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Systemic Pathology > Pathology Of The Heart > Flashcards

Pathology Of The Heart Flashcards

1
Q

What is CCF

A

Heart is unable to maintain an output sufficient for the metabolic requirements of the tissues and organs of the body.
•It can appear as the end stage of many forms of chronic heart disease

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2
Q

What are some causes of CCF

A

A) Loss of cardiac myocytes
•1) Myocardiac infarction
•2) Myocarditis e.g chaga’s disease
•3) Toxic damage e.g diphtheritic myocarditis

•B) Impaired contractility
•1) Amyloidosis
• 2) Beriberi
• 3) Hurler’s disease

C) Mechanical cardiac overload
• 1) Hypertension
• 2) Valvular heart disease
• 3) High output state eg:- thyrotoxicosis, anaemia, beriberi
• D) Impaired filling of the chambers
• 1) cardiac tamponade
• 2) constrictive pericarditis.

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3
Q

What are some causes of a left sided heart failure

A

Ischaemic heart disease
*Systemic hypertension( acute LVF)
*Rheumatic heart diseasei.e mitral &aortic valvular dx
*Myocardial diseases

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4
Q

What are some changes in organ mechanisms in a left cardiac failure

A

Lungs
Increased hydrostatic pressure
Pulmonary oedema and congestion
Heart failure cells
Brown induration of the lungs

Kidneys
Stimulation of the renin-angiotensin system
•Salt and water retention
•Acute tubular necrosis
•Pre-renal azotaemia

Brain
•Cerebral hypoperfusion
•Hypoxic symptoms e.g irritability, stupor & coma

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5
Q

What are some causes of right sided heart failure

A

•Cor pulmonale.
•Triscuspid & pulmonic valve lesions
•Congenital heart dx associated with left to right shunt
•Left heart failure.

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6
Q

What are some organ changes in a RSHF

A

Liver
Congestive hepatomegaly
*Central haemorrhagic necrosis
*Nutmeg appearance
*Cardiac sclerosis
*Cardiac cirrhosis

Spleen
Congestive splenomegaly ie reactive fibrosis
*Siderofibrotic nodules ( Ghandy-Gamna bodies)

Subcutaneous tissue
*Pitting pedal eodema
*Anasarca

Body cavities
*Pleural, pericardial & peritoneal effusion

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7
Q

What is hypertensive heart disease

A

Def. -Response of the heart to the increased demands induced by systemic or pulmonary hypertension

Systemic hypertensive heart disease
•LVH (usually concentric) in the absence of other vascular pathology
•History of hypertension

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8
Q

What is systemic hypertension

A

DEF—-sustained diastolic pressure >90mmHg or systolic > 140mmHg
•Classified as mild, moderate & severe.

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9
Q

What are the two causes of systemic hypertension

A

Essential hypertension 90-95%
Secondary hypertension 5- 10%

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10
Q

What are some genetic factors for essential hypertension

A

Genetic factors: Familial cluster,genetic defect in renal sodium excretion, etc

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11
Q

What are some environmental factors for essential hypertension

A

Stress, obesity, increased salt intake

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12
Q

Describe secondary hypertension

A

Renal diseases—acute GN,CGN,renal art. stenosis, renin producing tumours.
•Endocrine :- Cushing sydrome, phaechromocytoma, thyrotoxicosis
•Vascular :- Coartation of the aorta, vasculitis
•Neurogenic :- Psychogenic, increased intracranial pressure.

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13
Q

What is the pathogenesis of a secondary hypertension

A

BP=COXPR
•Increased PR —-pressure overload—myocardial hypertrophy
•Cardiomegaly & LV thickness

•Most pt.with hypertension has coronary atherosclerosis. This predisposes to ischaemic injury

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14
Q

What are some characteristics of a compensated heart

A

LVH (Concentric)
*No dilatation
*No valvular lesions

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15
Q

What are some characteristics of a decompensated heart

A

Cardiac dilatation
•Hypertrophy
•LV dilatation
•Cardiomegaly

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16
Q

What is cor pulmonale

A

DEF. RVH secondary to primary structural or functional lung disease.
It is also called RHF

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17
Q

What are some causes of cor pulmonale

A

Pulm hypertension
•COPD
•Intestitial lung dx
•Massive pulm. embolism
•Kypho-scoliosis
•Poliomyelitis

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18
Q

What is rheumatic fever

A

DEF An acute systemic febrile illness caused by Lancefield group A β-haemolytic streptococci.
•Pharyngitis 2-3weeks prior to the onset of symptoms.
•In the tropics skin infection may precede onset of symptoms
•Affects children between 6-16years(F>M)
•May occur in adults.
•Low Socio-economic group.

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19
Q

What are the major criteria for RF

A

Migratory poly arthritis & arthralgia of large joints
•Pan-carditis
•Erythema marginatum of the skin
•Sydenham’s chorea
•Subcutaneus nodules

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20
Q

What are the minor criteria for RF

A

Fever
•Increased ESR
•Increased ASO titre
•Leucocytosis

Jones criteria:-
•2major
•1major + 2 minor

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21
Q

What is RHD

A

Not directly caused by the organism
•Antibodies to strept. Cross-react with tissues of the heart, kidneys, etc.
•Commoner in blacks, and in Warmer climates
•Common among the poor.
•Usually a pan-carditis

Pericardium:-
•Fibrinous or Sero-fibrinous exudate
•Bread and butter pericarditis.
•Aschoff bodies not common
•Fibrin & mononuclear exudate
•May resolve completely or get organised, results in scarring adhesions without restriction.

Myocardium: Aschoff bodies are abundant in the perivascular space.
•Death may occur in acute R.F from CCF
•Chronic R.F —–fibrosis & lymphocytic infiltration.

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22
Q

What’s the morphology of an RHD

A

The diagnostic anatomic lesions of RHD is the Aschoff body.
•They are foci of fibrinoid necrosis surrounded by lymphocytes, macrophages, occasional plasma cells & plump activated histiocytes called Anitschkow cells or caterpillar cells because of the arrangement of the chromatin pattern of the nucleus

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23
Q

Describe Antischkow’s cells

A

Is pathognomonic of RH
•Also called caterpillar cells
•Are histiocytes with abundant cytoplasm and central round to ovoid nuclei in which the chromatin is disposed in a central, slender wavy ribbon
•Sometime the histiocytes are multinucleated

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24
Q

What is rheumatic endocarditis

A

Acute valvulitis; hyperaemia,oedema & thickening of the valves
•Verrucae : these are small friable vegetations deposited along the free edge of the cusps.
•Chronic valvulitis; there is progessive scarring & deformity of the valve leaflets.
•Mc Callum’s plaque are fibrous plaques seen on the subendocardium of the left atrium.
Fish- mouth” or “button hole” stenotic deformity may occur.
•Dystrophic calcification may occur in affected valves.

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25
Q

What are extra-cardiac lesion of RF

A

Subcutaneous nodules
•Polyarthritis( migratory)
•Pleural oedema and fibrinous exudates
•CNS Sydenham’s chorea characterized by rapid, irregular and purposeless movement ( basal ganglia haemorrhage,oedema,perivascular lymphocytic reaction)

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26
Q

What is a valvular heart disease

A

•Stenosis of the valve implies narrowing of the valve.
•Isolated mitral & aortic stenosis account for close to half of all valvular heart lesions.
•Stenotic valve impose volume overload as well as pressure overwork on the heart chamber involved.

Insufficiency or regurgitation occurs when a valve fails to close completely during systole.
•May occur as a result of intrinsic valvular dx or damage to the supporting structures
•Stenosis & regurgitation produce noisy movement of blood because of turbulence called cardiac murmur.
•Right heart valve disease is due to Carcinoid syndrome or congenital malformations.

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27
Q

What is IE

A

Invasion of the heart valve or the mural endocardium by infective agents.
2 FORMS.
•Acute – fatal fulminant infection. Occurs in a previously normal valve with highly virulent organism.
•Subacute. – smouldering, indolent illness. occurs in previously damaged valve.
•Distinction vague because of antibiotics.

Xterised by deposition of friable bulky, bacterial-laden (infective) vegetations on the heart valve.
Epidemiology &pathogenesis.
•Congenital heart dx e.g Tetralogy of Fallot,PDA.
•RHD
•Valvular defects.

Prosthetic valve
•Immunosuppresion eg HIV,drug induced
•Diabetes Mellitus
•Chronic alcoholics
•Intravenous drug abuse
•Commoner in males above 50yrs

Commoner in males.
•50-75% affect previously damaged valve
•Valves distorted by congenital malformations.

Factors predisposing to development of IE
•Seeding of blood with microbes.
•Haemodynamic disturbance occuring across deformed heart valve

Activation of clotting cascade
•Production of agglutinating antibodies leading to clumping of organism within the vegetation.

Heart—perforation of valve
•myocardial abscess
•suppurative pericarditis
•Congestive cardiac failure
•Fragmentation& embolization of septic vegetation to sites like brain, spleen, coronary arteries & kidneys
•Immune complex dx-focal GN
•OSTEOMYELITIS

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28
Q

What are the two types of non-infective endocarditis

A

Marantic endocarditis or non-bacteria thrombotic endocarditis

•Libman-Sacks dx or non-bacteria verrucous endocarditis.

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29
Q

What is marantic endocarditis

A

Debilitated and Cachetic patients
•Vegetations on line of closure of valves.
•Larger and softer than those of RF
•Frequency: mitral, aortic, tricuspid and pulmonary.
•Source of emboli to brain, lungs, kidney and spleen.
•Most common cause of coronary emboli.

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30
Q

What is Libman-Sacks endocarditis

A

Granular flat verrucae, both surfaces of valves.
•Mitral and Tricuspid valves commonly.
•Fibrinous, granular, sterile vegetations
•Valvulitis, immune complex mediated
•May appear in patients with SLE(50%).
•Usually does not deform the valves.

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31
Q

What are the types of pericarditis

A

Fibrinous
•Serous
•Serofibrinous
•Fibrinopurulent
•Purulent
•Haemorrhagic
•Cholesterol
•Granulomatous
•Adhesive
•Constrictive.

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32
Q

What are the etiologies of pericarditis

A

Infections: Bacterial,viral & fungal.
•Neoplastic
•Systemic disease
•Rheumatic fever
•Uraemia
•Myocardial infarction

33
Q

What is ischemic heart disease

A

Heart disease caused by reduction in blood supply to the myocardium assoc. with diseases of the coronary arteries.

In IHD, coronary atherosclosis is diffuse involving more than one major arterial branch typically involving the proximal 2cm in the epicardial region
•Due to presence of collateral vessels, the cross-sectional area of the vessels must be reduced by >75% to significantly affect perfusion
•Hypertension is an important risk factor for coronary atherosclerosis.

34
Q

What are the four clinico-pathological syndromes of IHD

A

Myocardial infarction (heart attack)
•Angina pectoris
•Chronic ischaemic heart dx
•Sudden cardiac death.

35
Q

What are some causes of coronary insufficiency

A

Coronary atherosclerosis 90-95%.
•Coronary vasospasm alone or superimposed on atherosclerosis
•Coronary artery embolism
•Ostial stenosis e.g syphilitic aortitis
•Coronary thrombosis
•Aneurysms. Medial Calcification.(rare)
•Congenital anomalies.

36
Q

What causes IHD

A

Caused by an imbalance between the myocardial blood flow and the metabolic demand
•In majority of cases, the reduction in coronary blood flow is related to progressive atherosclerosis with increasing occlusion of the coronary arteries
•Coronary artery perfusion depends on the differences between the pressure at the ostia and the coronary sinus
•Due to compression of intramuscular arteries and coronary orifices during systole, Cardiac Blood Flow reduces in systole

37
Q

What are some factors reducing coronary blood flow

A

Decrease aortic diastolic pressure
•Increased intraventricular pressure & myocardial contraction
•Coronary artery stenosis
–Fixed coronary stenosis
–Acute plague rupture or haemorrhage
–Coronary artery thrombosis
–Vasoconstriction
•Aortic valve stenosis and regurgitation
•Increased atrial pressure

38
Q

What are the patterns of IHD

A

Angina pectoris
–Stable angina-
–Variant or prinzmetal angina
–Unstable angina-
–Sudden cardiac death
•Myocardial infarction

39
Q

What is pectoral angina

A

Stable angina-
•subendocardial ischaemiaparoxysms of pain related to exertion and reduced by vasodilators(ST-segment depression on ECG)
–Variant or prinzmetal angina-
•reversible spasm in normal to severe atherosclerotic coronary Apain occurs at rest(ST-segment elevation or depression)
–Unstable angina-
•prolonged pain at rest in a patient with stable angina or worsening of pain of stable angina(usually ST-segment depression)
–Sudden cardiac death-
•high stroke stenosis with acute coronary changesunexpected death within an hour of a cardiac event

40
Q

What is the pathogenesis of an MI

A

Occlusive intracoronary thrombus-i.e complicated atheromatous plaque either by ulceration or fissured (90%)
•Vasospasm of CA with or without atherosclerosis (platelet aggregation implicated)
•Emboli from:
–Left sided mural thrombus
–Vegetative endocarditis
–Paradoxical emboli from right side of the heart(foramen ovale)

41
Q

What is the gross morphology of an MI

A

Transmural infarct-
–involve entire thickness of the LV wall from endocardial to epicardium
–usually anterior free wall
•Posterior free wall and septal infarct with extension into the RV wall
•Subendocardial infarct-multifocal areas of necrosis confined to inner 1/3-1/2 of the LV wall
•Isolated infarcts of the RV and RA are extremely rare
•The last 3 do not show the same evolution with transmural infarct

42
Q

What are the evolution of the gross morphological changes in MI

A

18-24hrs—pallor of the myocardium
•24-72hrs—pallor with some hyperaemia
•3-7days—central yellowish area surrounded by hyperaemic borders
•10-21days—maximally yellow and soft with vascular margins
•7weeks—white area of fibrosis

43
Q

What is the evolution of microscopic changes of MI

A

1-3hrs-wavy myocardial fibers
•2-3hrs-staining defect with tetrazolium or basic fuschin dye– nitro blue tetrazolium test
•4-12hrs-
–coagulative necrosis with loss of cross striations and contraction bands,
–oedema, haemorrhage and early neutrophilic infiltrate
•18-24hrs-
–continuing coagulative necrosis with nuclear Pyknosis
–marginal macrophage and mononuclear inflammatory cell infiltrate and
–Fibrovascular tissue response begin

10-21days-fibrovascular response with prominent granulation tissue
•7weeks-fibrosis
•These changes can vary depending on the size of the infarct, being slower in larger ones

44
Q

What are the complications of MI

A

Arrhythmias and conduction defects with possible sudden death
•Extension of infarct or re-infarction
•Congestive Cardiac Failure
•Cardiogenic shock
•Pericarditis
•Mural thrombus with possible Embolization
•Myocardial wall rupture with possible valvular insufficiency
•Ventricular aneurysm

Sudden death-
–death occurring within an hour of onset of symptoms
–Occurs in severe coronary atherosclerosis with >75% Lumina narrowing
–Associated complication such as thrombus or plaque haemorrhage or rupture
–Mechanism is usually an arrhythmia
•Aortic dissection can also cause sudden collapse.

Ishaemic cardiomyopathy- can also be a complication
severe atherosclerosis of all major arteries
inadequate vascular supply
myocyte loss + fibrosis
decreased compliancecompensatory hyperplasia & hypertrophydecompensation and heart failure

45
Q

What are some factors which eventually determine infarct size

A

Size of the myocardial bed at risk and its metabolic/oxygen needs
• Duration of obstruction
• Coronary artery anatomy,dominance/collaterals
• Site of coronary artery obstruction
• Severity of obstruction
• Rate at which obstruction developed

46
Q

What are the signs and symptoms of an MI

A

Signs and symptoms of severe pump failure/cardiogenic shock generally occur with large infarcts (> 40% of the left ventricle involved).
•Cardiogenic shock indicates
–a poor prognosis (70% mortality) and
–accounts for 2/3 of hospital deaths.

47
Q

What are the laboratory diagnosis of an MI

A

It is important to consider these:
•None of the available test is specific nor sensitive
•The tests must be correlated with clinical symptoms, ECG and angiography
•Timing is very important

48
Q

Describe the creatine kinase lab diagnosis for MI

A

Total creatinine is from both skeletal and cardiac origin; non specific
•MB, MM,BB fractions
–MM-cardiac & skeletal- has isoenzymes
–MB-specific for cardiac, 2% is skeletal
–BB-found in brain, bowel & bladder and not measured routinely)
•CK-MB-is measured every 2-4hrs for 9-12hrs after patient is first seen. Rising levels indicates myocardial injury
•Useful to diagnose re-infarction as level falls after a day dissipating in 1-3days

49
Q

Describe the troponin lab diagnosis for MI

A

Troponins-I and T are structural components of cardiac muscle and released into blood with myocardial injury
•Very specific; much more than CK-MB
•Begins to rise within 3-12hrs, remain elevated to 5-9days for troponin I and up to 2weeks for troponin T
•Difficult to diagnose re-infarction because of the above
•Troponin T not very specific as it can appear with skeletal myopathies or renal failure

50
Q

Describe the myoglobin lactate dehydrogenase test for MI

A

Myoglobin
–is a protein found in skeletal & cardiac muscle
–It is elevated before CK-MB but not specific
•LD-
– begins to rise in 12-24hrs, peaks in 2-3days and dissipating in 5-14days
–LDH isoenzymes is more specific.
–Normally isoenzyme 2 is higher than 1, but in MI, this is reversed.
–LDH-5 is from liver and may increase in centrilobular necrosis of chronic liver congestion that follows CCF

51
Q

What are some prevention methods for MI

A

Control of hypertension & diabetes
•Drug and dietary treatment of hypercholesterolemia
•Dietary reduction of plasma cholesterol & LDL
•Reduction of fat intake
•Avoidance of obesity
•Moderation of salt intake
•Cessation of smoking
•Exercise

52
Q

What are some complications of MI

A

Sudden cardiac death
•Acute ventricular fibrillation
•Myocardial rupture
•CCF
•Thrombo-embolism
•Aneurysm of the heart muscle wall

53
Q

What are some diseases of the cardiac muscle

A

Myocarditis
Cardiomyopathies

54
Q

What is the etiology for myocarditis

A

Viruses
•Riketssia.
•Chlamydia
•Bacteria eg diphtheria.
•Fungi eg candida
•Parasites: Trypanosoma cruzi
Toxoplasma

•Trichinella.
•Echinococcus.
•African Trypanosomiasis
Incidence variable, depends on the endemicity of certain diseases. Trypanosomiasis, diphteria.

55
Q

What are some causes of myocarditis

A

Immune mediated reactions
•RHD
•SLE
•Transplant rejection

TOXINS eg alcohol ,cytotoxic drugs

56
Q

What is the morphology of myocarditis

A

Acute phase —-enlarged, flabby heart
•Cut surface shows mottling of venticular wall, microhaemorrhages

57
Q

What is the histology of myocarditis

A

Histology depends on the causative agent.
•Chronic fibrosis & burnt out inflamm reaction.

58
Q

What are the three cardiomyopathies

A

•DILATED

•HYPERTROPHIC

•RESTRICTIVE

59
Q

What is a dilated CM

A

Xterised by gradual development of heart failure associated with 4 chamber hypertrophy & dilatation of the heart
•Familial occurrence 20%
•AD in most cases, AR, X-Linked mitochondrial inheritance less common
•X-linked has been associated with Duchene muscular dystrophy.
•Previous myocarditis
•Alcohol or toxins.
•Child bearing or peripartum

60
Q

What is the morphology of a dilated CM

A

Cardiomegaly
•Dilated chambers
•Hypertrophy of myocytes
•Patchy atrophy
•Mural thrombi
•Primary abnormality is impaired LV myocardial contractility.

61
Q

What is a hypertrophic CM

A

Asymmetrical septal hypertrophy
•Xterised by heavy hypercontracting heart
•AD in 50% of cases
•Associated With HLA B12,&HLA B5
•Most cases of mutation are due to mutation in the heavy chain of B myosin protein

62
Q

What is the morphology of a hypertrophic CM

A

Dis-proportional hypertrophy of LV muscle predominantly affecting the septum
•Reduction in chamber volume
•Microscopy myofibers disarray

63
Q

What is a restrictive CM

A

Endomyocardial fibrosis EMF
•Loeffler’s endocarditis
•Endocardial fibroelastosis

•EMF& Loeffler’s endocarditis are xterised by fibrosis of the ventricular endocardium and the subendocardial tissue.extends from the apex to the outflow tract.

64
Q

What is endomyocardial fibrosis

A

Has been associated with malnutrition, viral infection & microfilaria infection
•Excessive consumption of plantain.
•Mural thrombi
•Eosinophilia.

65
Q

What is endomyocardial fibroelastosis

A

Xterised by focal or diffuse cartilage-like fibroelastic thickening usually involving the mural LV endocardium
•Most common first 2years of life
•Associated with cong.heart anomaly most often aortic valve obstruction.

66
Q

What are some tumors of the heart

A

Primary tumours are rare
•Metastatic tumours –5% of patients dying of cancer
•Metastasis commonly affect the pericardium.

67
Q

What are the primary tumors of the heart in decreasing order of frequency

A

Myxoma
•Fibroma
•Lipoma
•Papillary fibroelastoma
•Rhabdomyoma
•Angiosarcoma

68
Q

What is a myoxoma

A

Most common primary tumour in adults
•90% occur in the atrial
•Lt :Rt 4:1
•Single tumour
•1-10cm in diameter
•Sessile or pedunculated, gelatinous mass
•Histology; stellate cells,myxoma cells & endothelial cells in a background of acid mucopolysaccharide.

69
Q

What is a rhabdomyoma

A

Most common primary heart tumour in infants
•Small gray-white myocardial masses protruding into ventricular chamber
•Histology: round to polygonal cells contain numerous glycogen vacuoles.

70
Q

What is a congenital heart disease (CHD)

A
71
Q

What is the etiology of a CHD

A

Trisomy 21 (Downs) VSD
•Trisomy 18 (Edward’s)
•Trisomy 13 (Patau’s)
•Turners synd. Coartation of the aorta

Environmental factors
• Maternal infection eg Rubella
•Cardiac teratogens: hypoxia,ionizing radiation,drugs eg thalidomide, alcohol.

72
Q

What are the classifications of CHDs

A
  1. Acyanotic with shunt (Lt to Rt shunt)
    • a) PDA, b) VSD, c) ASD
    •2) Cyanotic (Rt to Lt shunt )
    • a) tetralogy of Fallot
    • b) late cyanotic VSD (Eisenmenger complex)
    • c) transposition of great vessel
    d) Total anomalous pulmonary venous connection
    e) Persistent truncus arteriosus
    f) Tricuspid atresia
    •3) Acyanotic (no shunt )
    • a) Coarctation of the aorta
    • b) Aortic stenosis and atresia
    C) Pulmonary stenosis and atresia
    •
73
Q

What are some clinical significance of CHD

A

CYANOSIS
•Pulmonary hypertension
•Myocardial hypertrophy/dilatation
•Failure to thrive
•Cerebral thrombosis
•Paradoxical embolism
•Predisposition to infective endocarditis

74
Q

What is the most common CHD

A

VSD

75
Q

What is a VSD

A

Most common CHD.
•The defect is most commonly in the membraneous part of the ventricular septum
•Xterised by loud systolic murmur
•Complication: pulm. hypertension
• Reversal of shunt

76
Q

What is coarctation of the aorta

A

Constriction of the ascending aorta or the arch
•Pre-ductal i.e constriction just proximal to the origin of ductus arteriosus. Survival depends on the patency of the ductus.
•Post-ductal i.e constrition is distal to the ductus. Less severe , may be asymtomatic.

77
Q

What are clinical symptoms of coarctation of the aorta with patent PDA

A

Differences in the blood pressure in the upper and lower extremities

•Development of collateral channels

•Dilatation of intercoastal vessel leading to rib notching

78
Q

What are the constituents of the tetralogy of Fallot

A

Large VSD
•Overriding aorta
•Pulm. stenosis
•RVH

79
Q

What are some clinical features of a tetralogy of Fallot

A

Central cyanosis
•Dyspnoea with blue spells
•Squatting
•Failure to thrive
•Recurrent respiratory infection.

Systemic Pathology (17 decks)

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