Valvular Disease Flashcards

1
Q

Only non-tricuspid valve

A

Mitral

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2
Q

Valves responsible for ventricular outflow

A

Semilunar valves

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3
Q

What are valves made of?

A

endocardium covering core of dense fibrous connective tissue. Lined with endothelial layers. AV have smooth muscle on atrial side.

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4
Q

Two reasons velocity is greater through the semilunar valves

A

Smaller openings

greater chamber pressure

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5
Q

What is insufficiency?

A

Failure to close completely, allowing regurg and backflow

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6
Q

What is stenosis?

A

a narrowing or constriction of an orifice

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7
Q

What is current formation?

A

Abnormal valve function that may cause jet streams.

This can damage vessels or current eddies that allow thrombosis and bacterial deposition on either side of valve

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8
Q

Four main types of left sided flow disruption

A

Mitral stenosis
Mitral regurg
Aortic Stenosis
Aortic Regurg

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9
Q

Important details about mitral stenosis

A

Usually from post-rheumatic fever scarring
Coexists with insufficiency
Takes decades to develop, well tolerated

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10
Q

Important details about mitral regurgitation

A

Caused by infection and papillary muscle abnormality

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11
Q

Important details from aortic stensois

A

Usually calcific degeneration of the bicuspid

Leads to pressure overload and LVH

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12
Q

Important details from aortic regurg.

A

Valvular disease or aortic root disease

Volume overload and LVH

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13
Q

Symptoms of insufficient cardiac output from valvular disease

A

Syncopal episodes
LVH
Increase water/salt retention + inc. in peripheral resisitance

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14
Q

Named type of mechanical damage associated with valvular damage

A

Jet stream damage to aortic and pulmonic outflow tracks.

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15
Q

Types of emboli associated with valvular damage

A

Infectious thrombi – vegetations in endocarditis

Thrombotic vegetations, small clots

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16
Q

When does Bicuspid Aortic Valve typically present

A

6th-7th decade

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17
Q

Pathogenesis of Bicuspid Aortic valve

A

Congenital bicuspid aortic valve –> Progressive calcification of cusps –> calcific aortic stenosis

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18
Q

Gross features of bicuspid aortic valve

A

Heaped up calcified masses w/in aortic cusps

Architectural distortion

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19
Q

Microscopic features of bicuspid aortic valve

A

Fibrosed + Thickened Cusps

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20
Q

In bicuspid aortic valve patients, _____ increases the likelihood of sudden death

A

Syncope

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21
Q

Pathogenesis of mitral valve prolapse

A

Floppy enlarged mitral leaflets balloon into left atrium during systole
Snapping or tending of everted cusps/chordae tendinae

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22
Q

Auscultation findings associated with mitral valve prolapse

A

Midsystolic click, late systolic click, holosystolic murmur

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23
Q

Gross features of mitral valve prolapse

A

Billowing of MV leaflets
Pathologic if more than 4mm above the base of the cusp
Stretched/elongated/ruptured chordae tendineae
Fibrosis/Calcification of valve/Ventricular surface

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24
Q

What would you see in a symptomatic MVP patietient

A

Angina, dyspnea, fatigue, depression, personality disorders, anxiety rxn

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25
Q

Four main concerns with MVP

A
  1. Infective Endocarditis
  2. MV Insufficiency
  3. Arrythmia
  4. Sudden Death
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26
Q

What is Rheumatic Heart Disease

A

An acute, recurrent inflammatory disease following pharyngeal infection with S. pyogenes
Mainly in children (leading cause of heart disease death from ages 5-25)

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27
Q

Pathogenesis of Rheumatic Heart disease

A

Immunological cross rxn

Lesions are sterile, not from direct bac. invasion

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28
Q

Gross features of Rheumatic Heart disease

A

Mitral and Aortic Valves
Mitral valvulitis –> Stenosis
Vegetations
Pericarditis

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29
Q

name for the vegetations associated with Rheumatic Heart disease

A

Verrucae

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30
Q

What are Aschoff bodies?

A

Foci of fibrinous necrosis surronded by lymphocytes and macrophages
PATHOGNOMIC for rheumatic myocarditis
(Anitschkow are not)

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31
Q

Describe valvular lesions associated with Rheumatic Heart disease

A

Verrucae vegs along lines of closure
Focal collagen degeneration surrounded by inflamm.
Ulceration of valve with fibrin deposits

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32
Q

Jones Criteria for Rheumatic fever?

A
Migratory Polyarthritis
Carditis
Subcutaneous Nodules
Erythema marginatum
Sydenham's chorea
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33
Q

Main cause of death in rheumatic fever

A

Congestive Heart Failure from Myocarditis

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34
Q

Where in the heart is acute rheumatic heart disease?

A

Any layer of the heart

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35
Q

Important associations with Chronic Rheumatic Heart Disease

A

Recurrent Attacks with different strep
Permanent valve deformity (esp. MV)
Conspicuous, irregular thickening/fusion of leaflets
MacCallum’s patches on posterior atrium

36
Q

Incidence of LSE?

A

in about half of SLE patients

37
Q

What are LSE vegetations made of?

A

Necrotic Debris, Fibrinoid Material, Disintegrating Fibroblasts, and Inflammatory Cells

38
Q

LSE effects on Cusps/Other

A

Fibrinoid Necrosis w/ neutrophils and mononuclear infiltrate

Myocardial arterioles/small arteries undergo necrosis

39
Q

Infective Endocarditis, Rheumatic Endocarditis, LSE.

Which Valves?

A

IE - Any
RE - Mitral
LSE – Mitral, tri, pulmonic

40
Q

Infective Endocarditis, Rheumatic Endocarditis, LSE.

Size of vegetations

A

IE – Large (5-20)
RE – Small
LSE – Small

41
Q

Infective Endocarditis, Rheumatic Endocarditis, LSE.

Distribution.

A

IE - Single Foci
RE – Lines of cusp closure, beading verrucae
LSE – Multiple, Random. Both sides of valve

42
Q

What is endocarditis?

A

Colonization or invasion of valves/mural endocardium by a microbial agent leading to friable vegetations

43
Q

Who should you suspect in Endocarditis patients?

A

Strep. viridans

Staph, enterococci, pneumococci, G- Rods

44
Q

What predisposes you to endocarditis?

A

Anything causing abnormal flow, shunting, exposure of collagen, or valve damage

45
Q

IV drug exposure predisposes you to…..

A

Right sided infections (S. aureus, Candida, Aspergillus)

46
Q

Pathogenesis of infective endocarditis w/ damaged valved/fucked up blood flow

A

Desposition of Fibrin and Agglutinated Organisms

47
Q

Pathogensiss of infective endocarditis in R to L shunt?

A

Bypass filtering of blood by lungs

48
Q

Gross features of infectiveendocarditis?

A

Friable, Bulky, bacteria laden vegetations on heart valves
Usually Mitral+Aortic
Not usually around whole free edge
Evetually becomes fibrotic/Calcified

49
Q

Microscopic Features of infective endocarditis

A

Vegetations – Irregular masses of fibrin,platelets, blood cell debris, organisms, and inflam. cells
Leaflets – Vascularization + Nonspecific Inflammation

50
Q

Intrinsic consequences of endocarditis?

A

Erosion, destruction of valve leaflets
Deformation of valve leaflets – stenosis, insufficiency
CHF
Suppurative pericarditis (penetration of heart wall, myocardial metastatic abscesses)

51
Q

Extrinsic consequences of endocarditis?

A

Seeding of Aorta, Kidney, Spleen, Brain w/ infective emboli

Arterial thrombotic emboli

52
Q

Acute Bacterial Endocarditis clinical circumstances

A

Destructive, tumultuous infection
Necrotizing, ulcerative, invasive valvular infections
Can occur in normal heart

53
Q

Acute Bacterial Endocarditis is associated with…

A

IV catheter, Prosthetic Valve

54
Q

Organisms typically responsible for Acute Bacterial Endocarditis

A

STAPH AUREUS

55
Q

Morphology of Acute Bacterial Endocarditis

A

Friable, Bulky, Bacteria laden vegetitations

56
Q

Clinical course of Acute Bacterial Endocarditis?

A

Diagnosis and Treatment Improve Prognosis
Fever most common sign
Stormy onset, rapid fever, chills
Murmurs

57
Q

How to confirm Acute Bacterial Endocarditis?

A

Blood Culture

58
Q

Clinical circumstances Subacute bacterial Endocarditis?

A

Previous Heart Disease (Congenital, RHD, Surgery, Endo)

Seeding to damaged valves

59
Q

Organisms typically responsible for Subacute bacterial Endocarditis?

A

STREP VIRIDANS

60
Q

Which bacteria is associated with previous SBE? Previous RHD?

A

SBE – Strep Viridans

RHD – Group A Hemolytic Strep

61
Q

Clinical course of Subacute bacterial Endocarditis?

A

Flu-like illness going on for months
Heart Murmur + Signs of Systemic Infection
Requires Antibiotics

62
Q

Complication for watch out for in Subacute bacterial Endocarditis?

A

Heart failure from valve scarring/damage

Also increased MI risk from embolization

63
Q

ABE, SBE, Non-bacterial thrombotic endocarditis.

Identify the most common organism.

A

ABE – S. Aureus
SBE – Strep Viridans
NBTE – None (SLE, Tumors)

64
Q

ABE, SBE, Non-bacterial thrombotic endocarditis.

Clinical Setting?

A

ABE – IV contamination
SBE – Dental Work
NBTE – SLE, Tumors

65
Q

ABE, SBE, Non-bacterial thrombotic endocarditis.

Clinical Presentation?

A

ABE – Fever, Stormy Course, Murmurs
SBE – Flu-like, Fever of unknown Origin
NBTE – Distant embolization

66
Q

ABE, SBE, Non-bacterial thrombotic endocarditis.

Clinical Association?

A

ABE – Healthy or damaged valves
SBE – Previously damaged valves
NBTE – From other diseases

67
Q

ABE, SBE, Non-bacterial thrombotic endocarditis.

Consequences?

A

ABE – Acute Heart Failure, Septic Embolization
SBE – Chronic Heart Failure, Septic Embolization
NBTE – Embolization; secondary infection

68
Q

Pathogenesis of Non-bacterial thrombotic endocarditis?

A

Endothelial Damage –> Platelet+Fibrin Deposition on Valve Leaflets –> Formation of Nodular Vegetations

69
Q

Non-bacterial thrombotic endocarditis is associated with..

A

SLE, Cachexia, Mucin-producing tumors, endothelium damage

70
Q

Non-bacterial thrombotic endocarditis vegetations embolize and cause infarcts in…

A

Spleen, Kidney, Brain, Gut, Extremities

71
Q

Clinical features of Carcinoid Heart Disease?

A

Distinctive Episodic flushing of skin, cramps,
Nausea, Vomiting, Diarrhea
1/2 get cardiac lesions

72
Q

Pathogenesis of Carcinoid Heart Disease?

A

Deposits of Pearly gray, uniform fibrosis on tri/pulm valves

Insufficiency+Stenosis

73
Q

Why do carcinoids only affect the right heart?

A

Metabolized in the lungs, don’t reach the L heart

74
Q

What causes the fibrous tissue rxn in Carcinoid Heart Disease?

A

Elaboration of Bioactive products by argentaffinomas (including seratonin, kallikrein, bradykinin, His, prostaglandins)

75
Q

Gross features of Carcinoid Heart Disease?

A

Plaque-like thickenings made of unusual fibrous tissue superimposed on the endocardium of the cardiac chambers and valvular cusps

76
Q

Microscopic features of Carcinoid Heart Disease?

A

Fibrous thickening resembling cellular atheromas

77
Q

Pathogenesis of Mitral valve annulus calcification?

A

Trauma –> Fibrotic Changes –> Calcification –> Hemodynamic Obstruction, murmur

78
Q

Gross features of Mitral valve annulus calcification

A

Calcium deposition transforms mitral ring into a rigid curved bar up to 2 cm in diameter
Posterior leaflet may be distorted/Upwardly displaced

79
Q

Microscopic Features of Mitral valve annulus calcification?

A

Amorphous masses of calcified material in connective tissue of valve ring.
Calcificaion can extend into base leaflets and the ventricular septum.

80
Q

Major source of morbidity and mortality in artifical heart valves? less common, but serious complication?

A

Thromboembolism

Infective Endocarditis

81
Q

With prosthetic valves, early infection is associated with ____ and late with ____

A

Early - Staph

Late – Strep

82
Q

Four things that cause immediate cyanosis

A

Tetralogy
Tricuspid Atresia
Truncus Arteroisis
Transposition of Great Arteries

83
Q

Causes of aortic stenosis…who usually presents in patient 60/70s? 70s? 80s/90s?

A

60/70s- Bicuspid Aortic Valve
70s - RHD
80s-90s - Senile Calcification

84
Q

What are Aschoff bodies?

A

Collections of reactive histiocytes

85
Q

Unique feature of Anitschkow myocytes?

A

Caterpillar chromatin pattern