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Pharmacology > Vasodilators > Flashcards

Vasodilators Flashcards

1
Q

What is enalapril?

A

Converting enzyme inhibitor

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2
Q

What is losartan?

A

Angiotensin receptor blocker

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3
Q

What is amlodipine?

A

CCB dihydropyridine

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4
Q

What is verapamil?

A

CCB non-dihydropyridine

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5
Q

What is diltiazem?

A

CCB non-dihydropyridine

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6
Q

What is clonidine?

A

alpha2-adrenergic receptor agonist

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7
Q

What is prazosin?

A

alpha1-adrenergi receptor antagonist

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8
Q

What is hydralazine?

A

Arteriolar dilator (may involve NO)

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9
Q

What is minoxidil?

A

Arteriolar dilator

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10
Q

What is sodium nitroprusside?

A

venous and arterial dilator (NO form parent compound)

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11
Q

What is thiosulfate?

A

Sulfur donor

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12
Q

What is nitroglycerin?

A

Venous dilator (NO from parent compound)

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13
Q

What does cardiac output depend on?

A

Contractility (how hard does the heart beat?)
Afterload
Preload

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14
Q

What is afterload?

A

The resistance to which the heart needs to expel the blood into the peripheral circulation (peripheral vasculature)

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15
Q

What is preload?

A

The load that’s put on the heart before the heart (vena cava)

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16
Q

What are the three compensatory responses to a decrease in BP (regardless of the cause)?

A

Sodium retention
Increase in renin, which increases AG-II and aldosterone release
Increase in SNS activity

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17
Q

When are the three compensatory responses to a decrease in BP physiologically useful?

A

Dehydration, hemorrhage, early heart failure

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18
Q

When are the three compensatory responses to a decrease in BP pathophysiologically harmful?

A

Renal artery stenosis, decompensated heart failure

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19
Q

What happens to renal perfusion pressure when there’s a decrease in BP?

A

The renal perfusion pressure decrease which causes an increase in Na retention. This increases blood volume

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20
Q

What happens to RAAS when there’s a decrease in BP?

A

The RAAS increases, which increases aldosterone (Na retention, increased blood volume) and AG-II (increased preload and afterload, increased cardiac output)

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21
Q

What happens to SNS activity when there’s a decrease in BP?

A

The SNS activity increases, which increases preload, afterload, isotropy and heart rate (increased cardiac output)

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22
Q

What are the three types of vasodilators?

A

Venodilators (decrease preload, decrease pulmonary congestion)
Arteriolar dilators (decrease afterload)
Mixed vasodilators

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23
Q

What is an example of venodilators?

A

Nitrates

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24
Q

What are examples of mixed vasodilators?

A

Nitroprusside
ACE inhibitors and ARBs
alpha-adrenergic blockers
alpha2-central agonists

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25
Q

What are examples of arteriolar dilators?

A

Hydralazine
Minoxidil
CCB

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26
Q

What is the RAAS system increased?

A

The renin angiotensin aldosterone system (RAAS) is increased when a need to increase blood pressure and/or blood volume (sodium retention) is sensed

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27
Q

What is renin?

A

Renin is released from the juxtaglomerular apparatus (JGA)
It is the rate limiting step in angiotensin II (AGII) formation
Renin release is increased by low sodium load to distal nephron (macula densa), low renal perfusion pressure and/or low blood pressure (increased beta1-adrenoreceptor stimulation to JGA)

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28
Q

What is AGII?

A

Angiotensin II is the major active product of the RAAS system
It also increases aldosterone secretion

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29
Q

What is ACE? What does it lead to?

A

AGI doesn’t do anything; it needs to be converted into AGII by angiotensin converting enzyme (ACE)
AGII is active and binds to AT1 receptor, which causes vasoconstriction, increases aldosterone release, increases SNS activity, increases vasopressin release, increases contractility, increases thirst

30
Q

How do ACEi and ARBs work?

A

They lower blood pressure by decreasing total peripheral resistance (decreasing AGII levels or blocking AGII receptor), decreasing Na absorption (by decreasing aldosterone secretion), increasing bradykinin (which vasodilates)

31
Q

What happens is a person is volume depleted (hypovolemic) and they are given an ACEi?

A

If someone is volume depleted, their BP will drop, but the baroreceptor reflex will detect this and activate RAAS (and SNS activity), which will increase the BP via AGII and aldosterone (increased TPR and sodium retention). BP will return to normal (even though the person is still volume depleted). If you give an ACEi and remove AGII, the BP will drop dangerously

32
Q

How do we determine if a patient is volume depleted?

A

Take their BP sitting down then standing up. If the patient is volume replete, there won’t much of a drop in BP. If the patient is volume depleted, there will be a larger drop in BP and the heart rate will increase

33
Q

Do ACEi and ARBs increase LDL or glucose levels?

A

No

34
Q

Why should we use caution when using ACEi or ARBs if plasma renin is high

A

They might be hypovolemic (diuretic use, hemorrhage, dehydration)
They might have renal artery stenosis (here AGII plays a major role in the high blood pressure and ACEi and ARBs might produce a dangerous fall in BP)

35
Q

Why are ACEi and ARBs first line single therapy in uncomplicated hypertension?

A

They have similar benefits and side effects
They are recommended if the patient has one of the following concurrent conditions: heart failure, left ventricle dysfunction, post MI, diabetes, systolic dysfunction, proteinuria (chronic kidney disease)
They may have benefits in addition to their blood pressure lowering (cardiovascular improvements when BP is normal?)

36
Q

How do ACEi and ARBs treat hypertension?

A

They decrease total peripheral resistance within minimal changes in the heart rate and cardiac output
There are few side effects (well tolerated)
They are the first line treatment (decreased morbidity and mortality)

37
Q

How do ACEi and ARBs treat congestive heart failure?

A

CHF is associated with increased renin/AGII levels (also increased SNS activity and decreased renal perfusion pressure)
They cause a blockade of AGII, which decreases preload, afterload and cardiac remodelling and it increases sodium excretion
They cause a first line treatment (decreased morbidity and mortality)

38
Q

How do ACEi and ARB treat post-myocardial infarction?

A

Decreases post infarction myocardial remodeling

First line treatment (decreased morbidity and mortality)

39
Q

How do ACEi and ARBs treat diabetic nephropathy?

A

First line treatment for preventing/delaying diabetic nephropathy
Decreases protein excretion and decreases renal deterioration
Effective at doses that do not decrease blood pressure

40
Q

What are the toxicities associated with ACEi and ARBs?

A

Hypotension (especially with high renin levels)
Hyperkalemia (decreased aldosterone, means less potassium excretion)
May produce proteinuria in a few patients with normal GFR (but it’s the drug of choice in diabetic nephropathy, as it decreases proteinuria)
Dry cough (ACEi)a
Angioedema (

41
Q

When should caution be taken with ACEi and ARBs, and when should they be avoided?

A

Contraindicated in pregnancy as it is harmful to the fetus
Combine cautiously with potassium sparing drugs
In renal artery stenosis (caution)
Diabetes with type 4 renal tubular acidosis (already hyporenin and hypoaldosteronism)

42
Q

What are calcium channel blockers (CCBs)?

A

They block L-type voltage gated calcium ion channels

43
Q

What are the two sub-classes of CCBs?

A

Dihydropyridines which block calcium channels in the vasculature (amlodipine, nifedipine)
Non-dihydropyridines in the cardiac tissue and a little bit in the vasculature (verapamil, diltiazem)

44
Q

What do dihydropyridine CCBs do?

A

They decrease cytoplasmic calcium (decreased influx into cell during depolarization)
For this group, long acting agents are preferred for hypertension

45
Q

What are dihydropyridine CCBs do?

A

They have greater affinity for vascular (arterial) calcium channels
They are used for angina, Raynauds and hypertension
They reduce TPR (and BP) without apparent cardiac actions (minimal reflex tachycardia)
They are used as single treatment for hypertension
They are also used for hypertensive crisis
Other tissue can be relaxed (GI tract, uterus, bronchioles)

46
Q

What do non-dihyropyridine CCBs do?

A

They decrease sarcoplasmic reticulum release of calcium during depolarization
Used in hypertension if also a concern about the rate of control in atrial fibrillation in patients with angina

47
Q

What does diltiazem do?

A

It works on both vascular and cardiac calcium channels

It is used to treat angina and hypertension

48
Q

What does verapamil do?

A

Blocks mainly in the heart (limited vascular tissue)
Should not be combined with a beta adrenergic receptor blocker (or cautiously as there is a potential to produce severe, or even total, AV nodal block)
It is contraindicated in heart failure

49
Q

How do calcium channel blocker treat angina pectoris?

A

It decreases myocardial oxygen demand, which decreases BP (afterload), contractility, heart rate (verapamil and diltiazem)
It increases myocardial oxygen supply by increasing coronary artery dilation

50
Q

How do CCBs treat coronary artery spasm?

A

Coronary artery vasodilation

51
Q

How do CCBs treat hypertension?

A

Arterial smooth muscle relaxation

52
Q

How do CCBs treat supraventricular tachycardia?

A

Verapamil/diltiazem decrease conduction velocity, increase AV node refractory period

53
Q

Why are CCBs first line single therapy in uncomplicated hypertension

A

They are recommended where beta blockers are contraindicated as they are not contraindicated in asthma or COPD (beta blockers are CI in asthma/COPD)
They are effective in the elderly and African Americans (they respond better to CCBs than ACEi and ARBs)
There is a low incidence of side effects (but expensive)
Neutral metabolic profile (don’t alter glucose of LDL levels)

54
Q

What are the side effects of CCBs?

A

There can be adverse effects related to vasodilation: headache, flushing, oedema, constipation (oedema may be less common in the presence of an ACEi)
Avoid rapid decreases in blood pressure
There is published concerns regarding an increased risk of cancer or increased GI bleeding, but they are unfounded

55
Q

CCBs can be used in the presence of other coexisting conditions, such as:

A

Angina pectoris
Raynaud phenomenon
Asthma and COPD

56
Q

What do alpha1 adrenergic receptor antagonists treat? Why should we be cautious?

A

Hypertension (and decreases LDL and VLDL levels; they are not given alone, they are given with at least a diuretic)
Benign prostatic hypertrophy (causes increased urine flow)
May relieve nightmares and sleep disturbances in post traumatic stress disorder (PTSD)
Caution: first dose effect of severe postural hypotension
May cause runny nose

57
Q

What do alpha2 adrenergic receptor agonists treat?

A

Lowers BP by acting on central vasomotor centres (decreases SNS; limited use as a hypertensive as it causes sedation and dry mouth)
Oral or intrathecal clonidine (or other alpha2 agonists) decreases the amount of general anesthetic required to reach a surgical plane (results in fewer side effects)

58
Q

What is the mechanism of hydralazine?

A

The exact mechanism is unknown; may partially involve NO

59
Q

What does hydralazine do? How do we use it?

A

It’s an arteriolar dilator (pre-capillary arterioles)
Give with a beta-adrenergic receptor blocker and diuretic (may precipitate myocardial ischemia via the baroreceptor reflex)
It is a third line medication in hypertension
Used as a single therapy in hypertension in pregnancy (safe and works)
May be combined with a venodilator (nitrate) in heart failure

60
Q

How is hydralazine metabolized?

A

There is an extensive first-pass effect
50% of Americans are fast acetylators, 50% are slow acetylators
Slow acetylators have an increased bioavailability

61
Q

What are problems associated with hydralazine?

A

May cause lupus like syndrome

Headache, flushing nausea, hypotension, tachycardia, angina pectoris

62
Q

What is minoxidil? What do we use it for?

A

Arteriolar dilator
It is used for severe hypertension (refractory)
It is given with beta-adrenergic receptor blocker and diuretic
Reflex activation of SNS could be problematic
Effective even if there is renal failure
May cause pericardial effusion (fluid in the pericardial cavity)
Hirsutism (abnormal hair growth)

63
Q

What are the problems with minoxidil?

A

Similar problems to hydralazine

64
Q

What is sodium nitroprusside? What do we use it for?

A

It is a venous and arteriolar dilator
It is useful in severe congestive heart failure (even though it increases SNS activity)
It decreases prelude and afterload, which decreases oxygen remain and increases cardiac output in heart failure
It can also be used for hypertensive encephalopathy

65
Q

How does sodium nitroprusside work?

A

It contains iron, cyanide and nitroso moiety which are metabolized in red blood cells to release nitric oxide, which increases cGMP and this causes dilation
It has a rapid onset (1 minute) and a rapid offset (5 minute)
It is given intravenously so the blood pressure can be titrated
There is a potential for cyanide toxicity

66
Q

Describe the metabolism of nitroprusside

A

It metabolized into nitric oxide and cyanide
Cyanide is converted to thiocyanate and then excreted by the kidney
With chronic use (and/or renal failure) the cyanide may accumulate causing blurred vision, tinnitus, disorientation, nausea
Treat toxicity with thiosulfate (sulfur donor)

67
Q

What are the preparations of nitrates available?

A 
Amyl nitrate - volatile liquid (inhaled; now obsolete)
Nitroglycerine (organic nitrate) - sublingual (popular), lingual spray (less popular); rapid onset, short duration - patch
Isosorbide dinitrate (sublingual, oral; longer acting)
68
Q

What is the mechanism of nitrates?

A 
Increase nitric oxide which increases cGMP levels
Relax veins (lower dose) and larger arteries (higher doses)
This causes decreased preload (decrease venous return), which decreases heart side (decreased wall stress), and may redistribute blood to ischemic areas. It will also decrease pulmonary artery resistance (useful in pulmonary hypertension seen in COPD)
69
Q

How do nitrates prevent coronary steal?

A

Smaller arterioles and pre capillary sphincters are less affected by nitrates, which prevents blood flow to “healthy” regions. Arterial vessels that are effected by nitrates tend to be larger, which increases blood flow to healthy and ischemic regions
Some vasodilators may worsen angina (i.e., hydralazine) because they dilate small arterioles

70
Q

Can tolerance develop with nitrates?

A

Yes

71
Q

What are the adverse effects of nitrates?

A

Orthostasis
Effects related to blood pressure lowering
Throbbing headache
Reflex activation of SNS
Salt and water retention
High doses may decrease BP and increase sympathetic nerve activity
Resultant increased O2 demand and decreased perfusion pressure which be problematic

Pharmacology (15 decks)

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