Pharm Flashcards

1
Q

What are the 3 principal alpha-blocker used to treat essential hypertension?

A

doxazosin, terazosin, prazosin

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2
Q

What 2 alpha blockers act on both alpha 1 and 2 receptors and therefore have limited use?

A

phenoxybenzamine, phentolamine

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3
Q

Where are alpha receptors located anatomically?

A

primarily blood vessels. Also skeletal muscles

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4
Q

Where are beta receptors located anatomically?

A

primarily the heart. Also beta-2 are found in skeletal muscle.

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5
Q

What is the difference in location of alpha1 and alpha2 receptors?

A

Alpha 2: presynaptically–> activation causes increase release of norepinephrine leading to tachycardia.
Alpha 1: downstream signaling at effector organ. Smooth muscle contraction

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6
Q

What are the subtypes of alpha-1 receptors and what is the significance of this?

A

a: found in prostate

b and d found in vasculature

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7
Q

What are the 2 main side effects associated with alpha blockers?

A

first dose orthostatic hypotension and sinus-tach, syncope, vertigo

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8
Q

First dose orthostatic hypotension associated with alpha blockers is most prominent with ____.

A

prazosin

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9
Q

Why do alpha blockers cause tachycardia?

A

Blocking alpha-2 presynaptic receptors augments release of NE causing tachycardia.

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10
Q

____ is a non-competitive, covalent, alpha1 and 2 antagonist.

A

Phenoxybenzamine

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11
Q

Indications for phenoxybenzamine

A

sympathetic excess due to pheochromocytoma, raynaud’s, frostbite, acrocyanosis

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12
Q

Adverse effects of phenoxybenzamine

A

sinus-tach, nasal congestion, drowsiness, fatigue, weakness, malaise, confusion, headache, xerostomia, ejaculation dysfunction

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13
Q

_____ is a short-acting, competitive antagonist at alpha 1 and 2 receptors.

A

phentolamine

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14
Q

Indications of phentolamine

A

pheochromocytoma, hypertensive emergency

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15
Q

Adverse effects of phentolamine

A

postural hypotension, reflex tachycardia–> arrhythmias

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16
Q

Describe the dose effect when taking phentolamine

A

Smaller doses alpha 2 predominates–> increase BP

Larger doses alpha 1 predominates causing peripheral vasodilation and decrease BP

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17
Q

How do alpha blockers affect NE treatment?

A

Decrease BP caused by NE because they block vascoconstriction.

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18
Q

How to alpha blockers effect EP Rx?

A

Decrease BP caused by EP resulting in hypotension. This is because EP also acts to beta receptors in muscles which vasodilate.

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19
Q

Describe the affinity of terazosin, doxazosin, prazosin?

A

alpha 1&raquo_space;»» alpha 2

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20
Q

Describe the affinity of phenoxybenzamine.

A

alpha 1 > alpha 2

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21
Q

Describe the affinity of phentolamine

A

alpha 1= alpha 2

22
Q

Describe the anatomical location of beta receptors?

A

heart (mostly B1) and JGA, skeletal muscle (B2, relax)

23
Q

How to B-blockers affect renin release?

24
Q

Describe the action of b-blocker pretreatment with NE.

A

No action- NE acts on a1 and 2 receptors.

25
Describe the action of b-blocker pretreatment with EP.
No big action. It may inhibit vasodilation in skeletal muscle.
26
Describe the action of b-blocker pretreatment with isoproterenol.
increase BP
27
What B-blockers have B1>>>>B2 receptor specificity
metoprolol, acebutolol, alprenolol, atenolol, betaxolol, celiprolol, esmolol, nebivolol
28
What B blockers have B1=B2 receptor specificity.
propranolol, carteolol, penbutolol, pindolol, timolol
29
____ is a competitive non-specific B-blocker that is the prototype by which other compared.
propranolol
30
classical non-selective blockers are _____ generation.
first
31
B1 selective blockers are ____ generation.
second
32
Non-selective blockers with additional actions are ____ generation.
third
33
B1 selective blockers with additional actions are ____ generation.
third
34
What drugs have high membrane stabilizing activity? what generation are they? These are also known as _____.
propranolol (1), acebutolol (2), carvedilol (3) ; Class 1 antiarrhythmic compounds.
35
Describe the mechanism of B-blockers in membrane stabilizing activity
Bind and block fast Na channels responsible for rapid depolarization .
36
What BB drugs have high intrinsic sympathomimetic activity? What class?
pindolol (1) , acebutolol (2), carteolol (3)
37
Describe intrinsic agonist activity of BB.
Function as agonists in absence of sympathetic activity and antagonists in presence of sympathetic activity.
38
What BB drugs have NO production?
carteolol, nebivolol (all 3rd generation)
39
What BB drugs have B2 receptor agonism?
carteolol
40
what BB drugs have a1 receptor antagonism?
carvedilol, betaxolol
41
What BB drugs have antioxidant activity?
carvedilol
42
Do BB reduce BP in normotensive pt?
no
43
Describe the role of reduction of renin release from JGA in the function of BB.
Proporanolol is most effective in pt with elevated plasma renin whereas pindolol is effective with little or no effect on plasma renin activity. This reduction may not be required.
44
Long term administration of BB leads to a fall in ______.
peripheral vascular resistance.
45
What are adverse effects for BB?
**abrupt discontinuation increases risk of sudden death. Change in peripheral flow may cause cold extremeties, bradycardia, worsening CHF
46
Describe off target pulmonary effects of BB?
Pt with bronchospastic disease need smooth muscle B2 receptors to promote bronchodilation. Dont give BB to these pt!
47
Describe the off target CNS effects of BB.
more lipophilic drugs do this, include depression, vivid dreams
48
Describe the off target glucose effects of BB.
B1 and B2 B can cause hypoglycemia. Be careful in diabetics
49
Describe the off target lipid profile effects of BB.
a1,b1,2,3 receptors mediate lipolysis. BB cause an increase in triglycerides and decrease in HDLS with little effect on cholesterole and LDL. Drugs with intrinsic agonist activity tend to have less effect on TG and HDL.
50
Describe BB toxicity.
heart and CNS related symptoms like bradycardia, hypotension, arrythmias, hypothermia, hypoglycemia, seizures. Co injestion with cardio-active and psychotropic drugs worsens prognosis as well as underlying disease.
51
Clinical uses of BB
1. CV conditions- HTN, acute MI 2. Non CV- termor, thyrotroxicosis, anxiety, migraine, bleeding with esophageal varices, glaucoma