Pharmacology Ch 11: Drugs Used In Hypertension

Front 1

baroreceptor reflex

Back 1

sensors in the carotid sinus that can detect changes in blood pressure homeostasis, involves both parasympathetic and sympathetic control

Front 2

essential hypertension

Back 2

elevated BP with an unknown origin

Front 3

false transmitter

Back 3

substances stored in vesicles that are released into the synaptic cleft but do not have a full true effect, (ocampine w/ noepinephrine)

Front 4

orthostatic hypertension

Back 4

elevated BP when in upright position

Front 5

postganglionic neuron blocker

Back 5

blocks actions in postganglionic neurons

Front 6

rebound hypertension

Back 6

where removal of an antihypertensive drug causes blood pressure to rise above original levels

Front 7

reflex tachycardia

Back 7

when BP is lowered to a point where baroreceptor reflex causes an increase in heart rate

Front 8

stepped care

Back 8

adding a variety of treatment options gradually as opposed to all at once

Front 9

two types of diuretics

Back 9

thiazide, loop diuretics

Front 10

with a thiazide, what is achieved at a lower dose, maximum antihypertensive effect or diuretic effect

Back 10

maximum antihypertensive effect

Front 11

what do sympathoplegic drugs affect

Back 11

sympathetic control of cardiovascular function

Front 12

how do alpha 2 selective agonists work

Back 12

decrease in sympathetic outflow by activation of A2 receptors in the CNS

Front 13

how do clonidine and methyldopa reduce blood pressure

Back 13

by reducing vascular resistance or cardiac output, or both

Front 14

what is the major compensatory response of A2 selective agents

Back 14

increased salt retention

Front 15

what is the major side effect with A2 selective agents associated with discontinuation of the drug

Back 15

severe rebound hypertension, drug must be stepped down

Front 16

what is one major side effect unique to methyldopa

Back 16

hemolytic anemia

Front 17

why are ganglion blocker drugs not used anymore

Back 17

powerfully good at lowering BP, but come with severe side effects related to both parasympathetic and sympathetic nervous system blocks

Front 18

how do post ganglionic sympathetic nerve terminal blockers work

Back 18

by emptying adrenergic nerve terminal of its noepinephrine stores

Front 19

how do MAO inhibitors work

Back 19

formation of a false transmitter (ocampine) in sympathetic post ganglionic neuron terminals

Front 20

how does ocampine differ from norepnephrine

Back 20

has a very low efficiacy, resulting in a less than normal increase in vascular tone

Front 21

why are MAO inhibitors no longer used for hypertensive treatment

Back 21

hypertensive crisis can result from ingestion of large amounts of tyramine which is normally metabolized by monoamine oxidase

Front 22

what do alpha 1 selective agents reduce

Back 22

venous return and vascular resistance

Front 23

why are non selective a blockers not useful in chronic hypertension

Back 23

excessive compensatory side effects

Front 24

what is one side effect of alpha 1 selective adrenoreceptor blockers

Back 24

orthostatic hypotension

Front 25

how do B blockers work

Back 25

reduction of cardiac output and vascular tone

Front 26

what are side effects of B blockers

Back 26

increased glucose, LDL, triglyceride and lowered HDL counts

Front 27

4 major mechanisms on how vasodilators work

Back 27

release of nitric oxide, opening of potassium channels, blocking of calcium channels and activation of D1 dopamine receptors

Front 28

hydralazine

Back 28

release nitric oxide from endothelial cells of arterioles, discontinued because of high side effects (causes drug induced lupus)

Front 29

minoxidil

Back 29

prodrug that is metabolized to open potassium channels and hyperpolarize muscle cells, can cause excessive hypotension

Front 30

what is unique about calcium channel blockers

Back 30

orally active so can be used in chronic use of hypertension of any severity, few compensatory responses

Front 31

nitroprusside

Back 31

extremely short acting vasodilator that acts to release nitric oxide from the drug itself, must be continually infused to work properly

Front 32

diazoxide

Back 32

opens potassium channels and relaxes vascular muscle, can cause reduced insulin release (hyperglycemia is a side effect)

Front 33

fenoldopam

Back 33

dopamine D1 receptor activator, short duration of action

Front 34

dopamine D1

Back 34

acts on the release of cGMP and hence forth nitric oxide

Front 35

ACE inhibitor

Back 35

inhibits angiotensin converting enzyme, kinase II, causes reduction in angiotensin II and aldosterone levels and an increase in vasodilator bradykinin

Front 36

what is a major contraindication for ace inhibitors

Back 36

pregnancy

Front 37

major side effects for ace inhibitors

Back 37

cough and renal damage in patients with existing renal damage

Front 38

what is the major difference between ACE inhibitor and receptor blockers

Back 38

receptors competitively inhibit angiotenin II, lower incidence of cough, still have renal damage

Front 39

aliskiren

Back 39

renin to angiotensin I inhibitor

Front 40

aliskiren side effects

Back 40

headache and diarrhea, unknown teratogen effects but still contraindicated

Front 41

relationship between ACE inhibitors and potassium

Back 41

can cause hyperkalemia in patients with a high potassium diet or renal impairment

Front 42

what is the order in which drugs are added on in stepped treatment

Back 42

life style changes, thiazide diuretics, sympathoplegics (b blocker), ACE inhibotors, Vasodilators

Front 43

which vasodilator is prescribed first

Back 43

calcium channel blocker

Front 44

propanolol is often prescribed with hydrazine for what reason

Back 44

reduce tachycardia

Front 45

what do old people respond better to

Back 45

diuretics and B blockers, not so much ACE inhibitors

Front 46

how is acute malignant hypertension treated

Back 46

vasodilator combined with diuretic to lower, then managed with less powerful drugs