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Rheumatic fever
Autoimmune inflammatory collagen disease, charecterized by degenerative changes in
connective tissue, following streptococcal infection
Predisposing factors: high incidence in Children 5-15 y (90% of heart dis. in children)
URT infection by group A Beta-hemolytic strept., e.g. tonsillitis(low immunity– crowding)
Herditery factor
Rheumatic Arthritis:
Site:Large joints , in Adults
Gross :acute inflammation with effusion , Migratory, fleeting poly-arthritis
Micro :Synovitis + mixed inflammatory cells + Aschoff nodules
Fate:Self limiting(Acute onlyno chronic joint lesion, no joint damage)
N.B.
Other Rheumatic lesions:- Arterial nodules in media and adventetia of small arteries, Plurisy,
peritonitis, interstetial pneumonia
Clinical Diagnosis (Jone'schriteria) for diagnosis:2 major signs or 1 major + 2 minor
signs
Major: Carditis, Arthritis, Chorea, Skin nodules, Erythema Minor: Fever, ASO, ESR, Arthralgia
Endocarditis
Inflammation of mural&valvular endocardium, with formation of vegetations
Non infectiveR A T
Rheumatic endocarditis
Atypical verrucous endocarditis( Libman-sackendocarditis of SLE)
Thrombotic non bacterial endocarditis
P.F :
-Dental extraction or Tonsillectomy
-Diseased valve
(e.g. Chronic Rheumatic – congenital – artificial)
-Defective shunt
(ASD, VSD, PDA)
-Drug abuse (mainly right sided SBE)
Pyogenic bacteria proliferate on healthy weak bacteria proliferate inside vegetations
valveSuppurative of diseased valve (enumerate)non
Pathogenesis inflammationSuppurative vegetations Suppurative inflammation
Valve: Valve:
-suppurative inflammation - non supp.inflammation
-ulceration perforation
Svere Toxemia
-Mild Toxemia
-Fever , anemia , leukocytosis
-Clubbing of fingers
-Degeneration in organs
-Peticheal hemorrhage in skin & retina
Fate Fatal within 2 months Fatal within 6-24 months if not treated
(Pyemia + valve perforation) (Chronic heart failure)
Valvular diseases
Mitral stenosis Mitral incompetence Aortic stenosis Aortic
incompetence
left atriumdilatation & left side dilatation& left ventricle left side dilatation&
hypertrophy Lung hypertrophyleft sided dilatation& hypertrophyleft
congestion pulmonary heart failure hypertrophy sided heart failure
hypertension Right vent right sided heart failure
dilatation& hypertrophy Lung congestion coronary&cerebral
Right sided heart failure pulmonary hypertension insufficiency
Effects Right vent dilatation&
hypertrophy Right
sided heart failure
Tricuspid incompetence and pulmonary incompetence : are very rare, could be caused by
same causes or ABE --> lead to right side dilatation and failure
Myocarditis
myocardial inflammation which may resolve or progress to HF
Intoxication
o Toxic (bacterial like diphteria or chemicals CO )
o Degenerated muscle + mixedinflammation + necrosis in severe cases
Infection (Viral)
o Immune response against Viralinfection (coxsacki, influenza, Hepatitis,
polio)
o Focal uscle necrosis + mixed inflammation with excess lymphocytes
Infective (Bactrial).
o septicemia and pyemia --> suppurative inflammation + degenration +
necrosis.
o TB, Syphilis, Chlamydia
Immunological
o Rheumatic,
o SLE
Idiopathic giant cell myocarditis (Fiedler’s): rare
In young adults, idiopathic
o Chronic inflammatory cells and giant cells + neutrophils
Angina
Retrosternal chest pain, referred to left shoulder, neck and jaw
mechanism Iscjemia Hypoxia Lack of ATP anerobic glycolysis Lactic acid Pain
Myocardial Infarction
Coagulative necrosis of myocardium due to ischemia
Incidence: Most common cause of disease-induced death. Male >female, >50 y
Sites:
Type of injury:
Sub-endocardial Transmural
Morphology:
0.5 -4 hours 4 hours – 1st day 1st – 3rd day 1st – 2nd week 2nd week-2nd
reversible month
Complications:: C H A M P
Congestive heart failure (Left S. heart failure lung congestion Rt. S. H.F.)
Hemopericardium (Tamponade) : due to ruptured weak muscle
Aneurismal dilatation (due to fibrosis) thrombosis& embolism
Arrhythmia (ischemia of conduction system)
Myocardial rupture during 7 days(muscle is weak and infiltrated by inflam. cells ,
before granulation tissue)
Pericarditis
---------------------------------------------------------------------------------------------
Cardio-myopathy
Pathological changes of myocardium, not caused by ischemia, inflammation, or valve disease
Morphological Patterns
Dilated (Congestive)
o The most common typeof cardiomyopaty
o Congenital, or 2ry to Toxins (Alcohol, ,Beri Beri, Congenital)
o All chambers are dilated with thin muscle, some fibers are hypertrophied
o Systolic dysfunction Heart Failure
Hypertrophic
o Congenitalautosomal dominant(B-myosin,Troponin T)
o Asymmetricalhypertrophy of left ventricle & ventricular septumbanana
shaped distorted ventricle
o Diastolic dusfunction H.F.
Restrictive
o Rare type
o Idiopathic fibrosis , or 2ry to Amyloidosis, sarcoidosis, endomyocardial
fibrosis,
o Thickening of endocardium limitation of diastolic filling H.F.
Shunt diseases
Left right shunt(non cyanotic) Right left shunt(cyanotic)
Effects:
-Right s. dilation and hypertrophy rt. S.H.F. Effects:
-SBE -Cyanosis
- Reversal of shunt--> (Eisnemenger) -Left s. hypertrophy and dilatation ,H.F.
-SBE
PDA:In normal infants DA is closed after 8th week of birth due to low Pg E2, & hypoxia.
Effects: Effects of left right shunt (enumerate)
VSD :
Small defect (Roger’s) Big defect
rare Common
Heart Failure
Maintained impairment of cardiac function, with insufficient cardiac output
Chronic:
Effects: Effects:
-Lung congestion brown induration? Chronic generalized venous congestion ?
-Right sided heart failure
Pericarditis
Acute
o Sero-fibrinous: infection– immunological (Rhumatic, SLE) – infarction
o Suppurative (bacteria -->direct, blood, lymphatic)
o Hemorrhagic (Bleeding tendency - trauma)
Chronic
o Adhesive : Adhesive mediastino-pericarditis H.F.
o Constrictive: extensive fibrous tissue around the heart (defective
diastole) and may obliterate orifices of vena cava generalized
congestion
o Tuberculous adhesive or constrictive
Gross:
Single - rounded - 1-10 cm
Micro:
Myxoid matrix + compressed and stellate cells
Fate:
Benign
Valve obstruction