AIAPGET Common Pre-Clinical & Para-Clinical Sciences (Shared across AYUSH UG) Syllabus

What is gluconeogenesis and where does it primarily occur?

The synthesis of glucose from non-carbohydrate precursors (lactate, glycerol, amino acids); occurs mainly in the liver (and kidney).

What is the role of the Krebs (citric acid / TCA) cycle?

It oxidizes acetyl-CoA to CO2 in the mitochondria, generating NADH, FADH2, and GTP/ATP for the electron transport chain.

Define beta-oxidation of fatty acids.

The mitochondrial catabolic process that breaks fatty acids into two-carbon acetyl-CoA units, generating NADH and FADH2 for ATP production.

What is the urea cycle and where does it occur?

The metabolic pathway in the liver that converts toxic ammonia (from amino acid deamination) into urea for excretion.

Define an enzyme and explain its mechanism of action.

A biological protein catalyst that speeds reactions by lowering activation energy, without being consumed, by binding substrate at its active site.

What do Km and Vmax represent in the Michaelis-Menten equation?

Km is the substrate concentration at half-maximal velocity (inversely reflects enzyme affinity); Vmax is the maximum reaction rate when the enzyme is saturated.

Differentiate water-soluble from fat-soluble vitamins with examples.

Water-soluble: B-complex and C (not stored, excreted in urine). Fat-soluble: A, D, E, K (stored in fat/liver, risk of toxicity).

Match these vitamin deficiencies: scurvy, beriberi, rickets, pellagra.

Scurvy = vitamin C; beriberi = vitamin B1 (thiamine); rickets = vitamin D; pellagra = vitamin B3 (niacin).

What are the five cardinal signs of acute inflammation?

Rubor (redness), calor (heat), tumor (swelling), dolor (pain), and functio laesa (loss of function).

Differentiate acute from chronic inflammation by predominant cell type.

Acute inflammation: neutrophils predominate. Chronic inflammation: lymphocytes, plasma cells, and macrophages predominate.

Differentiate a benign from a malignant neoplasm.

Benign: well-differentiated, slow-growing, encapsulated, non-invasive, does not metastasize. Malignant: poorly differentiated, rapid, invasive, no capsule, metastasizes.

What is metastasis and name its main routes of spread.

The spread of malignant tumor cells to distant sites; routes are lymphatic, hematogenous (blood), and transcoelomic (across body cavities).

Differentiate reversible cell injury from irreversible cell injury.

Reversible: cellular swelling, fatty change, no membrane damage (recovers). Irreversible: severe membrane damage, mitochondrial dysfunction, leading to necrosis or apoptosis.

Differentiate necrosis from apoptosis.

Necrosis: pathological, affects cell groups, causes inflammation, cell swelling and lysis. Apoptosis: programmed/physiological, single cells, no inflammation, cell shrinkage and fragmentation.

Name the four major blood groups in the ABO system and the universal donor/recipient.

A, B, AB, and O. O negative is the universal donor; AB positive is the universal recipient.

Differentiate Gram-positive from Gram-negative bacteria by cell wall.

Gram-positive: thick peptidoglycan layer, stain purple/violet. Gram-negative: thin peptidoglycan with an outer lipopolysaccharide membrane, stain pink/red.

What are the four classical morphological shapes of bacteria?

Cocci (spherical), bacilli (rod-shaped), spirilla/spirochetes (spiral), and vibrio (comma-shaped).

Differentiate active from passive immunity.

Active immunity: the body produces its own antibodies (after infection or vaccination), slow onset, long-lasting. Passive immunity: ready-made antibodies transferred (e.g., mother to fetus, antiserum), immediate but short-lived.

Name the five classes of immunoglobulins and note the most abundant.

IgG, IgA, IgM, IgE, IgD. IgG is the most abundant in serum; IgM is the largest and first produced in an immune response.

Differentiate a virus from a bacterium.

Bacteria: living prokaryotic cells, have cell walls, reproduce independently, often respond to antibiotics. Viruses: non-cellular obligate intracellular parasites of nucleic acid in a protein coat, need a host to replicate, treated with antivirals.

Define a parasite and differentiate ectoparasite from endoparasite.

An organism living on/in a host at the host's expense. Ectoparasite lives on the body surface (e.g., lice); endoparasite lives inside the body (e.g., roundworms, Plasmodium).

In forensic medicine, what is rigor mortis and its typical time course?

Post-mortem stiffening of muscles due to ATP depletion; begins ~1-2 hours after death, fully established in ~12 hours, persists ~12 hours, and passes off in ~12 hours.

Differentiate the four classic post-mortem changes used to estimate time of death.

Algor mortis (cooling of body), livor mortis/hypostasis (gravitational pooling of blood/discoloration), rigor mortis (muscle stiffening), and decomposition/putrefaction.

What is the difference between an antemortem and a postmortem wound?

Antemortem (during life): shows signs of vital reaction such as bleeding, clotting, inflammation, and healing. Postmortem (after death): no vital reaction, minimal/no bleeding, gaping without retraction.

Define LD50 in toxicology.

The median lethal dose: the amount of a substance that kills 50% of a test population; a measure of acute toxicity (lower LD50 means more toxic).

What is the universal antidote concept, and name a common chelating agent and its use.

There is no true universal antidote; activated charcoal is used to adsorb many poisons. Chelating agents like BAL (dimercaprol) or EDTA treat heavy metal poisoning (e.g., arsenic, lead).

Define pharmacokinetics and its four components (ADME).

What the body does to a drug: Absorption, Distribution, Metabolism (biotransformation), and Excretion.

Define pharmacodynamics and the terms agonist and antagonist.

What the drug does to the body (mechanism of action). An agonist binds a receptor to produce a response; an antagonist binds but blocks/prevents the response.

Define drug half-life (t1/2) and its significance.

The time required for the plasma concentration of a drug to fall to half its value; it determines dosing frequency and time to reach steady state (~4-5 half-lives).

Which Indian statutory bodies regulate AYUSH medical education and practice, and under which framework?

The National Commission for Indian System of Medicine (NCISM) regulates Ayurveda, Siddha, Unani, and Sowa-Rigpa, and the National Commission for Homoeopathy (NCH) regulates Homoeopathy, under the Ministry of AYUSH (replacing the former CCIM and CCH).