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Renal MS2 > Vasodilators and Sympathoplegics > Flashcards

Vasodilators and Sympathoplegics Flashcards

1
Q

What are calcium channel blockers used for?

A

Long-term outpatient therapy of hypertension
Hypertensive emergencies
Angina

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2
Q

2 major subclasses of CCB

A

Dihydropyridines (DHP) - blocks L-type Ca channels in vasculature (less effect on cardiac channels)

Non-dihydropyridines - nonselective block of vascular AND cardiac L-type calcium channels

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3
Q

Prototypes for DHPs

A

Nifedipine and amlodipine

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4
Q

Prototypes for non-dihydropyridines

A

Verapamil and diltiazem

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5
Q

Where are L-type Ca channels found?

A

They are voltage-gated and responsible for Ca2+ influx into smooth muscle cells, cardiac myocytes, SA/AV nodes

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6
Q

Effects of CCBs on smooth muscle

A

Vasodilation –> decreases peripheral resistance and afterload/O2 demand by the heart
Arterioles are more sensitive than veins and orthostatic hypotension is not typically a problem

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7
Q

Effects of CCBs on cardiac muscle

A

Reduced contractility and decreased SA pacemaker rate and AV node conduction velocity

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8
Q

Do CCBs undergo first pass metabolism?

A

Extensively

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9
Q

Which CCB has the longest half life?

A

Amlodipine = 35-50 hours compared to 2-12 hours for other CCBs

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10
Q

Adverse effects of DHPs

A

Excessive hypotension, dizziness, HA, peripheral edema, flushing, tachy, rash, gingival hyperplasia

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11
Q

Why should you not use nifedipine for management of chronic HTN?

A

Because it is a short-acting DHP and it can cause MI, stroke or death – pick a slow release and longer-acting DHP

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12
Q

Adverse effects of non-dihydropyridines

A

dizziness, headache, peripheral edema, constipation (verapamil), AV block, BRADY, heart failure, lupus-like rash (diltiazem), pulmonary edema, coughing, wheezing

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13
Q

What class of drug is contraindicated in patients taking Beta blockers?

A

Non-DHPs – specifically verapamil > diltiazem since they can slow HR, slow atrioventricular conduction and cause heart block

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14
Q

What DHP can be used in the presence of AV conduction abnormalities?

A

Nifedipine - does not decrease AV conduction

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15
Q

Why are CCBs not indicated for their use in heart failure?

A

They have a negative ionotropic effect – but can use amlodipine and felodipine if necessary for another indication like angina/HTN (safer)

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16
Q

Contraindications of DHPs and non-DHPs

A

DHP - with other vasodilators

non-DHP - with other cardiac depressants and hypotensives

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17
Q

What are the 2 K channel openers?

A

Diazoxide (hypertensive emergencies) and Minoxidil (long-term outpatient therapy of severe HTN)

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18
Q

MOA of diazoxide - pharmacodynamics/kinetics?

A

K channel opener in smooth muscle
Hyperpolarizes membrane and reduces probability of contraction; arteriolar dilator resulting in reduced systemic vascular resistance/MAP
Relatively long acting (4-12 hrs) - usually injections
Has high protein binding

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19
Q

Adverse effects/contraindications of diazoxide

A

Excessive hypotension –> stroke and MI (this is worse in renal failure and patients taking B-blockers)
Hyperglycemia (again, in renal insufficiency)
Contraindicated in pts with ischemic heart disease
Causes sodium/H20 retention but insignificant

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20
Q

MOA of minoxidil

A

Its active metabolite (minoxidil sulfate) opens K channels in smooth muscle - dilates ARTERIOLES, not veins

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21
Q

Adverse effects of minoxidil

A

Headache, sweating, hypertrichosis (abn hair growth)
Tachy, palpitations, angina, edema (since it causes Na/H20 retention) –> use with B-blocker and loop diuretic to avoid these effects

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22
Q

MOA/pharmacodynamics/kinetics/use of fenoldopam

A

D1 agonist that is a peripheral arteriolar dilator and natriuretic
Usually administered IV (half life 10 min)
Used for hypertensive emergencies, peri/post op HTN

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23
Q

3 NO modulators

A 
Hydralazine (long term therapy of HTN)
Sodium nitroprusside (HTN emergencies + acute heart failure)
Organic nitrates (HTN emergencies + angina + heart failure)
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24
Q

MOA of hydralazine

A

Stimulates release of NO from endothelium –> increased cGMP levels
Dilates arterioles not veins
Bioavailability depends amongst individuals due to acetylation

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25
Q

First line therapy for HTN in pregnancy

A

Hydralazine and methyldopa

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26
Q

What should be used to treat HTN in African Americans with both HTN and heart failure?

A

Hydralazine and nitrates

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27
Q

MOA of sodium nitroprusside

A

Stimulates release of NO –> increased cGMP
Dilates arterial AND venous vessels – reduces PVR and then BP (in the absence of heart failure)
Administered IV with BP monitoring

28
Q

Adverse effects of sodium nitroprusside

A

Excessive hypotension
Releases cyanide and thiocyanate during metabolism (but usually not problematic unless infusions are administered for several days)

29
Q

Prototype for organic nitrates

A

NTG

isosorbide dinitrate and isosorbide mononitrate are others

30
Q

Pharmacodynamics/kinetics for organic nitrates?

A

Release of NO that relaxes veins over arteries of smooth M with NO DIRECT EFFECT on cardiac/skeletal muscle

  • -> increases venous capacitance
  • -> decreases ventricular preload, pulmonary vascular pressures and heart size
  • -> decreases CO in absence of heart failure
  • -> decreases platelet aggregation

Usually administered subL but can use oral/transdermal/buccal for longer durations
Tolerance is possible (esp NTG - so wait 8 hrs between doses)

31
Q

Adverse effects of organic nitrates

A

Orthostatic hypotension, syncope, throbbing headache

32
Q

Mechanisms that may contribute to tolerance of organic nitrates

A

Diminished release of NO
Reduced availability of sulfhydryl donors
Increase generation of O2 free radicals
Diminished availability of CGRP
Tachy, increased cardiac contractility, salt and water retention

33
Q

Contraindications for organic nitrates

A

If intracranial pressure is elevated

34
Q

Drug interactions for organic nitrates

A

PDE5 inhibitors

35
Q

What can you use sympathoplegic agents with to increase their efficacy?

A

Diuretic

36
Q

What 2 beta blockers can also block a1 receptors?

A

Carvedilol (non-selective non-ISA) and labetalol (non-selective ISA)

37
Q

What 3 beta blockers have vasodilating activity?

A

Carvedilol, Labetalol and Nebivolol (B1 selective ISA)

38
Q

Which beta blocker is also a B3 agonist

A

Nebivilol (B1 selective ISA)

39
Q

What are beta blockers used for and what’s the prototype?

A

Preventing reflex tachy that results from tx with direct vasodilators
Reduces mortality after MI and in some patients with HF
Propranolol

40
Q

Pharmacodynamics/kinetics of B-blockers

A

They decrease CO –> decreases BP (do not cause hypotension in healthy, normotensive pts)
Blocking B1 also inhibits renin release

All are available as oral preps except esmolol

41
Q

Which beta blockers are available as extended release

A

Carvedilol, metoprolol and propranolol

42
Q

Which beta blockers are available parenterally

A

Atenolol, esmolol, labetolol, metoprolol and propranolol

43
Q

Which 2 beta blockers can cross the BBB

A

Propranolol and penbutolol

44
Q

Adverse effects of B-blockers in asthma/COPD

A

Blockade of B2 can cause increase in airway resistance and should avoid beta blockers in general bc there is no drug that completely avoids B2 blockage

Can give in COPD because benefits outweigh risks (esp in ischemic heart disease)

45
Q

Adverse effects of B-blockers in diabetes

A

B2 blockage inhibits glycogenolysis partially and it can also mask signs of hypoglycemia; delays recovery from insulin-induced hypoglycemia

46
Q

Most common side effects of beta blockers

A

Brady and fatigue

Sexual dysfunction and depression sometimes

47
Q

What is chronic use of beta blockers associated with

A

Increased VLDL and reduced HDL

48
Q

What happens in sudden withdrawal from beta blockers

A

Rebound HTN, angina – possibly MI

49
Q

What should you not combine with beta blockers

A

Verapamil or diltiazem (CCBs) – slowed conduction leading to heart block

50
Q

Clinical use of beta blocker in HTN

A

Metoprolol and atenolol

51
Q

Clinical use for beta blocker in heart failure

A

Carvedilol, bisoprolol and metoprolol reduce mortality in long term use but can worsen ACUTE CHF!!!!

52
Q

Clinical use of B-blockers in ischemic heart disease

A

Reduce frequency of angina and improve exercise tolerance

53
Q

Clinical use of B-blockers in cardiac arrhythmias

A

Effective in supraventricular and ventricular ararrhythmias

54
Q

Clinical use of B-blockers in glaucoma

A

Timolol, betaxolol and carteolol reduce intraocular pressure

55
Q

When is B1-blocking selectivity advantageous?

A

Asthma, diabetes, peripheral vascular disease

56
Q

When would you use a beta blocker that has partial B2 agonist activity?

A

Patients with bradyarrhythmias or PVD –> d/t ISA

Like Labetolol

57
Q

Prototype for a1 blockers and the MOA

A

Prazosin

reversible antagonist

58
Q

Pharmacodynamics of a1-blockers

A

Prevents vasoconstriction of arteries and veins – reducing PVR and then BP
Relaxes smooth M in prostate
Retention of salt/H20 when used without diuretic
Can increase HDL

59
Q

Adverse effects of a1-blockers

A

Generally well tolerated
Orthostatic hypotension, dizziness, palpitations, HA
Less incidence of reflux tachy since a2 receptors can still inhibit NE release

60
Q

Clinical uses for a1-blockers

A

Usually men with concurrent HTN and BPH

61
Q

Prototypes for a2-agonists and MOA

A

Clonidine, methyldopa
Reduce sympathetic outflow from vasomotor centers in brainstem but allow centers to retain/increase sensitivity to baroreceptor control

62
Q

Clinical use of a2-agonists

A

Methyldopa for HTN during pregnancy

Clonidine for lowering BP

63
Q

Adverse effects of methyldopa

A

Sedation, dry mouth, lack of concentration, seuxal dysfunction

64
Q

Pharmacodynamics and adverse effects of clonidine

A

Reduces CO, PVD and then BP
Sedation, dry mouth, depression, sexual dysfunction
Can give transdermally to lessen sedation but then may get skin rxn

Abrupt withdrawal = life threatening HTN crisis

65
Q

General MOA for vasodilators

A

Relax smooth muscle of arterioles –> decreases peripheral vascular resistance –> arterial pressure

Renal MS2 (3 decks)

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