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Cardio-boards Flashcards

1
Q

A Anitschkow cell is hallmark for?

A

Acute Rheumatic Fever

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2
Q

What are the Diagnosis Major criteria for Acute Rheumatic Fever?

A

JONES; J = joints O= heart, N= subQ nodules, E= Erythema marginatum, S= Sydenham chorea

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3
Q

What is the key clinical problem with acute rheumatic fever?

A

Heart problems (pancarditis- each of the heart layers are inflamed)

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4
Q

What is molecular mimicry in reference to Acute rheumatic fever?

A

The way in which the M protein (VF in rheumatic fever), resembles a human tissue

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5
Q

What is Infantile coarctation of the aorta associated with?

A

Turner’s Syndrome and a PDA

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6
Q

How will someone with adult coarctation of the aorta present clinically?

A

They will present with HTN in the UE and hypotension in the LE. Also on X-ray you will see “RIB NOTCHING” due to engorged intercostal vessels receiving excess blood.

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7
Q

What is Tricuspid atresia associated with?

A

ASD

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8
Q

What is Truncus arteriosus?

A

Where there is a large vessel arising from both ventricles (there is not separate aortic or pulmonic artery)

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9
Q

How do you maintain a PDA until you can surgically repair it?

A

PGE (alprostadil, etc.)

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10
Q

What is transposition of the great vessels?

A

where the pulmonary artery arises from the L. ventricle, and the aorta arises from the R. ventricle

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11
Q

What is associated with transposition of the great vessels?

A

Maternal diabetes

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12
Q

How do you close a PDA?

A

Indomethacin

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13
Q

What is Patent Ductus Arteriosus associated with?

A

Congenital Rubella

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14
Q

How will the heart sound in someone with a PDA?

A

continuous “machine-like” murmur

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15
Q

What is tetralogy of Fallot?

A

PROV; P= pulmonary artery stenosis, R= Right ventricular hypertrophy, O= overriding aorta, V= VSD

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16
Q

How do patients with a Tetralogy of Fallot present?

A

Early cyanosis (due to a R–> L shunt), the patient learns to squat in response to the cyanotic spell

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17
Q

How will you be able to tell on X-ray that someone has a Tetralogy of Fallot?

A

It will appear “Boot-shaped” on x-ray

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18
Q

What is the most common ASD?

A

Ostium secundum

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19
Q

What is associated with a Ostium primum ASD?

A

Down syndrome

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20
Q

What is a paradoxical emboli?

A

Where the embolus forms on the R. side of the heart and due to a ASD can cross and lodge on the L. side of the heart

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21
Q

What is the most common congenital heart defect?

A

VSD

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22
Q

What is associated with a VSD?

A

Fetal Alcohol syndrome

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23
Q

How do you treat a VSD?

A

Small defects may close spontaneously, Large defects need surgery

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24
Q

What is Eisenmenger syndrome?

A

This is where you have a VSD which causes a Left to Right shunt. This in turn increases the blood flow to the lungs resulting in pulmonary HTN. This pulmonary HTN will then result in a Right to Left shunt and you get deoxygenated blood mixing with oxygenated blood and being sent out to the body resulting in cyanosis.

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25
Q

What is the most common cause of Right sided heart failure?

A

Left sided heart failure

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26
Q

What are some clinical features of Right sided heart failure?

A

JVD, “nutmeg” liver, dependent pitting edema

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27
Q

What is the main way to treat Left sided heart failure?

A

ACE inhibitor

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28
Q

Where do you see “heart failure” cells (hemosiderin laden macrophages)

A

Left-sided heart failure

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29
Q

What is Dressler syndrome?

A

where you get autoimmune antibodies against the pericardium. This occurs 6-8 weeks post MI and results in pericarditis.

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30
Q

What is the Gold standard cardiac enzyme for MI?

A

Troponin I

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31
Q

What is CK-MB useful for as a cardiac enzyme?

A

Detects reinfarction (because it disappears in 72 hours while Troponin I stays for 7-10 days, it is possible to see if it is the same MI or a reinfarction)

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32
Q

Why can the patient appear worse hours after treatment for a MI?

A

Reperfusion injury (due to free radicals further damaging the myocytes) and Contraction band necrosis (damaged cells cause Ca+ influx and contraction)

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33
Q

How will the initial phase of the MI appear on the EKG?

A

ST segment depression (subendocardial necrosis–> hasn’t involved the whole wall yet)

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34
Q

How will the continued ischemia of an MI appear on the EKG?

A

ST segment elevation ( transmural necrosis–> involving the whole wall)

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35
Q

What will you see microscopically 4-24 hours post MI?

A

Coagulative necrosis (pyknosis, karrohlexis, karyolysis)

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36
Q

How will the heart appear 4-24 hours post MI?

A

Dark discoloration (complications can be arrhythmic)

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37
Q

How will the heart appear 1-3 days post MI?

What microscopic changes will be seen?

A
  • Yellow

- Neutrophils

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38
Q

What will the microscopic changes be 4-7 days post MI?

What will the heart look like?

A

Macrophages

Yellow

39
Q

What will the heart look like 1-3 weeks post MI?

What microscopic changes will be seen?

A

Red border emerging from the edge of infarct

Granulation tissue

40
Q

What will the heart look like months post MI?

What microscopic changes are occurring?

A

White scar

Fibrosis

41
Q

What is a possible complication of the white scar post MI?

A

Aneurysm, mural thrombus, dressler syndrome

42
Q

What is a possible complication of 4-7 days post MI with macrophages?

A

Rupture of the ventricular free wall, IV septum, or papillary muscle (papillary muscle rupture is associated with Right coronary artery infarction)

43
Q

What is the most commonly involved artery in MI?

A

LAD

44
Q

what is the 2nd most common artery involved in an MI?

A

RCA (right coronary artery)

45
Q

What is stable angina?

How will it appear on EKG?

A

Chest pain arising with exertion or emotional stress

ST segment depression

46
Q

How do you treat stable angina?

A

Rest or nitroglycerin

47
Q

How will stable angina present?

A

chest pain <20 minutes radiating to the left arm or jaw

48
Q

What is unstable angina?

A

Chest pain occurring at rest

49
Q

What causes unstable angina?

A

Rupture of the atherosclerotic plaque with thrombus (which occurs due to the collagen of the basement membrane being exposed). It is an INCOMPLETE occlusion of the coronary artery

50
Q

How will the EKG look when someone has unstable angina?

How do you treat it?

A

ST segment depression

Nitroglycerin

51
Q

What is prinzmetal angina

A

episodic chest pain unrelated to exertion (due to coronary artery vasospasm)

52
Q

How will the EKG look on someone with prinzmetal angina?

A

ST segment elevation

53
Q

How do you treat prinzmetal angina?

A

Nitroglycerin or CCB’s

54
Q

What is an MI?

A

Necrosis of cardiac myocytes (irreversible injury and cell death)

55
Q

What usually causes an MI?

A

rupture of atherosclerotic plaque with thrombis and COMPLETE occlusion of the coronary artery

56
Q

How will someone with an MI present?

A

severe crushing chest pain lasting >20 minutes hat radiates to the left arm or jaw

57
Q

What is chronic rheumatic heart disease?

A

scarring that arises as a consequence of repeated exposure to Group A strep

58
Q

How does the valve appear in someone with chronic rheumatic heart disease?

A

“fish mouth” appearance

59
Q

What is the valve that is almost always involved with chronic rheumatic heart disease?

A

Mitral valve (occasionally the aortic valve)

60
Q

How can you tell aortic stenosis by itself from chronic rheumatic heart disease?

A

Chronic rheumatic heart disease ALWAYS has mitral stenosis and can have aortic as well, whereas aortic stenosis by itself won’t have mitral stenosis

61
Q

What complication can arise from acute rheumatic disease ?

What complication can arise from chronic rheumatic disease?

A

Mitral regurgitation

Mitral stenosis

62
Q

What bug is the most common overall cause of endocarditis?

A

Strep Viridans

63
Q

What bug is the most common cause of endocarditis in IV drug users?

A

Staph Aureus

64
Q

What bug is associated with endocarditis of prosthetic valves?

A

Staph Epidermidis

65
Q

What Bug is associated with endocarditis in patients with underlying colorectal cancer?

A

Strep Bovis

66
Q

What bug(s) are associated with endocarditis and have a negative blood culture?

A

HACEK; H= haemophilus, A= actinobacillus, C= cardiobacterium, E= eiknella, K= kingella

sx’s= Osler nodes, Janeway lesions and splinter hemorrhages

67
Q

What is the difference in endocarditis caused by Strep Viridans vs Staph aureus?

A

Endocarditis with Strep Viridans= low-virulence organism that infects previously damaged valves (doesn’t destroy valves); Endocarditis with Staph Aureus= High-virulence organism that infects normal valves (tricuspid) (destroys the valve)

68
Q

What is Libman-Sacks endocarditis?

A

Endocarditis where you get sterile vegetations that arise in association with SLE (on both sides the surface and undersurface)

69
Q

What is the test to detect endocarditis lesions on the valves?

A

TEE (transesophageal echocardiogram)

70
Q

What is the most common form of cardiomyopathy?

A

Dilated Cardiomyopathy

71
Q

This cardiac tumor appears gelatinous and has abundant ground substance on histology

A

Myxoma

72
Q

What area of the heart does a myxoma affect?

A

It is a pedunculated mass in the LEFT ATRIUM and causes obstruction of the mitral valve

73
Q

What is the most common primary cardiac tumor in children?

A

Rhabdomyoma

74
Q

What is the most common primary cardiac tumor in adults

A

Myxoma

75
Q

What is associated with rhabdomyoma?

A

Tuberous sclerosis (it arises in the ventricles)

76
Q

This is more common than primary tumors in the heart?

A

Metastasis

77
Q

What tumors like to metastasize to the heart?

A

Breast, lung, melanoma, lymphoma

78
Q

What part of the heart is usually affected by metastasis?

A

pericardium

79
Q

What is the usual cause of Hypertrophic cardiomyopathy?

A

Genetic mutations in SARCOMERE PROTEINS

80
Q

This disease usually presents as sudden death in young athletes

A

Hypertrophic cardiomyopathy

81
Q

How will someone’s heart with hypertrophic cardiomyopathy look histologically?

A

Myofiber disarray

82
Q

What type of dysfunction will hypertrophic cardiomyopathy cause?

A

diastolic dysfunction (can’t fill the heart)

83
Q

What can cause dilated cardiomyopathy?

A

genetic (AD), coxsackie A or B, Alcohol abuse, doxorubicin & cocaine, pregnancy, hemochromatosis

84
Q

What is restrictive cardiomyopathy?

A

Decreased compliance of ventricular endomyocardium

85
Q

What is restrictive cardiomyopathy in kids called?

A

endomyocardial fibrosis

86
Q

backflow of blood from aorta into L. ventricle during diastole

A

aortic regurgitation

87
Q

What is the most common cause of aortic regurgitation?

A

Isolated root dilation

88
Q

Clinical features of aortic regurgitation

A

Wide pulse pressure (systolic increases, diastolic decreases), water hammer pulse, Austin flint characteristic, head bobbing, pulsating nail bed

89
Q

what is mitral valve prolapse?

A

ballooning of mitral valve into left atrium during systole

90
Q

what type of pts can you see mitral valve prolapse with?

A

Ehlers-danlos and Marfans

91
Q

Mid systolic click followed by regurgitation murmur (becomes softer with squatting)

A

Mitral valve prolapse

92
Q

Holosystolic “blowing murmur” (louder with squatting and expiration)

A

Mitral regurgitation

93
Q

Acute rheumatic heart disease can cause

A

Mitral regurgitation

94
Q

Volume overload resulting in dilation of the L. atrium (usually due to chronic rheumatic heart disease)

A

Mitral stenosis

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