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Pharmacology > CH 11: Anti-hypertensives > Flashcards

CH 11: Anti-hypertensives Flashcards

1
Q

Hypertension

A

disease processes that result in a sustained elevation of blood pressure from:

  • Renal artery stenosis
  • Aortic coarctation
  • Pheochromocytoma, Cushing’s or Hyperthyroidism
  • Variety of drugs/ chemicals
    U- Unknown (called PRIMARY HYPERTENSION” (most cases; 90%))
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2
Q

What is hypertension? (JNC 7)

A 
Normal BP < 120 % < 80
Prehypertensive/elevated 120-129 & <80
Hypertensive
* stage 1 = 130-139 or 80-89
* stage 2 = >139 or >89
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3
Q

How do we lower B.P?

A

with stage 1 or 2 hypertension, we could start with one or two medications

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4
Q

Why should we lower B.P?

A

If we lower B.P. we decrease morbidity and mortality (health costs, etc)

Hypertension is associated with:

  • stroke
  • cerebral hemorrhage
  • CHF
  • renal failure
  • hypertensive crisis
  • end organ damage
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5
Q

BP data

A

for every 20 mmHh systolic or 10 mmHg diastolic increase in BP over 115/75, there is a doubling of mortality for both ischemic heart disease and stroke

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6
Q

Hypertension Factoids:

A
  1. in 2000, 1 billion people worldwide had hypertension
  2. hypertension is leading risk factor for cause of death worldwide (51% of strokes and 45% of ischemic heart disease deaths attributable to hypertension
  3. in U.S., 1 in 3 adults over 20 have it, and estimated 30% are pre-hypertensive
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7
Q

pathophysiology

A

genetic factors:
we see families and groups where it is more prevalent, and various groups respond to different treatments

environment:
smoking, caffeine, alcohol, obesity, vit. D deficiency

neural effects:
Symp NS, others

renal effects:
reduced sodium excretion

hormonal effects:
RAAS, others

vascular effects:
vasoconstrictors, atherosclerosis, remodeling, etc

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8
Q

Strategies to lowering B.P

A

REDUCE TOTAL PERIPHERAL RESISTANCE (TPR) BY:

  • decrease ANS (automatic nervous system)
  • decrease RAAS (renin angiotensin aldosterone system)
  • decrease endothelin or vasoactivity (Ca blockers)

REDUCE CARDIAC OUTPUT (CO)

  • decrease heart rate (HR)
  • decrease blood volume (diuretics)
  • increase venous capacitance (alpha blockers)
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9
Q

what are some types of antihypertensives

A
  • Diuretics
  • Blockers of Sympathetic N.S
    (sympathoplegics)
  • Blockers of RAS (RAAS)
  • Vasodilators
  • Calcium Channel Blockers
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10
Q

Diuretics

A
  • increase urine output and reduce blood volume, thus lowering CO
  • Can be used alone or * with other anti-hypertensives
  • Look at normal kidney functioning
  • Glomerulus: forms plasma filtrate
  • Proximal tubule:
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11
Q

What are some types of Diuretics?

A

Carbonic anhydrase inhibitors
Thiazide diuretics
Loop Diuretics/ High Ceiling diuretics
Potassium sparing

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12
Q

Carbonic anhydrase inhibitors

a type of diuretic

A

NOT VERY efficacious at lowering B.P
ex: Acetazolamide

  • work at proximal tubule to block CA
  • mostly for glaucoma & metabolic alkalosis

Effects:
decrease HCO3- reabsorption
alkaline urine
increased K+ excretion

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13
Q

Thiazide diuretics

A

INTERMEDIATE efficacy

  • Hydrochlorothiazide, chlorthalidone, and others
  • inhibit Na+Cl- symporter in distal tubule
  • increase K+ loss (Na-K exchanger in collecting duct)

Side effects:
Hypokalemia
Hyperuricemia (compete with uric acid for prom tubule secretion… can lead to gout)

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14
Q

Loop Diuretics/ High Ceiling Diuretics

A

MOST efficacious

  • Bumetanide, furosemide
  • inhibit Na-K-2CL transporter in asc. Loop
  • Cal lead to profound diuresis, but also to electrolyte imbalance

Side effects:
Hypokalemia, Hypocalcemia, Hypomagnesemia
Metabolic alkalosis (due to H+ loss)

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15
Q

Potassium Sparing

A

MILD efficacy

  • Amiloride, triamterene, spironolactone
  • act in collecting duct to decrease K+ and increase Na+ excretion (some compete with aldosterone)
  • Ofter used with Loop or Thiazide diuretics

Side effects:
Hyperkalemia (reduce K+ supplements)

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16
Q

What should you watch for using Diuretics?

A
  • Orthostatic hypotension
  • Tachycardia (reflex)
  • Increased vascular resistance (baroreflex)

** These are often used with other anti-hypersensitive (body may compensate for others by retaining water or sodium)

17
Q

Sympathetic System Nervous System Blockers

A

Alpha-2 agonists
Adrenergic neuron blockers
Alpha (alpha-1) blockers
Beta Blockers

18
Q

Alpha-2 agonists

A
  • Clonidine, guanabenz, methyldopa (not used too much as anti-hypertensives)
  • DECREASE sympathetic outflow
  • decrease NE release (reduce resistance)
  • decrease renin release (reduce resistance)
  • decrease HR and CO

** Can cause dry mouth, drowsiness, dizziness

19
Q

Adrenergic neuron blockers

A
  • Resperine, guanethidine
  • Prevent NE release (usually used with others or rarely for hypertension
  • Can cause orthostatic hypotension
20
Q

Alpha (alpha-1) blockers

A
  • Prazosin, Terazosin
  • Decrease resistance, increase v. capacitance
  • Can cause H2O & Na pretension (use w. diuretics); usually not used as mono therapy
  • ALSO: orthostatic hypo, dizziness, tachycardia
21
Q

Beta Blockers

A
  • Decrease HR, contractility, renin release (often first line agents)
  • B1/B2: Propranolol, timolol, nadolol (1x daily); pindolol and carvedilol also have sympathomimetic activity

B1 selective: metoprolol, atenolol (1x daily)

** Can cause bronchoconstriction (B2), some CNS effects (hallucinations, nightmares)

22
Q

RAS

A
  • Renin is released from juxtaglomerular cells of kidney, converts angiotensinogen to angiotensin I
  • Angio I is then converted to Angio II in the plasma and tissues by ACE (angiotensin converting enzyme)
  • ANG II acts at ATI receptors to cause vasoconstriction, Aldosterone release
  • ANG II acts on AT2 receptors, but has no strong effects (maybe dipsogenesis and vasodilation)
23
Q

Blockers of RAS

A
  1. Renin inhibitors:
    Aliskiren (similar to ACEI)
  2. ACE inhibitors
    - Captopril, enalapril, benazepril, lisinopril
    * * decrease TPR
    * * decrease aldo (promote NA excretion)
    * * increase renal blood flow (diuresis)

Can cause: Hypotension (not common) & dry cough (common)

3. Angiotensin receptor blockers (ARBs) 
(AT1 blockers)
- losartan, valsartan, candesartan
- similar, strong efficacy as ACE inhibitors 
- no dry cough side effect

** CAN NOT use ACE inhibitors or AT receptor blockers (or renin inhibitors) during pregnancy (And dilates umbilical arteries)

24
Q

Vasodilators

A

Dilate vascular smooth muscle (increase GC activity and cGMP)

Usually, if used, used in combination
a. arteriolar: hydralazine: can cause headache,
Lupus-like disorder
- Minoxidil: headache, hypertrichosis

b. arteriolar/venous dilators: nitroprusside
- only in emergency/ hypertensive crisis
- postural hypotension, reflex tachycardia

25
Q

Calcium Channel Blockers

A

Block calcium entry in vascular smooth muscle and cardiac tissue

Reduce TPR and (in some) CO

  • Nifedipine, felodipine, nicaradipine; verapamil, diltiazem
  • the dihydropyridines mostly impact peripheral tissue, while verapamil and diltiazem also impact the heart. Thus, they could also reduce CO as needed, but be unlikely to be used for left ventricular dysfunction

Side effects:
Orthostatic hypotension, tachycardia, dizziness, headache

26
Q

Anti-Hypertensives

A
  • most can cause hypotension and/or orthostatic hypotension
  • watch for exercise that increase peripheral vasodilation or muscle vasodilation
  • watch for loss of exercise tolerance w/ B-blockers
  • often prescribed now to improve lipid profile too
  • often use stepped care approach and/or poly pharmacy
27
Q

which Anti-Hypertensives

A

Stage 1: thiazides, ACEI or ARB, BB, CCB
Stage 2: usually combo of thiazide plus ACEI or ARB
Stage 3: as needed

Pharmacology (17 decks)

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