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Pharmacology > Hypertension > Flashcards

Hypertension Flashcards

(47 cards)

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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

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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

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A

Block sodium & chloride reabsorption in the Loop of Henle

21
Q

Potassium-Sparing agents MOA

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A

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

22
Q

Loops

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A

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

23
Q

Potassium Sparing

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A

-Weak anthtn alone when used in combo with thiazides

24
Q

Adrenergic Inhibitors

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A

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

25
MOA of BB (adrenergic inhibitors)
-decrease cardiac output (cardiac β1 receptor blockade) and renin release (renal β2 receptor blockade)
26
MOA of alpha 1 receptor blockers (adrenergic inhibitors)
-block post-synaptic α1 receptors causing vasodilation
27
MOA of alpha-beta blockers (adrenergic inhibitors)
-possess properties of both β and α1 receptor blockers
28
BB classes: Cardioselective B1
Atenolol, Betaxolol, Bisoprolol, Metoprolol | -At higher doses may exacerbate asthma/COPD via B2 receptor blockade
29
BB classes: Non-cardioselective (B1, B2)
Nadolol, Propranolol, Timolol
30
BB classes: Cardioselective (B1) & Vasodilatory
Nebivolol
31
BB Classes: Intrinsic Sympathomimetic Activity (ISA)
Acebutolol (also cardioselective) Carteolol, Penbutolol, Pindolol -Rarely indicated
32
BB s/e
-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
BB drug interactions
- 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
BB contraindications and precautions
- 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
Alternate Therapies
- 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
Alpha 1 receptor blockers
- Doxazosin, prazosin, | - MOA: peripheral vasculature, inhibit uptake of catecholamines in smooth muscles cells resulting in vasodilation
37
Alpha 1 receptor blockers S/E
orthostatic hypotension, first dose syncope (less with doxazosin), dizziness, weakness, palpitations, headache, drowsiness, anticholinergic effects
38
Renin Inhibitor (Aliskiren)
- 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
S/E Renin Inhibitor
-Rash, increase uric acid levels, gout, cough, dose related GI effects (diarrhea, abdominal pain, dyspepsia, reflux)
40
Drug interactions of Renin inhibitors
- 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
Central Alpha-2 adrenergic agonists
- Clonidine, guanfacine, methyldopa | - MOA: Stimulate central alpha-2 receptors, inhibit efferent sympathetic activity, decrease CNS sympathetic outflow
42
Central Alpha 2 adrenergic agonists s/e
Drowsiness, sedation, dry mouth, fatigue, depression, orthostasis, withdrawal hypertension
43
Central Alpha 2 adrenergic agonists Drug interactions and precautions
-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
Alpha-Beta Blockers
- Carvedilol, Labetalol - MOA: non-selective beta & alpha-1 receptor blockade - s/e: orthostatic hotn, dizziness, hepatotoxicity - Precautions similar to BB
45
Direct Vasodilators
Hydralazine, minoxidil | -MOA: Cause direct vascular smooth muscle relaxation and vasodilation (primarily arteriolar)
46
Direct vasodilators s/e
Headache, reflex tachycardia, aggravation of angina, fluid retention; nasal congestion, dizziness; drug induced Lupus syndrome, hepatitis (hydralazine); Hirsutism (Minoxidil), possible pericardial effusion
47
Htn urgency and emergency
180/120 | -Avoid rapid decrease

Pharmacology (24 decks)

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