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Pharm (Fall 2022) > 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
Which β-blocker is best used intraoperatively and why?
Esmolol due to short duration (5-15 min)
26
What 4 factors would help determine what β-blocker should be selected? Why might each of these factors produce a better drug?
1. β-selectivity (aka cardioselectivity) 2. ↑ half-life (once-a-day dosage) 3. Partial Agonism (better tolerated) 4. α-antagonism (↓ SVR)
27
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?
No, they affect venous capacitance vessels too. When used with a β-blocker or diuretic.
28
Does body positioning help determine the effectiveness of α-1 antagonists?
Yes, more effectiveness in an upright position
29
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?
- Hydralazine and Minoxidil - Nitroprusside and Fenoldopam - CCB's
30
Which two drugs release Nitric Oxide (NO) to produce Vasodilation? What is the difference in the mechanism of action between these two?
Nitroprusside and Hydralazine Nitroprusside releases NO itself. Hydralazine ↑ NO production.
31
How does minoxidil produce its vasodilatory effects?
↑ pK+ thus increasing threshold of activation for smooth muscle contraction.
32
Which vasodilator works through the activation of dopamine-receptors? What makes this drug unique?
Fenoldopam Fenoldopam ↑ renal blood flow and diuresis.
33
Vasodilators reduce SVR and MAP, what compensatory response occurs from this? What does this mean for vasodilator use in general?
Reflex Tachycardia. Vasodilators are best used in conjunction w/ other anti-hypertensives.
34
By what mechanism does NO produce vasodilation?
NO → endothelium → ↑ GC → ↑ cGMP → Ca2+ Channels blocked. *need to verify*
35
What should be known about hydralazine's susceptibility to first pass metabolism & bioavailability? Should it be used with other drugs?
-Rapid first pass metabolism w/ bioavailability of 25% -Subject to tachyphylaxis (best used alongside other drugs)
36
What s/s present with hydralazine toxicity? By what mechanism is hydralazine metabolized in the liver?
Headaches, nausea, sweating, and flushing Acetylation via Phase II reactions.
37
What symptomology might occur in slow acetylators if given hydralazine?
Lupus symptoms (just the symptoms not actual SLE condition).
38
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?
Minoxidil 4 hours
39
What are the symptoms of minoxidil toxicity?
Headaches, sweating, palpitations, tachycardia, angina **Hypertrichosis (Hair Growth)**
40
What drug is used for hypertensive emergencies? What is its mechanism of action?
Nitroprusside Vasodilation from ↑ NO release causing ↑ cGMP
41
What is the source of toxicity with nitroprusside use? What condition exacerbates nitroprusside toxicity? How can nitroprusside toxicity be counteracted?
- CN (cyanide) - Renal Insufficiency or Failure - Sodium Thiosulfate will ↑ CN metabolism
42
What are symptoms of CN (cyanide) accumulation?
Metabolic acidosis, arrhythmias, & death
43
In what clinical situation is fenoldopam particularly useful? How quickly is fenoldopam metabolized? What are signs of fenoldopam toxicity?
- Post-operative HTN - T1/2= 5 minutes - Reflex ↑HR, Flushing, Headache
44
What is the mechanism of action of CCB's? What other uses do CCB's have?
Inhibition of Ca2+ influx in arterial smooth muscle Antianginal and antiarrhythmic
45
Which CCB's are **not** dihydropyridines? What does this mean in terms of what these drugs treat?
Verapamil and Diltiazem * Verapamil is an antiarrhythmic * Diltiazem is an antiarrhythmic and ↓ BP
46
What 4 factors induce renin release by the kidneys?
1. ↓ MAP 2. ↓ Na+ delivery 3. ↑ Na+ at renal tubule 4. SNS stimulation
47
When can kidney damage occur from Aliskiren?
In diabetics or patients taking ACE inhibitors and/or ARBs.
48
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?
↑ bradykinin production 10% get persistent dry cough due to inflammatory effects on ACE receptors in the lungs.
49
What drug is used as an alternative to ACE inhibitors? How would these drugs elicit their effects?
Angiotensin Receptor Blockers (ARBs) By blocking Angiotensin II, ARBs will vasodilate and suppress aldosterone secretion.
50
Which ACE inhibitor is prototypical? Which ACE inhibitors are prodrugs with longer acting effects?
Captopril Enalapril, Lisinopril, and Benazapril
51
Can ACE inhibitors be given during pregnancy?
No, teratogenesis noted in 1st trimester
52
What two ARBs should be known? Do ARBs cause inflammation in the same manner as ACE inhibitors?
Losartan and Valsartan No. No effect on bradykinin = no inflammatory effect.
53
What is the prognosis for pulmonary hypertension?
Bad (2-3 years survival rate from diagnosis)
54
What IV drug is used to treat Pulmonary Hypertension? What is notable about this drug? Are there alternatives?
- 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
What do Endothelin Receptor Antagonists treat? Are these drugs generally effective? Which drugs of this class should be known?
* Pulmonary Hypertension * Very effective, ↑ life expectancy for pHTN patients. * Bosentan and Tezosentan
56
What are the adverse effects of endothelin receptor antagonists?
headache, edema, rash, hepatotoxicity, and teratogenesis.
57
What non-pharmacologic options exist for treating hypertension?
1. ↓ Na+ intake 2. Exercise 3. Weight reduction
58
What Blood pressure parameters indicate a **Hypertensive Urgency/Emergency**? What differentiates the two conditions?
> 180/110 mmHg - HTN urgency = No organ damage, hours to days to treat. - HTN emergency = Organ damage occurring, needs to be treated immediately.
59
What drugs are most commonly used to treat hypertensive emergencies? What others might be used?
* Nitroprusside and Fenoldopam * Labetolol, nicardipine, hydralazine, and methyldopa

Pharm (Fall 2022) (23 decks)

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