Vasodilators & Vasoactive Peptides

Front 1

Nitrate Drugs

Back 1

Isosorbide nitrate

nitroglycerine

nitroprusside

Front 2

Phosphodiesterase V inhibitor

Back 2

Sildenafil

Front 3

Angiotensin-Converting enzyme inhibitors (ACE Inhibitors)

Back 3

lisinopril

ramipril

Front 4

Angiotensin Receptor Blocker (ARBs)

Back 4

losartan

Front 5

4 factors that effect blood pressure

Back 5

Cardiac output
Resistance arterioles
Capacitance venules
Volume of fluid retention

Front 6

4 primary mechanisms in which vasodilators relax VSM

Back 6

increase intracellular cGMP
prevent depolarization
increase intracellular cAMP
decrease intracellular Ca2+

Front 7

Nitric Oxide donors (Nitrates)

Back 7

Release NO when metabolized
Relax smooth muscle (vascular, corpus cavernosa)
Inhibit platelet aggregation

Front 8

Myosin light chain promotes _____ after being broken dow n.

Back 8

relaxation (of smooth muscle)

Front 9

Primary effect of nitrites and nitrates if on _______ ____, because it is the main place of their breakdown.

Back 9

capacitance venules

Front 10

____ acts on both capacitance venules and resistance arterioles.

Back 10

Nitroprusside

*equal effect on arteries and veins

Front 11

Isosorbide dinitrate clinical use

Back 11

angina
heart failure

Front 12

nitroglycerin clinical use

Back 12

hypertensive emergency
hypotension induction
perioperative hypertension
postoperative hypersion

as well as acute MI, angina, HF, pulmonary edema,& unstable angina

Front 13

nitroprusside clinical use

Back 13

hypertensive emergency

Front 14

Angina is...

Back 14

ischemia for short amount of time

Front 15

Infarction (cell death) occurs when ischemia is greater than ____ mins.

Back 15

20

Front 16

Stable angina

Back 16

exertion

decreased lumen of coronary aa.

Front 17

Unstable angina

Back 17

plaque

ruptured plaque blocking coronary aa.

Front 18

Variant angina

Back 18

spasm

defect in Smooth muscle of coronary aa.

Front 19

factors contributing to O2 supply

Back 19

AV oxygen difference
regional myocardial distribution
coronary blood flow

Front 20

factors contributing to O2 demand

Back 20

contractility
HR
preload
afterload

Front 21

Oxygen supply must be _____ than oxygen demand.

Back 21

greater than or equal to

Front 22

Short-acting NO donors

Back 22

nitroglycerin, nitroprusside

Front 23

Long-acting NO donors

Back 23

nitoglycerin, isosorbide dinitrate

Front 24

IV Nitroglycerin onset/duration of action

Back 24

immediate/3-5 min

Front 25

Sublingual Nitroglycerin onset/duration of action

Back 25

1-3min/ 30-60 min

Front 26

Nitroglycerin fate and excretion

Back 26

60% bound to plasma protein, metabolized in liver to inorganic nitrate, extensive first pass effect for oral form, eliminated in urine

Front 27

IV nitroprusside onset/duration of action

Back 27

immediate/5-10 min

Front 28

Nitroprusside fate and excretion

Back 28

metabolized by intraerythrocytic reaction w/ hemoglobin, further metabolism in liver, metabolites excreted in urine

Front 29

Oral nitroglycerin onset/duration

Back 29

20-45min/4-8 hr

Front 30

Topical ointment nitroglycerin onset/duration

Back 30

15-60min/ 2-12 hr

Front 31

Transdermal nitroglycerin onset/duration

Back 31

40-60min/ 8-24 hr

Front 32

oral Isosorbide dinitrate onset/duration

Back 32

1hr/6-8 hr

Front 33

Isosorbide dinitrate fate and excretion

Back 33

extensive first pass effect, metabolized in liver, excreted in urine

Front 34

Continuous 24-hr plasma levels of organic nitrates results in ___

Back 34

tachyphylaxis (insurmountable tolerance)

Front 35

Nitrate-free period greater than ___ hours are necessary to prevent or attenuate tolerance.

Back 35

10

Front 36

Mechanism for tolerance poorly understood but may include:

____ release of endogenous NO
____sympathetic tone
____salt/H2O retention
____NO degradation

Back 36

decreased
increased
increased
increased

Front 37

tolerance is NOT developed to nitroprusside, likely due to fact that it involves a different pathway for metabolic activation than that of ______.

Back 37

nitrates/nitrites

Front 38

adverse effects of isosorbide dinitrate and nitroglycerin

Back 38

dizziness, headache, dysrhythmias, CV collapse, crescendo angina, methemoglobinemia, hemolytic anemia, flushing, postural hypotension, and reflex tachycardia

Front 39

Nitroprusside has all of the adverse effects of isosorbide and nitroglycerin as well as _____ toxicity.

Back 39

cyanide

Front 40

Isosorbide and nitroglycerin tolerance can lead to:

Back 40

restrictive cardiomyopathy
increased intracranial pressure

Front 41

Isosorbide, nitroglycerin and nitroprusside are all pregnancy category ___.

Back 41

C

Front 42

Hydralazine works on the ___ ____ and decreases afterload.

Back 42

resistance arterioles

Front 43

Hydralazine is clinically used for:

Back 43

hypertension and CHF

Front 44

Side effects of hydralazine

Back 44

dizziness, headache, angina, tachycardia, peripheral edema, nausea, lupus-like syndrome, pronounced arteriole dilation=reflex tachycardia

Front 45

hydralazine administered with ____ does not cause tachyphylaxis.

Back 45

nitroglycerin

Front 46

Hydralazine cannot be used for angina due to

Back 46

coronary steal phenomenon

--will dilate good arteries but cannot help damaged ones, leading to even further decrease in O2 in damaged vessels.

Front 47

onset/duration of oral hydralazine

Back 47

45min/3-8hrs

Front 48

_____ is well absorbed and undergoes 1st pass metabolism; bioavailability is 50% for slow acetylators and 30% for fast acetylators.

Back 48

Hydralazine

Front 49

Nitrate work well for _____

Back 49

venous vasodilation

Front 50

Nitroprusside works well for _____ and _____.

Back 50

arterial vasodilation, venous vasodilation

Front 51

Hydralazine works well for ____.

Back 51

arterial vasodilation

Front 52

Sildenafil clinical use:

Back 52

erectile dysfunction

pulmonary hypertension

Front 53

Sildenafil pregnancy category___.

Back 53

B

Front 54

Sildenafil adverse reactions:

Back 54

severe hypotension and death if combined w/ nitrates, dyspepsia, priapism

Front 55

Vasoactive peptides responsible for vasoconstriction

Back 55

Endothelin
vasopressin
Angiotensin II

Front 56

Vasoactive peptides responsible for vasodilation

Back 56

bradykinin
natriuretic peptides

Front 57

___ has direct effect on CNS, BVs, and sympathetic neurons.

Back 57

Angiotensin II

Front 58

Angiotensin converting enzymes produces ________ and breaks down bradykinin.

Back 58

Angiotensin II

Front 59

Biological effects of Angiotensin II

Back 59

volume expansion
direct vasoconstriction
increased sympathetic tone
cell proliferation, migration, & hypertrophy

Front 60

Vascular effects of ACE-I and ARB

Back 60

Vasorelaxation
Decrease in arterial resistance
Progressive reduction in BP
Reverse hypertrophy
Augment vascular distensibility
Decreased oxidative stress

Improved endothelial function
antiplatelet effect (ACE-I greater)
Stabilizes plaques
Decrease neutrophils & mononuclear cell prolif.

Front 61

Cardiac effects of ACE-I and ARB

Back 61

decreased preload and afterload
no change/increase in cardiac output
reverse hypertrophy

Front 62

Renal effects of ACE-I and ARB

Back 62

renoprotective
decreased proteinuria
increased renal blood flow
decreased kaliuresis that may result in hyperkalemia
preferential dilation of efferent arterioles, which reduces intraglomerular pressure

Front 63

ACE-I and ARB... (other effects)

Back 63

decreased pulmonary vascular resistance
decreased capillary wedge pressure (preload)
decreased sympathetic outflow
decreased aldosterone production
improved insulin sensitivity

Front 64

ACE-I class effect

Back 64

Hypertension, acute MI

Front 65

ACE-I + thiazide diuretics

Back 65

additive effect

Front 66

ACE-I + B-blockers/ACE-I/ARBs

Back 66

less than additive effect

Front 67

____ renin producers (e.g. African-Americans) respond less favorably to ACE inhibitors at low (ACE-I) monotherapy.

Back 67

low

Front 68

Losartan clinical uses

Back 68

HTN with LVH-left ventricular hypertrophy (to reduce stroke), Diabetic nephropathy, proteinuria

Front 69

ACE-I and ARBs are ___ line drugs.

Back 69

first

Front 70

A combination of 2 first line drugs may be considered as initial therapy if the blood pressure is >_____systolic or >10 diastolic above target.

Back 70

20

Front 71

ACEI and ARBs are good for

Back 71

....Everything!

HF, postMI, High CAD risk, With CAD, Diabetes, Chronic Kidney Disease (caution w/ arterial stenosis), Stroke prevention

Front 72

Preferred antihypertensive combinations...

Back 72

ACE-I/ARB + Thiazide
ACE-I/ARB + DHP CCB

Front 73

Lisinopril

Back 73

Active agent
1x day
excreted unchanged in urine

Front 74

Ramipril

Back 74

Prodrug, converted to active metabolite in liver
1 or 2x day
metabolized in liver, excreted in urine

Front 75

Losartan

Back 75

1xday
metabolized in liver, excreted in urine

Front 76

With ARBs, maximum effects in BP reduction occur ___ weeks after initiation of therapy.

Back 76

2-6

Front 77

ACE-I adverse effects

Back 77

dry cough
bronchospasm
angioedema
proteinuria
hypotension
tachycardia
chest pain
palpitations
hyperkalemia

Front 78

ACE-I contraindications

Back 78

Renal artery stenosis, K+sparing diuretics, ARB, NSAIDs

Front 79

ARB adverse effects

Back 79

dry cough
angioedema
hypotension
hyperkalemia

Front 80

ARB contraindications

Back 80

renal artery stenosis
K+ sparing diuretics, ACEI, NSAIDs

Front 81

Abrupt withdrawal of ACE-I and ARBs ______ been associated with rapid increase in blood pressure.

Back 81

has NOT

Front 82

ACE-I and ARBs are pregnancy category ___.

Back 82

D