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Cardiology > Autonomic Pharm I > Flashcards

Autonomic Pharm I Flashcards

1
Q

primary result of alpha-1 activation?

A

vasoconstriction by activation of smooth muscle

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2
Q

alpha-1 specific antagonists?

A

Doxazosin, Terazosin, Prazosin

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3
Q

balanced alpha-1/alpha-2 antagonists?

A

Phenoxybenzamine, Phentolamine

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4
Q

subtypes of alpha-1 receptors?

A

alpha-1a, alpha-1b, alpha-1d

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5
Q

location of alpha-1a receptors?

A

bladder neck and prostate, blockade can improve symptoms of BPH and improve urine flow

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6
Q

Stimulation of alpha-1 receptors induces vasoconstriction in these in vessels

A

vasculature of the skeletal muscle and skin, and the splachnic vessels

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7
Q

synaptic location of alpha-1 receptors?

A

post-synaptic membrane, mediates downstream events

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8
Q

synaptic location of alpha-2 receptors?

A

pre-synaptic terminal, functions as auto-receptor to terminate further NE release

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9
Q

activation of alpha-2 receptors produces?

A

agonists produce bradycardia and hypotension, they terminate further NE release

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10
Q

blockade of alpha-1 receptors causes?

A

lower blood pressure, prevents NE-stimulated smooth muscle contraction in the vasculature

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11
Q

Which alpha antagonist requires more than one daily dosing?

A

Prazosin

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12
Q

Alpha antagonist most correlated with first dose orthostatic hypotension?

A

Prazosin

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13
Q

Alpha antagonists that are more likely to cause sinus tachycarida?

A

Non-specific blockers, by virtue of augmenting action of endogenous NE release by inhibiting alpha-2

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14
Q

Phenoxybenzamine mechanism?

A

Binds covalently (me last you long time) to both alpha-1 and alpha-2

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15
Q

Phenoxybenzamine effect on blood pressure?

A

reduction via vasodilation, but less substantially than alpha-1 specific antagonists due to increased cardiac output seen with alpha-2 inhibition

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16
Q

Indications of Phenoxybenzamine?

A

Pheochromocytoma and “off label” use for Raynaud’s Syndrome

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17
Q

Mechanism of Phentolamine?

A

Non-specific, competitive alpha antagonist (short-acting)

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18
Q

Cardio-stimulation with Phentolamine?

A

Yes, due to antagonism of alpha-2

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19
Q

Phentolamine at low doses?

A

Blood pressure RISES due to cardio-stimulatory effect predominating

20
Q

Phentolamine at high doses?

A

Blood pressure falls due to alpha-1 mediated vasodilation

21
Q

Indications for Phentolamine?

A

Pheochromocytoma and hypertensive emergency (only hospital use)

22
Q

Precipitous fall in blood pressure causes what response?

A

Baroreceptors initiate sympathetic stimulation of the heart and subsequent tachycardia

23
Q

Are alpha antagonists very common in the treatment of HTN?

A

No, they are no longer used much due to better drugs

24
Q

Main locations of beta receptors?

A

the heart (B1), skeletal muscle vasculature (B2), bronchial smooth muscle (B2), and juxtaglomerular apparatus in the kidney (B1)

25
Q

Stimulation of beta-2 in vasculature of muscles causes?

A

inhibitory action, prevents calcium entry into vascular smooth muscle–> relaxation/increased perfusion of skeletal muscle (vasodilation)

26
Q

Stimulation of beta-1 causes?

A

acceleration of heart rate and increase in contractile force

27
Q

subtype of beta receptors in juxtaglomerular cells?

A

Beta-1

28
Q

stimulation of beta-1 receptors in the kidney causes?

A

release of renin, which eventually makes angiotensin II and induce potent vasoconstriction

29
Q

What is sympathomimetic activity?

A

the drug agent functions as a weak partial agonist that will provide some cardio-stimulation (but prevent excessive stimulation via endogenous NE/E)

30
Q

What types of patients would sympathomimetic drugs be useful?

A

the elderly, stroke patients, and others very susceptible to bradycardia caused by beta-blockers

31
Q

Most common CNS adverse effect seen in highly lipophilic beta antagonists?

A

Bad dreams

32
Q

Beta antagonists with names “A-M”

A

beta-1 selective

33
Q

Beta antagonists with names “N-T”

A

non-selective

34
Q

Beta antagonists ending in “ILOL” and “ALOL”

A

possess extended actions in preventing alpha-mediated reflex vasoconstriction (act as alpha 1 antagonists)

35
Q

Beta antagonist that also blocks calcium channels?

A

Carvedilol, Betaxolol

36
Q

Mechanism of beta-blocker antihypertensive effect?

A

Inhibit stimulation of renin production by catecholamines. Inhibition of presynaptic B-adrenoceptors that reduces sympathetic vasoconstrictor activity

37
Q

How must beta blockers be discontinued? Why?

A

They must be tapered off the medication. Chronic therapy causes up-regulation of the beta receptors that can cause rebound HTN if the medication is abruptly d/c

38
Q

Effects of Propranolol overdose?

A

Seizures and coma (highly lipophilic)

39
Q

Effects of Sotalol overdose?

A

prolongs the QT interval and can cause ventricular fibrillation and Torsade de Pointes

40
Q

Rescue drug therapy used in beta antagonist overdose?

A

Glucagon or high-dose Insulin/Glucose (cannot use Beta agonists, receptors are blocked)

41
Q

Non-specific beta blockers are contraindicated in?

A

patients with asthma (advised against in those with COPD)

42
Q

Beta receptor with important role in tx of bronchospasm?

A

Beta-2

43
Q

Beta blockers used cautiously in these patients?

A

Diabetics, B-1 antagonism masks hypoglycemic induced tachycardia–> patients unaware of low Blood sugar
Also patients on the borderline of decompensating CHF

44
Q

Effects of Beta-2 antagonism on glucose metabolism?

A

inhibits hepatic glycogenolysis and pancreatic glucagon release

45
Q

Beta blocker effect on Lipid profile?

A

can increase TAGs and decrease HDL; little/no effect on total cholesterol or LDL

Cardiology (14 decks)

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