium is multi-layered, allowing it to withstand friction from swallowed food.
2. Chemical Protection – While the esophagus does not secrete digestive enzymes, its epithelium provides a barrier against minor irritants (e.g., hot or acidic foods).
3. No Significant Absorption – Unlike the small intestine, the esophagus does not absorb nutrients.
4. No Major Secretory Role – Mucus is secreted by submucosal glands (not the epithelium itself) to aid lubrication, but the lining epithelium is not primarily secretory.

Thus, the dominant and essential function is protection.

Why the Other Options Are Incorrect:

1. A) Protective & Absorptive – Incorrect because the esophagus does not absorb nutrients. Absorption occurs in the stomach and intestines.
2. B) Secretory & Protective – Incorrect because secretion is not a primary epithelial function (mucus comes from submucosal glands, not the surface epithelium).
3. C) Absorptive – Incorrect for the same reason as A; the esophagus is not designed for absorption.
4. E) Secretory – Incorrect because while some lubrication occurs, it is not produced by the lining epithelium itself but by specialized glands beneath it.

Why “Beliefs” is Correct:
Beliefs are the core tenets or convictions that a group of people accept as true. They are deeply embedded in a community’s culture and shape its worldview. Examples include religious doctrines, societal assumptions (e.g., “hard work leads to success”), or superstitions. Beliefs influence values (what is considered good/bad) and norms (expected behaviors), but they are distinct as they represent the underlying truths a community holds.

Why the Other Options Are Incorrect:

1. A) Culture – While beliefs are part of culture, culture itself is broader, encompassing language, traditions, art, and social structures. The question asks specifically about tenets held as true, not the entire cultural system.
2. B) Values – Values are principles or standards a community considers important (e.g., honesty, equality). They stem from beliefs but are more about judgments of worth rather than convictions of truth.
3. C) Norms – Norms are rules or expectations for behavior (e.g., shaking hands when greeting). They are influenced by beliefs but are about actions, not the tenets themselves.
4. D) Architect – This is a distractor with no relevance. An architect designs buildings and does not relate to cultural tenets.

• Secretin, released by S-cells in the duodenum, is the main regulator of exocrine pancreatic secretion rich in bicarbonate.

• Trigger: Acidic chyme (low pH) from the stomach entering the duodenum.

• Function: Stimulates the ductal cells of the pancreas to secrete a watery, bicarbonate-rich fluid.

• Purpose: Neutralizes gastric acid in the duodenum, creating the optimal pH for pancreatic enzymes (like lipase, amylase, proteases) to function.

Why the Other Options Are Wrong

Gastrin ❌

• Secreted by G-cells in the stomach.

• Its main function is to increase gastric acid secretion and promote gastric motility.

• No direct effect on pancreatic bicarbonate secretion.

Cholecystokinin (CCK) ❌

• Secreted by I-cells in the duodenum/jejunum in response to fats and amino acids.

• Stimulates pancreatic acinar cells to release enzyme-rich secretions.

• But bicarbonate-rich fluid comes from ductal cells, which are regulated by secretin.

VIP (Vasoactive Intestinal Peptide) ❌

• Causes relaxation of intestinal smooth muscle and stimulates intestinal secretions.

• Does not specifically control pancreatic bicarbonate secretion.

GIP (Gastric Inhibitory Peptide / Glucose-dependent Insulinotropic Peptide) ❌

• Stimulates insulin secretion in response to oral glucose.

• It also mildly inhibits gastric acid secretion.

• Not involved in pancreatic bicarbonate secretion.

Bile secretion from the liver is primarily stimulated by the hormone secretin.

• Secretin is released from S-cells in the duodenum in response to acidic chyme entering from the stomach.

• Its major role is to increase bicarbonate-rich watery secretion from the bile ducts and pancreas, which helps neutralize acid in the small intestine.

• Thus, secretin directly promotes hepatic bile secretion.

Why the Other Options Are Wrong

ANP (Atrial natriuretic peptide) ❌

• ANP is a cardiac hormone involved in sodium and water excretion by the kidneys.

• It has no direct role in bile secretion.

CCK (Cholecystokinin) ❌

• CCK is released by I-cells of the duodenum and jejunum in response to fats and amino acids.

• Its role is to stimulate contraction of the gallbladder and relaxation of the sphincter of Oddi, releasing stored bile.

• Important: CCK causes bile release from the gallbladder, but not secretion from the liver.

VIP (Vasoactive intestinal peptide) ❌

• VIP stimulates intestinal secretions and smooth muscle relaxation.

• It does not regulate bile secretion from the liver.

GIP (Gastric inhibitory peptide / Glucose-dependent insulinotropic peptide) ❌

• GIP stimulates insulin release in response to oral glucose.

• It has no direct action on bile secretion.

The screening diagnostic test for hepatitis C virus (HCV) infection is the detection of anti-HCV antibodies in the blood.

• This is usually done using ELISA (enzyme-linked immunosorbent assay).

• If positive, it indicates exposure to the virus, either current or past.

• Since antibodies can persist, a confirmatory test (like HCV RNA PCR) is required to detect active infection.

So in screening, we look for antibodies (cost-effective and practical). In confirmation, we look for viral RNA.

Why the Other Options Are Wrong

HCV antigen ❌

• HCV core antigen tests exist and can indicate infection earlier than antibodies.

• But they are not the standard initial screening test; antibody testing remains first-line.

RNA levels ❌

• HCV RNA PCR is the confirmatory test to prove active infection and viral load.

• It is too expensive and not practical as a first-line screening tool.

Serum IgG antibodies ❌

• Hepatitis C does not typically use “IgM vs IgG” distinction the way hepatitis A or B does.

• General “anti-HCV antibody” testing (not specifically IgG) is used for screening.

Ultrasound ❌

• Ultrasound is used to assess liver damage, cirrhosis, or hepatocellular carcinoma.

• It does not detect HCV infection itself.

A liver biopsy is most commonly performed by inserting the needle in the right 8th or 9th intercostal space in the mid-axillary line.

• The needle is directed upward, inward, and slightly forward to reach the liver.

• This site is chosen because it provides a safe approach to the liver while avoiding injury to the lungs, pleura, or gallbladder.

• The patient is usually asked to hold breath in expiration during the procedure — this pushes the diaphragm upward, bringing the liver into a safer position.

Why the Other Options Are Wrong

Subcostal space ❌

• Not a defined anatomical space like the intercostal spaces.

• Subcostal (just below the costal margin) is not a standard approach due to higher risk of bowel or gallbladder injury.

5th intercostal space ❌

• Too high. At this level on the right side, the needle would risk puncturing the lungs and pleura, leading to pneumothorax.

Right 10th intercostal space ❌

• Too low. At this level, the risk of injuring colon, kidney, or gallbladder is increased.

• The liver may not extend this far down in some individuals.

Right 7th intercostal space ❌

• Slightly higher than the ideal site.

• In some individuals it might still be used, but the 8th intercostal space is safer and more standard.

The most reliable method for diagnosis and staging of gastric carcinoma is contrast-enhanced CT scan of the abdomen and chest.

• Diagnosis: While endoscopy with biopsy is the gold standard for confirming the diagnosis histologically, when the question combines diagnosis with staging, it refers to imaging choice. CT scan is the best modality to evaluate the extent of the primary tumor, local invasion, lymph node involvement, and distant metastases (especially liver and lungs).

• Chest CT is included because lung metastasis is a common route of spread.

Why the Other Options Are Wrong

Ultrasound abdomen ❌

• Useful for detecting liver metastases or ascites.

• However, it is not sensitive enough to evaluate local invasion, nodal spread, or small metastases.

• Cannot reliably stage gastric carcinoma.

MRI abdomen ❌

• Provides excellent soft tissue contrast and can be used for liver metastases or local staging in special cases.

• However, it is not routinely used as the first-line staging tool. CT is more practical and widely available.

PET scan ❌

• PET can detect metabolically active lesions and distant metastases.

• However, gastric carcinoma sometimes has low FDG uptake, making PET less reliable.

• PET may be used as an adjunct but not as the primary staging tool.

X-ray ❌

• Plain X-ray of the abdomen or chest is not useful for diagnosing or staging gastric carcinoma.

• It may show nonspecific findings (e.g., mass effect, obstruction, or lung nodules), but it cannot define extent or staging.

The root of the mesentery is a fan-shaped attachment of the small intestine’s mesentery (jejunum and ileum) to the posterior abdominal wall.

• It extends obliquely from the duodenojejunal flexure (left side of L2 vertebra) down to the ileocecal junction in the right iliac fossa.

• As it travels across the posterior abdominal wall, it crosses several retroperitoneal structures, the most important being the third part of the duodenum, as well as the aorta, inferior vena cava, and right ureter.

• Among the given options, the key organ that lies directly in its path is the third part of the duodenum.

Why the Other Options Are Wrong

Suprarenal glands ❌

• These are located superior to the kidneys and much higher than the course of the root of the mesentery.

• The root does not cross them.

Pancreas ❌

• The pancreas lies above the root of the mesentery (mostly at the level of L1–L2).

• The root begins below the pancreas at the duodenojejunal flexure and does not directly cross it.

Transverse colon ❌

• The transverse colon is an intraperitoneal structure, not retroperitoneal.

• It is attached by the transverse mesocolon, not by the root of the mesentery.

First part of the duodenum ❌

• The first part of the duodenum lies higher, at the level of L1.

• The root of the mesentery begins just distal to this, so it does not cross here.

In a research report, the Discussion section is where the researcher:

• Explains the significance of the findings

• Interprets results in the context of previous studies

• Discusses implications, limitations, and possible future directions

This is the analytical part of the report. Simply presenting numbers or outcomes isn’t enough — researchers must explain what those results mean. That’s the role of the Discussion section.

Why the Other Options Are Wrong

Results ❌

• The Results section only presents data (tables, graphs, statistical outcomes).

• It does not include interpretation, arguments, or meaning.

Abstract ❌

• The Abstract is a summary of the entire paper (background, methods, results, and conclusions).

• It’s concise and doesn’t provide detailed arguments or explanations.

Objective ❌

• The Objective states the purpose of the study or what the researchers aimed to achieve.

• It does not discuss or explain findings.

Introduction ❌

• The Introduction explains the background, rationale, and importance of the study.

• It sets up the research question but does not explain findings.

Ankylosing spondylitis (AS) is a seronegative spondyloarthropathy strongly associated with HLA-B27. These conditions often have systemic manifestations beyond the joints. One of the most important associations is with inflammatory bowel disease (IBD), especially ulcerative colitis and Crohn’s disease.

• The link is immunological: both AS and IBD involve dysregulation of the immune system with overlapping genetic risk factors (e.g., HLA-B27, IL-23 pathway).

• Up to 5–10% of patients with AS have clinically apparent IBD, while subclinical gut inflammation may be present in even more cases.

• Among the given options, ulcerative colitis is the key gastrointestinal manifestation to suspect.

Why the Other Options Are Wrong

Celiac disease ❌

• Celiac disease is an autoimmune disorder associated with HLA-DQ2/DQ8, not HLA-B27.

• It is linked more with dermatitis herpetiformis and other autoimmune conditions, not ankylosing spondylitis.

Peptic ulcer ❌

• Peptic ulcers are primarily associated with Helicobacter pylori infection, NSAID use, or hypersecretory states.

• No direct immunological or clinical association with ankylosing spondylitis exists.

Gastritis ❌

• While NSAID use in AS patients can cause gastritis as a complication of treatment, it is not a characteristic gastrointestinal manifestation of the disease itself.

Carcinoid syndrome ❌

• Carcinoid tumors produce serotonin and lead to flushing, diarrhea, and right-sided valvular heart disease.

• This syndrome has no relation to ankylosing spondylitis.

Saliva has a unique ionic composition compared to plasma. While plasma is rich in sodium (Na⁺) and chloride (Cl⁻), saliva undergoes active modification as it passes through the salivary ducts. The ducts reabsorb Na⁺ and Cl⁻ but secrete K⁺ and HCO₃⁻. As a result, final saliva is:

• Hypotonic compared to plasma

• High in K⁺ and HCO₃⁻

• Low in Na⁺ and Cl⁻

This is important because bicarbonate helps neutralize acids in the oral cavity, while potassium reflects the active transport processes of ductal cells.

Why the Incorrect Options Are Wrong

Potassium ❌

• Yes, potassium is increased in saliva compared to plasma.

• But bicarbonate is also significantly increased.

• Hence, choosing only potassium makes the answer incomplete.

Magnesium ❌

• Saliva does contain magnesium, but only in trace amounts.

• It is not a defining abundant electrolyte.

Calcium ❌

• Calcium is important for tooth enamel remineralization.

• However, its concentration is not as high as potassium and bicarbonate.

Na and Cl ❌

• In saliva, sodium and chloride are actually reabsorbed in ducts.

• Their levels are lower than plasma, so saliva is not abundant in these ions.

Concept

• Peliosis hepatis is characterized by blood-filled cavities in the liver.

• In AIDS patients, this condition is strongly linked to Bartonella henselae infection (the same pathogen responsible for bacillary angiomatosis and cat scratch disease).

• Bartonella organisms localize in the perisinusoidal space (Space of Disse), where they induce vascular proliferation and blood-filled cystic lesions.

Why the others are incorrect

• Gonorrhea ❌ – Causes urethritis, PID; not linked to peliosis.

• Salmonella ❌ – Associated with bacteremia in AIDS, but not peliosis.

• Shigella ❌ – Causes dysentery; no hepatic peliosis association.

• Plasmodium ❌ – Causes malaria with liver involvement, but not peliosis.

Clinical Relevance

• Bartonella in AIDS patients can cause peliosis hepatis, bacillary angiomatosis, and bacteremia.

• Diagnosis: Warthin–Starry silver stain shows organisms in tissue.

• Treatment: Macrolides (azithromycin, clarithromycin) or doxycycline.

✅ Final Answer: Bartonella (B)
💡 Tip: “Peliosis in AIDS = think Bartonella henselae (cat scratch/angiomatosis bug).”