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Pathology of the cardiovascular system

Dr. Haytham Aly

• Pericardium, epicardium • Myocardium • Endocardium

Coronary fat and bl. vsl.

Post-mortem changes (Normally found during necropsy) • Left ventricle is empty from blood. • Post mortem clots (Current jelly & Chicken fat clot ) are present in the right atrium, right ventricle and large veins (lack contraction). • Chicken fat clot sepsis, leukemia, sever anaemia, long agonal period.

• Hemoglobin imbibition. • Euthanasia solution cause crystalline deposits on the endocardium

Terms • An increase in myocardial mass is termed hypertrophy (valvular stenosis). • An increase in chamber volume is termed dilation. (flabby, due to myocardial degeneration)

• An overall increase in cardiac size is termed cardiomegaly.

Cardiac anomalies • Acardius heart absence • Ectopia cordis  displacement of the heart a. Dextroheart heart present in the right side b. Ectopia cordis cervicalis ”neck” c. Ectopia cordis pectoralis –defect in the sternum d. Ectopia coridis abdominalis – defect in the diaphragm

• • • •

Multiple hearts  chickens Valves stenosis or incompetency Dextro –aorta aorta in the right side Valvular hematocyst

Persistent fetal structures

Normal fetal circulation Notice 2 blood shunts 1. Oval foramen 2. Ducts arteriosus

Persistent fetal structures

Persistent ductus arteriosus

Tetralogy of Fallot

Persistent foramen ovale

Ventricular septal defect

Persistent ductus arteriosus

Persistent foramen ovale

Ventricular septal defect

Disturbance in growth 1. Aplasia 2. Atrophy a. Physiological  senile b. Pathological brown atrophy

3. Hypertrophy a) Physiological (racing horses, hunting dogs) b) Adaptive  valvular stenosis

Disturbance in metabolism • Cloudy swelling, vacuolar and hydropic degeneration • Mucoid and hyaline degeneration • Gout—(visceral gout in birds, reptiles) • Glycogen infiltration • Fatty change • Melanosis • Mineralization • Serous atrophy of coronary fat (cachectic animals, starvation)

Disturbance in the circulation • Hypremia • Embolism, thrombosis • Infarction occlusion of a branch of coronary artery small area (Organized); Large area (cardiac muscle degeneration) cardiac aneurysm rupture

• Cardiac tamponade rupture of the atrial wall hemopericardium prevent heart movement death

• Hydropericardium “oedema” • Petechial and ecchymotic hemorrhages

Pericardial diseases • • • • •

Hydropericardium Hemopericardium Pneumopericardium Pyopericardium Pericarditis

• Hydropericardium: Accumulation of fluid; either exudate (inflammatory) or transudate (noninflammatory) inside the pericardial sac. Cause: Increase blood pressure, increase permeability , African horse sickness

• Hemopericardium (Cardiac tamponade)

• Accumulation of blood in the pericardial sac. Stop the movement of the heartdeath. • Duet to: o Trauma by a sharp object o Rupture of a cardiac aneurysm o Rupture of an aortic aneurysm o Rupture of the coronary artery

Pneumopericardium • Accumulation of gas in the pericardial sac. • Due to: o Putrefaction of the exudate by a gas producing organism. o Broken ribs (Donkeys) o Gas pass from reticulum (TRPC)

Pyopericardium • It is accumulation of pus in the pericardial sac. • Due to: Pyogenic bacteria, TRPC

Pericarditis (Inflammation of the pericardium, usually secondary) • Infectious – Haematogenous as in septicemia (Mannheimosis, black leg) – By extension following myocarditis or pleuritis. – Types: serous, serofibrinous, fibrinous, hemorrhagic, (suppurative, gangrenous usually associated with TRPC) and granulomatous. – Macroscopic= type of exudate (fluid, blood, pus, yellowish fibrin ‘’Shaggy heart”) – Microscopic= Dilated bl. vsl., exudate (RBCs, neutophils, fibrin threads) and leukocytes.

Fibrinous pericarditis (Shaggy heart)

Gangrenous pericarditis

Granulomatous pericarditis (T.B.)

Fate of pericarditis:

1. Liquefaction of the exudate by neutrophils, absorption and regeneration. 2. Organization of exudate adhesion between parietal an visceral layer of the pericardium. 3. Calcification may occur if the exudate is extensive. 4. Rate of fluid accumulation in the pericardium:

1. Rapid rise in the pericardial pressure cardiac tamponade  death

2. Slow rising pressure heart compensate (hypertrophy) if continueddeath

Traumatic reticulopericarditis (Hardware disease) Def.: It is inflammation of the pericardium due to the penetration of a sharp object to the wall of the reticulum, diaphragm and pericardium. Common in cattle due to prehension of food by tongue.

Pathogenesis: Nail or wire penetrate reticulum fixed by granulation (Forming canal)penetrate diaphragm pericardium. Violent pentrationheart or coronary artery  cardiac tamponade Mild irritation serofibrimous  infected  suppurative

• Lesions: – Thoracic cavity filled with exudate “hydrothorax” – Thickening of the pericardium with dirty yellowish layers of fibrin (Shaggy heart). – When the fibrin is separated from each other by suppuration (pus) it is called butter and bread appearance

Fate of traumatic reticulopericarditis:

1.Mild serofibrinous pericarditis Resolution 2.Sever fibrinous pericarditis  may resolve with focal areas of adhesion “organization” 3.Invaded by pyogenic m. o. Suppurative pericarditis resolution doesn’t happen  massive adhesion Constrictive pericarditis 4.Constrictive pericarditis : chronic fibrous tissue proliferation and adhesion between the two layers of the pericardium following suppurative form leading to congestive heart failure due to cardiac hypertrophy.



Pathology of th ecardiovascular system