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• CARDIOVASCULAR SYSTEM
Pathology Tutorial
31st batch
A patient is found to have a mid-diastolic murmur
and is diagnosed as having mitral stenosis. He has a
past history of Rheumatic fever.
 List 2 other possible causes for mitral stenosis? (20)
 List 2 complications of mitral stenosis? (20)
 Describe the microscopic and macroscopic changes
of the heart in acute rheumatic fever (50)
 List 2 other organs / tissues involved in acute
rheumatic fever (10)
• Calcification
• Congenital heart disease
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Pulmonary hypertension
Pulmonary oedema
Right heart failure
Atrial fibrillation
Thrombo-embolism- cerebral/ renal/
peripheral/ intestinal infarction
• Affects all three layers of the heart
• Involvement of the endocardium
 Heart valves become edematous (thickened) and loss the
translucency.
 Small multiple wart like vegetations seen along the line of closure.
These are firmly attached to valvular leaflet and appear as irregular
ridges of valve
◦ left sided valves> right sided valves
◦ On atrial surface of AV valves and ventricular surface of
semilunar valves
 Microscopically , Infiltration lymphocyte and plasma cells is diffuse;
Aschoff bodies with central fibrinoid necrosis also seen. tiny (1-2mm)
vegetation along the lines of closure of the heart valve. Vegetation
contains fibrin and super added small thrombi (free of micro
organism)
• Mural endocarditis induces irregular thickenings of endocardial surface
called MacCallum plaques
 Myocarditis – ventricles becomes soft and flabby at early stage.
microscopically aschoff bodies are characteristic. Aschoff body is foci of
fibrinoid necrosis surrounded by anitschkow cells and multi nucleated
aschff cells and infiltration of lymphocytes and plasma cells.
 Loss of normal shiny and serofibrinous pericardial exudate in the
pericardial sac described as "bread-and-butter" pericarditis.
Microscopically contains fibrin deposits and cellular infiltrate mainly
lymphocytes and plasma cells. Ashoff bodies may be seen.
joints/ skin /central nervous system
• 2.1Define aneurysm (10)
• 2.2Classify aneurysms (40)
• 2.3Describe the clinical presentations of an
abdominal aneurysm and the underlying
pathological basis (50)
is a localized, abnormal dilatation of blood vessel / heart.
Classification of aneurysm
Depending on composition of wall
◦ True aneurysm - when it involve all 3 layers of vessels/
heart
 Atherosclerotic
 Congenital
 Infection – mycotic aneurysm ,Syphilitic
 Inflammation - vasculitis
 Ventricular aneurysm follows transmural MI
◦ False aneurysm - extra vascular hematoma that freely
communicate with the intravascular space
 Usually due to trauma
Depending on their shape and size
 Saccular aneurysm – spherical out pouching
 Fusiform – diffuse circumferential dilatation of
long segment of vessel
Clinical presentation AAA and its pathological basis (compression,
rupture and thrombo embolic phenomena and arterial occlusion)
 Pulsating abdominal mass
 Backache – compression of nerves / erosion of vertebra,
 Ureteric colic – compression of ureter
 Abdominal pain, distension, pallor- leaking aneurysm irritates the
peritoneum
 Hypovolumic shock – rupture leads to massive intra abdominal
heamorrage
 Acute onset severe pain in lower limb , pulse less , pale/ gangrene
-Limb ischemia due to thrombo embolism
 Abdominal pain , vomiting – intestinal ischemia due to mesenteric
artery occlusion by emboli
 Heamaturia – renal infarct / erosion of ureter
• 3.1 Discuss the serum enzyme changes in
myocardial infarction (40)
• 3.2 What type of necrosis would you see in a
myocardial infarction (10)
• 3.3 Describe the macroscopic and microscopic
appearance of myocardial infarct (30)
• 3.4 List 4 possible complications that can
occur after myocardial infarction? (20)
 Coagulative necrosis
• Macroscopic and microscopic appearance depends o age of the infarct
 MI less than12 hours - not apparent macroscopically
 12- 24 hours – reddish blue in colour due to stagnated blood.
 48 -72 hrs-Progressively becomes pale and
 3- 7 days - more sharply demarcated yellow , soft area
 10 – 14 days infarct is rimmed by hyperemic area
 4-6 weeks – grey and become contracted thin fibrous scar.
• microscopic
 Coagulative necrotic features seen in 4 to 12 hours, odema heamorrage few
neutrophils
 At the periphery of infarct – wavy fibers seen
 Sub lethal cells at the periphery shows myocyte vacuolization
 In 1 -3 days – acute inflammation dense PMNL infiltration
 5-10days – macrophages remove cell debris
 2-3 weeks – granulation tissue with loose collagen and
abundant capillaries
 4- 6 weeks – become less cellular and decreased vascularity.
 8weeks collagenous scar
Complications
 Cardiogenic shock due to impaired contractility
 Congestive heart failure
 Arrhythmias
 mitral regurgitation due to papillary dysfunction
 Ventricular septal defect due to myocardial rupture
 Pericarditis
 Mural thrombus and emboli
 Dressler’s syndrome
 Ventricular aneurysm
 Progressive late heart failure
 Explain the pathological basis
presence of embolic phenomenon in infective endocarditis and absence in
rheumatic endocarditis (25)
• Infective endocarditis
– Forms friable bulky and potentially destructive
vegetation on the heart valves, vegetation contains
micro organisms
• Rheumatic endocarditis
– Cardiac manifestation of rheumatic fever associated
with inflammation of the endocardium which results
valvular deformities
– vegetations are small 1-2 mm that are firmly
attached to the valves
4. Write short notes on the macroscopic
appearance of heart in
• 4.1 Acute rheumatic fever (30)
• 4.2 Infective endocarditis (30)
• 4.3 Acute myocardial infarction (40)
Acute rheumatic fever
 Affects all three layers of heart
 Small vegetation along the site of closure of valves
 Sub endothelial plaques may be seen
 Diffuse involvement of myocardium leads to soft
,flabby myocardium
 Pericardium- looses its shiny appearance; contain
fibrinous or serofibrinous exudate in the pericardial
sac gives bread and butter appearance , usually
heals without any sequale
Infective endocarditis
 Only the involve endocardium
 Aortic and mitral valves are commonly affected
 Forms friable bulky and destructive vegetation
containing fibrin, inflammatory cells and
microorganism
 Size of vegetation varies with type of organism (few
mm – cm)
 Single /multiple
 Potentially destructive
 Can erode into myocardium and cause ring abscess
• Acute myocardial infarction
5. A patient is diagnosed to have acute
rheumatic fever
• 5.1 Describe the pathological changes
that could be seen in the heart of this
patient? (50)
• 5.2 List 2 other causes for endocardial
vegetation? (20)
• 5.3 Name 3 extra cardiac manifestations
of rheumatic fever? (30)
◦ It is type II hypersensitivity reaction which follows Group A
streptococcus infection .
◦ Causes inflammation of all three layers of heart
◦ Discrete inflammatory lesion called aschoff bodies are the
pathognomic lesion
◦ Endocarditis - Involvement of the endocardium typically results in
fibrinoid necrosis and tiny (1-2mm) vegetations along the lines of
closure of the heart valve, which do not have much effect on cardiac
function in acute phase
 left sided valves> right sided valves
 Mitral valve is affected commonly
◦ subendothelial lesions may induce irregular thickenings called
MacCallum plaques
◦ Myocarditis - diffuse involvement of myocardium with aschoff bodies
scattered in the intertitial space may lead to cardiac dilatation ,
arrhythmia and congestive heart failure
◦ Pericarditis- contain fibrinous or serofibrinous exudates , heals without
any sequale
• Causes of endocardial vegetation
– Infective endocarditis
– Non bacterial thrombotic endocarditis
– libman-sacks endocarditis
• Extra cardiac manifestations
– Migrating polyarthritis
– Erythema marginatum
– Subcutaneous nodule
– Rheumatic chorea
6. A patient presenting with left sided chest pain of 48hours
duration is diagnosed as having
myocardial infarction.
 6.1 define infarction (10)
 6.2 What type of necrosis would you see in this patient? (10)
 6.3 Describe the macroscopy and microscopy of this patient’s
infarct (30)
 6.4 List 2 biochemical investigations that would help in the
diagnosis (20)
 6.5 List 4 possible complication this patient can develop (30)
• Infarction
– Necrosis of heart muscle due to ischemia
• Coagulative necrosis
• Macroscopy- infarcted area is soft yellow tan colour
Microscpically – coagulative necrotic features ………..,
with wavy fibers at the periphery
• loss of nuclei and striation of myocytes,
• neutrophil infiltrationin the intertitrial space
• Serum Troponin I , CK-MB levels
Complications
◦ arrhythmia
◦ Pericarditis
◦ Papillary muscle dysfunction results in mitral
regurgitation
◦ Myocardial rupture – VSD
◦ Mural thrombus formation and thromboembolism
◦ Later progressive heart failure
• What is arteriosclerosis?
• It is a general term includes
atherosclerosis, medial calcification
(occur in old people), and arteriosclerosis
• Thickening and loss of elasticity is
common feature
• What is atherosclerosis?
• Large arteries and medium sized arteries
• Formation of atheroma in intima of
vessels
• Can lead to obstruction and weakening of
wall
• Explain the pathogenesis of atherosclerosis /
formation of uncomplicated atheroma.
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Several theory –cellular proliferation in the intima, repetitive thrombi
formation and organization
• Response to injury theory - mostly accepted
• Chronic inflammatory process (of arterial
wall) in response to endothelial injury.
• Risk factors – induces endothelial injury (
usually chronic )
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Endothelial dysfunction
Increased permeability
Leucocytes adhesion
Accumulation of oxidized LDL in the sub endothelial space
Monocytes adhesion to endothelium and migration and
transformation into macrophages
Factors released from activated platelet ,macrophages and vascular
wall induces Smooth muscle cells recruitment to sub endothelium
Smooth muscle proliferates and produces collagen and other extra
cellular matrix ( which forms the fibrous cap of the plaque)
macrophages engulf lipid and become as foam cell
Smooth muscle cells also take up lipid
Accumulation of intracellular and extra cellular lipid
Endothelial
dysfunction
Leucocyte ,monocyte,
platelet adhesion
Increased
permeability
Prothrombotic
tendency
Lipoprotein
insudation
Accumulation of EC
lipids
oxidization
Monocyte
migration into
sub endothelial
space
Release of chemical
mediators
Migration of smooth
muscle cell into intima
Lipid taken up by
macrophages and
smooth muscle cells
Foam cells
Proliferation of
smooth muscle cells
Deposition of ECM
(collagen and
proteoglycans)
Fibrous
cap
• Risk factors for atherosclerosis
– Age
– Male
– Hyperlipidemia
– Family history
– Hypertension
– Diabetes mellitus
– Unhealthy diet ??
– smoking
– Lack of exercise
– Homocystinuria
– obesity
• What is atherogenesis?
• Describe the appearance of a uncomplicated
atherosclerotic plaque?
• Macroscopy
• Large vessel and medium sized artery, usually around
the origin of branches.
• White-yellowish raised focal lesion on in the luminal
surface
• Few mm-1-2cm
• Usually eccentric and multiple
• Soft core covered by firm fibrous tissue
New vessel
What are the complication of atherosclerotic
plaque?
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Rupture , ulceration, and erosion
Heamorrage into the plaque
Athero embolism
Critical stenosis
Aneurysm formation due to atrophy of
media
• Calcification
• What is arteriolosclerosis?
• Occurs in small vessels
• Thickening of vessel lumen and
narrowing
• Causes ??
• Types
– Hyaline arteriolosclerosis
– Hyperpalstic arteriolosclerosis
• Describe the pathogenesis of Hyaline
arteriolosclerosis.
• Chronic endothelial dysfunction /damage
due to certain factors
• Leakage of plasma
• Excessive deposition of ECM by smooth
muscle cells – hyaline thickening of
arterioles,> luminal narrowing
• Hyperplastic arteriolosclerosis
 Occurs in malignant hypertension
 Increased permeability of small vessels to fibrinogen and
other plasma proteins
 Platelet deposition at the site of injury
– Plasma and platelet derived growth factors induces
smooth muscle hyperplasia
• Fibrinoid necrosis is also
associated in malignant HT
• Describe the vascular changes in systemic
hypertension?
• Large and medium sized artery –
atherosclerosis and degenerative changes
• Small vessels - arteriosclerosis