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Pharmacology > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Diseases that can increase BP

A 
CKD
CUSHINGS
Coarctatation of the aorta 
OSA
Parathyroid disease
pheochromocytoma
primary aldosteronism
thyroid disease
renovascular disease
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2
Q

Drugs that can increase BP

A 
Corticosteroids
NSAIDS
Estrogen and caffeine
decongestants-phenylephrine, pseudophedrine
stimulants
calcineruin inhibitors-cyclosprine, tacrolimus
Erythropoietin 
illicit drugs
foods 
etoh
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3
Q

Pathophysiology

A
  • Malfunctions in RAAS
  • Vasodepressor mechanisms
  • neuronal mechanisms
  • defects in peripheral autoregulation
  • Disturbances in sodium, calcium; and natriuretic hormones
  • SBP-achieved during cardiac contraction
  • DBP-achieved after contraction when the chambers are filling
  • Difference between is the pulse pressure and measures arterial wall tension
  • MAP-average pressure throughout the cardiac cycle
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4
Q

Clinical presentation

A
  • Occipital HA
  • Visual disturbances
  • fatigue
    severe: stroke, dementia, retinopathy, LV hypertrophy, angina, MI, CKD, PAD
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5
Q

Routine labs to antihypertensive therapy

A

BUN, creatinine with EGF

  • Lipid panel
  • Fasting blood glucose
  • serum electrolytes
  • hgb and hct
  • ECG
  • ASCVD risk
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6
Q

First line antihtn

A
  • Thiazides
  • CCB
  • ACEi
  • ARBS
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7
Q

Secondary class Antihtn

A
  • Diuretics (loop, potassium sparing)
  • BB
  • Alpha/Beta blockers
  • Alpha 1 blockers
  • Central alpha 2 agonists
  • Direct vasodilators
  • Direct renin inhibitors
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8
Q

Thiazides

A
  • Chlorthalidone (preferred), hydrochlorothiazide, indapamide
  • Consider using loop w/ resistant htn w/ compromised kidney function <30ml/min/1.73)
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9
Q

ACEi

A

-End in PRIL

MOA: Inhibit angiotensin converting enzyme. Blocks formation of angio II from angio I. Reduces breakdown of bradykinin

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10
Q

ACEi S/E

A
  • Cough (common)
  • Hyperkalemia
  • Acute renal failure (consider holding therapy is SCr increases >30% from baseline
  • Angioedema
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11
Q

ACEi Drug interactions

A
  • NSAIDs (decrease BP control)
  • Diuretics (excessive hypotensive effect)
  • Potassium supplements
  • Lithium
  • Precaution in pregnancy
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12
Q

ARBs

A
  • End in ARTAN
  • MOA: Inhibit binding of angiotensin II to AT-1 receptors in blood vessels and other tissues causing vascular smooth muscle relaxation
  • Increased salt and water excretion, reduced plasma volume, and decreased cellular hypertrophy. – Inhibit the raas more completely and selectively than ACEI
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13
Q

ARBS s/e

A

dizziness, couhg, increase serum aminotransferase activity, neutropenia, hyperkalemia, angioedema

  • Precaution in pregnancy
  • Drug interactions (potassium sparing diuretic)
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14
Q

CCB: Dihydropyridines (DHP) & S/E

A
  • Amlodipine, felodipine, isradipine, nicardipine, nifedipine, nislodipine
  • S/E: HA, dizzy, peripheral edema, reflex tachy, gingival hyperplasia
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15
Q

CCB: Non-dihydropyridines (Non-DHP) & s/e

A
  • Diltiazem
  • Verapamil
  • Wil block calcium movement across cells as well as block slow channels in the heart, reducing HR and can produce a block
  • Can cause rash (lupus like)
  • Can cause constipation, AV block, bradycardia, heart failure
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16
Q

CCB MOA

A

Block inward movement of calcium ions across cells causing vascular smooth muscle relaxation.

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17
Q

CCB drug interactions

A

-hepatic enzyme inducers (rifampin, phenobarb, phyentoin, carbamazepine)

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18
Q

Diuretics

A
  • Thiazides (hctz, chlorthialidone, indapamide, metolazone)
  • Loop (furosemide, bumetanide, torsemide)
  • K sparing (amiloride, triamterne, adlosterone antagonists, spironolactone, eplerenone)
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19
Q

Diuretics MOA of Thiazides

A
  • Block reabsorption of sodium & chloride in the early distal tubule
  • During chronic therapy, thiazides decrease peripheral vascular resistance via arteriolar smooth muscle, lowering blood pressure
20
Q

Diuretics MOA of Loop

A

Block sodium & chloride reabsorption in the Loop of Henle

21
Q

Potassium-Sparing agents MOA

A

-Decrease both sodium reabsorption and potassium excretion in the distal tubule

22
Q

Loops

A

-Most potent for diuresis-preferred for htn w/ CKD and symptomatic HF

23
Q

Potassium Sparing

A

-Weak anthtn alone when used in combo with thiazides

24
Q

Adrenergic Inhibitors

A

-Includes beta blockers, alpha-beta blockers, and alpha-1 receptor blockers

25
Q

MOA of BB (adrenergic inhibitors)

A

-decrease cardiac output (cardiac β1 receptor blockade) and renin release (renal β2 receptor blockade)

26
Q

MOA of alpha 1 receptor blockers (adrenergic inhibitors)

A

-block post-synaptic α1 receptors causing vasodilation

27
Q

MOA of alpha-beta blockers (adrenergic inhibitors)

A

-possess properties of both β and α1 receptor blockers

28
Q

BB classes: Cardioselective B1

A

Atenolol, Betaxolol, Bisoprolol, Metoprolol

-At higher doses may exacerbate asthma/COPD via B2 receptor blockade

29
Q

BB classes: Non-cardioselective (B1, B2)

A

Nadolol, Propranolol, Timolol

30
Q

BB classes: Cardioselective (B1) & Vasodilatory

A

Nebivolol

31
Q

BB Classes: Intrinsic Sympathomimetic Activity (ISA)

A

Acebutolol (also cardioselective) Carteolol, Penbutolol, Pindolol
-Rarely indicated

32
Q

BB s/e

A

-Pulmonary, Bronchospasm
-Cardiovascular: Bradycardia
fatigue, reduced exercise tolerance, decreased AV node conduction, aggravation of peripheral arterial insufficiency
- CNS • Insomnia, vivid dreams or hallucinations, depression
-Metabolic: Hypertriglyceridemia, slight decrease in HDL,
-Mask symptoms of and delay recovery from insulin-induced hypoglycemia (non-selective > selective agents)
-Other-sexual dysfunction

33
Q

BB drug interactions

A
  • Antidiabetic Agents - BB may prolong hypoglycemic reactions, blunt hypoglycemic-induced tachycardia
  • NSAIDS - decrease b-blocker effect
  • Rifampin, phenobarbital (hepatic enzyme inducers) decrease b-blocker serum levels
34
Q

BB contraindications and precautions

A
  • Contraindications: 1st degree heart block, or sick sinus syndrome; severe sinus bradycardia; bronchospastic disease
  • Precautions: Acute HF with systolic dysfunction; Diabetes; peripheral vascular disease; physically active patients
  • Avoid abrupt withdrawal (may exacerbate angina or cause MI)
35
Q

Alternate Therapies

A
  • Add-on in patients who are being treated with combination therapy that includes a first line antihypertensive
  • Alpha-1 Receptor Blockers
  • Aliskiren (only direct renin inhibitor)
  • Central A-2 Agonist
  • Direct Arterial Vasodilator
36
Q

Alpha 1 receptor blockers

A
  • Doxazosin, prazosin,

- MOA: peripheral vasculature, inhibit uptake of catecholamines in smooth muscles cells resulting in vasodilation

37
Q

Alpha 1 receptor blockers S/E

A

orthostatic hypotension, first dose syncope (less with doxazosin), dizziness, weakness, palpitations, headache, drowsiness, anticholinergic effects

38
Q

Renin Inhibitor (Aliskiren)

A
  • binds renin, reducing conversion of angiotensinogen to angiotensin I, the first & rate limiting step in the renin-angiotensin-aldosterone system.
  • End result is ↓ levels of angiotensin I, angiotensin II & aldosterone, thereby decreasing BP.
39
Q

S/E Renin Inhibitor

A

-Rash, increase uric acid levels, gout, cough, dose related GI effects (diarrhea, abdominal pain, dyspepsia, reflux)

40
Q

Drug interactions of Renin inhibitors

A
  • Should not be used in combination with ACE or ARB (higher risk of adverse effects without decreasing BP)
  • Ketoconazole and Atorvastin may increase Aliskiren levels
  • Aliskiren may decrease furosemide levels
41
Q

Central Alpha-2 adrenergic agonists

A
  • Clonidine, guanfacine, methyldopa

- MOA: Stimulate central alpha-2 receptors, inhibit efferent sympathetic activity, decrease CNS sympathetic outflow

42
Q

Central Alpha 2 adrenergic agonists s/e

A

Drowsiness, sedation, dry mouth, fatigue, depression, orthostasis, withdrawal hypertension

43
Q

Central Alpha 2 adrenergic agonists Drug interactions and precautions

A

-Drug interactions: Tricyclic antidepressants (antihypertensive effects)
BB (­ severity of clonidine withdrawal). MAO inhibitors (may cause htn)
-Precautions: Don’t d/c abruptly (rebound htn), avoid w/ non-compliant patients, long-term use results in Na and water retention

44
Q

Alpha-Beta Blockers

A
  • Carvedilol, Labetalol
  • MOA: non-selective beta & alpha-1 receptor blockade
  • s/e: orthostatic hotn, dizziness, hepatotoxicity
  • Precautions similar to BB
45
Q

Direct Vasodilators

A

Hydralazine, minoxidil

-MOA: Cause direct vascular smooth muscle relaxation and vasodilation (primarily arteriolar)

46
Q

Direct vasodilators s/e

A

Headache, reflex tachycardia, aggravation of angina, fluid retention; nasal congestion, dizziness; drug induced Lupus syndrome, hepatitis (hydralazine); Hirsutism (Minoxidil), possible pericardial effusion

47
Q

Htn urgency and emergency

A

180/120

-Avoid rapid decrease

Pharmacology (24 decks)

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