Hypertension Flashcards
Diuretic agents mode of action
Drugs that increase excretion rate of water
- mechanism secondary to increased excretion of sodium
- decrease extracellular fluid volume without reducing plasma volume
Types of diuretics
- Thiazides
- loop diuretics
- potassium sparing diuretics
Thiazide mechanism
Inhibt NaCl symporter in cortical diluting site of the distal convoluted tubule
- Increase Na, Cl, and K excretion
- decrease Ca excretion
Therapeutic uses of thiazides
Edema
Hypertension: first choice in treatment of mild to moderate hypertension
Major side effects of thiazides
- Increased distal Na delivery leads to increased K excretion
- Elevation of plasma renin, Angiotensin II, and aldosterone due to volume and sodium depletion
- may result in hypokalemia
loop diuretics mechanism of action
- inhibit Na-K-2Cl symporter in thick ascending limb
- increase Na,Cl excretion
- increase distal K excretion in exchange for Na reuptake
loop diuretics therapeutic use
- Acute pulmonary edema
- edema for cardiac, hepatic and renal causes
- Hypertension refractory to other diuretics
Side effects of loop diuretics
- electrolyte abnormalities (hypokalemia)
- Worsening of incontinence
- drugs interaction(NSAIDs and antibiotics)
potassium sparing diuretics mechanism of action
- Inhibit Na reabsorption by principal cells of late distal tubules and collecting ducts
- Decrease K excretion
- Act directly on epithelial Na channel(amiloride)
- act indirectly by antagonism of aldosterone a mineralocorticoid receptor(spironolactone)
Indications of Potassium sparing diuretics
- both types used in combination with thiazides or loop diuretics to decrease hypokalemia
- Aldosterone receptor antagonists in combo with loop diuretics and ACE inhibitors in heart failure to enhance survival
List the types of sympatholytic
- β blockers
- CNS Alpha-2 agonists
- Selective α1 adrenoceptor antagonists
How do the β-blockers work?
- Block cardiac β1 receptors –> decreases HR, contractility and cardiac output
- Block renal β1 receptors–> Decrease plasma renin, ANG II, and TPR
How is a β-blocker useful for MI
Antiarrhythmic, Anti-ischemic, Antiatherogenic, Reverses cardiac remodeling
Why are CNS Alpha-2 agonists not used as a first line?
Can be troublesome in elderly patients because orthostatic hypertension and CNS effects
How do selective α1 adrenoceptor antagonists work
They block vascular α1 receptors causing vasodilatation, decreased TPR and MAP
When are selective α1 adrenoceptor antagonists used?
The yare not used as a fir line for antihypertensive therapy
maybe usedful as adjunctive therapy in resistant hypertension
Adverse effects-Tachycardia, Don’t use in CHF
Types of vasodilator agents
- Calcium channel blockers (CCBs)
- alpha-1 antagnoists
Target tissue eor CCBs
- Arterial Smooth muscle
- Cardiac tissue
Arterial smooth muscle CCB action and adverse effects
CCB block L-type voltage gated calcium channels and therefore prevent calcium entry into arterial VSM
-Adverse effects: reflex tachycardia,’ ankle edema due to selective arterial vaso dilatation
Cardiac tissue CCB action and drug interaction
- “non-dihydropyridine” CCBs block calcium entry into myocytes
- drug interactions: may precipitate AV block with drugs that decrease AV node conduction(e.g., Beta-blockers)
Direct acting vascular smooth muscle (vasodilator) action
- Binds to and activates potassium channels
- evokes potassium efflux and cell hyperpolarization
- prevents calcium-mediated smooth muscle contraction and evokes vasodilation
- -Triggers baroreflex evoked tachycardia and vasoconstriction -used in combination with beta blockers
Agents affecting RAAS
- ACe inhibitors(ACEI)
- AT1 antagonists(ARBs)
- Aldosterone antagonists
Main types of ACE inhibitors
- Sulfhydryl-containing
- Dicarboxyl-containing
- Phosphorous-containing
Primary method of clearance of ACE inhibitors
Cleared by kidney
