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Pharmacology > Vasodilators > Flashcards

Vasodilators Flashcards

1
Q

What is enalapril?

A

An angiotensin converting enzyme inhibitor (pro drug)

Mixed vasodilator

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2
Q

What is losartan?

A

An angiotensin receptor blocker (the receptor that AII binds to)
Mixed vasodilator

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3
Q

What are two examples of CCB hydropyridines?

A

Amlodipine and nifedipine

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4
Q

What are two examples of CCB non-dihydropyridines?

A

Verapamil and Diltiazem

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5
Q

What is clonidine?

A

An alpha 2 adrenergic receptor agonist

Mixed vasodilator

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6
Q

What is prazosin?

A

An alpha 1 adrenergic receptor antagonist

Mixed vasodilator

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7
Q

What are some examples of only arteriolar dilators? Which ones involve NO?

A

Hydralazine (may involve NO) and minoxidil

Increases cardiac output, decreases afterload

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8
Q

What is sodium nitroprusside?

A

A venous and arterial dilator that releases NO (increases cGMP) and cyanide
Used in severe congestive heart failure (decreases preload and afterload to decrease O2 demand and increase CO)
Rapid onset and offset, given IV

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9
Q

What is thiosulfate?

A

A sulfur donor used to treat cyanide toxicity possibly from sodium nitroprusside

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10
Q

What do nitrates do?

A 
Increase NO which increases cGMP levels. Relaxes veins (low dose) and larger arteries (high dose) to decrease preload and heart size and prevent coronary steal
Decrease pulmonary artery resistance (good for pulmonary hypertension in COPD)
Tolerance develops (12 hour treatment intervals)
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11
Q

Which receptors affect preload? How?

A

Increasing alpha 1 activity vasoconstricts and increases blood pressure
Decreasing beta 2 activity relaxes the heart to allow for more filling

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12
Q

What receptors affect contractility?

A

Increasing beta 1 receptors increases the force of the muscles

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13
Q

What happens when you increase or decrease preload?

A

Stroke volume increases or decreases proportionally. More preload, more stretching of the cardiac muscle, more contraction to push it out

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14
Q

What receptors affect afterload?

A

Increasing alpha 1 activity causes vasoconstriction to push blood out harder
Decreasing beta 2 activity
Decreasing D1 activity

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15
Q

What happens when you increase or decrease afterload?

A

Stroke volume increases or decreases inversely

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16
Q

What are the blood pressure compensatory responses?

A

The sympathetic nervous system, renin-angiotensin-aldosterone system and the amount of sodium and water in the body.

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17
Q

When are the blood pressure compensatory responses physiologically useful?

A

Dehydration, hemorrhage and early heart failure

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18
Q

When are the blood pressure compensatory responses pathophysiologically harmful?

A

Renal artery stenosis and decompensated heart failure

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19
Q

What happens in response to a decrease in blood pressure?

A

Renal perfusion pressure decreases to increase Na retention and thus increase blood volume.
Renin is increased to cause the formation of aldosterone which helps retain Na and the formation of angiotensin II which increases afterload and preload
SNS activity is increased to increase afterload, preload, inotropy and heart rate. This increases cardiac output. Causes a correction in blood pressure.

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20
Q

What can cause a decrease in blood pressure?

A

Standing up and hypovolemia (minor) and shock (severe)

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21
Q

How does arteriolar dilation affect afterload?

A

Increases cardiac output and decreases afterload

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22
Q

How does venous dilation affect preload?

A

Decreases preload and pulmonary congestion

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23
Q

When does the RAAS system come into play?

A

When a drop of blood pressure, blood volume (renal perfusion pressure) or sodium load to distal nephron is sensed

24
Q

What is renin?

A

An enzyme that is released from the JGA. The rate limiting step in angiotensin II formation

25
Q

What is angiotensin II?

A

Major product of the RAAS system that increases aldosterone secretion, vasoconstriction, SNS and has trophic effects (thickens heart, vessels)

26
Q

What is bradykinin?

A

Causes vasodilation, inactivated by ACE

27
Q

What is does angiotensin converting enzyme do?

A

Converts angiotension I to AII and deactivates bradykinin

28
Q

What do agiotensin converting enzyme inhibitors (ACEI) and angiotenin receptor blockers (ARBs) do?

A

Lower blood pressure by decreasing total peripheral resistance, decreasing Na reabsorption and increasing bradykinin

29
Q

How are ACEIs and ARBs metabolically?

A

Metabolically neutral. Don’t increase lipids (LDLs) or glucose

30
Q

When are ACEIs and ARBs most effective?

A

When plasma renin is high during hypovolemia or renal artery stenosis

31
Q

Why would the use of ACEIs and ARBs be dangerous during renal stenosis?

A

The stenosis decreases RPP which causes an increase RAAS to try to correct RPP even though the blood pressure in the rest of the body is okay. High blood pressure. The drugs can cause a dangerous fall in BP

32
Q

How do ACEIs and ARBs treat post MI?

A

Decreases the post infarction myocardial remodeling

First line treatment

33
Q

How do ACEIs and ARBs treat hypertension?

A

Decrease peripheral resistance with minimal changes in heart rate and cardiac output
First line treatment

34
Q

How do ACEIs and ARBs treat congestive heart failure?

A

Decreases the increased renin/AII levels associated with CHF

First line treatment

35
Q

How do ACEIs and ARBs treat diabetic nephropathy?

A

Decreases protein excretion and renal deterioration
Effective at doses that don’t decrease blood pressure
First line treatment to prevent/delay

36
Q

What are some possible problems with the use of ACEIs and ARBs?

A

Hypotension, hyperkalemia (less aldosterone means less K excretion), may increase protein excretion in normal patients and dry cough (ACEIs)

37
Q

In what individuals should ACEIs and ARBs be avoided?

A

Pregnancy or those of child bearing age, cautiously combine with K sparing drugs, renal artery stenosis and diabetes with type 4 tubular acidosis (already no renin or aldosterone)

38
Q

What do Ca channel blockers do?

A

Block L type voltage gated Ca channels

39
Q

What are dihydropyridine calcium channel blockers?

A

Greater affinity for arterial Ca channels
Decrease cytoplasmic Ca to reduce TPR, CO and BP with out apparent cardiac actions (reflex tachycardia)
Relaxes other tissues (GI tract, uterus, bronchioles)- use in IBS
Want long acting agents

40
Q

What are non-dihydropyridine calcium channel blockers? When are they used?

A

Cardiac and some vascular action, decrease sarcoplasmic reticulum release of Ca during depolarization. Decreases contractility Used in hypertension if there is also a concern about rate control in atrial fibrillation or angina
Neutral metabolic profile

41
Q

What are dihydropyrines used for?

A

Hypertension, hypertensive crisis, Raynauds, angina

42
Q

What is diltiazem used for?

A

Angina and hypertension

43
Q

What are some cautions or contraindications with verapamil?

A

Contraindicated in heart failure

Should not be combined with a beta adrenergic receptor blocker (potential for severe or total AV node block)

44
Q

What are some adverse effects of Ca channel blockers?

A

Headache, edema, constipation, flushing

45
Q

What are alpha 1 adrenergic antagonists used for?

A

Hypertension (lowers LDL and VLDL too)
Benign prostatic hypertrophy (increases urine flow)
Relief of nightmare in PTSD
Caution: First dose may cause postural hypotension

46
Q

How do alpha 2 adrenergic receptor agonists work? When is it used?

A

Lower blood pressure by decreasing SNS

Used oral or intrathecally to decrease the amount of general anesthetic needed foe surgery

47
Q

What are usually given with vasodilators and why?

A

Given with a diuretic and beta-adrenergic receptor blocker because Na retention and increased SNS and RAAS activity will decrease the vasodilation effects

48
Q

What is hydralazine?

A

An arteriolar dilator (may involve NO)
May preceipitate myocardial ischemia (increases O2 consumption)
Extensive first pass metabolism

49
Q

What is hydralazine used for?

A

3rd line for hypertension
1st line for hypertension in pregnancy
Combine with a nitrate in heart failure

50
Q

What are some side effects of hydralazine and minoxidil?

A

Headache, flushing nausea, hypotension, tachycardia, angina
May cause a lupus like syndrome (hydralazine)
Hirsutism (hair growth) and pericardial effusion (minoxidil)

51
Q

What is minoxidil?

A

An arteriolar dilator (reflex activation of SNS could cause problems)
For severe hypertension when others won’t work, effective even if patient has renal failure

52
Q

What are the forms of nitrates that are available?

A 
Nitroglycerin (rapid onset, short duration)
Isorbide dinitrate (longer acting)
53
Q

How do nitrates prevent coronary steal?

A

Don’t affect smaller arterioles and precapillary sphincters as much. Thus, prevents blood flow to healthy region and increases blood flow to ischemic regions. Want to dilate larger vessels so we get blood flow to both.

54
Q

How may hydralazine worsen angina?

A

By dilating small arterioles

55
Q

What are some adverse effects of nitrates?

A

Orthostasis
Blood pressure lowering
Throbbing headache

Pharmacology (11 decks)

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