Cardio USMLE Flashcards

1
Q

pregnant woman in 3rd trimester has normal BP when standing and sitting. When supine BP drops to 90/50.
what is the dx?

A

compression of the IVC

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2
Q

35 y/o man has high BP in arms and lowBP in his legs.

what is the dx

A

coarction of teh aorta

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3
Q

5 y/o boy presents weith a systolic murmur and a wide fixed split S2. what is the dx

A

ASD

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4
Q

During a game a young football player collapses and dies immediately. What is the most likely type of cardiac dz

A

hypoertrophic cardiomyopathy

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5
Q

pt has a stroke after incurring multiple long bone fractures in trauma stemming from a MVA. What caused the infarct

A

fat emboli

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6
Q

elderly woman presents with a headache and jaw pain. labs show elevated ESR. what is teh dx

A

temporal arteritis

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7
Q

80 y/o man presents w/ systolic crescendo-decrescendo murmur. What is the most likely cause?

A

aortic stenosis

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8
Q

Man starts a medication for hyperlipidemia. He then develops a rash, pruritis, and GI upset. What drug was it

A

Niacin

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9
Q

Pt developes a cough and must discontinue captopril. What is a good replacement drug and why doesn’t it have the same side effects?

A

losartan, an angiotensin II receptor antagonist, does not increase bradykinin as captopril does.

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10
Q

What are the 3 sx inside the carotid sheath

A

1) Internal jugular Vein (lateral)
2) Common carotid Artery (medial)
3) Vagus Nerve (posterior)

mneu: VAN

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11
Q

In the majority of cases, the SA and AV nodes are supplied by this carotid artery?

A

Right coronary artery

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12
Q

80% of the time the Right coronary artery is “dominant”, suppplying the left ventricle via the _________ branch

A

Posterior descending artery

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13
Q

cardiac output =

A

SVxHR

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14
Q

During exercise, CO ↑ initially as a result of an ↑ in ____. After prolonged exercise, CO ↑ as a result of an ↑ in ____.

A

SV

HR

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15
Q

Mean argerial Pressure (MAP)=
give 2 equasions:
1) CO, TPR
2) systolic, diastolic

A

1) CO x TPR

2) 1/3 systolic +2/3 diastolic

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16
Q

CO=

rate of O2 consumption, aa O2 content, vv O2 content

A

rate of O2 consumption
_______________________
aa O2 content-vv O2 content

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17
Q

Pulse pressure =

systolic, diastolic

A

systolic-diastolic

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18
Q

pulse pressure ≈

A

stroke volume

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19
Q

SV=
(2 equasions)
1) CO, HR
2)EDV,ESV

A

1) =CO/HR

2) =EDV-ESV

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20
Q

Coronary Artery Anatomy [pic]

A

1) Right Coronary aa (RCA)
2) Left main coronary aa (LCA)
3) Circumflex artery (CFX)
4) Left anterior descending aa (LAD
5) Posterior descending aa (PD)
6) Acute marginal aa

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21
Q

Stroke volume is affected by what 3 things

mneu: SV CAP

A

Contractility, Afterload, and Preload

mneu: SV CAP

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22
Q

↑Preload →__SV

A

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23
Q

↑Afterload→ __SV

A

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24
Q

↑contractility→ __SV

A

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25
Q

SV ___ in anxiety, exercise, & pregnancy

A

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26
Q

a failing heart has a ___ SV

A

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27
Q

Contractality (and SV), ____ with catecholemines

A

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28
Q

Contractality (and SV), ____ with ↑ intracellular Ca++

A

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29
Q

Contractality (and SV), ____ with ↓ extracellular sodium

A

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30
Q

Contractality (and SV), ____ with digitalis

A

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31
Q

Contractality (and SV), ____ with β1 blockade

A

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32
Q

Contractality (and SV), ____ with heart failure

A

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33
Q

Contractality (and SV), ____ with acidosis

A

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34
Q

Contractality (and SV), ____ with hypoxia/hypercapnea

A

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35
Q

Contractality (and SV), ____ with Ca++ channel blockers

A

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36
Q

Myocardial demand is ___ by ↑ afterload (diastolic BP)

A

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37
Q

Myocardial demand is ___ by ↑ contractility

A

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38
Q

Myocardial demand is ___ by ↑ heart rate

A

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39
Q

Myocardial demand is ___ by ↑ heart size

A

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40
Q

ventricular EDV

A

Preload

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41
Q

Systolic arterial pressure

A

afterload

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42
Q

proportional to peripheral resistance

A

afterload

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43
Q
venous dialators (e.g. nitroglycerine) ↓ \_\_\_\_\_\_\_
(preload or afterload)
A

preload

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44
Q
vaso dialators (e.g. hydralazine) ↓ \_\_\_\_\_\_\_
(preload or afterload)
A

afterload

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45
Q

______ ↑ w/ exercise, ↑ blood volume, exitement (sympathetics)

(preload or afterload)

A

Preload

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46
Q

Starling Curve: Force of _______ is proportional to initial length of cardiac mm fiber (preload)

A

contraction

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47
Q

contraction state of the myocardium is ____ by circulating catecholamines
(+,-)

A

+

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48
Q

contraction state of the myocardium is ____ by digitalis

+,-

A

+

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49
Q

contraction state of the myocardium is ____ by sympathetic stimulation
(+,-)

A

+

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50
Q

contraction state of the myocardium is ____ by pharmacologic depressants
(+,-)

A

-

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51
Q

contraction state of the myocardium is ____ by loss of myocardium (MI)
(+,-)

A

-

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52
Q

EF=
(give 2 equasions)
1) SV, EDV
2) EDV, ESV, EDV

A

1) SV/EDV

2) EDV-ESV/EDV

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53
Q

this is an index of ventricular contractility

A

EF

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54
Q

EF is normally > ___%

A

55

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55
Q

Place condition on the Starling curve [pic p.219]

A

1) exercise
2) CHF + digitalis
3) CHF

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56
Q

(driving Pressure)ΔP=

Q (flow) ,R (resistance)

A

Q x R

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57
Q

Resisitance (R) =
Give 2 equasions:
1)ΔP(driving pressure),flow(Q)
2)n(viscosity), length(l), radius (r)

A

1) =ΔP/Q

2) 8nxl/Πr(^4)

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58
Q

viscosity depends mostly on _______

A

hematocrit

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59
Q

increased ______ in:

1) Polycythemia
2) Hyperproteinemic states (e.g., multiple myeloma)
3) hereditary spherocytosis

A

viscosity

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60
Q

resistance is ________ to viscosity

proportional or inversely proportional

A

proportional

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61
Q

resistance is ________ to the radius to the 4th power

proportional or inversely proportional

A

inversely proportional

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62
Q

cardiac and vascular fx curves [pic p.219]

A

1) (+) inotropy
2) (-) inotropy
3) (↑) blood volume
4) (↓) blood volume

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63
Q

cardiac cycle image [p. 220]

A

1) isovolumetric contraction
2) aortic valve opens
3) ejection
4) aortic valve closes
5) isovolumetric relaxation
6) mitral valve opens
7) ventricular filling
8) mitral valve closes

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64
Q

Name the phase of the cardiac cycle:

period between mitral valve closure and aortic valve opening.

A

isovolumetric contraction

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65
Q

Name the phase of the cardiac cycle: period of highest O2 consumption

A

isovolumetric contraction

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66
Q

Name the phase of the cardiac cycle: period between aortic valve opening and closing

A

systolic ejection

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67
Q

Name the phase of the cardiac cycle: period between aortic valve closing and mitral valve opening

A

isovolumetric relaxation

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68
Q

Name the phase of the cardiac cycle: period just after mitral valve opening

A

rapid filling

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69
Q

Name the phase of the cardiac cycle: period just before mitral valve closure

A

slow filling

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70
Q

name the heart sound: mitral and tricuspid valve closure

A

S1

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71
Q

name the heart sound: aortic and pulmonary valve closure

A

S2

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72
Q

name the heart sound: at the end of rapid ventricular filling

A

S3

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73
Q

name the heart sound: high atrial pressure/stiff ventricle

A

S4

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74
Q

this heart sound is associated w/ dilated CHF

A

S3

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75
Q

this heart sound AKA “atrial kick” is associated with a hypertrophic ventricle

A

S4

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76
Q

Jugular venous pulse waves:

a wave

A

Atrial contraction

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77
Q

Jugular venous pulse waves: c wave

A

RV Contraction (tricuspid valve bulging into atrium)

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78
Q

Jugular venous pulse waves: v wave

A

increaseed atrial pressure due to filling against closed tricuspid Valve

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79
Q

jugular venous distention is seen in ___________

A

right heart failure

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80
Q

when the aortic valve closes before the pulmonic this heart sound abnormality results

A

S2 splitting

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81
Q

S2 splitting is increased upon ________

A

inspiration

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82
Q

Paradoxical splitting (S2 split increasd upon expiration is associated with what?

A

aortic stenosis

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83
Q

cardiac mm contraction is dependent on extracellular ________, which enters the cells during plateau of action potential and stimulates ______ release from the cardiac mm sarcoplasm reticulum.

A

calcium
calcium

calcium induced calcium release

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84
Q

In contrast to skeletal mm, cardiac mm action potential has a plateau, which is due to ____ influx.

A

Ca+

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85
Q

In contrast to skeletal mm, cardiac nodal cells ________ depolarize, resulting in automaticity

A

spontaneously

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86
Q

In contrast to skeletal mm, cardiac myocytes are electrically coupled to each other by ________

A

gap junctions

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87
Q

myocardial action potential occurs in atrial and ventricular myocytes and ________

A

perkinje fibers

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88
Q

In a myocardial action potential, this phase is the rapid upstroke, when voltage gated Na+ channels open

A

phase 0

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89
Q

In a myocardial action potential, this phase is the initial repolarization-inactivation of voltage0gated Na+ channels. Voltage gated K+ channels begin to open

A

Phase 1

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90
Q

In a myocardial action potential, this phase is the plateu–Ca++ influx through voltage-gated Ca++ channels balances K+ efflux. Ca++ influx triggers another Ca++ release from sarcoplasmic reticulum and myocyte contraction.

A

phase 2

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91
Q

In a myocardial action potential, this phase is the rapid repolarization–massive K+ efflux due to opening of voltage-gated slow K_ channels and closure of voltage gated Ca++ channels.

A

Phase 3

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92
Q

In a myocardial action potential, this phase is the resting potential–high K+ permeability through K+ channels.

A

phase 4

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93
Q

Pacemaker action potentials occur where

A

SA & AV nodes

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94
Q

In a pacemaker action potential this phase is the upstroke phase–it involves opening of voltage-gated Ca++ channels. These cells lack fast voltage-gated Na+ channels. Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles.

A

phase 0

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95
Q

In a pacemaker action potential this phase, the plateau is absent.

A

phase 2

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96
Q

In a pacemaker action potential this phase, the slow diastolic depololarization results in membrane potential spontaneously depolarizing as Na+ conductance increases. This accounts for automaticity of SA and AV nodes. The slope of this phase in the SA node determines the heart rate. ACh decreases and catecholamines increasee the rate of diastolic depolarization decreasing or increasing heart rate respectively.

A

phase 4

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97
Q

electrocardiogram: atrial depolarization

A

P wave

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98
Q

electrocardiogram: conduction delay through AV node (normally <200 msec)

A

PR segment

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99
Q

electrocardiogram: vetricular depolarization (normally < 120 msec)

A

QRS complex

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100
Q

electrocardiogram: mechanical contraction of the ventricles

A

QT interval

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101
Q

electrocardiogram: ventricular repolarization

A

T wave

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102
Q

electrocardiogram:

atrial repolarization is masked by _______

A

QRS complex

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103
Q

electrocardiogram: isoelectric, ventricles depolarized

A

ST segment

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104
Q

electrocardiogram: These waves caused by hypokalemia

A

U wave

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105
Q

this syndrome is caused by an accessory conduction pathway from atria to vetricle (bundle of kent), bypassing AV node. As a result, ventricles begin to partially depolarize earlier, giving rise to characteristic delta wave on ECG. May result in reentry current leading to supraventricular tachycardia [image p.223]

A

Wolff-Parkinson-White syndrome

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106
Q

This ECG tracing has a chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes (pic. p 224)

A

Atrial fibrillation

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107
Q

This ECG tracing has a rapid succession of identical, back to back atrial depolarization waves. The identical appearance accounts for the “sawtooth” appearance of the flutter waves. (pic. p 224)

A

Atrial flutter

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108
Q

In this condition PR interval is prolonged (>200 msec). Asymptomatic.
(pic. p 224)

A

1st degree AV block.

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109
Q

Progressive lenthening of the PR interval until a beat is “dropped” (a P wave not followed by a QRS complex). Usually asymptomatic. (pic. p 224)

A

2nd degree AV block

Mobitz type I (Wenckebach)

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110
Q

On ECG shows dropped beats that are not preceded by a change in the length of the PR interval. These abrupt, nonconducted P waves result in a pathologic condition. It is often found as a 2:1 block, where there are 2 P waves to 1 QRS response. May progress to 3rd degree block.(pic. p 225)

A

Mobitz type II AV block

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111
Q

In this condition, the atria and ventricles beat independently of each other. Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes. The atrial rate is faster than the ventricular rate. Usually treat with pacemaker.

A

3rd degree AV block (complete)

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112
Q

completely erratic rhythm with no identifiable waves. Fatal arrhythmia without immediate CPR and defibrillation. (pic. p 225)

A

Ventricular Fibrillation

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113
Q

________receptor transmits via vagus nn to medulla (responds only to increase blood pressure)

A

aortic arch receptor

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114
Q

________ receptor transmits via glossopharyngeal nn to medulla

A

carotid sinus

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115
Q

decreased firing by aroreceptors during hypotension results in an increase in efferent ________ firing

A

sympathetic

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116
Q

In a carotid massage, the increased pressure on carotid aa results in increased stretch and ____ in heart rate

A

decrease

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117
Q

Peripheral chemoreceptors in the carotid and aortic bodies respond to (3 things)

A

decreased PO2 (<60mmHg), increased PCO2 and decreased pH of blood

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118
Q

Central chemoreceptors respond to what changes (2)

A

changes in pH and Pco2 (not Po2)

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119
Q

This chemoreceptor is responsible for Cushing reaction, response to cerebral ischemia, response to increase intracranial pressure leads to hypertension (sympathetic response) and bradycardia (parasympathetic response)

A

Central chemoreceptor

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120
Q

This orgen gets the largest share of systemic cardiac output

A

liver

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121
Q

this organ gets the highest blood flow per gram of tissue

A

kidney

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122
Q

this orgen has a large arteriovenous O2 differnece. Increased O2 demand is met by increased coronary blood flow, not by increased extraction of O2.

A

heart

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123
Q

this is a good approximation of L atrial pressure and measured with a Swan-Ganz catheter

A

Pulmonary capillary wedge pressure

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124
Q

blood flow is altered to meet demands of tissue

A

autoregulation

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125
Q

Name the organ regulated by the local metabolites:

O2 adenosine, NO

A

heart

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126
Q

Name the organ regulated by the local metabolites:

CO2 (pH)

A

brain

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127
Q

Name the organ regulated by the local metabolites: Myogenic and tubuloglomerular feedback

A

kidneys

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128
Q

Name the organ regulated by the local metabolites: hypoxia causes vasoconstriction

A

lungs

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129
Q

_______ vasculature is unique in that hypoxia causes vasoconstriction (in other organs hypoxia causes vasodilation)

A

pulmonary

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130
Q

Name the organ regulated by the local metabolites: lactate, adenosine, K+

A

skeletal mm

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131
Q

Name the organ regulated by the local metabolites: sympathetic stimulation most important mechanism–temp control

A

skin

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132
Q

______ forces determine fluid movement by osmosis throug capillary membranes

A

starling

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133
Q

moves fluid out of capillary

A

P(c) capillary pressure

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134
Q

moves fluid into capillary

A

P(i) interstitial fluid pressue

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135
Q

moves fluid into capillary

A

π(c) plasma colloid osmotic pressure

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136
Q

moves fluid out of capillary

A

π(i) interstitial fluid colloid osmotic pressure

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137
Q

net filtration pressure=Pnet=

A

[Pc-Pi)-(πc-πi)]
capillary pressure -interstitial pressure
-
plasma colloid osmotic presure - interstitual fluid colloid osmotic pressures

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138
Q

Kf=

A

filtration constant (capillary permeability)

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139
Q

excess fluid outflow into interstitium

A

edema

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140
Q

edema is commonly caued by ___ capillary pressure (give example)

A

↑ P(c)

Heart failure

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141
Q

edema is commonly caued by ___ plasma protiens(give example)

A

↓π(c) plasma proteins

nephrotic syndrome, liver failure

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142
Q

edema is commonly caused by ___ capillary permeability (give example)

A

↑Kf

infections, burns

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143
Q

edema is commonly caued by ___ interstitial fluid colloid osmotic pressure
(give example)

A

↑ πi

lymphatic blockage

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144
Q

right-to-left shunts (early cyanoisis) “blue babies”

A

3 Ts
Tetrology
Transposition
Truncus

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145
Q

Children with this type of shunt may squat to increase venous return

A

right to left shunts

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146
Q

Right-to Left shunts (early cyanosis) - “blue babies”

A

1) Tetrology of fallot
2) Transposition of great vessels
3) Truncus arteriosis

The 3 Ts

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147
Q

children with this type of shunt may squat to increase venous return.

A

right to left shunt

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148
Q

Left to right shunts (late cyanosis) - “blue kids”

A

1) VSD
2) ASD
3) PDA

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149
Q

this is the most common cause of early cyanosis

A

tetralogy of fallot

150
Q

this is the most common congenital cardiac anomaly

A

VSD

151
Q

this congenital heart dz manifests itself with a loud S1 and a wide, fixed split S2

A

ASD

152
Q

this congenital heart defect is closed with indomethacin

A

PDA

153
Q

give the frequency of occurance with
PDA
VSD
ASD

A

VSD>ASD>PDA

154
Q

Uncorrected VSD, ASD or PDA leads to progressive pulmonary hypertension. As pulmonary resistance increases, the shunt reverses from L to R to R to L, which causes late cyanosis (clubbing & polycythemia). [pic p. 228]

A

eisenmenger’s syndrome

155
Q

Tetrology of Fallot [pic. p 228]

A

1) Pulmonary stenosis
2) RVH
3) Overiding aorta (overides VSD)
4) VSD

mneu: PROVe

156
Q

most important determinant for prognosis of tetrology of fallot

A

pulmonary stenosis

157
Q

ON x-ray TOF looks ________

A

boot shaped

158
Q

give the frequency of occurance with
PDA
VSD
ASD

A

VSD>ASD>PDA

159
Q

Aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior)leading to separation of systemic and pulmonary circulations.

A

Transposition of great vessels

160
Q

Transposition is not compatable with life unless a _____is present to allow adequate mixing of blood
[pic p. 229]

A

shunt (e.g. VSD, PDA or patent foramen ovale)

161
Q

transposition of great vessels is due to failure of the _________ septum to spiral

A

aorticopulmonary

162
Q

this type of coarction of aorta is aortic stenosis proximal to insertion of ductus arteriosus (preductal)

A

infantile

INfantile: IN close to the heart

163
Q

this type of coarction of aorta is aortic stenosis is distal to ductus arteriosus (postductal) it is associated with notching of the ribs, hypertension in upper extremities, weak pulses in lower extremities.

A

adult type

aDult: Distal to Ductus

164
Q

Coarction of aorta has a male: female ratio of ____

A

3:1

165
Q

what is best way to diagnose coartation of aorta

A

femoral pulses on pysical exam

166
Q

In fetal period, shunt is right to left. In neonatal period, lung resistance decreases and shunt becomes L to R w/ subsequent RVH and failure. [pic p. 229]

A

patent ductus arteriosis

167
Q

______ is used to closed a PDA

A

indomethacin

168
Q

______ is used to keep a PDA open, which may be necessary to sustain life in conditions such as transposition of the great vessels

A

PGE

169
Q

Congenital cardiac defect associations:

22q11

A

truncus arteriosus, tetralogy of Fallot

170
Q

Congenital cardiac defect associations:

Down syndrome

A

ASD, VSD

171
Q

Congenital cardiac defect associations:

Congenital rubella

A

septal defects, PDA

172
Q

Congenital cardiac defect associations:

Turners syndrome

A

coarctation of aorta

173
Q

Congenital cardiac defect associations:

Marfan’s syndrome

A

aortic insufficiency

174
Q

Congenital cardiac defect associations: Offspring of diabetic mother

A

transposition of great vessels

175
Q

Hypertension

A

BP >140/90

176
Q

HTN risk factors

A

increase age, obesity, diabetes, smoing, genetics, blck>white>asians

177
Q

90% of hypertension is this kind

A

essential

178
Q

essentail hypertention is related to either one of these two factors

A

increased CO or TPR

179
Q

10% of HTN is mostly secondary to ______ dz

A

renal

180
Q

this type of HTN is severe and rapidly progressing

A

malignant

181
Q

HTN predisposes pts to (give 3)

A

athrosclerosis, stroke, CHF, renal failure, retinopathy, & aortic dissection

182
Q

Hyperlipidemia signs:

Plaques in blood vessel walls

A

Atheromata

183
Q

Hyperlipidemia signs:

plaques or nodules composed of lipid-laden histocytes in the skin, especially the eyelids

A

Xanthoma

184
Q

Hyperlipidemia signs: lipid deposits in the tendon, esp. the achilles

A

Tendinous xanthoma

185
Q

Hyperlipidemia signs: lipid deposit in cornea, nonspecific (arcus senilis)

A

corneal arcus

186
Q

This type of arteriosclerosis is in the media of the arteries, esp radial or ulnar. Usually benign.

A

Monckeberg

187
Q

This type of arteriosclerosis is hyalin thickening of small arteries in essential hypertension. Hyperplastic “onion skinning” in malignant hypertension.

A

Arteriolosclerosis

188
Q

This type of arteriosclerosis is when fibrous plaques and atheromas form in intima of arteries

A

atherosclerosis

189
Q

this is a disease of elastic arteries and large and medium sized mm arteries (image 79)

A

atherosclerosis

190
Q

risk factors for atherosclerosis

A

smoking, hypertension, dbts, hyperlipidemia, family hx

191
Q

progression of atherosclerosis

complex atheromas, fatty streaks, proliferative plaque

A

fatty streaks to proliferative plaque to complex atheromas

192
Q

complications of atherosclerosis (give 3)

A

aneurisms, ischemia, infarcts, peripheral vascular dz, thrombus, emboli

193
Q

most common location of atherosclerosis

A

abdominal aorta> coronary artery>popliteal artery>carotid artery

194
Q

symptoms of atherosclerosis

A

angina, claudication, but can be asymptomatic

195
Q

CAD narrowing >75%

A

angina

196
Q

retrosternal chest pain with exertion , mostly secondary to atherosclerosis

A

stable angina

197
Q

chest pain occurring at rest secondary to corony artery spasm

A

prinzmetal’s variant (unstable angina)

198
Q

worsening of chest paiin due to thrombosis but no necrosis

A

unstable/crescendo angina

199
Q

most often acute thrombosis due to coronary artery atherosclerosis. Results in myocyte necrosis

A

myocardial infarction

200
Q

death from cardiac causes within 1 hour of onset of symptoms, most commonly due to a lethal arrythmia

A

sudden cardiac death

201
Q

progressive onset of CHF over many years due to chronic ischemic myocardial damage

A

chronic ischemic heart dz

202
Q

infarcts occuring in loose tissues with collaterals, such as lungs, intestine, or follwing reperfusion

A

red (hemorrhagic) infarcts

REd=REperfusion

203
Q

infarcts occur in solid tissues with single blood supply, such as brain, heart, kidney and spleen.

A

pale infacts

204
Q

give order of highest frequency of coronary artery occlusion

CFX, LAD, RCA

A

LAD>RCA>CFX

205
Q

symptoms of MI (give 4)

A

diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm or jaw, shortness of breath, fatigue, adrenergic symptoms.

206
Q

How long ago did the MI occur?

Occluded artery but no visable change by light microscopy

A

2-4 hours

207
Q

How long ago did the MI occur?

Gross: dark mottling; pale with tetrazolium stain.

Micro: coagulative nocrosis. coagulation bands visable. release of contents of necrotic cells into bloodstream and the begining of neutrophil emigration.

A

after 4 hrs. 1st day

208
Q

How long ago did the MI occur?

Gross: hyperemic border; central yellow-brown softening.

Micro: outer zone (ingrowth of granulation tissue), macrophages, & neutrophils

A

5-10 D

209
Q

How long ago did the MI occur?

Gross: grey-white
Micro: scar complete

A

7 weeks

210
Q

dx of MI what is gold standard in the 1st 6 hrs

A

ECG

211
Q

This lab test rises after 4 hours and is elevated for 7-10D.

A

troponin I

212
Q

this lab test is more specific than other protein markers

A

troponin I

213
Q

This is predominantly found in myocardium but can also be relased from skeletal mm

A

CK-MB

214
Q

This is nonspecific and can be found in cardiac, liver and skeletal mm cells

A

AST

215
Q

ECG changes include ST elevation which indicates

A

transmural infarct

216
Q

ECG changes include ST depression which indicates

A

subendocardial infarct

217
Q

ECG changes include pathological Q waves

A

transmural infact

218
Q

This MI complication is the most important cause of death before reaching hosptial; it is common in the 1st few days

A

cardiac arrhythmia

219
Q

This MI complication results in pulmonary edema

A

LV failure

220
Q

This MI complication has a high risk of mortanilty and occurs when there is a large infarct

A

cardiogenic shock

221
Q

Rupture of ventricular free wall, interventricular septum, or paillary mm, usually occurs _____ post MI

A

4-10D

222
Q

This MI complication of an MI results in decreased CO, a risk of arrythmia, and embolus from mural thrombus

A

aneurism formation

223
Q

this MI complication is also known as a friction rub and occurs 3-5 D post MI

A

fibrinous pericarditis

224
Q

This MI complication is an autoimmune phenomenon resulting in fibrinous pericarditis, several weeks post-MI

A

dresslers syndrome

225
Q

This is the most common cardiomyopathy (90%)

A

dialated (congestive) cardiomyopathy

226
Q

In dialated (congestive) cardiomyopathy ________ dysfunction ensues

A

systolic

227
Q

In this type of cardiomyopathy, the heart looks like a baloon on chest x-ray

A

dialated (congestive) cardiomyopathy

228
Q

etiology of dialated (congestive) cardiomyopathy

A
Alcohol 
Beriberi
Coxsackie B
Cocaine
Chagas dz
Doxorubicin
peripartum
hemochromatosis
229
Q

this type of cardiomyopathy often involves an asymetric enlargement of the intraventricular septum

A

hypertrophic cardiomyopathy

230
Q

In hypertrophic cardiomyopathy ______ disfunction occurs

A

diastolic

231
Q

hypertrophic cardiomyopathy is a __________ trait, and 50% are familial

A

autosomal dominant

232
Q

This is a very common cause of sudden death in young athletes.

A

hypertrophic cardiomyopathy

233
Q

What are the heart sound findings with hypertrophic cardiomyopathy

A

loud S4, apical impulses, systolic murmur

234
Q

How do you tx hypertrophic cardiomyopathy

A

Beta blocker

235
Q

major causes of this type of cardiomyopathy include sarcoidosis, amyloidoss, postratdiation fibrosis, endocarrdial fibroelastosis, and endomyocardial fibrosis (Loffler’s)

A

restrictive/obliterative cardiomyopathy

236
Q

Heart Murmurs:

holostolic, high piched “blowing murmur” loudest at apex[pic. p 234]

A

mitral regurgitation

237
Q

Heart Murmurs: crecendo-decrescendo systolic ejection murmur following ejection click. radiates to carotids/apesx. “pulsus parvus et tardus” pulses weak compared to heart sounds
[pic. p 234]

A

aortic stenosis

238
Q

Heart Murmurs:
holosystolic murmur
[pic. p 234]

A

VSD

239
Q

Heart Murmurs:
Late systolic murmur with midsystolic click. Most frequent valvular lesion
[pic. p 234]

A

mitral prolapse

240
Q

Heart Murmurs:
immediate high-pitched “blowing” diastolic murmur. Wide puse pressure
[pic. p 234]

A

aortic regurgitation

241
Q

Heart Murmurs: follows opening snap. delayed rumbling late diastolic murmur.
[pic. p 234]

A

mitral stenosis

242
Q

Heart Murmurs: Continuous machine like murmur. Loudest at time of S2
[pic. p 234]

A

PDA

243
Q

most common primary cardiac tumor in adults. Usually described as a “ball-valve” obstruction in the LA

A

myxomas.

244
Q

90% of myxomas occur in the _____

A

atria (mostly LA)

245
Q

Most frequent primary cardiac tumor in children, associated with tuberous sclerosis

A

rhabdomyomas

246
Q

Most common heat tumor (see color image 88)

A

metasteses

247
Q

Given the pathophysiology tell me the symptom of CHF:

failure of LV output to increase during exercise

A

dyspnea on exertion

248
Q

Given the pathophysiology tell me the symptom of CHF: greater ventricular end-diastolic volume

A

cardiac dilation

249
Q

Given the pathophysiology tell me the symptom of CHF:
Lv ventrical failure leads to increased pulmonary venous pressure which leads to pulmonary venous distention and transudation of fluid.

A

pulmonary edema (paroxysmal nocturnal dyspnea)

250
Q

this CHF abnormality is associated with presence of hemosiderin-laden macrophages

A

pulmonary edema

251
Q

Given the pathophysiology tell me the symptom of CHF: increase venous return in supine position exacerbates pulmonary vascular congestion

A

orthopnea (shortness of breath when supine)

252
Q

Given the pathophysiology tell me the symptom of CHF: increased central venous pressure leading to increased resistance to portal flow.

A

hepatomegaly (nutmeg liver)

253
Q

Given the pathophysiology tell me the symptom of CHF: RV failure leads to increased venous pressure which leads to fluid transudation

A

ankle , sacral edema

254
Q

embolus types

A

Fat, Air, Thrombus, Bacteria, Amniotic fluid, Tumor

mneu: an embolus moves like a a FAT BAT

255
Q

this type of emboli are associated with long bone fractures and liposuction.

A

fat

256
Q

approximately 95% of pulmonary emboli arise from where?

A

deep leg veins

257
Q

this type of emboli can lead to DIC, especially postpartum

A

amniotic fluid

258
Q

this type of embolus is associated with chest pain, tachypnea, and dyspnea

A

pulmoary embolus

259
Q

compression of heart by fluid (i.e.,blood) in pericardium, leading to decreased cardiac output and equilibration of pressures in all four chambers.

A

cardiac tamponade

260
Q

youre pt presents with hypotension, JVD, and distant heart sounds. He shows pulsus paradoxus and ECG shows electrical alternans

A

cardiac tampanad

261
Q

pulsus paradoxus

A

(exaggeration of nml variation in the systemic arterial pulse volume with respiration– becoming weaker with inspiration and stronger with expiration)

262
Q

electrical alternans

A

(beat to beat alterations in QRS complex height)

263
Q

Symptoms of bacterial endocarditis

A
Fever
Roth spots
osler nodes
Murmur (new)
Janeway lesions
Anemia
Nail-bed hemorrhage
Emboli

mneu: bacteria FROM JANE

264
Q

osler nodes

A

tender raised lesions on finger or toe pads

265
Q

Roth’s spots

A

round white spotss on retina surrounded by hemorrhage

266
Q

Janeway lesions

A

small erythematous lesions on palm or sole

267
Q

What is the most frequently involved valve in bacterial endocarditis

A

mitral valve

268
Q

What valve is associated with endocarditis associated with IV drug abuse

A

tricuspid valce

269
Q

what are some of the complications associated with bacterial endocartitis (give 2)

A

chordae rupture
glomerulonephritis
supportive pericarditis
emboli

270
Q

acute endocarditis has a rapid onset. It results from large vegetations on previously normal valves. It is most often caused by this bug.

A

S. aureus (high virulence)

271
Q

Subacute bacterial endocarditis has a more insidious onset. It consists of smaller vegetations on congentitally abnormal or diseased valves. It can be a sequela of dental procedures. Often caused by this bug

A

viridans streptococcus (low virulence)

272
Q

endocarditis may also be nonbacterial and secondary to these 2 conditions

A

metastasis or renal failure (marantic/ thrombotic endocarditis)

273
Q

In this condition, associated with lupus, vegetations develop on both sides of valve leading to mitral valve stenosis but do not embolize

A

libman-sacks endocarditis

mneu: SLE causes LSE

274
Q

Rhematic heart dz is a late consequence of pharyngeal infection with this organism

A

a beta hemolytic streptococci

275
Q

rhematic heart dz affects heart valves in this order

A

mitral>aortic»tricuspid

mneu: high pressure valves associated most.

276
Q

Give the symptoms of rheumatic heart dz

A
Fever
Erythema marginatum
Valvular damage
ESR (high)
Red-hot joints (polyartheritis)
Subcutaneous nodules
St. Vitus' dance (chorea)

mneu: FEVERSS

277
Q

This is associated with Aschoff bodies, migratory polyarthritis, erythema marginatum, elevated ASO titers.

A

Rheumatic heart dz

278
Q

is rheumatic heart dz immune mediated or the direct effect of bacteria

A

immune mediated

279
Q

Associated ith Aschoff bodies and Anitschkow’s cells

A

rheumatic heart dz

mneu: think of 2 RHussians with RHeumatic heart dz (Aschoff & Anischkow)

280
Q

Aschoff bodies

A

granuloma with giant cell

281
Q

Anitschkow’s cells

A

activated histiocytes

282
Q

This condition presents with pericardial pain, friction rub, ECG changes (diffuse ST elevation in all leads) pulsus paradoxus, distant heart sounds

A

pericarditis

283
Q

pericarditis can resolve without scarring however, scarring can lead to this

A

chronic adhesive or chronic constrictive pericarditis

284
Q

this type of pericarditis is caused by SLE, rheumatoid arthritis, infection, or uremia

A

serous pericarditis

285
Q

this type of pericarditis is caused by uremia, MI, rheumatic fever

A

fibrinous pericarditis

286
Q

this type of pericarditis is caused by TB or malignancy (e.g., melanoma)

A

hemorrhagic

287
Q

this dz disrupts the vasa vasora of the aorta with consequent dilation of the aorta and valve ring. It often effects the aortic root and results in calcification of ascending arch of the aorta

A

syphalitic heart dz (tertiary syphalis)

288
Q

This dz can result in aneurism of the ascending aorta or aortic arch and aortic valve incompetence.

A

syphalitic heart dz (tertiary syphalis)

289
Q

This Rx used for HTN has the adverse effect of HYPOKALEMIA, slight hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia

A

hydrochlorothiazide (diuretic)

290
Q

This Rx used for HTN has the adverse effect of potassium wasting, metabolic alkalosis, hypotension, ototoxicity

A

loop diuretics

291
Q

This sympathoplegic used in the tx of HTN has the adverse effect of dry mouth, sedation, severe rebound HTN

A

clonidine

292
Q

This sympathoplegic used in the tx of HTN has the adverse effect of sedation, positive Coomb’s test

A

methyldopa

293
Q

This sympathoplegic used in the tx of HTN has the adverse effect of severe orthostatic hypotension, blurred vision, constipation, sexual disfunction

A

hexamethonium

294
Q

This sympathoplegic used in the tx of HTN has the adverse effect of sedation, depression, nasal stuffiness, diarrhea

A

reserpine

295
Q

This sympathoplegic used in the tx of HTN has the adverse effect of orthostatic and exercise hypotension, sexual dysfunction, diarrhea

A

Guanethidie

296
Q

This sympathoplegic used in the tx of HTN has the adverse effect of 1st dose orthostatic hypotension, dizziness, headache

A

Prazosin

297
Q

This sympathoplegic used in the tx of HTN has the adverse effect of impotence, asthma, bradycardia, CHF, AV block, sedation & sleep alterations

A

B blockers

298
Q

This vasodialator used in the tx of HTN has the adverse effect of nausea, headache, lupus-like syndrome, reflex tachycardia, angina, salt retension

A

hydralazine

299
Q

This vasodialator used in the tx of HTN has the adverse effect of hypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retension

A

minoxidil

300
Q

This vasodialator used in the tx of HTN has the adverse effect of dizziness, flushing, constipation, nausea

A

nifidipine, veripamil (constipation)

301
Q

This vasodialator used in the tx of HTN has the adverse effect of cyaide toxicity (releases CN)

A

nitroprusside

302
Q

This ACE inhibitor used in the tx of HTN has the adverse effect of
Hyperkalemia, Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II

A

Captopril

mneu:CAPTOPRIL-Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II

303
Q

This angiotensin II receptor inhibitor has theadverse effect of fetal renal toxicity, hyperkalemia

A

Losartan

304
Q

This vasodialator used in the tx of HTN has the adverse effect of hypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retension

A

minoxidil

305
Q

This vasodialator used in the tx of HTN has the adverse effect of dizziness, flushing, constipation, nausea

A

nifidipine, veripamil (constipation)

306
Q

This vasodialator used in the tx of HTN has the adverse effect of cyaide toxicity (releases CN)

A

nitroprusside

307
Q

This ACE inhibitor used in the tx of HTN has the adverse effect of
Hyperkalemia, Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II

A

Captopril

mneu:CAPTOPRIL-Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II

308
Q

The MOA of this drug used for severe HTN & CHF is that it increases cGMP leading to smooth mm relaxation. It vasodilates arterioles > veins resulting in a reduction of afterload

A

hydralazine

309
Q

Toxicity of this drug for severe HTN & CHF include compensitory tachycardia, fluid retension, & lupus like syndrome

A

hydralazine

310
Q

The druges Nifedipine, verapamil & diltiazem belong to this category

A

calcium channel blockers

311
Q

The MOA of these drugs is that they block voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce mm contractilty

A

calcium channel blockers

312
Q

give the order of potency of the 3 CCBs (nifedipine, verapamil, diltiazem) in

1) the heart
2) vascular smooth mm

A

heart-verapamil>diltiazem>nifedipine
vascular sm mm–
nifedipine>diltiazem>verapamil

313
Q

CCBs are used in hypertension but also in these 2 conditions

A

angina, arrythymias (not nifedipine)

314
Q

These drugs produce a toxicity of cardiac depression, peripheral edema, flushing, dizziness, & constipation

A

CCBs

315
Q

These 2 drugs used for angina, pulmonary edema, and as an erection enhancer have a MOA of vasodilating by releasing NO in smooth mm, causing an increase in cGMP and smooth mm relaxation. They dialate vv»arteries resulting in a decrease in preload

A

nitroglycerine, isosorbide dinitrate

316
Q

toxicity of these drugs include tachycardia, hypotension, headache, “Monday dz” in industrial exposure, development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend, resulting intahycardia, dizziness, and headache.

A

nitroglycerin, isosorbide dinitrate

317
Q

What are the 2 major Rxs used in the tx of antianginal therapy

A

nitrates & B blockers

318
Q

In antianginal therapy the goal is to do what?

A

reduce myocardial O2 consumption.

319
Q

In order to reduce myocardial O2 consumption you need to decrease 1 or more of the determinants of MVO2 which are give 2(5)

A

1) EDV
2) BP
3) HR
4) contractility
5) ejection time

320
Q

Used for antianginal therapy Nitrates reduce _______ (preload or afterload)

A

preload

321
Q

Used for antianginal therapy B-blockers reduce _______ (preload or afterload)

A

afterload

322
Q

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have.

EDV

A

N (preload):↓
BB (afternoad):↑
C: no effect or ↓

323
Q

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have.

BP

A

N (preload):↓
BB (afternoad):↓
C:↓

324
Q

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have.

Contractility

A

N (preload):↑ (reflex response)
BB (afternoad):↓
C:little or no effect

325
Q

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have.

HR

A

N (preload):↑ reflex response
BB (afternoad):↓
C:↓

326
Q

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have.

Ejection time

A

N (preload):↓
BB (afternoad):↑
C:little or no effect

327
Q

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have.

MVO2

A

N (preload): ↓
BB (afternoad): ↓
C: ↓↓

328
Q

CCBs: Nifedipine is similar to ________ (nitrates or B blockers); Verapamil is similar to ________nitrates or B blockers)

A

Nitrates

B blockers

329
Q

Cardiac drugs: sites of action

A

1) Digitalis (-)
2) CCB (-)
3) B blockers
4) Ryanodine (+)
5) Ca++ sensitizers

330
Q

This cardiac drug inhibits Na+/K+ ATP ase

A

digitalis

331
Q

These 2 cardiac drugs inhibit on voltage gated Ca++ channels

A

CCBs

B blockers

332
Q

This cardiac drug sensitizes Ca++ release channel in the SR

A

Ryanodine

333
Q

These cardiac drug is a site of Ca+ interaction with troponin-tropomyosin system

A

Ca++ sensitizers

334
Q

This cardiac glycoside has 75% bioavalibility, is 20-40% protein bound, has a half life of 40 hours and is excreted in the urine

A

digoxin

335
Q

the MOA of this drug is that it inhibits the Na+/K+ ATPase of the cardiac sarcomere, causing an increase in intracellular Na+. Na+-Ca++antiport does not function as efficiently, casing an increase in intracellular Ca++, leading to positive inotropy.

A

digoxin

336
Q

this drug may cause an elevated PR, a depressed QT, a scooping of ST segment, and a T-wave inversion on ECG

A

digoxin

337
Q

The clinical uses for this drug include 1) ________ due to increased contractility 2) _______ due to decreased conduction at AV node

A

1) CHF

3) atrial fibrillation

338
Q

toxicity of this drug includes N/V/D. Blurry yellow vision. Arrhythmia.

A

digoxin

339
Q

Digoxins toxicities are increased by _________(decreased excretion), _______(potentiates drug’s effects) , and _________ (decreases digoxin clearance and displaces dignoxin from tissue binding sites

A

renal failure
hypokalemia
quinidine

340
Q

What is the treatment for digoxin toxicity

A

slowly normalize K+
lidocaine
cardiac pacer
anti-dig Fab fragments

341
Q

antiarrythmics (Class I) are _____ channel blockers

A

Na+

342
Q

antiarrythmics (Class II) are _____ blockers

A

Beta

343
Q

antiarrythmics (Class III) are _____ channel blockers

A

K+

344
Q

Thhs class of antiarrhthmics are local anesthetics. They act by slow or decreasd conduction. They decrese the slope of phase 4 ddepolarization and increase threshhold for firing in abnormal pacemaker cells.

A

antiarrhythmics-Na+ channel blockers (class I)

345
Q

antiarrhythmics-Na+ channel blockers (class I) are state dependent meaning what

A

they selectively depress tissue that is frequently depolarized (e.g., tachycardia

346
Q

this class of antiarrhythmics has 3 subcategories A, B, & C

A

antiarrhythmics-Na+channel blockers (class I)

347
Q

this class of antiarrythmics includes Quinidine, Amiodarone, Procainamide, Disopyramide.

A

Class IA

mneu: Queen Amy Proclaims Diso’s PYRAMID

348
Q

This class of antiarrhytmics has an ↑ AP duration, ↑ effective refractory period (EERP, ↑ QT interval. It can affect both atrial and ventricular arrhythmias

A

IA

349
Q

This member of class IA antiarrhytmics has toxicities that include (cinchonism-headache, tinnitis, thrombocytopenia, torsades de pointes due to prolonged QT interva)

A

quinidine

350
Q

This member of class IA antiarrhytmics has toxicities that include reverible SLE-like syndrome

A

procainamide

351
Q

This class of antiarrythmics include lidocaine mexiletine, tocainide

A

IB (Na+ channel blockers)

352
Q

this class of antiarrythmics acts to decrease AP duration. It effects ischemic or depolarized purkinje and ventricular tussue. It is useful in acute ventricular arrhytmias (especially post-MI) and i digitalis-induced arrhythmias.

A

IB (Na+ channel blockers)

353
Q

This class of antiarrhytmics has toxicities that include local anesthetic effects, CNS stimulation/depression, cardiovascular depression

A

IB (Na+ channel blockers)

354
Q

This class of antiarrhythmics includes flecainide, encainide, propafenone.

A

class IC (Na+ channel blockers.

355
Q

This class of antiarrhythmics has no effect on AP duration. It is useful in V-tachs that progress to VF and intractable SVT. Usually used only as last result in refractory tachyarrythmias.

A

class IC (Na+ channel blockers.

356
Q

Toxicities of this class of antiarrhythmics includes arrythmias, especially post MI (CONTRAINDICATED)

A

class IC (Na+ channel blockers.

357
Q

This clas of antiarrythmics includes propanolol, esmolol, metroprolol, atenolol, timool.

A

Beta Blockers (Class II)

358
Q

This class of antiarrythmics acts by ↓ cAMP, ↓ Ca+ currents, and by supressing abnormal pacemakers by ↓ slope of phase 4. The AV node is particularly sensitive resulting in increaed PR interval

A

B-blockers (Class II antiarrythmics)

359
Q

this is the shortest acting B blocker

A

esmolol

360
Q

Toxicities of this class of antiarrythmics include impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). It may mask signs of hypoglycemia.

A

B-blockers (Class II antiarrythmics)

361
Q

This class of antiarrythmics includes Sotalol, ibutilide, bretylium, & amiodarone

A

K+ channel blockers (class III)

362
Q

This class of antiarrythmics acts by ↑ AP duration, ↑ERP. It thends to ↑ QT interval. It is used when other antiarrhythmics fail.

A

K+ channel blockers (class III)

363
Q

This class III antiarrythmic has toxicities which include torsades de pointes and excessive beta block

A

sotalol

364
Q

This class III antiarrythmic has toxicities which include new arrhytmias& hypotension

A

bretylium

365
Q

This class III antiarrythmic has toxicities which include PULMONARY FIBROSIS, HEPATOTOXICITY, HYPOTHYROIDSIM/HYPERTHYROIDISM, corneal deposits, skin depsits resulting in photodermatiitis, neurologic effects, constipation, CV effects (bradycardia, heart block, CHF

A

amiodarone

mneu: remember to check PFTs, LFTs, and TFTs when using amiodarone.

366
Q

This class of antiarrythmics include the drugs verapamil, and diltiazem.

A

Ca++ channel blockers (class IV)

367
Q

The MOA of this class of antiarrythmics is primarily on AV nodal cells. They ↓ conduction velocity, ↑ ERP, ↑ PR interval.

A

Ca++ channel blockers (class IV)

368
Q

this class of antiarrythmics is used in prevention of nodal arrhythmias (e.g., SVT)

A

Ca++ channel blockers (class IV)

369
Q

Toxicity of this class of antiarrythmics can include constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression, & torsades de pointes.

A

Ca++ channel blockers (class IV)

370
Q

Other antiarrythmics: this antiarrhythmic is the drug of choice in diagnosing/abolishing AV nodal arrhythmias

A

adenosine

371
Q

Other antiarrythmics: this antiarrhythmic depresses ectopic pacemakers, especially in digoxin doxicity

A

K+

372
Q

Other antiarrythmics: this antiarrhythmic is effective in torsades de pointes and digoxin toxiciity

A

Mg+