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Pharm 2024 > PPT 11: antihypertension > Flashcards

PPT 11: antihypertension Flashcards

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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
What are more common uses for clonidine?
ADHD, Tourettes, Withdrawal symptoms - Off label use: Anxiety, PTSD; Sedative – prolong anesthesia
26
What are the side effects of clonidine?
Sedation, Dry Mouth
27
Which adrenoceptor antagonists can be used to lower BP?
Beta Blockers - Propanolol, Metropolol, Atenolol, Esmolol, Labetolol Alpha 1 blockers - Phentolamine, Prazosin, Terazosin, Doxazosin
28
How do alpha 1 blockers lower BP?
- 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
29
How do beta blockers lower BP?
- Lowers BP, prevents reflex tachycardia - Decreases cardiac output - Inhibits renin production
30
Differentiate between beta selectivity of beta blockers and their use in lowering BP
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
31
What are the 4 mechanisms of action of vasodilators? Give examples of drugs
32
What are the two main ways vasodilators lower BP?
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
Describe the effects of combination therapy of beta blockers and diuretics in lowering blood pressure
34
What are the important vasodilators to know for lowering BP?
1. Hydralazine 2. Minoxidil 3. Sodium Nitroprusside 4. Fenoldopam 5. Calcium channel blockers - Verapamil, Diltiazem, Dihydropyridines
35
How does hydralazine lower BP?
Dilates arterioles – induces NO production in endothelium
36
What are the symptoms of hydralazine toxicity?
- HA, nausea, sweating, flushing - Worse in slow acetylators (Symptoms resemble SLE)
37
What are the pharmacokinetics for hydralazine?
- A: Well absorbed - M: Rapid first pass metabolism (low bioavailabilty PO ~ 25%) - Tachyphylaxis – may be beneficial in combination (B blocker)
38
How does minoxidil lower BP?
- Opens K+ channels in smooth muscles; Stabilizes potential, less likely to contract - Dilates arteries, arterioles
39
What are the pharmacokinetics for minoxidil?
- A: Well absorbed orally, topically (Rogaine) - M: Initially converted to active metabolite in liver, then degraded in liver (4 hours)
39
What are the symptoms of minoxidil toxicity?
- HA, sweating, palpitations - Tachycardia - Angina - Hypertrichosis (hair growth)
40
What are the clinical indications for Sodium Nitroprusside?
HT emergencies and Cardiac failure
41
How does Sodium Nitroprusside lower BP?
Relaxes vascular smooth muscle, dilating arterial and venous vessels - Breaks down in blood to release NO - Increases intracellular cGMP
42
What is the upside and downside of Sodium Nitroprusside use?
Upside - Rapidly lowers BP; Effects disappear 1-10 min after d/c Downside - CN accumulation, slowly eliminated by kidney
43
What are the symptoms of CN accumulation? Which medication can cause this? Which medication helps remove CN?
- Metabolic acidosis, arrhythmias, death (Worse in patients with renal insufficiency) - Sodium Nitroprusside - Sodium thiosulfate facilitates metabolism of cyanide
44
How does Fenoldopam lower BP?
Peripheral arteriolar dilator - Agonist of D1 receptors - dilates renal vascular bed (lowers BP, diuresis)
45
What are the clinical indications for Fenoldopam use?
HTN emergencies, post-op HTN
46
What are the symptoms associated with Fenoldopam toxicity?
Reflex tachycardia, flushing, HA
47
How is Fenoldopam metabolized?
Rapidly metabolized by conjugation - T1/2 = 5 minutes
48
What are the clinical indications for Ca++ channel blockers?
- HTN - Antianginal - Antiarrhytmic
49
How do Ca++ channel blockers lower BP?
Dilate peripheral arterioles by inhibiting Ca2+ influx in arterial smooth muscle
50
Which Ca++ channel blockers target the heart vs the periphery?
- Verapamil - more targeted to heart - Diltiazem - both heart and periphery - Dihydropyridine family - more targeted to periphery
51
What are the types of Inhibitors of Angiotensin?
ACE inhibitors (-pril) Angiotensin competitive inhibitors (angiotensin receptor blockers, ARB) (-artan)
52
Compare the mechanisms of ACE inhibitors and ARBs in lowering BP
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
______ is the prototype drug of ACE inhibitors
Captopril
54
Renin release in kidney stimulated by what 4 mechanisms?
- Reduced arterial pressure - Reduced sodium delivery - Increased sodium concentration - Sympathetic stimulation (beta receptors)
55
What are the symptoms of toxicity of ACE inhibitors and ARBs? What is the main difference?
- 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
Why is a persistent, non-productive cough a symptom for ACE inhibitors but not ARBs?
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
Which angiotensin inhibitors do we need to know?
ACE inhibitors - Captopril Angiotensin receptor blockers – Losartan, Valsartan
58
Define pulmonary HTN
Increased pressure in pulmonary arteries
59
How is pulmonary HTN diagnosed?
echocardiogram, cardiac cath
60
How is pulmonary HTN treated?
Prostaglandins - Prostacyclin (Epoprostanol) – continuous IV infusion Endothelin Receptor Antagonists - more effects on hypertension in lungs than periphery
61
What are the causes of pulmonary HTN? What is the prognosis?
- Causes: HBP, congenital, emphysema, clots, HF - Prognosis - poor
62
Which drug is the primary endothelin receptor antagonist? What does it treat?
Bosentan, pulmunoary HTN
63
What are the adverse effects of bosentan?
- HA, edema, rash - Hepatotoxicty - Teratogenic
64
Why is pulmonary HTN prognosis poor?
Proliferation os smooth muscle in the lungs
65
How does low shear stress result in proliferation of smooth muscle in the vasculature?
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
How does increased endothelin result in pulmonary HTN?
Vasoconstriction when endothelin bound to endothelin receptors
67
How does high shear stress result in vasodilation?
High sheer stress - NO, PGI3, ANP Inhibits endothelin production, preventing proliferation
68
Describe the endothelin negative feedback loop
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
How do Endothelin Receptor Antagonists treat pulmonary HTN?
Prevent endothelin from binding to receptors, preventing proliferation of smooth muscle, and further vasoconstriction and HTN
70
Where are endothelin receptors found?
Primarily in lungs, little in the periphery
71
What are the nonpharmacologic interventions for HTN?
- Decrease sodium intake (Average American = 200 mEq/day) - Exercise - Weight reduction (↓ BP in 75% of obese patients)
72
What meds can increase BP?
Decongestants, NSAIDs, contraceptives, some herbal medications
73
What are the first line drugs for HTN?
- Low dose diuretic - Beta blocker - CCB - Dual therapy
74
What are the 2 types hypertensive crisis?
Hypertensive Urgency Hypertensive Emergency
75
Differentiate between Hypertensive Urgency and Emergency
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
What is the treatment for HTN emergencies?
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)

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