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38 Cards in this Set

  • Front
  • Back
drugs that enters the CNS and causing decreased SANS outflow resulting in lowered BP and HR
a2 agonists:
Clonidine
Methyldopa
Adverse effects of clonidine
rebound HTN
sedation
adverse effects of methyldopa
hemolytic anemia (positive Coomb's test)
sedation
a2 agonist DOC during pregnancy
methyldopa
irreversibly blocks the vesicular monoamine transporter (VMAT) that normally transports free norepinephrine, serotonin, and dopamine from the cytoplasm of the presynaptic nerve terminal into storage vesicles for subsequent release into the synaptic cleft
reserpine
blocks the reuptake of norepinephrine and depletes the stores
Guanethidine
adverse effects of postganglionic neuron blockers: resperine and guanethidine
sedation, severe psychiatric depression
a1 antagonist
prazosin
adverse effects of prazosin
1st dose hypotension
drug of choice in patients with HTN and BPH
prazosin
two effects associated with B blockers
decrease cardiac output
decrease renin release
adverse effects of B blockers
bronchospasm seen in propanolol
avoid use in patients with SA/AV nodal dysfunction
raised risk of stroke in patients over 60
Effects of ACE inhibitors
blocks conversion of ATN I to ATN II
blocks inactivation of bradykinin which is also a vasodilators
Blocks ATN II receptor
Losartan
Adverse effects of ACE inhibitors
Hyperkalemia (decreased ENaC usage in DCT)
Teratogen - contraindicated in pregnancy
Cough and Angioedema - both due to increased bradykinin
Adverse effects of ATN II receptor blocker
Hyperkalemia
teratogen
Ca channel blockerd with greater vasodilatory effect than cardiacdepressent effect
Nifedipine
amlidopine
finoldipine
Ca channel blockers with combined vasodilatory and cardiodepressent action
Verapamil
Diltiazem
Which drugs should be avoided to use in combination with B-blockers
Verapamil and Diltiazem
**Can result in extreme cardiac depression
Adverse effects of Verapamil/Diltiazem
excessive cardiac depression
constipation
avoid in patients with cardiac conduction disturbances
Opens K channel in smooth muscle resulting in decreased Ca entry and smooth muscle relaxation
Minoxidil
increaes eNOS release causing arteriolar dilation
Hydralazine
associated with lupus-like syndrome
hydralazine
associated with hirsutism
Minoxidil
why should hydralazine/minoxidil not be used as monotherapies
because they trigger baroreceptor-mediated tachycardia and RAAS activation
*need to be used in combination with B-blockers and diuretics
Releases NO from drug molecule resulting in increased cGMP resulting in vasodilation of both arteries and veins
Nitroprusside
associated with cyanide toxicity
Nitroprusside
Drug of choice for HTN emergency
nitroprusside
First-line DOC for HTN always
Thiazide diuretics
physiologic axn of each:
a1, a2, B1, B2
a1 - increases IP3 and intracellular Ca leading to vasoconstriction
a2 - decreases cAMP leading to decreased NE release from presynaptic neurons or contracts vessels directly if postsynaptic
B1 - increases cAMP and intracellular Ca leading to increased HR and contractility of the heart
B2 - increased cAMP and intracellular Ca causing vasodilation
patient population that respond less well to ACE inhibitors
Blacks
Elderly
selective B1 blockers
atenolol
metoprolol
acebutolol - can be B-agonist at high concentrations
nonselective B blockers
propanolol
timolol
pindolol - can be B agonists at high concentrations
3 drugs associated with increased vascular compliance
thiazide diuretics
Nitrates
ACE inhibitors
Why would ACE inhibitors still help in people with low renin levels
because increase bradykinin availability
differentiate cardiovascular effects of amlidopine vs. nifedipine
amlidopine has no affect on contracility while nifedipine decreases contractility - both are good vasodilators
vasodilator least likely to induce orthostatic hypotension
hydralazine - only dilates arterioles, NOT veins
combined alpha and Beta blockers
carvedilol
labetalol