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The Heart > Cardiomyopathy > Flashcards

Cardiomyopathy Flashcards

1
Q

Cardiomyopathy

A

Disease of cardiac muscle which interferes with pump function

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2
Q

Classification of cardiomyopathy

A

Dilated- enlarged heart/sys dysfunction
Hypertrophic- LV thickening/Dias dysfunction
Restrictive- Dias dysfunction
Arrythmogenic RV dysplasia- fibrofatty replacement
Unclassified- fibroelastosis/LV non compaction (epicardial compaction/endocardial Non compaction» lower left chamber develops incorrectly affecting pump function

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3
Q

Dilated CM

A

Dilation and impaired contraction of LV/RV
Characterised by myocyte damage (idiopathic)
Usually asymptomatic but can be ass. To HF
increased in African males (whites M=F) 20-60years

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4
Q

CM Etiology General

A

Ischemic/valvular/hypertensive/idiopathic/inflammatory
Toxic- alcohol/cocaine/anthracyclins (reversible with abstinence) increased myocyte cell death and fibrosis leads to inhibition of FA ox and Mit ox phos
Metabolic- DM/acromegaly/pheochromocytoma
Nutritional- deficiency of thiamine/selenium/carnitine
Neuromuscular- X linked DMD

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5
Q

CM Etiology infectious/non infectious/familial

A

Virus- picornaV/CMV/coxBV/echovirus (self limiting infection in children & can cause immune mediated myocyte necrosis and fibrosis)
Bacteria-rickettsiae and Lyme disease
Parasites- Chagas’ disease and toxoplasmosis
Peripartum/RA/SLE/collagen and vascular disorders
Familial- AD/AR/X linked transmission (genes encoding myosin and actin affected) and 30% idiopathic (altered E production and contractile force generation)

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6
Q

CM prognosis

A

Peripartum> idiopathic> ischemic HD> infiltrative HD> HIV

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7
Q

Peripartum CM

A

1month pre birth- 5months post birth
Affect 1/4000
Ass. To TNF/IL-6/fas apo-1 (PIC) and LV dysfunction/reduced end Dias diameter and ejection fraction

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8
Q

Hypertrophic CM

A

Affects 1/500
Disorganised and chaotic myocyte arrangement
LV hypertrophy not due to P overload
Other hypertrophy- (a)symmetric septal and apical
Vigorous sys function and reduced Dias function (impaired ventricular relaxation increase Dias P)

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9
Q

Hypertensive hypertrophic CM

A

Familial (AD)
Ass. To mutation of genes encoding beta myosin/trop T/myosin binding protein C/alpha tropomyosin
Primary COD in young people
Results in LV thickening > SCD (increased if Dx is early/family history/syncope/ischemia/VA)

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10
Q

Morphology of hypertrophic CM

A

Myocardial disarray
Myocytes are not aligned parallel
Myocytes for circles around CT foci
(Unspecific)

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11
Q

Restrictive CM

A

Impaired ventricular filling due to stiff ventricle
Normal systole and abnormal diastole
Increased intraventricular P with small increase in volume
Primary causes- (idiopathic/familial) fibrosis/myocardial infiltration of FA/hypertrophy/scleroderma/toxins/sarcoidosis/LSD/MPSoses/cancer

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12
Q

Endomyocardial fibrosis

A

Increased in Africa/Asia/south and Central America
Ass. To hypereisinophillic syndrome (Leofflers endocarditis)
Poor prognosis death in 1-2 years
Morphology- thick basal inferior wall/elastomyofibrosis/thrombi I’m endocardium/mitral regurgitation/apical obliteration

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13
Q

ARVD

A

RV free wall undergoes FFR (total/partial)
Reduction in motion and function of wall
Ass. To SCD in young people and arrhythmia
Occurs in young people <40yrs and increased in males

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14
Q

ARVD Dx/symptoms/genetics

A

Myocardial biopsy at interventricular septum to show FFR
Ventricular tachycardia/syncope/cardiac arrest
Familial in 30-50% (AD) ass. To chr 1/2/3/10/12/14 and plakophillin2 mutations
AR variant (Naxos disease-palmar keratosis and woolly hair)- alteration at chr 17 encoding desmoplakin/plakoglobin cell-cell junctions/PM impaired leading to cell death/FFR

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15
Q

ARVD histology

A

Diffuse and segmental LO RV myocytes
FFR and RV wall thinning
FFR begins at subepiC/mediomural/subendoC
Endo/myoC of trabeculae are spared

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16
Q

ARVD anatomic malformations

A

Mild- severe RV dilation/aneurysm/segmental hypokinesia
Mains sites of involvement- RV outflow tract/apex/infundibulum leading to electrophysiological hole and arrhythmia
FFR pattern- RV>IV SEPTUM>LV>posterior septum>posterolateral areas

17
Q

ARVD Etiology

A

Unknown/disontogenetic/degenerative/inflammatory/apoptotic/transD theory Mm—WAT

18
Q

ARVD natural history

A 
5% ass. to SCD 
25% ass. To exercise related deaths
Cardiac electrical instability 
Right bundle branch block 
RV dysfunction> RV and LV dysfunction> HF
19
Q

LV non compaction

A

Dx criteria- prominent trabeculae/deep recess in LV Alex/thick epiC and endoC
Increases risk of thrombosis/vent tachycardia/CHF/SCD
Maybe ass. To pregnant or congenital heart defect/mitochondrial disease/trisomy 13/Barth syndrome/NM diseases
Hereditable component

The Heart (12 decks)

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