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46 Cards in this Set

  • Front
  • Back
baroreceptor reflex
sensors in the carotid sinus that can detect changes in blood pressure homeostasis, involves both parasympathetic and sympathetic control
essential hypertension
elevated BP with an unknown origin
false transmitter
substances stored in vesicles that are released into the synaptic cleft but do not have a full true effect, (ocampine w/ noepinephrine)
orthostatic hypertension
elevated BP when in upright position
postganglionic neuron blocker
blocks actions in postganglionic neurons
rebound hypertension
where removal of an antihypertensive drug causes blood pressure to rise above original levels
reflex tachycardia
when BP is lowered to a point where baroreceptor reflex causes an increase in heart rate
stepped care
adding a variety of treatment options gradually as opposed to all at once
two types of diuretics
thiazide, loop diuretics
with a thiazide, what is achieved at a lower dose, maximum antihypertensive effect or diuretic effect
maximum antihypertensive effect
what do sympathoplegic drugs affect
sympathetic control of cardiovascular function
how do alpha 2 selective agonists work
decrease in sympathetic outflow by activation of A2 receptors in the CNS
how do clonidine and methyldopa reduce blood pressure
by reducing vascular resistance or cardiac output, or both
what is the major compensatory response of A2 selective agents
increased salt retention
what is the major side effect with A2 selective agents associated with discontinuation of the drug
severe rebound hypertension, drug must be stepped down
what is one major side effect unique to methyldopa
hemolytic anemia
why are ganglion blocker drugs not used anymore
powerfully good at lowering BP, but come with severe side effects related to both parasympathetic and sympathetic nervous system blocks
how do post ganglionic sympathetic nerve terminal blockers work
by emptying adrenergic nerve terminal of its noepinephrine stores
how do MAO inhibitors work
formation of a false transmitter (ocampine) in sympathetic post ganglionic neuron terminals
how does ocampine differ from norepnephrine
has a very low efficiacy, resulting in a less than normal increase in vascular tone
why are MAO inhibitors no longer used for hypertensive treatment
hypertensive crisis can result from ingestion of large amounts of tyramine which is normally metabolized by monoamine oxidase
what do alpha 1 selective agents reduce
venous return and vascular resistance
why are non selective a blockers not useful in chronic hypertension
excessive compensatory side effects
what is one side effect of alpha 1 selective adrenoreceptor blockers
orthostatic hypotension
how do B blockers work
reduction of cardiac output and vascular tone
what are side effects of B blockers
increased glucose, LDL, triglyceride and lowered HDL counts
4 major mechanisms on how vasodilators work
release of nitric oxide, opening of potassium channels, blocking of calcium channels and activation of D1 dopamine receptors
release nitric oxide from endothelial cells of arterioles, discontinued because of high side effects (causes drug induced lupus)
prodrug that is metabolized to open potassium channels and hyperpolarize muscle cells, can cause excessive hypotension
what is unique about calcium channel blockers
orally active so can be used in chronic use of hypertension of any severity, few compensatory responses
extremely short acting vasodilator that acts to release nitric oxide from the drug itself, must be continually infused to work properly
opens potassium channels and relaxes vascular muscle, can cause reduced insulin release (hyperglycemia is a side effect)
dopamine D1 receptor activator, short duration of action
dopamine D1
acts on the release of cGMP and hence forth nitric oxide
ACE inhibitor
inhibits angiotensin converting enzyme, kinase II, causes reduction in angiotensin II and aldosterone levels and an increase in vasodilator bradykinin
what is a major contraindication for ace inhibitors
major side effects for ace inhibitors
cough and renal damage in patients with existing renal damage
what is the major difference between ACE inhibitor and receptor blockers
receptors competitively inhibit angiotenin II, lower incidence of cough, still have renal damage
renin to angiotensin I inhibitor
aliskiren side effects
headache and diarrhea, unknown teratogen effects but still contraindicated
relationship between ACE inhibitors and potassium
can cause hyperkalemia in patients with a high potassium diet or renal impairment
what is the order in which drugs are added on in stepped treatment
life style changes, thiazide diuretics, sympathoplegics (b blocker), ACE inhibotors, Vasodilators
which vasodilator is prescribed first
calcium channel blocker
propanolol is often prescribed with hydrazine for what reason
reduce tachycardia
what do old people respond better to
diuretics and B blockers, not so much ACE inhibitors
how is acute malignant hypertension treated
vasodilator combined with diuretic to lower, then managed with less powerful drugs