Autonomic Pharm III

Question 1

General adverse effect/reason Ganglionic blockers are no longer being used?

Answer 1

They lack specificity, induce sporadic adverse effects

Question 2

Mechanism of cholinergic nicotinic receptor activation?

Answer 2

Preganglionic nerve releases Ach–> when 2 molecules bind the receptor, conformational change is induced–> ion pore forms conducting inward Na+ and possible Ca2+ current–> subsequent EPSP/IPSP

Question 3

What tone predominates in the vasculature at rest?

Answer 3

Sympathetic

Question 4

What tone predominates in the heart?

Answer 4

Parasympathetic

Question 5

Effects of Ganglionic blockers on the vasculature?

Answer 5

Vasodilation of both arteries and veins–> hypotension and peripheral blood pooling with decreased venous return/cardiac output

Question 6

Effects of Ganglionic blockers on the heart?

Answer 6

Tachycardia

Question 7

Mechanism of action of Ganglionic blockers?

Answer 7

Compete with Ach for binding at the nicotinic receptor, if two Ach don’t bind–> ion channel does not open, no EPSP

Question 8

Indication for Trimethaphan?

Answer 8

Acute dissecting Aortic aneurysms (you’re all assholes and I hate you all) (TR-imethaphan is for Tyler Reid)

Question 9

Indication for Mecamylamine

Answer 9

Shown indication in treating Tourette’s Syndrome, Cocaine and Nicotine addiction

Question 10

General adverse effects of Ganglionic blockers?

Answer 10

Postural hypotension, tachycardia/arrhythimas, visual disturbances, dry mouth, constipation, paralytic ileus, urinary retention, impotence, CNS effects, neuromuscular blockade

Question 11

Adverse effect specific to Trimethaphan?

Answer 11

Asthma due to excessive Histamine release–> massive bronchoconstriction (don’t give to asthmatics)

Question 12

Mechanism of action of Clonidine?

Answer 12

Clonidine is an alpha-2 agonist, given orally. Lowers blood pressure because at low doses, the CNS hypotensive action predominates over the peripheral vasoconstriction

Question 13

Activation of central alpha2 receptors causes?

Answer 13

limits release of Norepi from sympathetic nerves and Epi from adrenal chromaffin cells

Question 14

Activation of central alpha2 heteroreceptors in non-adrenergic neurons causes?

Answer 14

Bradycardia and hypotension via Vagal activation

Question 15

Why are diuretics commonly used with alpha2 agonists?

Answer 15

they help overcome the tolerance to the alpha2 agonist and may permit lowering of dose

Question 16

Long term therapy with agonists like clonidine causes?

Answer 16

down-regulation of receptor expression for alpha2 agonists (common w/ many GCPRs), either by increased degradation or decreased synthesis –> leads to the phenomenon known as resistance

Question 17

What will happen if you rapidly d/c clonidine on a patient?

Answer 17

A malignant rebound HTN

Question 18

Advantage alpha2 agonists have over other HTN meds (lack of certain adverse effects)

Answer 18

no effect upon glucose (use in DM patients) and no effect on lung function (asthmatics)

Question 19

Major adverse effects seen with alpha2 agonists?

Answer 19

Dry mouth (xerostomia) and drowsiness

Question 20

Drug used to treat Preeclampsia?

Answer 20

Methyldopa

Question 21

Mechanism of action of Reserpine?

Answer 21

Binds tightly (long-lasting) to adrenergic storage vesicles; inhibits VMAT2 (catecholamine transporter) which causes inability to concentrate Norepi and dopamine in the cytoplasm–> they’re degraded–> no adrenergic neurotransmitters

Question 22

Major adverse effect seen in Reserpine toxicity?

Answer 22

Significant CNS effects. Can cause psychotic depression–> depression (contraindicated in pts with depression or suicidal ideations)

Question 23

Metyrosine mechanism of action?

Answer 23

Blocks the rate-limiting step in the synthesis of catecholamines from Tyrosine –> rate limiting step is Tyrosine hydroxylase, conversion of tyrosine to DOPA

Question 24

Indication for Metyrosine?

Answer 24

Pheochromocytoma