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Pharm > PPT 11: antihypertension > Flashcards

PPT 11: antihypertension Flashcards

1
Q

What is the equation to calculate MAP

A

DBP+1/3(SBP-DBP)

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2
Q

What are factors that affect blood pressure?

A

peripheral resistance
vessel elasticity
blood volume
cardiac output

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3
Q

What is the Hydraulic equation

A

BP=CO x PVR

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4
Q

What are the 3 main sources of peripheral resistance?

A

blood vessel diameter
Blood viscosity
total vessel length (overweight ppl have inc. # of vessels)

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5
Q

where are baroreceptors located?

A

carotid arteries
aortic arch

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6
Q

How do the kidneys attempt to fix hypotension?

A

RAA cascade: hypotension in renal arterioles stimulates renin production. Renin -> angiotensin 1 -> angiotensin 2

angiotensin 2 causes vasoconstriction, stimulates aldosterone (inc. sodium absorption, intravascular volume)

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7
Q

What are the 4 types of antihypertensive agents?

A

diuretics
sympathoplegics (a2 agonists)
direct vasodilators
anti-angiotensins

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8
Q

Why is methyldopa better than clonidine for pregnant women?

A

Doesn’t cross the placental barrier like clonidine does

used for 2nd and 3rd trimester HTN

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9
Q

BP maintained by regulating:

A
  • cardiac output (systolic)
  • peripheral vascular resistance (diastolic)
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10
Q

What is systolic pressure? What is the normal range?

A

peak arterial pressure (120 mmHg)

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11
Q

What is diastolic pressure? What is the normal range?

A

lowest arterial pressure (70 - 80 mm Hg)

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12
Q

______ propels the blood to the tissues

A

MAP

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13
Q

What are the causes of primary hypertension?

A
  • CV disease - most common
  • obesity, age (over 40), diabetes, heredity, stress, smoking, renal failure, CV disease, stroke
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14
Q

Differentiate between the stages of hypertension

A

Normal - 120/80
Prehypertension (between)
Hypertension 140/90
Stage 1 (between)
Stage 2 - 160/100

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15
Q

What is driving venous pressure?

A

back pressure driving venous tone
skeletal muscle squeezes veins
one way valves

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16
Q

Cardiac output equation

A

CO = SVxHR

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17
Q

What are the four anatomic sites of BP control?

A
  1. Resistance - arterioles
  2. capacitance - venules
  3. pump output - heart
  4. volume - kidneys
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18
Q

Cardiac output is a function of what 3 things?

A
  • Stroke volume
  • Heart rate
  • Venous capacitance (Preload)
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19
Q

How much do diuretics typically lower BP?

A

Lower BP – 10-15 mm Hg in most patients

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20
Q

What are the main sympathoplegics used for lowering BP?

A

Clonidine and methyldopa
Dexmedetomidine (sedation)

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21
Q

How do sympathoplegics lower BP?

A
  • Primary antihypertensive activity due to α agonist activity in brainstem, decreasing sympathetic stimulation
  • Bind more tightly to α2 than α1
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22
Q

What kind of agonist is clonidine?

A

Partial agonist

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23
Q

Why can’t clonidine be given to a pregnant patient?

A

Lipid soluble, rapidly enters brain

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24
Q

Clonidine works to lower BP by stimulating the alpha receptors in the ________

A

arterioles

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25
Q

What are more common uses for clonidine?

A

ADHD, Tourettes, Withdrawal symptoms
- Off label use: Anxiety, PTSD; Sedative – prolong anesthesia

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26
Q

What are the side effects of clonidine?

A

Sedation, Dry Mouth

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27
Q

Which adrenoceptor antagonists can be used to lower BP?

A

Beta Blockers - Propanolol, Metropolol, Atenolol, Esmolol, Labetolol
Alpha 1 blockers - Phentolamine, Prazosin, Terazosin, Doxazosin

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28
Q

How do alpha 1 blockers lower BP?

A
  • Block α1 receptors in arterioles and venules
  • Dilates both resistance and capacitance vessels
  • BP is reduced more in upright position
  • Retention of salt and water
  • Most effective when used with a β blocker or a diuretic
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29
Q

How do beta blockers lower BP?

A
  • Lowers BP, prevents reflex tachycardia
  • Decreases cardiac output
  • Inhibits renin production
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30
Q

Differentiate between beta selectivity of beta blockers and their use in lowering BP

A

Propanolol - Antagonizes β1 & β2 receptors
β1 selective - Metoprolol, Atenolol, Esmolol (ultra-short acting), and Labetolol
- β1 has less systemic side effects and more selective for cardiac β1 receptors

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31
Q

What are the 4 mechanisms of action of vasodilators? Give examples of drugs

A
32
Q

What are the two main ways vasodilators lower BP?

A
  1. Relax smooth muscle of arterioles (all) and veins (nitroprusside and nitrates)
  2. Reduction of PVR and MAP - Elicits compensatory responses; Best when given in conjunction with other hypertensives that combat these mechanisms
33
Q

Describe the effects of combination therapy of beta blockers and diuretics in lowering blood pressure

A
34
Q

What are the important vasodilators to know for lowering BP?

A
  1. Hydralazine
  2. Minoxidil
  3. Sodium Nitroprusside
  4. Fenoldopam
  5. Calcium channel blockers - Verapamil, Diltiazem, Dihydropyridines
35
Q

How does hydralazine lower BP?

A

Dilates arterioles – induces NO production in endothelium

36
Q

What are the symptoms of hydralazine toxicity?

A
  • HA, nausea, sweating, flushing
  • Worse in slow acetylators (Symptoms resemble SLE)
37
Q

What are the pharmacokinetics for hydralazine?

A
  • A: Well absorbed
  • M: Rapid first pass metabolism (low bioavailabilty PO ~ 25%)
  • Tachyphylaxis – may be beneficial in combination (B blocker)
38
Q

How does minoxidil lower BP?

A
  • Opens K+ channels in smooth muscles; Stabilizes potential, less likely to contract
  • Dilates arteries, arterioles
39
Q

What are the symptoms of minoxidil toxicity?

A
  • HA, sweating, palpitations
  • Tachycardia
  • Angina
  • Hypertrichosis (hair growth)
40
Q

What are the clinical indications for Sodium Nitroprusside?

A

HT emergencies and Cardiac failure

41
Q

How does Sodium Nitroprusside lower BP?

A

Relaxes vascular smooth muscle, dilating arterial and venous vessels
- Breaks down in blood to release NO
- Increases intracellular cGMP

42
Q

What is the upside and downside of Sodium Nitroprusside use?

A

Upside - Rapidly lowers BP; Effects disappear 1-10 min after d/c
Downside - CN accumulation, slowly eliminated by kidney

43
Q

What are the symptoms of CN accumulation? Which medication can cause this? Which medication helps remove CN?

A
  • Metabolic acidosis, arrhythmias, death (Worse in patients with renal insufficiency)
  • Sodium Nitroprusside
  • Sodium thiosulfate facilitates metabolism of cyanide
44
Q

How does Fenoldopam lower BP?

A

Peripheral arteriolar dilator - Agonist of D1 receptors
- dilates renal vascular bed (lowers BP, diuresis)

45
Q

What are the clinical indications for Fenoldopam use?

A

HTN emergencies, post-op HTN

46
Q

What are the symptoms associated with Fenoldopam toxicity?

A

Reflex tachycardia, flushing, HA

47
Q

How is Fenoldopam metabolized?

A

Rapidly metabolized by conjugation - T1/2 = 5 minutes

48
Q

What are the clinical indications for Ca++ channel blockers?

A
  • HTN
  • Antianginal
  • Antiarrhytmic
49
Q

How do Ca++ channel blockers lower BP?

A

Dilate peripheral arterioles by inhibiting Ca2+ influx in arterial smooth muscle

50
Q

Which Ca++ channel blockers target the heart vs the periphery?

A
  • Verapamil - more targeted to heart
  • Diltiazem - both heart and periphery
  • Dihydropyridine family - more targeted to periphery
51
Q

What are the types of Inhibitors of Angiotensin?

A

ACE inhibitors (-pril)
Angiotensin competitive inhibitors (angiotensin receptor blockers, ARB) (-artan)

52
Q

Compare the mechanisms of ACE inhibitors and ARBs in lowering BP

A
  1. ACE inhibitors - Block conversion of angiotensin I → angiotensin II
    - Inhibits breakdown of bradykinins (stimulates PG synthesis) → vasodilation (decreased PVR)
  2. ARBs - Block angiotensin II receptors blood vessels and the adrenal cortex
53
Q

______ is the prototype drug of ACE inhibitors

A

Captopril

54
Q

Renin release in kidney stimulated by what 4 mechanisms?

A
  • Reduced arterial pressure
  • Reduced sodium delivery
  • Increased sodium concentration
  • Sympathetic stimulation (beta receptors)
55
Q

What are the symptoms of toxicity of ACE inhibitors and ARBs? What is the main difference?

A
  • Severe hypotension
  • Contraindicated in hypovolemic patients and pregnancy
  • Altered sense of taste
  • Rashes
  • Drug interactions (K+ supplements can lead to hyperkalemia; NSAIDS block some effects)
  • COUGH (ACE inhibitors only)
56
Q

Why is a persistent, non-productive cough a symptom for ACE inhibitors but not ARBs?

A

ARBs have no effect on bradykinin - no cough
ACE inhibitors - inhibit breakdown of bradykinins, which stimulate PG synthesis - excess bradykinin causes non-productive cough

57
Q

Which angiotensin inhibitors do we need to know?

A

ACE inhibitors - Captopril
Angiotensin receptor blockers – Losartan, Valsartan

58
Q

Define pulmonary HTN

A

Increased pressure in pulmonary arteries

59
Q

How is pulmonary HTN diagnosed?

A

echocardiogram, cardiac cath

60
Q

How is pulmonary HTN treated?

A

Prostaglandins - Prostacyclin (Epoprostanol) – continuous IV infusion
Endothelin Receptor Antagonists - more effects on hypertension in lungs than periphery

61
Q

What are the causes of pulmonary HTN? What is the prognosis?

A
  • Causes: HBP, congenital, emphysema, clots, HF
  • Prognosis - poor
62
Q

Which drug is the primary endothelin receptor antagonist? What does it treat?

A

Bosentan, pulmunoary HTN

63
Q

What are the adverse effects of bosentan?

A
  • HA, edema, rash
  • Hepatotoxicty
  • Teratogenic
64
Q

Why is pulmonary HTN prognosis poor?

A

Proliferation os smooth muscle in the lungs

65
Q

How does low shear stress result in proliferation of smooth muscle in the vasculature?

A

Low shear stress - ANG II, cytokines, thrombin
- stimulates preproET (precursor to ET)
Endothelin comes from vascular endothelium (cells that line blood vessels produced by low shear stress)

66
Q

How does increased endothelin result in pulmonary HTN?

A

Vasoconstriction when endothelin bound to endothelin receptors

67
Q

How does high shear stress result in vasodilation?

A

High sheer stress - NO, PGI3, ANP
Inhibits endothelin production, preventing proliferation

68
Q

Describe the endothelin negative feedback loop

A

Not only does endothelin bind to peripheral vascular smooth muscle, it also binds the endothelial cells themselves, stimulating the production of NO - vasodilation, preventing further proliferation

69
Q

How do Endothelin Receptor Antagonists treat pulmonary HTN?

A

Prevent endothelin from binding to receptors, preventing proliferation of smooth muscle, and further vasoconstriction and HTN

70
Q

Where are endothelin receptors found?

A

Primarily in lungs, little in the periphery

71
Q

What are the nonpharmacologic interventions for HTN?

A
  • Decrease sodium intake (Average American = 200 mEq/day)
  • Exercise
  • Weight reduction (↓ BP in 75% of obese patients)
72
Q

What meds can increase BP?

A

Decongestants, NSAIDs, contraceptives, some herbal medications

73
Q

What are the first line drugs for HTN?

A
  • Low dose diuretic
  • Beta blocker
  • CCB
  • Dual therapy
74
Q

What are the 2 types hypertensive crisis?

A

Hypertensive Urgency
Hypertensive Emergency

75
Q

Differentiate between Hypertensive Urgency
and Emergency

A

Hypertensive Urgency (>180/110, without acute end organ damage)
- Lower BP in hours to days
Hypertensive Emergency (>180/110, with acute end organ damage (kidney failure, infarct, stroke, etc)
- Need immediate lowering of BP

76
Q

What is the treatment for HTN emergencies?

A
  1. ICU monitoring with continuous BP - Monitor fluid intake, output, body weight
  2. Parenteral antihypertensives to lower BP rapidly: Sodium nitroprusside, Fenoldopam (increase kidney perfusion)
77
Q

What are the pharmacokinetics for minoxidil?

A
  • A: Well absorbed orally, topically (Rogaine)
  • M: Initially converted to active metabolite in liver, then degraded in liver (4 hours)

Pharm (16 decks)

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