Heart Pathology - Patho Colloq 5
Inflammations in the Heart
Endocarditis
Infective septic endocarditis
valvular damage due to microorganism colonisation and inflammation
Etiology: bacteria, fungi, Ricketsia. chlamydia
Vegetations - fibrin, inflammatory cells. microorganisms
Overtime: chronic inflammation, fibrosis, calcinosis
Myocarditis
Myocardial damage due to inflammation
Etiologic factors: infections (HIV, chlamydia, candida), immune reactions (pos-tviral, rheumatic fever, lupus), diseases of unknown etiology (sarcoidosis, giant cell myocarditis)
Rheumatic Fever
Immunologically mediated
After Streptococcus A pharyngitis
Many organ systems are affected
Hypersensitivity or Streptococcus-induced autoimmunity
Heart damage: acute rheumocarditis, chronic valvular damage esp. mitral stenosis
Main manifestation: Pancarditis
Acute rheumatic fever: Pancarditis
Aschoff granulomas in all layers of heart
Fibrinous exudate in pericardium
Fibrinoid necrosis and small vegetations in endocardium
Chronic rheumatic fever: heart
Valvular fibrosis and deformity
Mitral Valve: thickened, chordae tendinae thickened and lack elasticity
Pericarditis
Acute: serous, fibrinous, purulent, haemorrhagic, (caseous)
Chronic: adhesive, constrictive
Etiology: infections (viruses, bacteria), immune mediated (LED, Dressler syndrome after myocardial infarction), other (uremia, tumour, trauma, irradiation)
Cardiomyopathies (CMP)
Primary myocardial pathology
Types:
Dilated CMP
Hypertrophic CMP
Restrictive CMP
Dilated CMP
Progressive dilation
Systolic dysfunction
Causes: genetic, toxic including ethanol, myocarditis, pregnancy-induced, idiopathic
Heart weight increased, Fiber hypertrophy and atrophy, Interstitial and subendocardial fibrosis
Hypertrophic CMP
Myocardial Hypertrophy
Diastolic dysfunction
1/3 outflow problems
Weight increased, wall thickened, hypercontractility, hypertrophy
Restrictive CMP
Primary decreased elasticity
Diastolic dysfunction
Mostly preserved systolic function
Normal size, myocardium dense, focal/diffuse interstitial fibrosis
Valvular Heart Diseases
Morphologic changes result in:
Stenosis: Mostly primary valvular pathology, usually chronic
Insufficiency: Primary valvular pathology, due to pathology in surrounding structures (aorta, papillary muscles), acute e.g. papillary muscle rupture, chronic
Combined lesion
Etiology:
Inborn
Acquired
Acquired mitral valvular disease
Mitral prolapse
Acquired aortic valvular disease
Complications after implantation of valvular prosthesis:
Thrombosis / thrombembolism
Bleeding due to anticoagulant use
Endocarditis
Mechanical wear-and-tear
Peri-implant pathology: granulations
Congenital Heart Pathologies
Atrial septal defect: Left-to-right shunt
Hyperload of pulmonary circulation
Insufficiency of right ventricle
Shunt reversal
Late-onset cyanosis
Eisenmenger syndrome
Fixed defect
Patent foramen ovale
Size adequate
Non-fusion
Transient flow
Paradoxical embolism is possible
Ventricular septal defect: left-to-right shunting
Most common congenital heart anomaly at birth
Patent ductus arteriosus
Tetralogy of Fallot: right-to-left shunt
Most frequent cyanotic congenital heart pathology
Stenosis in truncus pulmonalis: subpulmonal stenosis, valve stenosis
Right ventricular hypertrophy
Ventricular septal defect
Aortic valve location above septal defect
Aortic coarctation
Infantile (preductal) coarctation
Adult (post-ductal) coarctation: most common
Truncus arteriosus
Truncus arteriosus = truncus pulmonalis + aorta
Tricuspid atresia
Closed tricuspid valve
Blood flow is possible through atrial and ventricular septal defects