Autonomic Pharm III Flashcards

1
Q

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

A

They lack specificity, induce sporadic adverse effects

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2
Q

Mechanism of cholinergic nicotinic receptor activation?

A

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

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3
Q

What tone predominates in the vasculature at rest?

A

Sympathetic

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4
Q

What tone predominates in the heart?

A

Parasympathetic

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5
Q

Effects of Ganglionic blockers on the vasculature?

A

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

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6
Q

Effects of Ganglionic blockers on the heart?

A

Tachycardia

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7
Q

Mechanism of action of Ganglionic blockers?

A

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

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8
Q

Indication for Trimethaphan?

A

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

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9
Q

Indication for Mecamylamine

A

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

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10
Q

General adverse effects of Ganglionic blockers?

A

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

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11
Q

Adverse effect specific to Trimethaphan?

A

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

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12
Q

Mechanism of action of Clonidine?

A

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

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13
Q

Activation of central alpha2 receptors causes?

A

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

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14
Q

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

A

Bradycardia and hypotension via Vagal activation

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15
Q

Why are diuretics commonly used with alpha2 agonists?

A

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

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16
Q

Long term therapy with agonists like clonidine causes?

A

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

17
Q

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

A

A malignant rebound HTN

18
Q

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

A

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

19
Q

Major adverse effects seen with alpha2 agonists?

A

Dry mouth (xerostomia) and drowsiness

20
Q

Drug used to treat Preeclampsia?

A

Methyldopa

21
Q

Mechanism of action of Reserpine?

A

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

22
Q

Major adverse effect seen in Reserpine toxicity?

A

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

23
Q

Metyrosine mechanism of action?

A

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

24
Q

Indication for Metyrosine?

A

Pheochromocytoma