THE CARDIOVASCULAR SYSTEM

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THE CARDIOVASCULAR SYSTEM

• PROF. W.O. ODESANMI

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PREVIEW

• Normal Weight 250-300g Female
• 300-350g male
  
• LV thickness 1.3-1.5cm
• RV thickness 0.3-0.5cm
• Blood supply Rt Lt coronary aa.
• Behave as end arteries functionally.

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CONGESTIVE CARDIAC FAILURE.

• Def.--Heart is unable to maintain an output
  sufficient for the metabolic requirements of the
  tissues and organs of the body.
• Decrease myocardial capacity
• Systemic venous congestion.

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Causes of congestive cardiac failure.

• A) Loss of cardiac myocytes
• 1) Myocardiac infarction
• 2) Myocarditis e.g chagas disease
• 3) Toxic damage e.g diphtheritic myocarditis
• B) Impaired contractility
• 1) Amyloidosis
• 2) Beriberi
• 3) Hurlers disease

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CAUSES OF CCF contd.

• 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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LEFT-SIDED HEART FAILURE

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

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ORGAN CHANGES

• LUNGS-
• Increased hydrostatic pressure
• Pulmonary oedema and Congestion
• Heart failure cells
• Brown induration of the lungs

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PULMONARY OEDEMA AND CONGESTION.
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HEART FAILURE CELLS.
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KIDNEYS

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

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BRAIN

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

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RIGHT SIDED HEART FAILURE(Causes)

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

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ORGAN CHANGES

• LIVER
• Central haemorrhagic necrosis
• Nutmeg appearance
• Cardiac sclerosis
• SPLEEN
• Congestive splenomegaly ie reactive fibrosis
• Siderofibrotic nodules ( Ghandy-Gamna bodies)

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Organ changes contd.

• Subcutaneous tissue
• Pitting pedal eodema
• Anasarca
• Body cavities
• Pleural, pericardial peritoneal effusion.

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CVC LIVER.
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CVC LIVER.
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HYPERTENSIVE HEART DISEASE

• 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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SYSTEMIC HYPERTENSION

• DEF----sustained diastolic pressure gt90mmHg or
  systolic gt 140mmHg
• Classified as mild, moderate severe.
• CAUSES
• 1) essential hypertension 90-95
• 2) secondary hypertension 5- 10

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Essential hypertension

• Genetic factors-
• Familial cluster,genetic defect in renal sodium
  excretion, etc
• Environment-
• Stress, obesity, increased sodium intake

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Secondary hypertension

• Renal diseasesacute 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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Pathogenesis

• BPCOXPR
• 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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HYPERTENSIVE HEART DISEASE

• A compensated heart has a steady cardiac output.
• LVH ( Concentric)
• No dilataion
• No valvular lesions

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LEFT VENTRICULAR HYPERTROPHY.
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HYPERTENSIVE H D. contd.

• Decompensated Heart-
• Cardiac dilatation
• Hypertrophy
• LV dilatation
• Cardiomegaly

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LVH. CCF.
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COR PULMONALE

• DEF. RVH secondary to primary structural or
  functional lung disease.
• CAUSES-
• Pulm hypertension
• COPD
• Intestitial lung dx
• Massive pulm. embolism
• Kypho-scoliosis
• Poliomyelitis

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RHEUMATIC FEVER

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

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CRITERIA

• MAJOR-
• Migratory poly arthritis arthralgia of large
  joints
• Pan-carditis
• Erythema marginatum of the skin
• Sydenhams chorea
• Subcutaneus nodules

• MINOR-
• Fever
• Increased ESR
• Increased ASO titre
• Leucocytosis
• Jones criteria-
• 2major
• 1major 1 minor

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RHEUMATIC HEART DISEASE

• 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
• Develops in 50-75 of childhood cases
• 35 of adults

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RHD CONTD.

• 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.

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PERICARDITIS
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RHD CONTD

• 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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MORPHORLOGY

• The diagnostic anatomic lesions of R.F 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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RHEUMATIC HEART DISEASE.
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RHEUMATIC MYOCARDITIS
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ASCHOFF NODULE.
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ANITSCHKOWS MYOCYTE.
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Rheumatic endocarditis

• 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 Callums patch are fibrous plaques seen on the
  posterior wall of the left atrium.

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RHD CONTD

• Fish- mouth or button hole stenotic
  deformity may occur.
• Dystrophic calcification may occur in affected
  valves.
• Mitral valve alone 65-70
• Mitral aortic 25
• Aortic valve alone
• Mitral Aortic and Tricuspid valve.
• Mitral, Aortic, Tricuspid and Pulmonary(rare).

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BICUSPID AORTIC VALVE
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CALCIFIED AORTIC VALVE.
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MITRAL VALVE
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EXTRA CARDIAC LESION OF RHEUMATIC FEVER.

• Subcutaneous nodules
• Polyarthritis( migratory)
• Pleural oedema and fibrinous exudates
• CNS Sydenhams chorea( basal ganglia
  haemorrhage,oedema,perivascular lymphocytic
  reaction.

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VALVULAR HEART DX

• GENERAL PRINCIPLE
• 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.
  

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Valvular dx contd

• Insufficiency or regurgitation occurs when a
  valve fails to close completely during diastole.
• 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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MITRAL AORTIC VALVES.
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INFECTIVE ENDOCARDITIS

• 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.

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IE CONTD

• 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.

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IEcontd

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

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IE CONTD

• ACUTE
• Highly virulent organism
• Staph aureus20
• Strept pneumonia

• SUB ACUTE
• Strept viridans 50
• Strept faecalis
• E.coli

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IE CONTD.

• Most affected patients about 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

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IE CONTD

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

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IE CONTD

• MORPHOLOGY
• The valves are affected in the following order of
  frequency
• Mitral valve 25-30
• Aortic valve 25-35
• Mitral aortic 10
• Triscuspid alone 10

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BACTERIAL ENDOCARDITIS
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BE (Perf.Aortic Valve)
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Pathologic sequelae

• Heartperforation 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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NON-INFECTIVE ENDOCARDITIS

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

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Marantic endocarditis(NBTE)

• 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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NBTE(Mitral valve)
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NBTE (Aortic valve)
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LIBMAN-SACKS ENDOCARDITIS (Endocarditis
Associated with SLE)

• 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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PERICARDITIS

• TYPES
• Fibrinous
• Serous
• Serofibrinous
• Fibrinopurulent
• Purulent

• Haemorrhagic
• Cholesterol
• Granulomatous
• Adhesive
• Constrictive.

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PERICARDITIS AETIOLOGY.

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

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TB PERICARDITIS.
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ISCHAEMIC HEART DX.

• Heart disease caused by reduction in blood supply
  to the myocardium assoc. with diseases of the
  coronary arteries.
• IHD consists of 4 clinicopathologic syndromes
• Myocardial infarction (heart attack)
• Angina pectoris
• Chronic ischaemic heart dx
• Sudden cardiac death.

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Causes of coronary insufficiency

• 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.

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EPIDEMIOLOGY

• Constitutes 60-75 of causes of cardiac death in
  industrialised nations
• Closely related to the incidence of
• Hypertension
• Cigarette smoking
• Obesity
• Consumption of saturated animal fat
• Lack of physical exercise

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NORMAL CORONARY ARTERY
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CORONARY ATHEROMA
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CORONARY THROMBOSIS.
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MYOCARDIAL INFARCTION

• Most important form of IHD.
• Acute myocardial necrosis brought about by total
  or subtotal occlusion of a major coronary artery.
• The left anterior descending branch of LCA in
  40-50 of cases.

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Morphology of MI

• Sub-endocardial infarct
• Transmural infarct
• Acute ischaemic event-------sudden death.
• 6-12 hrs ---no apparent changes grossly
• Pale area with triphenyl-tetrazolium chloride

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MI contd

• 18-24 hrs grey-brown area
• 2-4 days yellowish brown area delineated by
  area of hyperaemia
• Inflam. Cells inflitration
• 4-10 days fibrous tissue deposition

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MYOCARDIAL INFARCTION.
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RUPTURED MI.
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NORMAL MYOCARDIUM
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MYOCARDIAL INFARCT.
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Complications of MI

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

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Dxes of the cardiac muscle

• Myocarditis
• Cardiomyopathies --primary heart muscle dx.

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MYOCARDITIS

• Aetiology. Infections
• 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.

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CAUSES OF MYOCARDITIS

• 2) Immune mediated reactions
• RHD
• SLE
• Transplant rejection
• 3) TOXINS eg alcohol ,cytotoxic drugs

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Myocarditis contd

• Morphology
• Acute phase ----enlarged, flabby heart
• Cut surface shows mottling of venticular wall,
  microhaemorrhages
• Histology depends on the causative agent.
• Chronic fibrosis burnt out inflamm reaction.

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ACUTE MYOCARDITIS
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MYOCARDITIS
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CARDIOMYOPATHIES

• DILATED
• HYPERTROPHIC
• RESTRICTIVE

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DILATED CM

• Xterised by gradual development of heart failure
  associated with 4 chamber hypertrophy
  dilatation of the heart
• Familial occurrence 20
• AD, AR, X-LINKED.
• X-linked has been associated with Duchene
  muscular dystrophy.
• Previous myocarditis
• Alcohol or toxins.
• Hypertension

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Morphology

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

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HYPERTROPHIC CARDIOMYOPATHY

• Asymmetrical septal hypertrophy
• Xterised by heavy hypercontracting heart
• AD in 50 of cases
• Associated With HLA B12,HLA B5
• IN some cases X14 heavy chain of cardiac myosin

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HCM contd

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

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ASH (HOCM)
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ASH.
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ASH
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RESTRICTIVE CM

• Endomyocardial fibrosis EMF
• Loefflers endocarditis
• Endocardial fibroelastosis
• EMF Loefflers endocarditis are xterised by
  fibrosis of the ventricular endocardium and the
  subendocardial tissue.extends from the apex to
  the outflow tract.

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EMF

• Common in children young adults n Africa
• Has been associated with malnutrition, viral
  infection microfilaria infection
• Excessive consumption of plantain.
• Mural thrombi
• Eosinophilia.

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Endocardial fibroelastosis

• 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.

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TUMOURS OF THE HEART

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

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Primary tumours in descending order of frequency

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

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MYXOMA

• Most common primary tumour in adults
• 90 occur in the atrial
• Lt Rt 41
• Single tumour
• 1-10cm in diameter
• Sessile or pedunculated
• Histology stellate cells,myxoma cells
  endothelial cells in a background of acid
  mucopolysaccharide.

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Rhabdomyoma

• 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.

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CONGENITAL HEART DISEASE

• DEF structural abnormalities of the heart or
  great vessels present at birth.
• Incidence 6-8/1000 live births
• Increase incidence in preterm stillbirths
• Aetiology Mostly unknown
• Associated factors include-
• Chromosomal abnormalities

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AETIOLOGY OF CHD

• Trisomy 21 (Downs) VSD
• Trisomy 18 (Edwards)
• Trisomy 13 (Pataus)
• Turners synd. Coartation of the aorta
• Environmental factors
• Maternal infection eg Rubella
• Cardiac teratogens hypoxia,ionizing
  radiation,drugs eg thalidomide, alcohol.

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Classification

• 1. Acyanotic with 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
• 3) Acyanotic (no shunt )
• a) Coarctation of the aorta
• b) Aortic stenosis

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Clinical significance of CHD

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

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ASD. (PrimumSecondum)
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TRANSPOSITION OF GREAT VESSELS.
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VSD

• 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

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COARCTATION OF THE AORTA

• 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.

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PDA
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Clinical symptoms

• Differences in the blood pressure in the upper
  and lower extremities
• Development of collateral channels
• Dilatation of intercoastal vessel leading to rib
  notching

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Tetralogy of Fallot

• Large VSD
• Overriding aorta
• Pulm. stenosis
• RVH

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Clinical features

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

115
Diseases of blood vessels lymphatics

• Preview
• Arteries veins
• Composed of-
• Intima
• Media
• Adventitia

116
ARTERIES.

• 3 main types
• Elastic art. eg aorta its main branches
• Muscular art. Medium sized arteries
• Arterioles also called resistance vessels.
• Veins contain little quantities of muscle
  elastic fibres. Also called capacitance vessels.

117
ARTERIOSCLEROSIS

• Simply means hardening of arteries
• 3 disease entities
• 1. Atherosclerosis
• 2.Monkebergs medial calcific sclerosis
• 3.Arteriolosclerosis

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Atherosclerosis

• Affects the elastic muscular arteries
• The basic lesion is an Atheroma( fibrofatty
  plaque) consists of a raised focal plaque within
  the initima with a lipid core covered by
  fibrous cap
• Starts as a focal lesion ,later becomes numerous

119
Risk factors

• MAJOR
• Diet Hyperlipidemia
• Hypertension
• Cigarette smoking
• DM
• MINOR
• OBESITY
• Increasing age
• Sex male gender Post Menopause Females.
• Family history
• Oral contraceptives
• Sedentary life style

120
Pathogenesis of Atherosclerosis

• 1. Excessive inflitration/retention of
  cholesterol-rich, plasma-derived lipid within the
  arterial intima
• 2. smooth mm cell proliferation associated with
  synthesis secretion of collagen fibers matrix
  protein. This leads to the formation of fibrous
  cap.
• 3.necrosis of cells, fibers matrix at the
  plaque base.

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Morphology of Atherosclerosis

• The first macroscopically visible lesion is fatty
  streak
• Small yellowish dots 1-2mm in diameter slightly
  raised above the surrounding intima. The dots
  coalesce to form streaks
• Atheromatous plaque appear as white to yellow
  lesion impinge on the lumen of the artery

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Atherosclerosis contd.

• Vary from 0.3-1.5cm in diameter
• Cut surface shows a superficial fibrous cap
  deep yellowish inner core.
• Distribution abdominal aorta, thoracic aorta
  its major branches
• Microscopically smooth mm macrophages,
  leucocytes ,collagen fat cells

123
ATHEROMA AORTA.
124
Complications

• Ulceration
• Thrombosis
• Haemorrhage
• Calcification
• Embolism
• Aneurysmal dilatation

125
Monckebergs medial sclerosis

• Affects muscular arteries e.g radial ulnar,
  femoral.
• Xterised by degeneration fragmentation of medial
  muscle fibres followed by ring-like calcium
  deposition within the media
• Rarely occurs below 50years

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Arteriolosclerosis

• Hyaline arteriolosclerosis
• Hyperplastic
• Fibrinoid arteriosclerosis or necrotising
  arteriolitis

128
Hyaline arterolosclerosis

• Seen in the kidney in benign hypertension
• DM
• Elderly Patients
• Deposition of homogenous pink, hyaline material
  in the wall of arterioles
• There is loss of underlying structural details
• Narrowing of lumen

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Pathogenesis

• Haemodynamic stress of hypertension
• Metabolic stress of DM
• Both accentuate endothelial injury, leads to
  leakage hyaline deposition

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Hyperplastic arteriolosclerosis

• Associated severe hypertension
• Xterised by cellular proliferation of the
  intima,hypertrophy hyperplasia of the media.
• Onion- skin appearance

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Necrotising arteriolitis

• Frequently associated with hyperplastic
  arteriolosclerosis
• Xterised by deposition of intensely eosinophilic
  amorphous material called fibrinoid in the wall
  a vessels
• Malignant Hypertension

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Aneurysm

• Localised abnormal dilatations of vessel wall.
• Aetiology
• Most aneurysm (of the aorta) are caused by
• Atherosclerosis
• Syphilis
• Cystic medionecrosis

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Aetiology contd

• Poly Ateritis Nodosa.
• Trauma
• Congenital
• Infection mycotic aneurysm

137
Classification

• 1. Berry aneurysm
• Small spherical dilatation 1-1.5cm
• 2. Saccular aneurysm 5-20cm
• 3. Fusiform .formed by gradual steady
  dilatation of vessel wall leading to a spindle
  shaped aneurysm
• 4. Dissecting. hypertension , Marfans
  syndrome or cystic medial necrosis.
• 5. False aneurysm. Usualy due to trauma.

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BERRY ANEURYSM
139
DISSECTING ANEURYSM.
140
DISSECTING ANEURYSM.
141
DISSECTING ANEURYSM.
142
ANEURYSM AORTA.
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ANEURYSM AORTA
144
Venous system

• Varicose veins
• Abn. Dilated tortuos veins which occur as a
  result of increased intraluminal press./or
  incompetent venous valves
• Superfical veins

145
Causes

• Portal Hypertension
• Pregnancy
• Intraabdominal tumour
• Common gt50yrs
• Fgtm

146
Complications

• Oedema of affected part
• Pain
• Thrombosis
• Bleeding
• Phlebothrombosis
• Thrombophlebitis
• Chronic Skin Ulcers

147
Dxes of lymphatics

• Lymphoedema
• Congenital e.g milroy dx
• Acquired-
• obstructive
• Tumours
• Infection filariasis
• Post radiation.
• Lymphangitis

148
Tumours of blood vessels

• Benign
• haemangioma
• Intermediate
• haemangioendothelioma
• Malignant
• angiosarcoma
• Kaposis sarcoma classic, African type,
  epidemic. Transplant associated
• Haemangiopericytoma.

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VASCULITIDES

• VASCULITIS
• Aetiology-
• Bacteria
• Physical trauma
• Radiation injury
• Immunological injury scleroderma, rheumatoid
  arthritis, SLE

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CLASSIFICATION

• Large vessel vasculitis
• Giant cell (temporal ) arteritis
• Takayasu arteritis
• Medium artery
• PAN
• Kawasaki dx

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Small vessels vasculitis

• Wegeners granulomatosus
• Microscopic polyangiitis
• Essential cryoglobunaemic vasculitis

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