Tamil Nadu HSE Second Year Biochemistry cheat sheet

Monosaccharides are classified by carbon number (triose to heptose) and by functional group: aldoses carry an aldehyde at C1, ketoses a keto group at C2; glucose and fructose are the standard examples.

Reducing sugars (glucose, fructose, maltose, lactose) reduce Cu2+ in Benedict's or Fehling's reagent because a free anomeric carbon is present; sucrose is non-reducing since its glycosidic bond links both anomeric carbons.

Glycosidic bond nomenclature: maltose = alpha-1,4; cellobiose = beta-1,4; lactose = beta-1,4 (galactose-glucose); sucrose = alpha-1,2; isomaltose = alpha-1,6 (branch point in glycogen and amylopectin).

Starch contains amylose (unbranched alpha-1,4) and amylopectin (alpha-1,4 with alpha-1,6 branches); glycogen is more highly branched than amylopectin and is the animal storage form.

Fatty acid shorthand: palmitic 16:0, stearic 18:0, oleic 18:1 (delta-9), linoleic 18:2 (omega-6, essential), linolenic 18:3 (omega-3, essential); arachidonic acid 20:4 is a precursor of prostaglandins.

Triacylglycerols are esters of glycerol with three fatty acids; phospholipids replace one fatty acid with a phosphate-containing polar head, making them amphipathic and suited to membranes.

The 20 standard amino acids share a common structure: a central alpha-carbon bearing an amino group, a carboxyl group, a hydrogen, and a variable R group; glycine is the only achiral one.

Essential amino acids: histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, valine (mnemonic PVT TIM HALL); arginine is semi-essential.

Protein structure levels: primary = sequence; secondary = alpha-helix and beta-sheet held by backbone hydrogen bonds; tertiary = overall 3-D fold; quaternary = assembly of subunits such as haemoglobin's four globin chains.

Nucleic acids: DNA is a double helix with antiparallel strands, deoxyribose, and bases A, G, C, T; RNA is single-stranded, uses ribose and uracil, and occurs as mRNA, tRNA and rRNA. Base pairing is A-T (A-U in RNA) and G-C with three hydrogen bonds.

Six IUB classes: oxidoreductases (oxidation-reduction), transferases (group transfer), hydrolases (hydrolytic cleavage), lyases (non-hydrolytic removal of groups forming double bonds), isomerases (intramolecular rearrangement), ligases (joining with ATP hydrolysis).

Michaelis-Menten equation: v = Vmax[S]/(Km + [S]). Km equals the substrate concentration at which v = Vmax/2; a low Km indicates high enzyme affinity for substrate.

Lineweaver-Burk plot (1/v versus 1/[S]): y-intercept = 1/Vmax, x-intercept = -1/Km, slope = Km/Vmax; used to distinguish inhibition patterns.

Competitive inhibition raises apparent Km with unchanged Vmax (overcome by more substrate); non-competitive inhibition lowers Vmax with unchanged Km; uncompetitive inhibition lowers both Km and Vmax.

Irreversible inhibitors bind covalently; examples include aspirin acetylating cyclooxygenase and organophosphates inhibiting acetylcholinesterase. Reversible inhibitors bind non-covalently.

Allosteric (non-Michaelis-Menten) enzymes show sigmoid kinetics and are regulated by effectors; phosphofructokinase-1 is activated by AMP and fructose-2,6-bisphosphate and inhibited by ATP and citrate.

Covalent modification regulation: phosphorylation by protein kinases and dephosphorylation by phosphatases switch enzyme activity; glycogen phosphorylase is activated by phosphorylation.

Zymogens are inactive precursors activated by limited proteolysis: trypsinogen to trypsin by enteropeptidase, pepsinogen to pepsin by HCl, proinsulin to insulin by cleavage of C-peptide.

Enzyme activity units: one IU converts 1 micromole of substrate per minute; katal converts 1 mole per second. Cofactors include metal ions and coenzymes such as NAD+, FAD, and coenzyme A.

ATP hydrolysis releases about 30.5 kJ/mol under standard conditions; ATP is the universal energy currency, and its terminal phosphoanhydride bonds are the energy-rich ones.

The electron transport chain complexes: I (NADH dehydrogenase), II (succinate dehydrogenase), III (cytochrome bc1), IV (cytochrome c oxidase); mobile carriers are coenzyme Q and cytochrome c.

Complex I, III, and IV pump protons into the intermembrane space, generating the electrochemical gradient; complex II does not contribute to proton pumping.

Standard reduction potentials determine electron flow: electrons pass from NADH (-0.32 V) to O2 (+0.82 V), releasing energy at each carrier.

Chemiosmotic theory (Mitchell): the proton gradient drives ATP synthase (complex V) to phosphorylate ADP; ATP synthesis is coupled to electron flow.

P/O ratios: NADH yields about 2.5 ATP and FADH2 about 1.5 ATP; total oxidation of one glucose gives roughly 30-32 ATP.

Inhibitors: rotenone blocks complex I, malonate blocks complex II, antimycin A blocks complex III, cyanide and carbon monoxide block complex IV; oligomycin blocks ATP synthase.

Uncouplers such as 2,4-dinitrophenol and thermogenin (UCP-1) carry protons across the inner membrane, dissipating the gradient so oxygen consumption rises while ATP synthesis falls and heat is produced.

Oxidative phosphorylation occurs in the inner mitochondrial membrane; substrate-level phosphorylation occurs in glycolysis and the succinyl-CoA synthetase step of the TCA cycle.

Glycolysis (Embden-Meyerhof pathway) occurs in the cytosol: glucose to 2 pyruvate, net gain of 2 ATP and 2 NADH; investment phase uses hexokinase/glucokinase and phosphofructokinase-1, payoff phase generates ATP via phosphoglycerate kinase and pyruvate kinase.

Key regulatory enzymes of glycolysis: hexokinase (inhibited by glucose-6-phosphate), phosphofructokinase-1 (activated by AMP and fructose-2,6-bisphosphate, inhibited by ATP and citrate), and pyruvate kinase.

Pyruvate dehydrogenase complex converts pyruvate to acetyl-CoA, releasing CO2 and forming NADH; cofactors are thiamine pyrophosphate, lipoic acid, CoA, FAD, and NAD+.

TCA cycle per acetyl-CoA: 3 NADH, 1 FADH2, 1 GTP, and 2 CO2; regulatory enzymes are citrate synthase, isocitrate dehydrogenase, and alpha-ketoglutarate dehydrogenase.

Anaplerotic reaction: pyruvate carboxylase converts pyruvate to oxaloacetate, replenishing TCA intermediates; it requires biotin and acetyl-CoA as an activator.

Gluconeogenesis occurs mainly in liver and kidney cortex: pyruvate to glucose requires four unique enzymes - pyruvate carboxylase, phosphoenolpyruvate carboxykinase, fructose-1,6-bisphosphatase, and glucose-6-phosphatase.

Cori cycle: muscle glycogen or glucose forms lactate during anaerobic glycolysis; lactate travels to the liver, is converted back to glucose, and returns to muscle.

HMP shunt (pentose phosphate pathway) is cytosolic and generates NADPH and ribose-5-phosphate; the oxidative phase uses glucose-6-phosphate dehydrogenase, and NADPH maintains reduced glutathione in red cells.

Glucose-6-phosphate dehydrogenase deficiency causes haemolytic anaemia after oxidant stress such as primaquine or fava beans, because NADPH and reduced glutathione fall.

Beta-oxidation occurs in the mitochondrial matrix: fatty acid is activated to acyl-CoA (consuming 2 ATP equivalents), transported as carnitine derivative by CPT-I and CPT-II, then undergoes repeated cycles of oxidation, hydration, thiolysis, and dehydrogenation, each cycle yielding 1 FADH2, 1 NADH, and 1 acetyl-CoA.

ATP yield: palmitate (16 C) gives 8 acetyl-CoA, 7 FADH2, and 7 NADH, totaling 129 ATP gross minus 2 for activation = 129; the standard accounting is 129 ATP per palmitate.

Ketogenesis occurs in liver mitochondria: acetyl-CoA to acetoacetyl-CoA to HMG-CoA to acetoacetate, which reduces to beta-hydroxybutyrate or decarboxylates to acetone; ketone bodies are used by extrahepatic tissues via succinyl-CoA transferase (thiophorase), absent in liver.

Ketosis arises in starvation and uncontrolled diabetes when oxaloacetate is depleted and acetyl-CoA accumulates; acetone gives the fruity breath odour.

Cholesterol synthesis: acetyl-CoA to HMG-CoA to mevalonate, the rate-limiting step catalyzed by HMG-CoA reductase, which is inhibited by statins and regulated by SREBP and feedback.

LDL carries cholesterol to peripheral tissues via the LDL receptor; HDL mediates reverse cholesterol transport to the liver; VLDL carries endogenously synthesized triacylglycerol; chylomicrons carry dietary fat via lymph.

Lipoprotein lipase, activated by apoC-II, hydrolyzes triacylglycerol in chylomicrons and VLDL; familial hypercholesterolaemia results from defective LDL receptors.

Essential fatty acids linoleic and linolenic acids cannot be synthesized by humans; arachidonic acid is derived from linoleic acid and yields prostaglandins, thromboxanes, and leukotrienes.

Transamination transfers an amino group to alpha-ketoglutarate, forming glutamate; enzymes are aminotransferases (ALT and AST), which require pyruvate as coenzyme derivative - pyridoxal phosphate (vitamin B6).

Oxidative deamination of glutamate by glutamate dehydrogenase releases free ammonia and regenerates alpha-ketoglutarate; it uses NAD+ or NADP+.

Urea cycle enzymes and location: carbamoyl phosphate synthetase I (mitochondria), ornithine transcarbamoylase, argininosuccinate synthetase, argininosuccinase, and arginase (cytosol); one urea cycle consumes 3 ATP and produces urea plus fumarate.

Rate-limiting step of the urea cycle is carbamoyl phosphate synthetase I, activated by N-acetylglutamate.

Nitrogen balance: positive in growth, pregnancy, and convalescence; negative in starvation, trauma, fever, and uncontrolled diabetes; urea is the main excretory nitrogen form in humans.

Glucogenic amino acids yield pyruvate or TCA intermediates; ketogenic amino acids are leucine and lysine; both glucogenic and ketogenic are isoleucine, phenylalanine, tyrosine, and tryptophan.

Phenylketonuria: deficiency of phenylalanine hydroxylase causes phenylalanine accumulation, phenylketones in urine, and intellectual disability if untreated; treatment is a low-phenylalanine diet.

Alkaptonuria: homogentisate oxidase deficiency causes dark urine on standing and ochronosis; maple syrup urine disease involves branched-chain alpha-keto acid dehydrogenase deficiency.

DNA replication is semi-conservative and bidirectional from origins; DNA polymerase synthesizes 5' to 3' and requires a primer; leading strand is continuous, lagging strand forms Okazaki fragments joined by DNA ligase.

De novo purine synthesis builds the ring on ribose-5-phosphate and yields IMP, the branch point to AMP and GMP; pyrimidine synthesis forms the ring first (carbamoyl phosphate to orotate to UMP).

Salvage pathways: HGPRT recycles hypoxanthine and guanine; its deficiency (Lesch-Nyhan syndrome) causes hyperuricaemia and self-mutilation; adenosine deaminase deficiency causes severe combined immunodeficiency.

Uric acid is the end product of purine catabolism in humans; allopurinol inhibits xanthine oxidase and is used in gout.

Transcription in eukaryotes: RNA polymerase I makes rRNA, II makes mRNA, III makes tRNA and 5S rRNA; RNA polymerase II requires the TATA-binding protein and transcription factors.

RNA processing: 5' cap of 7-methylguanosine, 3' poly-A tail, and splicing of introns by the spliceosome; alternative splicing produces multiple proteins from one gene.

Translation: mRNA codons are read 5' to 3'; initiation uses Met-tRNA and the AUG start codon; elongation at the A, P, and E ribosomal sites; termination at UAA, UAG, or UGA stop codons.

The genetic code is degenerate and nearly universal; wobble base pairing at the third codon position allows one tRNA to recognize several codons.

Gene expression control includes promoters, enhancers, operons (lac operon induction by allolactose, repression by glucose via cAMP-CAP), and epigenetic mechanisms such as DNA methylation and histone acetylation.

Fat-soluble vitamins A, D, E, and K are stored in liver and adipose tissue; water-soluble B-complex and C are not stored and excess is excreted in urine.

Vitamin A deficiency causes night blindness and xerophthalmia; vitamin A is required for rhodopsin formation and epithelial integrity. Vitamin D deficiency causes rickets in children and osteomalacia in adults.

Vitamin K is a cofactor for gamma-carboxylation of glutamate residues in clotting factors II, VII, IX, and X; deficiency prolongs prothrombin time.

Thiamine (B1) deficiency causes beriberi and Wernicke-Korsakoff syndrome; thiamine pyrophosphate is a coenzyme for pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and transketolase.

Niacin (B3) deficiency causes pellagra with dermatitis, diarrhoea, and dementia; tryptophan can be converted to niacin at 60 mg tryptophan per 1 mg niacin equivalent.

Vitamin B12 and folate deficiencies both cause megaloblastic anaemia; B12 deficiency additionally causes neurological damage from defective myelin, and intrinsic factor from parietal cells is needed for B12 absorption.

Vitamin C is required for proline and lysine hydroxylation in collagen; deficiency causes scurvy with bleeding gums and poor wound healing.

Iron deficiency causes microcytic hypochromic anaemia; iodine deficiency causes goitre and cretinism; calcium and phosphorus are needed for bone mineralization, and zinc is required for many enzymes and wound healing.

Dietary reference values: energy is expressed in kcal or kJ (1 kcal = 4.184 kJ); protein provides 4 kcal/g, carbohydrate 4 kcal/g, and fat 9 kcal/g.

Insulin from pancreatic beta cells lowers blood glucose by promoting glucose uptake in muscle and adipose via GLUT4, stimulating glycogen synthesis, lipogenesis, and protein synthesis.

Glucagon from pancreatic alpha cells raises blood glucose by stimulating glycogenolysis and gluconeogenesis in liver; it is counter-regulatory to insulin, as are cortisol, adrenaline, and growth hormone.

Insulin signalling uses the insulin receptor tyrosine kinase, IRS proteins, and PI3K-Akt; secretion is stimulated by glucose via GLUT2 and ATP-sensitive potassium channel closure.

Thyroid hormones T3 and T4 increase basal metabolic rate, oxygen consumption, and thermogenesis; T4 is converted to the more active T3 in peripheral tissues; deficiency causes hypothyroidism with low BMR and weight gain.

Steroid hormones (cortisol, aldosterone, sex hormones) derive from cholesterol and act on intracellular receptors to alter gene transcription; cortisol raises gluconeogenesis and causes negative nitrogen balance.

Catecholamines from the adrenal medulla stimulate glycogenolysis and lipolysis through cAMP and protein kinase A; they are part of the fight-or-flight response.

Diabetes mellitus: type 1 is insulin deficiency from beta-cell destruction; type 2 is insulin resistance with relative deficiency; both cause hyperglycaemia, and chronic hyperglycaemia leads to glycation and microvascular complications.

Metabolic integration in fasting: glycogenolysis supplies glucose for the first hours, then gluconeogenesis in liver and kidney, then lipolysis and ketogenesis; the brain uses ketone bodies in prolonged starvation.

Normal fasting blood glucose is about 70-100 mg/dL; diabetes is diagnosed at fasting glucose of 126 mg/dL or more, 2-hour post-load glucose of 200 mg/dL or more, or HbA1c of 6.5% or more.

HbA1c reflects average glycaemia over about 2-3 months because it measures non-enzymatic glycation of haemoglobin; it is not useful when red cell survival is abnormal.

Liver function tests include ALT and AST (transaminases), alkaline phosphatase, bilirubin, albumin, and prothrombin time; ALT is more liver-specific than AST, and alkaline phosphatase rises in biliary obstruction.

Jaundice classification: prehepatic (unconjugated hyperbilirubinaemia from haemolysis), hepatic (mixed), and posthepatic (conjugated hyperbilirubinaemia from obstruction with pale stools and dark urine).

Kidney function tests: serum creatinine, blood urea nitrogen, urinalysis, and estimated glomerular filtration rate; creatinine is a better marker than urea because it is less affected by diet.

Urine analysis: glucose and ketones in diabetes, protein in nephrotic syndrome, blood and casts in glomerulonephritis; urine specific gravity reflects concentrating ability.

Myocardial infarction markers include troponin I and T (most specific), CK-MB, and myoglobin; troponin remains elevated for several days after infarction.

Serum enzymes in disease: amylase and lipase rise in acute pancreatitis, acid phosphatase in prostatic carcinoma, and creatine kinase in muscle damage.

Lipid profile interpretation: total cholesterol, LDL cholesterol, HDL cholesterol, and triacylglycerol; high LDL and low HDL increase atherosclerotic risk, and statins lower LDL by inhibiting HMG-CoA reductase.