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STEP > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Romano-Ward syndrome

A

Q from the bond is a giant standing in the back/form of congenital long QT syndrome. Femdom chick whipping him/autosomal dominant. /pure cardiac phenotype (no deafness). Arthur spinning/can predispose to torsades de pointes, causing syncopal episodes + sudden cardiac death. /thought to result from mutations in a K= channel protein that contributes to the delayed rectifier current (Ik) of the cardiac action potential.

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2
Q

Jervell and Lange-Nielsen syndrome

A

Q from the bond is a giant /form of congenital long QT syndrome. Tyrion running down the hall/autosomal recessive. Nelson has big headphones on/sensorineural deafness. /common presentation = syncope in an otherwise healthy person. Arthur spinning/can predispose to torsades de pointes + sudden cardiac death. /thought to result from mutations in a K+ channel protein that contributes to the delayed rectifier current (Ik) of the cardiac action potential.

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3
Q

Brugada syndrome

A

Tuong: he’s being whipped by a FEMDOM/autosomal dominant disorder most common in Asian males. Huge bundle of sticks in the right corner + mountains on backwall with hat bone on left and hambone on right/ECG pattern of pseudo-right bundle branch block + ST elevations in V1-V3. Jonny kenser dead on the floor + /increased risk of ventricular tachyarrhythmias + SCD (sudden cardiac death). He has an implanted cardioverter-defibrillator/prevent SCD with implantable cardioverter-defibrillator (ICD).

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4
Q

Wolff-Parkinson-White syndrome

A

o Parker from woodlands. Electric shock to the chest and lightning bolt that has down wall and across floor and up to Parker/very common ventricular pre-excitation syndrome. Abnormally fast accessory conduction pathway from atria to ventricle bypasses the rate-slowing AV node ventricles begin to partially depolarize earlier. May result in reentry circuit SVT. Camouflaged delta commanders coming out of the ground that have suffered strokes and are slurring their words + a morbidly obese Q from James bond (QRS complex code) + a midget media crew shooting photos on left/ECG = characteristic delta wave, described as “slurred upstroke of the QRS complex” + widened QRS complex + shortened PR interval on ECF. Amy young riding her hippo is there + vera wing in the back + Aidan Melville juggling in front of door/treatment = amiodarone + adenosine + verapamil. Tigger firing rocket launcher at parker/digoxin is contraindicated (can enhance transmission of impulses through accessory pathways by reentry or possible triggered membrane activity) extremely fast ventricular rate OR Vfib.

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5
Q

Potassium channel problem in romano-ward

A

DELAYED rectifier potassium channel.

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6
Q

truncus arteriosus gives rise to…

A

ascending aorta + pulmonary trunk

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7
Q

bulbus cordis gives rise to

A

smooth parts (outflow tract) of left and right ventricles

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8
Q

endocardial cushions give rise to

A

1) atrial septum
2) membranous inter ventricular septum
3) AV and semilunar valves

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9
Q

AV valves

A

mitral and tricuspid

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10
Q

semilunar valves

A

aortic + pulmonary valves

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11
Q

Primitive atrium gives rise to…

A

Trabeculated part of left and right atria

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12
Q

Primitive ventricle gives rise to

A

trabeculated part of left and right ventricles

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13
Q

Primitive pulmonary vein gives rise to…

A

smooth part of left atrium

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14
Q

Left horn of sinus venosus gives rise to…

A

coronary sinus

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15
Q

Right horn of sinus venosus gives rise to…

A

Smooth part of right atrium (sinus venarum)

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16
Q

What is SVC derived from

A

right common cardinal vein + right anterior cardinal vein

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17
Q

When does cardiac looping begin?

A

Week 4

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18
Q

Dextrocardia etiology

A

Defect in left-right dynein (dynes are involved in L/R asymmetry)

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19
Q

PFO etiology

A

Failure of septum premum and septum secundum to fuse.

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20
Q

underlying etiology of paradoxical emboli

A

1) ASD
2) VSD
3) PFO

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21
Q

Separation of cardiac chambers

A

1) septum primum grows toward endocardial cushions, narrowing foramen primum.
2) Foramen secundum forms in septum premum (foramen premium disappears)
3) Septum secundum develops as foramen secundum maintains right-to-left shunt.
4) septum secundum expands and covers most of the foramen secundum. Residual foramen is foramen ovale.
5) Remaining portion of septum premum forms valve of foramen ovale.

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22
Q

Most common location of VSD

A

membranous septum

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23
Q

Ventricle formation/morphogenesis

A

1) Muscular inter ventricular septum forms. Opening is inter ventricular foramen
2) Aorticopulmonary septum rotates and fuses with muscular ventricular septum to form membranous inter ventricular septum, closing inter ventricular foramen.
3) Growth of endocardial cushions separates atria from ventricles and contributes to both atrial septation and membranous portion of interventricular septum.

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24
Q

Outflow tract formation

A

Neural crest and endocardial cell migrations lead to truncal and bulbar ridges that spiral and fuse to form aorticopulmonary septum. Lead to ascending aorta and pulmonary trunk.

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25
Q

Persistent truncus arteriosus etiology

A

Failed neural crest migration

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26
Q

Tetralogy of fallot etiology

A

failed neural crest migration

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27
Q

transposition of great vessels etiology

A

failed neural crest migration

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28
Q

aortic/pulmonary valve origin

A

derived from endocardial cushions of outflow tract.

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29
Q

Mitral/tricuspid origin

A

Derived from fused endocardial cushions of the AV canal.

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30
Q

PO2 of umbilical vein blood

A

30 mm HG

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31
Q

umbilical vein blood saturation

A

80%

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32
Q

Path of most highly oxygenated blood reaching heart…

A

Most of the highly oxygenated blood reaching the heart via the IVC is directed through the foramen ovale and pumped into the aorta to supply the body.

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33
Q

path of deoxygenated blood from the SVC

A

SVC –> RA –> RV –> main pulmonary artery –> PDA –> descending aorta.

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34
Q

closing of foramen ovale mechanism

A

Decreased resistance in pulmonary vasculature leads to increased left atrial pressure vs. right atrial pressure –> closes.

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35
Q

Closure of ductus mechanism

A

Increase in O2 + decrees in prostaglandins (from placental separation)

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36
Q

Remnant of ductus arteriosus

A

Ligamentum arteriosum

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37
Q

What can you use to maintain the PDA?

A

PGE1 + PGE2

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38
Q

Median umbilical ligament derived from…

A

urachus

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39
Q

Remnant of ductus venosus…

A

ligamentum venosum

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40
Q

Remnant of foramen ovale

A

Fossa ovalis

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41
Q

Remnant of notochord

A

nucleus pulposus

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42
Q

Medial umbilical ligaments derived from

A

umbilical arteries

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43
Q

remnant of umbilical vein

A

ligamentum teres hepatis (contained in falciform ligament)

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44
Q

What supplies the SA and AV nodes usually?

A

RCA

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45
Q

Which circulation type is more common

A

Right-dominant

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46
Q

When does coronary blood flow peak?

A

Early diastole

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47
Q

Most posterior part of the heart

A

Left atrium

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48
Q

Layers of pericardium (from outer to inner)

A

1) Fibrous pericardium
2) Parietal layer of serous pericardium
3) Visceral layer of serous pericardium

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49
Q

Where is the pericardial cavity?

A

Lies between parietal and visceral layers

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50
Q

How is CO maintained in early and late stages of exercise?

A

Early –> increased HR + SV

Late –> increased HR only (SV plateaus)

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51
Q

Examples of increased pulse pressure

A

1) hyperthyroidism
2) aortic regurgitation
3) aortic stiffening (isolated systolic hypertension in elderly)
4) OSA (due to increased sympathetic tone)
5) Exercise (transient)

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52
Q

Examples of decreased pulse pressure

A

1) aortic stenosis
2) cardiogenic shock
3) cardiac tamponade
4) advanced heart failure (HF)

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53
Q

Catecholamines and increased contractility mechanism

A

Inhibition of phospholamban leads to increased calcium entry into sarcoplasmic reticulum –> increased calcium induced calcium release.

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54
Q

What increases contractility?

A

1) catecholamines
2) increased intracellular calcium
3) decreased extracellular sodium (decreased activity of Na/Ca exchanger)
4) digitalis

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55
Q

digitalis mechanism

A

Blocks Na/K+ pump, leading to increased intracellular sodium, decreased Na/Ca exchanger activity, and increased intracellular calcium.

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56
Q

Causes of decreased contractility

A

1) Beta-blockade
2) HF with systolic dysfunction
3) acidosis
4) hypoxia/hypercapnia
5) non-dihydropyridine Ca2+ channel blockers

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57
Q

Wall tension (Laplace’s law)

A

Wall tension = (pressure x radius)/(2 x wall thickness)

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58
Q

What approximates afterload?

A

MAP

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59
Q

Drugs that decrease both preload and after load…

A

ACE inhibitors and ARBs

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60
Q

Normal EF

A

greater than 55%

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61
Q

EF in systolic vs diastolic HF

A

Decreased in systolic HF, normal in diastolic HF

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62
Q

Other things that decrease contractility

A

1) Beta-blockers (acutely)
2) non-dihydropyridine Calcium channel blockers
3) narcotic overdose
4) uncompensated HF

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63
Q

Volumetric flow rate (Q)

A

Q = flow velocity (v) x cross-sectional area (A)

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64
Q

Total resistance of vessels in series

A

Rt = R1 + R2 + R3

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65
Q

What does viscosity depend on?

A

Primarily hematocrit

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66
Q

When is viscosity increased?

A

1) polycythemia

2) hyperproteinemic states (eg multiple myeloma)

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67
Q

Where is flow velocity lowest?

A

Capillaries

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68
Q

What is the effect of removing organs in parallel (eg nephrectomy)?

A

1) decreased TPR

2) increased CO

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69
Q

Factors that would cause a left shift in venous return graph

A

1) acute hemorrhage

2) spinal anesthesia

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70
Q

Exercise on cardiac function curve

A

1) increased inotropy
2) decreased TPR
* think about how this would affect graph

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71
Q

Compensated heart failure

A

Isotropy drops in order to maintain fluid retention and increase preload to maintain CO.

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72
Q

What will decrease TPR

A

1) exercise

2) AV shunt

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73
Q

vasopressor?

A

Antihypotensive meds. Anything that raises reduced blood pressure.

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74
Q

JVP: a wave

A

atrial contraction

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75
Q

JVP: c wave

A

RV contraction

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76
Q

JVP: x descent

A

atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction?

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77
Q

Absent x was on JVP?

A

tricuspid regurgitation

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78
Q

Prominent x wave on JVP indicates…

A

1) Tricuspid insufficiency

2) right HF

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79
Q

V wave on JVP

A

Increased right atrial pressure due to filling against closed tricuspid valve.

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80
Q

Y descent on JVP?

A

RA emptying into RV

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81
Q

When is y descent prominent?

A

Constrictive pericarditis

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82
Q

When is y descent absent?

A

Cardiac tamponade

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83
Q

What is S1?

A

Mitral and tricuspid valve closure.

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84
Q

What is S2?

A

Aortic and pulmonary valve closure.

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85
Q

atrial kick?

A

S4

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86
Q

Isovolumetric contraction?

A

Period between mitral valve closing and aortic valve opening.

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87
Q

When is O2 consumption highest in cardiac cycle?

A

Isovolumetric contraction.

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88
Q

Systolic ejection on PV loop?

A

Period between aortic valve opening and closing.

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89
Q

Isovolumetric relaxation on PV loop?

A

Period between aortic valve closing and mitral opening.

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90
Q

Rapid filling on PV loop?

A

Period just after mitral valve opening.

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91
Q

Reduced filling on PV loop?

A

Period just before mitral valve closing

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92
Q

How will increased contractility affect PV loop?

A

FA 270

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93
Q

How will increased afterload affect PV loop?

A

FA 270

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94
Q

How will increased preload affect PV loop?

A

FA 270

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95
Q

What causes normal splitting?

A

Inspiration –> drop in intrathoracic pressure –> increased venous return –> increased RV filling –> increased RV stroke volume –> increased RV ejection time –> delayed closure of pulmonic valve.

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96
Q

pulmonary impedance?

A

capacity of the pulmonary circulation

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97
Q

When is wide splitting seen?

A

Conditions that delay RV emptying.

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98
Q

What does wide splitting indicate?

A

Delayed pulmonic, as seen in…

1) pulmonic stenosis
2) right bundle branch block

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99
Q

Why does fixed splitting occur in ASDs?

A

Delay in pulmonic closure due to increased flow through pulmonic valve due to left-to-right shunt.

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100
Q

When does paradoxical splitting occur?

A

Conditions that delay aortic valve closure.

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101
Q

Conditions in which paradoxical splitting is seen…

A

1) aortic stenosis

2) left bundle branch block

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102
Q

What is paradoxical splitting?

A

Normal order of valve closure is reversed so that P2 sound occurs before delayed A2 sound. Therefore in inspiration, P2 closes later and moves closer to A2, thereby “paradoxically” eliminating the split.

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103
Q

VSD – systolic or diastolic?

A

systolic (holosystolic)

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104
Q

ASD – systolic or diastolic?

A

diastolic

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105
Q

Where are ASD’s best auscultated?

A

tricuspid area

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106
Q

Where are VSD’s best auscultated?

A

tricuspid area

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107
Q

holosystolic murmurs…

A

1) Tricuspid regurgitation
2) VSDs
3) mitral regurgitation

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108
Q

Affect of hand grip?

A

Increase afterload

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109
Q

What will hand grip increase intensity of?

A

1) MR + AR + VSD murmurs

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110
Q

diastolic heart sounds

A

1) aortic/pulmonic regurgitation

2) mitral/tricuspid stenosis

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111
Q

Affect of increased after load on MVP?

A

Later onset of click/murmur

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112
Q

What will hand grip decrease intensity of?

A

hypertrophic cardiomyopathy

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113
Q

Affect of Phase II valsalva?

A

Decreased preload

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114
Q

What will valsava decrease intensity of?

A

Most murmurs (including AS)

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115
Q

Affect of valsalva on MVP?

A

Earlier onset of click/murmur.

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116
Q

What will valsava increase intensity of?

A

hypertrophic cardiomyopathy

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117
Q

Affect of rapid squatting?

A

1) increased venous return
2) increased preload
3) increased afterload

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118
Q

Affect of squatting on HOCM?

A

decrease intensity

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119
Q

Affect of squatting on AS?

A

increase intensity

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120
Q

Affect of squatting on MVP?

A

Later onset of click/murmur

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121
Q

AS radiation

A

Loudest at base; radiates to carotids.

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122
Q

“Pulses parvus et tardus”

A

Pulses are weak with a delayed peak.

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123
Q

AS presentation

A

syncope + angina + dyspnea on exertion

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124
Q

Murmur radiating to right sternal border

A

tricuspid regurg

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125
Q

Rheumatic fever caveat

A

Can cause either MR or TR

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126
Q

MVP murmur

A

Late systolic crescendo murmur with mid systolic click

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127
Q

What is mid systolic click due to

A

Sudden tensing of chordae tendinae.

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128
Q

Most frequent valvular lesion?

A

MVP

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129
Q

MVP best location for auscultation?

A

Apex

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130
Q

When is MVP loudest?

A

Just before S2.

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131
Q

Some causes of MVP

A

1) Marfan’s
2) Ehlers-Dalos
3) rheumatic fever
4) chordae rupture

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132
Q

When are PDAs loudest?

A

S2

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133
Q

Most common causes of PDAs

A

1) congenital rubella

2) prematurity

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134
Q

Where are PDAs best heard?

A

Left infraclavicular area

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135
Q

aortic regurg murmur description

A

High-pitched blowing early diastolic decrescendo murmur.

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136
Q

aortic regurg characteristics

A

1) long diastolic murmur
2) hyperdynamic pulse
3) head bobbing when severe or chronic
4) wide pulse pressure

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137
Q

Aortic regurg causes

A

1) aortic root dilation
2) bicuspid aortic valve
3) endocarditis
4) RF

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138
Q

What causes opening snap in mitral stenosis?

A

Abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips.

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139
Q

What correlates with severity in mitral stenosis?

A

Decreased interval between S2 and OS.

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140
Q

Sequela of chronic mitral stenosis

A

LA dilatation

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141
Q

What underlies phase 1 in myocardial action potential?

A

1) inactivation of voltage-gated Na channels

2) voltage-gated K+ channels begin to open.

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142
Q

What underlies phase 2 in myocardial action potential?

A

Plateau..

1) Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux.
2) Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction.

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143
Q

What underlies phase 3 in myocardial action potential?

A

Rapid repolarization–massive K+ efflux due to opening of voltage-gated slow potassium channels and closure of voltage-gated Ca2+ channels.

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144
Q

What underlies phase 4 in myocardial action potential?

A

Resting potential–high K+ permeability through K+ channels.

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145
Q

What are the differences between myocardial action potential and skeletal muscle action potential?

A

1) Cardiac muscle action potential has a plateau, which is due to Ca2+ influx and K+ efflux.
2) Cardiac muscle contraction requires Ca2+ influx from ECF to induce Ca2+ release from sarcoplasmic reticulum (Ca2+ induced Ca2+ release).
3) electrical coupling with gap junctions.

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146
Q

Phases of pacemaker action potential…

A

Phase 0, phase 3, phase 4.

*NO phase 1 or 2.

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147
Q

What underlies phase 0 in pacemaker action potential?

A

Upstroke–opening of voltage-gated Ca2+ channels. Results in a slow conduction velocity that is used by the AV node to prolong transmission.

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148
Q

What underlies phase 3 in pacemaker action potential?

A

Inactivation of Ca2+ channels + increased activation of K+ channels leading to potassium efflux.

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149
Q

What underlies phase 4 in pacemaker action potential?

A

Slow spontaneous diastolic depolarization due to If (funny current).

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150
Q

If channels (funny current)

A

Slow, mixed Na/K inward current

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151
Q

What accounts for automacity of SA and AV nodes?

A

If channels (funny current)

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152
Q

What determines heart rate?

A

Slope of phase 4 in SA node.

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153
Q

Affect of adenosine on pacemaker action potential?

A

Decreases the rate of diastolic depolarization and decreases HR.

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154
Q

How does sympathetic stimulation increase HR?

A

Increases the chance that If channels are open and thus increases HR.

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155
Q

Conduction pathway in heart

A

SA node –> atria –> AV node –> bundle of His –> right and left bundle branches –> Purkinje fibers –> ventricles.

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156
Q

Why is the SA node the dominant pacemaker?

A

slow phase of upstroke

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157
Q

AV node location

A

Posteroinferior part of intertribal septum.

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158
Q

Pacemaker rates

A

SA, AV, bundle of His/Purkinje/ventricles

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159
Q

Speed of conduction

A

Purkinje, atria, ventricles, AV node

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160
Q

PR interval

A

Time from start of atrial depolarization to start of ventricular depolarization

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161
Q

Normal PR interval

A

Less than 200 msec

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162
Q

Normal QRS

A

less than 120 msec

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163
Q

What does QT interval represent?

A

ventricular depolarization + mechanical contraction of the ventricles + ventricular depolarization.

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164
Q

What does T wave represent?

A

Ventricular repolarization

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165
Q

What does a T-wave inversion indicate?

A

Recent MI.

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166
Q

What is the J point?

A

Junction between end of QRS complex and start of ST segment.

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167
Q

What does the ST segment represent?

A

Isoelectric period in which ventricles are depolarized.

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168
Q

When is a U wave prominent?

A

1) hypokalemia

2) bradycardia

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169
Q

treatment for torsades de pointes?

A

magnesium sulfate

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170
Q

What causes torsades de pointes?

A

1) long QT syndromes
2) drugs
3) hypokalemia
4) hypomagnesemia

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171
Q

Drugs causing torsades de pointes?

A

1) antiarrhythmics (class IA, III)
2) macrolides
3) haloperidol
4) TCAs
5) ondansetron

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172
Q

Wolff-Parkinson-White syndrome etiology

A

Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses rate-slowing AV node. This causes ventricles to depolarize early.

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173
Q

What is a delta wave?

A

shortened PR interval (due to early depolarization)

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174
Q

Wolff-Parkinson-White sequela

A

Reentry circuit leading to SVT.

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175
Q

Most common RF’s for afib

A

1) HTN

2) CAD

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176
Q

definitive treatment for atrial flutter

A

catheter ablation

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177
Q

1st degree AV block

A

Prolonged PR interval. Benign and asymptomatic condition that doesn’t require treatment.

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178
Q

Mobitz type I (wenckebach)

A

Type of 2nd degree heart block. Progressive lengthening of PR interval until a beat is “dropped” (a P wave not followed by a QRS complex). Variable RR interval with a pattern (regularly irregular)

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179
Q

Mobitz type I prognosis

A

usually asymptomatic

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180
Q

Mobitz type II

A

Form of second degree that block. Dropped beats that aren’t preceded by a change in length of PR interval.

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181
Q

Mobitz type II sequela

A

Can progress to 3rd degree block.

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182
Q

Mobitz type II management

A

Often treated with a pacemaker.

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183
Q

3rd degree heart block pathophys

A

atria and ventricles beat independently of each other.

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184
Q

3rd degree heart block on ECG

A

P waves and QRS complexes not rhythmically associated.

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185
Q

3rd degree heart block management

A

pacemaker

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186
Q

ANP effects

A

1) vasodilation
2) decreased Na+ reabsorption at *collecting tubule
3) dilates afferent arterioles + constricts efferent arterioles, promoting diuresis and contributing to aldosterone escape.

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187
Q

Difference between ANP and BNP?

A

BNP has a longer half-life.

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188
Q

nesiritide

A

recombinant BNP

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189
Q

Diagnostic relevance of BNP?

A

Blood test used for diagnosing HF (very good negative predictive value)

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190
Q

aortic chemoreceptor pathway

A

Transmits via vagus nerve to solitary nucleus of medulla.

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191
Q

Carotid sinus pathway

A

Transmits via glossopharyngeal nerve to solitary nucleus of medulla.

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192
Q

Carotid massage mechanism

A

Increased pressure on carotid sinus leads to increased stretch –> increased afferent baroreceptor firing –> increased AV node refractory period –> decreased HR.

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193
Q

Cushing reaction setting

A

Triad of HTN + bradycardia + respiratory depression

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194
Q

Cushing reaction pathophys

A

Increased ICP constricts arterioles leading to cerebral ischemia leading to increased PCO2 and decreased pH –> central reflex sympathetic increase in perfusion pressure (HTN) –> increased stretch –> increased peripheral reflex baroreceptor-induced bradycardia.

Better explanation:
With increased ICP, cushing reflex increases MAP in an attempt to restore cerebral perfusion pressure. Bradycardia occurs because baroreceptors in the carotid and aortic arch don’t know what’s going on in brain and just ease hypertension.

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195
Q

What triggers peripheral chemoreceptors?

A

1) decreased Po2
2) increased PCO2
3) decreased pH

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196
Q

What triggers central chemoreceptors?

A

Changes in pH and pCO2 of brain interstitial fluid (which are influenced by arterial CO2).

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197
Q

How do you determine mitral stenosis from cardiac pressures?

A

PCWP greater than LV EDV.

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198
Q

Normal cardiac pressures

A

FA 280

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199
Q

cardiac pressures from codebook

A

o Code: covered in ivy/right atrium = 0,8. Covered in hair + nails pounded in everywhere/right ventricle = 4,25. Nails + big hoops/pulmonary artery = 9,25. Hens + walls made out of tin cans/left atrium = 2,12. Hoops on walls + mice drinking mimosas/left ventricle = 9,130. Mice drinking mimosas + carrying briefcases/aorta = 70,130. Wedge of tissue sitting in middle of road covered in tin cans/wedge pressure = 12 (remember that wedge pressure is an indication of left atrial pressure).
o Location: Intersection of montview and colorado

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200
Q

what determines auto regulation in the heart?

A

Local vasodilatory metabolites: adenosine, NO, CO2, decreased O2.

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201
Q

What determines auto regulation in the brain?

A

CO2 (pH)

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202
Q

What determines auto regulation in the kidney?

A

Myogenic + tubuloglomerular feedback

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203
Q

Tubuloglomerular feedback

A

just macula dense and RAAS mechanism

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204
Q

myogenic mechanism

A

reflex vasoconstriction that occurs when perfusion pressure increases

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205
Q

what determines skeletal muscle regulation with exercise?

A

local metabolites: lactate, adenosine, K+, H+, CO2

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206
Q

what determines skeletal muscle regulation at rest?

A

sympathetic tone

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207
Q

what determines auto regulation in the skin?

A

sympathetic stimulation most impt

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208
Q

Thing to remember about about capillary oncotic pressure

A

Pushes fluid into capillary.

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209
Q

Why does lymphatic blockage cause edema?

A

Increased interstitial fluid colloid osmotic pressure because proteins aren’t drained into lymphatics

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210
Q

Managing early cyanosis

A

urgent surgery + maintain PDA

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211
Q

congenital heart diseases presenting with early cyanosis

A 
5 Ts:
Truncus arteriosus
Transposition
Tricuspid atresia
Tetralogy of ballot
TAPVR
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212
Q

Persistent truncus arteriosus etiology

A

Truncus fails to divide into pulmonary trunk and aorta due to lack of aorticopulmonary septum formation; most patients have accompanying VSD.

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213
Q

Etiology of transposition of great vessels

A

Failure of aorticopulmonary septum to spiral.

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214
Q

hypoplastic RV in cyanotic newborn suggests…

A

tricuspid atresia

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215
Q

TOF etiology

A

anterosuperior displacement of the infundibular septum.

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216
Q

shunt in TOF

A

Pulmonary stenosis forces right-to-left flow across VSD leading to RVH

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217
Q

What are “tet spells”

A

characteristic of TOF. exacerbation of RV outflow obstruction.

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218
Q

Why does squatting help TOF patients?

A

Increased SVR, decreased right to left shunt, improves cyanosis.

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219
Q

TAPVR mechanism

A

Pulmonary veins drain into right heart circulation.

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220
Q

Epstein anomaly associations

A

Tricuspid regurgitation + right HF.

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221
Q

Relative frequency of ASD, PDA, VSD

A

VSD, ASD, PDA

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222
Q

difference in presentation between right-to-left and left-to-right shunts?

A

Right-to-Left shunts: eaRLy cyanosis.

Left-to-Right shunts: “LateR” cyanosis.

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223
Q

Most common congenital cardiac defect

A

VSD

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224
Q

How does VSD present in terms of O2 saturation?

A

Increased in RV and pulmonary artery.

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225
Q

More common defect in ASD

A

Ostium secundum defects most common.

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226
Q

Difference between ASD and PFO

A

In ASDs, septa are missing tissue rather than unfused.

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227
Q

Increased O2 sat in RA, RV, and pulmonary artery?

A

ASD

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228
Q

What happens to PDA in neonatal period?

A

With decreased pulmonary vascular resistance, shunt becomes left to right, leading to progressive RVH and/or LVH and HF.

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229
Q

Eisenmenger mechanism

A

Uncorrected left-to-right shunt (VSD, ASD, PDA) leads to increased pulmonary blood flow –> pathologic remodeling of vasculature –> increased pulmonary arterial HTN and compensatory RVH –> shunt switches to become right to left.

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230
Q

Eisenmenger presentation

A

Late cyanosis + clubbing + polycythemia.

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231
Q

aortic coarctation associations

A

1) bicuspid aortic valve
2) congenital heart defects
3) Turner syndrome

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232
Q

Complications of aortic coarctation…

A

1) HF
2) Increased risk of cerebral hemorrhage (berry aneurysm)
3) aortic rupture
4) endocarditis.

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233
Q

fetal alcohol syndrome congenital cardiac defect associations

A

ASDs, VSDs, PDA, TOF

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234
Q

congenital rubella congenital cardiac defect associations

A

1) PDA
2) pulmonary artery stenosis
3) septal defects

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235
Q

Infant of diabetic mother: congenital cardiac defect associations

A

transposition of great vessels

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236
Q

Marfan syndrome: congenital cardiac defect associations

A

1) MVP
2) aortic regurgitation
3) thoracic aortic aneurysm and dissection

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237
Q

Williams syndrome: congenital cardiac defect associations

A

supravalvular aortic stenosis

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238
Q

22q11 syndromes: congenital cardiac defect associations

A

1) truncus arteriosus

2) TOF

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239
Q

HTN ethnic incidence

A

AA, caucasian, asian

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240
Q

HTN definition

A

persistent systolic greater than 140 and/or diastolic greater than 90

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241
Q

most hypertension is primary (essential) and due to..

A

Increased CO or increased TPR

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242
Q

Classic radiologic finding in FMD

A

“string of beads” appearance of arteries

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243
Q

hypertensive urgency

A

severe (greater than 180 or greater than 120) HTN without acute end-organ damage.

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244
Q

Hypertensive emergency

A

Severe HTN with evidence of acute end-organ damage (eg encephalopathy, stroke, retinal hemorrhages and exudates, papilledema, MI, HF, aortic dissection, kidney injury, microangiopathic hemolytic anemia, eclampsia).

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245
Q

Post-MI murmur?

A

Probably mitral regurg due to papillary muscle rupture.

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246
Q

Note – don’t assume VSD with holosystolic murmur.

A

OK

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247
Q

Flow rate expressed in…

A

L/min

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248
Q

calculation note: DO NOT forgot to convert units

A

OK.

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249
Q

Cubic centimeter in liter

A

1000 cubic cm = 1 liter

250
Q

Pericarditis presentation

A

Sharp pain aggravated by inspiration + relieved by sitting up and leaning forward.

251
Q

Characteristic physical exam finding in pericarditis

A

Friction rub (described as harsh as scratchy sound present in both systole and diastole)

252
Q

Pericarditis associations

A

1) Idiopathic (presumed viral)
2) coxsackievirus
3) neoplasia
4) SLE
5) arthritis
6) uremia
7) cardiovascular (acute STEMI or Dressler syndrome)
8) radiation therapy

253
Q

Hagemann factor Function

A

part of intrinsic pathway, activates kallikrein.

254
Q

Important complication of horseshoe kidney

A

Variant arterial supply. Anomalous origins of multiple renal arteries to each kidney.

255
Q

What do xanthomas consist of ?

A

lipid-laden histiocytes

256
Q

xanthelaasma?

A

xanthomas in the eyelids

257
Q

corneal arcus

A

Lipid deposits in cornea. Looks like ring around eye. Don’t confuse with Kaiser-Fleischer rings.

258
Q

Arteriosclerosis finding in essential HTN

A

Hyaline arteriolosclerosis

259
Q

Diabetes mellitus arteriosclerosis finding

A

hyaline arteriolosclerosis

260
Q

Severe HTN arteriosclerosis finding and etiology

A

Hyperplastic arteriosclerosis (onion skinning with proliferation of smooth muscle cells).

261
Q

Monckeberg description

A

medial calcific sclerosis

262
Q

Classic radiologic finding of Monckeberg’s

A

pipestem appearance.

263
Q

Monckeberg etiology

A

Calcification of internal elastic lamina and media. ***no intimal involvement.

264
Q

atherosclerosis epidemiology location

A

abdominal aorta, coronary artery, popliteal, carotid

265
Q

nonmodifiable RF’s for atherosclerosis

A

1) Age
2) Sex
3) Family history

266
Q

Sex at increased risk for atherosclerosis?

A

Increased in men + postmenopausal women

267
Q

claudication is a sign of…

A

atherosclerosis.

268
Q

atherosclerosis pathogenesis.

A

Inflammation impt. endothelial cell dysfunction –> macrophage and LDL accumulation –> foam cell formation –> fatty streaks –> smooth muscle cell migration, proliferation, and ECM deposition –> fibrous plaque –> complex atheroma.

269
Q

What causes smooth muscle cell migration in atheroma formation?

A

PDGF and FGF

270
Q

If someone has abdominal and/or back pain and a bulge/aneurysm what does this indicate?

A

Aneurysm is leaking, dissected, or rupture is imminent.

271
Q

AAA RF’s

A

1) tobacco use
2) increased age
3) male sex
4) family history

272
Q

RF’s for thoracic aortic aneurysms

A

1) HTN
2) bicuspid aortic valve
3) connective tissue disease (Marfan’s)

273
Q

abdominal vs thoracic aneurysms?

A

Abdominal associated with atherosclerosis, thoracic associated with HTN and cystic medial degeneration.

274
Q

Aneurysm type in tertiary syphilis?

A

thoracic aortic aneurysm

275
Q

cystic medial degeneration?

A

Degenerative breakdown of collagen, elastin, and smooth muscle.

276
Q

Where does traumatic aortic rupture most commonly occur?

A

Aortic isthmus

277
Q

What is the aortic isthmus?

A

Proximal descending aorta just distal to origin of left subclavian

278
Q

Aortic dissection associations

A

1) HTN
2) **bicuspid aortic valve
3) inherited connective tissue disorders

279
Q

Markedly unequal BP in arms suggests….

A

Aortic dissection

280
Q

CXR finding of aortic dissection

A

Mediastinal widening.

281
Q

Aortic dissection:

Stanford type A

A

Proximal aortic dissection; involves Ascending aorta. May extend to aortic arch or descending aorta.

282
Q

Stanford type A treatment

A

surgery

283
Q

Stanford type A complications

A

Acute aortic regurgitation or cardiac tamponade

284
Q

Stanford type B aortic dissection

A

Distal. Involves descending aorta and/or aortic arch.

285
Q

Stanford type B aortic dissection management.

A

B-blockers then vasodilators.

286
Q

Angina caveat

A

No myocyte necrosis.

287
Q

Stable angina on ECG

A

ST depression

288
Q

Variant (prinzmetal) angina triggers

A

1) tobacco
2) cocaine
3) triptans

289
Q

variant angina treatment

A

1) Ca2+ channel blockers
2) nitrates
3) smoking cessation

290
Q

unstable angina pathophys

A

Thrombosis with incomplete coronary artery occlusion.

291
Q

Unstable angina on ECG + markers

A

+/- ST depression and/or T wave inversion buT NO cardiac biomarker elevation.

292
Q

How do you distinguish NSTEMI from unstable angina?

A

biomarker elevation with NSTEMI, none with unstable.

293
Q

difference in presentation from stable and unstable angina

A

Stable usually exertion chest pain; unstable is either increase in frequency or intensity of pain or pain at rest.

294
Q

coronary steal syndrome pathophy

A

Distal to coronary stenosis, vessels are maximally dilated at baseline. Administration of vasodilators dilates normal vessels and shunts blood toward well-perfused areas leading to decreased flow and ischemia in poststenotic region.

295
Q

regadenoson

A

vasodilator

296
Q

dipyridamole use and MOA

A

1) vasodilator, inhibits clot formation

2) phosphodiesterase inhibitor

297
Q

SCD definition

A

death from cardiac causes within 1 hour of onset

298
Q

large majority of cases of SCD are caused by…

A

CAD

299
Q

What is chronic ischemic heart disease?

A

Progressive onset of HF over many years due to chronic ischemic myocardial damage.

300
Q

STEMI pathophys

A

Transmural infarct. Full thickness of myocardial wall involved.

301
Q

STEMI on ECG

A

ST elevation + Q waves

302
Q

NSTEMI pathophys

A

subendocardial infarcts

303
Q

commonly occluded coronary arteries

A

LAD, RCA, circumflex

304
Q

finding I don’t often think of with MI’s

A

Pain in left arm and/or jaw

305
Q

0-24 MI timeframe light microscopy

A

1) Early coagulative necrosis
2) release of necrotic cell contents into blood
3) edema, hemorrhage, wavy fibers.
4) neutrophils appear

306
Q

0-24 MI etiology

A

Repercussion injury, associated with generation of free radicals, leads to hyper contraction of myofibrils through increased free calcium influx.

307
Q

0-24 hr timeframe complications

A

1) ventricular arrhythmias
2) HF
3) cardiogenic shock

308
Q

1-3 day timeframe complication

A

Postinfarction fibrinous pericarditis.

309
Q

macroscopic appearance of heart in 1-3 day timeframe

A

hyperemia

310
Q

hyperemia

A

increased blood flow to different tissues in body

311
Q

1-3 day microscope chagnes

A

1) coagulative necrosis

2) *tissue surrounding infarct shows acute inflammation + neutrophils.

312
Q

3-14 day macroscopic appearance

A
  • hyperemic border; central yellow-born softening.

- maximally yellow and soft by 10 days.

313
Q

Papillary muscle rupture leads to…

A

mitral regurgitation

314
Q

morphologic appearance 2 weeks to several months

A
  • Reanalyzed artery.

- Gray-white appearance

315
Q

True vs false ventricular aneurysms

A

True occur later (after 2 weeks), false in 3-14 day timeframe.

316
Q

complication of true ventricular aneurysm

A

Mural thrombus.

317
Q

MI diagnosis and timeframe

A
  • In the first 6 hours, ECG is the gold standard.

- Biomarkers afterward.

318
Q

Troponin timeframe

A

1) Rises after 4 hours
2) Peaks at 24 hours
3) elevated for 7–10 days

319
Q

CK-MB timeframe

A

1) Rises after 6-12 hours
2) Peaks at 16-24 hours
3) Returns to baseline at 48 hours

320
Q

CK-MB downfall and use

A

It’s also found in skeletal muscle so not as specific, but good at diagnosing reinfarction since levels fall earlier.

321
Q

hyperacute T waves

A

peak T-waves

322
Q

Other ECG findings related to MI’s

A

1) hyper acute T waves
2) T-wave inversion
3) new left bundle branch block
4) pathologic Q waves
5) poor R wave progression

323
Q

What does poor R wave progression on ECG indicate?

A

evolving or old transmural infarct. R wave should become progressively taller, but remains low.

324
Q

Anteroseptal leads

A

V1-V2

325
Q

Anteroapical leads

A

V3-V4

326
Q

Anterolateral leads

A

V5-V6

327
Q

Lateral leads

A

I, aVL

328
Q

What leads will be elated with an anteroseptal (LAD) infarct?

A

V1-V2

329
Q

What leads will be elated with an anteroseptal (distal LAD) infarct?

A

V3-V4

330
Q

What leads will be elated with an anterolateral (LAD or LCX) infarct?

A

V5-V6

331
Q

What leads will be elevated with a lateral (LCX) infarct?

A

I, aVL

332
Q

What leads will be elated with an inferior (RCA) infarct?

A

II, III, aVF

333
Q

What leads will be elated with a posterior (PDA) infarct?

A

V7-V9, ST depression in V1-V3 with tall R waves

334
Q

tall R waves suggests..

A

posterior infarct

335
Q

most impt complication within first 24 hours post-MI?

A

arrhythmia

336
Q

What does a friction rub post MI indicate?

A

post infarction fibrinous pericarditis

337
Q

Where is papillary muscle rupture most likely to occur and why?

A

Posteromedially, due to single blood supply from PDA.

338
Q

When do inter ventricular septal ruptures occur?

A

3-5 days post MI

339
Q

What mediates interventricualr septal ruptures?

A

Macrophages

340
Q

Complications of ventricular pseudoaneurysms…

A

1) decreased CO
2) increased risk of arrhythmia
3) embolus from mural thrombus

341
Q

sequela of free wall rupture

A

cardiac tamponade

342
Q

How do true ventricular aneurysms present?

A

Outward bulge with contraction (“dyskinesia”) associated with fibrosis.

343
Q

Sign of LV infarction?

A

pulmonary edema

344
Q

Sign of papillary muscle rupture?

A

mitral regurg leading to pulmonary edema

345
Q

Unstable angina/NSTEMI management

A

1) heparin for anticoagulation
2) anti platelet therapy (aspirin + clopidogrel)
3) beta-blocker
4) ACE inhibitor
5) statins

346
Q

clopidogrel mechanism

A

ADP receptor inhibitor

347
Q

How do you control symptoms with unstable angina/NSTEMI?

A

Nitroglycerin + morphine.

348
Q

STEMI management?

A

Same as NSTEMI but you need repercussion therapy with PCI (preferred over fibrinolysis).

349
Q

Most common cardiomyopathy?

A

Dilated cardiomyopathy

350
Q

Common dilated cardiomyopathy etiologies

A

1) chronic alcohol abuse
2) wet beriberi
3) coxsackie B
4) chronic cocaine use
5) Chagas disease
6) doxorubicin
7) hemochromatosis
8) sarcoidosis
9) peripartum cardiomyopathy

351
Q

Murmur with dilated cardiomyopathy?

A

Systolic regurgitant murmur.

352
Q

hypertrophy associated with dilated cardiomyopathy?

A

Eccentric hypertrophy.

353
Q

Dilated cardiomyopathy treatment?

A

1) Na restriction
2) ACE inhibitors
3) beta-blockers
4) diuretics
5) digoxin
6) ICD
7) heart transplant

354
Q

Eccentric hypertrophy etiology

A

sarcomeres added in series.

355
Q

Concentric hypertrophy?

A

There’s no overall enlargement of ventricle. The walls are thickened.

356
Q

concentric hypertrophy associations

A

Volume overload, such as which HTN or aortic stenosis.

357
Q

Auscultation findings in HOCM

A

1) S4
2) systolic murmur
3) Mitral regurg possible due to impaired mitral valve closure.

358
Q

HOCM management

A

1) no high intensity sports
2) b-blocker or non-dihydropyridine Ca-blocker (verapamil)
3) ICD if high risk

359
Q

HOCM macroscopic findings

A

myofibrillar disarray + fibrosis

360
Q

Obstructive HOCM

A

subtype of HOCM characterized by asymmetric septal hypertrophy + systolic anterior motion of mitral valve, leading to outflow obstruction, dyspnea and possible syncope

361
Q

infiltrative cardiomyopathy?

A

restrictive cardiomyopathy

362
Q

What are some major causes of restrictive cardiomyopathy?

A

1) sarcoidosis
2) amyloidosis
3) postradiation fibrosis
4) endocardial fibroelastosis
5) Loffler syndrome
6) hemochromatosis

363
Q

endocardial fibroelastosis?

A

thick fibroelastic tissue in endocardium of young children.

364
Q

Loftier syndrome

A

Endomyocardial fibrosis with a prominent eosinophilic infiltrate.

365
Q

ECG and restrictive cardiomyopathy

A

Low-voltage ECG

366
Q

rales?

A

another name for crackles

367
Q

systolic dysfunction characteristics

A

Reduced EF + increased EDV + decreased contractility

368
Q

Diastolic dysfunction characteristics

A

Preserved EF + *normal EDV + decreased compliance (secondary to myocardial hypertrophy)

369
Q

Most common cause of right HF

A

Left HF

370
Q

cor pumonale

A

Isolated right HF due to pulmonary cause

371
Q

Drug contraindicated in acute decompensated HF?

A

beta-blockers

372
Q

What decreases mortality with heart failure?

A

1) ACEIs
2) ARBs
3) beta-blockers (except in acute decompensated)

373
Q

What drugs improve both symptoms in mortality in HF patients?

A

Hydralazine with nitrate therapy.

374
Q

Orthopnea etiology?

A

Increased venous return from redistribution of blood (gravity effect)

375
Q

paroxysmal nocturnal dyspnea etiology

A

same as orthopnea, increased venous return from redistribution of blood

376
Q

Rare complication of hepatomegaly?

A

cardiac cirrhosis

377
Q

Causes of hypovolemic shock?

A

1) hemorrhage
2) dehydration
3) *burns

378
Q

Obstructive shock

A

reduced CO due to cardiac tamponade or PE

379
Q

Distributive shock and causes

A

Inadequate organ perfusion due to…

1) sepsis
2) anaphylaxis
3) CNS injury

380
Q

Skin findings that distinguish distributive vs. other types of shock

A

Distributive shock presents with warm or dry skin. Other forms of shock present with cold, clammy skin.

381
Q

Hypovolemic shock treatment

A

IV fluids

382
Q

Cariogenic shock treatment

A

Inotropes + diuresis

383
Q

Obstructive shock treatment?

A

Relieve obstruction

384
Q

Sepsis, anaphylaxis, CNS injury shock treatment?

A

IV fluids + pressors

385
Q

hypovolemic shock

1) PCWP
2) CO
3) SVR

A

1) very reduced. Remember - this is preload
2) reduced.
3) Increased. this is afterload

386
Q

PCWP importance

A

= preload

387
Q

obstructive shock

1) PCWP
2) CO
3) SVR

A

1) increased
2) decreased a lot
3) increased

388
Q

SVR significance

A

afterload

389
Q

cardiogenic shock

1) PCWP
2) CO
3) SVR

A

1) increased
2) decreased a lot
3) increased

390
Q

Sepsis, anaphylaxis..

1) PCWP
2) CO
3) SVR

A

1) decreased
2) increased
3) severely decreased

391
Q

Shock related to CNS injury..

1) PCWP
2) CO
3) SVR

A

1) decreased
2) **decreased
3) severely decreased

392
Q

Skin findings with shock related to CNS injury

A

dry

393
Q

Skin findings with shock related to sepsis, anaphylaxis…

A

warm

394
Q

Roth spots description

A

Round white spots on retina surrounded by hemorrhage

395
Q

osler nodes description

A

tender raised lesson on finger or toe pads

396
Q

Janeway lesions description

A

Small, painless, erythematous lesions on palm or sole

397
Q

caveat about bacterial endocarditis

A

You need multiple blood cultures for diagnosis.

398
Q

vegetations in acute vs subacute endocarditis

A

With acute you get large vegetation on previously normal valves, with subacute you get smaller vegetations on congenitally abnormal or diseased valves.

399
Q

Causes of nonbacterial endocarditis?

A

1) malignancy
2) hyper coagulable state
3) lupus

400
Q

bugs causing tricuspid valve endocarditis

A

1) S aureus
2) pseudomonas
3) candida

401
Q

bugs causing culture negative endocarditis

A

1) Coxiella brunette
2) bartonella
3) HACEK bugs

402
Q

HACEK bugs

A 
Haemophilus
Aggregatibacter (formerly actinobacillus)
Cardiobacterium
Eikenella
Kingella
403
Q

Valves affected in RF in order

A

mitral then aortic then tricuspid (high-pressure valves affected most)

404
Q

Anitschkow cells

A

Rheumatic fever

405
Q

Anitschkow cell description

A

enlarged macrophages with ovoid, wavy, rod-like nucleus

406
Q

rheumatic fever pathophys

A

Type II hypersensitivity. Antibodies to M protein cross-react with self antigens (molecular mimicry)

407
Q

Rheumatic fever treatment

A

penicillin

408
Q

joint presentation of rheumatic fever

A

migratory polyarthritis

409
Q

common complication of acute pericarditis

A

Pericardial effusion

410
Q

physical exam finding for pericarditis

A

friction rub

411
Q

ECG for pericarditis

A

Widespread ST-segment elevation and/or PR depression

412
Q

Causes of acute pericarditis

A

1) idiopathic (presumed viral)
2) coxsackie
3) neoplasia
4) SLE
5) RA
6) uremia
7) acute STEMI
8) dressler
9) radiation therapy

413
Q

what happens to pressure in cardiac chambers with tamponade?

A

Equilibration of pressure in all 4 chambers.

414
Q

ECG in tamponade

A

low-voltage QRS + electrical alternans

415
Q

what is pulsus paradoxus?

A

Decrease in amplitude of systolic BP by greater than 10 mm Hg during inspiration.

416
Q

Pulsus paradoxes seen in..

A

1) cardiac tamponade
2) asthma
3) OSA
4) pericarditis
5) croup

417
Q

Most common heart tumor…

A

metastasis

418
Q

What is kussmaul sign?

A

Increase in JVP on inspiration instead of a normal decrease.

419
Q

JVD pathophys

A

inspiration –> negative intrathoracic pressure not transmitted to heart –> impaired filling of right ventricle –> blood backs up into venae cavae

420
Q

Kussmaul sign + elevated JVP associations

A

1) constrictive pericarditis
2) restrictive cardiomyopathies
3) right atrial or ventricular tumors

421
Q

Pathophys of eye injury with GCA

A

Ophthalmic artery can become occluded

422
Q

What arteries are most commonly affected by GCA?

A

Branches of carotid

423
Q

Takayasu affects..

A

Large-vessels: aortic arch and proximal great vessels

424
Q

Takayasu presentatoin

A

1) “pulseless disease” (weak upper extremity pulses)

2) fever + night sweats + arthritis + myalgias + skin nodules + ocular disturbances

425
Q

Takayasu treatment

A

corticosteroids

426
Q

polyarteritis nodosa classic demographic

A

young adults

427
Q

PAN presentation

A

Fever + weight loss + malaise + headache + abdominal pain + melon.
HTN + neurologic dysfunction + cutaneous eruptions + renal damage.

428
Q

what arteries are usually involved in PAN?

A

Renal and visceral vessels, NOT pulmonary arteries.

429
Q

Hypersensitivity type in PAN?

A

immune complex mediated

430
Q

PAN treatment

A

1) corticosteroids

2) cyclophosphamide

431
Q

Impt findings in PAN

A

1) transmural inflammation with fibrinoid necrosis
2) different stages of inflammation coexisting in different vessels
3) innumerable renal micro aneurysms and spasms on arteriogram.

432
Q

Other name for Kawasaki

A

mucocutaneous lymph node syndrome

433
Q

kawasaki presentation

A

conjunctival injection + rash (desquamating) + cervical adenopathy + strawberry tongue + hand foot changes + fever

434
Q

strawberry tongue medical term

A

oral mucositis

435
Q

Kawasaki treatment

A

IVIG + aspirin

436
Q

Other name for Buerger’s…

A

Thromboangiitis obliterans

437
Q

other impt finding in Buerger’s…

A

superficial nodular phlebitis

438
Q

Wegener’s upper respiratory presentation

A

1) perforated nasal septum
2) chronic sinusitis
3) otitis media
4) mastoiditis

439
Q

mastoiditis

A

mastoid sits behind the ear (battle sign)

440
Q

renal presentation of Wegener’s

A

hematuria + red cell casts

441
Q

wegener’s triad

A

focal necrotizing vasculitis + necrotizing granulomas in lung and upper airway + necrotizing glomerulonephritis.

442
Q

other term for c-ANCA

A

anti-proteinase 3

443
Q

CXR in wegener’s

A

large nodular densities

444
Q

Wegener’s treatment

A

Cyclophosphamide + corticosteroids

445
Q

microscopic polyangiitis presentation

A

Necrotizing vasculitis commonly involved lung + kidneys + skin with pauci-immune glomerulonephritis and palpable purpura.

446
Q

How do you differentiate microscopic polyangiitis from wagerer’s?

A

in microscopic polyangiitsis, there’s no nasopharyngeal involvement + no granulomas.

447
Q

other name for p-ANCA

A

anti-myeloperoxidase

448
Q

microscopic polyangiits treatment

A

cyclophosphamide + corticosteroids

449
Q

Churn-Strauss presentation

A

asthma + sinusitis + skin nodules or purpura + peripheral neuropathy. Can involve heart, GI, kidneys.

450
Q

churg-strauss path

A

Granulomatous, necrotizing vasculitis with eosinophilia.

451
Q

Labs in churg-strauss

A

1) *increased IgE

2) MPO-ANCA/p-ANCA

452
Q

HSP pathophys

A

IgA immune complex deposition

453
Q

Essential HTN management

A

1) thiazides
2) ACEIs/ARBs
3) *dihydropyridine Ca2+ channel blockers

454
Q

HTN with heart failure management

A

1) diuretics
2) ACEI’s/ARBs
3) b-blockers (compensated) (to prevent cardiac remodeling)
4) aldosterone antagonists (to prevent from being fluid overloaded)

455
Q

HTN with DM management

A

1) ACE/ARBs (both are protective against diabetic nephropathy)
2) Ca2+ channel blockers
3) thiazides
4) beta-blockers

456
Q

Drugs for HTN in pregnancy?

A

1) hydrazine
2) labetalol
3) methyldopa
4) nifedipine

457
Q

dihydropyridines vs nondihydropyridines

A

dihyropyridines act on vascular smooth muscle, non-dihydropyridines act on heart

458
Q

dihydropyridines

A

all the -pines

459
Q

non-dihydropyridines

A

dilimiazem + verapamil

460
Q

Ca-channel blocker mechanism

A

Block voltage-dependent *L-type calcium channels of cardiac and smooth muscle leading to decreased contractility.

461
Q

order of action of calcium channel blockers on vascular smooth muscle

A

Amlodipine + nifedipine, then diltiazem, then verapamil

462
Q

order of efficacy of calcium channel blockers on heart

A

verapamil, diltiazem, amlodipine = nifedipine (verapamil for ventricle)

463
Q

dihydropyridine you can’t use for HTN, angina, or Raynaud’s

A

nimodipine

464
Q

clevidipine clinal use?

A

hypertensive urgency or emergency.

465
Q

other use for non-dihydropyridines

A

afib/ a flutter

466
Q

AE’s of non-dihydropyridines

A

cardiac depression + AV block + hyperprolactinemia + constipation

467
Q

AE’s of dihydropyridines

A

peripheral edema + flushing + dizziness + gingival hyperplasia

468
Q

hydrazine mechanism

A

increases cGMP leading to smooth muscle relaxation. Vasodilates arterioles more so than veins, leading to after load reduction.

469
Q

when is hydralazine contraindicated?

A

angina/CAD (due to compensatory tachycardia)

470
Q

hydralazine AE’s

A

fluid retention + headache + angina + lupus-like syndrome

471
Q

hypertensive emergency drugs

A

1) clevidipine
2) fenoldopam
3) labetalol
4) nicardipine
5) nitroprusside

472
Q

Nitroprusside MOA

A

short acting, increases cGMP via direct release of NO.

473
Q

Nitroprusside AE

A

can cause cyanide toxicity (releases cyanide)

474
Q

Fenoldopam MOA

A

Dopamine D1 receptor agonist– coronary, peripheral, renal, and splanchnic vasodilation. Decreases BP, increases natriuresis

475
Q

What drug is commonly used postop for anti hypertension?

A

fenoldopam

476
Q

Fenoldopam SE’s

A

hypotension + tachycardia

477
Q

nitrates effect on veins or arteries?

A

Dilate veins more than arteries, thus DECREASING preload

478
Q

other use for nitrates

A

pulmonary edema

479
Q

nitrates AE’s

A

reflex tachycardia + hypotension + flushing + headache.

480
Q

Describe Monday disease

A

exposure to nitrates leads to development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend. So they show up to work and become tachy, dizzy, and have a headache upon exposure.

481
Q

MVO2

A

myocardial oxygen consumption

482
Q

What beta-agonists are contraindicated in angina?

A

pindolol and acebutolol

483
Q

pindolol MOA

A

partial B-antagonist (Only partial among nonselective)

484
Q

B-blocker effect on EDV?

A

no effect or increased

485
Q

Nitrate effect on ejection time?

A

decrease

486
Q

Beta-blocker effect on ejection time?

A

Increase

487
Q

Combined effect of nitrates + beta-blockers on

1) EDV
2) BP
3) contractility
4) HR
5) ejection time
6) MVO2

A

1) no effect or decreased
2) decreased
3) little/no effect
4) no effect or decreased
5) little/no effect
6) decreased significantly

488
Q

**Ranolazine MOA

A

Inhibits the late phase of sodium current thereby reducing diastolic wall tension and oxygen consumption. *No affect on HR or contractility.

489
Q

What is ranolazine used for?

A

angina refractory to other medical therapies

490
Q

Ranolazine AE’s

A

constipation + dizziness + headache + nausea + QT prolongation

491
Q

Statin mechanism

A

HMG-CoA reductase inhibitors: inhibit conversion of HMG-CoA to mevalonate

492
Q

Mevalonate

A

precursor to cholesterol

493
Q

when is myopathy a concern with statins?

A

When used with fibrates or niacin.

494
Q

Name bile acid resin drugs

A

1) cholestyramine
2) colestipol
3) colesevelam

495
Q

Bile acid resins affect on…

1) LDL
2) HDL
3) triglycerides

A

1) decrease (2 arrows)
2) slight increase
3) slight increase

496
Q

Bile acid AE’s

A

1) GI upset

2) decrease absorption of other drugs and fat-soluble vitamins

497
Q

Ezetimibe MOA

A

Prevents cholesterol absorption at small intestine brush border.

498
Q

1) LDL
2) HDL
3) triglycerides

A

1) decrease (2 arrows)
2) null
3) null

499
Q

Ezetimibe AE’s

A

rare hepatoxicity + diarrhea

500
Q

Fibrate affect on…

1) LDL
2) HDL
3) triglycerides

A

1) decrease
2) increase
3) major decrease

501
Q

fibrate mechanism

A

1) up regulate LPL leading to increased TG clearance

2) activates PPAR-alpha to induce HDL synthesis

502
Q

Vibrate AE

A

myopathy + cholesterol gallstones

503
Q

Niacin affects on…

1) LDL
2) HDL
3) triglycerides

A

1) significant decrease (2 arrows)
2) significant increase
3) decrease

504
Q

Niacin mechanism as a lipid lowering agent

A

1) Inhibits lipolysis (HSL) in adipose tissue. Thus this prevents FFA from getting into the bloodstream and uptake into liver where cholesterol synthesis occurs.
2) reduces hepatic VLDL synthesis

505
Q

Other niacin AE’s

A

hyperglycemia + hyperuricemia

506
Q

Cholesterol synthesis pathway

A

Acetyl CoA –> HMG-CoA –> mevalonate –> cholesterol

507
Q

digoxin affect on vagus nerve

A

Stimulates vagus nerve leading to decreased HR.

508
Q

Factors predisposing to digoxin toxicity

A

1) renal failure
2) hypokalemia (this leads to increase binding at K+ binding site on ATPase because there’s less potassium).
3) decreased clearance with verapamil, amiodarone, and quinidine

509
Q

Management of digoxin toxicity

A

1) Slowly normalize K+
2) cardiac pacer
3) anti-dig FAB
4) Mg2+

510
Q

Class IA antiarrhytmics

A

Quinine + procainamide + disopyramide

511
Q

Class IA affects

A

1) Increased AP duration
2) increase effective refractory period
3) increase QT interval

512
Q

When are class IA’s used?

A

atrial and ventricular arrhythmias

513
Q

Treatment for re-entrant and ectopic SVT and VT?

A

Class IA’s

514
Q

cinchonism

A

headache + tinnitus with quinidine

515
Q

disopyramide AE

A

HF

516
Q

Other 1A SE’s

A

thrombocytopenia + torsades de pointes

517
Q

1B drugs

A

Lidocaine + mexiletine + (phenytoin)

518
Q

1B affects on action potential

A

Decrease AP duration.

519
Q

1B MOA

A

Preferentially affect ischemic or depolarized Purkinje and ventricular tissue.

520
Q

Best anti-arrhythmic post-MI?

A

IB’s (IB is Best post MI)

521
Q

Arrhythmias for digitalis induced?

A

1B’s (lidocaine or mexiletine)

522
Q

1B AE’s

A

CNS stimulation/depression + cardiovascular depression

523
Q

IC drugs

A

fleicanide + propafenone

524
Q

IC mechanism

A

Significantly prolong ERP in AV node and accessory bypass tracts. No effect on ERP in purkinje and ventricular tissue.
- No affect on AP duration.

525
Q

antiarrhythmics contraindicated post-MI?

A

IC (IC Contraindicated post MI)

526
Q

antiarrhythmics contraindicated in structural and ischemic heart disease?

A

IC (IC contraindicated)

527
Q

beta-blocker mechanism

A

Decrease SA and AV nodal activity by decreasing cAMP and Ca2+ currents.

528
Q

How do beta-blockers suppress abnormal pacemakers?

A

Decreasing slope of phase 4.

529
Q

esmolol caveat

A

very short acting

530
Q

Why is PR interval increased with beta-blockers?

A

AV node particularly sensitive

531
Q

metoprolol other AE

A

dyslipidemia

532
Q

propranolol other AE

A

Can exacerbate vasospasm in prinzmetal angina

533
Q

carvedilol and labetalol MOA

A

nonselective alpha and b-antagonists

534
Q

Problem with giving b-blockers for cocaine toxicity or pheochromocytoma?

A

Cause unopposed alpha1 agonism if given alone.

535
Q

Beta-Blocker overdose management

A

saline + atropine + glucagon

536
Q

Class III antiarrhytmics mechanism

A

Increase AP duration + increase ERP + increase QT interval

537
Q

Class IIIs used for V tach

A

amiodarone + sotalol

538
Q

antiarrhythmics for afib

A

Anything except 1B or 1C

539
Q

Sotalol AE’s

A

torsades de pointes + excessive betablockade

540
Q

Ibutilide AE’s

A

torsades de pointes

541
Q

amiodarone AE’s

A

1) PF
2) hepatotoxic
3) hypothyroidism
4) *hyperthyroidism (amiodarone is 40% iodine by weight)
5) corneal deposits + blue/gray skin deposits resulting in photo dermatitis
6) neurologic effects
7) constipation
8) bradycardia + heart block + HF

542
Q

What will class III look like on action potential graph?

A

markedly prolonged repolraization

543
Q

Why does amiodarone cause corneal deposits and skin deposits?

A

Acts as a happen.

544
Q

Caveat about amiodarone

A

Lipophilic and has class I, II, III, and IV effects.

545
Q

Class IV mechanism

A

Decreased conduction velocity + increased ERP + increased PR interval

546
Q

What do you use for rate control in fib?

A

Class IV channel blockers

547
Q

Which anti arrhythmic can depress the sinus node?

A

class IV - verapamil, diltiazem.

548
Q

adenosine

A

Moves K+ out of cells leading to hyper polarization of cell and decreased caclium

549
Q

Drug of choice in diagnosing/terminating certain forms of SVT?

A

adenosine (very short acting)

550
Q

Adenosine contraindications

A

theophylline + caffeine will blunt effects because both are adenosine receptor antagonists

551
Q

Adenosine AE’s

A

flushing + hypotension + chest pain + sense of impending doom + bronchospasm

552
Q

What do you use to treat torsades de points?

A

Mg2+

553
Q

Displaced PMI indicates…

A

cardiomegaly

554
Q

Mixed osteolytic and blastic lesions

A

1) gastric

2) breast

555
Q

acute decompensated heart failure

A

Decompensation of chronic stable heart failure. Eg from illness, MI, abnormal rhythm, uncontrolled HTN, or increased fluids.

556
Q

Where do internal thoracics come off of?

A

subclavian

557
Q

Pathophys of rib notching

A

with increased flow through the internal thoracic-anterior intercostal arterial system, retrograde flow through the posterior intercostal arteries develops, providing oxygenated blood to the descending aorta distal to the coarctation. /this is what causes rib notching (increased flow through the intercostals enlarges the arteries resulting in resorption of bone along the lower borders of the ribs.

558
Q

murmur in aortic coarctation

A

harsh systolic ejection murmur.

559
Q

carotid occlusion

A

procedure in which occlusion of the carotid results in less stretch of the carotid baroreceptors and less afferent nerve activity. Basically tricks body into thinking it has a lower blood pressure than it actually has. /thus, a baroreceptor reflex is elicited, leading to an increase in sympathetic tone increasing mean blood pressure + HR.

560
Q

What happens to preload when CO decreases?

A

Increases because blood is redistributed to the veins. Blood flow ceases, and then flows from high pressure arterial system to low pressure venous system.

561
Q

MCFP

A

mean circulatory filling pressure. Equilibrated pressure when pressure is equal throughout CV system.

562
Q

Mean systemic filling pressure (MSFP)

A

Measure of volume of blood and compliance of vessels.

563
Q

Relation of venous compliance to preload

A

Decreased compliance = increased preload.

564
Q

Bainbridge reflex

A

Increase in HR due to increase in CVP.
Increased blood volume –> increased volume sensed by baroreceptors –> B-fibers reflex with heart affecting sympathetic and parasympathetic pathways –> increased HR.

565
Q

Auto regulation of blood flow in heart?

A

ATP consumption increases with increased work –> increased adenosine –> vasodilation –> increased oxygen delivery.

566
Q

What happens to arterial PO2 and arterial O2 sat at high elevation?

A

Low. Even with acclimatization since these are independent of hematocrit. Just depend on O2 availability.

567
Q

Changes with acclimatization…

A

1) arterial PO2 and O2 sat stay low
2) systemic arterial O2 content increases to normal
3) pH normal (increased ventilation)

568
Q

acute changes to altitude

A

decreased PAO2 and PaO2 + decreased PACO2 and PaCO2 + increased systemic arterial pH + decreased Hb% sat + decreased systemic arterial O2.

569
Q

What happens to compliance and CVP with exercise?

A

Increased sympathetic activity causes venous smooth muscle constriction –> decreased compliance –> increased CVP –> increases CO

570
Q

adenosine half-life

A

minutes

571
Q

TPR and CO changes with dynamic, endurance exercise?

A

Increased CO + decreased TPR due to metabolic vasodilation.

572
Q

static exercise changes in…

1) blood flow
2) MAP
3) ATP/ADP ratio

A

Contraction of skeletal muscles compress blood vessels and decreases blood flow. This increases vascular resistance + profound increase of MAP.
3) decreased.

573
Q

What happens to blood flow with dynamic exercise?

A

Increased blood flow due to metabolic vasodilation of arterioles due to local vasodilator actions.

574
Q

PV loop changes with LV dilation

A

Only slightly increased EDP (compliance increases but not a significant change in pressure).

575
Q

Hypertonic contraction

A

Loss of hypotonic fluid

576
Q

Hypertonic expansion

A

Excessive intake of sodium chloride.

577
Q

Approach to Darrow Yannett diagrams

A

Just draw cell and think about osmolar effect.

578
Q

Causes of isotonic fluid loss

A

1) hemorrhaging
2) diarrhea
3) vomiting

579
Q

Affect of isotonic fluid loss on:

1) osmolarity
2) ICF volume
3) ECF volume

A

1) no change
2) no change (no force pushing fluid out of cell)
3) decreased

580
Q

Causes of hypotonic fluid loss:

A

1) dehydration
2) DI
3) alcoholism

581
Q

Affect of hypotonic fluid loss on:

1) osmolarity
2) ICF volume
3) ECF volume

A

1) Increased
2) decreased
3) decreased

582
Q

Affect of isotonic fluid gain on:

1) osmolarity
2) ICF volume
3) ECF volume

A

1) no change
2) no change
3) increased

583
Q

Causes of hypotonic fluid gain

A

1) hypotonic saline

2) water intoxication

584
Q

Affect of hypotonic fluid gain on:

1) osmolarity
2) ICF volume
3) ECF volume

A

1) decreased
2) increased
3) increased

585
Q

Premature contraction of the ventricle (PVC) on ECG

A

no P wave

586
Q

Premature contraction of the ventricle (PVC)

A

presentation = either asymptomatic or palpitations or syncopale episodes. /can present after MIs in which tissue damage in ventricular tissue produces ectopic (non-SA node) sites of electrical activation. When these sites depolarize the ventricles contract independently and generate premature and abnormal QRS patterns seen on ECG.

587
Q

afib on ECG

A

absent P waves + irregularly irregular QRS

588
Q

premortem thrombi (lines of zahn) suggests…

A

afib prior to death

589
Q

treatment of choice for V tach?

A

amiodarone

590
Q

AV fistula

1) presentation
2) scenario
3) findings

A

1) coldness of extremity (due to lack of arterial flow)
2) post surgery
3) palpable thrill over area of wound. Continuous murmur. Diminished pulse. Doppler showing turbulence.

591
Q

Nutmeg appearance of heart may also indicate…

A

right heart failure

592
Q

Adult pressures in the cardiac chambers (minimum, maximum)

A

Code: covered in ivy/right atrium = 0,8. Covered in hair + nails pounded in everywhere/right ventricle = 4,25. Nails + big hoops/pulmonary artery = 9,25. Hens + walls made out of tin cans/left atrium = 2,12. Hoops on walls + mice drinking mimosas/left ventricle = 9,130. Mice drinking mimosas + carrying briefcases/aorta = 70,130. Wedge of tissue sitting in middle of road covered in tin cans/wedge pressure = 12

593
Q

Common treatment for bradycardia?

A

atropine (decreases vagal influence on the SA and AV nodes).

594
Q

valsalva maneuver pathophys

A

pathophys: pressure increase in chest forces blood out of pulmonary circulation into left atrium. ALSO return of systemic blood to the heart is impeded by increased pressure in chest. /effect = decreases preload + decreases afterload

595
Q

What signifies the development of a complicated atheromatous plaque?

A

Calcification

596
Q

“foci of calcification”

A

atherosclerotic plaque

597
Q

ruptured free wall presentation

A

profound hypotension + dyspnea + muffled hear sounds and elevated JVP.

598
Q

What does coronary sinus dilation often suggest

A

pulmonary hypertension.

599
Q

bronchiolitis obliterans

A

lymphocytic inflammation and necrosis of bronchiolar walls, leading to scarring and progressive obliteration of small airway lumens.

600
Q

SERCA proteins

A

Sarcoplasmic reticulum Ca ATPase. Pump Ca, and thus a net positive charge out of the cytosol into the sarcoplasmic reticulum (thus sequester Calcium)

601
Q

sarcoplasmic reticulum

A

stores calcium

602
Q

Ryanodine receptor functions

A

Mediates calcium-induced calcium release

603
Q

When does ischemic injury become irreversible?

A

half hour

604
Q

When does loss of cardiomyocyte contractility occur with ischemia?

A

after 60 seconds.

605
Q

If radius of an artery decreases by 50%, what is change in blood flow?

A

Decreases by 1/16 (flow is proportional to radius ^ 4th power) so (1/2)^4 = 1/16

606
Q

Systolic pressure in downstream arteries is actually slightly higher than in aorta.

A

So renal artery pressure is actually higher than aorta.

607
Q

What happens with extra systolic beats?

A

There’s more calcium in the myocyte so contractility increases. Thus, pulse pressure increases.

608
Q

What does 2 P waves breeding each QRS complex indicate?

A

Only every other P wave is conducted through AV node to ventricle. Thus, conduction velocity through AV node must be decreased.

609
Q

What determines pulse pressure?

A

Stroke volume

610
Q

When is the aortic pressure highest in the cardiac cycle?

A
  • Reduced ventricular filling (diastasis).

- Aortic pressure reaches its highest level immediately after rapid ejection of blood during systole.

611
Q

Affect of histamine on vasculature

A

1) vasodilation of arterioles, thus increasing filtration.

2) constriction of veins

612
Q

Hodgkin’s lytic or blastic mets?

A

blastic

613
Q

What happens to TPR during exercise?

A

Decreases. Although there is increased sympathetic flow to blood vessels, there is an overriding vasodilation of skeletal muscle arterioles.

614
Q

During which phase of the cardiac cycle is ventricular volume lowest?

A

Isovolumetric ventricular relaxation (ventricle is relaxed just before filling occurs).

615
Q

Why does standing cause an increase in HR?

A

Blood pools and due to decreased venous return, baroreceptors sense this and stimulate increased HR.

616
Q

During which phase of ventricular action potential is membrane potential closest o K+?

A

Phase 4

617
Q

What receptors mediate slowing of the heart?

A

Muscarinic (via ACh in the SA node)

618
Q

Other cause of decreased inotropy…

A
  • Acetylcholine (on atria)
619
Q

How do sympathetic stimulation and NE increase contractility?

A

Increasing calcium entry during the plateau phase and increasing storage of Ca by the sarcoplasmic reticulum.96

620
Q

pulses finding in AS

A

“pulses parvus et tardus”– pulses are weak with a delayed peak.

STEP (85 decks)

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