USMLE Pharmacology Flashcards

24 sample cards from the Pharmacology deck

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

1. Identify the antidotes for iron poisoning, copper/Wilson disease, lead poisoning, and cyanide.

   Iron: deferoxamine or deferasirox. Copper/Wilson: penicillamine or trientine. Lead: EDTA, dimercaprol, succimer (DMSA for children). Cyanide: hydroxocobalamin, sodium thiosulfate, nitrites (induce methemoglobin).

2. What receptors do sympathomimetics act on, and what are the second messengers for each adrenergic receptor subtype?

   $\alpha_1$: $G_q$ → increased IP3/DAG/$Ca^{2+}$. $\alpha_2$: $G_i$ → decreased cAMP. $\beta_1$, $\beta_2$, $\beta_3$: $G_s$ → increased cAMP. Sympathomimetics mimic the effects of endogenous catecholamines at these G-protein-coupled receptors.

3. Compare the receptor selectivity and clinical use of epinephrine, norepinephrine, and isoproterenol.

   Epinephrine: $\alpha_1=\alpha_2$, $\beta_1=\beta_2$ (low dose $\beta$ predominates) — anaphylaxis, cardiac arrest. Norepinephrine: $\alpha_1 > \alpha_2 > \beta_1$ (minimal $\beta_2$) — septic shock/vasopressor. Isoproterenol: $\beta_1=\beta_2$ (no $\alpha$) — nonselective $\beta$-agonist, causes reflex tachycardia.

4. Explain the 'epinephrine reversal' phenomenon caused by alpha-blockade.

   Normally epinephrine raises blood pressure via $\alpha_1$ vasoconstriction. After an $\alpha$-blocker (e.g., phentolamine), epinephrine's remaining $\beta_2$-mediated vasodilation dominates, so blood pressure paradoxically falls. Phenylephrine (pure $\alpha_1$) shows only a blunted response, not reversal.

5. What is the mechanism and clinical use of dobutamine?

   Dobutamine is a predominantly $\beta_1$-selective agonist ($\beta_1 > \beta_2$) that increases myocardial contractility (positive inotrope) and heart rate. It is used in acute decompensated heart failure and cardiogenic shock, and as a pharmacologic cardiac stress test.

6. Compare the actions of low-dose versus high-dose dopamine.

   Low dose: activates $D_1$ receptors (renal/mesenteric vasodilation, increased renal blood flow). Medium dose: activates $\beta_1$ (increased contractility and heart rate). High dose: activates $\alpha_1$ (vasoconstriction, increased blood pressure). Used in shock and heart failure.

7. What are the clinical uses of the selective $\beta_2$-agonists albuterol and terbutaline?

   Albuterol (short-acting) and salmeterol/formoterol (long-acting) cause bronchodilation for acute asthma/COPD. Terbutaline and ritodrine relax the uterus (tocolysis) to delay preterm labor. $\beta_2$ agonism also shifts $K^{+}$ intracellularly, useful in hyperkalemia.

8. How do amphetamine, ephedrine, and cocaine act as indirect sympathomimetics?

   Amphetamine releases stored catecholamines and reverses the reuptake transporter. Ephedrine releases stored norepinephrine (and has direct action). Cocaine blocks presynaptic reuptake of norepinephrine/dopamine. All increase synaptic catecholamine levels indirectly rather than binding receptors directly.

9. What is the mechanism and primary use of phenylephrine?

   Phenylephrine is a selective $\alpha_1$-agonist causing vasoconstriction (raises blood pressure, causes reflex bradycardia), mydriasis without cycloplegia, and nasal decongestion. Used for hypotension, as a decongestant, and to dilate the pupil for eye exams.

10. Describe the mechanism and uses of the $\alpha_2$-agonist clonidine.

    Clonidine is a central $\alpha_2$-agonist that reduces central sympathetic outflow, lowering blood pressure. Uses: hypertension (especially with renal disease), ADHD, Tourette syndrome, and to blunt opioid/alcohol withdrawal. Abrupt cessation causes rebound hypertension.

11. How do non-selective ($\alpha_1 = \alpha_2$) alpha-blockers phentolamine and phenoxybenzamine differ?

    Phentolamine is a reversible/competitive non-selective $\alpha$-blocker (short-acting). Phenoxybenzamine is an irreversible non-selective $\alpha$-blocker (long-acting). Phenoxybenzamine is used preoperatively for pheochromocytoma; phentolamine treats catecholamine/tyramine-induced hypertensive crisis. Both cause reflex tachycardia and orthostatic hypotension.

12. What are the clinical uses of the selective $\alpha_1$-blockers ('-osin' drugs) and their key side effect?

    Prazosin, terazosin, doxazosin, and tamsulosin block $\alpha_1$ to relax vascular and prostatic/bladder-neck smooth muscle. Uses: BPH (urinary symptoms) and hypertension; prazosin also treats PTSD nightmares. Key side effect: first-dose orthostatic hypotension. Tamsulosin is uroselective.

13. Distinguish cardioselective from non-selective beta-blockers, and name the '-olol' mnemonic split.

    Cardioselective ($\beta_1$) blockers (A–M): atenolol, betaxolol, esmolol, metoprolol, acebutolol — safer in asthma/COPD. Non-selective ($\beta_1 = \beta_2$) blockers (N–Z): nadolol, propranolol, timolol, pindolol. Labetalol and carvedilol also block $\alpha_1$.

14. List the major clinical uses and mechanisms by which beta-blockers help in cardiovascular disease.

    Beta-blockers reduce heart rate, contractility, and renin release (decreasing cAMP). Uses: angina, hypertension, post-MI/heart failure (reduce mortality), arrhythmias (SVT rate control), thyroid storm symptom control, glaucoma (timolol reduces aqueous humor), and migraine prophylaxis.

15. Why must beta-blockers be avoided or used cautiously in a patient with a pheochromocytoma before alpha-blockade?

    Giving a beta-blocker first blocks $\beta_2$-mediated vasodilation while leaving $\alpha_1$-mediated vasoconstriction unopposed, causing a hypertensive crisis (unopposed alpha stimulation). Alpha-blockade (e.g., phenoxybenzamine) must be established before adding a beta-blocker. The same caution applies to cocaine-induced hypertension.

16. What is the effect of beta-blockers in a diabetic patient regarding hypoglycemia?

    Non-selective beta-blockers mask the adrenergic warning symptoms of hypoglycemia (tremor, tachycardia, palpitations), leaving sweating intact, and can blunt glycogenolysis-mediated recovery. This masking effect can delay recognition of hypoglycemia.

17. Compare the muscarinic and nicotinic acetylcholine receptors, including their signaling.

    Muscarinic ($M_1$–$M_5$) are G-protein-coupled: $M_1, M_3, M_5$ use $G_q$ (IP3/DAG); $M_2$ uses $G_i$ (decreased cAMP, slows heart). Nicotinic ($N_N$ ganglia/CNS, $N_M$ neuromuscular junction) are ligand-gated $Na^{+}/K^{+}$ ion channels causing fast depolarization.

18. What is the mechanism and clinical use of bethanechol?

    Bethanechol is a direct muscarinic agonist resistant to acetylcholinesterase. It activates the bowel and bladder (increased motility/tone) and is used for postoperative ileus and urinary retention (non-obstructive, e.g., neurogenic bladder). 'Bethanechol activates the Bowel and Bladder.'

19. Describe the mechanism and clinical uses of pilocarpine.

    Pilocarpine is a direct muscarinic agonist resistant to cholinesterase that contracts the ciliary muscle (open-angle glaucoma) and pupillary sphincter (closed-angle glaucoma), and stimulates secretions. Used for glaucoma (potent, enters eye) and for xerostomia/dry mouth in Sjögren syndrome.

20. How does neostigmine differ from physostigmine, and give a clinical use of each.

    Both are reversible acetylcholinesterase inhibitors that increase acetylcholine. Neostigmine is charged and does NOT cross the blood-brain barrier — used for myasthenia gravis, postoperative ileus/urinary retention, and reversal of neuromuscular blockade. Physostigmine is uncharged and crosses into the CNS — used for anticholinergic (atropine) toxicity.

21. What are the signs of cholinergic (muscarinic) excess, and give a mnemonic.

    DUMBBELSS / SLUDGE: Diarrhea, Urination, Miosis, Bradycardia/Bronchospasm, Emesis, Lacrimation, Salivation, Sweating (or Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis). Caused by organophosphates or cholinergic overdose; treat with atropine (+ pralidoxime for organophosphates).

22. What is edrophonium and how was it historically used in myasthenia gravis?

    Edrophonium is a very short-acting acetylcholinesterase inhibitor. In the historical Tensilon test, it transiently improved muscle strength in myasthenia gravis (diagnostic); it also distinguished myasthenic crisis (improves) from cholinergic crisis (worsens). Largely replaced by antibody testing today.

23. What is the mechanism of botulinum toxin, and how does it relate to the cholinergic system?

    Botulinum toxin is an indirect anticholinergic that cleaves SNARE proteins, preventing presynaptic release of acetylcholine at the neuromuscular junction and cholinergic terminals. This causes flaccid paralysis. Clinically used for dystonias, spasticity, blepharospasm, hyperhidrosis, chronic migraine, and cosmesis.

24. Summarize the direct-acting cholinergic agonists and their target-organ mnemonic ('Bethanechol, Carbachol, Methacholine, Pilocarpine').

    Bethanechol → bladder and bowel (urinary retention, ileus). Carbachol → eye (glaucoma, constricts pupil, resistant to cholinesterase). Methacholine → challenge test for bronchial hyperreactivity (asthma diagnosis). Pilocarpine → glaucoma and dry mouth (potent, crosses into eye, stimulates secretions/sweat).

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