Pre Unified Pharmacology

Question 1

Botulinum Toxin (Botox)

Answer 1

Mechanism: Degrades SNARE, prevents vesicle fusion/exocytosis. Prevents ACh release
Effect: Muscle relaxation
Clinical Use: Increased Skeletal muscle tone, focal dystonia, Diagnosis of Lambert-Eaton Syndrome
Side Effects: Paralysis

Question 2

Edrophonium

Answer 2

Mechanism: AChase inhibitor SHORT DURATION
Effect: Allows for more ACh effects by preventing ACh breakdown.
Clinical Use: Diagnosis of Myasthenia Gravis or Lambert-Eaton Syndrome.
Side Effects: Can cause muscle paralysis, cramps.

Question 3

Neostigmine

Answer 3

Mechanism: AChase inhibitor, LONGER DURATION. Hydrolized by AChE so that covalent bond forms. Prevents AcH Breakdown.
Clinical Use: Treatment of Myasthenia Gravis
, reversal of neuromuscular blockers.
Side Effects: muscle paralysis, weakness, cramps. Salivation, lacrimation, miosis, diarrhea, bradycardia

Question 4

Physostigmine

Answer 4

Mechanism: AChase inhibitor LONGER DURATION, CROSSES BBB (Can affect CNS), prevents ACh breakdown.
Clinical Use: Treatment of Myasthenia Gravis, Reversal of Atropine poisoning,
Side Effects: muscle paralysis, weakness, cramps. Salivation, lacrimation, miosis, diarrhea, bradycardia

Question 5

Malathion

Answer 5

Mechanism: AChase Inhibitor, IRREVERSIBLE. (Phosphate group irreversibly binds AchE to form stable complex, no AcH breakdown, only overcome via synthesis of new AchE (~6 weeks)
Clinical Use: NONE. Toxic, pesticides.
Side Effects: muscle paralysis, weakness, cramps. Salivation, lacrimation, miosis, diarrhea, bradycardia

Question 6

Pilocarpine

Answer 6

Mechanism: Muscarinic agonist

Clinical Use: Glaucoma (Miosis causing increased drainage, reduces intraocular pressure, Dry mouth in Sjogrens Syndrome.

Question 7

Methacholine

Answer 7

Mechanism: Muscarinic agonist (3x more stable vs. AchE), little affinity for nicotinic receptors
Clinical Use: diagnosis of asthma (causes increased bronchial secretion)
Side Effects: Salivation, lacrimation, miosis, diarrhea, bradycardia

Question 8

Bethanecol

Answer 8

Mechanism: Muscarinic agonist (completely selective)
Clinical Use: promotes GI/Urinary tract motility, bladder empying, Post Op, post partum, counteract drug related urine retention
Side Effects: Salivation, lacrimation, miosis, diarrhea, bradycardia

Question 9

Atropine

Answer 9

Mechanism: muscarinic ANTagonists (allows sympathetic to predominate)
Clinical Use:myadriasis (opthalamic exam), sinus bradycardia, inhibit salivation/mucus secretion during surgery, counteract muscarine poisining, reduce GI motility and tone, bladder motility, sweating.
Decreases SLUDGE: Salivation, Lacrimation, Urination, Diaphoresis, GIT motility, Emesis
Side effects: SLUDGE (lol)

Question 10

Succinylcholine

Answer 10

Mechanism: Depolarizing Neuromuscular Blocker (holds channels open) Keeps muscles from contracting SHORT DURATION (MIN)
Clinical Use: Muscle relaxant in surgery, paralysis of pharyngeal muscles for intubation, ventilation
Side effects: Bradycardia, K+ release, prolonged paralysis, malignant hyperthermia.

Question 11

Pancuronium

Answer 11

Mechanism: Non-depolarizing Neuromuscular blocker (Holds channels closed) can be overcome with ACh (Reverse with AChE inhibitor) LONG DURATION (Hours)
Clinical Use: relax muscles during surgery, anesthesia, ventilation.

Question 12

Phenylephrine

Answer 12

Mechanism: alpha one agonist
Clinical Use: Nasal decongestant, treatment of shock,
Side Effects: hypertension.

Question 13

Prazozin

Answer 13

Mechanism: Alpha one antagonist
Clinical Use: hypertension, benign prostatic hyperplasia
Side Effects:postural/orthostatic hypotension

Question 14

Tamsulosin

Answer 14

Mechanism: alpha one antagonist
Clinical Use: BPH, more selective for GU muscle receptor subtype.
Side effects: postural/orthostatic hypotension

Question 15

Clonidine

Answer 15

Mechanism: alpha two agonists
Clinical use: hypertension, opioid withdrawal
Side EffectsL bradycardia hypotension

Question 16

Oxymethaxoline

Answer 16

Mechanism: Alpha one agonist, alpha two partial agonist (overall vasoconstriction) NON Selective
Clinical Use: Topical/nasal decongestant ocular hyperemia (eye redness)

Question 17

Phenoxybenzamine

Answer 17

Mechanism: Alpha One AND alpha two ANTagonist
Prevents vasoconstriction, decreases BP IRREVERSIBLE
Clinical Use: Manage hypertension from pheochromocytoma

Question 18

Phentalomine

Answer 18

Mechanism: Apha One AND alpha Two ANTagonist
REVERSIBLE, competitive
Clinical Use: Manage hypertension from pheochromocytoma.

Question 19

Dobutamine

Answer 19

Mechanism: selective beta one agonist
ionotropic. increased contractility and cardiac output, NOT heart rate. SHORT ACTING (COMT Metabolism)
Clinical Use: Acute management of heart failure.

Question 20

Albuterol

Answer 20

Mechanism: beta two agonist, avoids cardiac and skeletal side effects. Rapid action (15 min) short duration (4-6 hours)
Clinical Use: Asthma reliever

Question 21

Pindolol

Answer 21

Mechanism: PARTIAL beta one agonist.

Clinical Use: Hypertension in pts with bradycardia or low cardiac reserve

Question 22

Atenolol

Answer 22

Mechanism: Beta One SELECTIVE ANTagonist
Clinical Use: Hypertension and angina, reduce BV (via decreased renin production)
Side Effects: Sedation and Dyspnea

Question 23

Propranolol

Answer 23

Mechanism: NONSELECTIVE Beta ANTagonist
Clinical Use: hypertension and angina
Side Effects: more severe sedation, bronchoconstriction, dyspnea

Question 24

Ephedrine/Pseudoephedrine

Answer 24

Mechanism: Inhibit NE storage, therefore increases activity at post synaptic alpha and beta receptors
Clinical Use: Nasal decongestant

Question 25

Cocaine

Answer 25

Mechanism: inhibits NE transporter and uptake. (Increases NE activity)
Clinical Use: None?

Question 26

Imipramine

Answer 26

Mechanism: Inhibits NE reuptake
Clinical Use: treat mild depression
Side Effects: Postural hypotension and tachycardia

Question 27

Iproniazid

Answer 27

Mechanism: Irreversible and nonselective Discontinued everywhere except France
Clinical Use: mild depression