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Pharmacology - Exam 3 > Anti-Adrenergics > Flashcards

Anti-Adrenergics Flashcards

1
Q

What kind of drugs are drugs ending in -olol

A

beta blocker

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2
Q

Phenoxybenzamine: alpha or beta blocker?

A

alpha blocker somewhat selective for A1 over A2 irreversible

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3
Q

Phentolamine: alpha or beta blocker?

A

alpha blocker non-selective: so A1 and A2 reversible

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4
Q

Atenolol: alpha or beta blocker?

A

selective B1 blocker

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5
Q

Esmolol: alpha or beta blocker?

A

selective B1 blocker

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6
Q

Prazosin: alpha or beta blocker?

A

selective A1 blocker reversible

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7
Q

What are Clonidine and Methyldopa?

A

A2 agonist acts as anti-adrenergic

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8
Q

physiological effect of prazosin

A

A1 blockade dec BP get reflex tachycardia

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9
Q

Why do you get reflex tachycardia with prazosin and phentolamine?

A

prazosin blocks A1 receptors/phentolamine blocks A1 receptors…get vasodilation…dec BP…baroreceptors activate vasomotor center…inc output signaling from vasomotor center…NE released…already got A1 receptors blocked from prazosin so NE acts only on heart…get tachycardia *remember phentolamine non-selective alpha blocker so also blocks A2 which will give you even greater tachycardia

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10
Q

Why is the duration of action longer for phenoxybenzamine?

A

irreversible alpha blocker duration of action 24 hours B/c must synthesize new receptor to recover A1 effect

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11
Q

physiological effect of phentolamine

A

reversible, non-selective alpha blocker A1 blockade…dec BP…reflex tachycardia A2 blockade…prevents feedback inhibition by released NE…causes more NE to be released onto B1 receptors in heart…even GREATER tachycardia than with selective blocker

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12
Q

So difference between selective (prazosin) and non-selective (phentolamine) alpha blocker?

A

tachycardia is WORSE with a non-selective alpha blocker than with a selective A1 blocker

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13
Q

Why even use non-selective alpha blocker (phentolamine) when get worse/double bad tachycardia?

A

phentolamine and phenoxybenzamine are used in combo with propranolol for pheochromocytoma (which is a tumor that dumps Epi and NE into system) management

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14
Q

What is prazosin used for?

A

HTN

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15
Q

What can be used for benign prostatic hypertrophy?

A

phenoxybenzamine, prazosin, and terazosin relax smooth muscle in bladder, prostate capsule, and prostatic urethra which improves urinary flow

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16
Q

Toxicity and side effects of alpha blockers

A

reflex tachycardia in both selective (prazosin) and non-selective (phentolamine) alpha blockers but worse with non-selective

postural hypotension is caused by A1 blockade

nasal stuffiness

inhibition of ejaculation

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17
Q

What is Epi reversal?

A

as concentration of Epi goes up at first BP is dec due to Epi’s effects on B2 but as inc Epi concentration more BP inc due to Epi’s effects on A1 (bi-phasic effect)

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18
Q

What happens when Epi is administered in the presence of an alpha blocker?

A

no pressor response of BP, don’t get bi-phasic effect, just get depressor response of BP, just get dec in BP due to effects on B2

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19
Q

Where are B1 receptors located?

A

heart

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20
Q

Where are B2 receptors located?

A

lungs

blood vessels

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21
Q

Do you ever want to be selective and block only for B2?

A

NO, causes bronchoconstriction and possible bronchospasm no particular reasons to want to antagonize B2 receptors

22
Q

Since don’t want to be selective for only B2 when say selective for B1 only relatively so

A

the best selectivity achieved is about 100 fold see picture

23
Q

What is Propranolol?

A

non-selective beta blocker both B1 and B2

24
Q

cardiac effects of non-selective beta blockers (propranolol)

A

cardiac effects due to blockage of B1

dec HR

dec cardiac output ( more pronounced during exercise)

dec conduction velocity

dec myocardial oxygen demand

dec spontaneous rate of depolarization

25
Q

vascular and BP effects of non-selective beta blockers (propranolol)

A

B2 block may inc TPR slightly

B1 block dec in plasma renin…so dec BP

net effect is dec in BP

MECHANISM: dec cardiac output…dec in plasma renin…dec in sympathetic tone via effects in CNS

26
Q

metabolic effects of non-selective beta blockers (propranolol)

A

no effect on plasma glucose levels in normal person

does slow recovery from hypoglycemia in diabetics (less of a problem with B1 selective)

inc plasma concentration of triglycerides and VLDL

dec plasma concentrations of HDL

27
Q

respiratory tract effects of non-selective beta blockers (propranolol)

A

blocks B2 so airway resistance increased can be life threatening to asthmatics

28
Q

What is Timolol?

A

non-selective beta blocker used in glaucoma

although non-selective used for B1 actions in the eye

29
Q

Drug of choice to treat glaucoma?

A

Timolol

30
Q

How does Timolol treat glaucoma?

A

dec aqueous humor produciton b/c B1 is responsible for production of aqueous humor in the eye

31
Q

Atenolol and Esmolol are both selective B1 blockers. When do you use Esmolol over Atenolol?

A

in emergency procedures because Esmolol has 8 min half-life

32
Q

cardiac effects of selective B1 blockers (Atenolol)

A

same as non-selective beta blockers:

cardiac effects due to blockage of B1

dec HR

dec cardiac output ( more pronounced during exercise)

dec conduction velocity

dec myocardial oxygen demand

dec spontaneous rate of depolarization

33
Q

Is there more or less danger of respirator side effects with selective B1 or non-selective beta blockers?

A

less danger with selective B1 blockers

34
Q

Are beta blockers really “selective” at high doses?

A

NO

Remember card with picture where when 100% B1 blockage saw 50% B2 blockage

35
Q

what do mixed alpha and beta blockers end with?

A

-alol or -ilol just not -olol (that’s beta blockers)

36
Q

What are therapeutic uses of beta blockers?

A

*recent reports suggest B blockers may inhibit cancer progression*

HTN (usually with diuretics and vasodilators)

Cardiac arrhythmias

Angina

Prophylaxis of migraine

Early in MI reduces high sympathetic tone

Prophylaxis to dec mortality after MI

Glaucoma

Performance anxiety

Pheochromocytoma (with alpha blocker)

Heart failure (carvedilol)

37
Q

Side effects and toxicity of beta blockers

A

B1 block= dec cardiac output, heart block, bradycardia

B2 block= bronchoconstriction

CNS: depression and lethargy

38
Q

Give example of a drug that works at presynapse

A

Guanethidine and Reserpine

39
Q

How does Guanethidine work?

A

enters via the NET (revolving hotel door) and concentrates in vesicles and depletes NE over time

40
Q

Therapeutic uses of Guanethidine

A

historically but not any more as antihypertensive used therapeutically as a BOARD QUESTION

41
Q

side effects of Guanethidine

A

postural hypotension

diarrhea

impaired sexual function

(all related to peripheral antiadrenergic actions)

42
Q

How does Reserpine work?

A

enters terminal, blocks VMAT, causing depletion of NE over time

43
Q

Therapeutic uses of Reserpine

A

historically used for hypertension

44
Q

Side effects of Reserpine

A

CNS: depression

Peripheral: orthostatic hypotension

45
Q

Mechanism of action of A2 agonists

A

A2 receptors at pre and post synaptic sites in the brain and block sympathetic outflow (A2 agonists acting on the presynaptic A2 receptors to inhibit NE release)

increases neg feedback = less NE released

functionally working as anti-adrenergic

46
Q

Give two examples of A2 agonists

A

Clonidine and alpa-methyl-dopa and dexmedetomide

47
Q

EXAM QUESTION: What is the difference between the two A2 agonists Clonidine and alpha-methyl-dopa?

A

Cloninine works directly at A2 receptors

alpha-methyl-dopa must be metabolized to alpha-methly-NE

48
Q

Therapeutic uses of Clonidine

A

essential HTN

reduction of unpleasant side effects associated with opioid withdrawal

ADHD

open angle glaucoma (apraclonidine: also dec production of aqueous humor)

49
Q

Therapeutic uses of alpha-methyl-dopa

A

essential HTN

safe in pregnancy

50
Q

toxicities and side effects of A2 agonists (Clonidine and alpa-methly-dopa)

A

dry mouth

sedation

hypertensive crisis may occur upon abrupt withdrawal from Clonidine

high incidence of autoimmune response with alpha-methly-dopa (positive Coombs test/antiglobulin test)

Pharmacology - Exam 3 (12 decks)

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