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Pharmacology fall 2024 > Antihypertensive Drugs Ch. 11 (Exam III) > Flashcards

Antihypertensive Drugs Ch. 11 (Exam III) Flashcards

1
Q

What is the formula for MAP?

A

dBP + 1/3(sBP - dBP)

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2
Q

What 4 factors affect blood pressure?

A
  1. Peripheral Resistance
  2. Vessel Elasticity
  3. Blood Volume
  4. Cardiac Output
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3
Q

Briefly describe Frank-Starlings law?

A

Increase stretch of cardiac muscle = increased Cardiac Output

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4
Q

What is the hydraulic equation of blood pressure?

A

BP = CO x SVR

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5
Q

What are the 3 main sources of Systemic Vascular Resistance (SVR) ?
What are the sub-factors governing each of these?

A
  1. Blood Vessel Diameter (α-agonism/antagonism)
  2. Blood Viscosity (dehydration, hyperlipidemia, etc.)
  3. Total Vessel Length (Obesity = more blood vessels)
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6
Q

What is the most common cardiovascular disease?

A

Primary Hypertension

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7
Q

How can blood pressure be modulated at the vasomotor center of the brain?

What are some drug examples?

A

Centrally Acting α-2 drugs.
- Methyldopa
- Clonidine
- Dexmedetomidine

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8
Q

Describe the process of the renal response to hypotension ending in angiotensin II formation.

A
  1. Hypotension → Renin Release
  2. Renin → angiotensinogen → angiotensin 1
  3. angiotensin 1 → ACE → angiotensin 2
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9
Q

How does Angiotensin II modulate blood pressure?

A
  • Arteriole Constriction
  • ↑ Aldosterone secretion in adrenal cortex
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10
Q

In what three ways, discussed in lecture, can the RAAS system be altered by drugs?

A
  1. Aliskiren inhibiting Renin
  2. ACE Inhibitors
  3. ARBs
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11
Q

What endogenous molecule of the RAAS has negative feedback capability on renin release?

A

Angiotensin II

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12
Q

What are the 4 target sites for blood pressure modulation?

A
  1. Heart
  2. Arteries
  3. Veins
  4. Kidneys
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13
Q

How do sympathoplegics treat HTN?

A

↓ SVR, ↓ CO

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14
Q

What drug class is first-line therapy for treating HTN?
How much of a BP reduction is usually noted with these?
What is the most common toxic side effect?

A
  1. Diuretics
  2. 10-15 mmHg reduction
  3. Hypokalemia
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15
Q

What is the mechanism of action of Clonidine and Methyldopa?

A

Both act on α-2 receptors of the Tractus Solaris and Rostral Ventrolateral Medulla to ↑ PSNS and ↓ SNS.

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16
Q

Is methyldopa a prodrug?
If so, what are it’s active metabolites?

A

Yes.
Methyldopa → α-methyldopamine + α-methylNE

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17
Q

Does methyldopa cross the BBB?

A

Yes

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18
Q

What is methyldopa used for? Why?
What is the primary side effect of methyldopa?

A
  • Pregnancy induced hypertension.
  • Methyldopa does not cross the placenta.
  • Sedation.
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19
Q

Which centrally acting sympathoplegic is a partial agonist?
What does this drug do to blood pressure?

A

Clonidine

Slight initial ↑ BP from α-1.
Prolonged ↓ BP from α-2.

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20
Q

Is Clonidine a first-line therapeutic for HTN?
What are the primary side effects from clonidine?

A

No

Sedation and dry mouth

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21
Q

What are more common uses for clonidine outside of HTN?

A
  • ADHD (↓ NE in frontal cortex)
  • Tourettes
  • Withdrawal symptoms
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22
Q

What off-label uses are there for clonidine? Which is most pertinent to CRNA’s?

A

Anxiety, PTSD

Prolongation of Anesthesia

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23
Q

Which β-blocker is considered the 1st?
Is this drug cardio-selective?

A

Propanolol
No, affects all β receptors.

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24
Q

Which two drugs are better selections for cardiac effects vs propanolol?

A

Metoprolol and Atenolol

25
Q

Which β-blocker is best used intraoperatively and why?

A

Esmolol due to short duration (5-15 min)

26
Q

What 4 factors would help determine what β-blocker should be selected?
Why might each of these factors produce a better drug?

A
  1. β-selectivity (aka cardioselectivity)
  2. ↑ half-life (once-a-day dosage)
  3. Partial Agonism (better tolerated)
  4. α-antagonism (↓ SVR)
27
Q

Do α-1 antagonists only work on the arterial system?
What drugs, when used in conjuction with α-1 antagonists, make α-1 antagonists more effective?

A

No, they affect venous capacitance vessels too.
When used with a β-blocker or diuretic.

28
Q

Does body positioning help determine the effectiveness of α-1 antagonists?

A

Yes, more effectiveness in an upright position

29
Q

What two oral vasodilators need to be known?
What two parenteral vasodilators need to known?
What drugs can be taken orally or parenterally for vasodilation?

A
  • Hydralazine and Minoxidil
  • Nitroprusside and Fenoldopam
  • CCB’s
30
Q

Which two drugs release Nitric Oxide (NO) to produce Vasodilation?
What is the difference in the mechanism of action between these two?

A

Nitroprusside and Hydralazine

Nitroprusside releases NO itself.
Hydralazine ↑ NO production.

31
Q

How does minoxidil produce its vasodilatory effects?

A

↑ pK+ thus increasing threshold of activation for smooth muscle contraction.

32
Q

Which vasodilator works through the activation of dopamine-receptors?
What makes this drug unique?

A

Fenoldopam

Fenoldopam ↑ renal blood flow and diuresis.

33
Q

Vasodilators reduce SVR and MAP, what compensatory response occurs from this?
What does this mean for vasodilator use in general?

A

Reflex Tachycardia.

Vasodilators are best used in conjunction w/ other anti-hypertensives.

34
Q

By what mechanism does NO produce vasodilation?

A

NO → endothelium → ↑ GC → ↑ cGMP → Ca2+ Channels blocked.

need to verify

35
Q

What should be known about hydralazine’s susceptibility to first pass metabolism & bioavailability?
Should it be used with other drugs?

A

-Rapid first pass metabolism w/ bioavailability of 25%
-Subject to tachyphylaxis (best used alongside other drugs)

36
Q

What s/s present with hydralazine toxicity?
By what mechanism is hydralazine metabolized in the liver?

A

Headaches, nausea, sweating, and flushing

Acetylation via Phase II reactions.

37
Q

What symptomology might occur in slow acetylators if given hydralazine?

A

Lupus symptoms (just the symptoms not actual SLE condition).

38
Q

What drug’s active form treats BP but the prodrug form produces hairgrowth?
What is the duration of action of this drug if taken PO?

A

Minoxidil
4 hours

39
Q

What are the symptoms of minoxidil toxicity?

A

Headaches, sweating, palpitations, tachycardia, angina

Hypertrichosis (Hair Growth)

40
Q

What drug is used for hypertensive emergencies?
What is its mechanism of action?

A

Nitroprusside
Vasodilation from ↑ NO release causing ↑ cGMP

41
Q

What is the source of toxicity with nitroprusside use?
What condition exacerbates nitroprusside toxicity?
How can nitroprusside toxicity be counteracted?

A
  • CN (cyanide)
  • Renal Insufficiency or Failure
  • Sodium Thiosulfate will ↑ CN metabolism
42
Q

What are symptoms of CN (cyanide) accumulation?

A

Metabolic acidosis, arrhythmias, & death

43
Q

In what clinical situation is fenoldopam particularly useful?
How quickly is fenoldopam metabolized?
What are signs of fenoldopam toxicity?

A
  • Post-operative HTN
  • T1/2= 5 minutes
  • Reflex ↑HR, Flushing, Headache
44
Q

What is the mechanism of action of CCB’s?
What other uses do CCB’s have?

A

Inhibition of Ca2+ influx in arterial smooth muscle

Antianginal and antiarrhythmic

45
Q

Which CCB’s are not dihydropyridines?

What does this mean in terms of what these drugs treat?

A

Verapamil and Diltiazem

  • Verapamil is an antiarrhythmic
  • Diltiazem is an antiarrhythmic and ↓ BP
46
Q

What 4 factors induce renin release by the kidneys?

A
  1. ↓ MAP
  2. ↓ Na+ delivery
  3. ↑ Na+ at renal tubule
  4. SNS stimulation
47
Q

When can kidney damage occur from Aliskiren?

A

In diabetics or patients taking ACE inhibitors and/or ARBs.

48
Q

How do ACE inhibitors increase inflammation?
What is the most notable side effect from ACE inhibitors, what percentage has this side effect, and why does it occur?

A

↑ bradykinin production

10% get persistent dry cough due to inflammatory effects on ACE receptors in the lungs.

49
Q

What drug is used as an alternative to ACE inhibitors?

How would these drugs elicit their effects?

A

Angiotensin Receptor Blockers (ARBs)

By blocking Angiotensin II, ARBs will vasodilate and suppress aldosterone secretion.

50
Q

Which ACE inhibitor is prototypical?

Which ACE inhibitors are prodrugs with longer acting effects?

A

Captopril

Enalapril, Lisinopril, and Benazapril

51
Q

Can ACE inhibitors be given during pregnancy?

A

No, teratogenesis noted in 1st trimester

52
Q

What two ARBs should be known?

Do ARBs cause inflammation in the same manner as ACE inhibitors?

A

Losartan and Valsartan

No. No effect on bradykinin = no inflammatory effect.

53
Q

What is the prognosis for pulmonary hypertension?

A

Bad (2-3 years survival rate from diagnosis)

54
Q

What IV drug is used to treat Pulmonary Hypertension?
What is notable about this drug?
Are there alternatives?

A
  • Epoprostenol
  • Prostaglandin is potent pulmonary vasodilator that has to be given via continuous IV infusion.
  • Inhaled alternatives that don’t last long and Endothelin Receptor Antagonists.
55
Q

What do Endothelin Receptor Antagonists treat?
Are these drugs generally effective?
Which drugs of this class should be known?

A
  • Pulmonary Hypertension
  • Very effective, ↑ life expectancy for pHTN patients.
  • Bosentan and Tezosentan
56
Q

What are the adverse effects of endothelin receptor antagonists?

A

headache, edema, rash, hepatotoxicity, and teratogenesis.

57
Q

What non-pharmacologic options exist for treating hypertension?

A
  1. ↓ Na+ intake
  2. Exercise
  3. Weight reduction
58
Q

What Blood pressure parameters indicate a Hypertensive Urgency/Emergency?
What differentiates the two conditions?

A

> 180/110 mmHg

  • HTN urgency = No organ damage, hours to days to treat.
  • HTN emergency = Organ damage occurring, needs to be treated immediately.
59
Q

What drugs are most commonly used to treat hypertensive emergencies?
What others might be used?

A
  • Nitroprusside and Fenoldopam
  • Labetolol, nicardipine, hydralazine, and methyldopa

Pharmacology fall 2024 (23 decks)

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