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Cardio > Cardio Path > Flashcards

Cardio Path Flashcards

1
Q

Most common sites for cardiac atherosclerotic disease

A

LAD > RCA > LCX > LCA

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2
Q

Leading cause of death in the US

A

Coronary artery disease (ischemic heart disease)

Most commonly caused by atherosclerosis (>90%)

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3
Q

Coronary artery disease risk factors

A 
Age, 
male, 
HTN, 
hyperlipidemia (especially LDL), 
smoking, 
diabetes
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4
Q

Crushing, substernal chest pain (crushing/stabbing/squeezing)
Radiates to neck, shoulder or jaw
Rapid, weak pulse
Profuse sweating (diaphoresis)

A

Clinical features of MI

*may also present with dyspnea, N/V, or be asymptomatic

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5
Q

Key events in ischemic cardiac myocytes

A

Hypoxia leads to ATP depletion

Loss of contractility occurs within 2 minutes

Irriversible cell injury occurs within 20-40 minutes

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6
Q

Most sensitive and specific cardiac biomarkers

A

Troponin T and I

cTnT and cTnI

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7
Q

Biomarker that is sensitive but not specific for cardiac myocyte injury

A

Creatine Kinase MB (CK-MB)

sensitive so negative CK-MB is likely a true negative for MI

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8
Q

CK-MB and cTnT, cTnI time to peak

A

3-12 hours

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9
Q

CK-MB normalizes after how long?

A

2-3 days (48-72 hours)

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10
Q

Troponins (cTnT and cTnI) normalize after how long?

A

> 5 days (about a week)

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11
Q

Occlusion of the LAD leads to infarct of which region(s) of the heart?

A

LAD occlusion => apex and anterior LV wall infarct

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12
Q

Occlusion of the LCX leads to infarct of which region(s) of the heart?

A

LCX occlusion => lateral LV wall

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13
Q

Occlusion of the RCA leads to infarct of which region(s) of the heart?

A

RCA occlusion => RV free wall, posterior 1/3 of septum and posterior LV wall (if right dominant)

RCA divides into PDA most commonly (right dominant heart)

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14
Q

Subendocardial infarct can occur after (2)

A
  1. Reperfusion of a transmural infarct (will be in same region as initial infarct)
  2. Global hypotension (diffuse subendocardial infarct)
    * subendocardium is furthest from blood supply, dies first, reperfusion saves more superficial myocytes, hypotension diffusely starves subendocardium
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15
Q

Gross morphologic changes in MI

0.5 - 4 hours
4 - 12 hours
12 -24 hours
1 - 3 days*
3 - 7 days
7 - 10 days
10 - 14 days
2 - 8 weeks
> 2 months
A 
0.5 - 4 hours = none
4 - 12 hours = Dark mottling
12 -24 hours = Dark mottling
1 - 3 days = yellow coloration*
3 - 7 days = hyperemic border with yellowing
7 - 10 days = depressed red margins, maximally yellow and soft
10 - 14 days = depressed red margins
2 - 8 weeks = gray/white scar
> 2 months = complete scarring
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16
Q

Gross morphologic changes in MI

0.5 - 4 hours
4 - 12 hours
12 -24 hours
1 - 3 days
3 - 7 days*
7 - 10 days
10 - 14 days
2 - 8 weeks
> 2 months
A 
0.5 - 4 hours = none
4 - 12 hours = Dark mottling
12 -24 hours = Dark mottling
1 - 3 days = yellow coloration
3 - 7 days = hyperemic border with yellowing*
7 - 10 days = depressed red margins, maximally yellow and soft
10 - 14 days = depressed red margins
2 - 8 weeks = gray/white scar
> 2 months = complete scarring
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17
Q

Gross morphologic changes in MI

0.5 - 4 hours
4 - 12 hours
12 -24 hours
1 - 3 days
3 - 7 days
7 - 10 days*
10 - 14 days
2 - 8 weeks
> 2 months
A 
0.5 - 4 hours = none
4 - 12 hours = Dark mottling
12 -24 hours = Dark mottling
1 - 3 days = yellow coloration
3 - 7 days = hyperemic border with yellowing
7 - 10 days = depressed red margins, maximally yellow and soft*
10 - 14 days = depressed red margins
2 - 8 weeks = gray/white scar
> 2 months = complete scarring
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18
Q

Gross morphologic changes in MI

0.5 - 4 hours
4 - 12 hours
12 -24 hours
1 - 3 days
3 - 7 days
7 - 10 days
10 - 14 days*
2 - 8 weeks
> 2 months
A 
0.5 - 4 hours = none
4 - 12 hours = Dark mottling
12 -24 hours = Dark mottling
1 - 3 days = yellow coloration
3 - 7 days = hyperemic border with yellowing
7 - 10 days = depressed red margins, maximally yellow and soft
10 - 14 days = depressed red margins*
2 - 8 weeks = gray/white scar
> 2 months = complete scarring
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19
Q

Microscopic morphologic changes in MI

0.5 - 4 hours*
4 - 12 hours
12 -24 hours
1 - 3 days
3 - 7 days
7 - 10 days
10 - 14 days
2 - 8 weeks
> 2 months
A

0.5 - 4 hours = waviness of fibers at border*
4 - 12 hours = coagulation necrosis and edema
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis
1 - 3 days = neutrophilic infiltrate
3 - 7 days = macrophages
7 - 10 days = granulation tissue
10 - 14 days = collagen deposition
2 - 8 weeks = increased collagen deposition
> 2 months = dense collagenous scar

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20
Q

Microscopic morphologic changes in MI

0.5 - 4 hours
4 - 12 hours*
12 -24 hours
1 - 3 days
3 - 7 days
7 - 10 days
10 - 14 days
2 - 8 weeks
> 2 months
A

0.5 - 4 hours = waviness of fibers at border
4 - 12 hours = coagulation necrosis and edema*
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis
1 - 3 days = neutrophilic infiltrate
3 - 7 days = macrophages
7 - 10 days = granulation tissue
10 - 14 days = collagen deposition
2 - 8 weeks = increased collagen deposition
> 2 months = dense collagenous scar

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21
Q

Microscopic morphologic changes in MI

0.5 - 4 hours
4 - 12 hours
12 -24 hours*
1 - 3 days
3 - 7 days
7 - 10 days
10 - 14 days
2 - 8 weeks
> 2 months
A

0.5 - 4 hours = waviness of fibers at border
4 - 12 hours = coagulation necrosis and edema
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis*
1 - 3 days = neutrophilic infiltrate
3 - 7 days = macrophages
7 - 10 days = granulation tissue
10 - 14 days = collagen deposition
2 - 8 weeks = increased collagen deposition
> 2 months = dense collagenous scar

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22
Q

Microscopic morphologic changes in MI

0.5 - 4 hours
4 - 12 hours
12 -24 hours
1 - 3 days*
3 - 7 days
7 - 10 days
10 - 14 days
2 - 8 weeks
> 2 months
A

0.5 - 4 hours = waviness of fibers at border
4 - 12 hours = coagulation necrosis and edema
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis
1 - 3 days = neutrophilic infiltrate*
3 - 7 days = macrophages
7 - 10 days = granulation tissue
10 - 14 days = collagen deposition
2 - 8 weeks = increased collagen deposition
> 2 months = dense collagenous scar

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23
Q

Microscopic morphologic changes in MI

0.5 - 4 hours
4 - 12 hours
12 -24 hours
1 - 3 days
3 - 7 days*
7 - 10 days
10 - 14 days
2 - 8 weeks
> 2 months
A

0.5 - 4 hours = waviness of fibers at border
4 - 12 hours = coagulation necrosis and edema
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis
1 - 3 days = neutrophilic infiltrate
3 - 7 days = macrophages*
7 - 10 days = granulation tissue
10 - 14 days = collagen deposition
2 - 8 weeks = increased collagen deposition
> 2 months = dense collagenous scar

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24
Q

Microscopic morphologic changes in MI

0.5 - 4 hours
4 - 12 hours
12 -24 hours
1 - 3 days
3 - 7 days
7 - 10 days*
10 - 14 days
2 - 8 weeks
> 2 months
A

0.5 - 4 hours = waviness of fibers at border
4 - 12 hours = coagulation necrosis and edema
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis
1 - 3 days = neutrophilic infiltrate
3 - 7 days = macrophages
7 - 10 days = granulation tissue*
10 - 14 days = collagen deposition
2 - 8 weeks = increased collagen deposition
> 2 months = dense collagenous scar

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25
Q

Microscopic morphologic changes in MI

0.5 - 4 hours
4 - 12 hours
12 -24 hours
1 - 3 days
3 - 7 days
7 - 10 days
10 - 14 days*
2 - 8 weeks
> 2 months
A

0.5 - 4 hours = waviness of fibers at border
4 - 12 hours = coagulation necrosis and edema
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis
1 - 3 days = neutrophilic infiltrate
3 - 7 days = macrophages
7 - 10 days = granulation tissue
10 - 14 days = collagen deposition*
2 - 8 weeks = increased collagen deposition
> 2 months = dense collagenous scar

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26
Q

Microscopic morphologic changes in MI

0.5 - 4 hours
4 - 12 hours
12 -24 hours
1 - 3 days
3 - 7 days
7 - 10 days
10 - 14 days
2 - 8 weeks*
> 2 months
A

0.5 - 4 hours = waviness of fibers at border
4 - 12 hours = coagulation necrosis and edema
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis
1 - 3 days = neutrophilic infiltrate
3 - 7 days = macrophages
7 - 10 days = granulation tissue
10 - 14 days = collagen deposition
2 - 8 weeks = increased collagen deposition*
> 2 months = dense collagenous scar

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27
Q

Microscopic morphologic changes in MI

0.5 - 4 hours
4 - 12 hours
12 -24 hours
1 - 3 days
3 - 7 days
7 - 10 days
10 - 14 days
2 - 8 weeks
> 2 months*
A

0.5 - 4 hours = waviness of fibers at border
4 - 12 hours = coagulation necrosis and edema
12 -24 hours = coagulation necrosis, pyknosis, eosinophilia, contraction band necrosis
1 - 3 days = neutrophilic infiltrate
3 - 7 days = macrophages
7 - 10 days = granulation tissue
10 - 14 days = collagen deposition
2 - 8 weeks = increased collagen deposition
> 2 months = dense collagenous scar*

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28
Q

General gross morphologic progression of MI

A
  • dark mottling during the first day
  • yellowing of infarct over the first few days
  • hyperemic border develops over 1 week - 10 days
  • scarring from 2 weeks onward
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29
Q

General microscopic progression of MI

A
  • waviness of fibers in the first 4 hours
  • coagulative necrosis over the first few days w/ neutrophils
  • macrophages after neutrophils up until 1 week
  • granulation tissue at 7-10 days
  • collagen deposition over the next several weeks
  • dense collagenous scar after 2 months
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30
Q

Early (within 24 hours) MI complications (2)

A

Arrhythmia: #1 cause of death, can occur within 1 hour

Contractile dysfunction: can lead to cardiogenic shock

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31
Q

Intermediate (within 2-4 days) MI complications (2)

A

Myocardial rupture: septal, free wall, papillary

Acute pericarditis: fibrinous or serofibrinous (tamponade)

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32
Q

Late (after 2 weeks) MI complications (3)

A

Dressler syndrome: febrile, autoimmune fibrinous pericarditis

Ventricular aneurysm: thin walled scar leads to dilation (remodeling can also cause arrhythmia)

Risk of CHF and life threatening arrhythmia

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33
Q

Angina induced by activity, stress

A

Stable angina

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34
Q

Episodic angina unrelated to physical activity, HR, or BP

A

Prinzmetal angina

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35
Q

Angina present at rest with a “cresendo” pattern (increasing in severity and duration)

A

Unstable angina

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36
Q

ECG and troponins in stable angina

A

Normal ECG and Troponins

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37
Q

ECG and troponins in unstable angina

A

ECG: Normal, inverted T-waves or ST depression

Troponins: Normal

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38
Q

ECG and troponins in NSTEMI

A

ECG: Normal, inverted T-waves or ST depression

Troponins: Elevated

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39
Q

ECG and troponins in STEMI

A

ECG: ST elevation

Troponins: Elevated

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40
Q

How long before troponins become elevated?

A

Approximately 3 hours

*important! STEMI presentation (ECG changes, chest pain and radiations etc.) for less than 3 hours should be assumed to be a transmural acute MI!!!

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41
Q

Blunt force to the heart in a MVA can cause

A

Cardiac contusion

If full thickness can cause rupture and blood filling into the pericardial space, causing cardiac tamponade

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42
Q

Most common aortic injury due to rapid deceleration in a MVA

A

Tearing of the aorta at the ligamentum arteriosum

*rapid deceleration can rip the ligamentum arteriosum from the aorta, causing massive hemorrhage

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43
Q

Most common cause of arrhythmia

A

Ischemic heart disease

*Almost any structural alteration to the heart can cause arrhythmia. others include cardiomyopathies, amyloidosis, sarcoidosis, myocarditis (autoimmune or infectious), congenital heart disease

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44
Q

Arrhythmia due to a damaged SA node, presents as bradycardia

A

Sick sinus syndrome

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45
Q

Arrhythmia due to independent and sporadic myocyte depolarization with variable AV node transmission, leading to an irregularly irregular HR

A

Atrial fibrillation

*can cause thrombus formation and thromboembolism

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46
Q

Arrhythmia due to dysfunctional AV node: prolonged PR interval

A

First degree heart block

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47
Q

Arrhythmia due to dysfunctional AV node: dropped beats (no QRS following some P waves)

A

Second degree heart block

  • Type 1: progressive PR lengthening leading to eventual dropped QRS
  • Type 2: Dropped QRS with normal PR
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48
Q

Arrhythmia due to dysfunctional AV node: P waves and QRS complexes are completely out of synch; independent beating of artia and ventricles

A

Third degree heart block

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49
Q

Hereditary channelopathy (Na or K channel dysfunction) that causes problems conducting electrical impulses throughout the heart

A

Long QT syndrome

*may progress to Torsades de Pointes

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50
Q

Most common cause of ischemia induced arrhythmia that leads to death

A

Coronary artery disease

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51
Q

Pressure overload on the heart (HTN, aortic stenosis) leads to

A

Hypertrophic cardiomyopathy

*cardiac myocytes grow in size in response to the need to increase contractile strength, the heart is now able to pump with more force but less volume

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52
Q

Pathologic vs Physiologic hypertrophic cardiomyopathy

A

Physiologic hypertrophic cardiomyopathy (due to exercise) leads to increased capillaries supplying the heart

Pathologic hypertrophic cardiomyopathy does not, leads to ischemia in severe cases

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53
Q

Volume overload on the heart leads to

A

Dilated cardiomyopathy

*increased volume stretches the chambers, decreasing the ability to pump blood

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54
Q

The inability of the heart to pump blood to meet the body’s demand for oxygen

A

Congestive heart failure

55
Q

CHF can result from diastolic dysfunction, which is

A

an inability to fill the ventricles during diatole

56
Q

CHF can result from systolic dysfunction, which is

A

an inability to sufficiently contract the ventricles during systole

57
Q

Systolic left sided heart failure causes (4)

A
  • Ischemic heart disease
  • HTN
  • Aortic stenosis
  • Dilated cardiomyopathy
58
Q

Systolic left sided heart failure leads to

A

decreased ejection fraction

59
Q

Diastolic left sided heart failure causes (4)

A
  • HTN
  • Aortic stenosis
  • Hypertrophic cardiomyopathy
  • Restrictive cardiomyopathy
60
Q

Diastolic left sided heart failure leads to

A

normal ejection fraction but lower volume output due to less filling

61
Q

Right sided heart failure causes (2)

A
  • Left sided heart failure (most common)

- Cor pulmonale (lung dysfunction)

62
Q

Diagnosis?

Paroxsymal nocturnal dyspnea
Pulmonary congestion (cough, crackles, wheezes, tachypnea)
Orthopnea
Tachycardia
Exertional dyspnea
Cyanosis
Kerley B lines on CXR (interstitial pulm edema)

A

Left heart failure

*inability of the LV to pump leads to pulmonary edema/congestion, decreased tissue perfusion (including brain and kidneys)

63
Q

Diagnosis?

Exertional dyspnea
Ascites
Hepatomegaly
Splenomegaly
Jugular venous distension
A

Right heart failure

*inability of the RV to pump causes the blood/fluid to back up into the venous system

64
Q

Chronic, slowly accumulating pericardial effusion
Typically asymptomatic
Appears as enlarged heart on CXR

A

Serous effusion

*from CHF

65
Q

Acute (<1 week) rapidly accumulating pericardial effusion
Symptomatic (hypotension, death)
Cardiac tamponade

A

Hemopericardium

*from trauma, ruptured MI, aortic dissection

66
Q

Clinical signs of what diagnosis?

Pleuritic chest pain (worsens with breathing)
Position dependent chest pain
Pericardial friction rub on auscultation

A

Pericarditis

67
Q

Fibrinous/ serofibrinous pericarditis causes (3)

  • increased fibrin = fibrinous
  • increased fibrin and fluid = serofibrinous
A
  • Acute MI (inflammation post-MI)
  • Dresslers syndrome (autoimmune 1-3d post MI)
  • Uremia (CKD pt who presents w/ pericarditis)
68
Q

Pericarditis caused by viral or noninfectious inflammatory diseases

A

Serous pericarditis

69
Q

Pericarditis caused by active microbial infection

A

Purulent/suppurative pericarditis

70
Q

Pericarditis caused by Tuberculosis, sometimes fungal

A

Caseous pericarditis

71
Q

Pericarditis caused by the spread of a malignant neoplasm or trauma

A

Hemorrhagic pericarditis

72
Q

Pericarditis where the heart is encased in a dense fibrous scar that limits diastolic expansion; mimics restrictive cardiomyopathy

A

Constrictive pericarditis

73
Q

Most common primary cardiac tumor in adults (benign)
Mesenchymal origin
Arise in the LA, in the septal region of the fossa ovalis
Pedunculated, moves like wrecking ball
Can embolize
Secretes IL-6 (fever and malaise)

A

Cardiac Myxoma

74
Q

Cardiac tumor comprised of fat (benign)

A

Cardiac lipoma

75
Q

Cardiac tumor that looks like a sea anemone

Resemble a larger version of Lambl excrescences (thrombi on valves of old people)

A

Papillary fibroelastoma

76
Q

Most common tumor of the pediatric heart (benign)
Hamartoma of developing cardiac myocytes
50% due to mutations in tuberous sclerosis genes (TSC1 or TSC2)

A

Cardiac rhabdomyoma

77
Q

Malignant endothelial neoplasm that primarily affects older adults

A

Angiosarcoma

78
Q

Heart transplant rejection in the first month

A
  • Cell mediated rejection (T-cells)
  • Antibody mediated rejection

*both due to immune response to foreign heart HLA Ags

79
Q

Most significant long term limitation to survival post heart transplant

A

Allograft vasculopathy

*immune response induces growth factors that eventually lead to occlusion and stenosis of coronary arteries

80
Q

How may allograft vasculopathy present?

A

Silent MI

(at +/- 10 years)

*no angina due to denervated heart

81
Q

Chronic immunosuppression in heart transplant patients put pts at risk for

A
  • Increased risk of skin cancers

- EBV positive lymphoproliferative disorder

82
Q

General effect of aging on the heart

A

Decreased compliance and elasticity of the heart and vessels

*fibrotic valves, calcific deposits, LV cavity size decrease, atrial dilation, atherosclerosis induced stenosis

83
Q

Shunt type in ASD, VSD and PDA

Typically asymptomatic unless large

A

Left to right shunt

  • oxygenated blood can move back to the right heart
  • ASD/VSD lead to increased RV outflow and pulm bloodflow
  • PDA increases only pulmonary bloodflow
84
Q

Shunt type in tetrology of fallot, transposition of the great vessels and tricuspid atresia

A

Right to left shunt

*deoxygenated blood bypasses the lungs

85
Q

Failure of the septum secundum to close
Asymptomatic until adulthood
Systolic ejection murmur

A

Ostium secundum ASD

  • L to R shunt
  • most common ASD
86
Q

Most common form of congenital heart disease
Malformation of the membranous part of the interventricular septum
Asymptomatic until adulthood
Holosystolic murmur

A

VSD

  • L to R shunt
  • Symptomatic VSD associated with other cardiac anomalies
  • Membranous type most common
87
Q

Failure of the ductus arteriosus to close after birth due to hypoxia or other heart defects
Increased pulmonary vascular resistance
Harsh machine like murmur
Typically asymptomatic

A

PDA

*L to R shunt

88
Q

Explain Eisenmenger Syndrome

A
  • Longstanding L to R shunt causes pulmonary HTN -Pulm vascular remodeling increases resistance
  • Shunt reversal (L to R becomes R to L)
  • Blood bypasses lungs
  • Hypoxia (cyanosis) and extreme dyspnea leads to death
89
Q

Patent foramen ovale in pt with a DVT can lead to

A

Paradoxical embolism

  • venous thrombosis => arterial thrombosis => end organ effects/stroke
  • paradoxical embolism due to PDA would lead to LE arterial occlusion
90
Q

Four features of Tetrology of Fallot

A
  • VSD
  • RVH
  • Subpulmonic stenosis
  • Overriding aorta (entrance to aorta centered over VSD)
91
Q

Clinical presentation of what diagnosis?

Cyanosis present since birth
Holosystolic murmur
Systolic ejection murmur
Cyanosis, syncope during emotional distress, excitement or activity
Compensatory squatting
Boot shaped heart on CXR
A

Tetrology of Fallot

  • Holosystolic murmur (VSD)
  • Systolic ejection murmur (subpulmonic stenosis)
  • Cyanosis, syncope during emotional distress, excitement or activity (Tet spell)
  • Compensatory squatting (increases systemic pressure)
92
Q

Aorta and pulmonary artery are switched
Incompatible with life
Cyanosis at birth

A

Transposition of the Great vessels

*Must keep PDA open or death (give PGE1), surgery necessary

93
Q

Complete absence of the tricuspid valve
Severe immediate cyanosis
Oxygenation maintained by ASD/PFO and VSD, otherwise incompatible with life
Severe immediate cyanosis

A

Tricuspid atresia

  • LV pumps to lungs and systemic circulation simultaneously
  • surgical correction necessary
94
Q

Infantile vs adult type of coarctation of the aorta (focal narrowing of the aorta)

A
  • Infantile form has PDA (creates shunt that bypasses lungs)

- Adult form without PDA

95
Q

Coarctation of the aorta is associated with what genetic abnormality in females?

A

Turner syndrome (45, X)

96
Q

Clinical presentation diagnosis?

  • Baby with cyanosis of lower half of body only
  • Adult with upper body HTN and lower body hypotension, rib notching
A

Coarctation of the aorta

*closure of the PDA leads to no cyanosis in adult form

97
Q

Clinical presentation diagnosis?

Cyanotic baby with left ventricular hypertrophy

A

Congenital aortic stenosis

98
Q

Most common septal defects in down syndrome (trisomy 21)

A

AVSD > VSD > ASD

99
Q

Marfan syndrome (tall, thin, lanky, Fibrillin-1 mutation) is at risk for what cardiovascular complication?

A

Aortic aneurysm/dissection

*Fibrillin-1 mutation leads to excessive TGF-B activity, increasing metalloproteases, leading to degradation of elastin

100
Q

DiGeorge syndrome is associated with what cardiac defect?

A

Conotruncal abnormalities (TOF, transposition, ASD, VSD)

*CATCH-22

101
Q

Hypertensive heart disease can lead to

A

CHF due to diastolic or systolic heart failure

  • HTN => LV hypertrophy
  • diastolic failure due to concentric LV hypertrophy, systolic failure due to increased O2 demand
102
Q

Pulmonary HTN due to pulmonary vessel diseases causes RV dilation then hypertrophy, eventually leading to right heart failure

A

Cor pulmonale

103
Q

Wear and tear of the aortic valve associated with HTN and hyperlipidemia

A

Calcific aortic stenosis

*chronic progressive injury leads to calcification of valve

104
Q

Bicuspid aortic valve is associated with what complications (3)

A
  • Accelerated onset of calcific aortic stenosis
  • Aortic valve prolapse
  • Infective endocarditis more likely
105
Q

Mitral annular calcification is associated with what complications (2)

A
  • Arrhythmia (heart block)
  • Infective endocarditis

*most common in elderly females with MVP

106
Q

Mitral valve prolapse can rarely occur in what genetic condition?

A

Marfan syndrome

*MVP is typically absent of an underlying cause

107
Q

Clinical presentation diagnosis?

Midsystolic click on auscultation
Mitral regurgitation
Dyspnea in chronic cases

A

Mitral valve prolapse

*may lead to arrhythmia (afib with atrial dilation) or infective endocarditis in severe cases

108
Q 
GAS
JONES criteria
M streptococcal antigen
Dx confirmed with Ab to Streptolysin O and DNase B
Valves affected = MAT
A

Rheumatic fever

109
Q

Acute infectious endocarditis presentation

A

Fever and chills that develop rapidy

110
Q

Subacute infectious endocarditis presentation

A

Low grade fever (<101F) and fatigue

111
Q

Organism that causes acute infectious endocarditis, specifically tricuspid valve in IVDU

A

S aureus

*can also infect prosthetic valves

112
Q

Organism that causes subacute infectious endocarditis after dental procedure/ poor dentition

A

S viridans, HACEK group

*Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella

113
Q

Organism that causes subacute infectious endocarditis, specifically prosthetic valves

A

S epidermidis

114
Q

Sterile, non-inflammatory valvular thrombi caused by hypercoagulable states like cancer, antiphospholipid syndrome, SLE

A

Nonbacterial Thrombotic Endocarditis

  • Cancer = mucinous adenocarcinomas
  • APS and SLE create anti-endothelial Ab, which is procoagulant
115
Q

What side of the heart can be affected in carcinoid heart disease and why?

A

Right heart (tricuspid, pulmonic, RV) because lungs catabolize serotonin, protecting the left heart

*Carcinoid tumor must mets to liver to affect heart

116
Q

Complications of prosthetic heart valves (mechanical and bioprosthesis)

A
  • Infectious endocarditis (both)
  • Lifelong risk of thromboembolism (mech)
  • Only last 10-15 years (bio)
  • RBC shearing (both)
  • Regurgitation (both)
117
Q

Cardiomyopathy definition

A

Structurally and functionally abnormal heart with mechanical or electrical dysfunction in teh absence of CAD, HTN, valvular disease, congenital heart disease

118
Q

Dilated cardiomyopathy with systolic dysfunction due to a mutation in TTN (Titin)

A

Familial dilated cardiomyopathy

119
Q

Dilated cardiomyopathy with systolic dysfunction due to volume overload that occurs in late pregnancy

A

Peripartum cardiomyopathy

120
Q

Dilated cardiomyopathy with systolic dysfunction due to direct cytotoxic effects of alcohol on cardiomyocytes, or thiamine deficiency (impaired cell metabolism)

A

Alcoholic cardiomyopathy

121
Q

Dilated cardiomyopathy with systolic dysfunction due to antracyclines doxorubicin and daunorubicin

A

Drug induced dilated cardiomyopathy

122
Q

Dilated cardiomyopathy with systolic dysfunction due to hemochromatosis

A

Iron overload dilated cardiomyopathy

123
Q

Classic presentation:

Otherwise seemingly healthy athlete dies of sudden cardiac death
May present with systolic ejection murmur
Hypertrophic ventrcular septum

A

Hypertrophic cardiomyopathy (diastolic dysfunction)

  • Mutations in sarcomere proteins, most commonly B-myosin heavy chain
  • Myocyte hypertrophy and disarray with septal prominence
124
Q

Myocardium of the right ventricular wall is replaced with adipose & fibrosis
Leads to Vtach, premature contractions, fibrillation
Sudden death

A

Arrythmogenic Right Ventricular Cardiomyopathy (ARVC)

125
Q

ARVC with plantar and palmar hyperkeratosis, wooly hair

Mutation in plakoglobin

A

Naxos syndrome

126
Q

Cardiomyopathy caused by deposition of material (amyloid) in heart wall
Diastolic dysfunction leads to enlarged atria with normal sized ventricles

A

Restrictive cardiomyopathy

  • AL amyloid from multiple myeloma
  • AA amyloid released from liver in chronic inflammatory states
127
Q

Most common myocarditis, seen in viral infection (most common) and autoimmune
Abundant lymphocytic infiltrate

A

Lymphocytic myocarditis

  • Viral infection: Coxsackie B and COVID-19
  • Coxsackie B presents as fever, headache, sore throat, GI distress, fatigue, chest pain, myalgias
128
Q

Myocarditis can also be caused by Chagas disease

A

Trypansoma cruzi

129
Q

Myocarditis after eating undercooked pork, also comes with myalgias and GI symptoms

A

Trichenella spiralis

130
Q

Myocarditis after tick bite, erythema migrans, bells palsy, heart block

A

Lyme disease, Borriela burgderofi

131
Q

Myocarditis with eosinophilia in the absence of parasitic infection
Caused by hypersensitivity to drug

A

Eosinophilic myocarditis

132
Q

Idiopathic myocarditis that is aggressive and poor prognosis

Enlarged multinucleated cells

A

Idiopathic giant cell myocarditis

133
Q

Idiopathic myocarditis

Giant cells with non-necrotizing granulomas

A

Myocardial sarcoidosis

Cardio (18 decks)

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