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Renal MS2 > Vasodilators and Sympathoplegics > Flashcards

Vasodilators and Sympathoplegics Flashcards

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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
First line therapy for HTN in pregnancy
Hydralazine and methyldopa
26
What should be used to treat HTN in African Americans with both HTN and heart failure?
Hydralazine and nitrates
27
MOA of sodium nitroprusside
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
Adverse effects of sodium nitroprusside
Excessive hypotension Releases cyanide and thiocyanate during metabolism (but usually not problematic unless infusions are administered for several days)
29
Prototype for organic nitrates
NTG | isosorbide dinitrate and isosorbide mononitrate are others
30
Pharmacodynamics/kinetics for organic nitrates?
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
Adverse effects of organic nitrates
Orthostatic hypotension, syncope, throbbing headache
32
Mechanisms that may contribute to tolerance of organic nitrates
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
Contraindications for organic nitrates
If intracranial pressure is elevated
34
Drug interactions for organic nitrates
PDE5 inhibitors
35
What can you use sympathoplegic agents with to increase their efficacy?
Diuretic
36
What 2 beta blockers can also block a1 receptors?
Carvedilol (non-selective non-ISA) and labetalol (non-selective ISA)
37
What 3 beta blockers have vasodilating activity?
Carvedilol, Labetalol and Nebivolol (B1 selective ISA)
38
Which beta blocker is also a B3 agonist
Nebivilol (B1 selective ISA)
39
What are beta blockers used for and what's the prototype?
Preventing reflex tachy that results from tx with direct vasodilators Reduces mortality after MI and in some patients with HF Propranolol
40
Pharmacodynamics/kinetics of B-blockers
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
Which beta blockers are available as extended release
Carvedilol, metoprolol and propranolol
42
Which beta blockers are available parenterally
Atenolol, esmolol, labetolol, metoprolol and propranolol
43
Which 2 beta blockers can cross the BBB
Propranolol and penbutolol
44
Adverse effects of B-blockers in asthma/COPD
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
Adverse effects of B-blockers in diabetes
B2 blockage inhibits glycogenolysis partially and it can also mask signs of hypoglycemia; delays recovery from insulin-induced hypoglycemia
46
Most common side effects of beta blockers
Brady and fatigue | Sexual dysfunction and depression sometimes
47
What is chronic use of beta blockers associated with
Increased VLDL and reduced HDL
48
What happens in sudden withdrawal from beta blockers
Rebound HTN, angina -- possibly MI
49
What should you not combine with beta blockers
Verapamil or diltiazem (CCBs) -- slowed conduction leading to heart block
50
Clinical use of beta blocker in HTN
Metoprolol and atenolol
51
Clinical use for beta blocker in heart failure
Carvedilol, bisoprolol and metoprolol reduce mortality in long term use but can worsen ACUTE CHF!!!!
52
Clinical use of B-blockers in ischemic heart disease
Reduce frequency of angina and improve exercise tolerance
53
Clinical use of B-blockers in cardiac arrhythmias
Effective in supraventricular and ventricular ararrhythmias
54
Clinical use of B-blockers in glaucoma
Timolol, betaxolol and carteolol reduce intraocular pressure
55
When is B1-blocking selectivity advantageous?
Asthma, diabetes, peripheral vascular disease
56
When would you use a beta blocker that has partial B2 agonist activity?
Patients with bradyarrhythmias or PVD --> d/t ISA | Like Labetolol
57
Prototype for a1 blockers and the MOA
Prazosin | reversible antagonist
58
Pharmacodynamics of a1-blockers
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
Adverse effects of a1-blockers
Generally well tolerated Orthostatic hypotension, dizziness, palpitations, HA Less incidence of reflux tachy since a2 receptors can still inhibit NE release
60
Clinical uses for a1-blockers
Usually men with concurrent HTN and BPH
61
Prototypes for a2-agonists and MOA
Clonidine, methyldopa Reduce sympathetic outflow from vasomotor centers in brainstem but allow centers to retain/increase sensitivity to baroreceptor control
62
Clinical use of a2-agonists
Methyldopa for HTN during pregnancy | Clonidine for lowering BP
63
Adverse effects of methyldopa
Sedation, dry mouth, lack of concentration, seuxal dysfunction
64
Pharmacodynamics and adverse effects of clonidine
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
General MOA for vasodilators
Relax smooth muscle of arterioles --> decreases peripheral vascular resistance --> arterial pressure

Renal MS2 (3 decks)

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