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BI13.1-5 | Miscellaneous — Gate Quiz
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Which nitrogenous bases are classified as purines?
Correct! Purines are double-ring nitrogenous bases: Adenine (A) and Guanine (G). Pyrimidines are single-ring bases: Cytosine (C), Thymine (T, in DNA), and Uracil (U, in RNA).
Mnemonic: PURe As Gold (PURines = Adenine, Guanine). CUT the PY (Pyrimidines = Cytosine, Uracil, Thymine). Purines have a double-ring structure (pyrimidine + imidazole). Pyrimidines have a single-ring structure. Purine synthesis: de novo (complex, requires PRPP, glutamine, glycine, THF, aspartate, CO2) or salvage pathway.
Incorrect. Purines = Adenine and Guanine (double ring). Pyrimidines = Cytosine, Thymine, Uracil (single ring).
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Gout is caused by hyperuricaemia. Uric acid is the final product of purine catabolism in humans. Which enzyme is deficient in Lesch-Nyhan syndrome, leading to severe hyperuricaemia?
Correct! Lesch-Nyhan syndrome is caused by HGPRT deficiency (X-linked recessive). Without HGPRT, hypoxanthine and guanine cannot be salvaged, leading to their degradation to uric acid and severe hyperuricaemia, plus neurological features (self-mutilation, intellectual disability, choreoathetosis).
HGPRT (Hypoxanthine-guanine phosphoribosyl transferase): salvage pathway enzyme. Converts hypoxanthine + PRPP to IMP; guanine + PRPP to GMP. Deficiency forces de novo synthesis, generating excess uric acid. Allopurinol (xanthine oxidase inhibitor) treats gout but is less effective in Lesch-Nyhan. Adenosine deaminase deficiency causes SCID (not Lesch-Nyhan).
Incorrect. HGPRT deficiency causes Lesch-Nyhan syndrome with severe hyperuricaemia.
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The rate-limiting enzyme of haem biosynthesis, which is inhibited by the end product haem (feedback inhibition), is:
Correct! ALA synthase (delta-ALA synthase) is the rate-limiting enzyme of haem synthesis. It is inhibited by free haem (feedback) and requires pyridoxal phosphate (B6) as a cofactor.
Haem synthesis pathway: ALA synthase (rate-limiting, in mitochondria) produces ALA from succinyl-CoA + glycine (requires PLP/B6). ALA transported to cytoplasm for steps 2-6, then back to mitochondria for final steps. Ferrochelatase inserts Fe2+ into protoporphyrin IX to form haem. Lead inhibits ALA dehydratase and ferrochelatase, causing porphyria-like picture.
Incorrect. ALA synthase is the rate-limiting, regulated enzyme of haem synthesis.
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Glucagon is released from alpha cells of the pancreatic islets in response to low blood glucose. Glucagon raises blood glucose by acting primarily on which organ?
Correct! Glucagon acts primarily on the liver to stimulate glycogenolysis (immediate) and gluconeogenesis (sustained), releasing glucose into the blood. Glucagon has minimal effect on muscle (muscle lacks glucagon receptors in significant number).
Glucagon mechanism: binds GPCR (liver), activates adenylyl cyclase, increases cAMP, activates PKA. PKA: (1) activates phosphorylase kinase (glycogenolysis), (2) inhibits glycogen synthase, (3) stimulates gluconeogenesis (phosphorylates and inactivates PFK-2, reducing fructose-2,6-bisphosphate). Net effect: glucose released into blood.
Incorrect. Glucagon acts primarily on the liver to stimulate glycogenolysis and gluconeogenesis.
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HbA1c (glycated haemoglobin) reflects average blood glucose over the preceding:
Correct! HbA1c reflects average blood glucose over the preceding 2-3 months, corresponding to the lifespan of red blood cells (approximately 120 days). ADA diagnostic criterion: HbA1c >=6.5% = diabetes.
HbA1c: Non-enzymatic glycation of haemoglobin (Hb A) to form HbA1c. Rate of formation proportional to average glucose concentration. Not useful in haemolytic anaemia (shortened RBC lifespan = falsely low), sickle cell disease, or haemoglobin variants. Normal HbA1c: less than 5.7%. Prediabetes: 5.7-6.4%. Diabetes: 6.5% or more.
Incorrect. HbA1c reflects average blood glucose over 2-3 months (RBC lifespan approximately 120 days).
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Epinephrine binds beta-adrenergic receptors (GPCRs) on the liver. Which second messenger is generated that activates PKA?
Correct! Beta-adrenergic receptors couple to Gs protein, which activates adenylyl cyclase to produce cAMP from ATP. cAMP activates protein kinase A (PKA), triggering glycogenolysis, lipolysis, and gluconeogenesis.
G-protein second messenger pathways: Gs (stimulatory): adenylyl cyclase increased, cAMP increased, PKA activated (beta-adrenergic, glucagon, TSH, PTH, ACTH, FSH, LH). Gi (inhibitory): adenylyl cyclase decreased, cAMP decreased. Gq: phospholipase C activated, IP3 + DAG increased, PKC activated, Ca2+ released (alpha-1 adrenergic, M1/M3 muscarinic, histamine H1).
Incorrect. Beta-adrenergic receptors use cAMP as the second messenger to activate PKA.
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Which enzyme is inhibited by non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen?
Correct! NSAIDs (ibuprofen, naproxen, diclofenac) inhibit cyclooxygenase (COX-1 and COX-2), blocking conversion of arachidonic acid to prostaglandins and thromboxanes. This reduces pain, fever, and inflammation.
NSAID mechanism: COX inhibition reduces prostaglandin synthesis. Prostaglandins: PGE2/PGI2 = pain sensitization, fever, inflammation, gastric protection. COX-1 (constitutive): gastric protection, platelet TXA2. COX-2 (inducible by inflammation): pain and fever mediators. Selective COX-2 inhibitors (celecoxib) spare gastric mucosa but increase cardiovascular risk (reduced prostacyclin). Aspirin: irreversible COX inhibition.
Incorrect. NSAIDs inhibit cyclooxygenase (COX), not lipoxygenase.
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The intrinsic pathway of coagulation is activated by contact with negatively charged surfaces (contact activation). The initial factor activated in the intrinsic pathway is:
Correct! The intrinsic pathway begins with Factor XII (Hageman factor) activation by contact with collagen or glass surfaces. This activates Factor XI, then IX, then X (converges with extrinsic pathway).
Coagulation cascade: Intrinsic (PTT/aPTT): XII, XI, IX, VIII, X. Extrinsic (PT/INR): VII, X. Common: X, V, prothrombin (II), fibrinogen (I). Vitamin K-dependent: II, VII, IX, X, Protein C, Protein S. Tests: PT prolonged = extrinsic/common pathway defect. aPTT prolonged = intrinsic/common pathway defect. Both prolonged = common pathway defect.
Incorrect. Factor XII (Hageman factor) is the initiating factor of the intrinsic (contact activation) pathway.
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In sickle cell anaemia, deoxygenated HbS polymerises due to a single amino acid substitution. Under hypoxic conditions at high altitude, a patient with sickle cell trait (HbAS) is MOST at risk of:
Correct! Sickle cell trait (HbAS) is generally benign at sea level. However, extreme hypoxia (high altitude, pressurized aircraft depressurization) can cause sickling in HbAS individuals. At normal conditions, the approximately 40% HbS present does not reach concentrations sufficient to polymerize.
HbAS (sickle cell trait): 40% HbS + 60% HbA. Protective against P. falciparum malaria (evolutionary selection for high prevalence in malaria-endemic regions like India, Africa). Generally no clinical disease at sea level. Extreme hypoxia (altitude, anaesthesia complications) can cause problems. HbSS = sickle cell disease with severe complications.
Incorrect. Sickle cell trait carriers can have vaso-occlusive crises under extreme hypoxic conditions.
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A 4-year-old child who ate paint chips from an old house presents with anaemia, abdominal pain, and elevated urinary delta-aminolevulinic acid (ALA). Lead poisoning is suspected. Which enzyme in haem synthesis is primarily inhibited by lead?
Correct! Lead inhibits ALA dehydratase (ALAD, step 2) and ferrochelatase (last step). This causes accumulation of ALA and zinc protoporphyrin (in RBCs). Elevated urinary ALA is a key diagnostic marker of lead poisoning.
Lead poisoning effects on haem synthesis: Inhibits ALAD (accumulates ALA and PBG) and Ferrochelatase (Fe2+ cannot be inserted; zinc is substituted = ZPP in RBCs). Clinical features: microcytic anaemia (basophilic stippling on blood film), abdominal colic, encephalopathy, peripheral neuropathy. Diagnosis: blood lead level, urinary ALA, ZPP. Treatment: chelation (DMSA, EDTA).
Incorrect. Lead inhibits ALA dehydratase and ferrochelatase in the haem synthesis pathway.
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