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PBL 2.2.4 > Path 12: Heart go brrrrrrrrr > Flashcards

Path 12: Heart go brrrrrrrrr Flashcards

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1
Q

Layers of tri-layer architecture of cardiac valves

A

Endothelium
Fibrosa
Ventricularis/Atrialis Layer

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2
Q

Cardiac myocytes rely on ________ for energy

A

oxidative phosphorylation

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3
Q

Diastole comprises ____ [fraction] of the cardiac cycle

A

2/3

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4
Q

With tachycardia, the relative duration of ____ decreases

A

diastole

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5
Q

Frank-Starling mechanism

A

1) Increased filling volumes dilate the heart
2) Actin-myosin crossbridge formation increases
3) Contractility increases

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6
Q

Normal EF

A

45-65%

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7
Q

Causes of hypertrophy

A

Pressure overload
Volume overload
Trophic signals (aka ß activation)

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8
Q

Hypertrophic myocyte cellular characteristics

A

1) increased protein synthesis
2) Increased mitochindira
3) Multiple/enlarge nuclei
4) DNA ploidy

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9
Q

Patterns of hypertrophy

A

Pressure overload: sarcomeres are PARALLEL to long axes of cells. Wall thickness increases

Volume overload: sarcomeres assembled in series with existing ones. Heart weight increases, but wall thickness does not. Dilation of ventricle

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10
Q

Why does hypertrophy make heart vulnerable to ischemia

A

1) Increased oxygen demand
2) Hypetrophic growth not accompanied by capillary growth
3) Fibrous tissue resists diastolic filling

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11
Q

Genes expressed in hypertrophic myocytes

A

FOS
JUN
MYC
EGR1

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12
Q

Most common left HF causes

A

1) Ischemia
2) HTN
3) Aortic/mitral dx
4) Primary myocardial dx

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13
Q

Pulmonary changes from pulmonary edema

A

1) Perivascular and interstitial edema
2) Progressive widening of alveolar septa
3) Accumulation of fluid in alveolar spaces

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14
Q

Histologic changes pointing to previous episodes of pulmonary edema

A

Hemosiderin laden macrophages

AKA Heart Failure Cells

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15
Q

Mechanism of hemosiderin laden macrophages

A

Extravasated red cells phagocytosed and accumulated iron is hemosiderin

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16
Q

CHF auscultation findings

A

1) Fine rales in bases (inspiratory)
2) S3 (volume overload)
3) S4 (increased myocardial stiffness

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17
Q

Mitral regurgitation in HF caused by

A

Dilation of heart outwardly displaces papillary muscle

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18
Q

Most common cause of right HF

A

Left HF

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19
Q

Isolated right HF caused by

A

Usually pulmonary pathologies

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20
Q

Marker used to quantitatively assess CHF progression

A

BNP

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21
Q

Cardiac cell embryologic origin

A

Mesoderm

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22
Q

First wave of cardiac folding in embryo produces

A

Left ventricle

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23
Q

Second wave of cardiac folding in embryo produces

A

Right ventricle, outflow tract, atria

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24
Q

Most common genetic cause of congenital heart dx

A

Down syndrome

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25
Q

Left-to-right shunts types

A

ASD
VSD
PDA

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26
Q

Atrial Septal Defect presentation

A

Usually silent till adulthood
Pulmonary valve murmur

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27
Q

Patent foramen ovale

A

Persistent foramen can open when right sided pressures are elavated, sometimes creating a right-left shunt or paradoxial embolism

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28
Q

90% of VSDs happen in

A

Membranous interventricular septum

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29
Q

VSD below pulmonary valve

A

Infundibular VSD

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30
Q

VSD presentation age

A

Manifest in children

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31
Q

VSD clinical features (morphology changes)

A

Irreversible pulmonary vascular disease
Right hypertrophy
Pulmonary hypertension

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32
Q

VSD treatment

A

Most close spontaneously so surgery is delayed
Surgery if no closure

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33
Q

PDA structure

A

PA joins aorta just distal to left subclavian

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34
Q

PDA auscultation

A

Persistent machinery like murmur

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35
Q

Mechanisms that close Ductus arteriosus

A

Increased atrial oxygenation
Decreased pulmonary vascular resistance
Declining prostaglandin E2 levels

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36
Q

Causes of PDA

A

Hypoxia in infant
Other defects increase pulmonary vascular resistance

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37
Q

Treatments to close PDA

A

Prostaglandin inhibitors
Percutaneous/surgical

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38
Q

When should a PDA be preserved

A

Co-occurring defects that obstruct pulmonary outflow tracts

Done by admin of Prostaglandin E1

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39
Q

Four features of Tetralogy of Fallot

A

1) VSD
2) Obstruction of the right ventricular outflow tract
3) Overriding aorta
4) Right ventricular hypertrophy (secondary to to pressure overload)

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40
Q

Tetralogy of Fallot classic presentation

A

Cyanotic at birth
Loud murmur

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41
Q

Transposition of great vessels types

A

L- uncommon, often well tolerated (corrected)
D- most common, leads to death without shunting

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42
Q

Cause of tricuspid atresia

A

unequal canal division makes tricuspid smaller and mitral larger

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43
Q

Tricuspid atresia symptom

A

Cyanosis

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44
Q
A
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45
Q

How is circulation maintained in tricuspid atresia?

A

VSD/ASD providing shunting

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46
Q

Coarctation of aorta patient population

A

Males and Turner syndrome

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47
Q

Infantile form of coarctation of aorta features

A

Tubular hypoplasia in aortic arch proximal to a PDA

48
Q

Adult coarctation of aorta features

A

Discrete, ridgelike folding of aorta opposite to closed ductus arteriosus

49
Q

4 step sequence in MIs

A

1) Plaque is disrupted exposing subedothelial collagen
2) Platelets adhere and realease TXA2 and ADP increasing aggregation and vasospasm
3) Tissue factor coagulation grows thrombus
4) Artery is occluded

50
Q

What are ultrastructural changes

A

Changes in heart that set in within a few minutes of ischemia

Glycogen depletion, myofibrillar relaxation, mitochondrial swelling

51
Q

How long to get irriversible MI damage

A

20-30 min

52
Q

Earliest detectable feature of myocyte necrosis

A

Disruption of sarcolemmal membrane. Macromolecules leak into blood (troponin)

53
Q

How long for infarct to reach full extent

A

3-6 hours

54
Q

Apex of heart supplied by

A

LAD

55
Q

Dominant coronary artery

A

RCA vs LCX

depends of on who supplies posterior 1/3 of septum

56
Q

Transmural infarction occurs when a ______ vessel is occulded

A

Epicardial

57
Q

Subendocardial infarcts occur

A

When there is lysis of plaque prior to transmural necrosis

58
Q

MI gross autopsy buzzword timeline

A

Less than 12 hours: Not many changes, can see necrosis with stain
12-24 hours: Reddish blue discoloration, extravasated blood
1-3 Days: acute inflammation
3-7 Days: Macrophages
7-10 Granulation tissue

59
Q

Myocyte vacuolization

A

Intracecullar accumulations of salt/water

Seen in infarct periphery

60
Q

How long to fully heal MI

A

6-8 weeks

61
Q

Factors contributing to reperfusion injury

A

1) mitochondrial dysfunction
2) Myocyte hypercontracture
3) Free radicals
4) Leukocyte aggregation

62
Q

Top marker for MI in past

A

CK-MB

63
Q

Clinically useful biomarkers of myocardial damage

A

CTnT and cTnI (troponin T and I)

64
Q

Troponins begin to rise in ______ and peak _____ after MI

A

2-4 hours

24-48 hours

65
Q

Intense pericarditis a week after MI name and MOA

A

Dressler syndrome

Due to a formation of antibodies agaisnt damaged myocardium

66
Q

Patients with greatest risk of free-wall rupture, expansion, mural thrombi

A

Anterior transmural

67
Q

Chronic IHD presentation

A

LVH, cardiomegaly, dilation

68
Q

Long QT genetics

A

K+ channel loss of function or NA+ gain of function

69
Q

Brugada genetics

A

NA+ loss of function SCNL genes

70
Q

hypertensive heart disease features

A

Pressure overload, ventricular hypertrophy

71
Q

Cor pulmonale aka

A

Right sided hypertensive heard disease

72
Q

Acute cor pulmonale ventricle morphology

A

Marked dilation w/o hypertrophy

73
Q

Most common valvular abnormality

A

Calcific Aortic Stenosis

74
Q

Calcific aortic stenosis caused by

A

Chronic injury from hyperlipidemia, htn , inflamation

75
Q

Morphological hallmark of calcific aortic stenosis

A

Mounded calfified masses on outflow surfaces that prevent cuspal opening

76
Q

Aortic stenosis sx

A

Narrow valve increases ventricular pressure. LVH goes on to CHF

77
Q

bicuspid aortic valve significance

A

Malformed valve gets stressed and calficies. cc: Aortic stenosis

78
Q

Bicuspid aortic valve course of symptoms

A

Assymptomatic early in life

Big risk for calcific stenosis, aortic regurg

79
Q

Where do mitral valve calcifications happen

A

Fibrous annulus

Done usually affect function… importantly can be thrombus formatio. site

80
Q

Mitral valve prolapse population

A

Old women

81
Q

Mitral valve prolapse in marfan cause

A

FBN1 fibrillin gene alter TGF-B signaling

82
Q

Histology of Mitral valve prolapse

A

myxomatous degeneration of spongiosa layer

83
Q

MVP heart sound

A

Mid systolic click

84
Q

Rheumatic fever cause

A

2-3 weeks after strep

Type 2 hypersensitivity. Cross reactivity

M proteins resemble cardiac antigens

85
Q

Rheumatic fever histo

A

Aschoff bodies: t lymphocyte foci (acute only)
Anitschkow cells: plump large macrophages

86
Q

Subendocardial lesions can can induce irregular thickenings called _______ plaques, usually in the ____

A

MacCallum

Left atrium

87
Q

Rheumatic fever anatomic changes

A

Mitral valve thickening, commisural fusion/shortening and thickening of the tendinous cords

88
Q

Rheumatic fever sx

A

Migratory polyarthritis
Pancarditis
Subcutaneous nodules
Erythema Marginatum
Sydenham Chorea

MPSES

89
Q

Most common endocarditis bug

A

S Viridans (cavities)
S. Areus (drugs)

90
Q

Morphology of Infectious endocarditis

A

Vegetations on heart valves

91
Q

Nonbacterial Thrombotic Endocarditis characterized by

A

Sterile thrombi on valve leaflets

92
Q

Nonbacterial Thrombotic Endocarditis happens in

A

Cancer/sepsis patients with hypercoagulable states

93
Q

Carcinoid syndrome sx

A

Flushing , diarrhea, dermatitis, bronchoconstriction

94
Q

Carcinoid heart disease happens after

A

Massive hepatic metastatic burden, bc liver normall metabolizes circulating mediators.

95
Q

Carcinoid syndrome heart lesion morphology

A

Glistening white intimal plaquelike thickenings of endocarcial surfaces

Tricuspid insuficiency and pulmonary stenosis

96
Q

Dilated Cardiomyopathy (DCM) is characterized morphologically and functionally by _______

A

progressive cardiac dilation and contractile (systolic) dysfunction, usually with concomitant hypertrophy.

97
Q

Arrhythmogenic right ventricular cardiomyopathy sx

A

Right sided HF and rhythm disturbances

Can cause sudden cardiac death

98
Q

Arrhythmogenic cardiomyopathy+hyperkeratosis =

A

Naxos syndrome

99
Q

Hypetrophic cardiomyopathy caused by (genetic)

A

Mutations to sarcomeric protein genes

100
Q

Restrictice cardiomyopathy characterized by

A

Impaired ventricular diastolic filling due to ventricular compliance decrease

101
Q

Amyloidosis cardiomyopathy features

A

Restrictive
β-pleate sheet accumulation

Either on congo red stain H&E

102
Q

Most common cause of myocarditis

A

Viruses

esp coxsackie A/B

103
Q

Chagas disease sx and histo

A

Myocarditis

scattered myofibers by trypanosomes accompanied by a mixed inflammatory infiltrate of neutrophils, lymphocytes, macrophages, and occasional eosinophils

104
Q

Chemotoxic agents for heart

A

Doxorubicin
Danorubicin

Chemo

105
Q

Serous pericarditis associated with

A

Inflammatory diseases

106
Q

Constricitve pericarditis

A

Happens when pericardium scars limiting diastolic expansion. No ability to increase output

107
Q

Most common primary heart tumor

A

Myxoma

108
Q

Mixoma pathogenesis

A

Benign

Primitive multipotent mesenchyme

109
Q

myxoma histo

A

stellate or globular myxoma cells with abundant ground substance

110
Q

Sea-anemone shape tumor in heart

A

Papillary fibroelastoma

111
Q

most common peds tumor in heart

A

Rhabdomyoma

112
Q

Rhabdomyoma disease course

A

Regresses sponatneously

113
Q

Prinzmetal angina due to

A

Smooth muscle hyperreactivity in coronary artery call

114
Q

What happens 1-3 days after MI

A

Coagulation necrosis, neutrophils, early pericarditis

115
Q

Concentric vs eccentric hypertrophy

A

Concentric: Sarcomeres add in parallel in response to increased afterload/pressure

Eccentric: adds sacomeres in series in response to volume overload

116
Q

Squating in TOF helps how

A

Increases SVR to force blood into pulmonary circulation

117
Q

PE in lung periphery causes

A

Wedge shape necrosis (infarction)

PBL 2.2.4 (13 decks)

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