Pharmacotherapy of HTN Flashcards

1
Q

Epidemiology of HTN

A

1/3 adults in US have HTN

About 70% of people with MI, CVA, or heart failure have BP >140/90

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2
Q

Normal BP

A

<120/80

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3
Q

Pre-HTN

A

120-139/80-89

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4
Q

Stage 1 HTN

A

140-159/90-99

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5
Q

Stage 2 HTN

A

>160/100

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6
Q

CVD risk doubles with what increase in BP?

A

20/10

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7
Q

Evaluation of elevated BP

A
  1. Asses lifestyle and identify other CV RFs or concomitant disorders
  2. Reveal identifiable causes of high BP (primary vs secondary HTN)
  3. Asses the presence or absence of target organ damage
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8
Q

JNC 7 Major Cardiovascular Disease RFs

A

HTN

Tobacco Use

Obesity

Physical inactivity

DM

Dyslipidemia

Microalbuminuria

Age (55/65)

FHx of premature CVD (MI/sudden death)– 55/65

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9
Q

Definable causes of HTN

(secondary HTN)

A

Sleep apnea

Chronic kidney disease

Primary aldosteronism

Renovascular disease

Chronic steroid therapy/Cushings syndrome

Pheochromocytoma

Coarctation of the aorta

Thyroid or parathyroid disease

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10
Q

Medications that can cause HTN

A

NSAIDs

Corticosteroids

Oral contraceptives

Cocaine, amphetamines

Sympathomimetics

Erythropoieten

Licorice

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11
Q

Target Organ Damage

A

Heart: LV hypertrophy, angina or prior MI, prior coronary revascularization, heart failure

Brain: stroke/TIA

Nephropathy

Peripheral artery disease

Retinopathy

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12
Q

Goal of HTN therapy

A

Reduce CVD and renal morbidity and mortality

Achieve SBP goal

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13
Q

Blood pressure goals for uncomplicated HTN

A

<140/90

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14
Q

Blood pressure goals if also have DM, renal disease, CAD, CAD equivalents, Framingham score >10%, or left ventricular heart failure

A

<130/80

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15
Q

The Big 5: Lifestyle Modifications to Manage HTN

A
  1. Weight reduction
  2. DASH diet
  3. Decrease Sodium intake
  4. Physical activity
  5. Moderation of alcohol consumption
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16
Q

Pharm treatment decreases the risk of what?

A

clearly decreases the incidence of cardiovascular morbidity and mortality

Dec BP by 5-6 leads to 42% dec in stroke and 14% in CHD

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17
Q

Potential additive favorable and unfavorable effects of thiazide diuretics

A

Useful in slowing osteoporosis

Should be used cautiously with history of gout or hyponatremia

18
Q

Potential additive favorable and unfavorable effects of BBs

A

Useful in treating atrial tachyarrhythmias/fib, migraine, essential tremor, perioperative HTN

Avoid in pts with asthma, reactive airways disease, or second/third degree heart block

19
Q

Potential additive favorable and unfavorable effects of CCBs

A

Useful in Raynuad’s syndrome and certain arrhythmias

20
Q

Potential additive unfavorable effects of ACEI

A

Do not use in women who are pregnant or may become pregnant

Do not use if hx of angioedema

21
Q

Preferred Combos of synergistic antihypertensives

A

ACEI + thiazide

ACEI + DHP CCB

ARB + thiazide

ARB + DHP CCB

22
Q

NOT preferred combos of antihypertensives

A

ACEI + ARB

BB + ACEI or ARB

BB + NDHP CCB

BB + Central acting

23
Q

Follow up in pts being treated for HTN

A

Patients should return of f/u and adjustment of meds until goal is reached:

  • Check BP 2-4 weeks after start or change in dose, assess response after 4-6wks
  • More frequent visits for stage 2 or if comorbid conditions

After BP at goal, f/u at 3-6 month intervals

Serum potassium and creatinine montitored 1-2times/year

May come in more frequently if other comorbid conditions

24
Q

Monitoring of pts being treated for HTN

  • Diuretics
  • Aldosterone antagonists
  • ACEI
  • ARBs
  • CCB
  • BB
A

Diuretics

  • K, Mg, UA, Cr, Na, BG

Aldosterone antagonists, ACEI, ARBs

  • Cr, K

CCB, BB

  • HR
25
Q

Antihypertensive Therapy Adherence Issues

A

One in four will take taking med withing 6 months. To improve this:

  1. Educate pts why its import to control BP
  2. Identify problems with drug tolerance as early as possible
  3. Address increased urination with diuretics; use low doses and advise that limiting salt will help decrease urination and improve thiazide efficiency
  4. Use generics or combo products to dec cost
26
Q

If patient is not responding to treatment, check causes of resistant HTN

A

Improper BP measurement

Volume overload

  • Excessive sodium intake
  • Volume retention from kidney disease
  • Inadequate diuretic therapy

Medication

  • Nonadherence
  • Inadequate doses
  • Drug interactoins

Associated conditions

  • Obesity, excess EtOH intake
  • Secondary HTN
27
Q

HTN Urgency

A

DBP > 130mmHg but no target organ damage

Can use oral agents

Reduce DBP to 100 mmHg within 24hrs

28
Q

HTN Emergency

A

DBP > 130mmHg and target organ damage present

Goal: reduce DBP to 110mmHg in 30 minutes, then to 100 within 12-24 hrs

Requies IV drug therapy: nitropusside, nicardipine, fenoldopam, nitroglycerin, enaliprilat, hydralazine, diazoxide

29
Q

What is the inital drug of choice for most patients, either alone or in combination?

A

Thiazide diuretics

30
Q

Classes of diuretics

A

Thiazides

Potassium sparing

Loop

31
Q

Thiazide Diuretics

Chorthalidone (Thalidone)

A

Work at distal tubule to

  • Inc Na excresion
  • Dec plasma volume and CO

Adverse Effects

  • Hypokalemia and hypomagnesemia
  • Hyperuricemia
  • Hyperglycemia

Effective in renal insufficiency, unless really severe (SCr)

32
Q

**Potassium Sparing Diuretics **

Spironolactone

A

Weak diuretic effects at collecting duct

Used with thiazides because will offset hypokalemia by conserving potassium

If used with ACEI may cause hyperkalemia

May cause gynecomastia because aldosterone antagonist

33
Q

**Loop Diuretics **

Furosemide

A

More potent diuretic effect at loop of Henle to

  • Inc Na excretion
  • Dec plasma volume

More effective than thiazide in pts with significant heart failure or renal insufficiency

Greater risk for hypokalemia, hypomagnesemia, overdiuresis, and metabolic alkalosis

34
Q

**ACE Inhibitors **

Lisinopril (Prinivil, Zestril)

A

Mechanism of Action

  • By inhibiting ACE, they…
  • Block formation of Angiotensin II (powerful vasoconstrictor)
  • Dec Aldosterone (dec Na retention)
  • Inc Bradykinin (vasodilator)

May cause hyperkalemia (especially with potassium sparing diuretic). Consider stopping diuretic to avoid excessive hypotension.

Adverse effects:

  • cough, hypotension, rash, angioedema, and acute renal failure in pts with bilateral renal artery stenosis
  • Do not use in pregnant women
35
Q

Angiotensin II Receptor Blockers (ARB)

Losartan

A

By blocking the angiotensin II receptor, they

  • cause vasodilation
  • Dec aldosterone (dec Na retention)

Adverse effects: Same as ACEI, except no cough or rash (hypotension, angioedema, acute renal failure)

Use in pts who cannot tolerate ACEI

36
Q

**Direct Renin Inhibitors **

Aliskiren

A

By directly inhibiting renin, they lead to

  • Vasodilation
  • Dec aldosterone (dec Na retention)

Adverse effects:

  • Diarrhea
  • Cough, angioedema
  • Do not use in pregnancy

ESPENSIVE

37
Q

**Calcium Channel Blockers **

Class effects

A

Block intracellular influx of calcium therby causing vascular smooth muscle relaxation or vasodilation

Adverse side effects:

  • headache
  • dizziness
  • peripheral (ankle) edema
  • eczema in elderly
  • Do not use in pts with HF because dec’s contractile force of heart
38
Q

Calcium Channel Blockers–Dihydropyridine class

**Amlodipine **

A

Contractility (-)

Peripheral Vasodilation (+++) Strong

May cause tachycardia–because heart compensating for fluid accumulating in LE

39
Q

Calcium Channel Blockers–Non-dihydropyridine Class

Diltiazem and Verapamil

A

Diltiazem

  • Contractility (- -)
  • Peripheral Vasodilation (++)

Verapamil

  • Contractility (- - -)
  • Peripheral Vasodilation (++)
  • May increase digoxin levels significantly,
  • May cause constipation

Both slow down HR, so use caution in pts with bradycardia, heart block, or sinus node disease

40
Q

**Beta Blockers **

Class adverse effects and comments

A

Beta 2 blockade may aggrave asthma

CI in patients with bradycardia, heart block, and sinus node disease due to decreased HR

Caution use in pts with uncontrolled HF

May cause:

  • fatigue
  • bradycardia
  • aggrevate PVD
  • masks signs of hypoglycemia
  • insomnia, nightmares

Do not stop abruptly in pts with IHD

41
Q

Beta Blockers Classes and MOA

Non-Selective (Propranolol)

Cardioselective (Atenolol, Metoprolol)

Mixed alpha-beta (Labetalol)

Intrinsic Sympathomimetic Activity (ISA) (Acebutolol)

A

Non-Selective (Propranolol)–beta 1 and 2

  • Block beta 1 in heart to…
  • Dec HR and CO, therefore dec BP
  • Also dec plasma renin activity

Cardioselective (Atenolol, Metoprolol)

  • Same as non-selective

Mixed alpha-beta (Labetalol)

  • Same as beta blocker with additional alpha blocking effects (vasodilation)

Intrinsic Sympathomimetic Activity (ISA) (Acebutolol)

  • Same, but only indicated for HTN
  • Does not confer cardioprotective effects
42
Q

Second line agents for HTN

A

Centrally Acting alpha-2 Agonists

Peripherally-acting Adrenergic Antagonists

Direct Vasodilators

alpha-1 Receptor Blockers