Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

N929 Pharmacology II > Cardiovascular agents II part 2 > Flashcards

Cardiovascular agents II part 2 Flashcards

1
Q

Phenoxybenzamine is a

A

non-selective (binds covalently) alpha antagonist alpha 1 activity> alpha 2
less alpha 2, so less associated tachycardia with decrease in SVR & cause vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Phenoxybenzamine is used for

A

preoperative control of BP in patients with pheochromocytoma (0.5-1.0 mg/kg) & for patients with Raynaud’s disease
PO medication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Phenoxybenzamine onset time & duration of action

A

1 hr. onset
elimination half-time of 24 hours (long-acting)
pro-drug- inactive substance until it is converted to something that works in the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Prazosin is considered a

A

selective alpha 1 antagonist
less likely to cause tachycardia
dilates both arterioles & veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Prazosin is used for

A

pre-op preparation of patients with pheochromocytoma, essential HTN (combined with thiazides), decreasing afterload in patients with HF
Raynaud phenomenon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Phentolamine is a

A

non-selective alpha antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Phentolamine is used for

A

intraoperative management of hypertensive emergencies (30-70 mcg/kg): pheochromocytoma manipulation & autonomic hyperreflexia
used subcutaneously for extravascular administration of sympathomimetic agents (2.5 to 5.0 mg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Phentolamine causes

A

peripheral vasodilation and a decrease in SVR

reflex mediated and alpha 2 associated increases in HR & CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Yohimibine is a

A

alpha 2 selective blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Yohimibine is used for

A

orthostatic hypotension & impotence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Yohimibine causes

A

increased release of norepi from post-synaptic neuron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Terazosin & tamsulosin are

A

long acting selective alpha 1 antagonists that are effective in prostatic smooth muscle relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

The biggest concern with terazosin & tamsulosin include

A

orthostatic hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Beta blockers work at

A

phase 4 to block antiarrhythmic effects due to excessive catecholamines
decrease HR, workload on heart, and increase time for CPP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Beta adrenergic receptor antagonists work on the heart to cause

A

bradycardia, decreased contractility, decreased conduction velocity, and improve O2 supply and demand balance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Beta adrenergic receptor antagonists work on the airway to cause

A

bronchoconstriction and can provoke bronchospasm in patients with asthma or COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Beta adrenergic receptor antagonists work on the blood vessels to cause

A

vasoconstriction in skeletal muscles, increased PVD symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Beta adrenergic receptor antagonists work on the juxtaglomerular cells to cause

A

decreased renin release–> indirect way of decreasing BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Beta adrenergic receptor antagonists work on the pancreas to cause

A

decreased stimulation of insulin release by epi/norepi at beta 2 and then mask symptoms of hypoglycemia beta 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Beta adrenergic receptor antagonists work by

A

selective binding to beta receptors (influence inotropy, chronotropy)
competitive and reversible inhibition- large doses of agonists will completely overcome antagonism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Chronic usage of beta antagonists is associated with

A

increased number of receptors (up-regulation)

if you have sudden stop perioperatively they’d have more of a response to SNS stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Non-selective beta adrenergic antagonists include

A

propranolol, nadalol, timolol, pindolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Beta 1 adrenergic antagonists include

A

metoprolol, atenolol, acebutolol, betaxolol, esmolol

large doses lose selectivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Clinical uses of beta blockers include

A

treatment of hypertension, management of angina, decrease mortality in tx of post MI patients, used periop & preop for pts at risk for MI, suppression of tachyarrhythmias, prevention of excessive sympathetic nervous system activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Relative contraindications to beta blockers include

A

hypovolemia (if you drop HR then cannot keep up CO)
diabetes mellitus (without BS monitoring) can mask s/s of hypoglycemia
reactive airway diseaes
pre-existing AV heart block or cardiac failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Side effects of beta blockers include

A

CV system- decrease HR, contractility, BP
exacerbation of peripheral vascular disease (block of beta 2 vasodilation)
airway resistance- bronchospasm
metabolism- alter carbohydrate and fat metabolism, mask hypoglycemic increase in HR
distribution of extracellular K-inhibit uptake of K into skeletal muscles
May have decreased BP with anesthetics
Nervous system- fatigue, lethargy
N/V & diarrhea
Eye- reduction in IOP d/t decreased aqueous humor production
decreased concentration of HDLs have been seen with chronic use that may increase risk for CAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Propranolol is considered

A

the prototype & is a non-selective beta blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Propranolol has (CV effects)

A

decreased HR & contractility (B1) and increased vascular resistance (B2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Propranolol goes through

A

extensive 1st pass effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

With patients who have been treated chronically with propranolol,

A

there is decreased clearance of amide local anesthetics & decreased pulmonary clearance of fentanyl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Propranolol is administered with a goal of

A

55-60 bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Cardiac effects of propranolol include

A

decreased HR, contractility, decreased CO
the above effects are especially prominent during exercise and sympathetic outflow
blockade of beta 2 receptors–> increased PVR, increased coronary vascular resistance
reduction in renin release (mainly through B1 antagonism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Propranolol is metabolized

A

in the liver

& highly protein bound

34
Q

Propranolol has elimination half time of

A

2-3 hours

35
Q

Propranolol dosage is

A

oral dose much larger than IV dose b/c undergoes significant first pass effect- 0.05 mg/kg IV or 1-10 mg (give slowly 1 mg q 5 min)

36
Q

Propranolol decreases clearance of

A

amide LAs due to a decrease in hepatic blood flow inhibiting metabolism in the liver- risk of systemic toxicity of amide local anesthetics

37
Q

Metoprolol is a

A

beta 1 selective (inotropic & chronotropic)

selectivity is dose related

38
Q

Metoprolol undergoes

A

significant first pass effect

39
Q

Metoprolol is metabolized

A

in the liver

40
Q

The elimination half time of metoprolol is

A

3-4 hours

41
Q

The dosage of metoprolol is

A

PO 50-400 mg

IV 1-15 mg (max dose)

42
Q

With metoprolol the beta 2 receptors

A

remain intact- bronchial dilation, vasodilation, and metabolic effects
patients with asthma would benefit from this selectivity

43
Q

Atenolol is the

A

most selective beta 1 antagonist and though to have the least CNS effects

44
Q

Atenolol elimination half time is

A

6-7 hours

45
Q

Atenolol is used for

A

oral drug to treat HTN (long lasting antihypertensive effects) & advantageous to those who need beta 2 receptor activity like asthmatics

46
Q

Metabolism for atenolol

A

not metabolized in the liver, excreted via renal system, therefore elimination half life is increased markedly in patients with renal disease

47
Q

Esmolol is

A

a short duration beta 1 selective beta blocker

has a rapid onset

48
Q

Esmolol (availability, onset of action, elimination half time & duration of action)

A

availability : IV
Onset of action: 60 seconds
elimination half time is 9 minutes
Duration of action is 10-30 minutes

49
Q

Esmolol is metabolized by

A 
plasma esterase (less than 1% of the drug is excreted unchanged in the urine)
not the same esterases as plasma cholinesterases responsible for metabolism of succinylcholine (no effect on succinylcholine metabolism or duration of action)
50
Q

Esmolol has poor

A

lipid solubility & does not cross the BBB or placenta

51
Q

Esmolol is used to treat

A

hyperdynamic effects of- pheochromocytoma, thyrotoxicosis, and thyroid storm
useful in treating HTN & tachycardia associated with laryngoscopy

52
Q

Treatment of hypotension includes

A

sympathomimetics- ephedrine, phenylephrine, vasopressin, epinephrine, norepinephrine, dopamine, dobutamine

53
Q

Side effects of centrally acting partial alpha 2 agonists include

A

bradycardia, sedation, xerostomia (dry mouth), impaired concentration, nightmares, depression, vertigo, lactation in men, EPS

54
Q

Clonidine results in

A

BP reduction from decreased CO due to decreased HR and peripheral resistance
rebound hypertension with abrupt cessation

55
Q

Centrally acting agents are metabolized via

A

hepatic metabolism and renal excretion

56
Q

Centrally acting agents are available as

A

PO or transdermal patch

57
Q

Withdrawal symptoms with centrally acting agents include

A

occurs with doses >1.2 mg/day
occurs 18 hours after acute discontinuation of drug
lasts for 24-72 hours
treatment rectal or transdermal clonidine

58
Q

Perioperative use of beta-blockers indicates

A

that beta blockers should only be given if patient is already on beta blockers and hasn’t already taken it prior to surgery

59
Q

Clinical uses of centrally acting agents include

A

hypertension, induce sedation, decrease anesthetic requirements, improve perioperative hemodynamics, and analgesia

60
Q

The mechanism of action of centrally acting agents includes

A

reduce sympathetic outflow from vasomotor centers in the brain stem; centrally acting selective partial alpha 2 adrenergic agoists

61
Q

The site of action of centrally acting agents

A

CNS non-adrenergic binding sites and alpha 2 receptor agonism

62
Q

Labetalol is used to treat

A

intraoperative HTN and hypertensive crisis

can be used in hypotensive technique without an increase in HR

63
Q

Labetalol causes a

A

decrease in systemic BP via alpha 1 with attenuated reflex tachycardia (beta 1 blockade)
decreased BP, SVR, HR; CO is unaffected

64
Q

Labetalol side effects include

A

orthostatic hypotension, bronchospasm, heart block, CHF, and bradycardia

65
Q

Timolol is considered to be a

A

non-selective beta blocker

66
Q

Timolol is used to treat

A

glaucoma- decreases intraocular pressure by decreasing production of aqueous humor

67
Q

Timolol side effects include

A

eye drops can cause decreased BP, HR, and increased airway resistance

68
Q

Nadolol is considered to be

A

non selective beta blocker

69
Q

Nadolol metabolism and elimination half-time

A

no significant metabolism (renal/biliary elimination)

20-40 hrs take 1x daily

70
Q

Betaxolol is considered to be a

A

cardioselective beta 1 blocker

71
Q

Betaxolol elimination half-life is

A

11-22 hours

72
Q

Betaxolol is used for

A

HTN
topical useful for glaucoma with less risk of bronchospasm as seen with timolol so good alternative choice in asthmatics with glaucoma

73
Q

Labetalol is considered to be a

A

combined non-selective antagonists
alpha 1, beta 1 & beta 2 receptors
IV: beta to alpha blockade 7:1
PO: beta to alpha blockade 3:1

74
Q

Labetalol is metabolized via

A

conjugation of glucuronic acid; <5% drug recovered unchanged in the urine

75
Q

The elimination half time is

A

5 to 8 hours; prolonged in liver disease not affected by renal dysfunction

76
Q

The maximum drop in blood pressure with labetalol occurs

A

5-10 minutes after IV administration

77
Q

Labetalol is usually given

A

5 mg at a time for mild hypertension in the OR

78
Q

Precautions with taking timolol/brimonidine

A

bronchospastic disease, diabetes mellitus, glaucoma-angle closure, myasthenia gravis, hepatic/renal impairment, pregnancy/lactation, thryodoxicosis

79
Q

Contraindications with taking timolol/brimonidine

A

sinus bradycardia, cardiogenic shock, hypersensitivity to drug and/or its components, heart failure uncompensated, heart block 2nd or 3rd degree, severe COPD/asthma, MAO inhibitor use with or within 14 days

80
Q

Indications for brimonidine/timolol include

A

to lower IOP such as open-angle glaucoma and ocular hypertension

N929 Pharmacology II (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions