1. Pathology Tutorial 31st batch
CARDIOVASCULAR SYSTEM
Pathology Tutorial 31st batch

2. 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)

3. Calcification
Congenital heart disease
Pulmonary hypertension
Pulmonary oedema
Right heart failure
Atrial fibrillation
Thrombo-embolism- cerebral/ renal/ peripheral/ intestinal infarction

4. left sided valves> right sided valves
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

5. joints/ skin /central nervous system
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

6. 2.1Define aneurysm (10)
2.2Classify aneurysms (40)
2.3Describe the clinical presentations of an abdominal aneurysm and the underlying pathological basis (50)

7. 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

8. 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

9. 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)

13. Coagulative necrosis
Macroscopic and microscopic appearance depends o age of the infarct
MI less than12 hours - not apparent macroscopically
hours – reddish blue in colour due to stagnated blood.
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

14. 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

15. Infective endocarditis
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

16. 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)

17. 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

18. 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

19. Acute myocardial infarction

20. 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)

21. Causes inflammation of all three layers of heart
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

22. Causes of endocardial vegetation
Infective endocarditis
Non bacterial thrombotic endocarditis
libman-sacks endocarditis
Extra cardiac manifestations
Migrating polyarthritis
Erythema marginatum
Subcutaneous nodule
Rheumatic chorea

23. 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)

24. Macroscopy- infarcted area is soft yellow tan colour
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

25. Complications arrhythmia Pericarditis
Papillary muscle dysfunction results in mitral regurgitation
Myocardial rupture – VSD
Mural thrombus formation and thromboembolism
Later progressive heart failure

26. 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

27. What is atherosclerosis?
Large arteries and medium sized arteries
Formation of atheroma in intima of vessels
Can lead to obstruction and weakening of wall

28. Response to injury theory - mostly accepted
Explain the pathogenesis of atherosclerosis / formation of uncomplicated atheroma.
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 )

29. 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

30. Endothelial dysfunction
Increased permeability
Prothrombotic tendency
Leucocyte ,monocyte, platelet adhesion
Lipoprotein insudation
Accumulation of EC lipids
oxidization
Release of chemical mediators
Monocyte migration into sub endothelial space
Migration of smooth muscle cell into intima
Lipid taken up by macrophages and smooth muscle cells
Proliferation of smooth muscle cells
Deposition of ECM (collagen and proteoglycans)
Fibrous cap
Foam cells

31. Risk factors for atherosclerosis
Age
Male
Hyperlipidemia
Family history
Hypertension
Diabetes mellitus
Unhealthy diet ??
smoking
Lack of exercise
Homocystinuria
obesity
Stressful life style

32. Describe the appearance of a uncomplicated atherosclerotic plaque?
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

33. New vessel

34. Rupture , ulceration, and erosion Heamorrage into the plaque
What are the complication of atherosclerotic plaque?
Rupture , ulceration, and erosion
Heamorrage into the plaque
Athero embolism
Critical stenosis
Aneurysm formation due to atrophy of media
Calcification

36. What is arteriolosclerosis? Occurs in small vessels
Thickening of vessel lumen and narrowing
Causes ??
Types
Hyaline arteriolosclerosis
Hyperpalstic arteriolosclerosis

37. Chronic endothelial dysfunction /damage due to certain factors
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

38. 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

39. Describe the vascular changes in systemic hypertension?
Large and medium sized artery –atherosclerosis and degenerative changes
Small vessels - arteriosclerosis