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Cardio > Ishemic Heart Disease 2/Valves > Flashcards

Ishemic Heart Disease 2/Valves Flashcards

1
Q

What is a stunned myocyte?

A

myocytes injured by acute ischemia, which look normal microscopically, but need time (several days) to repair before they work normally again

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2
Q

What is reperfusion injury?

A

hemorrhage and other injurious phenomena associated with bringing oxygen and calcium to injured tissue, attributed to reactive oxygen species and metabolic effects of calcium

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3
Q

Why is there an oxidative burst after reperfusion of ischemic cardiomyocytes?

A

In ischemic cardiomyocytes, lack of oxygen causes the electron transport in mitochondria to back up, thereby priming various components of the electron transport chain to generate oxygen free radicals when oxygen returns

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4
Q

What occurs at the same time as the oxidative burst during reperfusion?

A

large influx of calcium

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5
Q

What is the prime target of the excess oxygen radicals and calcium in reperfusion injury?

A

mitochondrial permeability transition pore (mPTP)

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6
Q

What happens when oxygen radicals and calcium bind to mPTP in reperfusion?

A

results in opening of the mPTP and collapsing of mitochondrial function (messes up membrane potential needed for mitochondria to make ATP)

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7
Q

What is the mitochondrial permeability transition pore (mPTP)?

A

is a voltage-dependent channel that is regulated by calcium and oxidative stress

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8
Q

What 3 proteins influence the function of the mPTP? Where are they?

A

1) voltage-dependent anion channel (VDAC): outer membrane
2) adenine nucleotide translocator (ANT): inner membrane
3) cyclophilin D (CypD): matrix side of inner membrane

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9
Q

The mPTP connects what parts of the mitochondria?

A

mitochondrial matrix and cytoplasm

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10
Q

What is the “no reflow phenomenon”?

A

failure of relieving obstruction at the arterial level to restore blood flow, attributed to microvascular obstruction or edema

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11
Q

What is “ischemic preconditioning”?

A

resistance to mild-moderate ischemia due to induction of protective proteins by brief episodes of ischemia

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12
Q

How does ischemic preconditioning begin?

A

the activation of various G-protein coupled receptors by various autocoids

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13
Q

What are autocoids? When are they released?

A

adenosine, bradykinin, and opioids, which are released during the brief periods of ischemia and reperfusion

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14
Q

In ischemic conditioning, activation of GPCR initiates a complex signaling cascade, including multiple kinases, that leads to what?

A

opening of potassium channels in the mitochondrial membrane and maintenance of the mPTP and the electrical potential of the inner mitochondrial membrane

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15
Q

What is the primary mechanism for the protective effect of conditioning?

A

preservation of mitochondrial function and ATP production

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16
Q

One of the protective mechanisms of conditioning involves turning on what pathway in the mitochondria?

A

reperfusion injury salvage kinase (RISK) pathway

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17
Q

What are the 2 arms of the RISK pathway?

A

1) Action of phosphatidylinositol-3 kinase (PI-3K) on Akt (protein kinase B) and on the mTOR
2) mitogen-associated protein kinase (MAPK) and p42/p44 ERK

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18
Q

The 2 arms of the RISK pathway converge on what?

A

p70s6 kinase to activate glycogen synthase kinase beta, which acts to prevent opening of the mPTP

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19
Q

What are hibernating myocytes?

A

chronically ischemic myocytes, which have cleared cytoplasm due to catabolism of their contractile proteins and need time to regenerate their contractile proteins before they work normally again

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20
Q

What is the word for light microscopic appearance of hibernating myocytes?

A

myocytolysis

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21
Q

What is acute rheumatic fever?

A

Acute, immunologically mediated, multisystem inflammatory disease that occurs after group A, beta-hemolytic streptococcal infections

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22
Q

What is rheumatic heart disease?

A

cardiac manifestation of rheumatic fever associated with inflammation of all parts of the heart, with valvular inflammation and scarring the most prominent clinical features

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23
Q

What is Jones criteria?

A

Diagnostic criteria for acute rheumatic fever (must have 2 or more):
1) carditis
2) migratory polyarthritis of large joints
3) Subcutaneous nodules
4) Erythema marginatum skin rashes
5) Sydenham chorea (neurological disorder)
MINOR: fever, migratory arthralgias, prolonged PR interval, High ESR or WBC count

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24
Q

Describe the gross pathology of acute rheumatic heart disease?

A

tiny (1-2 mm) verrucous (wartlike) vegetations lined up on line of valve closure. Fibrinous pericarditis.

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25
Q

Describe the microscopic pathology of acute rheumatic heart disease?

A

fibrin + platelet thrombi on valves and Aschoff bodies with Anitschkow cells (caterpillar cells)

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26
Q

What is an Aschoff body? Where are they found?

A

collecitons of lymphocytes (T cells), scattered plasma cells, and Anitschkow cells occasionally punctuating zones of fibrinoid necrosis– can be found in any of hte 3 layers of the heart

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27
Q

What are Anitschkow cells?

A

plump activated macrophages with abundant cytoplasm and central nuclei with chromatin in slender, wavy ribbon shape

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28
Q

Acute rheumatic fever typically occurs in who? What is the major symptom?

A

children, carditis

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29
Q

In adults, what is the major symptom of rheumatic fever?

A

arthritis

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30
Q

How long does it take for symptoms of rheumatic fever to start?

A

2-3 weeks after infection

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31
Q

True or false: actue rheumatic heart disease is more common than chronic.

A

FALSE: chronic is more common

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32
Q

What are the symptoms of chronic rheumatic heart disease?

A

recurrent carditis, severe carditis and carditis at an early age

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33
Q

When do you first see symptoms of chronic rheumatic heart disease?

A

average 20 years after carditis

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34
Q

What is the ONLY cause of acquired mitral stenosis?

A

rheumatic heart disease

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35
Q

Describe the gross pathology of chronic rheumatic heart disease.

A

1) Slitlike fishmouth or round buttonhole stenosis with fibrous thickening and rigidity of valve
2) +/- fusion of commissures
3) Thickening, retraction and fusion of chordae

36
Q

What is another name for Marantic Endocarditis?

A

Nonbacterial Thrombotic Endocarditis (NBTE)

37
Q

Who gets marantic endocarditis (NBTE)?

A

people with:

1) cancer (especially adenocarcinomas)
2) disseminated intravascular coagulation
3) hypercoagulable states
4) long-term central venous catheterization

38
Q

Describe the gross patholgoy of marantic endocarditis.

A

Small (1-5 mm) fibrin + platelet thrombi usually on line of valve closure,

  • most common on atrial side of mitral valve,
  • second most common on ventricular side of aortic valve
39
Q

True or false: NBTE is very destructive.

A

false, sterile and nondestructive usually

40
Q

What are the 2 major complication of marantic endocarditis?

A

1) Embolization causes strokes (cerebral infarcts with irreparable brain losses), and infarcts of heart, kidneys, spleen and other organs.
2) Precursor for infective endocarditis

41
Q

What is the most common valve disease in the US and is usually benign?

A

mitral valve prolapse

42
Q

What is myxomatous mitral valve?

A

“floppy mitral valve” that leads to mitral valve prolapse

43
Q

What is mitral valve prolapse?

A

billowing of redundant mitral valve into the left atrium during systole

44
Q

What is the basis for primary myxomatous degeneration?

A

possibly an intrinsic defect in CT synthesis or remodeling (common feature of CT diseases like Marfan syndrome)

45
Q

Describe the gross pathology of myxomatous degeneration.

A
  • Billowing, ballooning, floppy leaflets (but look normal)

- Elongated, attenuated chordae tendineae that are vulnerable to rupture

46
Q

Describe the microscopic pathology of myxomatous degeneration.

A

degeneration and attenuation of outer zona fibrosa of valve and expansion of inner zona spongiosa layer owing to increased deposition of myxomatous (mucoid) material

47
Q

What heart sounds are associated with myxomatous degeneration?

A

midsystolic click and late systolic murmur

48
Q

What are some complications associated with myxomatous degeneration?

A

1) regurgitation (most common)
2) infection of valve (endocarditis)
3) rupture of chorda
4) Atrial/ventricular arrhythmias

49
Q

What is associated with Libman-Sacks endocarditis?

A

SLE (occurs in 50% of patients along with pericarditis)

50
Q

Describe the gross pathology of Libman-Sacks endocarditis.

A

Small to MEDIUM verrucous, berrylike or flat vegetations commonly on multiple valves (mitral and tricuspid mostly) on either or both sides

51
Q

Describe the microscopic pathology of Libman-Sacks endocarditis.

A

necrotic debris, fibrinoid material, degenerating leukocytes, fibroblasts and hematoxylin bodies

52
Q

What are hematoxylin bodies?

A

condensed, naked nuclei of dead degenerated cells ingested by phagocytes

53
Q

Infective endocarditis most commonly effects what part of the heart?

A 
creates friable (tan, grey, red, or brown) vegetations on valves (usually along line of valve closure)
(Atrial side of AV valve, ventricular side of semilunar valves)
54
Q

What is in a vegetation?

A

necrotic debris, thrombus, and infecting organisms

Friable masses of infecting organisms and blood clot

55
Q

What is the pathogenesis of infective endocarditis?

A

1) Valvular endothelial injury
2) Platelet and fibrin deposition
3) Microbial seeding
4) Microbial mltiplications

56
Q

Why is infective endocarditis a must not miss hypothesis?

A

100% fatal if undiagnosed/untreated

20% fatal if treated with IV antibiotics/surgery

57
Q

What are the 2 “clinical course” classifications of infective endocarditis?

A

1) Acute bacterial endocarditis

2) Subacute bacterial endocarditis

58
Q

Which type of infective endocarditis is caused by highly virulent organisms (staph aureus) attacking a previously normal valve with substantial morbidity and mortality?

A

acute bacterial endocarditis

59
Q

Which type of infective endocarditis is caused by low virulence organsims (strep viridans) involving sarred or deformed valves and has an insiduous onset of weeks?

A

subacute bacterial endocarditis

60
Q

What are the two most common valves affected by infective endocarditis?

A

mitral (35%) and aortic (20%) or both (20%)

61
Q

What complication occurs 7 days after a large myocardial infarct?

A

stroke from mural thrombus

62
Q

What are the three layers of the mitral valve (inner to outer)?

A

Inner: zona fibrosa
Middle: zona spongiosa
Outer: zona atrialis (or fibrosa)

63
Q

True or false: Embolization is a common complication of Libman-Sacks endocarditis.

A

False: rarely embolizes

64
Q

Incidence of infection, marantic endocarditis and rheumatic disease on a valve correlate with what?

A

Resting pressure on the closed valve

65
Q

What are the causative agents of infective endocarditis?

A

42% staph

40% strep

66
Q

What are some portals of entry for infective endocarditis?

A

Central venous catheter

Mouth (dental procedures, gingivitis, etc.)

67
Q

True or false: smaller vegetations are more likely it is to be infective.

A

False

68
Q

What are the complications of infective endocarditis?

A 
Heart failure (67%)
-perforation of valve
-adjacent abscess 
-fibrotic scarring
-calcification
Septic Emboli (55%) to kidney, heart, spleen, brain
Myocardial abscess
69
Q

Describe the early microscopic pathology of infective endocarditis.

A

Platelets, masses of organisms, +/- necrosis and neutrophils

70
Q

Describe the later microscopic pathology of infective endocarditis.

A

+/- lymphocytes, macrophages, fibroblasts, fibrosis

71
Q

What are the common symptoms of infective endocarditis?

A 
Fever (80%)
Chills
Weakness
Dyspnea
(cough, sweats, weight loss, malaise, etc.)
72
Q

What are the common signs of infective endocarditis?

A 
Fever (90%)
Heart murmur (85%)
Splenomegaly
Petechiae
Osler nodes (tender on fingers/toes)
Janeway lesions (uncommon)
Roth spots (uncommon)
73
Q

What are the common lab findings of infective endocarditis?

A

High ESR
Anemia
Proteinuria
Rheumatoid Factor (50%)

74
Q

How to you test for infective endocarditis?

A 
Transesophageal echocardiograaphy (90% sens)
Transthoracic echocardiography (60% sens)
75
Q

What else do you need (other than murmur and visualization of vegetations) to diagnose infective endocarditis?

A 
blood cultures (to detect low-grade bacteremia)
3 (from 3 different sites, 30-60 minutes apart, BEFORE starting antibiotics)
76
Q

Why should you alert the microbiology lab that endocarditis is expected?

A

Because some bacteria causing endocarditis are fastidious or slow-growing or both, so the microbiology laboratory will use extra “special” culture media and hold the cultures longer, but only if you alert them of the need.

77
Q

What is the problem with treating infective endocarditis with surgical valve replacement?

A

Life-saving if acute.
Replacing one chronic disease with another (life-long anticoagulation), and bioprosthesis deteriorate by 10 years in 50% of patients.

78
Q

True or false: in infective endocarditis, less pathogenic bugs produce smaller vegetations?

A

FALSE: larger vegetations indicate less pathogenic bugs (subacute bacterial endocarditis)

79
Q

What heart sound do you hear in mitral valve stenosis?

A

opening snap and diastolic rumble after

80
Q

Mitral valve stenosis predisposes to what condition? Why?

A

stasis in the left atrium predisposes to thrombus formation

81
Q

What is Virchow’s Triad?

A

3 conditions necessary to make a thrombus:

1) endothelial injury
2) abnormal blood flow
3) hypercoagulability

82
Q

What is carcinoid syndome?

A

carcinoid syndrome results from bioactive compounds such as serotonin released by carcinoid tumors

83
Q

What are the systemic manifestations of carcinoid syndrome?

A

flushing, diarrhea, dermatitis and bronchoconstriction

84
Q

What is carcinoid heart disease?

A

the cardiac manifestations caused by the bioactive compounds and occurs in half of carcinoid syndrome patients: endocardium and valves of the right heart are primarily affected

85
Q

What is the gross pathology of carcinoid heart disease?

A

distinctive, glistening white intimal plaquelike thickenings

86
Q

What is the microscopic pathology of carcinoid heart disease?

A

smooth muscle cells and sparse collagen fibers embedded in an acid mucopolysaccharide-rich matrix

87
Q

What happens if a septic embolus goes to the spleen? The liver?

A 
Splenic infarcts (abscesses of liquefactive necrosis that must be DRAINED)
Liver metastases

Cardio (24 decks)

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