Hypertension Flashcards
Diseases that can increase BP
CKD CUSHINGS Coarctatation of the aorta OSA Parathyroid disease pheochromocytoma primary aldosteronism thyroid disease renovascular disease
Drugs that can increase BP
Corticosteroids NSAIDS Estrogen and caffeine decongestants-phenylephrine, pseudophedrine stimulants calcineruin inhibitors-cyclosprine, tacrolimus Erythropoietin illicit drugs foods etoh
Pathophysiology
- 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
Clinical presentation
- Occipital HA
- Visual disturbances
- fatigue
severe: stroke, dementia, retinopathy, LV hypertrophy, angina, MI, CKD, PAD
Routine labs to antihypertensive therapy
BUN, creatinine with EGF
- Lipid panel
- Fasting blood glucose
- serum electrolytes
- hgb and hct
- ECG
- ASCVD risk
First line antihtn
- Thiazides
- CCB
- ACEi
- ARBS
Secondary class Antihtn
- Diuretics (loop, potassium sparing)
- BB
- Alpha/Beta blockers
- Alpha 1 blockers
- Central alpha 2 agonists
- Direct vasodilators
- Direct renin inhibitors
Thiazides
- Chlorthalidone (preferred), hydrochlorothiazide, indapamide
- Consider using loop w/ resistant htn w/ compromised kidney function <30ml/min/1.73)
ACEi
-End in PRIL
MOA: Inhibit angiotensin converting enzyme. Blocks formation of angio II from angio I. Reduces breakdown of bradykinin
ACEi S/E
- Cough (common)
- Hyperkalemia
- Acute renal failure (consider holding therapy is SCr increases >30% from baseline
- Angioedema
ACEi Drug interactions
- NSAIDs (decrease BP control)
- Diuretics (excessive hypotensive effect)
- Potassium supplements
- Lithium
- Precaution in pregnancy
ARBs
- 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
ARBS s/e
dizziness, couhg, increase serum aminotransferase activity, neutropenia, hyperkalemia, angioedema
- Precaution in pregnancy
- Drug interactions (potassium sparing diuretic)
CCB: Dihydropyridines (DHP) & S/E
- Amlodipine, felodipine, isradipine, nicardipine, nifedipine, nislodipine
- S/E: HA, dizzy, peripheral edema, reflex tachy, gingival hyperplasia
CCB: Non-dihydropyridines (Non-DHP) & s/e
- 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
CCB MOA
Block inward movement of calcium ions across cells causing vascular smooth muscle relaxation.
CCB drug interactions
-hepatic enzyme inducers (rifampin, phenobarb, phyentoin, carbamazepine)
Diuretics
- Thiazides (hctz, chlorthialidone, indapamide, metolazone)
- Loop (furosemide, bumetanide, torsemide)
- K sparing (amiloride, triamterne, adlosterone antagonists, spironolactone, eplerenone)
Diuretics MOA of Thiazides
- 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
Diuretics MOA of Loop
Block sodium & chloride reabsorption in the Loop of Henle
Potassium-Sparing agents MOA
-Decrease both sodium reabsorption and potassium excretion in the distal tubule
Loops
-Most potent for diuresis-preferred for htn w/ CKD and symptomatic HF
Potassium Sparing
-Weak anthtn alone when used in combo with thiazides
Adrenergic Inhibitors
-Includes beta blockers, alpha-beta blockers, and alpha-1 receptor blockers
MOA of BB (adrenergic inhibitors)
-decrease cardiac output (cardiac β1 receptor blockade) and renin release (renal β2 receptor blockade)
MOA of alpha 1 receptor blockers (adrenergic inhibitors)
-block post-synaptic α1 receptors causing vasodilation
MOA of alpha-beta blockers (adrenergic inhibitors)
-possess properties of both β and α1 receptor blockers
BB classes: Cardioselective B1
Atenolol, Betaxolol, Bisoprolol, Metoprolol
-At higher doses may exacerbate asthma/COPD via B2 receptor blockade
BB classes: Non-cardioselective (B1, B2)
Nadolol, Propranolol, Timolol
BB classes: Cardioselective (B1) & Vasodilatory
Nebivolol
BB Classes: Intrinsic Sympathomimetic Activity (ISA)
Acebutolol (also cardioselective) Carteolol, Penbutolol, Pindolol
-Rarely indicated
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
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
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)
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
Alpha 1 receptor blockers
- Doxazosin, prazosin,
- MOA: peripheral vasculature, inhibit uptake of catecholamines in smooth muscles cells resulting in vasodilation
Alpha 1 receptor blockers S/E
orthostatic hypotension, first dose syncope (less with doxazosin), dizziness, weakness, palpitations, headache, drowsiness, anticholinergic effects
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.
S/E Renin Inhibitor
-Rash, increase uric acid levels, gout, cough, dose related GI effects (diarrhea, abdominal pain, dyspepsia, reflux)
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
Central Alpha-2 adrenergic agonists
- Clonidine, guanfacine, methyldopa
- MOA: Stimulate central alpha-2 receptors, inhibit efferent sympathetic activity, decrease CNS sympathetic outflow
Central Alpha 2 adrenergic agonists s/e
Drowsiness, sedation, dry mouth, fatigue, depression, orthostasis, withdrawal hypertension
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
Alpha-Beta Blockers
- Carvedilol, Labetalol
- MOA: non-selective beta & alpha-1 receptor blockade
- s/e: orthostatic hotn, dizziness, hepatotoxicity
- Precautions similar to BB
Direct Vasodilators
Hydralazine, minoxidil
-MOA: Cause direct vascular smooth muscle relaxation and vasodilation (primarily arteriolar)
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
Htn urgency and emergency
180/120
-Avoid rapid decrease
