1. CARDIOVASCULAR SYSTEM PATHOLOGY-1.ppt

Pathology of the cardiovascular system

1. CARDIOVASCULAR
PATHOLOGY
By: Josphine
PhD Epidem. McM. Forensic Med.,Bsc. Clin. Med., Dip Clin Med.
2025

4. Normal Features
•250-300 grams
•40% of all deaths (2x cancer)
•Wall thickness ~ pressure
•(i.e., a wall is only as thick as it has to be)
•LV=1.5 cm
•RV= 0.5 cm
•Atria =0.2 cm
•Systole/Diastole
•Starling’s Law
NB; The above stated wall thickness measurements may differ depending on the
anatomical site , please check from anatomy references .

5. Cardiac Diseases

6. Pathology of the Heart
•All problems are eventually expressed as
inadequate cardiac output.
•Leaks in the system
•Electrical Conduction, irregular rhythm
•Obstruction to flow
•Valve problems, obstruction or incompetence
•Cardiac muscle weakness and failure

7. 1.Heart Failure
•Def; pathophysiologic state in which
impaired cardiac function is unable to
maintain an adequate circulation for the
metabolic needs of the tissues of the body.

8. Heart Failure
•Diminished out volume of either ventricle.
•Systolic failure
•Loss of pumping strength.
•Backup of blood behind weakened
ventricle.
•Atherosclerosis leading to chronic
ischemia.
•Diastolic failure
•Reduced ability of ventricle to fill.
•Constriction of trapping of ventricle

9. Etiology of Heart failure
1. Intrinsic pump failure
•Weakening of ventricular muscle
a)Ischaemic heart disease
b)Myocarditis
c)Cardiomyopathies
d)Metabolic disorders e.g.beriberi-
decreased cardiac function from
impaired cellular metabolism.
e) disorders of rhythm e.g. atrial
fibrillation and flutter

10. 2. Increased workload on the heart
•Increased mechanical workload – increased
myocardial demand- myocardial failure.
•Can either be; pressure load or volume load
(a)Increased pressure load
I.Systemic and pulmonary arterial
hypertension
II.Valvular diseases- mitral stenosis,
aortic stenosis, pulmonary stenosis
III.Chronic lung diseases

11. (b) Increased volume load
•Occurs when the ventricle is required to eject
more than normal volume of the blood-
cardiac failure
I.Valvular insufficiency
II.Severe anaemia
III.Thyrotoxicosis
IV.Arteriovenous shunts
V.Hypoxia due to lung diseases

12. 3. Impaired filling of cardiac chambers
a)Cardiac tamponade e.g. haemopericardium,
hydropericardium
b)Constrictive pericarditis

13. Types of heart failure

14. 1. Left Sided Failure
•Low output vs. congestion
•Lungs
•pulmonary congestion and edema
•Kidneys
•pre-renal azotemia
•salt and fluid retention
•renin-aldosterone activation
•natriuretic peptides
•Brain: Irritability, decreased attention, hypoxic
encephalopathy, stupor, coma
•Muscular weakness and fatigue

15. Left Heart Failure Symptoms
•Dyspnea
•on exertion
•at rest
•Orthopnea
•redistribution of peripheral edema fluid
•Paroxysmal Nocturnal Dyspnea (PND)
•Brain: Irritability, decreased attention,hypoxic
encephalopathy stupor,coma
•Muscular weakness and fatigue

16. Left Heart Failure
Dyspnea
Orthopnea
PND (Paroxysmal Nocturnal Dyspnea)
Blood tinged sputum
Cyanosis
Elevated pulmonary “WEDGE”
pressure (PCWP) (nl = 2-15 mm Hg)-
Pulmonary capillary wedge pressure (PCWP) is
frequently used to assess left ventricular filling,
represent left atrial pressure, and assess mitral valve
function.

17. Right Sided Heart Failure
•Aetiology
•left heart failure
•cor pulmonale
•Symptoms and signs
•Liver and spleen
•passive congestion (nutmeg liver)
•congestive splenomegaly
•ascites
•Kidneys failure
•Pleura/Pericardium
•pleural and pericardial effusions
•transudates
•Hypoxia in Peripheral tissues

18. Right Heart Failure
FATIGUE
edema
Jugular vein Distension
Hepatomegaly (congestion)
ASCITES, PLEURAL EFFUSION
GI symptoms
Cyanosis
Increased peripheral venous pressure
(CVP) (nl = 2-6 mm Hg)

19. Congestive Heart Failure
•Diminished
pumping ability of
left ventricle.
•Back up of blood
in pulmonary
vasculature.
•Pulmonary edema
•Peripheral edema

21. Pulmonary Edema

22. Liver Chronic Passive Congestion

23. Pitting Edema

24. •2. ACUTE AND CHRONIC HEART FAILURE.
• Depending upon whether the heart
failure develops rapidly or slowly, it may
be acute or chronic
•Acute heart failure.
•Sudden and rapid development of heart
failure occurs in the following conditions:
•i) Larger myocardial infarction
•ii) Valve rupture
•iii) Cardiac tamponade

25. •iv) Massive pulmonary embolism
•v) Acute viral myocarditis
•vi) Acute bacterial toxaemia.
•In acute heart failure, there is
sudden reduction in cardiac output
resulting in systemic hypotension
but oedema does not occur.
• Instead, a state of cardiogenic shock
and cerebral hypoxia develops.

26. Chronic heart failure.
•More often, heart failure develops slowly
as observed in the following states:
•i) Myocardial ischaemia from
atherosclerotic coronary artery disease
•ii) Multivalvular heart disease
•iii) Systemic arterial hypertension
•iv) Chronic lung diseases resulting in
hypoxia and pulmonary arterial
hypertension
•v) Progression of acute into chronic
failure.

27. •In chronic heart failure,
compensatory mechanisms like
tachycardia, cardiac dilatation and
cardiac hypertrophy try to make
adjustments so as to maintain
adequate cardiac output.
• This often results in well-
maintained arterial pressure
and there is accumulation of oedema.

28. 3. BACKWARD AND FORWARD HEART FAILURE.
•The mechanism of clinical manifestations
resulting from heart failure can be explained
on the basis of mutually interdependent
backward and forward failure.
•Backward heart failure.
•According to this concept, either of the
ventricles fails to eject blood normally,
resulting in rise of end-diastolic volume in the
ventricle and increase in volume and pressure
in the atrium which is transmitted backward
producing elevated pressure in the veins.

29. •Forward heart failure.
• According to this hypothesis, clinical
manifestations result directly from failure
of the heart to pump blood causing
diminished flow of blood to the tissues,
especially diminished renal perfusion
and activation of renin-angiotensin.

30. Compensatory mechanism
1.Hypertrophy
Increase in size and weight of the myocardium
2.Cardiac dilatation
Stress leading to accumulation of excessive volume of blood in
the chamber of the heart
Increase myocardial fibers length
3. Tachycardia
increased heart rate due to activation of neurohumoral system e.g
release of norepinephrine
release of atrial natriuretic peptide
activation of renin-angiotensin aldosterone mechanism
(READ AND WRITE SHORT NOTES ON THESE
NEUROHUMORAL SYSTEMS)

31. 2. Ischemic Heart Disease
Etiology
1.Atherosclerosis of coronary arteries.
2.Superadded changes in coronary atherosclerosis
3.Non-atherosclerotic cause
i.Vasospasm
ii.Stenosis of coronary ostia
iii.Arteritis
iv. embolism
v.Thrombotic diseases
vi.Trauma
vii.Aneurysms
viii.compression

32. Ischemic Heart Disease
•Acute vs. chronic ischemia.
•Four basic patterns
•Angina pectoris
• Acute Myocardial infarction
•Chronic ischemia leading to CHF
•Sudden death from arrhythmia

33. Coronary Atherosclerosis

34. Coronary Atherosclerosis
•Focal narrowing

35. ANGINA PECTORIS
•Clinical syndrome resulting from transient
myocardial ischaemia
•Paroxysmal (sudden) pain
•Recurrent
•Aggravated by increase in demand of the heart
•Relieved by decrease in work of the heart
•15 sec.-15 min.
•Reduced perfusion, but NO infarction

36. ANGINA PECTORIS
•THREE TYPES
•STABLE: pain following exertion, relieved by
rest
•PRINZMETAL: SPASM is main feature, pain
at rest, no relationship with physical activity,
responds to nitroglycerine,
•Xterised- S-T elevation.
•UNSTABLE (crescendo pain at rest, PRE-
infarction, ): perhaps some thrombosis, perhaps
some non transmural necrosis, perhaps some
embolization, but DISRUPTION of PLAQUE
is universally agreed upon

37. Acute Myocardial Infarction
•Incidence;
•Age- all ages but more in the elderly
•Sex- more in males
•Most are TRANSMURAL, and MOST are caused by
coronary artery occlusion
•In the 10% of transmural MIs NOT associated with
atherosclerosis:
•Vasospasm
•Emboli, e.g., mural thrombus
•UNexplained

38. Acute Myocardial Infarction
•Etiopathogenesis
1.Myocardial ischeamia
2.Emboli
3.Acute plaque rupture
4.Non- atherosclerotic causes;
•Vasospasm
•Arteritis
•Coronary ostial stenosis
•trauma

39. Types of infarcts
•Anatomical site;
anterior, posterior, lateral, septal , circumferential
•Degree of thickness; fullthicknes/transmural,
subendocardial
•Age of infarcts;
•newly formed-acute, recent, fresh
•old, healed, organised

40. Morphology of infarcts
•Gross
•0-6hrs= no change or pale
•24hrs= cyanotic red-purple area of
haemorrhage
•48-72hrs= pale, hyperaemic
•3
rd
-7
th
= hyperaemic border,centre yellow
and soft
•10
th
day= red- purple periphery
•4
th
-6
th
week= thin, grey-white, hard,
shrunken fibrous scar
•Size= 4 to 10 cm.

41. Diagnosis of acute myocardial
infarction
1.Clinical features
1.Pain- sudden, severe, crushing, prolonged, substernal in
location, unrelieved by rest nor nitroglycerin, radiates to
one or both arms, neck and back
2.Indigestion-epigastric discomfort interpreted as
heartburn with nausea and vomiting
3.Apprehension-terrified, restless,- great fear of death
4.Shock- systolic bp <80mmhg, lethargy, cold clammy,
cyanosis, weak pulse, /bradycardia
5.Oliguria-urine flow< 20ml per hour
6.Low grade fever-
7.Acute pulmonary oedema- dyspnoea, orthopnea,and
bubbling respiration

44. •2. ECG changes
•ST segment elevation in AMI
( STEMI)
•T- wave inversion
•Wide deep Q wave

45. NORMAL ECG WAVE

49. •3. Serum Cardiac Markers
•1.Elevated Creatinine Phosphokinase (CK) –CK-MB2
•More sensitive in the first 4-6 hrs, at 48 hrs it disappears
• 2. Elevated Lactate Dehydrogenase (LDH)- LDH 1
•Begins to rise after 24 hrs, return to normal in 14 days
3. Elevated cardiac specific troponins (cTn)
cTnI - 7-10 days
cTnT – 10-14 days
4. Myoglobin – elevated within first 24hrs, excreted in urine-
not specific

51. Myocardial Infarction

52. Myocardial Infarction

55. Acute Myocardial Infarction
•Complications of MI
Cardiogenic heart failure
Sudden loss of pumping strength.
Arrhythmias
Irritable conduction system.
Valvular dysfunction
involvement of papillary muscle
Rupture and tamponade
Cardiogenic shock
Mural thrombosis and thromboembolism
pericarditis

56. 3. Hypertension
•Essential (majority)
•No known cause
•Stress perhaps
•Modifiable causes
•Endocrine tumors
•Aldosterone
•Cushing's Syndrome
•Vascular related
•Narrowing of renal a.
•Primary Renal disease
•Excess renin
production
•Lead to hypertensive
heart disease

57. hypertensive heart disease
•Left ventricular hypertrophy
•Abnormal orientation of
hypertrophied cells.
•Wt 500gm or more
•Normal 300gm
•Thickness-20mm or more
•Normal thickness- 13-
15mm
•Initially only hypertrophy-
concentric hypertrophy
•Later-hypertrophy +
dilatation with thinning of
ventricular wall-eccentric
hypertrophy
• lead to Heart failure

58. Left Ventricular Hypertrophy

59. 4. Cor Pulmonale
•Right-sided failure
secondary to intrinsic
pulmonary disease.
•Xterised by rt
ventricular dilatation
or hypertrophy or
both
•Emphysema
•Scaring conditions
of the lung
•Chronic
embolization

60. Cor pulmonale
•Acute cor pulmonale
• massive pulmonary embolism resulting in sudden
dilation of the pulmonary trunk and right ventricle
•Chronic cor pulmonale
Chronic lung disease
•Chronic emphysema
•Chronic bronchitis
•Pulmonary TB
•Pneumoconiosis

61. 5. Rheumatic Fever
•Beta haemolytic
Streptococcalof group
A, infection starts it.
•Antibodies are made
against Strep wall.
•Antibodies cross react
with connective tissue.
•Type II
hypersensitivity.
•Many systems become
involved.

63. Rheumatic Fever
•Antibodies cross react
with connective tissue.
•Joint
•Skin
•Heart
•CNS
•R/S

64. Rheumatic fever
morphology
•1. Cardiac lesions
•(1) Aschoff nodules or bodies-spheroidal, 1-2mm in size,in the intestitium of
the heart, in the vicinity of small blood vessels in all layers of the heart.
( 2) Rheumatic pancarditis
(i) Rheumatic endorcaditis
•(a) Rheumatic valvulitis- acute RF.
•thickening & loss of translucency of valve leaflets/cusps
•Multiple warty vegetations/verrucae along line of closure
•Vegetations are grey brown , transluscent, FIRMLY attached
•In chronic RHD- mitral valve- ‘fish mouth” or “button hole”
•(b). mural endocarditis
•Mac callum’s patch –left atrium, & posterior wall= appears as a map
•Thickened
•Roughened
•wrinkled

65. Rheumatic fever
morphology
•(ii) rheumatic myocarditis
•Early-lt ventricle soft and flabby
•Intermediate-small foci of necrosis
•Late aschoff bodies
•(iii) rheumatic pericarditis
•Loss of normal shiny pericardial surface- fibrin
deposition
•Fibrin deposition & fibrinous exudate in
pericardial sac
•Two surfaces shuggy with “ bread and butter”
appearance

66. Rheumatic fever
morphology
•2. EXTRACARDIAC LESIONS
•(A) Polyarthritis-
• acute and painful inflammation of synovial membranes –
larger joint of limbs,
•As pain and swelling subside in one joint others tend to
get involved
•(B) Subcutaneous nodules
•Spherical/ovoid & painless
•Attached to tendons, ligaments. Fascia or periosteum
•Extensor surfaces- wrists, elbows, ankles, knees

67. •(C) Erythema Marginatum
•Non-pruritic erythematous rash on trunk and proximal
parts of extremities
•Central clearing with elevated red margins
•(D) Rheumatic arteritis
•Coronary, aorta, renal, mesenteric, cerebral

68. Extracardiac lesions cont.
•(E) Chorea minor/Sydenham’s chorea/ saint
vitus dance
•Involvement of CNS- late
•Xterised- disordered and involuntary jerky
movement of trunk & extremities,
•Emotional instability
•(F) Rheumatic pneumonitis and pleuritis
•Lungs- large, firm and rubbery

69. ACUTE:
-Inflammation
-Aschoff bodies
-Pancarditis
-Vegetations on
chordae tendinae at
leaflet junction
CHRONIC:
THICKENED VALVES
COMMISURAL FUSION
THICK, SHORT,
CHORDAE TENDINAE

70. Rheumatic Carditis
•All parts of the heart are
involved.
•Endocardium
•Valves
•Myocardium
•Pericardium
•To the right are sterile
vegetations on acutely
inflamed valves
•Can embolize
•Will lead to scaring

71. Healed Rheumatic Carditis
•Scared and stenotic
mitral and aortic valves.
•Old sites of
inflammation in
myocardium
•Aschoff nodules
•Scars of pericarditis

72. Healed Rheumatic Mitral Valve
•Scarred valve.
•Both stenotic and
incompetent.
•‘Fish mouth’
•This valve is a set
up for infections.

73. Rheumatic Valvular Disease

74. Clinical features of RHD
Jones criteria
A. Major criteria
1. carditis
2. polyarthritis
3. chorea minor
4. erythema marginatum
5. subcutaneous nodules
B. Minor criteria
1. fever
2. arthalgia
3. previous history of RF
4.Lab. Elevated ESR, raised C-reactive protein,
Leucocytosis
5. prolonged PR interval in ECG

75. Clinical Features
•Migratory Polyarthritis
•Myocarditis
•Subcutaneous nodules
•Erythema marginatum
•Sydenham chorea

76. C. Supportive evidence
•Preceding group A streptococcal infection;
•Positive throat culture
•Raised titres of streptococcal antibodies
•Antistreptolysin O and S
•Antistreptokinase
•Anti strepto hyaluronidase
•Anti DNAse B
•DX OF RF
•LAB + 2 MAJOR CRITERIA
•OR
•LAB + ONE MAJOR + 2 MINOR CRITERIA

77. 6. Infective Endocarditis
•Living bacteria on the
valves
•Previously damaged
valves are at greater risk
•.
•Destroys valve
•Embolize the vegetations

78. TYPES OF INFECTIVE ENDOCARDITIS
•A. ACUTE BACTERIAL ENDOCARDITIS (ABE)
•Fulminant and destructive acute infection by highly
virulent bacterias in a previously normal heart
•Staphylococcus aureus
•Pneumococci
•Gonococci
•Beta streptococci
•enterococci
B. SUBACUTE BACTERIAL ENDORCARTIS (SABE)
•Caused by less virulent bacteria in a previously diseased heart
•Streptococcus viridans
•Streptococcus bovis
•Streptococcus pneumoniae
•Staphylococcus epidermidis

79. Predisposing factors of infective
endocarditis
•1. Underlying heart disease
•2. Impaired host defense

80. Morphology- ABE & SABE
Typical vegetation/verrucae on valve
cusps/leaflets
Grey-tawny to greenish in colour
Irregular in shape
Single or multiple
Typically friable

81. Infective Endocarditis

82. complications
•A. Cardiac complications
•Valvular stenosis or insufficiency
•Perforation, rupture & aneurysm of valve leaflets
•Abscess in the valve ring
•Myocardial abscess
•Suppurative pericarditis
•Cardiac failure

83. complications
•B. Extracardiac complications
Emboli- lt side of heart to systemic circulation
Emboli – rt to pulmonary circulation
Petechiae on skin and conjunctiva (roth’s spots)
In SABE- osler’s nodules- tender nodules on finger tips and
feet
In ABE –Janeway’s spots – painless non tender lesion on pulp
of fingers
Focal necrotising glomerulonephritis- circulating immune
complexes

85. 7. Valvular Diseases
•Stenosis- failure of a valve to open
completely during diastole resulting in
obstruction to the forward flow of the blood
•Incompetency/insufficiency/ regurgitation-
failure of valve to close completely during
systole resulting in back flow of blood

86. Mitral stenosis
•Secondary to RHD ( commonly) or infective endocarditis
( rare)
• majority are women
•Morphology
•Leaflets diffusely thickened towards closing margin
•Fibrous adhesion of mitral commissures and fusion and
shortening of chordae tendinae
•Slit like or oval mitral opening
•“Button hole” or “fish mouth”
•Effects;
•Dilatation and hypertrophy of lt atrium
•Atrophic lt ventricle
•Pulmonary hypertension

89. Mitral insufficiency
•Etiology
RHD
non-inflammatory calcification
Morpholgy
rigidity, deformity & retraction of valve leaflets
fusion of comissures & shortening of chordae
tendinae
Effects;
dilation & hypertrophy of lt ventricle
marked dilation of lt atrium
pulmonary hypertension

93. Aortic stenosis
•Etiology
•Chronic RHD
•Congenital valvular & subaortic stenosis
•Bacterial endocarditis
Morphology
•Fibrous thickening & calcific nodularity of closing edges
Effects;
3 cardinal features;
 exertional dyspnea- elevation of pulmonary capillary
pressure
 angina pectoris- increased demand of hypertrophied
myocardium
 syncope- coronary insufficiency
NB; sudden death may occur

96. Aortic insufficiency
•Etiology
•RHD
•Syphilitic valvulitis
•Infective endocarditis
•Congenital subaortic stenosis
•Traumatic rupture of valve cusps,
•Marfan’s syndrome
•Morphology
•Aortic valves deformed, shortened , fail to
close

97. Aortic insufficiency
•Effects
•Hypertrophy & dilatation of lt ventricle
•Pulmonary hypertension
•Eventually rt heart failure
•NB; xterised
•Awareness of the heart beats pounding in the head with
each heartbeat
•Low diastolic and high pulse pressure
•Corrigan's pulse is characterized by the abrupt distension
and quick collapse of carotid arteries in aortic
regurgitation,

98. •water hammer pulse is the characteristic pulse observed in
peripheral arteries-feel like a tapping impulse through the
patient's forearm due to the rapid emptying of blood from
the arm during diastole.
•Systolic and diastolic murmur-heard over femoral when
lightly compressed-( durozier’s sign)
•Angina pectoris- increased myocardial demand

101. Marfan’s Syndrome
•Inherited disorder of elastic
tissue-Marfan syndrome prevents
connective tissue from growing and
developing normally. This makes the
tissues in your aorta and heart valves
become weak and inelastic. A lack of
elasticity can cause your aorta to
widen or bulge. It can also result in
your heart valves not opening and
closing properly.
•Dilated aorta, dissection
and rupture.
•Incompetent aortic valve.
•Mitral valve stretches
•Lenses can’t accommodate.

102. •Many people with Marfan syndrome will
need glasses because they will develop
myopia (nearsightedness) or have
astigmatism (abnormal curvature of the
eye).
• Patients with Marfan syndrome may also
have a higher chance of developing cataracts,
glaucoma, strabismus and retinal
detachment.

103. 8. Myocarditis
•Viruses mostly in US
•Rarely bacteria of TB.
•Parasites
•Toxoplasmosis gondii
•Trypanosoma cruzi
•Complications
•Heart failure
•Rhythm disturbances
•Scarring of muscle
•Mural thrombus and
embolization

104. 9. Cardiomyopathy
•Any disorder that affects the heart
muscle is called a cardiomyopathy.
Cardiomyopathy causes the heart to
lose its ability to pump blood well. In
some cases, the heart rhythm also
becomes disturbed. This leads to
arrhythmias
•Weakened and,
paradoxically, hyperplastic
myocardium
•‘Primary’ means we don’t
know what causes it.

105. •Secondary to something else.
•Genetic-mutation in x-chromosome
•Alcohol
•Heavy metals -cobalt
•Virus?

106. Morphology of cardiomyopathy
•Heart is enlarged and wt increase upto 1kg
•Dilatation of the 4 chambers
•Thickening of ventricular walls
•Endocardium thickened
•Mural thrombi in ventricles and atria
•Valves – normal
•Types
•Idiopathic dilated- when the heart chambers
enlarge and lose their ability to contract. It
often starts in the left ventricle (bottom
chamber). As the disease gets worse, it may
spread to the right ventricle and to the atria
(top chambers). -

108. •Idiopathic hypertrophic-A condition in which
the heart muscle becomes abnormally thick.
•Hypertrophic cardiomyopathy makes it hard
for the heart to pump blood. It often goes
undiagnosed.
•Most people with the condition have no
symptoms and experience no significant
problems.
•For some, it can cause dyspnea, chest pain or
(arrhythmias).
•-

110. Restrictive cardiomyopathy- refers to a set of
changes in how the heart muscle functions.
These changes cause the heart to fill poorly

113. 11. Pericardial Disease
•Inflammation
•Viral
•Lyme disease
•Renal Failure
•Cancer
•Effusions
•CHF
•Cancer
•Fibrosis leading to
restriction of heart
motion

114. Pericarditis
•Inflammation of
epicardium and
pericardium
•Effusion (fluid) of
pericardial space
•Tamponade
•May lead to serious
scarring and
restriction of heart
motion.

115. Hemopericardium
•Ruptured or
perforated heart
•MI
•Penetrating wounds
•Lacerated aortic root
•Auto accident
•Rotatory motion
unscrews heart from
aorta

116. 12. TUMORS
•90% benign “mesenchymal”, i.e., stromal
•MYXOMAS (LEFT ATRIUM MOST
COMMON)
•FIBROMAS
•LIPOMAS
•FIBROELASTOMAS (valvular, usually
papillary)
•RHABDOMYOMA (Most common cardiac
tumor in children)
•10% SARCOMAS

117. MORPHOLOGY
•Single but may be multiple
•<1 to 10cm
•Polypoid,pedunculated, spherical
•Soft and haemorrhagic

118. MYXOMA

119. Revision question
1.Discuss the three etiologies of heart failure
2.Discuss the pathologoy of three types of heart failure stating their clinical features
3.Describe the 3 compensatory mechanisms of a failing heart
4.List the four patterns of ischaemic heart diseases
5.Describe the types of angina pectoris
6.Give a detailed explanation of how to make a diagnosis of acute myorcadial infarction
and with aid of diagrams illustrate.
7.List the complications acute myocardial infarction
8.Discuss the pathology of rheumatic fever
9.Discuss the morphology of rheumatic heart disease
10.Explain how to make a diagnosis of rheumatic heart disease
11.Describe the types of infective endocarditis listing their etiology
12.Describe the cardiac and extracardiac morphology of ABE and SABE lesions
13.List the cardiac and the extra-cardiac complications of infective endocarditis
14.Discuss mitral stenosis, mitral insufficiency, aortic stenosis, aortic insufficiency ( each )
under; etiology, morphology, effects.
15.Describe 3 types of cardiomyopathy and with aid of diagrams illustrate
16.Describe 3 causes of pericardial diseases
17. state the most common tumour of the heart and describe its morphology.

120. A POSITIVE ATTITUDE ,
DISCIPLINE AND SELF DRIVE
ARE PART OF THE MOST
IMPORTANT INGREDIENTS
THAT YOU NEED TO ACHIEVE
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THESE VIRTUES.
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