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Renal 2 > PostMT, Vasodilators and Sympathetics > Flashcards

PostMT, Vasodilators and Sympathetics Flashcards

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1
Q

What are three vasodilators (NO modulators) that release NO from drug or endothelium? When are they each used clinically?

A

Nitroprusside, used in HTN emergencies
Nitrates, used in HTN emergencies and angina
Hydralazine, used in long term outpatient therapy of severe or resistant HTN

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2
Q

What are four vasodilators that reduce calcium influx (Calcium Channel Blockers). When are they all clinically used?

A

Verapamil, Diltiazem, Nifedipine, Amlodopine.

Used in long term outpatient therapy of HTN, HTN emergencies, and angina.

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3
Q

What are two vasodilators that cause hyperpolarization of smooth muscle membrane through opening of potassium channels (potassium channel openers)? When are is each used clinically?

A

Minoxidil, used for long term outpatient therapy of severe or resistant HTN.

Diazoxide, used for HTN emergencies.

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4
Q

What is a vasodilator that activates dopamine receptors? When is it used clinically?

A

Fenoldopam, used in HTN emergencies.

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5
Q

Two major subclasses of Calcium Channel Blockers. Two examples of each.
What do CCBs block?

A

DiHydroPyridines. Nifedipine and Amlodipine
Non-DiHydroPyridines. Verapamil and Diltiazem.

CCBs block L-type VCCC.

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6
Q

MOA of DHPs

A

Block L-type calcium channels in VASCULATURE > cardiac channels.

Not as large an effect on cardiac muscle as non-DHPs; but they block smooth muscle at much lower concentrations, so cardiac effects are negligible at effective therapeutic concentrations.

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7
Q

MOA of non-DHPs

A

Nonselective block of VASCULAR AND CARDIAC L-type calcium channels.

non-DHPs have MORE CARDIAC EFFECT THAN DHPs!

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8
Q

Why do DHPs and non-DHPs differ in effects on vascular v. cardiac tissues?

A

While all CCBs bind to L-type calcium channels, DHPs and non-DHPs bind to DIFFERENT SITES on the channel proteins.

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9
Q

CCB (DHP primarily) effects on smooth muscle.

A

VASODILATION, which decreases peripheral resistance, arterioles are more sensitive than veins, orthostatic hypotension not usually problem.
RELAXATION of arteriolar smooth muscle leads to decreased afterload and decreased oxygen demand by the heart.

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10
Q

CCB (non-DHP primarily) effects on cardiac muscle

A

Reduced contractility, decreased SA node pacemaker rate, decreased AV node conduction velocity.

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11
Q

General MOA of vasodilators used for HTN.

A

Relax smooth muscle of arterioles, decreasing the peripheral vascular resistance and thus, the arterial blood pressure; sodium nitroprusside and the nitrates also relax veins.

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12
Q

In what form are all CCBs active?

A

Orally

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13
Q

What 4 CCBs can be administered by IV, as well as orally?

A

nifedipine, clevidipine, verapamil, diltiazem

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14
Q

What CCB has the longest half life?

A

Amlodipine, 35-50 hours

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15
Q

Adverse effects of DHPs

A 
Excessive hypotension
Dizziness
HA
Peripheral edema
Flushing
Tachycardia
Rash
Gingival Hyperplasia
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16
Q

What is a contraindication for use of nifedipine?

A

Don’t use in patients with chronic HTN

Nifedipine is a SHORT acting DHP and has increased risk for MI, stoke, death.

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17
Q

What should be used for treatment of chronic HTN?

A

SLOW RELEASE and long acting DHPs.

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18
Q

Adverse effects of non-DHPs.

A

*Constipation with Virapamil
* peripheral edema
Dizziness, HE, AV block, bradycardia, heart failure.
Lupus-like rash with Diltiazem
Pulmonary edema, coughing, wheezing possible.

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19
Q

*When are non-DHPs contraindicated?

A

**When a person is also taking a BETA-BLOCKER.

Non-DHPs (verapamil>diltiazem) slows HR, can SLOW AV CONDUCTION, can cause heart block.

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20
Q

When should nifedipine be used?

A

Use in the presence of AV conduction abnormalities because it does not slow AV conduction.

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21
Q

CCBs are not indicated for use in what?

But which 2 can be used if necessary for another indication? What indication?

A

HF
Amlodipine and felodipine can be used for indicated angina or HTN because of their relatively neutral vasoselective effects.

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22
Q

What drug-drug interaction can verapamil have with digoxin?

A

Increase digoxin levels through phrmacokinetic interaciton.

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23
Q

What drug-drug interaction do DHPs have?

What drug-drug interaction do non-DHPs have?

A

Additive with other vasodilators.

Additive with other cardiac depressants and hypotensive drugs.

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24
Q

What are the clinical uses of CCBs?

A

Long term outpatient therapy of HTN (counteract reflex CV responses)
HTN emergencies
Angina

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25
Potassium Channel Openers
Diazoxide | Minoxidil
26
Diazoxide and Minoxidil MOA
Opens potassium channels in smooth muscle.
27
Diazoxide and Minoxidil Pharmacodynamics (2).
(1) Increasing potassium permeability that hyperpolarizes smooth muscle membrane, reducing probability of contraction. (2) Arteriolar dilator, resulting in reduced systemic vascular resistance and mean arterial pressure. (minoxidil does NOT dilate veins)
28
Diazoxide Pharmacokinetics (3).
(1) Relatively long acting (4-12 hours after injection). (2) High protein binding - metabolism not well understood (3) Administered as 3-4 injections, 5-15 min apart, prn. Sometimes by IV
29
Diazoxide: 1. Adverse effects 2. Contraindications
1. Excessive hypotension resulting in stroke and MI. Hyperglycemia in patients with renal insufficiency 2. Contraindicated in patients with ischemic heart disease - increases propensity for angina, ischemia, cardiac failure.
30
How should dosing of diazoxide be changed in a patient with renal failure or pretreated with beta blockers to prevent reflex tachycardia?
Smaller doses because hypotensive effects are greater in theses patients.
31
Minoxidil Adverse Effects/Contraindications
HA, sweating, hypertrichosis (abnormal hair growth). Associated with reflex sympathetic stimulation and sodium and fluid retention resulting in tachycardia, palpations, angina, and edema.
32
What must minoxidil be used with to avoid reflex sympathetic stimulation and sodium/fluid retention?
Loop diuretics and B-blocker
33
A person has abnormal hair growth and on meds for severe HTN. What med?
Minoxidil
34
Clinical uses for minoxidil.
(1) Long term outpatient therapy of severe hypertension | (2) Topical formations (i.e. Rogaine) used to stimulate hair growth.
35
Clinical uses for diazoxide.
Hypertensive emergencies
36
MOA of fenoldopam.
D1 Receptor Dopamine Agonist
37
Fenoldopam pharmakokinetics
Peripheral arteriolar dilator, natriuretic
38
Fenoldopam pharmacokinetics
Continuous IV infusion due to rapid metabolism and short half life of 10 min.
39
Fenoldopam Adverse Effects and Contraintidcation
(1) tachycardia, HA, flushin | (2) AVOID in patients with GLAUCOMA due to increases in intraocular pressure
40
Fenoldopam clinical uses
Hypertensive emergencies | Peri and postoperative hypertension
41
Hydralazine MOA
Stimulates NO fro endothelium = Dilation of arterioles (a>v) | Reflex tachy
42
Hydralazine pahramcokinetics
1. Well absorbed, but high first pass effect results in low bioavailabilty 2. Metabolism occurs via acetylation, so bioavailability is variable among individuals dependent on rate of acetylation
43
Clinical uses of Hydralazine | What two demographics in particular?
Long term outpatient HTN therapy, Parenteral formulation useful in HTN EMERGENCIES. Combo with nitrates for HF, esp in AFRICAN AMERICANS who have both HTN and HF. **First line for HTN in PREGNANCY, with methyldopa.
44
Adverse effects/contraindications of Hydralazine
HA, nausea, anorexia, palpitations, sweating, flushing Rare - peripheral neuropathy and drug fever May provoke angina or ischemic arrhythmias in patients with ischemic heart disease, reflex tachycardia, and sympathetic stimulation.
45
Sodium Nitroprusside MOA
Drug metabolism releases NO resulting in increased cGMP levels.
46
Sodium Nitroprusside pharmacodynamics
*Powerful DILATION of arterial and venous vessels, reduces peripheral vascular resistance and venous return *Decreased preload and afterload. In absence of heart failure, BP decreases and CO does not change. When CO already low due to HF, CO often increases due to afterload reduction.
47
Sodium Nitroprusside pharmacokinetics
Rapid metabolism results in rapid onset and short duration of effect. Administer by IV
48
Sodium Nitroprusside Adverse effects
Excessive hypotension. | **Long term IV admin = cyanide poisoning.
49
Sodium Nitroprusside clincial uses
hypertensive emergencies | Acute decompensated HF
50
Nitroglycerin - what type of vasodilator? MOA pharmakodynamics
Organic nitrate (also isosorbide dinitrate, isosorbide mononitrate) MOA: Release NO via enzymatic metab. Relaxes smooth muscle and veins>arteries. Heart size and pulm vascular pressure reduced. In absence of HF, CO is reduced. Decreases platelet aggregatino.
51
Nitroglycerin pharmakokinetics.
Administer sublingual route to avoid first pass. Therapeutic blood vessels reached within mintues and last 15-30 min. Oral, tansdermal, buccal preparations have longer duration. Can build TOLERANCE!
52
Nitroglycerin adverse effects/contraindications
Orthostatic Hypotension, syncope, throbbing HA. TOLERANCE Contraindicated if ICP increased. Can SAFELY use in presence of intraocular pressure (glaucoma).
53
Nitroglycerin drug-drug interactions
hypotension with PDE5 inhibitors (sildenafil, tadalafil, vardenafil)
54
Nitroglycerin clincial uses
Hypertensive emergencies, angina, HF
55
When to use BETA BLOCKERS.
Prevent reflex tachy that results form tx of direct **peripheral VASODILATORS (in severe HTN.) Reduce mortality after MI.
56
Propranolol MOA
Non-selective Bblocker
57
Propranolil Pharmacodynamics
Decreases BP by decreasing CO Do not cause hypotension in normotensive, healthy patients. Blocks B1 receptors in kidney = decrease renin release Some have LOCAL anesthetic action by blocking Na channels and resultant membrane stabilization.
58
Propranolol pharmacokinetics
All bblockers (except esmolol) are oral.
59
Which bblocker is availabel as extended release tablets?
carvedilol, metopralol, propranolol
60
Which bblocker is available as parenteral?
atenolol, esmolol, labetalol, metoprolol, propanolol
61
Which bblockers can readily cross BBB?
propranolol, penbutolol. | All others are quite lipophilic
62
Contraindications of Bblockers
* Asthmatics/COPD - cannot avoid the blockade of B2 receptors in bronchial smooth muscle, which would lead to increased airway resistance. * Diabetic risk - glycogenolysis is inhibited by B2 blckage
63
Adverse side effects of Bblockers
bradycardia, fatigue Sexual dusfunction Depression Chronic use associated with unfavorable plasma lipid profiles - increased VLDL and reduced HDL
64
What is chronic use of bblockers associated with?
Unfavorable plasma lipid profiles - increased VLDL and reduced HDL.
65
What can sudden withdrawl of bblockers cause?
Rebound hypertension, angina, possibly MI
66
B-blocker drug-drug interactions
heart block if combined with CCBs verapamil or diltiazem - they also slow heart conduction
67
Clinicial uses for Bblockers
HTN - metoprolol and atenolol HF - long term, NOT for acute CHF (carvedilol, bisoprolol, metoprolol) Ischemic Heart Disease - reduce freq of angina episodes and improve exercise tolerance (timolol, metoprolol, propranolol) Cardiac Arrhythmias Glaucoma - reduce intraocular pressure with topical drops (timolol, betaxolo, carteolol) Use B1 selectivity for Co-morbid asthma, Diabetes, or peripheral vascular disease. Partial B2 agonist activity good for people with bradyarrhythmias or Peripheral Vascular Disease.
68
MOA of alpha1-blockers | Prototype
Prototype - Prazosin | MOA - reversible antagonist at alpha1 receptor
69
alpha1-blocker pharmacodynamics
Prevents vasoconstricion of arteries and veins, BP reduced by lowering peripheral vascular resistance Relaxes smooth muscle in the PROSTATE. If used without diuretic, Na and water retention will occur. No change or improvement in plasma lipid profile (possible increased HDL).
70
alpha1-blockers adverse effects/contraindications
Generally well tolerated. Orthostatic hypotension, dizziness, palpations, HA, lassitude (physical/mental weariness). Less incidence of reflex tachy than non-selective alpha blockers because alpha2 receptor inhibition of NE release is unaffected.
71
alpha1-blockers drug-drug interactions
Most effective when used in combo with bblocker or diuretic.
72
Clinical uses of alpha1-blockers
Used in MEN with concurrent HTN and benign prostatic hyperplasia.
73
MOA of centrally acting agents (alpha2 agonists) | Prototypes (2)
Clonidine, methyldopa. MOA - reduce sympathetic outflow from vasomotor centers in brainstem but allow these centers to retain or even increase their sensitivity to baroreceptor control AGONISTS AT CENTRAL ALPHA2 RECEPTORS
74
Clinical use of centrally acting alpha2 agonists
rarely used today, except: Clonidine Methydopa
75
Clonidine pharmacodynamics and adverse effects
alpha2 r agonist lowers BP by decreasing CO and reducing vascular resistance. Adverse effects - sedation, dry mouth, depression, sexual dysfunction
76
Administration of clonidine
(1) transdermal has less sedation than (2) oral | (3) patch
77
What don't you want to do during clonidine withdrawl?
**Abrupt withdrawl can lead to life threatening HTN crisis
78
Methyldopa pharmacodynamics, kinetics, adverse effects
Lowers BP by REDUCING peripheral vascular resistance analog of L-dopa, parallels synthesis of NE from L-dopa Adverse effects - sedation, dry mouth, lack of concentration, sexual dysfunction.
79
When are Bblockers used for HTN tx?
1. HF 2. Recent MI 3. REduced Left vent function
80
Labelalol
selective a1 blocker NS B1/B2 blocker Partial B2 agonist
81
Labelalol clinical use
IV for severe HTN | HTN during pregnancy
82
Carvedilol
NS B/a1 blocker
83
Esmolol onset and DOA
* Rapid onset * Short DOA B1 selective
84
When are a1 selective R blockers used?
men with concurrent HTN and BPH

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