Anti Hypertensive Flashcards
What is essential hypertension
Without a cause, 90% of cases
How does reduced renal blood flow increase blood pressure
RAAS activated, more renin, more angiotensin 2, increase peripheral resistance
Decrease gfr, RAAS, Nat+ and h2o retention, increase cardiac output
Mechanism of thiazides
Diuretic ie excrete more sodium to increase water excretion
At DCT, blocks Na/Cl cotransporter to block NaCl reabsorption, increased ca reabsorption
At PCT, increased urea reabsorption (diuretic induced hyperuricemia)
How do NSAIDS interfere with thiazide
Action of thiazide dependent on renal prostaglandin synthesis which NSAIDS reduce
What are the adverse effects of thiazide
Hypokalemia
Hyponatremia (block na absorption)
Hyperglycemia (diabetes)
Hyperlipidemia
Hyperuricemia (gout; pct increased urea reabsorption)
Hypercalcemia (DCT)
Thiazides are contraindicated in what patients
Patients with diabetes, hyperlipidemia, gout
Action of loop diuretics
Work at the ascending loop (25% of Na reabsorption vs 5% at DCT hence more potent than thiazide)
Inhibit na/k/cl transporter
What do beta blockers do to reduce hypertension
B blockers decrease rate and force, decreasing cardiac output, hence decreasing bloo pressure
Examples of b blockers
Propranolol (non selective heart and lungs), atenolol (b1 selective)
When are beta blockers used
Hypertension, angina, following MI (reduce cardiac function for heart to relax)
What do angiotensin inhibitors do
Inhibit angiotensin converting enzyme
Hence no conversion of Ang 1 to Ang 2, which is responsible for vasoconstriction (increase peripheral vascular resistance) and aldosterone which increases na/h2o retention
Hence bradykinin not broken down. Bradykinin able to form more NO and PG, causing vasodilatation and reducing bp
In which patients are ace inhibitors contraindicated
Pregnant women
What are the adverse effects of ace inhibitors
Severe hypotension, hyperkalemia, angioedema, dry cough due to bradykinin accumulation, acute renal failure
