INI CET Para-Clinical Sciences Flashcards

24 sample cards from the Para-Clinical Sciences deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. What is the difference between cirrhosis micronodular and macronodular patterns?

   Micronodular cirrhosis (<3 mm uniform nodules) is typically due to alcohol and metabolic causes. Macronodular cirrhosis (>3 mm variable nodules) is typically post-viral hepatitis or post-necrotic.

2. Differentiate nephrotic from nephritic syndrome.

   Nephrotic: heavy proteinuria (>3.5 g/day), hypoalbuminemia, edema, hyperlipidemia, bland urine. Nephritic: hematuria with RBC casts, hypertension, oliguria, mild-to-moderate proteinuria, azotemia.

3. What are the histologic features of papillary thyroid carcinoma?

   Orphan-Annie eye nuclei (optically clear, ground-glass), nuclear grooves, intranuclear pseudoinclusions, and psammoma bodies. It is the most common thyroid malignancy with excellent prognosis.

4. What receptor status defines triple-negative breast cancer and why is it significant?

   Negative for estrogen receptor (ER), progesterone receptor (PR), and HER2/neu. It is significant because it does not respond to hormonal or anti-HER2 therapy and carries a poorer prognosis.

5. What is the difference between Gram-positive and Gram-negative bacterial cell walls?

   Gram-positive bacteria have a thick peptidoglycan layer that retains crystal violet (stain purple). Gram-negative bacteria have a thin peptidoglycan layer plus an outer LPS membrane, lose crystal violet, and counterstain pink with safranin.

6. What is the difference between exotoxins and endotoxins?

   Exotoxins are secreted proteins from gram-positive and gram-negative bacteria, often highly toxic and antigenic (form toxoids). Endotoxin is lipopolysaccharide (LPS) in gram-negative cell walls, released on lysis, causes fever/shock, poorly antigenic, no toxoid.

7. Name the obligate intracellular bacteria and one disease for each genus.

   Rickettsia (typhus/spotted fever), Chlamydia (trachoma, urethritis), and Coxiella (Q fever). They cannot make their own ATP (except Chlamydia which lacks it; Rickettsia can synthesize some).

8. What virus causes which: classic Koplik spots, Negri bodies, Owl-eye inclusions?

   Koplik spots: measles (rubeola) virus. Negri bodies: rabies virus. Owl-eye intranuclear inclusions: cytomegalovirus (CMV).

9. Differentiate DNA and RNA viruses by genome and give two examples of each.

   DNA viruses (mostly double-stranded, replicate in nucleus): Herpesviruses, Hepatitis B, Adenovirus, Papillomavirus. RNA viruses (mostly single-stranded, replicate in cytoplasm): Influenza, HIV, Hepatitis C, Rabies, Poliovirus.

10. What stain and microscopic feature identify Cryptococcus neoformans?

    India ink preparation shows a wide clear capsule; mucicarmine stains the capsule red. It is an encapsulated yeast causing meningitis, especially in AIDS patients.

11. Name the malaria species causing the most severe disease and the species with relapses.

    Plasmodium falciparum causes the most severe (cerebral) malaria. P. vivax and P. ovale cause relapses due to dormant hypnozoites in the liver.

12. Define pharmacokinetics and pharmacodynamics.

    Pharmacokinetics is what the body does to the drug (absorption, distribution, metabolism, excretion — ADME). Pharmacodynamics is what the drug does to the body (mechanism of action and effect, e.g., receptor binding, dose-response).

13. What is the equation for volume of distribution (Vd) and what does a large Vd indicate?

    Vd = amount of drug in body / plasma drug concentration. A large Vd indicates extensive distribution into tissues (low plasma concentration), typical of lipophilic drugs.

14. What is the difference between zero-order and first-order kinetics?

    Zero-order: a constant amount of drug is eliminated per unit time regardless of concentration (e.g., ethanol, phenytoin at high doses, aspirin). First-order: a constant fraction is eliminated per unit time, proportional to concentration (most drugs).

15. Define therapeutic index and which drugs have a narrow one.

    Therapeutic index = TD50/ED50 (or LD50/ED50), the ratio of toxic to effective dose. A high index means a safer drug. Narrow-index drugs include digoxin, warfarin, lithium, phenytoin, theophylline, and aminoglycosides.

16. Compare the effects of muscarinic vs nicotinic acetylcholine receptors.

    Muscarinic (GPCRs) mediate parasympathetic effects on smooth muscle/glands/heart (e.g., bradycardia, salivation). Nicotinic (ligand-gated ion channels) are at neuromuscular junction (Nm) and autonomic ganglia (Nn), causing muscle contraction and ganglionic transmission.

17. What are the cardinal autonomic effects of beta-1 vs beta-2 adrenergic receptor stimulation?

    Beta-1: increased heart rate, contractility, AV conduction, and renin release. Beta-2: bronchodilation, vasodilation (skeletal muscle), uterine relaxation, and glycogenolysis.

18. What is the mechanism of action of benzodiazepines vs barbiturates on GABA-A receptors?

    Benzodiazepines increase the frequency of chloride channel opening; barbiturates increase the duration of channel opening. Barbiturates can also directly open the channel at high doses, making them more dangerous in overdose.

19. What is the mechanism and a key adverse effect of ACE inhibitors?

    ACE inhibitors block conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone, lowering blood pressure. Key adverse effects: dry cough (bradykinin accumulation), hyperkalemia, angioedema, and teratogenicity.

20. Classify diuretics by site of action with one example each.

    Loop (thick ascending limb): furosemide. Thiazide (distal convoluted tubule): hydrochlorothiazide. Potassium-sparing (collecting duct): spironolactone, amiloride. Carbonic anhydrase inhibitor (proximal tubule): acetazolamide. Osmotic: mannitol.

21. What is the difference between cell cycle-specific and cell cycle-nonspecific chemotherapy agents?

    Cell cycle-specific agents act on dividing cells in a particular phase (e.g., antimetabolites in S phase, vinca alkaloids/taxanes in M phase). Cell cycle-nonspecific agents act on cells in any phase including resting (e.g., alkylating agents, cisplatin).

22. What are the time-of-death estimation features: algor, rigor, and livor mortis?

    Algor mortis: cooling of the body (~1°C/hour, faster early). Rigor mortis: stiffening from ATP depletion, begins 1-2 hr, full by 12 hr, passes off by 24-36 hr. Livor mortis (lividity): bluish-purple skin discoloration from blood settling, fixed by ~6-8 hr.

23. In medical jurisprudence, what is the difference between consent and informed consent, and what is the legal age of consent for medical examination in India?

    Consent is voluntary agreement; informed consent requires the patient understand the nature, risks, benefits, and alternatives of the procedure. In India, the age of consent for a medical examination/treatment is 12 years; for valid independent consent it is generally 18 years (12 for examination/general procedures).

24. What is the lethal/fatal dose and antidote for organophosphate poisoning, and its mechanism?

    Organophosphates inhibit acetylcholinesterase, causing accumulation of acetylcholine (cholinergic crisis: SLUDGE - salivation, lacrimation, urination, defecation, GI distress, emesis, plus miosis). Antidotes: atropine (blocks muscarinic effects) and pralidoxime/oximes (reactivate cholinesterase if given early).

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