Hypertension Pharmacology Flashcards
1
Q
Targets of antihypertensive therapy
A
- fluid balance (sodium & water)
- renin angiotensin system (RAS)
- central & peripheral control of SNS
- tone of vascular smooth muscle
2
Q
Classes of antihypertensive drugs
A
- Diuretics
- RAS blockers
- Ca+ channel blockers
- Sympatholytics
- Vasodilators
3
Q
Diuretics: initial & long term use
A
- initial use: decrease extracellular fluid volume and CO
- long term use: decrease vascular resistance; decreased response of VSM to vasoconstrictors, impaired release of NE/Epi
- cellular mechanism: decrease in VSM Na+ & secondarily decrease in Ca2+
4
Q
Diuretics: major use & adverse effects
A
- use: alone of in combination, use in treatment of heart failure
- adverse effects: most deplete K+ (except for K+ sparing diuretics)
5
Q
Thiazide diuretics
A
- chlorothiazide & hydrochlorothiazide
- mechanism: block Na+Cl- symporter in distal convoluted tubule
- effect: moderate diuresis, reduced by NSAIDs
- adverse effects: hypkalemia, decreased uric acid & calcium excretion, thiazides & sulfonamides cross reactivity
6
Q
High ceiling LOOP diuretics
A
- furosemide, bumetanide, torsemide
- mechanism: block Na, K+2Cl- co transporter in thick ascending limb of Loop of Henle
- effect: use with edema, MOST EFFECT DIURETICS
- adverse effects: hyokalemia, decreased uric acid excretion, deafness
7
Q
Aldosterone receptor blockers
A
- spironolactone & eplerenone
- mechanism: collecting duct; block Na+ & water reabsorption, K+ sparing
- use: resistant HTN, CHF HTN
- adverse effects: HYPERKALEMIA*** not hypo
8
Q
Potassium sparing diuretics
A
- triameterene, amiloride
- mechanism: late distal tubule & collecting duct Na+ channel blockers
- diuretic effect in combo w/ thiazides: mild diuresis, weak HTN effect
- adverse effects: HYPERKALEMIA
9
Q
RAS inhibitors & HTN
A
- blood levels of drugs & renin don’t correlate w/ effects
- non renal RAS: vascular & brain
- ACE/aldosterone escape: increased renin release, loss of negative feedback, RAAS and non RAAS mediated mechanism
10
Q
Angiotensin II actions
A
- vasocontriction–increasing blood pressure
- stimulate thirst & secretion of aldosterone/ADH, increasing fluid/Na+
- increase SNS: increasing cardiac activity and PVR
- cardiac and vascular remodeling
- feedback inhibition of renin release
11
Q
ACE inhibitors
A
- captopril, enalapril, lisinopril, fosinopril (PRILs)
- mechanism: block conversion of angiotensin I to II, elevate bradykinin levels, decreased PVR, decreased aldosterone (increasing Na+/water excretion), reverse or reduce CV remodeling, increase plasma renin & renin activity
12
Q
ACE inhibitors: use & adverse effects
A
- use: mild/moderate HTN & heart failure
- adverse effects: DRY COUGH (20%), hyperkalemia, angioedema, hypotension, rash, pregnancy problems,
13
Q
Angiotensin receptor antagonists (ARBs)
A
- losartan, valsartan, candesartan, irbesartan
- mehcanism: AT1 antagonist, vasodilation, increased Na+/water excretion, reduced plasma volume & cellular hypertrophy, increased plasma renin & renin activity
14
Q
ARBs use and adverse effects
A
- use: HTN & heart failure
- adverse effects: hypotension, cough or angioedema but less than ACEIs (don’t start w/ this b/c don’t have as good long term effects, not used in combo w/ ACEIs), hyperkalemia, fetal renal toxicity
15
Q
Renin inhibitor
A
- aliskiren
- mechanism: direct competitive inhibitor, increase plasma renin but NOT renin activity
- use: HTN (not first line since long term CV outcome unclear)
- adverse: diabetic/renal impairment, hypotension, dry cough, angioedema, hyperkalemia