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Hypertension (week 1) > Anti-HTN Pharmacology > Flashcards

Anti-HTN Pharmacology Flashcards

1
Q

Formula for blood pressure

A

BP = CO xSVR

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2
Q

Targets for decreasing blood pressure with drug therapy

A
  • SVR

- CO = HR X SV = speed x (contractility &venous return)

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3
Q

What alters venous return (2)

A
  1. Intravascular (blood volume) - determined by ECF volume filtered by renal output of fluids and electrolytes and net intake of fluid, electrolytes.
  2. Vascular tone
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4
Q

Drugs that alter blood pressure (6 categories)

A
  1. Diuretics
  2. RAAS inhibitors (ACE inhibitors, ARBs, renin inhibitors)
  3. Ca2+ Channel Blockers
  4. Sympatholytics: beta blockers, alpha- antagonists
  5. Vasodilators
  6. CNS central agents
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5
Q

Diuretics MOA

A
  • draining off fluids via Na+ & K+
  • Na+ = effector; inhibit re-uptake in kidney = natriuresis
  • K+ = impt. b/c it gets adjusted by body to compensate for changing Na+ levels and may lead to hypo-/hyper-kalemia
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6
Q

Benefits of diuretics (2)

A
  • cheapest

- safest (generally)

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7
Q

Types of diuretics (3)

A

1) Thiazide (hydrocholorothiazide)
2) Loop diuretics (furosemide)
3) K+ sparing diuretics (spironolactone)

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8
Q

Actions of thiazide (2)

A
  1. Vasodilation (MOA unknown)

2. Diuretic effect

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9
Q

Renin Angiotensin System (RAS)

A
  1. Stimulation B1 receptors releases renin
  2. Renin converts angiotensinogen to angiotensin I
  3. Angiotensin converting enzyme converts angiotensin I to angiotensin II
  4. Angiotensin II binds to AT1 receptors and causes release of aldosterone (leading to Na+ retention) and leads to vasoconstriction.
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10
Q

How to inhibit RAAS system (5)

A
  1. Block B1 receptors (inhibit release of renin)
  2. Block ACE to reduce production of Ang II
  3. Direct renin inhibitors
  4. AT1 receptor antagonist
  5. Block aldosterone receptor via spirolactone (K+ spring diuretic)
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11
Q

ACE inhibitors example

A

Ramipril

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12
Q

ACE inhibitor effects

A

-inhibit aldosterone secretion
-inhibit NaCl reabsorption
- increased vasodilation (bradykinin breakdown inhibited)
Net effect = decreased SVR + natiuresis/diuresis

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13
Q

Important protective effect of ace inhibitors in kidneys (2)

A
  • Delay onset of diabetic nephropathy because reduce intraglomerular pressure (dilation of efferent arteriole)
  • Decrease oxidative stress on blood vessels caused by Ang II over time
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14
Q

Adverse effects of ACE inhibitors (4)

A
  1. Hacking, dry cough (attributed to bradykinin)
  2. Angioedema -rare but serious (fatal) swelling especially around the mouth
  3. Hyperkalemia (due to reduced aldosterone; exchange of Na+ for K+ to increase natiuresis can lead to hyperkalemia)
  4. Renal dysfunction - ATII maintains GFR by constricting efferent arteriole if hypovolemic or have compromised renal arterial blood flow (renal artery stenosis) without this ACEi may cause acute renal failure
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15
Q

Example of ARBs

A

Losartan (-sartan)

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16
Q

Effect of ARBs (4)

A
  • inhibit vasoconstriction (less than ACEi)
  • inhibit alosterone secretion
  • inhibit NaCl reabsorption
  • no effect on bradykinin
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17
Q

Renin inhibitors example

A

Aliskiren (-ren)

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18
Q

Renin inhibitor advantage

A
  • non-ACE pathway exists to generate ATII
  • this pathway is stronger in certain populations
  • without plasma renin activity no ATI is made so can block the production of ATII more universally
19
Q

Ca+ Channel blocker MOA

A

-decrease contraction by decreasing influx of Ca+ into vascular smooth muscle to decrease sympathetic tone

20
Q

Categories of Ca+ channel blockers (2)

A

1) Dihydropyridines (DHPs)

2) Non-DHPs

21
Q

Dihydropyridines example

A

-amlodipine (-ipine)

22
Q

Effect of DHP

A
  • act on vascular more than heart
  • dilate
  • reduce contractility (weakly)
23
Q

Adverse effects of DHP

A

-reflex tachycardia because of rapid onset when first introduced

24
Q

Example of non-DHP (2)

A
  • benzothiazepines (Dialtiazem- tiaz)

- Phenylalkylamines (Verapamil -ami)

25
Q

Effects of Non-DHP

A
  • both have greater effects on heart than vasculature
  • less selective than DHPs
  • reduce heart rate & contractility
26
Q

Adverse effect of non-DHPs

A

-cardio depressant (be careful of drug intake)

27
Q

Beta Antagonist example

A

Propranolol (-lol)

28
Q

Effects of beta antagonist (3)

A
  • decrease heart rate, contractility
  • decrease renin secretion
  • decrease SNS activity
29
Q

Adverse effects of beta antagonists

A
  • bronchoconstriction (contraindicated in asthma)

- fatigue -reduced cardiac output (problem for you active person)

30
Q

Alpha-1 blocker example

A

-prazosin (-zosin)

31
Q

Effect of alpha-1 blocker

A

-vasodialtory and venodilatory effect

32
Q

Adverse effect of alpha-1 blocker

A

Orthostatic hypotension

33
Q

Vasodilator example

A

-hydralizine

34
Q

MOA of vasodilators (2)

A

Open K+ channels

-decreases total peripheral resistance

35
Q

Example of CNS agents

A

-clonidine

36
Q

MOA of CNS agents

A

-feedback inhibition of norepinephrine release

37
Q

Effects of CNS agents

A
  • decreased HR, SV, SVR

- very messy drug

38
Q

Combination therapies

A

-counteract changes in RAAS pathway (i.e. increase SNS = increase RAS)
by giving ACEi, ARBs, renin inhib or B-blocker in combination
-to maximize efficacy and minimize toxicity

39
Q

Endothelin antagonist ex

A

Bosentan (-entan)

-in development

40
Q

Indications for endothelin antagonist

A

-primary pulmonary HTN

41
Q

Vasopeptidate inhibitors ex

A

Omepatrilat

  • also in development
  • concerns over toxicity (especially angioedema)
42
Q

ALLHAT trial

A

-antihypertensive & lipid lowering Tx to prevent heart attack trial
-used chlorithalidone (thiazide), lisinopril, amlodipine, doxazosin (A-blocker)
Results:
1. Daxazosin bad when stopped early
2. All 3 equally well with mortality
3. Fewer strokes with thiazides vs ACEi
4. More heart failure with CCBs
5. More incidence withdrawal due to adverse events w ACEi (cough)

43
Q

DASH-diet benefit

A

Comparable BP lowering effects as anti-HTN drugs

Hypertension (week 1) (4 decks)

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