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Rapid Review Pathology > Chapter 11 - Heart Disorders > Flashcards

Chapter 11 - Heart Disorders Flashcards

0
Q

What is afterload?

A

Afterload: resistance ventricle contracts against to eject blood in systole

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1
Q

How does wall stress affect gene expression in the heart?

A

Wall stress increases gene-controlled sarcomere duplication

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2
Q

What is the effect of increased afterload on sarcomeres and muscle?

A

↑Afterload: sarcomeres duplicate parallel to long axis; muscle is thicker

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3
Q

Increased afterload results in what type of hypertrophy?

A

↑Afterload: concentric ventricular hypertrophy

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4
Q

What are the causes of concentric LVH?

A

Concentric LVH: essential HTN, AV stenosis, hypertrophic cardiomyopathy

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5
Q

What are the causes of concentric RVH?

A

Concentric RVH: PH, PV stenosis

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6
Q

What is preload?

A

Preload: volume of blood ventricle must expel during systole

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7
Q

How does increased preload affect sarcomeres and muscle fibers?

A

↑Preload: sarcomeres duplicate in series; muscle fibers longer/wider

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8
Q

Increased preload causes what type of hypertrophy?

A

↑Preload causes eccentric ventricular hypertrophy

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9
Q

What are the causes of eccentric LVH?

A

Eccentric LVH: MV/AV regurgitation; left-to-right shunt

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10
Q

What are the causes of eccentric RVH?

A

Eccentric RVH: TV/PV regurgitation

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11
Q

What are the consequences of ventricular hypertrophy?

A

Consequences: heart failure, S4, angina (subendocardial ischemia)

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12
Q

What does the S4 heart sound indicate?

A

S4: blood entering noncompliant ventricle (concentric/eccentric hypertrophy)

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13
Q

What does the S3 heart sound indicate?

A

S3: blood entering volume overloaded ventricle

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14
Q

What is the most common cause of hospital admission for persons >65 years old?

A

CHF: MCC hospital admission for persons >65 years old

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15
Q

What are the types of heart failure?

A

Types heart failure: left/right, biventricular, high output

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16
Q

Where does blood back up into in LHF?

A

LHF: blood backs up into lungs

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17
Q

Where does blood back up into in RHF?

A

RHF: blood backs up into venous system

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18
Q

What type of edema is caused by LHF?

A

LHF → pulmonary edema

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19
Q

What is the most common type of LHF? What is the pathogenesis of LHF?

A

SHF: MC type LHF; ↓ventricular contraction

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20
Q

What are the causes of SHF? Which cause is the most common?

A

SHF: ischemia MCC; myocarditis, post-MI, dilated cardiomyopathy

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21
Q

What is DHF?

A

DHF: noncompliant LV (stiff ventricle) with impaired relaxation; ↑LVEDP

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22
Q

What is the most common cause of DHF?

A

DHF: MCC essential HTN

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23
Q

How is the EF affected in SHF?

A

SHF: ↓EF

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24
Q

How is the EF affected in DHF?

A

DHF: normal EF at rest

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25
Q

What are the microscopic findings of LHF?

A

LHF: heart failure cells; alveolar macrophages with hemosiderin

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26
Q

What is dyspnea?

A

Dyspnea: cannot take full inspiration

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27
Q

How do the pulmonary capillary HP and OP compare in pulmonary edema?

A

Pulmonary edema: pulmonary capillary HP > OP

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28
Q

What causes cardiac asthma?

A

Cardiac asthma: peribronchiolar edema

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29
Q

What is a physical exam finding in LHF?

A

LHF: bibasilar inspiratory crackles (edema)

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30
Q

What are the chest radiograph findings in LHF?

A

LHF X-ray: bat-wing configuration, fluffy alveolar infiltrate, Kerley lines, air bronchograms

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31
Q

What is the first cardiac sign of LHF?

A

S3: first cardiac sign LHF

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32
Q

What type of regurgitant murmur may be present in LHF?

A

LHF: functional MV regurgitation

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33
Q

What is the cause of PND/orthopnea?

A

PND/orthopnea: ↑venous return to right side of heart at night → failed left heart → pulmonary edema

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34
Q

Describe how pillows relieve orthopnea.

A

Pillow orthopnea: pillows ↑gravitational effect → ↓venous return to right heart

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35
Q

What is BNP useful in?

A

BNP: useful in confirming/excluding LHF; predicting survival

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36
Q

How is ANP affected in LHF?

A

ANP: ↑with left atrial dilatation in LHF

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37
Q

How is the venous HP affected in RHF?

A

RHF → ↑venous hydrostatic pressure

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38
Q

What is the most common cause of RHF?

A

MCC RHF: ↑afterload from LHF

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39
Q

What are the causes of decreased RV contraction in RHF?

A

RHF: ↓RV contraction; e.g., myocarditis, RV infarction

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40
Q

What are the causes of a noncompliant RV in RHF?

A

RHF: RV noncompliant; e.g., restrictive cardiomyopathy, concentric RVH

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41
Q

What are the causes of increased RV preload in RHF?

A

RHF: ↑RV preload; e.g., valvular regurgitation; left-to-right shunt

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42
Q

What are the clinical findings in RHF?

A

RHF: prominence internal jugular veins; function TV regurgitation
RHF: S3/S4 heart sounds
RHF: painful hepatomegaly; centrilobular hemorrhagic necrosis
RHF: dependent pitting edema, ascites, cyanotic mucous membranes

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43
Q

What is the nonpharmacologic therapy for CHF?

A

Restrict sodium & water

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44
Q

What are two pharmacologic treatments for CHF? How do they work?

A

ACE inhibitor: ↓afterload, ↓preload

β-Blocker: ↓myocardial O2 consumption; ↓heart rate

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45
Q

Describe the pathogenesis and causes of high-output heart failure.

A

HOF: ↑SV; e.g., hyperthyroidism
HOF: ↓blood viscosity; e.g., severe anemia
HOF: vasodilation PVRs; e.g., septic shock, thiamine deficiency
HOF: arteriovenous fistula

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46
Q

What is ischemic heart disease?

A

IHD: imbalance in demand of O2 and supply

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47
Q

When do coronary arteries normally fill?

A

Coronary arteries: fill in diastole

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48
Q

How does tachycardia affect diastole and the filling of coronary arteries?

A

Tachycardia: ↓diastole and filling of coronary arteries

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49
Q

What is the distribution of the LAD?

A

LAD: anterior portion LV; anterior IVS; apex

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50
Q

What is the most common site of coronary artery thrombosis?

A

LAD: MC site coronary artery thrombosis

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51
Q

What is the distribution of the RCA?

A

RCA: posterior LV; posterior IVS; RV; posteromedial papillary muscle; SA/AV nodes

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52
Q

What is the distribution of the left circumflex coronary artery?

A

Left circumflex: lateral wall LV

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53
Q

IHD is a major cause of what in the U.S.?

A

IHD: major cause of death in U.S.

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54
Q

What is the most common manifestation of coronary artery disease?

A

Angina pectoris: MC manifestation coronary artery disease

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55
Q

What is the most important risk factor for angina pectoris?

A

Angina pectoris: age most important risk factor

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56
Q

Which gender is more affected by angina pectoris?

A

Angina: males > females

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57
Q

What is the most common variant of angina?

A

Chronic (stable) angina: MC type of angina

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58
Q

What is the most common cause of stable angina?

A

Stable angina: MCC fixed atherosclerotic coronary artery disease

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59
Q

What are other causes of stable angina?

A

Stable angina: AV stenosis/HTN with concentric LVH

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60
Q

Describe the pathogenesis of stable angina.

A

Pathogenesis: subendocardial ischemia; ↓coronary artery blood flow/concentric hypertrophy

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61
Q

What is a clinical finding of stable angina?

A

Exercise-induced substernal chest pain; relieved by rest/nitroglycerin

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62
Q

How does subendocardial ischemia appear on a stress test?

A

Subendocardial ischemia: ST-segment depression on stress test

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63
Q

What is Prinzmetal angina?

A

Prinzmetal angina: vasospasm with transmural ischemia/ST-segment elevation

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64
Q

What is unstable angina?

A

Unstable angina: angina at rest; multivessel disease; disrupted plaques

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65
Q

What is the treatment for Prinzmetal variant angina?

A

Prinzmetal variant angina: calcium channel blockers vasodilate coronary arteries

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66
Q

What is CIHD?

A

CIHD: muscle replaced by noncontractile fibrous tissue; progressive CHF

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67
Q

What is sudden cardiac death? What is its most important risk factor?

A

SCD: unexpected death within 1 hour after symptoms; IHD most important

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68
Q

What is a NSTEMI?

A

NSTEMI = non-ST elevation myocardial infarction

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69
Q

What is the most common cause of SCD in children?

A

SCD in children: AV stenosis MCC

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70
Q

Describe the pathogenesis of SCD in adults.

A

SCD: coronary artery thrombosis not usually present; ventricular arrhythmia

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71
Q

What is the most common cause of death in adults in the U.S.?

A

AMI: MCC death in adults in U.S.

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72
Q

Describe the pathogenesis of developing an AMI.

A

Rupture of disrupted plaque → platelet thrombus → AMI

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73
Q

Describe the coronary arteries in a cocaine-induced AMI.

A

Cocaine: AMI with normal coronary arteries

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74
Q

What is a STEMI?

A

STEMI = ST wave elevation myocardial infarction; Q waves

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75
Q

What is the effect of early reperfusion following AMI?

A

Early reperfusion (<3 hr): ↑short- and long-term survival

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76
Q

What is reperfusion injury?

A

Reperfusion injury: ischemic myocardial cells not already irreversibly damaged become so after reperfusion
Reperfusion injury: previously ischemic cells become irreversibly damaged

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77
Q

What is reversible after reperfusion?

A

Myocardial stunning after reperfusion is reversible

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78
Q

Describe the mechanism of irreversible myocardial injury.

A

Irreversible injury: superoxide FRs

Neutrophils contribute to irreversible myocardial injury

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79
Q

When does coagulation necrosis occur following an AMI?

A

AMI: coagulation necrosis within 24 hours

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80
Q

What period following an AMI is the risk for rupture the greatest?

A

AMI: heart softest 3–7 days; danger of rupture

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81
Q

What are the clinical findings of an AMI?

A

AMI: retrosternal pain >30 minutes, radiation to left inner arm/shoulder, diaphoresis

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82
Q

What are the nerves to the heart?

A

Nerves to heart: T1–T5

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83
Q

Inner arm pain is in the distribution of which nerve?

A

Inner arm pain: T1 distribution

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84
Q

The epigastrium is in which nerve distribution?

A

Epigastrium radiation: T4–T5 distribution

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85
Q

How does the early mortality rate of a STEMI compare to that of an NSTEMI?

A

STEMI: ↑early mortality rate

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86
Q

Having an NSTEMI increases the risk of what?

A

NSTEMI: ↑risk for SCD

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87
Q

What is the most common arrhythmia post-STEMI?

A

Ventricular premature contractions MC arrhythmia

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88
Q

What is the most common cause of death in a STEMI?

A

Ventricular fibrillation: MCC death in STEMI

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89
Q

When is myocardial rupture most common post-AMI?

A

Myocardial rupture: MC at 3–7 days

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90
Q

What is posteromedial papillary muscle rupture associated with? How does it present?

A

Posteromedial papillary muscle rupture: RCA thrombosis; MV regurgitation

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91
Q

What is the most common cause of an IVS rupture? What does it produce?

A

IVS rupture: left-to-right shunt; LAD thrombosis MCC

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92
Q

There is danger of what with a mural thrombus?

A

Mural thrombus: danger of embolization

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93
Q

Describe the characteristics of fibrinous pericarditis following STEMI AMI.

A

Fibrinous pericarditis: early (acute inflammation); late complication (autoimmune)

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94
Q

Describe the characteristics of ventricular aneurysm following STEMI AMI.

A

Ventricular aneurysm: precordial bulge with systole; CHF MCC death

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95
Q

What is a right ventricular AMI associated with? What are its clinical findings?

A

RV AMI: RCA thrombosis; hypotension, RHF, preserved LV function

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96
Q

How is reinfarction of the heart defined?

A

Reinfarction: reappearance of CK-MB after 3 days

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97
Q

What are the cardiac troponins tested for in an AMI? Can they be used to diagnose reinfarction?

A

cTnI, cTnT: cannot diagnose reinfarction

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98
Q

What is the gold standard for diagnosis of an AMI?

A

cTnI, cTnT: gold standard for diagnosis of AMI

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99
Q

What are the ECG findings in a STEMI?

A

ECG findings in STEMI: inverted T waves, elevated ST segments, Q waves

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100
Q

What do inverted T waves correlate with in an AMI?

A

Inverted T waves: correlates with ischemia at periphery of infarct

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101
Q

What does ST elevation correlate with in an AMI?

A

ST elevation: correlates with injured myocardial cells surrounding area of necrosis

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102
Q

What do new Q waves correlate with in an AMI?

A

Q waves: correlates with area of coagulation necrosis

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103
Q

Describe the role of the chorionic villus in the fetal circulation.

A

Chorionic villus: primary site O2 exchange; vessels become umbilical vein

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104
Q

Describe the role of the umbilical vein in the fetal circulation.

A

Umbilical vein: highest PO2 in fetal circulation

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105
Q

What keeps the ductus arteriosus open?

A

Ductus arteriosus kept open by PGE2, a vasodilator synthesized by placenta

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106
Q

Which two structures are patent in the fetal circulation but not the adult circulation?

A

Fetal circulation: foramen ovale and ductus arteriosus are patent

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107
Q

The presence of a single umbilical artery increases the risk for what?

A

Single umbilical artery: ↑risk congenital abnormalities

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108
Q

What are the changes in the fetal circulation at birth?

A

Ductus arteriosus becomes ligamentum arteriosum after birth

Newborn: foramen ovale and ductus arteriosus are closed

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109
Q

What type of heart disease is the most common in children?

A

CHD MC heart disease in children

110
Q

Which are the most common causes of congenital heart disease?

A

Genetic-environmental causes MCC CHD

111
Q

How does the risk for CHD change with maternal age?

A

CHD: ↑risk with ↑maternal age

112
Q

What are the maternal risk factors for CHD?

A

Previous child with CHD; poorly controlled DM
Alcohol; congenital infections (rubella)
Aspirin, diphenylhydantoin, SLE

113
Q

Describe the spectrum of CHD.

A

CHD: valvular disorders, shunts (acyanotic, cyanotic)

114
Q

What are the systemic complications of CHD?

A

Complications: 2° polycythemia, clubbing, infective endocarditis, metastatic abscesses

115
Q

What are the types of shunts in CHD?

A

CHD shunts: left-to-right; right-to-left (often cyanotic)

116
Q

Describe the effect of left-to-right shunts on SaO2.

A

Left-to-right shunts: step up of SaO2 in right heart

117
Q

Describe the effect of right-to-left shunts on SaO2.

A

Right-to-left shunts: step down of SaO2 in left heart

118
Q

What is shunt reversal due to in left-to-right shunts?

A

Shunt reversal due to PH and RVH

119
Q

What is there danger of if a left-to-right shunt is uncorrected?

A

Left-to-right shunts: danger of shunt reversal if uncorrected

120
Q

What is the most common type of CHD?

A

VSD: MC CHD

121
Q

Which type of VSD is most common?

A

VSD MC a defect in membranous portion of IVS

122
Q

What are the associations of VSD with other congenital heart diseases?

A

VSD associations: cri du chat syndrome, fetal alcohol syndrome

123
Q

How is the SaO2 affected in a patient with a VSD?

A

VSD: step up SaO2 in RV and PA

124
Q

What percentage of VSDs spontaneously close?

A

VSD: ~50% spontaneously close

125
Q

What is the most common CHD in adults?

A

ASD: MC CHD in adults

126
Q

What is the most common cause of ASD?

A

ASD: MCC patent foramen ovale

127
Q

What are the associations of ASD with other CHDs?

A

ASD associations: fetal alcohol syndrome, Down syndrome (primum type)

128
Q

What is the physical exam finding of ASD?

A

ASD: wide and fixed split of S2 very characteristic

129
Q

ASD is associated with which type of embolism?

A

ASD: paradoxical embolism (venous clot in system circulation)

130
Q

How is the SaO2 affected in a patient with an ASD?

A

ASD: step up SaO2 in RA, RV, PA

131
Q

What are the associations of PDAs?

A

PDA associations: congenital rubella, RDS, transposition

132
Q

What is the physical exam finding of a PDA? How is the SaO2 affected in a patient with a PDA?

A

PDA: continuous machinery murmur; step up SaO2 in PA

133
Q

What is the physical exam finding of a shunt reversal in PDA?

A

Reversal of shunt in PDA: differential cyanosis (pink on top, blue on bottom)

134
Q

What is the treatment for a PDA?

A

PDA: closed with indomethacin

135
Q

What is the most common cyanosis CHD after one year of age?

A

Tetralogy of Fallot: MC cyanotic CHD after age 1 year

136
Q

What are the defects in tetralogy of Fallot?

A

VSD, infundibular pulmonic stenosis, dextrorotation of aorta, RVH

137
Q

What does the degree of PV stenosis correlate with in tetralogy of Fallot?

A

Degree of PV stenosis correlates with presence or absence of cyanosis

138
Q

What is the effect of severe PV stenosis in tetralogy of Fallot?

A

Severe PV stenosis → cyanosis; mild PV stenosis → no cyanosis

139
Q

How is the SaO2 affected in patients with tetralogy of Fallot?

A

Step down in SaO2 in LV and Ao

140
Q

What are the cardioprotective shunts in tetralogy of Fallot?

A

Cardioprotective shunts in tetralogy: ASD, PDA

141
Q

What are tet spells? Describe the mechanism of compensation.

A

Tet spells (hypoxemic episode): squatting ↑PVR → reverses shunt → ↑PaO2

142
Q

What is transposition of the great arteries?

A

Transposition: abnormal formation of truncal and aortopulmonary septa

143
Q

What are the defects of complete transposition?

A

Transposition: Ao empties RV; PA empties LV; atria normal

144
Q

What are the cardioprotective shunts in transposition?

A

Cardioprotective shunts: ASD, VSD, PDA

145
Q

Describe the characteristics of infantile coarctation.

A

Infantile coarctation: preductal; constriction proximal to ligamentum arteriosum; associated with Turner syndrome

146
Q

Describe the characteristics of adult coarctation.

A

Adult coarctation: constriction distal to ligamentum arteriosum

147
Q

What is commonly present in patients with an adult coarctation?

A

Adult coarctation: bicuspid AV commonly present

148
Q

What are the clinical findings and possible complications proximal to the coarctation in adult coarctation?

A

↑Upper extremity systolic blood pressure (SBP); ↑cerebral blood flow (risk for berry aneurysms)

148
Q

What are the clinical findings and possible complications distal to the coarctation in adult coarctation?

A

Disparity between upper/lower extremity blood pressure >10 mm Hg
Leg claudication: pain in calf/buttocks when walking
HTN due to activation of RAA system from ↓renal blood flow

149
Q

Describe the collateral circulation that develops in coarctation.

A

Coarctation collaterals: anterior ICAs → posterior ICAs → Ao; superior epigastric artery → inferior epigastric artery → external iliac artery

150
Q

What causes rib notching?

A

Rib notching from enlarged ICAs

151
Q

Acute rheumatic fever only occurs after what?

A

Acute RF: only after group A streptococcal pharyngitis

151
Q

Describe the pathogenesis of RF.

A

Type II HSR (most common); cell-mediated immunity type IV HSR
M protein antibodies cross-react with human tissue (mimicry)

152
Q

What is the most common initial presentation of RF?

A

Migratory polyarthritis MC initial presentation

153
Q

What types of carditis may be present in acute RF?

A

Carditis: pericarditis, myocarditis, endocarditis (valves)

154
Q

What is the most common cause of death in acute RF?

A

Myocarditis MCC death in acute RF

155
Q

Describe the characteristics of endocarditis in RF.

A

Endocarditis: MV most often involved, followed by AV; sterile vegetations

156
Q

How does valvular disease differ between acute RF and chronic RF?

A

MV regurgitation in acute RF; MV stenosis in chronic RF

157
Q

The subcutaneous nodules in RF are comparable to those in what disease?

A

Subcutaneous nodules similar to rheumatoid arthritis nodules

158
Q

Describe the physical exam findings in erythema marginatum.

A

Erythema marginatum: circular or C-shaped areas of erythema around normal skin

159
Q

Describe the characteristics of Sydenham chorea in acute RF.

A

Sydenham chorea: late manifestation; reversible

160
Q

How is acute RF diagnosed?

A

Acute RF: diagnose with revised Jones criteria

161
Q

What are the major criteria of the revised Jones criteria?

A

Acute RF: carditis, arthritis, chorea, erythema marginatum, subcutaneous nodules

162
Q

What are the lab findings and ECG finding of acute RF?

A

Acute RF: carditis, arthritis, chorea, erythema marginatum, subcutaneous nodules

163
Q

What is the most common cause of MV stenosis?

A

MV stenosis: MCC is recurrent RF

164
Q

What are the effects on the LA caused by MV stenosis?

A

MV stenosis: LA dilated/hypertrophied

165
Q

What are the pulmonary clinical findings in MV stenosis?

A

Dyspnea; rust-colored sputum from pulmonary congestion

Pulmonary venous hypertension → RVH → RHF

166
Q

What are the cardiovascular clinical findings in MV stenosis?

A

Atrial fibrillation: common in MV stenosis; danger thrombus formation/embolization
MV stenosis: opening snap followed by an early to middiastolic rumble

167
Q

What are the gastrointestinal clinical findings in MV stenosis?

A

Dysphagia for solids from LA dilation

168
Q

What is MV regurgitation?

A

MV regurgitation: retrograde blood flow into LA during systole

169
Q

What is the most common cause of mitral valve regurgitation?

A

MVP: MCC of MV regurgitation

170
Q

What is the effect of MV regurgitation on cardiac output and the LA?

A

MV regurgitation: ↓cardiac output; LA dilated/hypertrophied

171
Q

What is the effect of MV regurgitation on the pulmonary vein, right ventricle, and right side of the heart?

A

Pulmonary venous hypertension → RVH → RHF

172
Q

How do the stroke volume and cardiac output change in chronic compensated mitral regurgitation?

A

Normalization of stroke volume/cardiac output in chronic compensated mitral regurgitation

173
Q

What is the effect of MV regurgitation on the left ventricle?

A

Eccentric LVH due to ↑LV volume

174
Q

What are the clinical findings of MV regurgitation?

A

Pansystolic murmur; S3/S4; no ↑intensity with deep held inspiration

175
Q

MVP is associated with what syndromes?

A

MVP: association with Marfan, Ehlers-Danlos, Klinefelter syndromes

176
Q

Describe the pathophysiology of MVP.

A

Bulging anterior and/or posterior leaflets into LA during systole
MVP: myxomatous degeneration; excess dermatan sulfate in MV

177
Q

What are the clinical findings of MVP?

A

MVP: systolic click followed by murmur; most patients are asymptomatic

178
Q

What does preload alter in MVP?

A

Preload alters click and murmur relationship to S1/S2

179
Q

What is the effect of decreasing preload on MVP? List three causes of decreased preload.

A

↓Preload (anxiety, standing, Valsalva) click/murmur closer to S1

180
Q

What is the effect of increasing preload on MVP? List three causes of increased preload.

A

↑Preload (reclining, squatting, sustained hand grip) click/murmur closer to S2

181
Q

What is the treatment for symptomatic MVP?

A

Symptomatic MVP: β-blockers

182
Q

What is the most common valve lesion in Western countries?

A

AV stenosis is MC valve lesion in Western countries

183
Q

What is the most common cause of stenosis in patients >60 years old?

A

Calcific AV stenosis: MCC of stenosis in patients >60 years old

184
Q

What is a major cause of stenosis <30 years old?

A

Congenital AV stenosis major cause of stenosis <30 years old

185
Q

How does obstruction to LV outflow tract in AV stenosis affect the left ventricle?

A

Obstruction to LV outflow tract → concentric LVH

186
Q

Describe the physical exam findings of AV stenosis.

A

Harsh systolic ejection murmur with radiation into neck; S4 heart sound

187
Q

What changes the murmur intensity in AV stenosis?

A

Changing preload changes murmur intensity

188
Q

How does the murmur intensity of AV stenosis change with preload?

A

↓Murmur intensity with ↓preload; ↑murmur intensity with ↑preload

189
Q

What is the most common valvular lesion causing syncope/angina with exercise?

A

MC valvular lesion causing syncope/angina with exercise

AV stenosis

190
Q

What is the most common cause of microangiopathic hemolytic anemia with schistocytes and hemoglobinuria?

A

MCC microangiopathic hemolytic anemia with schistocytes and hemoglobinuria
AV stenosis

191
Q

What is the most common cause of AV regurgitation?

A

Isolated AV root dilation MCC AV regurgitation

192
Q

What are the other causes of AV regurgitation?

A

Chronic RF, syphilitic aortitis, infective endocarditis, aortic dissection, coarctation

193
Q

How are LVEDP, SBP, pulse pressure and cardiac output affected in acute AV regurgitation?

A

Acute AV regurgitation: ↑LVEDP, ↓SBP, normal/↓pulse pressure, ↓cardiac output

194
Q

How are LVEDP, SBP, DBP, pulse pressure and cardiac output affected in chronic AV regurgitation?

A

Chronic AV regurgitation: normal LVEDP, ↑SBP, ↓DBP, ↑pulse pressure, normal cardiac output

195
Q

How does AV regurgitation affect the left ventricle?

A

AV regurgitation: eccentric LVH

196
Q

What are the clinical findings of AV regurgitation?

A

Early diastolic murmur; S3, S4; no ↑intensity with inspiration
Wide pulse pressure → bounding pulses, head nodding, pulsating nail bed
Austin Flint murmur: sign for AV replacement

197
Q

What is the most common cause of TV regurgitation in adults?

A

TV regurgitation: functional (stretching of ring), MCC in adults
RHF

198
Q

What is the most common cause of TV regurgitation in adolescents/young adults?

A

Adolescents/young adults: CHD MCC

199
Q

What is the most common cause of TV regurgitation in IVDA?

A

IVDA: infective endocarditis of valve MCC

200
Q

Describe the pathophysiology of TV regurgitation.

A

Retrograde blood flow into RA during systole

RA dilatation/hypertrophy; eccentric RVH; ↑pressure in venous system

201
Q

What are the clinical findings of TV regurgitation?

A

Pulsating liver; ascites; ↑portal vein pressure

Giant c-v wave; pansystolic murmur + S3/S4 that ↑in intensity with deep held inspiration

202
Q

What is PV stenosis associated with?

A

PV stenosis: CHD, carcinoid heart disease

203
Q

What is the most common cause of PV regurgitation?

A

PV regurgitation: MCC stretching of ring from PH

204
Q

Describe the characteristics of carcinoid heart disease.

A

Must be liver metastasis to produce carcinoid heart disease; serotonin causes valve fibrosis
Carcinoid heart disease: PV stenosis, TV regurgitation

205
Q

IE is most frequent at what age?

A

IE most frequent at age 45–65 years

206
Q

What is the most common cause of IE?

A

Acute IE: Staphylococcus aureus MCC

207
Q

What is the most common cause of IVDA IE?

A

IVDA IE: Staphylococcus aureus MCC

208
Q

What is the most common cause of subacute IE?

A

Subacute endocarditis: viridans Streptococcus MCC

209
Q

What are the most common overall pathogens causing IE?

A

Viridans group of Streptococcus: overall MCC IE

210
Q

What is the most common cause of early IE associated with prosthetic heart valves?

A

Prosthetic valve IE early: Staphylococcus epidermidis (coagulase negative) MCC

211
Q

What are the causes of late IE associated with prosthetic heart valves?

A

Prosthetic valve IE late: Staphylococcus aureus, enterococci, group D streptococci

212
Q

What is the most common cause of nosocomial IE in patients with intravenous catheters?

A

Nosocomial IE intravenous catheters: Staphylococcus aureus MCC

213
Q

What is the most common cause of nosocomial IE in patients with indwelling urinary catheters?

A

Nosocomial IE indwelling urinary catheters: enterococci MCC

214
Q

What is the cause of IE associated with ulcerative bowel lesions?

A

IE associated with ulcerative bowel lesions: Streptococcus bovis

215
Q

What is the most common valve involved in IE?

A

MC valve involved in IE: MV

216
Q

What are the valvular lesions in IVDA IE?

A

IVDA IE: TV regurgitation/AV regurgitation

217
Q

What do the viridans group of streptococci infect in IE?

A

Viridans group of streptococci infect previously damaged valves

218
Q

What does Staphylococcus aureus infect in IE?

A

Staphylococcus aureus infects normal or damaged valves

219
Q

What type of murmurs are the most common in IE?

A

Regurgitant murmurs MC in IE

220
Q

What is the most consistent sign in IE?

A

Fever is most consistent sign in IE

221
Q

What are the immunocomplex signs in IE?

A

Immunocomplex signs: glomerulonephritis (nephritic), Roth spot in eyes

222
Q

What are the microembolization signs in IE?

A

Microembolization signs: splinter hemorrhages, Janeway lesions (painless), Osler nodes (painful), infarctions

223
Q

What are the other clinical findings in IE?

A

Changing heart murmurs, splenomegaly (only subacute)

224
Q

What are the lab findings in IE?

A

Positive blood culture majority of cases

225
Q

Describe the characteristics of Libman-Sacks endocarditis.

A

Libman-Sacks endocarditis: associated with SLE; MV regurgitation

226
Q

Describe the characteristics of NBTE.

A

NBTE: sterile vegetations MV; paraneoplastic syndrome; mucin-producing tumors

227
Q

Myocarditis is a major cause of sudden death in what age group worldwide?

A

Major cause sudden death in adults <40 years old

228
Q

What is the most common cause of acute myocarditis in the U.S.?

A

Viruses: MCC acute myocarditis U.S.

229
Q

What is the most common cause of myocarditis leading to CHF in Central/South America?

A

Chagas disease: MCC myocarditis leading to CHF in Central/South America

230
Q

What type of RF is an etiology of myocarditis?

A

Myocarditis in acute RF

231
Q

Which toxins are etiologies of myocarditis?

A

Toxins: diphtheria, carbon monoxide, black widow and scorpion venoms

232
Q

Which drugs are etiologies of myocarditis?

A

Drugs: doxorubicin, daunorubicin, cocaine, alcohol

233
Q

Which systemic and collagen vascular diseases are etiologies of myocarditis?

A

SLE, systemic sclerosis, Kawasaki disease, radiation, sarcoidosis

234
Q

Describe the pathology of myocarditis.

A

Myocarditis: global enlargement of heart; dilation of all chambers

235
Q

What are the clinical findings of myocarditis?

A

Myocarditis: fever, dyspnea, chest pain
Myocarditis: arrhythmias, pericarditis, biventricular CHF, MV regurgitation

236
Q

What are the lab findings in myocarditis?

A

Myocarditis: ↑CK-MB, troponin I/T

237
Q

Describe the etiology of most cases of pericarditis.

A

Pericarditis: most cases are idiopathic

238
Q

What are the clinical findings in pericarditis?

A

Precordial friction rub; pain relieved by leaning forward; worse when leaning back

239
Q

A young woman with pericarditis and effusion most likely has what?

A

Young woman with pericarditis and effusion most likely has SLE

240
Q

What is the physical exam findings of a pericardial effusion? How is the cardiac output affected?

A

Effusion: muffled heart sounds
Effusion: ↓cardiac output; neck vein distention with inspiration
Effusion: hypotension with pulsus paradoxus on inspiration

241
Q

What is the pericardial effusion triad?

A

Effusion triad: muffled heart sounds, neck distention on inspiration, pulsus paradoxus on inspiration

242
Q

What are the chest x-ray findings of pericardial effusion?

A

Effusion: chest X-ray shows water bottle configuration of heart silhouette

243
Q

What is the most common cause of constrictive pericarditis worldwide?

A

Constrictive pericarditis: TB MCC worldwide

244
Q

Most cases of constrictive pericarditis are due to what in the U.S.?

A

Constrictive pericarditis U.S.: idiopathic or post open heart surgery

245
Q

Describe the pathophysiology of constrictive pericarditis.

A

Constrictive pericarditis: incomplete filling of chambers; pericardial knock

246
Q

What are the findings of constrictive pericarditis on chest x-ray?

A

Constrictive pericarditis: calcification pericardium on x-ray

247
Q

What are the types of cardiomyopathy?

A

Cardiomyopathies: dilated, hypertrophic, restrictive

247
Q

What is the most common cardiomyopathy in young people?

A

Dilated: MC cardiomyopathy

247
Q

What is the most common known cause of dilated cardiomyopathy?

A

Dilated: myocarditis MC known cause

247
Q

What are the other causes of cardiomyopathy?

A

Dilated: alcohol—direct toxic effect; thiamine deficiency (↓ATP)
Dilated: drugs—doxorubicin, daunorubicin, cocaine
Dilated: postpartum, organic solvents, acromegaly, myxedema heart

248
Q

Describe the pathophysiology of dilated cardiomyopathy.

A

Dilated: global enlargement of heart

249
Q

What are the clinical findings in dilated cardiomyopathy?

A

Dilated: signs/symptoms biventricular failure
Dilated: narrow pulse pressure; arrhythmias

250
Q

How is dilated cardiomyopathy diagnosed?

A

Dilated: echocardiography—EF <40%

251
Q

What is the most common cause of sudden death in young athletes?

A

HCM: MCC sudden death in young athletes

252
Q

What is the most common type of HCM? Describe its characteristics.

A

Familial type HCM: AD with complete penetrance; MC type

253
Q

Who is affected by the sporadic type of HCM?

A

Sporadic type HCM: elderly population

254
Q

Describe the pathophysiology of HCM.

A

HCM: obstruction outflow tract below AV
HCM: aberrant myofibers in conduction system cause fatal arrhythmia, sudden death
HCM: noncompliant LV—diastolic dysfunction

255
Q

What are the clinical findings in HCM?

A

HCM: palpable double apical impulse

256
Q

How do preload changes in HCM compare to preload changes in AV stenosis?

A

HCM: preload changes are opposite those for AV stenosis

257
Q

What are the clinical findings when exercising in HCM? These findings also occur in what condition?

A

HCM: angina/syncope with exercise similar to AV stenosis

258
Q

What is the cause of sudden death in HCM?

A

HCM: sudden death due to ventricular tachycardia/fibrillation

259
Q

What is the treatment for HCM?

A

HCM: treat with β-blockers

260
Q

Which is the least common cardiomyopathy?

A

Restrictive: least common cardiomyopathy

261
Q

What is the most common cause of restrictive cardiomyopathy?

A

Restrictive: amyloidosis MCC

262
Q

Describe the pathophysiology of restrictive cardiomyopathy.

A

Restrictive: ↓ventricular compliance; biventricular heart failure

263
Q

What are the ECG findings of restrictive cardiomyopathy?

A

Restrictive: characteristic low voltage ECG

264
Q

Describe the epidemiology of heart tumors.

A

Heart tumors: metastasis > primary tumors

264
Q

Where is the most common site for metastasis in the heart?

A

Pericardium MC site for metastasis

264
Q

What is the most common adult primary tumor of the heart? Where in the heart is its most common site?

A

Cardiac myxoma: MC adult primary tumor; MC in LA

265
Q

What are the complications of cardiac myxoma?

A

Myxoma: embolization; syncopal episodes

266
Q

Describe the characteristics of rhabdomyomas.

A

Rhabdomyomas: associated with tuberous sclerosis in children; hamartoma

Rapid Review Pathology (14 decks)

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