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CPR Exam 1 > Heart PT 2 > Flashcards

Heart PT 2 Flashcards

1
Q

Rhythmic disorders are most caused by?

A

ischemia

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2
Q

What is sick sinus syndrome and what does it cause

A

SA node is damaged d/t ischemia => causing bradycardia

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3
Q

What is a-fib? What can it cause and describe the heartbeat?

A
  • Sporadically depolarizing atrial myocytes d/t atrial dilation, causing variable transmission through the AV node, which can cause clots and an irregular irregular heartbeat
    • Thus, give blood thinners
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4
Q

What is an AV block?

A

Fucked up AV node causes abnormal heart rhythm that causes the heart to beat too slowly (heart block)

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5
Q

What is the difference between first, second and third degree heart block?

A
  • First degree heart block has a prolonged PR interval
  • Second degree heart block has intermittent transmission
  • Third degree heart block has complete heart failure.
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6
Q

What causes arrhythmias?

A
  • Abnormalities in structure of gap junction/ spatial relationship,
  • Ischmia/hypertrophy/ inflammation,
  • Amyloid deposits or scarring/
  • Genetics (AD)
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7
Q

What is the most common inherited arrhythmogenic disease?

A
  • Long QT syndrome: arrythmias d/t with too much prolongation of cardiac repolarization d/t K+/Na+ channelopathy
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8
Q

Most common inherited arrhythmogenic disease have what pattern of genetic inheritance?

A

AD

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9
Q

What are 4 genes implicated in long QT syndrome?

A
    • KCNQ1
    • KCNH2
    • SCN5A
    • CAV3
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10
Q

Long QT syndrome is associated with ____ of K+ channels or _____ of Na+ channels

A

LOF of K+

GOF of Na+

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11
Q

arrhythmias associated with short repolarization intervals.

What is this and what can patients experience

A

Short QT syndrome

palpitations, syncome, sudden cardiac death

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12
Q

What syndrome has ECG abnormalities (ST-elevation; RBBB) without a structural defect in the heart?

What do they present with?

A

Brugada syndrome;

-syncope/SCD during rest, sleep or large meals

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13
Q

Pablo came into ER and was pronounced death after an unexpected cardiac cause within 24 hours of onset of symptoms. What can we diagnose this patient as? Are symptoms always required?

A
  • Sudden cardiac death (SCD)
  • No
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14
Q

Pablo was diagnosed with SCD (sudden cardiac death). SCD is due to?

A

fatal arrhythmia d/t damage of the myocardium d/t ischemia.

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15
Q

Pablo, who suffered from SCD, was able to be resuscitated. Based on statistics, what will his lab/ECG show?

A
  • 80-90% of resuscitated patients have NO lab or ECG changes because they have no long-term damage.
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16
Q

What is the leading cause of SCD?

A
  • CAD in 80-90% of patients: patients will usually have >75% stenosis of 1 or more of 3 main coronary arteries.
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17
Q

What is OFTEN first sign of IHD (ischemic heart disease)?

A

Sudden cardiac death :(

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18
Q

Hypertrophy of the heart is an adaptive response to chronically elevated pressures; with continued overload, the result can be

A

dysfunction, dilation, CHF or SCD.

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19
Q

What criteria are required to diagnose a patient with left-sided hypertensive heart diseases (systemic hypertensive heart disease)?

A
  • 1. HTN
    1. LV hypertrophy that is concentric w no other probs => decrease lumen size
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20
Q

In systemic hypertensive heart disease, how will the heart adaptively response?

A
  • Wall of LV thickens to more than 1.5 cm => weighs more than 500 grams.
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21
Q

In Systemic (left-sided) HHD as the LV wall continues to increase in thickness, what associated morphological changes occur?

A
  • ↑ interstitial CT –> stiffness = impaired diastolic filling; LV does not fill with blood –> LEFT ATRIAL ENLARGEMENT => a-fib
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22
Q

In many pt’s, systemic HHD comes to attention due to what signs/sx’s?

A
  • L atria enlarged => causes A-fib => leads to CHF, a risk factor for SCD.
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23
Q

Isolated pulmonary (right-sided) HTN heart disease (cor pulmonale) arises in the setting of what?

A
  • Pulmonary HTN
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24
Q

What is the most common cause of pulmonary HTN?

A
  • Left-sided heart disease.
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25
Q

How can we distinguish whether right-sided hypertensive disease (pulmonary hypertensive disease) is acute or chronic?

A
  • Acute pulmonary HHD is caused by a large PE => pulmonary HTN => RV dilation w/t hypertrophy
  • Chronic pulmonary HHD is caused primary pulmonary HTN or chronic dz that affects parynchma (COPD, CF, emphysema) => pulmonary HTN => RV wall thickens
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26
Q

Aubrey comes in and we suspect pulmonary HHD. What morphological changes will tell us whether or not it is acute or chronic?

A
  • Acute: RV dilation without hypertrophy
  • Chronic: RV wall thickens
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27
Q

What are 5 diseases affecting the lung parenchyma => cor pulmonale?

A

1. COPD

2. Diffuse pulmonary intersitial fibrosis

3. Pneuoconiosis

4. CF

5. Bronchostasis

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28
Q

________ can lead to cor pulmonale because of the physical pressure on the rib cage from being hunched over.

A

Kyphoscoliosis

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29
Q

Pathologic changes of valves include what 3 types?

A
  1. Damage to collagen that weakens leaflets
    1. Mitral valve prolapse
  2. Nodular calcification that beings in interstitial cells
  3. Fibrotic thickening
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30
Q

Why are valves so vulnerable to damage?

A
  • Because they are so thin and receive nourishment via diffusion, they have little BS.
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31
Q

When do we begin to clinically notice a valvular disease?

If chronic, what can these diseases cause

A

when they begin to cause clinical problems.

  1. Stenosis
    1. Stenosis is stiffening/thickening of a valve, causing failure of a valve to open completely, which disrupts forward flow.
    2. Chronic stenosis can cause what? Pressure-overload hypertrophy => CHF
  2. Insufficiency/regurgitation/incompetence
    1. Insufficiency: valve does NOT CLOSE completely, which reverses flow
    2. Chronic regurgitation may cause volume-overload hypertrophy => CHF
  3. Both
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32
Q

Other words for regurg

A
  1. incompetence
  2. insuffiiency
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33
Q

Chronic stenosis** may cause what type of overload hypertrophy vs. **chronic insufficiency?

A
  • Chronic stenosis = cause pressure-overload hypertrophy
  • Chronic insufficiency= cause volume- overload hypertrophy
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34
Q

Incompetence of a valve due to a abnormality in one of its support structure, NOT the valve itself is called?

A
  • Functional regurgitation
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35
Q

Functional mitral valve regurg is clinically important in what 2 conditions?

A
  1. IHD
  2. Dilated cardiomyopathy
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36
Q
  1. What is the major etiology causing mitral stenosis?
A
  1. Rheumatic heart disease (post-inflammatory scarring)
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37
Q
  1. What is the major etiology causing mitral regurgitation?
A
  • Problems in leaflets/commissures due to: post-inflammatory scarring and infective endocarditis
  • Mitral valve prolapse
  • Drugs
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38
Q
  1. What is the major etiology causing aortic stenosis?
A
  1. Abnormalities in leaflets/commissures due to rheumatic heart disease (RHD)
  2. Senile calcification aortic stenosis
    1. Normal aortic valve that undergoes calcification. Thus, not bicuspid
  3. Calcification of a congenitally deformed valve (bicuspid or unicuspid)
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39
Q
  1. What is the major etiology causing aortic regurgitation?
A
  1. RHD that causes post-inflammatory scarring => damages leaflets and commissures
  2. Aortic insufficiency: dilation of ascending aorta, often due to HTN or aging.
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40
Q

Abnormalities of the tensor apparatus that cause aortic Regurgitation may be caused by what 4 things?

A

a. -Syphilitic aortitis *

b. Ankylosing spondylitis
c. Rheumatoid arthritis

d. Marfan Syndrome *

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41
Q

What is aortic insuffiency?

A

Dilation of ascending aorta, often d/t a HTN or aging => can cause aortic regurg

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42
Q

Aortic stenosis is a stiff aortic valve, causing obstruction of _________outflow and decrease ____. Thus, it is a ____ problem.

A
  • LV outflow
  • CO
  • systemic => decrease blood going to body
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43
Q

3 cardiac signs of aortic stenosis.

A
  1. Exertional dizziness or syncope
  2. Exertional dyspnea
  3. Exertional angina
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44
Q

What is the most common valve abnormality?

A
  • Calcific aortic stenosis; mounds of calcification prevent the cusps from completely opening.
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45
Q

When are you most likely to get calcific aortic stenosis and what is it usually due to?

A
  • 60-80 yo
  • “Wear and tear” due to. w/ chronic HTN, hyperlipidemia, and inflammation
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46
Q

Calcification, leading to aortic stenosis of previously normal valve differs in onset from calcification of a abnormal bicuspid aortic valve (BAV) how?

A

Senile calcific aortic stenosis occurs 60-80 YO, however if the patient has a bicuspid valve, onset occurs 1-2 decades earlier because it faces more stress.

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47
Q

How does valve injury of calcific aortic stenosis differ from atherosclerosis?

A

Abnormal valves contain osteoblast-like cells–> make bone matrix and deposit Ca2+=> ossifies

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48
Q

In contrast to rheumatic (and congenital) aortic stenosis, what are 2 major differences seen in nonrheumatic, calcific aortic stenosis?

A
    • Commissural fusion is NOT usually seen
    • Mitral valve = normal
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49
Q

What are the 3 main symptoms of calcific aortic stenosis? What do you see on XR?

A
  1. Angina
  2. CHF
    1. Patients with calcific aortic stenosis + CHF will die in 2 years
  3. Syncope
  4. On XR, patients will have LV hypertrophy d/t increased pressure
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50
Q

If present, which site on the cusp is a major site of Ca2+ deposits in those with congenital bicuspid aortic valves (BAV)?

A

Midline raphe

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51
Q

Calcium deposits in the mitral valve tend to accumulate in the _______, resulting in _______\_

A
  • Fibrous annulus
  • Mitral annular calcification
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52
Q

As opposed to the cuspal involvement in aortic valve calcification, where do calcific deposits occur in the mitral valve?

A

Mitral annulus

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53
Q

What is the gross morphology of the calcific deposits in mitral annular calcification?

A
  • Irregular, stony, hard ulcerated nodules.
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54
Q

How does mitral annular calcification affect valve function?

A

Valve function is usually NOT affected. However, it can cause:

    1. Stenosis by preventing opening
    1. Regurg by impaiing physio contraction
    1. Arrhythmia and sudden death if Ca2+ deposits fuck with the AV node
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55
Q

Ca2+ nodules in mitral annular calcification may provide a site for what complications?

Pt’s are at greater risk for what?

A

for thrombi or infective endocarditis

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56
Q

Mitral annular calcification is most common who?

A
  • Females over 60 with mitral valve prolapse.
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57
Q

Mitral valve prolapse has a higher incidence in what gender?

A

F (7:1)

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58
Q

Mitral Valve Prolapse is often discovered incidentally by hearing what during ausculation?

A

Mid systolic click sometimes followed by mid-to-late systolic murmur

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59
Q

What occurs to the valve leaflets in Mitral Valve Prolapse?

A

“Floppy” leaflets balloon back into the LA during systole

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60
Q

Which heritable disorder of CT is associated with Mitral Valve Prolapse?

A

Marfan Syndrome

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61
Q

The leaflets in Mitral Valve Prolapse become thickened and rubbery due to what?

A
  1. Deposits of proteoglycans (myxomatous degeneration)
  2. Fucking up of elastic fibers
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62
Q

What is the characterstic anatomic change in mitral venous prolapse?

A

Interchordal ballooning (hooding) of mitral leaflets

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63
Q
  • Majority of patients with Mitral Valve Prolapse are asymptomatic, but a small minority may develop which 4 serious, but RARE complications?
A
  • 1. Infective endocarditis
    1. Mitral insufficiency
    1. Stroke or thromboembolism
    1. Arrythmias
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64
Q

2’ changes reflecting the stresses and tissue injury incident to the billowing leaflets in mitral valve prolapse include thickening of what 3 structures?

A
  • Fibrous thickening of valve leaflets
  • Linear fibrous thickening of LV endocardial surface
  • Thickening of the mural endocardium of the LV or LA
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65
Q

How can the diagnosis/confirm of mitral valve prolapse be made?

A
    • Auscultation
    • Confirmed w/ Echocardiography
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66
Q

What is the most common cause for mitral valve surgery in the US?

A

MVP (mitral valve prolapse)

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67
Q

Rheumatic heart disease is virtually the only cause of what cardiac disorder?

A

mitral stenosis

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68
Q

What is rheumatic fever?

A

autoimmune reaction (type 2) that causes inflammation of joints, muscles and fibrous tissue. I can damage heart muscle => lead to rheumatic heart disease.

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69
Q

What is the pathogenesis of RF?

A
  • CD4+ T cells that attack M-proteins on group A strep cross-react with cardiac self-antigens in a processes called molecular mimicry.
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70
Q

What bacteria causes rheumatic fever and when does it occur?

A
  • Weeks after streptococcal pharyngitis “strep throat” due to group A strep.
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71
Q

Rheumatic heart disease is most common in who?

A

chilren

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72
Q

When does acute RF occur and what enzymes can we detect in these patients?

A
  • 10 days – 6 weeks after group A strep
  • Anti-streptolysin O
  • Anti-Dnase B
73
Q

How do we diagnose rheumatic fever?

A
  • JONES CRITERIA
    • Joints: polyarthritis in at least 5 joints
    • <3: Carditis: valvulitis, myocarditis, pANcarditis
    • Nodules; subcutaneous
    • Erythema marginatum (ring rash) on the trunk
    • Sydenham chorea: a jerking movement disorder
74
Q
  • Rheumatic heart disease is damage to the heart valves by rheumatic fever. __________ is most commonly affected
A

mitral valve

75
Q

What are the distinctive lesions found in the heart during acute RF, and what do these lesions consist of?

A
  • Pancarditis (inflammation of ENTIRE heart) with aschoff bodies (granuloma inflammation with giant cells) with:
    • T-cells
    • Plasma cells
    • Anitschow cells (“caterpillar cells” activated MO that look wavy)
  • Fibrinoid necrosis of the endocardium and left sided valves with vegetations (verecae
    *
76
Q

Which cells are pathognomonic for RF?

A
  • Anistchow cells (activated MO) located in aschoff bodies.
77
Q

What changes do we see in the heart and valves with acute rheumatic fever.

A
  1. Fibrinoid necrosis of endocardium
  2. Vegetation of fibrin and platelets on left-sided valves (mitral and aortic) called verrucae, that overlie necrotic area.
78
Q

What heart changes occur in chronic rheumatic heart disease?

A

mitral stenosis

  • Mitral leaflets become thicker and can fuse together (commissural fusion)
    • Chordae tendineae become thick and short and fuse
  • LA enlarges > a-fib
79
Q

With tight mitral stenosis seen in RHD what compensatory changes occur in the left atrium and it may harbor what?

A

Left atrium DILATES and may harbor mural thrombi that can embolize

80
Q

Chronic RHD can lead to what changes in the LUNGS, that will result in…

A

Pulmonary congestion => RV hypertrophy

81
Q

Which 2 antibodies to streptococcal enzymes may be detected in the sera of pt with RF?

A

anti-streptolysin 0

anti DNAse B

82
Q

What is infective endocarditis?

A
  • infection of the endocardium and heart valves that forms vegetations (made up of microbes and debris) underlying tissue damage.
83
Q

How are acute IE and subacute IE different from one another? and txs

A
  • Acute IE is a RAPID infection of a previously NORMAL valve.
    • Treatment: surgery + ABX
  • Subacute IE is slower infection of a previously DEFORMED valve.
    • Treatment: ABX
84
Q

How does acute infective endocarditis differ from subacute infective endocarditis in the type of organism involved?

A

§ - Acute IE = infection by highly virulent bacteria (i.e., S. aureus)

§ - Subacute IE = infection w/ lower virulence bacteria (i.e., Viridians strep)

85
Q

What are 6 predisposing conditions which increase the risk of developing infective endocarditis?

A
  • Valvular abnormalities: such as
    • prosthetic valves
    • RHD
    • MV prolapse
    • calcific stenosis/bicuspid AV
  • Bacteremia (dental work, infection, contaminated needle)
86
Q

The most important among the risk factors for infective endocarditis are those that can cause microorganisms to do what?

A

get into bloodstream (bacteremia/fungemia) => spread infection

87
Q

Which organism is most often responsible for infective endocarditis of native but previously damaged or abnormal valves?

A

Streptococcus viridians

88
Q

Which bacteria is responsible for a majority of the mortality associated with infective endocarditis and is common in IV drug abusers?

89
Q

Which bacteria is causes infectious endocarditis in those with prosthetic valves?

A
  • S. epidermidis (coagulase-neg staph)
90
Q

Which organisms are implicated in infective endocarditis?

A
  • HACEK (gram - bacteria)
  • Hemophilus, actinobacillus, cardiobacterium, eikenella, kingella
91
Q

IE causes vegetations to build up on endocardium and valves.

What valve is most commonly affected?

A
  • Left-sided valves (aortic and mitral)
  • Right-sided valves in IV drug users (tricuspid and pulmonary)
    • Don’t “tri” drugs.
92
Q

Describe the vegetations IE caues and what they can result in.

A
  • Friable, bulky and destructive valvular vegetations
  • Left sides valves (mitral and aorta) => septic emboli
  • Right sided valves (tri/pul) => pulmonary empolism
93
Q

Microscopically, the vegetations of subacute IE typically exhibit what that is indicative of healing?

A

granulation tissue, which can fibrosis and calcify

94
Q

What is the clinical presentation (signs/sx’s) of infective endocarditis?

What may be heard upon auscultation in a patient with IE.

A
    • Rapidly developing fever + Chills
    • Weakness + Malaise
  • - Left sided IE = MURMUR
95
Q

What are the 4 major forms of vegetative endocarditis?

in RHD, IE, LSE, and NBTE

A
  1. Rheumatic heart disease
    1. Small vegetations that look like warts along the line of valve closure
  2. Infective endocarditis
    1. Large irregular masses on cusps that extend into chordae
  3. Non-bacterial thrombotic endocarditis (NBTE)
    1. Small vegetations on line of closure
  4. Libman-sacks endocarditis (LSE)
    1. Small or medium sized vegetation on both side of valve leaflet (often involving the mitral valve)
    2. Assx with SLE
96
Q

What happens if a vegetation in infective endoarditis erodes into underlying tissue?

A

Ring abcess

97
Q

Which type of infective endocarditis is more likely to form emboli? What can these emboli cause

A
  • Acute IE
  • Septic infarcts or mycotic aneurysms
98
Q

What are signs of IE?

A
  • FROM JANE
  • Fever
  • Roth Spots: retinal hemorrhages in eye w pale centers
  • Osler nodes (subcutaneous nodes on fingers and toes that persist for hours/days)
  • Murmur (if left-sided IE)
  • Janeways lesions: non-tender lesions on palms or soles
  • Anemia
  • Nail-bed hemorrhage: splinter
  • Emboli
99
Q

Although non-bacterial thrombotic endocarditis (NBTE) has small, sterile vegetations along the line of closure that are not invasive** and **not inflammatory, why can they pose a problem?

A
  • They are loosely attached and can emboli => produce infarcts
100
Q

NBTE (non-bacterial thrombotic endocarditis) has a striking association with what?

A

MUCINOUS ADENOCARCINOMAS

101
Q

carcinoid syndrome; what is it?

A

a paraneoplastic syndrome that causes SOB (bronchoconstriction), flushing of face, diarrhea and dermatitis d/t release of 5HT from carcinoid tumors

102
Q

50% of pts with carcinoid syndrome develop carcinoid heart disease, what part of the heart is more protected and why?

A

Right endocardium and valves because the L side is protected by the lungs metabolizing 5HT and mediators

103
Q

Cardiac lesions of carcinoid syndrome ususally only occur after there is a massive burden where and why?

A

Liver, because the liver metabolizes 5-HT before it reaches the heart.

104
Q

What is the morphology of cardiac lesions that occur in carcinoid heart disease?

A
  • Mucopolydsacchardie builds up on endocardium and valve= > producing glistening plaque-like intimal thickenings
105
Q

What is the major complication associated with the use of mechanical prosthetic valves?

A

Thromboembolism –> thrombotic occlusion of the prosthesis or emboli released from thrombi formed on the valve

106
Q

Due to the major risk of thromboembolism associated with mechanical prosthetic valves, what long-term therapy must be given?

A

Long-term anti-coagulation tx

107
Q

Which type of prosthetic valve (mechanical or bioprostheses) almost always undergoes structural deterioration?

A

Almost ALL bioprostheses eventually become incompetent due to calcification and/or tearing

108
Q

Pt’s with mechanical prosthetic valves must be on long-term anticoagulant therapy to prevent thromboembolism, but this puts them at a risk of what complication?

A

Hemorrhagic stroke

109
Q

Infective endocarditis is a potentially serious complication associated with what type of prosthetic valve (mechanical or bioprostheses)?

110
Q

Cardiomyopathy is a disease of the _______ (_______disease).

  • ________ cardiomyopathy: occurs when disease of myocardium is genetic or acquired.
  • _______ cardiomyopathy: occurs when cardiomyopathy occurs to compensate for another disease.
A
  • myocardium (heart muscle disease)
  • Primary
  • Secondary
111
Q

What are our cardiomyopathies? 6

A
    1. Dilated
    1. Hypertrophic
    1. Restrictive
    1. Takotsubo
    1. Arrhythmogenic RV cardiomyopthy (ARVC)
    1. Amyloid
      *
112
Q

The mechanism of heart failure in dilated cardiomyopathy (DCM) is an impairment in what?

A

Contractility (systolic dysfunction)

113
Q

The mechanism of heart failure in hypertrophic and restrictive cardiomyopathy is an impairment in what?

A
  • Compliance (diastolic dysfunction)
    • Compliance=> how easily something expands when it fills with blood
114
Q

90% of cardiomyopathies are of what kind?

What is the least common?

A

Dilated cardiomyopathy

Least: Restrictive

115
Q

What is a dilated cardiomyopathy?

A
  • Dilation of all 4 chambers and dilation hypertrophy => causing systolic dysfunction, because the heart now has a problem contracting.
116
Q

What are the common gross morphological features of Dilated CM?

Which type of thrombi are common and valvular alterations?

A
  • All 4 chambers are dilated & interstitial fibrosis
  • Mural thrombi
  • No innate problems w valves; but functional regurg can occur
117
Q

Familial cases of dilated cardiomyopathy (30-50%) are linked to mutations in what gene?

Major inheritance pattern?

118
Q

Dilated cardiomyopathy typically manifests during what ages? What signs or sxs does it present with?

A
  • 20-50 YO
  • Slowly progressive signs of CHF => dyspnea, easy tired and decrease EJ
119
Q

What does it mean that DCM causes a systolic dysfunction?

A
  • If you stretch the heart => will not be able to contract properly => will not empty => biventricular CHF
120
Q

Most commonly, DCM is idiopathic. Other causes include what?

A
  1. Alcohol
  2. Myocarditis d/t coxsackie B
  3. Drugs: doxorubicin, cobalt, iron overload d/t hereditary hemochromatosis (HFE mutation)
121
Q

Myocarditis can progress to what type of cardiomyopathy and is often associated with what virus?

A
  • DCM; coxsackie B
122
Q

What serious complications are associated with dilated cardiomyopathy?

A
  • Thrombus 2’ to stasis –> embolism (stroke)
  • Arrhythmias –> sudden cardiac death
123
Q

What is “broken heart syndrome”?

A
  • Takotsubo cardiomyopathy is a dilated cardiomyopathy of the LV(octopus trap) that occurs afterextreme emotionsorpsychological stress d/t too much catecholamines.
124
Q

Who is most likely to get broken heart syndrome?

Sx are similar to what?

A
  • 90% W that are 58-75
  • Acute MI
125
Q

How does the <3 change in Takosubo cardiomyopathy?

A
  • Apical ballooning of the LV
126
Q

Which type of cardiomyopathy has a 100% genetic cause?

A

Hypertrophic cardiomyopathy d/t mutations in sarcomere proteins (B-myosin heavy chain)

127
Q

How is the gross morphology and contractility of hypertrophic cardiomyopathy different from dilated cardiomyopathy?

A
    • Heart is thick-walled, heavy, and HYPERcontracting in HCM
  • Compared to flabby + HYPOcontractingheart in DCM
128
Q

In classic hypertrophic cardiomyopathy what disproportionate thickening do we see and what is a possible consequence?

A

Ventricular septum becomes WAY THICCER than the left ventricle free wall, termed asymmetric septal hypertrophy => can block aorta (outflow)

129
Q

What does hypertrophic cardiomyopathy look like on histo?

A
  • Septum is hypertrophied
  • Myocyte disarray
130
Q

What do you hear upon ausculatation during hypertrophic cardiomyopathy and why?

A

Harsh ejection fraction d/t obstraction in ventricular outflow as the mitral leaflets move toward the ventricular septum during systole

131
Q

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

A

Hypertrophic Cardiomyopathy

132
Q

Which phase of the cardiac cycle is dysfunctional in Hypertrophic Cardiomyopathy?

133
Q

In hypertrophic cardiomyopathy, the LV is poorly compliant => abnormal diastolic filling and can lead to intermittent what?

A

Ventricular outflow obstruction

134
Q

What is the essential morphological feature of Hypertrophic Cardiomyopathy?

A

Massive myocardial hypertrophy, usually W/O ventricular dilation

135
Q

What are the 3 most important histologic features of hypertrophic cardiomyopathy?

A

1. Myocyte hypertrophy

2. Myofiber disarray

3. Interstitial and replacement fibrosis

136
Q

In hypertrophic cardiomypothay, what is the thickeniing of th eventricular septum called

A

Asymmetric septal hypertrophy

137
Q

What is a consequency of hypertrophic cardiomyopathy?

A
  1. Dilation of left atria
  2. MURAL THROMBUS => emboli and stroke
  3. sudden death
138
Q

Arrhythmogenic right ventricular cardiomyopathy (ARVC) shows what characteristic morphology of the right ventricle?

A

VERY thin wall replaced with fat and fibrosis

139
Q

Arrhythmogenic right ventricular cardiomyopathy leads to failure of what and is associated with what rhythm disturbances?

A
  • RV failure
  • V-tach or v-fib => sudden death
140
Q

Arrhythmogenic right ventricular cardiomyopathy (ARVC) has what inheritance pattern?

A
  • AD
  • defect in the desmosomes that link cardiac myocytes.
141
Q

What is Naxos syndrome?

Caused by what mutation?

A
  • Arrhythmogenic right ventricular cardiomyopathy, with hyperkeratosis of the sole of foot and palm of hand
  • Plakoglobin: encodes desmosome-assx protein
142
Q

What is restrictive cardiomyopathy

A

Decreased ventricular compliance (stiff), causing diastolic dysfunction (impaired filling).

often d/t amyloid deposit in the wall or increased fibrsosis in radiation

143
Q

What do the myocardium, ventricles and atria look like in Restrictive Cardiomyopathy?

A
  • Ventricles = NL
  • Myocardium = firm and noncompliant
  • Atria: BOTH dilated
  • have to work harder to fill ventricles
144
Q

Restrictive cardiomyopathy is typically due to __________ (deposition of __________) in what part of the heart. _______ is often the misfolded culprit that leads to the disease.

A
  • Amyloidosis (deposition of β-pleated sheets).
  • INTERSTITIUM OF THE MYOCARDIUM
  • Transthyretin
145
Q

Amyloidosis results from the extracellular accumulation of protein fibrils which form?

A

Insoluble β-pleated sheets

146
Q

Amyloidosis of the heart can appear as a consequence of what 2 underlying conditions?

A
  • Systemic amyloidosis = myeloma
  • Restricted to heart of older pt’s w/ senile cardiac amyloidosis via transtheyretin
147
Q

Remember that _______stain is the stain for amyloidosis. Amyloid appears _____

A

Remember that congo red stain is the stain for amyloidosis. Amyloid appears apple green.

148
Q

Inflammation of the myocadrium, most likely d./t virus cocksackie A and B

A

Myocarditis

149
Q

Other causes of Myocarditis include what?

A
  • 1. Chagas disease (trypanasoma cruzi)
  • 2. Immune mediated (noninfective) RF, SLE, drug hypersensitivity
150
Q

What is the distinct morphology of the myocarditis of Chagas disease?

A

Parasite invasion of scattered myofibers: trypanosomes w/ mixed inflammatory infiltrate (neutrophils, lymphocytes, MO, and some EOS)

151
Q

Chagas disease is 10% fatal during the acute attack, and many progress to cardiac insufficiency in 10 - 20 years. Eosinophils will be present due to the infection, and we can see ____ in the myocytes themselves.

A

amistagotes

152
Q

What stain is used for Chagas?

A

Giemsa stain typansoma cruzi

153
Q

Lymphocytic myocarditis ≡ _______

Eosinophils myocarditis ≡ ________

Giant cell myocarditis ≡ ________.

Amastigotes mycardidits ≡ ______

A
  • Virus (cocksackie)
  • Chagas/hypersensitivty to drug
  • Chronic myocarditis
  • Chagas
154
Q

What type of infiltrates are seen in Hypersensitivity Myocarditis?

A

Perivascular, composed of lymphocytes, macrophages, and high proportion of eosinophils

155
Q

Giant-cell myocarditis is characterized by widespread inflammatory infiltrates composed of?

A

Multinucleate giant cells + lymphocytes, eosinophils, plasma cells, and macrophages

156
Q

Non-infectious causes of myocarditis are due to what conditions?

A
  • Hypersensitivity –> Post-strep (RF), SLE, drug hypersensitivity, and transplant rejection
  • Idiopathic –> Giant cell myocarditis
157
Q

Acute, rapidly developing fluid collections of 200-300 mL in the pericardial sac can cause what fatal complication?

A

Cardiac Tamponade

158
Q

Serous pericarditis is characteristically produced by what 5 non-infectious inflammatory diseases?

A
  1. - Rheumatic fever
  2. - SLE
  3. - Scleroderma
  4. - Tumors
  5. - Uremia
159
Q

What are the most frequent types of pericarditis?

A

Fibrinous and serofibrinous pericarditis

160
Q

What are the most common causes of Fibrinous and Serofibrinous pericarditis?

A
  • Acute MI

- Postinfarction (Dressler) syndrome

- Uremia

  • Chest radiation
  • RF, SLE, and trauma
161
Q
  • _______ pericarditis is dry, and finely granular.
  • _______ is charactarized by a yellow-brown, turbid fluid with WBC, RBC, and fibrin
A
  • Finrinous
  • Serofibrinous
162
Q

The most striking finding suggesting pericardial disease is a ________

A

loud pericardial friction rub.

163
Q

Purulent or suppurative pericarditis reflecting an active infection is most often a result of microbial invasion via what 4 routes?

A
    1. Direct extension
  • 2. Seed from blood
  • 3. Lymphatic extension
  • 4. Direct introduction
164
Q

The intense inflammatory rxn of purulent or suppurative pericarditis eventually causes scarring and commonly leads to what?

A

Constrictive pericarditis: heart is encased in fibrous scar => limits expansoin in diastole, CO

165
Q

Constrictive pericareditis mimics what

A

restrictive cardiomyopthy

166
Q

What type of pericarditis is caused by the spread of a malignant neoplasm into the pericardial space?

A

Hemorrhagic pericaridits

167
Q

Inflammatory diseases produce ____ pericarditis.

Infections produce ____ pericarditis.

Tuberculosis produces ____ pericarditis.

Cancer produces a ____ pericardidit

A
  • Serous
  • Purulent/suppurative
  • Caseous
  • Hemorrhagic
168
Q

______ exudate is described as “bread and butter” pericarditis

A

fibrous;

AMI, postinfarction, uremia,

169
Q

the top 5 PRIMARY tumors in the heart are all _____

170
Q

Top 5 tumors in the heart

A

1. Myxoma

2. Fibroma

3. Lipoma

4. angiosarcoma

171
Q

Myxocoma are the most common primary cardiac tumor.

They are originate from the _______, are _______ (sit on a stalk), and can are called a “ball valve” why?

A

fossa ovalis

pedunculated

  • Often mobile and cause intermittent obstruction of AV valve during systole
  • May exert “wrecking ball” effect, damaging valve leaflets
172
Q

Which cytokine elabortated by Myxomas is responsible for the consititutional sx’s, such as fever and malaise?

173
Q

what do we hear on auscultation of myxoma?

A

tumor plop

174
Q

Histologically myxomas are composed of what cells?

Which peculiar structures are characteritics findings?

A

- Stellate or globular myxoma cells w many nuclei

  • Peculiar vessel-like or gland-like structures
175
Q

top malignant cancer of heart

A

angiosarcoma

176
Q

Most common cause of heart transplant _______

Major complication: __________

A

Dilated cardiomyopathy or IHD

Allograft rejection

177
Q

Virtually all heart transplants develop ____________ presenting as intimal proliferation => causes stenosis => ischemia

A

Allograft arteriopathy

178
Q

What is a silent MI?

A

A transplanted heart is denervated, so if the pt has an MI, they won’t feel it

No angina either

CPR Exam 1 (19 decks)

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