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Heart

Banha 2018 -2019


Systemic Pathology [ HEART DISEASES]

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

Pathogenesis: After 2-5 weeks  elevated ASO antibody


 Antigenic similarity: Ab against bacterial (M protein) --> reacts with cardiac muscle
 Altered Antigenecity: of collagen by bacterial toxin. Collagen became antigenic
 Immune complex theory: deposition of Ag-Ab complex in the heart (NOT
identified)

Pathology : Ashoff'snodule: the pathognomonic lesion


 Sites:Heart– Joint – Skin – CNS - serous sacs
 Gross:rounded – small (1-2mm) – pale grey - firm
 Micro:
o Early:
 Fibrinoidnecrosis (dmamged collagen + fibrindeposts)
 Mixed Inflammatory cells (lymphocyte & macrophages)
 (Anitskow or Aschoff’scell) :Activated macrophage
 Aschoff'sgiantcells(multinucleated giant cells 2-8 neuclei, abundant
basophilic cytoplasm)
 Fibroblasts
o Chronic lesion( in heart only) :Fibrosis + Calcification

2 Dr. Abdelrahman Khalifa , MD., PhD.


Systemic Pathology [ HEART DISEASES]

Acute Rheumatic heart disease: (Pan-carditis)


common site is posterior wall of left atrium, para vascular and left valves (M, A)

Myocarditis Pericarditis Endocarditis


In Acute: In Acute: In Acute:
MultipleAschoffnodules Gross: fibrin between layers -Mural endocarditis:
(describe) (Bread & Butter) Ashoff body + swollen endocardium
muscles fibers are degenerated Micro: Sero-
--> dilated chamber
Chronic--> fibrosis
fibrinousinflammation rough patch(Mc Callum
patch)mural thrombosis

-Valve:75% mitral and aortic


- swollen red valve , endothelial
In Chronic: damage
Fibrosis of Aschoff nodules In Chronic:
Vegetations:
-Resolution Gross:multiple - Small – pale – adherent
-(organization) on top of the valve
Fibrosis Thick white patch along line of closure
(milky patches) Adhesive
mediastino-pericarditis micro: platelets + fibrin
endothelial damage + subendothelial
or adhesion between layers
ashoff nodules + swollen vascular
cusps

Chronic Rheumatic Valvulitis:


 Valve  fibrosis & calcification  thick, white & deformed
 Commissural adhesionFish mouth or button hole
 Cordae tendenae thick & short Funnel shaped valve
 Valve stenosis , or incompetence , or both (double lesion)
Complications of Rhuematic heart disease:A F S H
 Arrhythmia
 Fibrosis
 Subacute Bacterial Endocarditis (SBE)
 Heart failure(due to chronic valve lesion)

3 Dr. Abdelrahman Khalifa , MD., PhD.


Systemic Pathology [ HEART DISEASES]

N.B. Embolism if occurs(from mural thrombosis – NOT from Rhuematic vegetations)

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 onlyno chronic joint lesion, no joint damage)

Rheumatic Skin lesion:


 Subcutaneous nodules (Aschoff): painless over bony prominence 2mm -2cm
 Erythema marginatum:red borders and pale center

Rheumatic Chorea (more in girls)


 Rheumatic lesion of Basal ganglia (perivascular nodules)
 Involuntary, purposeless, jerky movementself limited

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

Types of Endocarditis = Types of cardiac vegetations:

 Non infectiveR A T
 Rheumatic endocarditis
 Atypical verrucous endocarditis( Libman-sackendocarditis of SLE)
 Thrombotic non bacterial endocarditis

 Infective acute – sub - chronic


 Acute bacterial endocarditis (ABE)
 Subacute bacterial endocarditis (SBE)
 Chronic T.B, Syphilis, viral

4 Dr. Abdelrahman Khalifa , MD., PhD.


Systemic Pathology [ HEART DISEASES]

Acute infective Subacute infective


Endocarditis endocarditis
Age >50 y(lower immunity) young
Highly virulent bacteria (pyogenic) low virulent bacteria (e.g.strept. veridance 95%
septicemia --> suppuration on valves of cases)
Aetilology Mostly left valves bacteremia

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
valveSuppurative of diseased valve (enumerate)non
Pathogenesis inflammationSuppurative vegetations Suppurative inflammation

Valve: Valve:
-suppurative inflammation - non supp.inflammation
-ulceration perforation

Morphology Vegetations: Vegetations:


-Large bulky -Less bulky
-Yellow -greyish red
-Friable (?) -less Friable
-Micro:
-upper zone: platelets - fibrin -Micro:
-middle zone: bacteria -upper zone: platelets - fibrin
-Lower zone: inflammatory cells – -middle zone: bacteria
Neutrophils & pus cells -Lower zone: inflammatory cells –valve Fibrosis
Severe myocardial degeneration Mild myocardial degeneration
Cardiac: Cardiac:
-Vlaveperforationacute heart failure -Vlavestenosis -incompetenceHeart failure
-Abscess in myocardium, pericardium -Degeneration of cardiac muscle due to toxins
Heart failure 6-18 months
Extra-cardiac (Embolic): Extra-cardiac (Embolic):
Complications
- Embolipyemia - Emboliinfarctions
-Cerebral, retinal, cardiac, Splenic, renal
-very small emboli in vasa vasorum of Arteries -
Mycotic aneurism

-Allergic vasculitis (Ag-Ab


mediated)&microemboli:
- Focal embolic GN (flea bitten kidney)
(glomerular necrosis and inflammation)
- Finger lesions (osler nodule – splinter
hemorrhage)

5 Dr. Abdelrahman Khalifa , MD., PhD.


Systemic Pathology [ HEART DISEASES]

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

- Rheumatic - Rheumatic - Rheumatic - Rheumatic


-SBE -SBE -SBE -SBE
-Congenital -Congenital valve prolapse -Congenital -Congenital (Marfan)

Causes -Dilated left ventricle -Senile(calcific -Syphilitic aneurism


(Hypertension – Healed Atherosclerotic
infarction – Anemia – stenosis) -dilated left side in
Aortic incompetence) H.F.

Morphology Similar to rheumatic valve Wide commisure Similar to MS Similar to MI


(describe)
Or prolapsed valve

left atriumdilatation & left side dilatation& left ventricle left side dilatation&
hypertrophy Lung hypertrophyleft sided dilatation& hypertrophyleft
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 Stenosis & pulmonary Stenosis:


caused by the same causes + carcinoid sndrome --> right side dilation and hypertrophy and
failure + pale anemic lung

Tricuspid incompetence and pulmonary incompetence : are very rare, could be caused by
same causes or ABE --> lead to right side dilatation and failure

6 Dr. Abdelrahman Khalifa , MD., PhD.


Systemic Pathology [ HEART DISEASES]

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

7 Dr. Abdelrahman Khalifa , MD., PhD.


Systemic Pathology [ HEART DISEASES]

Ischemic heart Disease


group of diseases resulting from insufficient flow to myocardium

Gradual ischemia Acute sudden occlusion

Coronary atherosclerosis Complicated coronaryAtherosclerosis


Anemia - Aortic valve disease -Coronary embolism
Hypertension - Hypertrophy -Coronary vasculitis (PAN)
-Coronary spasm
-Aneurism of Syphilitic aortitis (narrow coronaries)
-Aortic Aneurism (dissecting type)
-Size of heart is mildly reduced Coagulaive necrosis
-Patchy pale areas of fibrosis
-Valve fibrosis or calcification
Effects: Effects:
-Arrhythmia and Heart failure -Myocardial infarction
-Angina - V.F.  sudden death
-Acute sudden occlusion (if complicated)

Angina
Retrosternal chest pain, referred to left shoulder, neck and jaw

causes Causes of ischemic Heart diseeases (enumerate?) - more in males

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

P.F.:causes of IHD, mainly Complicated atherosclerosis

Sites:

 Leftanterior coronary occlusion (40-50%) infarction of anterior wall of left


ventricle, ant 2/3 of septum & apex (the commonest)
 Right coronary occlusion (30 -40%) infarction of posterior wall of left ventricle ,
right ventricle, post 1/3 of septum.
 Left circumflexocclusion (15-20%) infarction of lateral wall of left ventricle

8 Dr. Abdelrahman Khalifa , MD., PhD.


Systemic Pathology [ HEART DISEASES]

Type of injury:

Sub-endocardial Transmural

-1/3 thickness , multifocal -Full thickness , unifocal


-stenosis but not occluded coronary -caused by coronary occlusion

Morphology:

0.5 -4 hours 4 hours – 1st day 1st – 3rd day 1st – 2nd week 2nd week-2nd
reversible month

Gross:none Pale , mottled Pale yellow Pale yellow Grayish white


Red margins Firm

Micro: Coagulative necrosis -no striations Granulation Collagen scar


non -eosinophilic fibers -no neuclei tissue at margin
- pyknosis -neutrophils
-neutrophils (describe)
E/M: glycogen -MQ appear 3-7 days
loss

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
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9 Dr. Abdelrahman Khalifa , MD., PhD.


Systemic Pathology [ HEART DISEASES]

Cardio-myopathy
Pathological changes of myocardium, not caused by ischemia, inflammation, or valve disease

Classification : 1ry (genetic) - 2ry ( e.g. Alcohol, Amyloid, Sarcoidosis)

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 septumbanana
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.

Congenital Heart diseases


 Incidence : 10% of heart diseases in children, starts in 5th to 8th gestational week
 Causes:Teratogenic Drugs– Trisomies (e.g. Trisomy 21) – D.M.- viral (Rubella, coxaci)-
syphilis
 Types:
 Non cyamotic left toright shut (ASD, VSD, PDA) , Stenotic (AS, PS,
Coarctation of Aorta)
 Cyanotic rightleft shunts (Fallot ,triology, tetralogy, Transposition of
A-P, Eisenmenger’s)

Aortic Coarctation:Focal stenosis in the wall of Aorta

10 Dr. Abdelrahman Khalifa , MD., PhD.


Systemic Pathology [ HEART DISEASES]

Shunt diseases
Left right shunt(non cyanotic) Right  left shunt(cyanotic)

-ASDpatent foramen ovale,(the most common) -Tetralogy of Fallot


-VSDLarge defect– Small defect of Roger Triology of Fallot
-PDA -Transposition of great vessles (A-P)
-Eisenmenger

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)

Tetralogy of Fallot:P.S. – Right ventr hypertrophy – Overriding of Aorta with


dextroposition – high VSD PROV . Effects of rtlft shunt (enumerate)

Triology of Fallot:P.S. – Right ventr hypertrophy – ASD


Effects of rtlft shunt (enumerate)

ASD :Patent foramen between both atria.


Effects: Effects of left right shunt (enumerate)

VSD :
Small defect (Roger’s) Big defect

rare Common

Muscular septum Membranous septum

11 Dr. Abdelrahman Khalifa , MD., PhD.


Systemic Pathology [ HEART DISEASES]

Heart Failure
Maintained impairment of cardiac function, with insufficient cardiac output

Acute:pulmonary embolism – Hemopericardium (tamponade) – Myocardia disease (?)

Chronic:

Left Sided H.F. Right sided H.F.


Causes:CAMPS Causes:

-Congenital (right  left shunts enumerate?) -Congenital (leftright shunts enumerate?)


-Aortic diseases -P.S.
-M.I(mitral incompetence- myocardial infarction) -M.S
-Pericardial disease (pericarditis – hemopericardium) -Pericardial disease (pericarditis – hemopericardium)
-Systemic hypertension -Pulmonary hypertension(lung fibrosis –
emphysema – lung congestion due to left sided HF)

Effects: Effects:
-Lung congestion  brown induration? Chronic generalized venous congestion ?
-Right sided heart failure

Mechanism of Heart Failure : Compansatory stage (High heart rate +


Physilologic dilatation) --> Decompansatory stage (Cardiac fatigue + Weak
contraction)

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

Hemopericardium(tamponade) is caused by: General causes of bleeding– Local


causes (injury – tumor – ruptured cardiac or aortic aneurism). Effect  limited diastole 
HF
Hydropericardium:Accumulation of serous fluid as a part of generalized edema 
Heart failure

12 Dr. Abdelrahman Khalifa , MD., PhD.


Systemic Pathology [ HEART DISEASES]

Tumors of the Heart:


Myxoma of left atrium(rare, but the most common in adults)

Rhabdomyoma (the most common in children) – Others: Lipoma – Fibroma- Angiosarcoma)


– metastatic(e.g.bronchial carcinoma ,leukemia, lymphoma, melanoma)
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Myxoma of the heart


Site: Mainly right atrium

Gross:
Single - rounded - 1-10 cm

Micro:
Myxoid matrix + compressed and stellate cells

Fate:
Benign
Valve obstruction

13 Dr. Abdelrahman Khalifa , MD., PhD.