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Pathology II PCC > Chapter 10 > Flashcards

Chapter 10 Flashcards

1
Q
A

acute myocarditis

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2
Q
A

Chronic, hypersensitivity myocarditis

Multinucleate giant cells

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3
Q
A

Atrial septal defect

L to R

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4
Q
A

Patent ductus arteriosus

L to R

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5
Q
A

Ventricular Septal Defect

42%

L to R

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6
Q
A

myxoma

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7
Q
A

rheumatic valvular disease

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8
Q
A

calcific aortic stenosis

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9
Q
A

scarlet fever

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10
Q

what are the two leading causes of death in the US?

A
  1. heart disease
  2. cancer
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11
Q

what’s the MC mechanism of heart disease?

A

contractile (pump) failure

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12
Q

Why, when a patient has heart failure/CHF, can they not meet tissue demands?

A
  1. decreased cardiac output (MC)
  2. increased tissue demands (hyperthyroidism, severe anemia, fistula – ‘high-output failure’)
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13
Q

what dysfunctions cause decreased cardiac output?

A
  1. systolic dysfunction: weak contraction
  2. Diastolic dysfunction: failure of relaxation/filling; females
  3. valvular dysfunction: stenosis, endocarditis
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14
Q

what are the risks for systolic dysfunction?

A

CAD, systemic HTN, decreased pH

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15
Q

what are the risks for diastolic dysfunction?

A

Females

myocardial fibrosis, amyloidosis, left-sided hypertrophy, pericardial tamponade

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16
Q

what is forward failure? backward failure? are they typically found together or separate? what organs do they affect?

A

forward: insufficient output = hypoxia
backward: venous congestion – increased venous volume/pressure

forward failure is almost always combined with backward failure – affects virtually every organ

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17
Q

what are 3 adaptations that occur with the heart?

A
  1. Frank-Starling mechanism
  2. Neurohumoral mechanisms
  3. Cardiac hypertorphy
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18
Q

what is the Frank-Starling mechanism?

A

increased ventricular stretch = stronger contraction

benefit: increased output
cost: increased O2 , increased tension

compensated heart failure

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19
Q

what are neurohumoral mechanisms of heart adapation?

A

NE: increased heart rate, increased contractility, R-A-A system (increase BP)

ANP: vasodilation (balances NE)

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20
Q

Why does cardiac hypertrophy occur?

A

when the heart gets overloaded.

can be physiological or pathological

increases O2 consumption

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21
Q

what are the symptoms of left sided heart failure? right sided?

A

left sided: short of breath, fatigue

right sided: edema in legs (pitting edema) and liver failure

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22
Q

what is the ‘good’ type of cardiac hypertrophy? the ‘bad’ type? How can you tell the difference?

A

good: eccentric hypertrophy
bad: concentric hypertrophy

can tell the difference by looking at the ratio of wall to chamber size

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23
Q

what causes left-sided heart failure?

A

IHD (CAD), HTN, valve disorders (mitral & aortic), primary myocardial disease

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24
Q

once the left ventricle hypertrophies, what else in the heart can dilate? which causes what?

A

the left atria– atria fibrillation atrial thrombi (stroke)

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25
Q

what are symptoms of left sided heart failure?

A

pulmonary edema

dyspnea

rales (cracking in lungs)

orthopnea (drowning when lying down)

cough

tachycardia

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26
Q

what is right sided heart failure most commonly caused by?

A

left sided heart failure

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27
Q

what is cor pulmonale?

A

only right sided heart failure

happens following pulmonary HTN

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28
Q

how common is congenital heart disease? what increases the risk?

A

30% of birth defects

prematurity increases risks

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29
Q

What opening is present at birth that connects the right and left atrium?

A

foramen ovale

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30
Q

what opening is present at birth that connects the left pulmonary artery and the aorta?

A

ductus arteriosus

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31
Q

What is known to cause congenital heart disease?

A
  1. genetic: trisomies (13, 18, 21), polygenic
  2. Environment: teratogens, maternal diabetes, infxn
  3. 90% are idiopathic–> septal defects make up over half of the cases, MC is ventricular septal defects
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32
Q

What happens with right-to-left shunts? what causes it?

A

blood bypasses the lungs

cyanosis

causes: tetralogy of Fallot (MC) & transposition of great arteries

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33
Q

What happens with left-to-right shunts? what are examples of them?

A

pulmonary HTN

caused by ASD, VSD & PDA

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34
Q

What are examples of obstruction of flow congenital heart disease?

A

valvular stenosis and aortic coarctation (narrowing)

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35
Q

Details about atrial septal defects

A

left-to-right shunt

MC asymptomatic until adulthood

rare spontaneous closure

10% of malformations

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36
Q

details about ventricular septal defects

A

MC structural abnormality – 42%

Left-to-right shunt

may spontaneously close

only 20-30% in isolation

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37
Q

Details about patent ductus arteriosus

A

left-to-right shunt

90% isolated

7% of malformations

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38
Q

What is the most common CHD to cause cyanosis?

A

Tetralogy of fallot –>bypasses the lungs

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39
Q

What defects cause Tetralogy of Fallot?

A
  1. Ventricular septal defects
  2. Right ventricular outflow obstruction (subpulmonic valve stenosis)
  3. Overriding aorta (over VSD) –> between ventricles, right ventricle to aorta (right to left shunt)
  4. right ventricular hypertrophy
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40
Q

What causes a ‘boot-shaped’ heart?

A

tetralogy of fallot

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41
Q

What changes occur with transposition of the great arteries?

A

arteries connect to wrong ventricles

right ventricle –> aorta

left ventricle –> pulmonary artery

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42
Q

Why is transposition of the great arteries so serious?

A

it separates pulmonary & systemic circulation

its incomplatible with postnatal life– sunts are required

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43
Q

Who is most likely to have aortic coarctation?

A

males

turner syndrome (45, X)

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44
Q

what defect to the aortic valve can occur with aortic coarctation?

A

>50% also have a bicuspid aortic valve

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45
Q

With infantile aortic coarctation, where does it occur? adult?

A

infantile: proximal to a PDA
adult: infolding near the ligamentum arteriosum, MC asymptomatic

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46
Q

features of aortic coarctation

A

upper extremity HTN

weak LE pulses

LE vascular claudication & cyanosis

systolic murmurs/thrills

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47
Q

with ischemic heart disease, what happens to the myocytes? how long until dysfunction? necrosis?

A

the cardiac myocytes use oxidative phosphorylation

dysfunction: 1-2 minutes
necrosis: 20-40 minutes

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48
Q

What disease makes up 90% of IHD? What else can cause IHD less commonly?

A

coronary artery disease – atheromas thromboemboli, vasospasm

also caused by increased tissue demand, decreased BV or hypoxia

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49
Q

What is the leading cause of death in the US, specifically?

A

Ischemic Heart Disease – CAD, pneumonia, CO poisoning, A-V fistula

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50
Q

What are cardiac syndromes the result of?

A

Myocardial ischemia

51
Q

What are the forms of acute coronary syndrome?

A

angina pectoris– chest pain; ischemia but NO cellular death

acute myocardial infarction (M.I.)

Chronic IHD –> CHF

sudden cardiac death (SCD)

52
Q

Angina pectoris means how much occlusion? Unstable angina?

A

Angina pectoris: >70% occluded –> critical stenosis

unstable angina: > or equal to 90% occluded

53
Q

What is the process of ischemic heart disease?

A
  1. inflammation – atherosclerosis, abrupt plaque changes
  2. Thrombosis – associated with ACS, sudden coronary artery occlusion
  3. Vasoconstriction– decreased arterial lumen, may rupture plaques –>risks: increase SNS, inflammation, endothelial dysfunction
54
Q

What do people describe as having ‘an elephant on their chest’?

A

angina pectoris

sub-sternal chest pain: crushing & squeezing

referred: jaw, left arm, back, shoulders

55
Q

Stable vs. variant angina vs. Unstable

A

stable: aka typical, episodic, exertional, relieved by rest and vasodilators
variant: aka Prinzmetal, vasospasm at REST, responds to vasodilators
unstable: aka crescendo/pre-infarction angina, increased frequency, intensity and duration; provoked by **decreased exertion, **90% occlusion

56
Q

cause of unstable angina

A

plaque disruption

thrombosis

embolization

vasospasm

57
Q

Angina pectoris in females

A

may have NO angina

dyspnea, unexplained fatigue

lower chest discomfort/pressure

back pain

nausea, dizziness

may mistake for an upset somach

58
Q

what’s another name for heart attack?

A

myocardial infarction

59
Q

what is the mc cause of MI?

A

90% cause by acute coronary artery thrombosis

pre-existing atheroma: rupture –> vasospasm & coagulation –> rapid/severe obstruction

60
Q

T/F: Myocardial infarctions cause rapid death and loss of contractility

A

F: MI cause rapid DYSFUNCTION and loss of contractility

61
Q

what are the risks for MI?

A

males

PM females

age

HTN

smoking

diabetes

sickle cell disease

amyloidosis

CHF (stasis)

62
Q

What is the most common cause of sudden cardiac death?

A

Ventricular fibrillation (80-90%)

63
Q

T/F: MI can cause arrhythmias

A

T: it can lead to coronary artery ischemia and cause electrical instability which can lead to ventricular fibrillation

64
Q

Reperfusion with myocardial infarction: how is it done? what does it cause?

A

Artifically done by thrombolytic meds, angioplasty and bypass

causes ROS, hemorrhage and endothelial swelling –> blocks capillaries, temporarily ‘stunned’ myocardium

may need temporary pump assistance

65
Q

What is special about the angina associated with Myocardial Infarction?

A

Unrelieved by nitroglycerine

66
Q

How are Myocardial infarctions diagnosed in the laboratory?

A

CK-MB and troponins

67
Q

after a myocardial infarction, what happens to the viable myocarium left? to the functioning of the heart?

A

it is overloaded

hypertrophy and dilation occurs which leads to failure

walls may rupture

contractile dysfunction – arrhythmia, CHF, cardiogenic shock

general pericarditis

68
Q

prognosis of M.I.

A

poor

2nd MI

arrhythmia (SCD)

CHF

69
Q

What is sudden cardiac death?

A

sustained arrhythmia

lethal arrhythmia: MC involves left ventricle

sudden unexpected death

no symptoms in previous 24 hours

typically caused by Ventricular fibrillation (MC) or asystole

70
Q

Commotio cordis

A

blow to sternal region disrupts heart rhythm

Adolescent males: avg 15 years

71
Q

What happens to the heart with hypertensive heart disease?

A

the heart hypertrophies to meet increased cardiac demands, the ventricles dilate

metabolic demand increases with no increase in blood supply to compensate

cardiac decompensation (CHF) –> eventual loss of contractility

72
Q

systemic hypertensive heart disease causes what other heart disease?

A

left sided heart disease, left ventricular hypertrophy

73
Q

what can help decrease the risks of systemic hypertensive heart disease?

A

blood pressure management– hypertrophy is reversible

74
Q

how does pulmonary hypertension affect the heart?

A

causes right sided heart failure – cor pulmonale

right ventricle hypertrophy and early dilation

75
Q

what can cause pulmonary hypertensive heart disease?

A

pulmonary fibrosis

cystic fibrosis

PE

kyphoscoliosis

76
Q

what causes acute pulmonary hypertensive heart disease?

what causes chronic pulmonary hypertensive heart disease?

A

acute: large pulmonary embolism; >50% occlusion
chronic: prolonged COPD or pulmonary fibrosis, right sided hypertrophy

77
Q

what are 2 types of valvular heart disease?

A
  1. stenosis
  2. insufficiency
78
Q

What causes stenosis? what is MC affected?

A

calcification and scarring

chronic

mitral valve is MC

79
Q

What causes insufficiency?

A

valvular destruction

abnormal suportive structures

80
Q

What is a murmur?

A

turbulent flow through diseased valve

Thrill: turbulence –> palpable vibration

81
Q

what is the MC cause of aortic valve stenosis?

A

calcific aortic stenosis

82
Q

what population does calcific aortic stenosis commonly occur in? what accelerates it? what condition changes the age group?

A

older adults –> 60-80 years old because of wear and tear

accelerated by HTN and inflammation

having a bicuspid aortic valve makes it occur earlier– 40-50 years

83
Q

rheumatic valvular disease is caused by what? when does it occur (time period)?

A

group A beta-hemolytic streptococcal pharyngitis

occurs 2-3 weeks post infection

84
Q

what is the most common sign in children with rheumatic valvular disease?

what is the most common sign in adults with rheumatic valvular disease?

what’s a general symptom of rheumatic valvular disease?

A

carditis

migratory polyarthritis

Sydenham’s chorea

85
Q

when is rheumatic valvular disease most commonly diagnosed?

A

between 5-15 years old

86
Q

What is the only acquired cause of mitral stenosis?

A

Rheumatic valvular disease

87
Q

What is pancarditis?

A

rheumatic heart disease

88
Q

what are aschoff bodies? where are they most commonly found?

A

nodules around the heart valve

found with acute pancarditis

MC found in the mitral valve

89
Q

what changes, of the heart specifically, occur with rheumatic valvular disease?

A

aschoff bodies (acute)

fibrosis (chronic)

fibrinoid necrosis of valve(s)

possible arrhythmias

90
Q

what causes scarlet fever? what is it a rxn to? where does the infxn occur?

A

Group A beta-hemolytic strep

it’s a rxn to erythrogenic toxins

infection is pharyngeal and cutaneous

1-4 days

91
Q

What is the hallmark of scarlet fever?

A

pink punctate skin rash

circumoral pallor rash on face

strawberry tongue

92
Q

What condition can scarlet fever transition into?

A

rheumatic fever

93
Q

infective endocarditis causes what?

A

infection of hear chambers or valves

bacteremia (MC)

94
Q

what are the symptoms of infective endocarditis?

A

flu-like symptoms: pyrexia, chills, fatigue, weight loss, murmur

or lethal: arrhythmia or renal failure

95
Q

which is easier to treat: acute or subacute infective endocarditis? why?

A

subacute has low virulence and is easier to treat –> present in previously abnormal tissue

acute is destructive, virulent and difficult to treat –>present in previously normal valve

96
Q

why are prosthetic cardiac valves used?

A

used as an intervention for valve disease

types:

  1. Mechanical (MC) –anti-coagulative
  2. Bioprosthetic– not anti-coagulative
97
Q

cardiomyopathy are mostly caused by:

A

they’re idiopathic, with genetic risks

98
Q

what is the most common type of cardiomyopathy? least common type?

A

MC: Dilated

LC: restrictive

99
Q

What physiologically happens with dilated cardiomyopathy?

A
  1. progressive dilation of all chambers
  2. systolic dysfunction: dyspnea, fatigue
100
Q

What condition mimics progressive CHF?

what are the risks for the answer above?

age group?

A

dilated cardiomyopathy

risks: genetics, viral infections, alcohol

20-50 years old

101
Q

What conditions can occur with dilated cardiomyopathy?

A
  1. mitral regurgitation
  2. Arrhythmia
  3. Thromboemboli
102
Q

Which cardiomyopathy is genetic?

A

Hypertrophic cardiomyopathy, beta-myosin mutation

103
Q

What are the signs of hypertrophic cardiomyopathy?

A
  1. Hyper-contractile sarcomeres
  2. Massive Left ventricular hypertrophy
  3. Diastolic dysfunction
  4. decreased stroke volume/CO
104
Q

What condition has asymmetrical septal hypertrophy?

A

hypertrophic cardiomyopathy

ventricular septum > ventricular wall

105
Q

With hypertrophic cardiomyopathy, what does the heart ventricle look like?

When does it typically occur?

A

elongated –> ‘banana like’

after puberty–> growth spurt

106
Q

What causes 1/3 of SCD among younger athletes?

A

Hypertrophic cardiomyopathy –> V-fib

107
Q

What are the symptoms of restrictive cardiomyopathy?

A

interstitial fibrosis: stiff myocardium

dyastolic dysfunction = decreased filling

45-90% ejection fraction

108
Q

What can cause restrictive cardiomyopathy? who’s at most risk for each cause?

A
  1. Amyloidosis: senile cardiac amyloidosis –>african americans
  2. Endomyocardial fibrosis: fibrosis of the ventricular endocardium, pediatrics/young adults in Africa
  3. Etc: irradiation, idiopathic
109
Q

What is the MC cause of myocarditis in the USA?

A

viral infection: coxsackievirus A & B, HIV, CMV and influenza

110
Q

What very serious condition does myocarditis cause?

A

arrhythmia/SCD

111
Q

Histology wise, what is the difference between acute and chronic/hypersensitivity myocarditis?

A

Chronic/Hypersensitivity myocarditis has multinucleate giant cells

112
Q

Which is more common, acute or chronic/hypersensitivity myocarditis?

A

Acute

113
Q

What is pericarditis? What causes primary pericarditis? Secondary?

A

pericarditis is pericardial inflammation

Primary: infection – viral (MC), bacterial, fungal

Secondary: MI, surgery, irradiation, rheumatic fever, SLE, CA

114
Q

what can severe pericarditis cause? What causes constrictive pericarditis?

A

cardiac tamponade- pericardial compression (decreased filling)

fibrosis causes constrictive pericarditis

115
Q

What type of inflammation occurs with pericarditis? what does that mean?

A

Fibrinous inflammation– severe increased permeability allows fibrin out of circulation

116
Q

T/F: MC metastasis to the heart is the MC cardiac neoplasm

A

True

117
Q

Cancer from where most commonly mets to heart?

A

Lung

118
Q

most common primary cardiac neoplasm?

A

Myxoma

119
Q

primary cardiac neoplasm of children

A

rhabdomyomas

120
Q

what is the MC primary malignant cardiac tumor?

A

Angiosarcoma

121
Q

where are Myxomas MC found?

what valve does it MC interfere with?

A

MC found on/near fossa ovalis (left atrium)

‘wrecking ball’ that interferes with MITRAL valve

122
Q

What is the MC long-term limitation of cardiac transplantation?

A

Allograft arteriopathy– silent MI

123
Q
A

Pathology II PCC (7 decks)

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