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MBBS Bio Chemistry Flashcards
62 question-and-answer cards covering Bio Chemistry as it is examined in MBBS. 24 of them are printed below, taken from across the deck — no signup, no paywall on the preview.
24 sample cards from the Bio Chemistry deck
Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.
What is the overall reaction, location, and net ATP yield of glycolysis?
Glycolysis converts one glucose to two pyruvate in the cytosol. Net yield per glucose: $2\ \text{ATP}$ (4 produced − 2 invested) and $2\ \text{NADH}$. Net equation: $$\ce{Glucose + 2 NAD+ + 2 ADP + 2 P_i -> 2 Pyruvate + 2 NADH + 2 H+ + 2 ATP + 2 H2O}$$
Name the three irreversible (regulatory) enzymes of glycolysis.
(1) Hexokinase/glucokinase (glucose → glucose-6-phosphate), (2) phosphofructokinase-1 (PFK-1; fructose-6-phosphate → fructose-1,6-bisphosphate) — the rate-limiting/committed step, and (3) pyruvate kinase (phosphoenolpyruvate → pyruvate).
What is the most important allosteric regulator of PFK-1, and what activates and inhibits this enzyme?
Fructose-2,6-bisphosphate is the most potent allosteric activator of PFK-1. PFK-1 is also activated by AMP and inhibited by ATP and citrate (high-energy signals). This makes PFK-1 the key control point of glycolysis.
What are the fates of pyruvate under aerobic versus anaerobic conditions?
Aerobic: pyruvate enters mitochondria and is oxidatively decarboxylated by pyruvate dehydrogenase to acetyl-CoA. Anaerobic: pyruvate is reduced to lactate by lactate dehydrogenase, regenerating $\ce{NAD+}$ to sustain glycolysis: $$\ce{Pyruvate + NADH + H+ -> Lactate + NAD+}$$
Define gluconeogenesis: its purpose, main site, and major precursors.
Gluconeogenesis is the synthesis of glucose from non-carbohydrate precursors, occurring mainly in the liver (and renal cortex). Major precursors are lactate, glucogenic amino acids (e.g. alanine), and glycerol. It maintains blood glucose during fasting.
Which four key enzymes allow gluconeogenesis to bypass the irreversible steps of glycolysis?
(1) Pyruvate carboxylase (pyruvate → oxaloacetate, mitochondrial, requires biotin), (2) PEP carboxykinase (oxaloacetate → phosphoenolpyruvate), (3) fructose-1,6-bisphosphatase (rate-limiting), and (4) glucose-6-phosphatase (G6P → glucose, in liver/kidney ER).
What is the main function of the pentose phosphate pathway and its two products?
The PPP (hexose monophosphate shunt) operates in the cytosol to produce NADPH (for reductive biosynthesis and antioxidant defense) and ribose-5-phosphate (for nucleotide and nucleic acid synthesis). Its rate-limiting enzyme is glucose-6-phosphate dehydrogenase (G6PD).
Why is NADPH from the pentose phosphate pathway important in red blood cells, and what disease results from its deficiency?
NADPH maintains reduced glutathione, which protects RBCs from oxidative damage. G6PD deficiency reduces NADPH, causing oxidative hemolysis (hemolytic anemia, Heinz bodies, bite cells) especially after oxidant stress (fava beans, infections, primaquine, sulfa drugs).
Describe glycogenesis and the key enzymes involved.
Glycogenesis is glycogen synthesis. Glucose-6-phosphate → glucose-1-phosphate → UDP-glucose (via UDP-glucose pyrophosphorylase). Glycogen synthase adds glucose via $\alpha\text{-}1,4$ linkages (the regulated step), and branching enzyme creates $\alpha\text{-}1,6$ branch points.
Describe glycogenolysis and its key enzymes.
Glycogenolysis is glycogen breakdown. Glycogen phosphorylase (rate-limiting; uses pyridoxal phosphate) cleaves $\alpha\text{-}1,4$ bonds to release glucose-1-phosphate. Debranching enzyme removes $\alpha\text{-}1,6$ branch points. Glycogen phosphorylase is activated by phosphorylation (via glucagon/epinephrine).
How do insulin and glucagon reciprocally regulate glycogen metabolism?
Insulin activates glycogen synthase (dephosphorylation) and inhibits phosphorylase, promoting glycogen synthesis. Glucagon/epinephrine activate phosphorylase and inhibit synthase (via cAMP-dependent phosphorylation), promoting glycogen breakdown. Phosphorylation activates phosphorylase but inactivates synthase.
What is the overall function of the citric acid (Krebs) cycle, its location, and the molecule that enters it?
The citric acid cycle oxidizes acetyl-CoA to $\ce{CO2}$ in the mitochondrial matrix, capturing energy as reduced coenzymes. Acetyl-CoA (2 carbons) condenses with oxaloacetate (4 carbons) to form citrate (6 carbons), the first step catalyzed by citrate synthase.
State the energy yield (per acetyl-CoA) of one turn of the citric acid cycle.
Per turn: $3\ \text{NADH}$, $1\ \text{FADH2}$, $1\ \text{GTP}$ (or ATP), and $2\ \ce{CO2}$ released. Through oxidative phosphorylation this corresponds to roughly $10\ \text{ATP}$ per acetyl-CoA.
Name the three regulatory (irreversible) enzymes of the citric acid cycle.
Citrate synthase, isocitrate dehydrogenase (the rate-limiting step), and the α-ketoglutarate dehydrogenase complex. They are inhibited by high ATP/NADH and activated by ADP/$\ce{Ca^2+}$ (signals of low energy).
Where does fatty acid β-oxidation occur, and how are long-chain fatty acids transported into this compartment?
β-oxidation occurs in the mitochondrial matrix. Long-chain fatty acyl groups are carried across the inner mitochondrial membrane by the carnitine shuttle (carnitine palmitoyltransferase I and II). CPT-I is the rate-limiting step and is inhibited by malonyl-CoA.
What are the products of one round of fatty acid β-oxidation, and the energy yield from palmitate?
Each cycle shortens the fatty acyl chain by 2 carbons, producing 1 acetyl-CoA, 1 FADH2, and 1 NADH. Complete oxidation of palmitate ($\ce{C16}$) yields about $106\ \text{ATP}$ net (8 acetyl-CoA, 7 FADH2, 7 NADH, minus 2 ATP for activation).
Where and from what is fatty acid synthesis carried out, and what is its committed regulatory step?
Fatty acid synthesis occurs in the cytosol using acetyl-CoA, NADPH, and the multienzyme fatty acid synthase. The committed/rate-limiting step is acetyl-CoA → malonyl-CoA by acetyl-CoA carboxylase (requires biotin; activated by citrate and insulin, inhibited by palmitoyl-CoA and glucagon).
What are ketone bodies, where are they made, and when are they produced?
Ketone bodies are acetoacetate, β-hydroxybutyrate, and acetone, synthesized in liver mitochondria (ketogenesis) from acetyl-CoA. They are produced during prolonged fasting, starvation, or uncontrolled diabetes when fatty acid oxidation exceeds the citric acid cycle's capacity, and serve as fuel for brain and muscle.
Describe the structure and main storage function of triacylglycerols (triglycerides).
A triacylglycerol is a glycerol backbone esterified to three fatty acids. It is the major storage form of energy, stored in adipose tissue, because the highly reduced, anhydrous fatty acids yield more than twice the energy per gram of carbohydrate or protein.
What enzymes mobilize and synthesize triacylglycerols, and how are they hormonally regulated?
Lipolysis: hormone-sensitive lipase (and adipose triglyceride lipase) hydrolyzes stored TAG, releasing free fatty acids and glycerol; it is activated by glucagon/epinephrine (cAMP) and inhibited by insulin. Synthesis (esterification) is promoted by insulin in the fed state.
List the major classes of lipoproteins in order of increasing density and decreasing triglyceride content.
Chylomicrons (lowest density, highest TG) < VLDL < IDL < LDL < HDL (highest density, highest protein, lowest TG). As density increases, the protein content rises and triglyceride content falls.
State the primary function of each major lipoprotein class.
Chylomicrons transport dietary (exogenous) triglycerides from the intestine. VLDL transports endogenous (liver-made) triglycerides. LDL delivers cholesterol to peripheral tissues ("bad" cholesterol). HDL performs reverse cholesterol transport, carrying cholesterol from tissues back to the liver ("good" cholesterol).
What is the role of lipoprotein lipase (LPL) and which apolipoprotein activates it?
Lipoprotein lipase, located on capillary endothelium, hydrolyzes triglycerides in chylomicrons and VLDL to release free fatty acids for uptake by tissues. It is activated by apolipoprotein C-II on the lipoprotein surface.
Outline the regulation and rate-limiting step of cholesterol synthesis.
Cholesterol is synthesized in the cytosol/ER from acetyl-CoA. The rate-limiting step is HMG-CoA reductase converting HMG-CoA to mevalonate. It is inhibited by cholesterol and statins, inhibited by glucagon (phosphorylation), and activated by insulin. This is the target of statin drugs.
What this deck covers
The Bio Chemistry deck follows the MBBS Bio Chemistry syllabus — 10 chapters and 32 topics — so questions land on material that is genuinely examinable rather than trivia around it. That works out to roughly 6.2 cards per chapter.
Answers are written to be recallable, not just readable — averaging about 261 characters, which is long enough to carry the reasoning and short enough to say out loud.
A deck like this earns its keep on the second and third pass. Read the syllabus first so you know the shape of the subject, then use the cards to find the specific facts that have not stuck.
Bio Chemistry flashcards FAQ
How many Bio Chemistry flashcards are in this MBBS deck?
62 cards. This page previews 24 of them, sampled evenly across the deck so you can judge the difficulty before installing anything.
Are these MBBS flashcards free?
Yes. The preview here is free to read with no signup, and the full 62-card deck is free inside the Examius app.
What do the Bio Chemistry cards cover?
They follow the MBBS Bio Chemistry syllabus — 10 chapters and 32 topics — so the questions track what is actually examinable.
How should I use these flashcards?
Read the syllabus first so you know the shape of the subject, then drill the deck. Examius schedules each card with spaced repetition, so cards you keep missing come back sooner and ones you know drift further apart.