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Pharmacology > Drugs Affecting the Cardiovascular Systems > Flashcards

Drugs Affecting the Cardiovascular Systems Flashcards

1
Q

what are the 4 factors that regulate cardiovascular disease?

A
  1. Autonomic NS
  2. Kidneys
  3. Heart
  4. Blood volume & composition
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2
Q

how is the autonomic NS involved in regulation of cardiovascular disease?

A

from the innervations of the parasympathetic and sympathetic divisions to the heart, BV, kidneys, and adrenal glands

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3
Q

how are the kidneys involved in regulation of cardiovascular disease?

A

maintenance of cardiac output by excretion & reabsorption of ions and water

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4
Q

how is the heart involved in regulation of cardiovascular disease?

A

through its effects on rate & force of contraction through the intrinsic NS

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5
Q

how is blood volume and composition involved in regulation of cardiovascular disease?

A

water and electrolyte balance

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6
Q

hypertension =

A

systolic pressure > 140 mm Hg

diastolic pressure > 90 mm Hg

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7
Q

what type of hypertension composes up to 90% of cases?

A

primary hypertension

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7
Q

primary hypertension’s specific cause is

A

unknown

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7
Q

BP =

A

cardiac output (CO) X Peripheral Vascular Resistance (PVR)

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7
Q

what is the cause of secondary hypertension

A

causative basis for elevation in pressure

eclampsia of pregnancy, renal artery disease, pheochromocytoma

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7
Q

CO=

A

heart rate (HR) X stroke volume (SV)

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7
Q

there is a _________ relationship between vascular resistance and blood pressure

A

direct

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8
Q

vasoconstriction can be described as a

A

decrease in lumen size

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8
Q

vasoconstriction will __________ resistance to blood flow therefore increasing _____________ ____________

A
  • increase
  • blood pressure
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9
Q

vasodilation can be described as an

A

increase in lumen size

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10
Q

vasodilation decreases resistance to __________ _______ and in turn _______ BP

A
  • blood flow
  • decreases
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11
Q

what are the 6 categories of antihypertensive agents?

A
  1. adrenergic agents
  2. angiotensin-converting enzyme inhibitors
  3. angiotensin II receptor blockers
  4. calcium channel blockers
  5. diuretics
  6. vasodilators
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12
Q

alpha 1 blockers are peripheral acting agents that block the

adrenergic agents

A

vasoconstricting effects through alpha 1 receptors

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13
Q

beta 1 blockers are cardio selective agents that

adrenergic agents

A

decrease the force of contraction in the heart

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14
Q

What may be a consequence of given a “non-selective” beta blocker to a patient that may also have asthma?

A

BAD RESULT
- severe bronchospasm
- fatalitites
- bronchoconstriction
- asthma exacerbations

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15
Q

give an example of alpha 2 agonists

A

clonidine

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15
Q

alpha 2 agonists stimulate what? to decrease what?

adrenergic agents

A

stimulate: alpha 2 receptors
decrease: sympathetic outflow from the CNS

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16
Q

ACE inhibitors block

angiotensin converting enzyme

A

the conversion of angiotensin 1 to angiotensin II

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17
Q

angiotensin II is a potent

A

vasoconstrictor

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18
Q

angiotensin II stimulates the release of

A

aldosterone

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18
Q

aldosterone is a vasoconstrictor that promotes the

A

reabsorption of H2O and Na in the renal tubules

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18
Q

what is the MOA of angiotensin II receptor blockers?

A

to block the receptors that receive AII inhibiting vasoconstriction and the release of aldosterone

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19
Q

calcium channel blockers cause

A

smooth muscle relaxation

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20
Q

how do calcium channel blockers cause smooth muscle relaxation?

A

by blocking the binding of calcium to its receptors

21
Q

vasodilators are

A

rapid acting

21
Q

how does calcium channel blockers affect PVR and BP?

A

decreases both of them

22
Q

vasodilators are powerful

A

antihypertensives

23
Q

vasodilators directly relaxes

A

smooth muscle

23
Q

what are the 4 categories of diuretics based on their pharmacodynamics?

A
  1. loop diuretics
  2. osmotic diuretics
  3. potassium-sparing diuretics
  4. thiazide diuretics
24
Q

diuretics decrease the

A

plasma and extracellular fluid volumes

24
Q

how do diuretics decrease the plasma and extracellular fluid volumes?

A

by increasing the rate of urine formation

24
Q

what is the result of diuretics?

A

decrease cardiac output and blood pressure

25
Q

loop diuretics are aka

A

lasix

26
Q

loop diuretics inhibit

A

sodium and chloride resorption

27
Q

loop diuretics increase

A

renal prostaglandins

28
Q

an increase in renal prostaglandins results in

A
  • BV dilation
  • decreased PVR

peripheral vascular resistance

29
Q

there is a tendency to loose _________ during excretion with loop diuretics.

A

calcium

30
Q

what is an example of osmotic diuretics?

A

mannitol

31
Q

osmotic diuretics do NOT

A
  • interact w/ receptors
  • block renal transport mechanisms
32
Q

osmotic diuretics produce an

A

osmotic gradient

33
Q

how do osmotic diuretics increase urine output?

A

by pulling water into the tubule system of the nephrons

34
Q

potassium-sparing diuretics prevent

A

potassium from being pumped into the tubules and excreted in the final urine product

35
Q

potassium-sparing diuretics have a….

this is why they are used in combination with other diuretics

A

weak overall effect

36
Q

thiazide diuretics inhibit the

A

reabsorption of sodium and chloride

37
Q

with thiazides there is a

A

decreased loss of calcium in the excretion

38
Q

where sodium goes…

A

water follows

39
Q

antiarrhythmic drugs are drugs used for the

A

treatment and prevention of cardiac rhythm disturbances

40
Q

action potential pathway describes the flow of

A

depolarization through the intrinsic NS of the heart

41
Q

describe the pathway known as action potential “Super Highway”

A

sinoatrial node -> atrioventricular node -> bundle of His -> L&R bundle branches -> purkinje network & papillary muscles

42
Q

ALL antiarrhythmic drugs have the potential to they themselves…

A

produce arrhythmias

43
Q

what are 4 common antiarrhythmic drugs

A
  1. sodium channel blockers
  2. beta blockers
  3. drugs prolonging the AP from the SA to AV node
  4. calcium channel blockers
43
Q

sodium channel blockers MOA is to

A

decrease the AP or electrical conductance within the heart

44
Q

beta blocker’s MOA is to

A

reduce stimulation to the sympathetic NS

45
Q

calcium channel blockers are commonly used for what conditions?

A
  • arrhythmias
  • tachycardia
46
Q

drugs that prolong the AP from the SA to the AV node are commonly used for

A
  • atrial arrhythmias
  • ventricular tachycardia
46
Q

calcium channel blocker’s MOA is to

A

decrease intracellular calcium that is required for cardiac muscle contraction

47
Q

define heart failure

A

a reduction in cardiac output resulting in a loss of blood pressure

48
Q

with heart failure there is an initial

A

compensatory response

49
Q

the compensatory response in heart failure is accompanied by

A

elevated sympathetic NS activity

50
Q

an elevation in SNS activity increases the

A

rate and force of contraction in the heart by stimulating beta1, 2, and alpha 1 receptors

51
Q

long term SNS produces…

A

hyperadrenergic state

51
Q

a hyperadrenergic state may lead to

A
  • irreversible myocyte damage
  • fibrotic buildup
  • death of cardio-myocytes (myocardial infarction)
52
Q

what are the 6 different pharmacological treatment options for heart failure

A
  1. ACE inhibitors
  2. angiotensin receptor blockers
  3. beta-adrenergic blockers
  4. aldosterone antagonists
  5. diuretics
  6. phosphodiesterase inhibitors
52
Q

what is the MOA of beta-adrenergic blockers

A

to reverse the effect of SNS activity and reduce cardiac workload

53
Q

what is the MOA of aldosterone antagonists

A

to inhibit sodium retention in the kidneys and sympathetic activity promoted by aldosterone binding to its receptors

53
Q

what is the MOA for phosphodiesterase inhibitors?

A

increase cAMP in cell and produce a positive inotropic force of contraction

Pharmacology (9 decks)

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