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Fall Pharm > Exam 3 review > Flashcards

Exam 3 review Flashcards

1
Q

Beta Blockers used in:

A
  • ***HTN
  • **CHF
  • **Arrhythmias
  • ***Angina
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2
Q

Ca++ channel blockers used in:

A
  • ***HTN
  • ***Arrhythmias
  • ***Angina
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3
Q

ACE-I/ARBs/Aliskiren used in:

A
  • ***HTN

* ***CHF

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4
Q

Diuretics/Thiazides used in:

A
  • ***HTN

* ***CHF

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5
Q

Cardiac glycosides/Digoxin used in:

A
  • *CHF

* Arrhythmias

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6
Q

Vasodilators used in:

A
  • **HTN
  • *CHF
  • ***Angina
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7
Q

Na+ channel blockers used in:

A

**Arrhythmias

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8
Q

Nitrates used in:

A
  • *CHF

* ***Angina

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9
Q

Blood volume for males and females:

A

Females: 4-5L
Males: 5-6L

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10
Q

Large proportion of blood volume is located..

A

..in the splanchnic bed.

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11
Q

Mean arterial pressure

A

pressure that propels blood into the tissues.

MAP = (SBP + 2DBP)/3

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12
Q

4 factors affecting BP:

A
  • Peripheral resistance
  • Vessel elasticity
  • Blood volume
  • Cardiac output
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13
Q

Cardiac output

A

SV x HR = CO

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14
Q

Preload

A

The amount of stretch due to the amount of blood in the heart at end diastole (EDV)

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15
Q

4 main anatomic sites that are targets for high BP:

A
  • Resistance arterioles
  • Capacitance venules
  • Pump output heart
  • Kidneys
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16
Q

Resistance arterioles

A

primarily targeted by alpha 1 agonism

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17
Q

Capacitance venules

A

Have a lot of volume

When contracted, will contribute considerably to preload/EDV

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18
Q

Kidneys role in BP:

A

Juxtaglomerular apparatus senses an increase in pressure and releases NO.
OR
Juxtaglomerular apparatus senses a decrease in volume and (or direct beta agonism) activates renin/angiotensin/aldosterone system.

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19
Q

Peripheral Resistance

A

Blood cells and plasma encounter resistance when they contact blood vessel walls.

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20
Q

3 main sources of peripheral resistance:

A
  • blood vessel diameter (most controllable via Alpha1)
  • blood viscosity
  • total vessel length
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21
Q

Primary HTN

A

Idiopathic

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22
Q

How is Renin stimulated?

A

Decreased pressure in renal arterioles
Reduced Na+ delivery
Increased Na+ concentration at distal renal tubule
Sympathetic stimulation

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23
Q

What does Angiotensin 2 do?

A
  • Constricts vessels
  • Stimulates aldosterone secretion in adrenal cortex
  • inhibits further renin release (negative feedback)
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24
Q

What does Aldosterone do?

A
  • increases renal Na+ absorption

- increases intravascular blood volume

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25
Q

How do diuretics decrease BP?

A

Deplete Na+

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26
Q

How do Sympathoplegics decrease BP?

A

Decrease PVR
Reduce CO
(Alpha-blockers, Beta-blockers, and Alpha 2 agonist in CNS)

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27
Q

How do direct vasodilators decrease BP?

A

relax vascular smooth muscle

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28
Q

How do anti-angiotensin decrease BP?

A

block activity or production of angiotensin

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29
Q

Sympathoplegic categories:

A
  • Central Acting
  • Ganglion Blocking
  • Adrenergic neuron blocking
  • Adrenoceptor antagonist
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30
Q

Central acting MOA:

A

Decrease sympathetic outflow from vasomotor center in brain. Binds to Alpha2 and Alpha 1 receptors in CNS.

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31
Q

Central acting drugs:

A

Clonidine and Methyldopa

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32
Q

Ganglion blocking MOA:

A

Block ACh of post-ganglionic autonomic neurons (sympathetic and parasympathetic)

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33
Q

Ganglion blocking drugs:

A

Hexamethonium

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34
Q

Adrenergic neuron blockers MOA:

A

Block NE release from post-ganglionic sympathetic neuron

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35
Q

Adrenergic neuron blocker drugs:

A

Guanethidine and Reserpine

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36
Q

Adrenoceptor antagonist MOA:

A

Antagonize catecholamines at alpha and beta receptors

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37
Q

Adrenoceptor antagonist drugs:

A

Prazosin (A1) and Propranolol (B)

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38
Q

Vasodilators

A

Relax smooth muscle of arterioles (all) and veins (nitroprusside and nitrates)
Reduce PVR and MAP

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39
Q

When MAP is decreased..

A

..there is a compensatory response by the body to increase MAP.

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40
Q

Angiotensin inhibitors:

A

ACE-I and ARBs

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41
Q

Outpatient therapy considerations:

A

Na+ intake
Weight
Current home meds that increase BP

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42
Q

1st line HTN drugs:

A

B-blockers

Diuretics

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43
Q

Best HTN med for DM patients:

A

ACE-I

no Beta blockers due to B3

44
Q

Best HTN med for Angina patients:

A

Beta blockers

Ca++ channel blockers

45
Q

Best HTN med for CHF patients:

A

Diuretic

ACE-I

46
Q

Best HTN med for African American patients:

A

Diuretic

Ca++ channel blockers

47
Q

Chinese population tend to be more sensitive to what HTN med?

A

Beta blockers.

48
Q

Types of vascular tone:

A

Arteriolar tone
Capillary tone
Venous tone

49
Q

Capillary function

A

Exchange of gasses.

has no smooth muscle

50
Q

Pre-capillary sphincters

A

Rings of smooth muscle around beginning of capillaries.

Respond to alpha 1 agonism.

51
Q

What happens when pre-capillary sphincters dilate?

A

There is more fluid loss (edema)

Happens in shock.

52
Q

What happens when pre-capillary sphincters constrict?

A

They shunt blood from arteries to veins

53
Q

Angina

A

Accumulation of metabolites due to myocardial ischemia.

Heart switches to deoxygenated energy metabolism and byproducts build up.

54
Q

2 Functions of venous system:

A
  • Conduct blood back to heart (maintains filling of heart despite changes in blood volume)
  • Reservoir for blood volume
55
Q

Compliance of veins VS arteries:

A

Veins have 30x more compliance

56
Q

The venous system contains ____% of total blood volume.

A

70%

20-30% is in splanchnic bed

57
Q

Splanchnic bed

A

Veins in intestins, stomach, spleen, liver

58
Q

Angina immediate relief:

A

Nitroglycerin (Artery and venous dilation)

59
Q

Angina prophylaxis:

A

Ca++ channel blockers

Beta blockers

60
Q

Stable Angina

A

“classic” or “Angina of effort”
Cause: plaque
Precipitating fx: Exercise, stress
Brief, relieved by rest

61
Q

Unstable Angina

A

“Acute Coronary Syndrome”
Cause: plaque
Precipitating fx: resting
Emergency

62
Q

Variant Angina

A

“Prinzmetal” or “Angina inversa”
Cause: hyperreactive vessels
Precipitating fx: resting
Rare (2% of angina)

63
Q

Microvascular Angina

A

“MVD”
Cause: Coronary microvascular disease
Precipitating fx: exercise, stress
Long lasting (>30 minutes)

64
Q

Tx for stable, unstable, MVD angina:

A

Reduce O2 demand

Easier to treat pharmacologically

65
Q

Tx for variant angina:

A

Vasodilators

Nitrates or CCB

66
Q

Factors effecting oxygen availability for the heart:

A

Arterial pO2 concentration
Hgb concentration
Coronary flow and distribution
O2 extraction and coronary microcirculation

67
Q

Factors effecting oxygen requirements of the heart:

A

HR
contractile state
wall tension

68
Q

Coronary blood flow is related to:

A

Perfusion pressure
Duration of diastole (no flow during systole)
Inversely proportional to coronary vascular bed resistance

69
Q

Targets to relax vascular tone:

A

Block Ca++ influx
Open K+ channels
Increase cAMP
Increase cGMP

70
Q

Increasing cAMP causes..

A

More phosphorylation of MLCK which inhibits phosphorylation of MLC preventing contraction

71
Q

Increasing cGMP causes..

A

Un-phosphorylation of MLC preventing it from interacting with actin

72
Q

Actions on vascular smooth muscle:

NO, Nitrates, Nitrites

A

Activates GC –> increases cGMP –> relaxation

best response is in large veins

73
Q

Actions on vascular smooth muscle:

Beta-2 Agonists

A

GPCR–> cAMP –> Relaxation (mainly respiratory)

74
Q

Actions on vascular smooth muscle:

Beta-blockers

A

Decrease demand of heart

75
Q

Actions on vascular smooth muscle:

CCB

A

less total Ca++ –> relaxation

76
Q

Actions on vascular smooth muscle:

Sildenafil

A

Blocks PDE5–>increases cGMP –> relaxation

77
Q

Nitrates and Nitrites action:

A 
(primary action: decrease venous return to heart)
Increase venous capacitance
Decrease ventricular preload
Decrease heart size
Decrease CO
78
Q

Nitrates and Nitrites SE:

A 
Orthostatic hypotension
Syncope
HA
Reflex tachycardia
hemoglobin interactions (meth-hgb)
79
Q

Nitrates and Nitrites tolerance:

A

continuous dose
long term exposure
workplace exposure

80
Q

Nitrates and Nitrites carcinogenicity:

A

nitrogen in foods

powerful carcinogen in animals

81
Q

Nitrates and Nitrites on Angina of effort:

A

Decrease venous return to heart

Reduction in intra-cardiac volume

82
Q

Nitrates and Nitrites on Variant angina:

A

Relax coronary arteries

Relieve coronary artery spasm

83
Q

Nitrates and Nitrites on unstable angina:

A

Dilation of coronary arteries

84
Q

Ca++ Channel Blockers (CCB) action:

Vessels

A

long lasting smooth muscle relaxation (mainly vascular)
Reduce BP
Decrease PVR
Decrease coronary arterial tone

85
Q

CCB action:

heart

A

Decrease contractility
Decrease SA node rate
Decrease AV node conduction velocity

86
Q

CCB toxicity:

A

Serious cardiac suppression (rare)

More toxicity with immediate acting

87
Q

CCB contraindicated in:

A 
AV block
arrhythmia
low BP
digoxin
unstable angina
CHF
88
Q

CCB in variant angina:

A

Decreased myocardial contractile force
Decreased myocardial oxygen demand

Decreased arteriolar tone
Decreased PVR

Decreased atrial/ventricular pressure
Decreased left ventricle wall stress

Decreased HR

Prevents coronary spasm

89
Q

Beta blockers

A 
Not vasodilators
Decrease O2 demand
Decrease HR
Decrease contractility
Decrease BP
90
Q

Beta blockers use in angina:

A

Angina of effort

Silent (ambulatory) ischemia

91
Q

Angina risk factors:

A

smoking
HTN
hyperlipidemia

92
Q

Tx for stable angina in HTN patient:

A

CCB

Beta blocker

93
Q

Tx for stable angina in normal BP patients:

A

longer-acting nitrates

94
Q

Tx for vasospastic angina:

A

Nitrates

CCB

95
Q

Systolic Heart failure

A 
reduced cardiac function (thinned walls)
decreased CO (bc of decreased force)
decreased EF
96
Q

Diastolic heart failure

A

reduced cardiac filling (heart or peripheral cause)
thickened walls (chronic HTN)
decreased CO (bc of decreased volume)
normal EF
(doesn’t respond well to positive inotropic drugs)

97
Q

Congestive heart failure

A

increased left ventricle pressure at end diastole.

results in increased pulmonary pressure and pulmonary edema

98
Q

Classes of heart failure: Stage A

A

High risk of HF, without structural heart disease/symptoms

99
Q

Classes of heart failure: stage B

A

Heart disease with asymptomatic left ventricular dysfunction

100
Q

Classes of heart failure: stage C

A

Prior or current symptoms of HF

101
Q

Classes of heart failure: stage D

A

Advanced heart disease and severely symptomatic or refractory HF

102
Q

Long-term tx of HF

A

therapy directed at non-carediac targets maybe more useful: ACE-I, ARB, B-Blockers, Aldosterone receptor antagonist, Vasodilators

103
Q

High output heart failure

A

not a heart issue, cause is in the periphery (Hyperthyroidism, beriberi, anemia, arteriovenous shunts)

104
Q

Cardiac performance: 4 factors

A

preload
afterload
contractility
heart rate

105
Q

Decrease Preload tx:

A

salt restriction
diuretics
vasodilation

Fall Pharm (8 decks)

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