ICAR AICE-JRF/SRF (PhD) · India · NTA for ICAR
Original practice questions written to the published syllabus · not past papersICAR AICE-JRF/SRF (PhD) is a PhD, fellowship and lectureship exam run by NTA for ICAR, for candidates in India. Computer-based, 2 hours, 120 questions: Part A 20 (general agriculture, animal husbandry, current events), Part B 50 (core group), Part C 50 (specialised subject). +4 / -1, maximum 480.
Source: icar.org.in.
Checked against the exam body's published information. Formats and fees change; confirm the current edition there before you book.
Deeper reasoning: redistribution and context-sensitive half-time, factors changing MAC, second-gas effect and diffusion hypoxia, pKa and local anaesthetic onset, partial agonism of buprenorphine, enzyme induction by phenobarbital, bromide-chloride interaction, Hofmann elimination and train-of-four.
Drugs acting on the central nervous system: sedatives, tranquillisers, alpha-2 agonists, general and local anaesthetics, opioids, anticonvulsants and muscle relaxants.
Our 15 ICAR AICE-JRF/SRF questions in this subject: 0 easy, 1 medium, 14 hard, across 9 units.
Choose an answer, then open the working. Each explanation says why the right answer is right and why the others are not.
These 10 were written to ICAR AICE-JRF/SRF and are not shown on any other exam's page.
Ketamine at subanaesthetic infusion rates is used as an analgesic adjunct mainly because it:
A. Blocks NMDA receptors involved in dorsal-horn central sensitisation (wind-up)
NMDA receptor activation in the dorsal horn amplifies pain after injury; ketamine blocks the channel and limits wind-up. It is not an opioid agonist or COX inhibitor, and GABA-A potentiation is the mechanism of propofol or barbiturates.
A sheep sedated with an alpha-2 agonist becomes hypoxaemic. The mechanism most often reported is:
B. Pulmonary interstitial oedema and intrapulmonary shunting
Alpha-2 agonists cause pulmonary oedema and hypoxaemia in sheep, with variation by breed and drug. It is not methaemoglobin formation.
Tiletamine-zolazepam gives a rough, tiletamine-dominated recovery in dogs but a calmer recovery in cats. The explanation is:
C. In dogs zolazepam is cleared before tiletamine; in cats tiletamine is cleared first
The two components have different species-specific clearance. In dogs the benzodiazepine component wears off first, leaving dissociative effects; in cats the benzodiazepine persists longer.
Approximately what fraction of absorbed halothane is metabolised, compared with isoflurane?
C. About 20–25% for halothane versus about 0.2% for isoflurane
Halothane undergoes extensive hepatic oxidative and reductive metabolism, linked to hepatotoxicity in people; isoflurane is barely metabolised. Sevoflurane is intermediate at a few per cent.
Lidocaine has a pKa of 7.9. Using Henderson-Hasselbalch, what fraction is un-ionised at pH 7.4 and at pH 6.9?
B. About 24% at pH 7.4 and about 9% at pH 6.9
For a base, un-ionised fraction = 1 / (1 + 10^(pKa − pH)). pH 7.4: 1/(1 + 10^0.5) = 1/4.16 = 0.24. pH 6.9: 1/(1 + 10^1) = 0.091. The 76/91% option gives the ionised fractions (equivalently, treats lidocaine as an acid); the 9/24% option swaps the two pH values; 50% at both would hold only if pH equalled the pKa.
Tramadol provides inconsistent analgesia in dogs. The main pharmacokinetic reason proposed is:
C. Dogs produce little O-desmethyltramadol, the active mu-agonist metabolite
Tramadol is a prodrug; its M1 metabolite is the main mu agonist. Dogs form little M1, while cats form it, which fits the clinical findings.
A dog received buprenorphine 1 hour ago but is still painful after surgery. Why may giving a full mu agonist now be less effective than expected?
A. Buprenorphine's high receptor affinity limits binding of the full agonist
Buprenorphine occupies mu receptors with high affinity and dissociates slowly, so a full agonist competes poorly until buprenorphine levels fall; higher doses may overcome this partially.
The half-life of phenobarbital in a dog is 48 hours. About how long after starting a fixed daily dose (without loading) is steady state reached, and what fraction of steady state is present after 3 half-lives?
A. About 10 days; about 87.5%
Steady state is reached after about 5 half-lives: 5 × 48 h = 240 h = 10 days. After n half-lives the fraction is 1 − 0.5^n; for n = 3, 1 − 0.125 = 0.875. 75% is the value after 2 half-lives, and about 97% the value after 5.
During a non-depolarising neuromuscular block, train-of-four stimulation shows:
D. Fade, with progressively weaker twitches from the first to the fourth
Non-depolarising block causes fade because presynaptic acetylcholine release is also reduced. A phase I depolarising block gives reduced equal twitches without fade.
Which non-depolarising blocker is long-acting and vagolytic, tending to raise heart rate?
C. Pancuronium
Pancuronium blocks cardiac muscarinic receptors, causing tachycardia. Cisatracurium has minimal cardiovascular effects; atracurium can release histamine.
This plan follows where our questions actually fall, so the time goes where the marks are likely to be. It is our reading of the syllabus, not the exam body's weighting.
Read the manual chapters for these first and do every worked question you can find on them.
Aim for one sitting per unit, then mixed questions across them.
Learn the definitions, classifications and standard numbers; these units are more often recalled than worked.
Come back to these after a first pass, untimed, and read every explanation, including for the options you rejected.
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