hypertension drugs Flashcards
beta blockers. give 2 examples nature action consequences S/Es
most effect on the heart.
proponolol – non selective beta antagonist B1 and B2 - used in HTN, arrhythmias and angina – cross BBB hence central effects -> nightmares, depression and insomnia
atenolol - cardioselective B1> B2 no central effect!
nature: beta adrenergic receptor antagonist
action: B1: act on heart affecting rate and force of contraction
B2: act on smooth muscles of blood vessels
consequences: gradual fall in BP, reduction in renin release, reduction of SNS activity
S/Es: bronchoconstriction exercise-induced hypoglycemia bradycardia cardiac failure fatigue, depression
what are the 7 groups of antihypertensive drugs used?
beta blockers alpha blockers calcium channel blockers AC-inhibitors angiotensin receptor antagonist vasodilators diuretics
explain alpha blockers give examples nature action consequence Side effects
nature: alpha adrenergic receptor antagonist
non-selective alpha antagonist:phenoxybenzanine
selective: prazosin (used only in severe HTN)
action: A1 - constrict SM BV and A2: constrict/dilate SM BV
consequence: vasodilator and reduce peripheral vascular resistance
S/Es: postural hypotension, dizziness, weakness and fatigue
calcium channel blockers 2 examples action consequence S/Es
nifidepine (SM)
verapamil (heart and SM)
action: binds to alpha subunit of L-type Ca channels
reduce the entry of Ca, (Ca)i reduced hence results in generalised arterial vasodilation –> reduce peripheral vascular resistance (PVR)
main effects on heart and smooth muscles
reduce force and rate of contraction – reduction of CO
S/Es:
headache, ankle swelling and constipation
ACE-inhibitor 3 examples nature action consequence and effects of bradykinin S/Es
captopril, lisinopril, ramipril
acts on: drugs mimic angiotensin I and competitively binds to ACE active site.
inhibits the conversion of AGI–>AGII
AGII effects:
- salt retension - via aldosterone secretion and Na reabsorption
- vasoconstriction - directly increase SNS noradrenaline which increases PVR and hence BP
- effects on bradykinin enhanced by ACE-I - ACE inactivates bradykinin and hence w ACE-I, no inactivation of bradykinin
bradykinin – (1)cause secretion og PGI2 and PGE2 (2) vasodilator –> reduce BP
hence effects/consequences of ACE-I
- reduce water retension hence reduce BV and BP
- reduce cardiac load – good for heart failure
affect capacitance and resistance vessels through vasodilation
S/Es:
- persistent dry cough (bradykinin)
- poor renal perfusion in renal artery stenosis
- hyperkalemia esp w renal failure
- rash and taste disturbacnes (esp w higher doses)
angiotensin receptor antagonist blockers 2 examples action consequence S/Es
lostartan, valsartan
used in patients intolerant to ACE-I
blocks the receptor from mediating effects of angiotensin II
AGII effects
1) salt retention via aldosterone secretion and Na reabsorption
2) directly increase SNS via noradrenaline – increase PVR and hence BP
consequence: similar to AC-I
water retention hence reduce BP
reduce cardiac load w reduced BV
affect capacitance and resistance vessels
just as effective as ACE-I
no dry cough
hyperkalemia
rash and taste disturbances
vasodilators - 3 types and the 3 different actions – 1 consequence and the different SEs
nitroprusside – intensive care unit, ST usage
- release of NO – reduce AP propagation and hence contraction
reflex tachycardia and hypotension
minoxidil – severe HTN and pregnancy
- open K channel -> reduce AP propagation
- severe tachycardia
hydralazine – pregnancy and HTN
- inhibit intracellular Ca release - reduce AP propagation
- lupus like syndrome
diuretics –2 types give short explanation
1) thiazides - eg hydrochlorothiazide - antagonist
block Na/Cl symporter
reduce BV and reduce PVR
toxicity - K depletion, alkolosis
2) loop diuretics - eg furosemide
antagonist - block Na/K/2Cl symporter
reduce BV and reduce PVR
K depletion and hypokalemia
