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Pathology > Cardiovascular: Pathoma, BRS, First Aid > Flashcards

Cardiovascular: Pathoma, BRS, First Aid Flashcards

1
Q

Ischemic heart disease is caused by what?

A

Partial or complete interruption of arterial blood flow to the myocardium

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2
Q

What is the main cause for interruption of arterial blood flow to myocardium?

A

Atherosclerosis of coronary arteries

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3
Q

Incidence of IHD increases with what?

A

Age

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4
Q

How will ischemia present? (6)

A
  1. Silent
  2. Angina pectoris
  3. Coronary steal syndrome
  4. Myocardial infarction
  5. Sudden cardiac death
  6. Chronic ischemic heart disease
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5
Q

Frequency of IHD increases in patients who manifest what?

A

Metabolic syndrome

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6
Q

What does metabolic syndrome include?

A
  1. Central obesity
  2. Artherogenic lipid patterns
  3. Hypertension
  4. Insulin resistance
  5. Proinflammatory state
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7
Q

What predisposes someone to metabolic syndrome?

A

Obesity
Physical activity
Genetic factors

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8
Q

What is angina pectoris?

A

Episodic chest pain that is caused by inadequate oxygenation of myocardium

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9
Q

How much stenosis or obstruction of a vessel is needed to cause angina?

A

> 70-75%

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10
Q

Is there myocyte necrosis in angina?

Why?

A

No

Reversible

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11
Q

What is the most common type of angina?

A

Stable angina

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12
Q

What precipitates stable angina?

Why?

A

Exertion or stress

Can’t get enough blood (oxygen) to heart

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13
Q

What causes stable angina?

A

CAD of coronary arteries greater than 70%

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14
Q

How does stable angina present? 3

A
  1. Chest pain less than 20 minutes that radiates to left arm or jaw
  2. Diaphoresis
  3. Shortness of breath
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15
Q

Why is the 20 minute interval important?

A

After that you get irreversible injury and cell death

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16
Q

What does an EKG show in stable angina?

Why?

A

ST segment depression

Subendocardial ischemia

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17
Q

What relieves stable angina? (2)

A
  1. Rest

2. Vasodilators like nitroglycerin

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18
Q

Function of nitroglycerin?

A

Vasodilation of veins mainly that decreases preload and decreases stress on myocardia

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19
Q

Unstable angina is chest pain that occurs when?

A

At rest

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20
Q

What causes unstable angina?

A

Rupture of atherosclerotic plaque with thrombosis and incomplete occlusion of coronary artery

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21
Q

What type of damage is occurring in unstable angina?

A

Reversible injury to myocytes

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22
Q

What does an EKG show on unstable angina?

A

ST segment depression

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23
Q

What relieves unstable angina?

A

Nitroglycerin: Vasodilation to decrease preload which decreases stress

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24
Q

What are unstable angina patients at risk for?

A

Progressing to full occlusion: Myocardial infarction)

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25
Q

Prinzmetal angina is due to what?

A

Coronary artery vasospasm

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26
Q

What is the timing of pain in prinzmetal angina?

A

Episodic/intermittent chest pain at rest

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27
Q

What type of damage occurs in prinzmetal angina?

A

Reversible injury to myocytes

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28
Q

What does prinzmetal EKG show?

Why

A

ST segment elevation

Transmural ischemia

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29
Q

What relieves prinzmetal angina? 2

A
  1. Nitroglycerin: Decrease preload

2. Calcium channel blockers: Decrease spasm

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30
Q

What is the most important cause of morbidity from IHD?

A

Myocardial infarction

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31
Q

What is myocardial infarction?

A

Necrosis of cardiac myocytes (so after 20 minutes)

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32
Q

What mainly causes a myocardial infarction?

A

Rupture of a atherosclerotic plaque with thrombosis and complete occlusion of coronary artery

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33
Q

Other causes of myocardial infarction? (3)

A
  1. Coronary artery vasospasm (Complete prinzmetal)
  2. Emboli
  3. Vasculitis (kawasaki’s disease)
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34
Q

Symptoms of myocardial infarction?

A
  1. Severe chest pain greater than 20 minutes that radiates to left arm/jaw
  2. Diaphoresis
  3. Dyspnea: Heart can’t pump –> Fluid in lungs
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35
Q

Will nitroglycerin relieve myocardial infarction pain?

A

No

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36
Q

What ventricle is usually involved in an MI?

A

Left

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37
Q

What is most common artery involved in MI?

Which causes an infarction where?

A

LAD

Infarciton of anterior wall of LV and anterior part of IV septum

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38
Q

What is 2nd most common artery involved in MI?

Which causes an infarction where?

A

Right coronary

Infarction of right ventricle, posterior wall of LV and anterior portion of IV septum

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39
Q

What is 3rd most common artery involved in MI?

Which causes an infarction where?

A

Left circumflex

Infarction of lateral wall of LV

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40
Q

What are the 2 types of infarction based on heart layers involved?
Which is more common

A
  1. Transmural: Entire ventricular wall from endo to epi. More common
  2. Subendocardial infarction: Just 1/3 of the wall
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41
Q

ECG shows what during myocardial infarction?

A
  1. During the initial subendocardial infarction, ST depression
  2. During later transmural infarction, ST elevation
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42
Q

Why are there biomarkers for MI?

A

Irreversible damage to myocytes causes membrane breakdown thus releasing markers

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43
Q

What is the most SENSITIVE and most SPECIFIC cardiac marker?

A

Troponin I

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44
Q

When does troponin I peak?

A

24 hours

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45
Q

How long does troponin I remain high after MI?

A

7 to 10 days

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46
Q

CK-MB is most useful for what?

A

Detecting re-infarction

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47
Q

When does CK-MB rise?

A

4-6 hours after infarction

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48
Q

When does CK-MB peak?

A

24 hours

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49
Q

When does CK-MB return to normal? 72 hours

A

72 hours

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50
Q

What is the gold standard for diagnosing MI in first 6 hours?

A

ECG

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51
Q

When does LDH peak?

How long does it last?

A

3 days

4-7 days

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52
Q

When does myoglobin peak?

How long does it last?

A

First 6 hours

24 hours

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53
Q

Treatment of MI includes what? 6

Describe each

A
  1. ASA/Heparin: limit more thrombosis
  2. Supplemental O2: minimize ischemia
  3. Nitrates: Vasodilate –> Decrease preload
  4. Beta-blocker: Slow heart rate –> Decrease O2 need + decrease arrhythmia
  5. ACE inhibitor: Decrease dilatation
  6. Fibrinolysis/Angioplasty: Destroy blockage/open up vessel
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54
Q

How does an ACE inhiabitor decrease LV dilatation? 2

A
  1. Blocks ANG II production –> prohibit constriction of peripheral arterioles –> Decrease afterload
  2. Block ANG II –> No aldosterone secreted –> No blood volume increase
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55
Q

Two injuries due to fibrinolysis and angioplasty?

A
  1. Contraction band necrosis

2. Reperfusion

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56
Q

What is contraction band necrosis?

A

Calcium will enter cell after blood flow is restored and cause contraction –> visible contraction bands

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57
Q

What is reperfusion injury?

A

Returning O2 rapidly to cell causes ROS to form –> Further damage the cells

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58
Q

What is a lab test for reperfusion injury?

A

See cardiac enzymes continue to rise after reperfusion

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59
Q

Less than 4 hours from infarction, what risks does patient have?

A
  1. Cardiogenic shock: Heart fails –> Hypofusion
  2. CHF: Dead tissue –> Can’t pump–> Backs up into heart –> Decreased ejection fracture
  3. Arrhythmia
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60
Q

Between 4 and 24 hours after infarction, what changes do you see macroscopically?

What risk?

A
  1. Dark discoloration
  2. Coagulative necrosis: Karyolysis, pyknosis, karyorrhexis

Arrhythmia

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61
Q

Between 1 and 3 days what change do you see? 2

What is patient at risk for?

A

Yellow pallor
Neutrophils on scene

Fibrinous pericarditis

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62
Q

How does fibrinous pericarditis present in days 1-3?

Why does it occur?

A

Chest pain with friction rub

Transmural infarction –> Neutrophils enlame entire wall –> Debris into pericardium –> Pericarditis

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63
Q

How does MI present in days 4-7? 2

A
  1. Yellow pallor

2. Macrophages on scene

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64
Q

What is important about days 4-7 after MI?

A

Cardiac wall is weakest due to macrophages eating all the dead material.

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65
Q

What are the 3 things a patient is at risk for 4-7 days after MI?

A
  1. Rupture of ventricular free wall –> Blood leaks into pericardium –> Compresses heart –> Cardiac tamponade
  2. Rupture of IV septum –> Shunt from LV to RV
  3. Rupture of papillary muscle –> Mitral insufficiency
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66
Q

What causes rupture of papillary muscle?

A

Occlusion of right coronary artery

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67
Q

In weeks 1-3, what are the macroscopic changes? (2)

A
  1. Red border as granulation tissue enters from edge

2. Granulation tissue with fibroblasts, collagen, and BV’s

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68
Q

Months after, what changes does MI patient have?

A
  1. White scar of Type 1 collagen

2. Fibrosis

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69
Q

What risks does a patient with an MI have after months? (3)

A
  1. Weak scar: leads to balloon like dilatation –> Aneurysm
  2. Scar along heart wall –> Stasis –> Mural thrombus
  3. Dressler syndrome
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70
Q

What happens in Dressler’s syndrome?

A

Transmural infarct –> Pericardium leaks –> Form imune response against pericardium antigens –> Pericarditis 6-8 weeks after infarction

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71
Q

What is most common cause of death in first several hours after infarction?

A

Arrhythmia

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72
Q

What is sudden cardiac death due to?

A

Cardiac disease

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73
Q

How does sudden cardiac death appear? 2

A
  1. Asymptomatic before

2. Less than 1 hour after symptoms arise

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74
Q

What usually causes sudden cardiac death?

A

Fatal ventricular arrhythmia

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75
Q

Most common etiology of sudden cardiac death?

A

Acute ischemia

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76
Q

90% of SCD patients have what pre-existing condition?

A

Severe atherosclerosis

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77
Q

Less common etiologies of SCD? 3

A
  1. Mitral valve prolapse
  2. Cardiomyopathy
  3. Cocaine abuse
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78
Q

Chronic ischemic heart disease is defined how?

A

Poor myocardial function

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79
Q

What is Chronic IHD due to?

A

Chronic ischemic damage (with or without MI)

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80
Q

What do chronic IHD patients progress to?

A

CHF

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81
Q

What is coronary steal syndrome?

A

Vasodilator may aggravate ischemia by shunting blood from area of critical stenosis to an area of higher perfusion.

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82
Q

Congestive heart failure may be failure of what ventricle?

A

Right, Left or both

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83
Q

Causes of Left sided heart failure?

Explain each

A
  1. Ischemia: Decrease blood flow –> Damage myocardium –> Can’t pump well
  2. Hypertension: Get concentric LV hypertrophy to deal with stress –> Extra O2 demands –> Ischemic damage –> Can’t pump well
  3. Dilated cardiomyopathy: Stretch all four chambers –> Can’t contract well
  4. Myocardial infarction: Nonfunctional tissue –> Can’t pump well
  5. Restrictive cardiomyopathy: Can’t fill heart well –> Can’t pump enough out
  6. Aortic and mitral valvular disease
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84
Q

Two main Clinical manifestations of LCHF?

A
  1. Pulmonary congestion

2. Decreased forward perfusion

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85
Q

Pulmonary congestion from LCHF is due to what?

A

Heart can’t pump blood forward –> Backs up –>blood accumulates in lung –> Pulmonary congestion

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86
Q

Why does pulmonary congestion result in dyspnea?

A

Increase in hydrostatic pressure –> Pulmonary edema –> Dyspnea

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87
Q

What is PND?

A

Dyspnea upon laying flat for several hours

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88
Q

What is othopnea?

A

Dyspnea if late flat for a few minutes?

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89
Q

What are crackles?

A

Fluid in lungs upon auscultation

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90
Q

Ruptured pulmonary capillaries in LCHF results in what?

A

Blood in alveoli –> Macrophages arrive to clean up –> Iron fills maccrophages –> Forms hemosiderin laden cells called heart failure cells.

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91
Q

What are the 5 clinical manifestations of pulmonary congestion?

A
  1. Dyspnea
  2. PND
  3. Orthopnea
  4. Crackles
  5. Heart failure cells
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92
Q

Decreased forward perfusion results in activation of what?

A

RAS

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93
Q

RAS activation has what two effects?

A

Decreased blood flow to kidneys activates juxtaglomerular apparatus –> Release renin –> Release Ang II –>

  1. Constrict arterioles –> Increase total peripheral resistance
  2. Go to adrenal gland –> Release aldosterone –> Cause resorption of sodium –> Water follows –> Increase blood volume

OVERALL = Increase resistance –> Exacerbates problem

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94
Q

Main treatment for LCHF?

A

ACE inhibitor

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95
Q

Right sided failure has what causes? 6

A
  1. Left sided heart failure
  2. Left-sided lesions
  3. Pulmonary hypertension: Chronic lung disease/cor pulmonale –> Vessel constriction
  4. Cardiomyopathy/Diffuse myocarditis
  5. Tricuspid or pulmonary valvular disease
  6. Left to right shunts
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96
Q

Most common cause of RCHF?

Why?

A

LCHF

Backup into pulmonary circuit –> Backups into right heart

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97
Q

Isolated RCHF is usually due to what?

A

Cor pulmonale

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98
Q

Clinical manifestations of RCHF? 4

A
  1. Jugular vein backup –> JVD
  2. Hepato and spleno congestion –> Hepatosplenomegaly + cardiac cirrhosis + nutmeg liver
  3. Pitting edema: Due to increased hydrostatic pressure in low extremities.
  4. Renal hypoxia: Fluid retention
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99
Q

Congenital defects arise when?

A

During embryogenesis weeks 3-8

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100
Q

Congenital heart defects are seen in what percentage of live births?

A

1%

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101
Q

Most congenital defects are caused by what?

A

Undetermined = Sporadic

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102
Q

Congenital defects overall usually result in what?

A

Shunting between left and right circulations

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103
Q

What is most common congenital heart defect?

A

Ventricular septal defect

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104
Q

VSD is a defect associated with what syndrome?

A

Fetal Alcohol Syndrome

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105
Q

What happens with blood flow in VSD?

A

Blood enters right atrium and can enters normal low pressure RV over high pressure LV. However upon returning to LA, blood chooses low pressure RV instead of high pressure LV resulting in LEFT TO RIGHT SHUNT

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106
Q

How does size of defect affect symptoms in VSD?

A

Small VSD = asymptomatic

Large VSD = large amounts of blood entering RV –> increase of blood in pulmonary circuit –> Pulmonary hypertension

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107
Q

What does pulmonary hypertension from VSD result in over time?

A

P-HTN –> Right side to become high pressure –> Blood now shunts from high pressure right to low pressure left ventricle –> Deoxygenated blood in systemic circulation –> Cyanosis

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108
Q

The reversal of a shunt due to a change in pressure from pulmonary hypertension is known as what?

A

Eisenmenger syndrome

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109
Q

3 consequences of Eisenmenger’s syndrome?

A
  1. RV hypertrophy: Due to pumping against higher pressure
  2. Polycythemia: Deox blood –> Hypoxemia –> Release EPO –> Increase RBC’s
  3. Clubbing: Change in fingernails from cyanosis
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110
Q

Treatment of VSD? (2)

A
  1. Small VSD close on their own

2. Surgical closure

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111
Q

Atrial septal defect includes what five types?

A
  1. Patent foramen ovale
  2. Septum primum
  3. Septum secundum
  4. Sinus venosus
  5. Lutembacher syndrome
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112
Q

Patent foramen ovale is clinically significant how?

A

It’s not. 20-30% of people have it.

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113
Q

Septum primum/Ostium primum is associated with what consequence?
What genetic disease is associated with this?

A

Affects lower part of septum so it can affect AV valves.

Down’s syndrome

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114
Q

Most common type of ASD is what?

A

Ostium/Primum secundum

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115
Q

Ostium/Primum secundum is a defect in what?

A

Fossa ovalis

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116
Q

Sinus venosus affects what area?

A

Upper part of septum near SVC

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117
Q

Lutembacher syndrome has what two components?

A
  1. ASD

2. Mitral stenosis

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118
Q

Atrial septal defect results in what type of shunt?

A

Left to right shunt

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119
Q

ASD presents how on auscultation? 2

A
  1. Split S2

2. Loud S1

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120
Q

Why does split S2 occur in ASD?

A

Blood from high pressure LA crosses to low pressure RA –> Extra volume on right side –> Delayed closure of pulmonic valve –> Split S2

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121
Q

What is the S2 sound?

A

Pulmonary and aortic valves closing

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122
Q

What is an important complication of ASD?

A

Paradoxical emboli: DVT emboli enters RA normally but crosses over to LA and lodges in brian or extremities.

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123
Q

When are ASD symptoms seen?

What is the main one?

A

Late in life

Cyanosis due to Eisenmenger’s syndrome from P-HTN

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124
Q

What is Patent ductus arteriosus?

A

Failure of ductus arteriosus to close.

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125
Q

PDA is associated with what situations? 2

A
  1. Congenital Rubella

2. People living in high altitudes

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126
Q

What is the mechanism of PDA?

A

Blood enters RA –> RV –> Enters pulmonary artery –> Chooses to enter low pressure lungs over high pressure aorta –> LA –> Enters LV –> Enters aorta –> Chooses low pressure lungs over high pressure systemic circulation –> LEFT TO RIGHT SHUNT

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127
Q

What happens over time in PDA patients?

A

P-HTN develops –> Blood now chooses low pressure aorta over high pressure lungs –> Deox blood goes to LOWER extremities –> Cyanosis in lower extremities in late life.

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128
Q

How does PDA appear at birth?

A

Asymptomatic left to right shunt

129
Q

What causes PDA to appear in adulthood?

A

Eisenmenger’s syndrome

130
Q

What keeps the PDA open? 2

A

Prostaglandin E

Low O2 tension

131
Q

What are treatments for PDA? (2)

A
  1. surgery

2. Indomethacin

132
Q

Function of indomethacin

A

Decrease prostaglandin E –> Close PDA

133
Q

What is the quality of murmur in PDA?

A

Machine-like murmur

134
Q

Tetralogy of Fallot is caused by what?

A

Anteriosuperior displacement of infundibular septum

135
Q

Tetralogy of Fallot has what four components?

A 
PROVe
Pulmonary infundibular stenosis
Right Ventricular Hypertrophy
Overriding aorta (of VSD)
Ventricular Septal Defect
136
Q

What is the flow of blood in tetralogy of Fallot?

A

RA –> RV –> Due to stenosis –> Shunt to aorta = Right to left shunt

137
Q

In babies, ToF results in what?

A

Cyanosis due to deoxygenated right sided blood entering systemic circulation.

138
Q

What is shape of heart in ToF?

A

Boot-shaped heart

139
Q

In adults, what will cause cyanosis to occur in ToF?

140
Q

How do patients deal with ToF?

A

Squat –> Increase left sided pressure –> Decrease shunt –> Oxygenate more blood –> less cyanotic

141
Q

The main point behind squatting with ToF?

A

Increased arterial resistance –> Decreases shunting

142
Q

Treatment of ToF?

A

Early surgery

143
Q

In transposition of great vessels, what happens?

A

Aorta comes off RV and Pulmonary artery comes off LV resulting in two independent circuits that do not connect.

144
Q

Can a person with transposition of great vessels live?

A

Only if they somehow form a shunt.

145
Q

How do you treat Transposition of great vessels?

Specifically? (2)

A

Cause open PDA so that blood can mix

  1. Give patient prostaglandin E
  2. Surgically repair problem
146
Q

What maternal condition is associated with Transposition of Great vessels?

A

maternal diabetes

147
Q

How do ToGV patients present?

A

Early cyanosis since deox blood from right side enters aorta –> Systemic circulation

148
Q

What is truncus arteriosus?

A

Truncus fails to divide providing one single large vessel coming from both ventricles.

149
Q

How does blood flow in truncus arteriosus?

A

One vessels drains both ventricles but divides later –> Deox and ox blood mix –> Deox blood enters systemic circulation –> Cyanosis

150
Q

What is tricuspid atresia?

A

Tricuspid valve orifice fails to develop

151
Q

What does atresia mean?

A

Fail to form lumen of tube

152
Q

In tricuspid atresia, how is the RV described?

A

Hypoplastic

153
Q

In tricuspid atresia, what is the situation associated with?
What is flow of blood?
How does it present?

A

ASD: Right to left shunt

Tricuspid fails to form –> No blood to RV –> ASD forms –> Deox blood enters left side

Cyanosis

154
Q

Coarctation means what?

A

Narrowing of aorta

155
Q

Coarctation of aorta is divided into what two forms?

A

Infantile and Adult

156
Q

Infantile CoA is associated with what?

157
Q

In infantile CoA, where is the coarctation?

A

Distal to aortic arch

Proximal to PDA

158
Q

Describe the pressures in infantile CoA?

A

High pressure above coarctation

Low pressure below coarctation

159
Q

What is mechanism of blood flow in infantile CoA?

A

RA–> RV –> PA –> Cross PDA to low pressure aorta below coarctation –> Deox blood in lower extremities –> Lower extremity cyanosis

160
Q

What disease is associated with infantile CoA?

A

Turner’s

161
Q

Is adult form of CoA associated with PDA?

162
Q

Where is coarctation in adult CoA?

A

Distal to aortic arch?

163
Q

Mechanism of blood flow in adult CoA?

A

Since narrowing is below arch –> High pressure above and low pressure below –> High pressure in UE + low pressure in LE

164
Q

How does adult CoA present?

A

HTN in upper extremity

Hyptension with weak pulses in lower extremity

165
Q

When is adult form of CoA found?

A

In adulthood

166
Q

What defect is adult CoA associated with?

A

Bicuspid aortic valve

167
Q

What X-ray feature is seen in adult CoA?

Why?

A

Notching of ribs

Collateral circulation develops across intercostal arteries –> Engorged arteries –> Notching of ribs

168
Q

What is Turner’s syndrome associated with in congenital heart defects?

A

Coarctation of Aorta (Infantile)

169
Q

What are congenital defects are Down syndrome patients known for?
Such as? 3

A

Endocardial cushion defects

ASD, VSD, AV septal defect

170
Q

Congenital rubella is associated with what congenital CV defects? 5

A 
Septal defects: VSD,
PDA
Pulmonary artery stenosis
Valvular stenosis
Aortic stenosis
171
Q

22q11 syndromes are associated with what CV defects? (2)

A
  1. Truncus arteriosus

2. Tetralogy of Fallot

172
Q

Marfan’s syndrome is associated with what CV defects?

A

Aortic insufficiency and dissection

173
Q

Infant of diabetic mother has what associated CV defects?

A

Transposition of great vessels

174
Q

Noncyanotic congenital CV defects include what two types?

A

No shunt

Left-to-right shunt

175
Q

What are the diseases of noncyanotic congenital CV defects?

A

No shunts = 1. Aortic stenosis 2. CoA

L-2-R shunts = 1. PDA, ASD, VSD

176
Q

Rank frequency of left to right shunt defects?

A

VSD > ASD > PDA

177
Q

Right to left shunts are known as what? 3

A

Blue babies
Early cyanosis
Cyanotic diseases

178
Q

What are the 5 T’s of right to left shunts?

A 
Tetralogy of Fallot
Transposition of great arteries
Truncus arteriosus
Tricuspid Atresia
Total anomalous pulmonary venous return
179
Q

What do most patients with truncus arteriosus also have?

180
Q

What is total anomalous pulmonary venous return?

A

Pulmonary veins return to RA

181
Q

Two types of valvular disease?

A

Stenosis and regurgitation

182
Q

Acute rheumatic fever is what?

A

Systemic complication of pharyngitis due to Group A beta-hemolytic strep

183
Q

How old are children usually with ARF?

How many weeks after strep throat is ARF seen?

A

5-15 years old

2-3 weeks

184
Q

What is the etiology of ARF?

A

The Bacterial M protein of Group A strep resembles human tissues and causes type II hypersensitivity against own heart tissues.

185
Q

What evidence prior to ARF must be had?

How is this accomplished? 2

A

Evidence of group A strep infection

ASO or anti-DNase B titer

186
Q

Minor criteria for ARF? 2

A

Fever

Elevated ESR

187
Q

Major criteria for ARF?

A 
JONES
J = Joint problems = Migratory polyarthritis
O = Heart problems (pan-carditis)
N = Nodules in Skin
E = Erythema marginatum
S = Sydenham's chorea
188
Q

What is first layer of heart to be affected in ARF?

Which results in what?

A

Endocardium

Tiny vegetations on mitral valve (possibly aortic as well) –> Regurgitation

189
Q

Myocardium is second layer to be affected in ARF, what forms here?

A

Aschoff bodies of: Giant cells + Fibrinoid material (degenerated collagen) + Anitschkow Cells

190
Q

How do anitschkow cells appear?

A

Slender wavy nuclei (Caterpillar nuclei)

191
Q

Pericarditis in ARF presents how?

A

Friction rub

192
Q

Which of the 3 layers of carditis is most likely to kill ARF patient?

A

Myocarditis

193
Q

What is erythema marginatum?

A

Rash that is more red on edges

194
Q

Sydenham’s chorea is what?

A

Rapid involuntary muscle movement

195
Q

What is the First Aid acronym for Rheumatic fever facts?

A

FEVERSS

F=Fever
E=Erythema Marginatum
V=Valvular damage (vegetation and fibrosis)
E=Elevated ESR
R = Red-hot joints (migratory polyarthritis)
S=Subcutaneous nodules
S=St. Vitus’ dance (Sydenham’s chorea)

196
Q

Rheumatic endocarditis has what happen in early stage?

A

Valve leaflets are red and swollen with tiny vegetations resulting in mitral valve regurgitation

197
Q

As a consequence of healing, what changes do valves have in ARF?

A

Valves become thickened, fibrotic and deformed.

198
Q

Chronic rheumatic valvular disease is result of what?

A

Valve scarring that results from rheumatic fever?

199
Q

Chronic rheumatic valvular disease results in what?

200
Q

Mitral valve stenosis leads to what?

A

Thickening of chordae tendinae and cusps

201
Q

Aortic valve in CRV results in what?

A

Fusion of comissures

202
Q

Fusion of comisures in aortic valve CRV results in what? (2)

A
  1. Small orifice –> FIshmouth appearance

2. Stenosis –> Can’t completely open valve

203
Q

Mitral stenosis causes what pressure difference to develop?

A

Diastolic pressure higher in left atrium than in left ventricle

204
Q

What is aortic stenosis

A

Narrowing of aortic valve orifice

205
Q

What is aortic stenosis due to mainly? (2)

A
  1. Fibrosis

2. Calcification

206
Q

When does aortic stenosis present?

A

Late adulthood (>60 years old)

207
Q

Two others causes of aortic stenosis?

A

Bicuspid aortic valve

Chronic rheumatic valve disease

208
Q

Aortic valve is usually what organization?

209
Q

What’s the problem with bicuspid aortic valves?

A

Two cusps do the work of 3 –> increases risk for aortic stenosis

210
Q

How does CRVD cause aortic stenosis?

A

It has mitral valve stenosis and fusion of aortic valve comissures

211
Q

What is difference between “wear-and-tear” aortic stenosis and CRVD caused aortic stenosis

A

Wear and tear aortic stenosis has only the aortic valve affected, CRVD = mitral + aortic valve

212
Q

Compensation in aortic stenosis leads to what? 2

A
  1. longer asymptomatic stage

2. Systolic ejection click followed by crescendo-decrescendo murmur

213
Q

Complications resulting from aortic stenosis? (3)

A
  1. LV Hypertrophy: Due to pumping against stenotic valve
  2. Angina and syncope with exercise: Stenosis reduces systemic blood flow –> Don’t get enough during exercise
  3. Microangiopathic hemolytic anemia: Blood cells rupture moving across bad valve
214
Q

Treatment of aortic stenosis?

A

Replace valve after symptoms appear

215
Q

Aortic regurgitation is what?

A

backflow of blood from aorta into LV during diastole

216
Q

AR arises due to what? 4

Which is most common

A
  1. Isolated aortic root dilation (Most common)
  2. Syphilitic aneurysm
  3. Valve damage (such as CRVD)
  4. Non-dissecting aortic aneurysm
217
Q

Why does aortic root dilatation cause AR?

A

Dilation of root –> Pulls valves apart –> Regurg occurs

218
Q

Clinical features of AR? 7

A

BE-PHILE

  1. Bounding pulses
  2. Early blowing diastolic murmur
  3. Pulsating nail bed
  4. Head bobbing
  5. Increasing pulse pressure
  6. LV dilation
  7. Eccentric hypertrophy of one part of ventricle
219
Q

Treatment of AR?

A

Valve replacement

220
Q

What is the most common valvular lesion?

A

Mitral valve prolapse

221
Q

What is mitral valve prolapse?

A

Ballooning of mitral valve into left atrium during systole

222
Q

Mitral valve prolapse is due to what?

A

Myxoid degeneration of valve making it floppy

223
Q

What diseases commonly have mitral valve prolapse? 2

A

Marfan and Ehlers Danlos

224
Q

Clinical features of MVP? 3

A
  1. Mid-systolic click with systolic regurgitation murmur
  2. Arrhythmia
  3. Can turn into infective endocarditis
225
Q

Treatment of MVP?

A

Valve replacement

226
Q

Mitral regurg involves what?

A

Reflux of blood from LV into LA during systole

227
Q

Mitral regurg is a complication of what prior problem usually?

A

Mitral valve prolapse

228
Q

Other causes of mitral regurg? 4

A
  1. LV dilation
  2. Infective endocarditis (Bad leaflets)
  3. ARF (Mitral valve)
  4. Papillary muscle rupture after MI
229
Q

Clinical features of mitral regurgitation? 3

A
  1. Holosystolic blowing murmur
  2. Louder with squatting and expiration
  3. volume overload and left-sided heart failure
230
Q

Why does squatting make mitral regurg louder?

A

Increase systemic resistance –> less blood forward –> more blood backwards –> Louder murmur

231
Q

Why does expiration make mitral regurg louder?

A

Increase in amount of blood entering LA –> Increase blood in LV –> increase in regurgitated blood

232
Q

What is mitral stenosis?

A

Narrowing of mitral valve orifice

233
Q

Cause of mitral stenosis?

234
Q

Clinical symptoms of mitral valve stenosis?

A
  1. Opening snap with diastolic rumble

2. Volume overload leads to dilation of LA

235
Q

Consequences of dilated LA in mitral valve stenosis?

A
  1. Pulmonary congestion: Overloading LA –> Blood backs up into pulmonary circuit –> Pulmonary congestion –> Edema + Alveolar hemorrhage –> Heart failure cells
  2. Pulmonary HTN: Excess blood in circuit –> Rt heart pumps against –> Right heart fails
  3. Atrial fibrillation: Dilation –> Abnormal wall movement –> Stasis –> Mural thrombi
236
Q

What syndrome is tricuspid valve involved in?

A

Carcinoid syndrome

237
Q

The pulmonary valve is normally affected by what

A

Congenital malformations

238
Q

Endocarditis is what?

A

Inflammation of endocardium (inner surface)

239
Q

Endocarditis is usually the result of what?

240
Q

General features of bacterial endocarditis? 3

A
  1. Large soft vegetations on valvular surfaces
  2. Ulceration and perforation of valves cusps
  3. Rupture of chordae tendineae
241
Q

Two classifications of bacterial endocarditis?

A

Acute endocarditis

Subacute endocarditis

242
Q

What is acute endocarditis caused by?

A

Highly virulent pathogens like staph aureus

243
Q

Staph aureus is most common cause of endocarditis in what demographic?

A

IV drug abusers

244
Q

Acute endocarditis like staph aureus is secondary to what?

A

Infection elsewhere

245
Q

What is state of valves that highly virulent bacteria like staph aureus inhabit?

A

Normal healthy

246
Q

What does acute endocarditis result in?

A

Large vegetations with rapid onset of symptoms due to destruction of valve

247
Q

Subacute endocarditis is caused by what?

A

Less virulent bacteria like strep viridans

248
Q

What is the most common cause of bacterial endocarditis?

A

Strep Viridans

249
Q

Subacute endocarditis occurs on what state of valves?

A

Previously damaged valves such as congenital heart disease or valvular heart disease

250
Q

What is result of subacute endocarditis?

A

subendocardium is exposed allowing for formation of thrombotic vegetations that do not destroy the valve.

251
Q

What allows for bacteria in subacute endocarditis to inhabit a valve?

A

Bacteremia such as during a dental procedure

252
Q

Staph epidermidis is most common in what?

A

Endocarditis of prosthetic valves

253
Q

Strep bovis is seen in what patients?

A

Endocarditis of patients with underlying colorectal carcinoma

254
Q

Endocarditis with negative blood cultures is due to what?

A

HACEK organisms

Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella

255
Q

Clinical features of bacterial endocarditis? 8

A

FROM JANE

  1. Fever
  2. Roth’s spots
  3. Osler nodes: Painful lesions on fingers/toes
  4. Murmur: Vegetations disrupt flow
  5. Janeway Lesions: nonpainful on palms/soles
  6. Anemia
  7. Nailbed hemorrhage
  8. Emboli (septic): Vegetations come off and lodge
256
Q

What valve is most frequently involved in bacterial endocarditis?

A

Mitral valve

257
Q

Tricuspid valve bacterial endocarditis is associated with what?

A

IV drug abuse (Don’t Tri Drugs)

258
Q

Lab features of bacterial endocarditis? 5

A
  1. Positive blood cultures
  2. Microcytic anemia: Low hemoglobin, low MCV
  3. Hepcidin traps iron
  4. Ferritin will be hidden (Low TIVC)
  5. TEE = best for detecting lesions on valves
259
Q

Nonbacterial thrombotic endocarditis is what?
Where do vegetations arise?
What do they cause?

A

Sterile vegetations that arise with hypercoagulable state or underlying adenocarcinoma

Mitral valve along lines of closure

Regurgitation

260
Q

Libman-Sacks endocarditis is what?

A

Sterile vegetations associated with SLE (lupus)

261
Q

What makes the vegetations in Libman-Sacks endocarditis special?
What does it result in?

A

Vegetations present on surface AND undersurface of mitral valve

Results in mitral regurgitation

262
Q

The cause of endocarditis of carcinoid syndrome is what?

A

Secretory products of carcinoid tumors (vasoactive peptides and amines)

263
Q

What does endocarditis of carcinoid syndrome result in?

A

Thickened endocardial plaques

264
Q

What is cardiomyopathy?

A

Disease of heart muscle that results in cardiac dysfunction

265
Q

What is most common form of cardiomyopathy?

A

Dilated cardiomyopathy (90%)

266
Q

Dilated cardiomyopathy involves dilation/stretching of what?

A

All four chambers of heart

267
Q

What are causes of dilated cardiomyopathy? (6)

A

MIDCAP BC

  1. Idiopathic (Most common)
  2. mutation (AD)
  3. Coxsackievirus
  4. Alcohol abuse
  5. Drugs: Doxorubicin, Cocaine
  6. Pregnancy: late or right after birth
  7. wet Beriberi
  8. Chagas disease
268
Q

Treatment of dilated cardiomyopathy?

A

Transplant

269
Q

Hypertrophic cardiomyopathy is what?

A

Massive hypertrophy of left ventricle

270
Q

What causes hypertrophic cardiomyopathy?

A

Genetic mutations in sarcomere proteins (autosomal dominant)

271
Q

Clinical features of hypertrophic cardiomyopathy? 3

A
  1. Decreased cardiac output: Too much muscle –> Lose compliance –> Diastolic dysfunction
  2. Sudden death due to ventricular arrhythmias
  3. Syncope with exercise: IV septum creates block in LV –> Blood can’t get out well
272
Q

What genetic disease is associated with hypertrophic cardiomyopathy?

A

Friedreich’s ataxia

273
Q

Microscopic features of hypertrophic cardiomyopathy?

A

Disoriented, tangled, hypertrophied myocardial fibers

274
Q

Treatment of hypertrophic cardiomyopathy?

A
  1. Beta blocker

2. Calcium channel blocker

275
Q

Restrictive cardiomyopathy is what?

A

Diastolic problem of not being able to fill due to decreased compliance of ventricular myocardium.

276
Q

Causes of restrictive cardiomyopathy?

A

A SHELF

Amyloidosis

Sarcoidosis: Granulomas in wall of heart
Hemochromatosis: Iron in wall of heart
Endocardial fibroelastosis: FIbrosis in endocardium
Loeffler Syndrome: Eosinophil infiltrate of heart
Fibrosis Postradiation

277
Q

Which cause of restrictive cardiomyopathy is seen in children?

A

Endocardial fibroelastosis

278
Q

How does restrictive cardiomyopathy present? (3)

A
  1. CHF: Can’t fill heart –> Backs up
  2. Low-voltage EKG
  3. Diminished QRS amplitudes
279
Q

Two cardiac tumor types?

A
  1. Myxoma

2. Rhabdomyoma

280
Q

Myxoma is what?

A

Mesenchymal proliferation with gelatinous appearance to tumor

281
Q

Myxoma has abundant what?

A

Ground substance

282
Q

Myxoma is most primary cardiac tumor in what demogrpahic?

283
Q

Can myocytes form tumors?

284
Q

How does myxoma present?

A

Pedunculated mass in left atrium obstructing the mitral valve –> Syncope

285
Q

What is rhabdomyoma?

A

Hamartoma of cardiac muscle

286
Q

Rhabdomyoma is most common primary cardiac tumor in what demographic?

287
Q

Rhabdomyoma is associated with what disease?

A

Tuberous sclerosis

288
Q

Where does rhabdomyoma grow?

289
Q

Are myxoma and rhabdomyoma benign or malignant?

290
Q

What is the most common heart tumor?

A

A metastasis

291
Q

Common metastases primary locations?

A
  1. Breast carcinoma
  2. Lung carcinoma
  3. Melanoma
  4. Lymphoma
292
Q

Metastases usually invade what layer of heart?

Resulting in what?

A

Pericardium

Pericardial effusion

293
Q

Myocarditis most often presents as what?

A

Biventricular heart failure in young people with no other major heart diseases

294
Q

Myocarditis morphological characteristics? 2

A
  1. Diffuse myocardial degeneration

2. Necrosis with inflammatory infiltrate

295
Q

Myocarditis has what etiology?

Specifically?

A

Viral

Coxsackievirus

296
Q

What causes myocarditis in south america?

A

Chagas disease

297
Q

What is hydropericardium?

A

Accumulation of serous transudate in pericardial space

298
Q

What causes hydropericardium?

Most often?

A

Anything that can cause systemic edema.

Hypoproteinemia like in nephrotic syndrome or chronic liver disease

299
Q

What is hemopericardium?

A

Accumulation of blood in pericardial sac

300
Q

What causes hemopericardium?

A

Traumatic perforation of heart or aorta by myocardial rupture associated with MI

301
Q

Five types of acute pericarditis?

A
  1. Serous
  2. Fibrinous/Serofibrinous
  3. Purulent/Suppurative
  4. Hemorrhagic
  5. Caseous
302
Q

Serous pericarditis is associated with what causes? (3)

A
  1. SLE
  2. Rheumatic fever
  3. Viral infections
303
Q

What is the liquid in acute pericarditis?

A

Protein-rich exudate with inflammatory cells

304
Q

What is fibrinous/serofibrinous pericarditis characterized by?

A

Fibrin-rich exudate

305
Q

What causes fibrinous/serofibrinous pericarditis? 5

A
  1. uremia
  2. Myocardial infarction
  3. ARF
  4. Dressler’s syndrome
  5. Radiation
306
Q

What is clinical finding in fibrinous/serofibrinous pericarditis?

A

Loud friction rub

307
Q

Purulent/suppurative pericarditis is characterized by what?

A

Inflammatory exudate

308
Q

What causes purulent/suppurative pericarditis?

A

Bacterial infection

309
Q

Hemorrhagic pericarditis is characterized by what?

A

Bloody inflammatory exudate

310
Q

What causes hemorrhagic pericarditis? 2

A
  1. Tumor invasion

2. TB or other bacterial infection

311
Q

Overall, acute pericarditis presents how? 5

A
  1. Sharp pain
  2. Aggravated by inspiration
  3. Relieved by sitting up and leaning forward
  4. Friction rub
  5. ST segment elevation or depression
312
Q

Chronic pericarditis has what etiology? 2

A
  1. TB

2. Pyogenic staph

313
Q

Characteristics of chronic pericarditis? 4

A
  1. Thickening and scarring of pericardium
  2. Loss of elasticity
  3. Mimics Right sided heart failure
  4. Proliferation of fibrous tissue
314
Q

Hypertrophy of left ventricle is caused by what? 2

A

HTN

Aortic or mitral valvular disease

315
Q

Hypertrophy of right ventricle causes? 4

A
  1. LV failure
  2. Chronic lung disease
  3. Mitral valve disease
  4. Congenital heart disease with L-2-R shunt
316
Q

Define cor pulmonale

A

Right ventircular hypertrophy secondary to prmary disease of pulmonary vasculature (P-HTN)

317
Q

What is cardiac tamponade?

A

Compression of heart by fluid in pericardium –> leading to decreased cardiac output.

318
Q

Findings in cardiac tamponade? 6

A
  1. Equilibration of diastolic pressure in all 4 chambers
  2. Hypotension
  3. Increased JVD
  4. Distant heart sounds
  5. Increase HR
  6. Pulsus paradoxus

Pathology (36 decks)

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