Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > Hypertension > Flashcards

Hypertension Flashcards

1
Q

types of cardiovascular disease:

A

hypertension

CHF

MI and angina pectoris

cardiac arrhythmias

thrombosis

hyperlidemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is hypertension?

A

high BP >140/90

normal= 120/80 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the stages of hypertension?

A

SBP:
I: 140-159
II: 160-179
III: 180-200

DBP:
I: 90-99
II:100-109
III:110-119

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is prehypertension?

A

BP between 120/80 - 139/89

a strong risk factor for developing HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is isolated systolic HTN?

A

SBP >140 and normal DBP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are risk factors for HTN?

A 
blood relatives with HTN
men > 55 y/o
post menopausal women
obesity
smoking
diabetes
high blood cholesterol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are complications of HTN?

A 
cerebrovascular hemorrhage
stroke
renal failure
heart failure
MI
retinal damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the types of HTN?

A

PRIMARY (idiopathic) HTN- 95%

SECONDARY HTN (5%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are possible contributors of primary HTN?

A
  • high sodium in diet or sodium retention
  • enhanced sympathetic nerve activity
  • perturbations in renin-angiotensin-aldosterone system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are possible contributors of secondary HTN?

A
  • precipitated by chronic renal disease (diabetic nephropathy)
  • pheochromocytoma
  • stress
  • aortic coarctation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is a nephron?

A

the functional unit of the kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is a diuretic?

A

For high blood pressure, diuretics, commonly known as “water pills,” help your body get rid of unneeded water and salt through the urine. Getting rid of excess salt and fluid helps lower blood pressure and can make it easier for your heart to pump.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the 3 major diuretics?

A

1- loop- high ceiling diuretics

2- thiazides and thiazide-like

3- K+ Sparing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are examples of loop diuretics?

A

Durosemide (Lasix)

Bumetanide (Bumex)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

where do loop diuretics work?

A

in the loop of Henle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the mechanism of action for a loop diuretic?

A

inhibition of Na+, K+, Cl reabsorption in the loop of Henle resulting in electrolyte and fluid excretion

excretion of water, sodium and chord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are indications for the use of loop diuretics?

A

treatment of:
acute pulmonary edema.
CHF
HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are adverse effects of loop diuretics?

A

electrolyte imbalances: hyponatremia (Na), hypokalemia (K) (leads to cardiac arrhythmia)

reactive increase in renin levels

alkalosis

hyperuricemia (uric acid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are examples of thiazide diuretics?

A

Chlorothiazide (Diuril)
Hydrochlorothiazide (Hydrodiurl)
Metolazone (Zaroxolyn(

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

where do thiazide diuretics work?

A

distal convoluted tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the mechanism of action for a thiazide diuretic?

A

inhibition of Na+, CL- reabsorption in the distal convoluted tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are indications for the use of thiazide diuretics?

A

either alone or in combo with other drugs in the treatment of HTN and/or CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are adverse effects of thiazide diuretics?

A

same as loop diuretics

electrolyte imbalance: hyponatremia, hypokalemia–>leads to cardiac arrhythmia

reactive increase in renin levels

alkalosis

hyperuricemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the 2 categories of K+ sparing diuretics?

A

1- mineralocroticoid receptor antagonists

2- renal Na+ channel inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are mineralocroticoid receptor antagonists?

A

Spironolactone (Aldactone)- blocks aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is aldersterone?

A

a hormone secreted from adrenal cortex and works on the collecting ducts to enhance exchange of Na+ and K+

retains sodium
secretes potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the mechanism of action of mineralocroticoid receptor antagonist?

A

competitive blocker of aldosterone receptors in collecting duct, decrease the Na+/K+ exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are indications for the use of mineralocroticoid receptor antagonists?

A

co-administered with thiazides or loop diuretics in tx of HTN and CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are adverse effects of mineralocroticoid receptor antagonists?

A

life threatening hyperkalemia

gynecomastia- enlarged breast in men

impotence- erectile dysfunction

decreased libido

acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are renal Na+ channel inhibitors?

A

amiloride (Midamor)

Triamterene (Dyrenium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is the mechanism of action of renal Na+ channel inhibitors?

A

inhibit Na+ channels in collecting duct, leading to inhibition of Na+ reabsorption, and K+ sparing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are indications for use of renal Na+ channel inhibitors?

A

in combination therapy with thiazides to treat HTN and CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are adverse effects of renal Na+ channel inhibitors?

A

hyperkalemia

acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what are examples of combination therapy?

A

amiloride & hydrocholorothiazide

spironolactone and isobutylhydrocholorthiazide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what are the 2 ways to manage hyperkalemia?

A

1- IV injection of insulin and dextrose

2- exchange resin (sodium polystryrene, kayexalate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is renin?

A

an enzyme secreted by renal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is RAS?

A

Renin-angiotensin II- Aldosterone System
a hormonal cascade that functions in the homeostatic control of arterial pressure, tissue perfusion, and extracellular volume. Dysregulation of the RAAS plays an important role in the pathogenesis of cardiovascular and renal disorders.

Liver produces a pre enzyme- angiotensinogen ->gets converted to angiotensin I (occurs thru the action of renin that is released by the kidney bc of low fluid volume –> converted to angiotensin II by ACE floating in the blood
Angiotensin II acts on the adrenal gland that causes it to release aldosterone (a steoid hormone) which then acts on the collecting ducts of the nephron within the kidney and causes the nephron to retain water

If the body retains water the BP goes up

angiotensin II leads to:
1- aldosterone –> increased blood volume

2- vascular smooth muscle–> vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

loop and thiazide diuretics increase:

A

sodium excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what are the therapeutic components of loop and thiazide diuretics?

A

decreased blood volume

decreased vascular resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what are the counter-therapeutic components of loop and thiazide diuretics?

A

increased renin production

increased angiotensin II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what are examples of ACE inhibitors?

A

Captopril (Capoten)
Enlapril (Vasotec)
Lisinopril (Prinivil)
Quinapril (Accupril)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is the mechanism of action of ACE inhibitors?

A

inhibition of angiotension converting enzyme (ACE), which reduces levels of vasoconstricting angiotensin II and increases levels of the vasodilator bradykinin.

diminished angiotensin II also decreases secretion of the sodium retaining, potassium secreting corticosteroid, aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what are indications for the use of ACE inhibitors?

A

diabetic hypertensive populations- slows development of diabetic neuropathy

hypertensive populations with L ventricular hypertrophy - reverse hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what are adverse effects of ACE inhibitors?

A

cough
dizzyness

can result in angioedema. ACE is responsible for breakdown of bradykinin- a mediator that increases permeability of blood vessels

hyperkalemia

renal insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what are examples of angiotensin-receptor blockers (ARB)?

A

Losartan (Cozaar)
Valsartan (DIovan)
Candesartan (Atacand)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what is the mechanism of action of ARBs?

A

competitive inhibitor of AT-1 receptor of vascular smooth muscle leading to smooth muscle relaxation and decrease vascular resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what are indications for the use of ARBs?

A

as efficacious as ACE inhibitors in tx of HTN when combined with a thiazide diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what are adverse effects of ARBs?

A

hypotension, generally well tolerated

should be discontinued in second and third trimesters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what are examples of Beta adrenergic blockers?

A

B1 selective:
Metoprolol (Lopressor)
Atenolol (Tenormin)
Esmolol (Brevibloc)

Non-selective:
Propranolol (Inderal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what is the MOA of beta adrenergic blockers?

A

decrease renin production and release in the kidney- ultimately decreasing angiotensin II formation– resulting in decrease of vascular resistance.

other contributing mechanisms including decrease in myocardial contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what are indications of use of beta adrenergic blockers?

A

hypertensive patients with angina, following heart attack (promotes survival)

should be avoided in diabetics as it masks hypoglycemic tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what are adverse effects of beta adrenergic blockers?

A

in patients with AC conduction defects, B1 blockers may cause life threatening bradyarrhythmias

abrupt discontinuation of long term B1 blockers use in angina can exacerbate and may increase risk of sudden heart attack

B2 receptors blockade can worsen bronchoconstriction in asthmatic populations.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what are examples of alpha1 adrenergic blockers?

A

Prazocin (minipress)
Doxazocin (Cardura)
Terazocin (Hytrin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what is the MOA of alpha1 adrenergic blockers?

A

interference with the ability of NE (sympathetic neurons) or epinephrine to activate alpha adrenoreceptors on vascular smooth muscle, thus demising their vasoconstriction and growth promoting actions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what are the indications for use of alpha1 adrenergic blockers?

A

a combination therapy with diuretics
B1 adreoceptor blockers to treat HTN

should not be used alone since they increase the risk of CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what are adverse effects of alpha1 adrenergic blockers?

A

characteristic first dose phenomenon

leads to orthostatic hypotension (seen in 50% of patients)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what are examples of Ca++ Channel Blockers

A

Verapamil (Isoptin)
Nifedpine (adalat)
Dilitiazem (Cardiazem)
Amlodipine (Norvasc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what is the MOA of Ca++ Channel Blockers?

A

block calcium channels in arteriolar smooth muscles, leading to block calcium entry into the cells.

entry of calcium from extracellular fluid to the cytosol is a requirement for smooth muscle contraction

net effect is a decrease in vascular resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what are the indications for use of Ca++ channel blockers?

A

mono therapy for elderly populations with low circulating renin levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what is the MOA of direct acting vasodilators?

A

direct relaxation of vascular smooth muscles thus decreasing vascular resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what are adverse effects of direct acting vasodilators?

A

reflex tachycardia

hypotension

fluid retention

hypertrichosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what are vasodilators used to treat outpatients?

A

Hydralazine (Apresoline)

Minoxidil (Loniten)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what are vasodilators used in emergency?

A

Sodium nitroprusside

diazoxide (hyperstat IV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what are the 2 centrally acting sympatholytic agents?

A

1- clonidine (catapress)

2- Reserpine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what is clonidine? what is its MOA?

A

(catapress)
centrall acting sympatholytic agent

MOA:
agonist of alpha2 receptor in brainstem resulting in reduction of sympathetic outflow from CNS – especially in emergency situations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what is reserpine? what is its MOA? Adverse effect?

A

a centrally acting sympatholytic agent

depletes CNS of NE which lowers BP (pretty dramatically)

MOA:
inhibit vascular storage of NE and dopamine in central adrenergic neurons

adverse effect:
depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what is CHF?

A

the inability of the heart to maintain adequate BF to meet the demands of peripheral tissues and itself

among the major causes of mortality

68
Q

the most common form of CHF is ____? characterized by:?

A

systolic heart failure

characterized by:
decreased CO
increased pressure and volume loads on R and L ventricles

69
Q

what are causes of CHF?

A

uncontrolled HTN
coronary artery diseases
idiopathic cardiomyopathy

70
Q

what are symptoms of CHF?

A 
orthopnea (SOB/ dyspnea)
paroxymal nocturnal dyspnea
tachypnea- rapid breathing 
peripheral edema
ankle swelling
weight gain
hepatomegaly - swelling of the liver
71
Q

as CO gets worse, what 2 compensatory mechanisms also get worse?

A

1- increased sympathetic nerve activity

  • tacycardia
  • vasoconstriction –> increased vascular resistance

2- decreased kidney perfusion

  • increased renin release–> increased angiotensin II release–> increased vascular resistance
  • decreased urine output –> edema

*really worried about the kidney- fluid is retained–>edema

idea of tx is to slow this down!

72
Q

what are 2 objectives to therapy?

A

1- increase CO
2-decrease ventricular filling volume
3- slow pathological remodeling of ventricles

73
Q

what drugs are used in CHF?

A

diuretics- to get rid of fluid

vasodilators- to decrease resistance problems with sympathetic activation

inotrophic agents- to stimulate the heart

74
Q

what is the problem with diuretics for CHF?

A

development of resistance to the actions of the loop diuretic when chronically used in patients with CHF

75
Q

how do you overcome the problem of diuretics with CHF?

A

a thiazide diuretic (Metolazone) can be given either before or with the loop diuretic

the loop is no longer as effective so you add a thiazide

76
Q

what are thiazides more frequently combined with for CHF?

A

can be used in mild CHF

most frequently combined with loop diuretics to overcome resistance problem

77
Q

how can spironolactone be used for CHF?

A

can be used in combination therapy (K+ sparing)

recent evidence indicates beneficial effects on advanced CHF (promotes survival) independent of its natriuretic effect

78
Q

What vasodilators are used for CHF?

A

ACE inhibitors

ARBs

Nitrovasodilators

Ca++ channel blockers

79
Q

ACE inhibitors for CHF=

A

first line therapy

shown to promote survival in CHF patients

80
Q

ARBs for CHF=

A

used as alternative to ACE inhibitors when side effects of ACE inhibitors are not tolerated

81
Q

how do nitrovasodilators work for CHF?

A

to increase BF to the heart (to get more oxygen to heart muscle itself

sodium nitroprusside
organic nitrates- isosorbide denigrate, nitroglycerin

82
Q

what is the MOA of nitrovasodilators?

A

release of nitric oxide (NO) - a potent vasodilator

83
Q

Ca++ for CHF=

A

second line option- have no been proven as efficacious as other vasodilators in the treatment of CHF

84
Q

what is the major benefit of using a beta blocker for CHF?

A

has the ability to slow down pathological remodeling of ventricles (slow down hypertrophy)

recommended for use in moderate forms of CHF where it was shown that they reduce mortality

decreases CO– decreases renin production

85
Q

what are inotropic drugs used in CHF?

A

Cardiac Glycosides (digitalis glycosides)

  • Digoxin (Lanoxin)
  • Digitoxin (Crystodigin)

inotropic= affects force of muscle contraction

86
Q

what is the MOA of inotrophic drugs?

A

1- inhibition of Na/K ATPase pump in ventricular myocytes leading to elevation of intracellular Ca++ and increased myocardial contractility

2- potentiation of vagal nerve effects on the heart
(slows the heart by stimulating vagus nerve)

87
Q

what problems are associated with digoxin use?

A

**narrow therapeutic index (fine line b/w positive effect and toxicity- has a long half life- have to be very careful about specific dosing

Cardiac arrhythmia (due to inhibition of Na/K pump
A: atrial arrhythmia (atrial fibrillation, sinus bradycardia)
B: ventrical arrhythmia (associated with angina or MI) ***bigger concern

K+ level monitoring during digoxin therapy (hypokalemia and hyperkalemia potentiate digoxin toxicity)

88
Q

what is the negative chronotropic effect of digitalis glycosides?

A

decreased heart rate

89
Q

what are the positive chronotropic effects of digitalis glycosides?

A

increased CO
increased kidney perfusion
increased urine output

90
Q

dopamine is a good inotropic because..

A

it is a good vasodilator

Dobutamine (dobutrex)

91
Q

what are indications for the use of doputamine?

A

short term support of circulation in advanced CHF

dopamine is a cardiac stimulant

92
Q

what is the MOA of dopamine/dobutamine?

A

inhibitors of phosphodiesterase enzyme leading to stimulation of myocardial contractility and acceleration of myocardial relaxation

also causes a decrease in vascular resistance

93
Q

how is heart failure staged?

A

ACC/AHA classification
stages A, B, C, D

based on disease progression

patients cannot revert back to a lower stage

emphasizes preventability

directs treatment approaches

94
Q

what is stage A of HF?

A

high risk for developing HF

but no structural heart disease

95
Q

describe stage B of HF:

A

structural heart disease is present but no symptoms

-asymptomatic LV dysfunction

96
Q

describe stage C of HF:

A

past or current symptoms of HF

CO is increased
tachycardia

97
Q

describe stage D of HF:

A

end stage HF

needs transplant

98
Q

what are non-pharmacologic managements to heart failure?

A

daily weight monitoring

encourage exercise as tolerated

sodium restriction <1.5 L per day

(sodium and fluid decrease will decrease amount of fluid build up)

99
Q

what are pharmacologic managements to heart failure?

A

appropriately manage and treat co-morbid illness

d/c drugs that may contribute to HF

recommend tx options based on ACC/AGA stage

100
Q

what are treatment options for stage A HF?

A

stage A= high risk for development of HF

drug therapy to slow disease progression

both classes shown to reduce morbidity and mortality

ACE inhibitors- first line therapy
ARB

101
Q

what are treatment options for stage B HF?

A

stage B=asymptomatic structural heart disease

all general measures for stage A

drug therapy
ACE inhibitors or ARB

PLUS
Beta blocker- to decrease BP

102
Q

what are 3 types of beta blockers?

A

bisoprolol

carvedilol

metoprolol succinate

103
Q

what is bisoprolol?

A

selective beta1 receptor blocker

104
Q

what is carvedilol?

A

non selective beta receptor blocker AND alpha adrenergic receptor blocker

105
Q

what is metoprolol succinate?

A

selective beta1 receptor blocker

106
Q

what are common adverse effects of beta blockers?

A

hypotension
bradycardia
fluid retention
fatigue

107
Q

what are relative contraindications for the use of BB?

A

HR <100mm Hg

108
Q

what are precautions for the use of BB?

A

asthma/COPD

peripheral vascular disease

109
Q

what happens if you give too much BB?

A

fluid retention

110
Q

what are treatment options for stage C of HF?

A

stage C= structural heart disease w/ prior or current symptoms

general measures for stages A and B

drug therapy for all patients

  • diuretics
  • ACE-I or ARB
  • BB

drug therapy for selected patients

  • aldosterone antagonist
  • digitalis
  • hydralizaine/nitrates

devices for selected patients:

  • biventricular pacing (BivP)
  • implantable cardioverter difibrillator (ICD)
111
Q

loop diuretics for HF:

A

more potent–> CHF

effective in renal dysfunction

shorter acting: T1/2: 4-6 hours for furosemide

effect potentiated by thiazides

112
Q

thiazide diuretics for HF:

A

sustained action–> HTN

only matolazone is effective in renal dysfunction

113
Q

what is a common adverse effect of diuretics?

A

urinary frequency

114
Q

what are contraindications for diuretics?

A

anuria- failure of kidneys to produce urine

renal decompensation –> renal failure

115
Q

what are monitoring parameters for diuretics?

A

electrolytes

renal function

weight

116
Q

what are aldosterone antagonists?

A

spironolactone
initial dose: 12.5-25 mg qd
max dose: 25 mg

Eplerenone
initial dose: 25
max dose: 50

117
Q

what are common adverse effects to aldosterone antagonists?

A

gynomastia- esp w/ spironolactone

118
Q

what are contraindications for the use of aldosterone antagonists?

A

hyperkalemia

119
Q

what are monitoring parameters for aldosterone antagonists?

A

renal function

K+

BP

120
Q

what is the usual dose for digitalis?

A

0.125-0.25 mg qd

121
Q

what is the half life for digitalis?

A

40h

122
Q

digitalis is excreted by the:

A

kidney

-maintenance dose depends on the patient

123
Q

what is the therapeutic range of digitalis?

A

NARROW

<1.2 ng/ml

124
Q

the toxicity of digitalis is enhanced by:

A

quinidine
amiodarone
low K
high Ca

125
Q

what is the MOA of digoxin?

A

inhibits Na/K+ ATPase

increases Na/Ca exchange

increases in intracellular calcium
-increased myocardial contractility

126
Q

what are side effects of digoxin?

A

visual disturbance, MI, dz, n/v/d

127
Q

what are precautions for digoxin?

A

narrow therapeutic index

128
Q

what are monitoring parameters for digoxin?

A

serum concentrations

129
Q

what is the MOA of hydrazine?

A

direct vasodilation of arterial smooth muscle

reduce afterload

130
Q

what is the MOA of long acting nitrates?

A

vasodilation

decrease cardiac oxygen consumption by increasing intracellular cyclic GMP

131
Q

what are side effects of hydralazines?

A

reflex tachycardia
lupus
headache
flushing

132
Q

what are side effects of nitrates?

A

headaches

133
Q

what are contraindications for nitrates?

A

use of PDE-5 inhibitors

head trauma

cerebral hemorrhage

134
Q

what are monitoring parameters for hydralazines/nitrates?

A

orthstasis

135
Q

what are treatment options for stage D HF?

A

stage D= refractory HF

appropriate measures for stages A, B, C

hospice care?

heart transplant?

136
Q

what are self care strategies ?

A

medication adherence
-pill organizer

dietary adherence:

  • fluid restriction
  • sodium restiction

monitoring of daily weights:

  • purchase scale
  • keep logbook
137
Q

what is myocardial ischemia?

A

insufficient blood flow through coronary arteries to heart leading to imbalance between oxygen supply and demand

138
Q

what is angina pectoris?

A

choking and squeezing pain in the chest produced by ischemia

139
Q

what is MI?

A

extreme form of ischemia leading to significant cardiac tissue damage and death

140
Q

what are the 3 types of angina?

A

1- stable angina (exertional)

2- unstable

3- prinzmetal (variant, vasospastic)

141
Q

what is stable angina?

A

exertional

simple blockage of coronary arteries by artherosclerotic lesions

pain and discomfort following exercise or stress

142
Q

what is unstable angina?

A

caused by arherosclerotic lesion and/or a clot that can occlude the smaller coronary vessels and is the most common cause of MI

143
Q

what is prinzmetal angina?

A

variant, vasospastic

caused by spasm of coronary arteries that are sudden and unpredictable

144
Q

myocardial oxygen demand depends on?

A

heart rate

preload, afterload

145
Q

myocardial oxygen supply depends on?

A

coronary blood flow

  • coronary vascular resistance
  • aortic pressure
146
Q

what drugs are used to treat angina?

A

organic nitrates –> relaxation of vascular smooth muscles

coronary arteries:
increased BF–> increased oxygen supply

peripheral arterioles:
reduction in afterload –>decreased o2 demand

veins:
reduction in preload–> decrease o2 demand

147
Q

what are examples of organic nitrates?

A

nitroglycerine
isosorbide dinitrate
isosorbide monoitrate
amyl nitrite

148
Q

what happens to organic nitrates taken orally?

A

subject to first pass metabolism

thereby greatly decreasing their efficacy

149
Q

what is organic nitrates effect on BP?

A

can produce severe drops in BP (sometimes fatal) either alone or when combined with other drugs

150
Q

what is the half life of organic nitrates?

A

nitroglycerin: 3 min

isosorbide dinitrate: 45 min

151
Q

sublingual tablets and inhalation sprays of organic nitrate are used for?

A

immediate relief of angina symptoms (onset of action is 1-2 min)

152
Q

oral nitrates are used for?

A

prophylaxis for patients having more than occasional angina attacks

153
Q

transmucosal or buccal organic nitrates are used for?

A

short term prophylaxis in anticipation of an angina attack

154
Q

IV nitroglycerine organic nitrate is used for?

A

acute management of unstable angina

155
Q

innervation of the heart and coupling of electrical signaling and muscle contraction:

A

signal is generated from SA node under the control of sympathetic and parasympathetic systems

signal travels to AV node resulting in atrial contraction

signal enters ventricles, travels through bundle of His and Purkinje fibers leading to ventricular contraction

156
Q

P wave:

A

atrial depolarization

157
Q

QRS complex:

A

ventricular depolarization

158
Q

T wave:

A

ventricular repolarization

159
Q

atrial fibrillation

A

skips a p wave

160
Q

ventricular tachycardia

A

all over

161
Q

what are the 4 classes of anti arrhythmic drugs?

A

Class I- Na+ channel blockers

Class II- beta adrenoceptor blockers

Class III- K+ channel blockers

Class IV- Ca+ channel blockers

162
Q

what is class I anti arrhythmic drugs?

A

Na+ channel blockers

Quindine, phenytonin, lidocaine, procainamide

these drugs decreases conduction velocity

163
Q

what are class II anti arrhythmic drugs?

A

beta adrenoreceptor blockers

Metoprolol, nadolol, propranolol

antagonize sympathetic nerve activity, decrease SA automaticity, negative inotropic effect

164
Q

what are class III anti arrhythmic drugs?

A

K+ channel blockers

bretylium, amiodarone, clofiliu

these drugs extend the duration of AP

165
Q

what are class IV anti arrhythmic drugs?

A

Ca++ channel blockers

verapamil, ditiazem

these drugs’ effects are restricted to SA and AV nodes and produce similar effects to class II drugs

166
Q

what is the MOA of digoxin and digitoxin?

A

enhance effects of vagus nerve on heart

this results in slowing of SA node, conduction through AV node

cardiac glycosides are used in treatment of atrial arrhythmia associated with tachycardia

Pharmacology (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions