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Pharm 3, Test 3 > Miscellaneous Anti HTN drugs > Flashcards

Miscellaneous Anti HTN drugs Flashcards

1
Q

What are the a1 blockers to know?

A

Prazosin, terazosin, and doxazosin

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2
Q

Whats the primary use of a1 blockers?

A

treating BPH

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3
Q

What it the MOA of a1 blockers on the peripheral tissue?

A

Activation of GPCR, leading to influx of Ca, stimulating vascular smooth muscle contraction through the whole myosin cascade stuff

They block this by reducing ca

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4
Q

What is the bodies response to blockage of a1?

A

Increased sympathetic outflow due to the reduces bp

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5
Q

What does a1 blockers indirectly do?

A

Reduces preload

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6
Q

What ADE will many pts experience with a1 blockers?

A

Orthostatic hypotension

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7
Q

What other ADEs do a1 have

A

Increases risk for CHF, stroke, and CVD

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8
Q

Are a1 preferred treatments for htn?

A

Nah

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9
Q

What is hydralazines MOA?

A

Activation of K channels, producing hyperpolarization, not responsing to stimuli and not contracting

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10
Q

What will happen if you use hydralazine solely as a htn treatment option?

A

The whole renin release, increased sympathetic outflow, stuff

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11
Q

What is a ADE of hyralazine and minoxidil related to the heart?

A

It does not dilate epicardial arteries leading to coronary steal. Basically it may redirect blood flow away from regions that have plaque build up, in favor of areas with less resistance

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12
Q

What is minoxidils MOA?

A

Relaxes vascular smooth muscle by activating K channels to promote K efflux, resulting in hyperpolarization

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13
Q

What is the ADE of minoxidil?

A

Hypertrichosis-sometimes used for this as a topical agent

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14
Q

Should minoxidil be used alone?

A

No, due to increase in renin and all that

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15
Q

What is the MOA of sodium nitroprusside?

A

Its a nitrovasodilator……

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16
Q

What does nitro do?

A

DIlates venous and arterial vessels, causing increased cardiac output

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17
Q

What is the main use for nitro?

A

Htn emergency, like actively dissecting aneyuresm

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18
Q

What is diazoxides MOA?

A

Like minoxidil, it is a K channel opener in vascular smooth muscle, leading to hyperpolarization

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19
Q

What is the ADE of diazoxide?

A

Hyperglycemia, pulm HTN

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20
Q

What is fenoldopams MOA?

A

Dopamine D1 agonist, causing dilation of peripheral arteries and natriuresis

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21
Q

What does Rostral mean? What does caudal mean?

A

Rostral-To the nose

Caudal-To the tail

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22
Q

What is clonidines moa?

A

Activates centrally acting a2 receptors

Reduces sympathetic outflow and increases parasympathetic outflow from the vasomotor region of the medulla oblongata

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23
Q

What is the ADEs of clonidine?

A

Bradycardia
Sedation/dry mouth (parasympathetic/cholinergic activation)
Withdrawal effects

24
Q

What is guanfacine basically identical to?

A

Clonidine

25
Q

What is guanfacines random therapeutic use?

A

ADHD

26
Q

What is methyldopa metabolized by?

A

L aromatic amino acid decarboxylase to a-methldopamine

Then that is metabolized by dopamine to a-methylnorepinephrine

27
Q

What is the use of methyldopa?

A

Same as clonidine, used for hypertension, causes build up of methylnorepinephrine, which is not broken down by Monoamine oxidase, therfore it results in more accumulation and activation of a2 receptors

28
Q

What is the MOA of endothelin receptor antagonists?

A

The normal action is -GPCR that lead to vascular smooth muscle contraction

This drug class blocks this, causing vasodilation. Same concept as a1 antagonists

29
Q

What is the ending for the endothelin receptor antagonists?

A

Sentan

30
Q

What are the endothelin receptor antagonists ADEs?

A

Pregnancy category X

Hepatotoxic-BBW for bosentan

31
Q

What is the MOA of PDE5 inhibitors?

A

Inhibit PDE-5, increasing cGMP, promotes smooth muscle relaxation

32
Q

What is Guanylyl cyclase stimulators MOA?

A

Stimulates soluble guanylyl cyclase directly and stabilized interaction with NO with sGC. Increases intracellular cGMP concentrations

33
Q

What is the one sGC mentioned?

A

Riociguat

34
Q

What is riociguat metabolized by?

A

CYP1A1

35
Q

Who is the ADEs of riociguat?

A

GI-heart burn and gastritis
HYPOtension- Contraindicated with nitrovasodilators, PDE inhibitors
Pregnancy category X

36
Q

What is the cause of angina?

A

Imbalance in myocardial oxygen supply and demand, caused by an increase in myocardial oxygen demand, a decrease in myocardial oxygen supply, or both

37
Q

What are the four drug classes mentioned for treatment of angina?

A

CCB, BB, nitrovasodilators, and sodium channel blockers

38
Q

Why are ccb and bb good for angina?

A

negative ionotropic and chronotropic, so reduction in myocardial oxygen

39
Q

Which drug class is specifically helpful in variant (prinzmetals) angina?

A

CCB

40
Q

What are the five things that ccb specifically do to help with angina?

A

Reduce contractility, HR, wall tension

Improve regional myocardial blood flow, improve coronary blood flow

41
Q

What do BBs do to make them effective for angina?

A

Reduce hr and contractility

42
Q

What is the MOA of nitrovasodilators?

A

When metabolized, they release NO. This leads to the cascade of events seen with PDE5 inhibitors. The excess NO activates soluble guanylyl cyclase, which formed cGMP from GTP. cGMP activates PKG, which phosphorylates MLCK. This removes a Phosphate from MLCK, which then removes a phosphate from MLC, which causes smooth muscle relaxation.

43
Q

What do nitrovasodilators do at low doses?

A

Relax smooth muscle on arteries AND veins. Veins are mainly effected at low doses. Overall, decreases chamber sizes and end diastolic pressure

44
Q

What do nitrovasodilators do at high doses?

A

Increased venous blood pooling, decrease in arteriolar resistance, causing decrease BP
Decrease in cardiac output, resulting in increase in sympathetic outflow

45
Q

What does the nitrovasodilator at high dose lead to in regards to increased sympathetic outflow?

A

Tachycardia, increased peripheral arteriolar vasoconstriction

46
Q

What are the effects on myocardial oxygen demand for nitrovasodilators at higher doses?

A

They reduce myocardial oxygen demand by decreasing preload and afterload, hr, and contractility

47
Q

What is the mechanism of benefit for nitrovasodilators?

A

Redistribution of coronary flow and decrease in O2 demand

48
Q

What are the other effects of nitrovasodilators?

A

They act on all smooth muscle cells, so bronchial smooth muscle relaxation, GI smooth muscle relaxation

49
Q

What are the overall ways in which nitrovasodilators work on the O2 demand and supply?

A

They reduce ventricular volume, reducing ventricular pressure, causing a reduction in wall tension. They also increase regional myocardial blood flow and coronary artery blood flow

50
Q

What are nitrovasodilators ADEs?

A

HA most common, most other effects are secondary to the actions of the drugs on the cardiovascular system/ So dizziness, weakness, hypotension

51
Q

Why cant we use PDE5 inhibitors with nitrovasodilators?

A

They work synergistically

52
Q

What is the major route of metabolism for isosorbide dinitrate?

A

Enzymatic denitration followed by formation of glucuronide conjugates

53
Q

What drug class is ranolazine?

A

Sodium channel blocker

54
Q

What is ranolazines MOA?

A

It inhibits late/slow sodium current, which normally leads to a build up of Na in the cell, activating the na-ca exchange. This leads to a buildup of ca inside the cell, which increases contractility, wall tension, and myocardial oxygen demand. So it blocks this

55
Q

What does the Na channel blockers work in regards to O2 demand and O2 supply?

A

Reduces wall tension and reduced myocardial oxygen demand

56
Q

What is ranolazine metabolized by?

A

CYP3A4 and CYP2D6-significant drug interactions like always

57
Q

What is ranolazines ADEs?

A

QTc prolongation, hypotension

Pharm 3, Test 3 (5 decks)

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