Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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
|
|
hydralazine
|
release nitric oxide from endothelial cells of arterioles, discontinued because of high side effects (causes drug induced lupus)
|
|
minoxidil
|
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
|
|
nitroprusside
|
extremely short acting vasodilator that acts to release nitric oxide from the drug itself, must be continually infused to work properly
|
|
diazoxide
|
opens potassium channels and relaxes vascular muscle, can cause reduced insulin release (hyperglycemia is a side effect)
|
|
fenoldopam
|
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
|
pregnancy
|
|
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
|
|
aliskiren
|
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
|