14 Cardiovascular Flashcards
Front (Term)
Back (Definition)
What are some anticoagulant and antithrombotic molecules produced by endothelial cells?
Prostacyclin
Thrombomodulin
Plasminogen activator
Heparin-like molecules
What are some prothrombotic molecules produced by endothelial cells?
Von willebrand factor Plasminogen activator inhibitor
What immunomodulatory molecules are produced by endothelial cells?
IL1, 6, 8, adhesion molecules, histocompatibilty antigens.
1.Maintenance of permeability barrier controlling transfer of molecules into and out of the vascular system.
- Regulation of thrombotic and antithrombotic prcesses
Formation of anticoagulant and antithrombotic molecules Prostacyclin
Thrombomodulin Plasminogen activator Heparin-like molecules
Formation of prothrombotic molecules Von willebrand factor Plasminogen activator inhibitor
- Modulation of blood flow and vascular reactivity
Formation of endothelin, ACE
Formation of prostacyclin, NO - Regulation of inflammation by controlling white cell interaction with vessel wall.
IL1, 6, 8, adhesion molecules, histocompatibilty antigens.
5. Formation of extracellular matrix Collagen Proteoglycans Regulation of growth of other cell types Production of growth stimulators and inhibitors PDGF, CSF, FGF Heparin, TNF beta Modification of lipoproteins LDL oxidation Metabolisation of hormones Angiotensin 1
What activates endothelial sells to produce mediators?
Cytokines
Complement products
Advanced glycosylation end products
Lipid products
Bacterial products, Viruses
Haemodynamic forces
Hypoxia
Activated endothelial cells respond by producing mediators listed above
What are the promoters and inhibitors of endothelial cell proliferation/synthesis of growth factors/matrix proteins?
Promotors
PDGF FGF IL1
Inhibitors
Heparin NO Gamma interferon
What is the response of endothelial cells to vascular injury?
Vascular injury stimulates intimal thickening due to
Smooth muscle cell migration from media to intima Smooth muscle cell mitosis
Production of extracellular matrix
Smooth muscle cells characteristically change from contractile phenotype to proliferative-synthetic phenotype
Define Atherosclerosis
Slowly progressive disease of large and medium arteries characterized by focal intimal fibrofatty plaques and predisposing to narrowing of the vessel lumen, thrombosis and aneurysm.
Global distribution, virtually ubiquitous in developed nations with significant consequences for health systems.
Risk inversely related to HDL.
Multiple risk factors are additive.
What is the pathogenesis of atherosclerosis?
Chronic endothelial injury:
Likely mostly due to haemodynamic disturbances and hypercholesterolaemia
Endothelial dysfunction
Increased vascular permeability including to LDL (with high cholesterol content)
Adhesion of platelets, monocytes, leukocytes
Monocyte migration
Macrophage activation, smooth muscle migration from media to intima.
Macrophages and smooth muscle cells engulf lipid.
Smooth muscle proliferation, extracellular matrix deposition, deposition of extracellular lipids.
What do atherosclerotic plaques look like morphologically?
Characteristic atheroma
Macroscopically
White/yellow intimal lesion up to 1.5cm diameter protruding into the vessel lumen.
Distribution (in order): Affect abdominal aorta, coronary arteries, popliteal arteries, descending thoracic aorta, internal carotids, circle of willis
What do atheromas look like under the microscope?
Superficial fibrous cap
containing smooth muscle cells, scattered white cells, and dense connective tissue.
Cellular zone
containing smooth muscle cells, macrophages, T lymphocytes.
Necrotic core
containing dead cells, lipid, cholesterol, foam cells and plasma proteins.
Atheroma may be preceeded by fatty streaks that are intimal collections of foam cells and smooth muscle cells.
Complicated plaques are calcified and fissured or ulcerated and predispose to cholesterol microemboli, local thrombosis, haemorrhage, medial thinning and aneurysm.
What % of hypertension is essential hypertension?
Essential hypertension (90-95%)
What are the renal causes of hypertension?
Acute glomerulonephritis Chronic renal disease Polycystic disease Renal artery stenosis Renal vasculitis Renin producing tumours
What is the pathogenesis of essential hypertension?
Essential hypertension occurs when there are changes that alter the relationship between blood volume (renal sodium homeostasis) and total peripheral resistance (vascular reactivity and vascular wall thickness).
Genetic factors:
Normal distribution in blood pressure.
Genetic differences control of blood volume
- Genes defects in the control of aldosterone metabolism
- Gene defects in proteins affecting sodium reabsorption
- Genetic variation in the renin angiotensin system. –Genetic variation in vascular smooth muscle growth.
Genetic differences in the control of TPR:
-Genetic variation in the renin angiotensin system. –Genetic variation in smooth muscle sensitivity to vasoconstrictor agents.
Environmental factors:
Stress, obesity, smoking, physical inactivity, salt consumption.
What are the small vessel diseases caused by essential hypertension?
Hyaline arteriolosclerosis
Hyperplastic arteriolosclerosis
What is a true aneurism?
Bounded by complete but generally attenuated arterial wall components. Blood always remains within the vascular space.
What is a false aneurism?
Extravascular haematoma that communicates with the intravascular space.
What is a mycotic aneurism?
Infection of an artery resulting in weakening of the arterial wall
May be due to:
Complication of infective endocarditis
Extension of an adjacent suppurative process Haematogenous spread of infection elsewhere in the body
What are the 3 morphological classifications of aneurisms?
Berry – spherical dilation due to congenital wall weakness, most common in the circle of willis.
Saccular aneurysm – large spherical dilatation up to 20cm diameter often partially filled with thrombus. Generally occur secondary to atherosclerosis.
Fusiform – cylindrical dilatation, most commonly seen in aorta. Generally occurs secondary to atherosclerosis.
Define a dissection?
Blood enters the wall of an artery and forms a false lumen.
What is the epidemiology of AAA
Severe atherosclerotic damage of the aortic wall; however, new evidence suggests this is not the only factor, and aneurysmal disease is probably a distinct arterial pathology.
Family history - there are probably strong genetic factors. About 15% of first-degree relatives of a patient with an abdominal aortic aneurysm (AAA), mainly men, will develop an aneurysm.[5]
Tobacco smoking is an important factor.
Male sex.
Increasing age.
Hypertension.
Chronic obstructive pulmonary disease.
Hyperlipidaemia.
In population-based studies, people with diabetes have a lower incidence of aneurysms than non-diabetics have.
Atherosclerosis is the most common cause Additional familial component (in addition to that associated with atherosclerosis itself)
Any factor which causes weakness of the arterial wall can be causative: Congenital defects Infection Trauma Systemic disease including vasculitis
Pathogenesis of AAA?
Atherosclerosis results in destruction of underlying tunica media and weakening of the arterial wall.
Hypertension is a risk factor both for atherosclerosis itself and subsequent aneurysm formation.
(note – syphilitic aneurysms affect ascending aorta and arc
Most likely location for AAA?
Classical location is the abdominal aorta between the renal arteries and common iliacs.
Other sites include renal artery, superior and inferior mesenteric artery, common iliac arteries.
Complications of AAA including % risk of rupture of 5 cm?
Rupture into peritoneal cavity or retroperitoneal tissues. (2% risk if 5cm
Occlusion of a branch by direct pressure or thrombus – particularly iliac, renal, mesenteric, vertebral.
Thromboembolism.
Compression of an adjacent structure – ureter, vertebrae
What causes Ascending thoracic or arch aneurysms?
uncommon, syphillis
Characteristic of tertiary syphilis. Obliterative endarteritis involves the vasa vasorum and causes ischaemia of the aortic media and loss of elastic support. Dissection is unusual due to scarring. Such syphilitic lesions tend to be complicated by atherosclerotic lesions.
Aneurysms less common that aortic valve defects that may result in severe insufficiency and ‘cor bovinum’
Epideiology of aortic dissection?
Most common in 40-60 year age group or in younger patients with Marfans
Csuse of aortic dissection?
Hypertension (causative factor in 90%)
Connective tissue abnormalities – Marfans Rare complication of pregnancy
What is the pathology of aortic dissection?
Intimal tear into the media usually occurs within 10cm of aortic valve. Dissection can extend proximally or distally.
Connective tissue disorders result in cystic medial degeneration characterized by elastic tissue fragmentation and separation of the elastic and fibromuscular components of the media by cystic spaces filled with extracellular matrix. (CMD may also occur in patients with hypertension but there is poor correlation between the presence of CMD and dissection)
Haematoma or false lumen forms between laminar planes between middle and outer third.
What are the types of aortic dissections?
What are the complications of aortic dissections?
Type A involve ascending aorta – more common and more dangerous
Type B involve descending aorta distal to the left subclavian artery
Dissection characterized by severe tearing chest and back pain.
Outcomes: Rupture into peritoneum, pericardium or pleural space. (most common cause of death)
Extension into arterial branches resulting in occlusion.
Retrograde extension resulting in disruption of aortic valve.
What is Virchow’s triad?
Endothelial injury Stasis or turbulence of blood flow Blood hypercoagulability
What are the genetic causes of hyper-coagulability?
Factor V mutations Antithrombin III deficiency Protein C or S deficiency Fibrinolysis defects Homocystinuria Allelic variations in prothrombin levels
Acquired: DIC Heparin induced thrombocytopenia Antiphospholipid antibody syndrome AF Cardiomyopathy Nephrotic syndrome COC Sickle cell anaemia Smoking
What is the prognosis of CCF?
Common Poor prognosis
50% 5-year mortality
The most frequent specific causes are hypertension and IHD
What is the pathogenesis of myocardial hypertrophy?
Hyperlasia cannot occur as myocytes cannot divide Hypertrophied heart has less capillary/myocyte ratio, increased fibrous tissue and dysfunctional proteins and itself contributes to pump failure
Pressure hypertrophy causes increased wall thickness with normal or reduced cavity diameter
Volume hypertrophy causes increased wall thickness accompanied by dilation and increased ventricular diameter.
What are the neurohumeral processes activated by heart failure?
Immediate sympathetic response mediated by baroreceptors
Inotropic and chronotropic response Peripheral vasoconstriction
Release of catecholamines Renin-angiotensin system Atrial natriuretic peptide
Morphology of left heart failure?
Left ventricular hypertrophy Left ventricular dilation. Secondary enlargement of left atrium. Pulmonary congestion and oedema Reduced renal perfusion Reduced brain perfusion.
Morphology of right heart failure?
Congestive hepatomegaly
Congestive splenomegaly Ascites
Renal congestion
Pleural and pericardial effusions Peripheral oedema
What causes cor pulmonale?
Right ventricular hypertrophy, dilation and potential failure secondary to pulmonary hypertension
Pulmonary hypertension - pulmonary blood pressure greater than 1/4 systemic blood pressure.
Preceeding disease results in endothelial cell injury. Endothelial cell dysfunction results in failure of regulation of pulmonary blood flow.
What does acute cor pulmonaele look like morphologically?
Marked dilation of the right ventricle without hypertrophy.
What does chronic cor pulmonale look like?
Ventricular wall thickening to 1cm or more plus thickening of outflow tract.
Compression of the left ventricle and tricuspid valve incompetence can also occur.
What does pulmonary hypertension look like morphologically?
Severe cases reusult in the formation of atheromas in the pulmonary artery and its major branches.
Arterioles and small arteries develop medial hypertrophy and intimal fibrosis.
Extreme cases characterised by plexogenic pulmonary arteriopathy.
Leading cause of death among men and women?
IHD
Aetoiology of IHD?
Atherosclerosis (90%)
Vasospasm Arteritis Systemic hypoperfusion
Increased myocardial demand: Tachycardia Hypertrophy
Reduced oxygen transport: Anaemia, Lung disease Congenital heart disease
Carbon monoxide poisoning.
What are the risk factors for acute plaque change?
Myocardial ischaemia is commonly precipitated by acute plaque change in a pre- existing chronic lesion due to: Haemorrhage into the atheroma expanding its volume. Rupture or fissuring resulting in exposure of thrombogenic constituents. Erosion or ulceration resulting in exposure of the thrombogenic basement membrane.
Moderate sized lesions (greatest risk of catastrophic event – 95% lesions cause reduced flow and therefore reduced mechanical stress)
Eccentric configuration
Large soft core
High density of macrophages
Thin fibrous cap. Hypertension Vasospasm.
Discuss the formation of thrombus in a coronary vessel?
Platelets adhere to exposed subendothelial collagen or necrotic plaque contects and undergo adhesion, aggregation, activation, and release of aggregators including thromboxane A2 and serotonin, resulting is vasospasm and activation of the clotting cascade.
Thrombus superimposed on a disrupted plaque can cause partial (unstable angina, subendocardial infarction, sudden cardiac death) or total (myocardial infarction) occlusion of the vessel lumen.
Thrombus formation may be exacerbated by local factors such as thromboxane A2.
Thrombus may embolise and is an activator of growth factors that result in growth of atherosclerotic lesions.
What other than plaque rupture and thrombus contributes to coronary ischemia during a heart attack?
Local vasoconstriction compromises lumen size and can create mechanical forces that contribute to acute plaque change.
Vasoconstriction can be stimulated by:
Circulated adrenergic agonists
Locally released platelet and mast cell contents Impaired secretion of nitric oxide
Define an MI?
‘ischaemic necrosis of the myocardium’
Epidemiology of MI?
Leading cause of death amongst men and women in western society
10% occur under the age of 40 years
45% occur under the age of 65 years
Time to irreversible injury (necrosis in MI)?
20-40 mins
Discuss transmural vs subendocardial MI?
Transmural
Ischaemic necrosis of the full myocardial thickness greater than 2.5cm diameter due to acute plaque change and superimposed thrombus.
Subendocardial
Ischaemic necrosis limited to the inner one third of the ventricular wall (subendocardial zone is least well perfused and therefore most susceptible to infarction) due to diffuse atherosclerosis but without superimposed thrombus.
Macroscopic changes in MI?
6-12 hours: Lesion may be slightly pale or be inapparent
18-24 hours: Infarcted tissue is pale or cyanotic
1 week: Infarct becomes more sharply defined, yellow and softened.
7-10 days: Rim of hyperaemic granulation tissue.
6 weeks: Infarct replaced by fibrous scar.
Microscopic changes in MI?
1 hour: Intercellular oedema, buckling of myocytes at edge of infarct. Border zone viable cells show fine lipid droplets and large cytoplasmic vacuoles
12-72 hours: Neutrophilic infiltrate and progressive evolution of eosinophilic coagulative necrosis.
7-10 days: Granulation tissue gradually replaces necrotic tissue ultimately generating scar.
What kind of myocyte necrosis is seen in reperfusion after thrombolysis?
(reperfusion after thrombolysis results in haemorrhagic necrosis.
Necrotic myocytes have necrosis with contraction bands – intensely eosimophilic transverse bands composed of hypercontracted sarcomeres)
Time course of myocardial enzymes?
Creatine kinase begins to rise at 2-4 hours, peaks at 24 hours and falls by 72 hours. Troponin follows a similar time course but stays elevated for 1 week
Complications of STEMI?
Fatal arrhythmia – 25%
Non-fatal arrhythmia
– 25-95%
CHF – 60%
Cardiogenic shock – 10% (more than 40% LV infarcted)
Mitral valve dysfunction due to papillary muscle infarction.
Fibrinous or haemorrhagic pericarditis
Ventricular rupture – 1-5%
Ventricular aneurysm
Overall mortality 35% in first year, 5-10% per year thereafter.
Infarct extension or expansion
What is rheumatic fever?
Acute immune mediated multisystem inflammatory disease occurring 1-5 weeks after infection by group A beta haemolytic streptococcus.
Age group for rheumatic fever?
Most common in children 5-15 years.
Occurs after 3% of episodes of acute streptococcal pharyngitis though reactivation can occur with further infections.
Pathogenesis of rheumatic fever?
Antistreptococcal antibodies cross react with tissue glycoproteins in heart, joints and other tissues.
Macro and microscopic lesions in rheumatic fever?
Acute rheumatic heart disease:
Aschoff bodies – foci of fibrinoid degeneration surrounded by lymphocytes, occasional plasma cells and plump macrophages (anitschkow cells) – found in pericardium, myocardium and endocardium.
Pericardial lesions associated with serofibrinous pericardial exudates (bread and butter pericarditis)
Myocardial lesions associated with myocarditis.
Endocardial lesions can form vegetations (verrucae) along the valve lines of closure.
Thickenings in the left atrium are called McCallum plaques.
What are the effects of chronic rheumatic heart disease?
Fibrosis results in valvular thickening, predominantly of the mitral valve.
Fish mouth or buttonhole stenosis may result. Causes >99% of mitral stenosis.
How do you diagnose rheumatic heart disease?
Diagnosis dependent on evidence of recent streptococcal infection and presence of 2 major or 1 major and 2 minor Jones criteria
Major
- Migratory large joint polyarthritis – 90% of adults, uncommon in children.
- Carditis – 50% of children, 35% of adults.
- Subcutaneous nodules
- Erythema marginatum – macular lesions with erythematous rim and central clearing, seen in 10-60%.
- Sydenham chorea - rapid involuntary purposeless movements
Minor
Fever Arthralgia Elevated acute phase proteins Leukocytosis
What are the major jones criteria for RHD?
- Migratory large joint polyarthritis – 90% of adults, uncommon in children.
- Carditis – 50% of children, 35% of adults.
- Subcutaneous nodules
- Erythema marginatum – macular lesions with erythematous rim and central clearing, seen in 10-60%.
- Sydenham chorea - rapid involuntary purposeless movements
What are the minor jones criteria for RHD?
Fever Arthralgia Elevated acute phase proteins Leukocytosis
What is the most common valvular abnormality?
Mitral valve prolapse (myxomatous degeneration of the mitral valve) affects
3% of adults – most common valvular abnormality
Causes of acquired mitral stenosis and regurg?
Mitral stenosis: Rheumatic heart disease
Mitral regurgitation:
Mitral valve prolapse
Rheumatic heart disease, Infective endocarditis Papillary muscle dysfuction, Papillary muscle rupture, Chordae tendonae rupture, Dilated cardiomyopathy, Calcification of mitral annulus
Causes of aortic stenosis?
Senile calcific aortic stenosis
Calcification of congenitally abnormal (bicuspid) valve Rheumatic heart disease
Causes of aortic regurgitation?
Degenerative aortic dilation Rheumatic heart disease Infective endocarditis Syphilitic aortitis Ankylosing spondylitis Rheumatoid arthritis Marfan syndrome
Morphology of senior calcific aortic stenosis?
Heaped up calcified masses within the bases of the aortic cusps that ultimately prevent full opening of the valve.
May extend down to the mitral valve or cause calcification of the mitral annulus but functionally the mitral valve is usually normal (in contrast to rheumatic aortic stenosis)
Aortic stenosis results in pressure overload hypertrophy of the left ventricle eventually progressing to angina and congestive heart failure.
What is the morphology of rheumatic mitral annular calcification?
Irregular stony hard nodules that lie behind the valve. Uncommonly affect valve function.
Also associated with arrhythmias, thrombosis and infective endocarditis.
Commonly associated with mitral valve prolapse.
Morphology of MVP?
One or more leaflets is enlarged, hooded, redundant or floppy and prolapse into the left atrium during systole. There may be elongation or rupture of the chordae tendonae.
Secondary changes include fibrous thickening of the valve leaflets, thickening of the LV endocardium at sites of friction, atrial thrombosis behind the ballooning cusps and calcifications.
Microscopic:
Thinning and degeneration of outer zona fibrosa and thickening of the inner zona spongiosa.
(tricuspid also involved in 40%, may also involve aortic and pulmonary) ?due to subtle abnormalities in structural proteins.
Mitral valve prolapse
Usually an incidental finding on clinical examination – causes a mid systolic click
May cause the following complications: Infective endocarditis Mitral insufficiency Thromboembolism Arrhyhthmia
What are the risk factors for infective endocarditis?
Any valvular disease predisposes to seeding of bacteria. Congenital abnormalities and tight stenoses most commonly affected.
Host factors include immunosuppression or deficiency, chronic disease, poor nutrition, alcohol.
What are the organisms that cause infective endocarditis?
Organisms
Streptococcus (alpha haemolytic) viridans, faecalis, bovis – 65% - mainly SBE
Staphylococcus aureus – 30% - mainly acute episodes.
Staphylococcus: epidermidis in prosthetic valves.
Enterococci : HACEK group from oral cavity - Haemophilus Actinobacillus Cardiobacterium Eikenella Kingella Candida Plus any other organism
What are the morphological features of infective endocarditis?
Bulky 0.5-2cm vegetations form on one or more valves.
Acute infective endocarditis causes erosions or perforations and may invade underlying myocardium to produce an abscess. IV drug abuse is associated with right sided lesions.
Features of subacute infective endocarditis?
Insidious onset malaise, low grade fever, weight loss.
Petechiae, subungal haemorrhages, roth spots may also occur.
Define primary cardiomyopathy?
Primary cardiomyopathy is defined as myocardial disease of unknown aetilology
What is the mosct common cardiomyopathy?
Dilated: Most common cardiomyopathy accounting for 90% of cases. May occur at any age Most common 20-60 years. May occur at any age. 75% 5 year mortality
Aetiology of dilated cardiomyopathy?
Idiopathic Genetic Alcohol - ?direct toxicity Pregnancy – nutritional deficiency, hypertension, volume overload, metabolic derangements – 50% resolve. Viral myocarditis Haemochromatosis Sarcoid
Causes of hypertrophic cardiomyopathy?
Idiopathic
Genetic - autosomal dominant transmission in 50% Friedrich ataxia
Storage diseases
Infants of diabetic mothers
Pathology:
Largely unknown.
Excessive myocyte response to catecholamines Myocardial ischaemia
Primary collagen disorder.
Causes of restrictive cardiomyopathy?
Cardiac amyloid Radiation Endomyocardial fibrosis – found typically in children and young adults in Africa Loeffler’s endocarditis Endocardial fibroelastosis
Morphology of dilated cardiomyopathy?
Characterized by gradual 4-chamber dilatation and cardiomegaly. Poor contraction (systolic dysfunction) and stasis leads to mural thrombi.
Macroscopic morphology of hypertrophic cardiomyopathy?
Hypercontractile, poorly compliant heart with poor diastolic relaxation and filling and rapid emptying. Characterized by a marked cardiomegaly with disproportionate (in 90%) thickening of the septum versus the LV free wall creating a banana like configuration.
Symmetric hypertrophy can also occur. Thickening of the septum at the level of the mitral valve causes outflow obstruction.
Microscopic morphology of HCM?
Septum shows ‘helter skelter myocyte disarray’ and diffuse interstitial fibrosis.
Morphology of restrictive cardiomyopathy?
Decrease in ventricular compliance leads to impaired ventricular filling in diastole. Ventricles are normal or slightly enlarged and the ventricular cavity is not dilated. There may be atrail dilation.
Clinical features of cardiomyopathies?
Dilated:
Main complications include progressive congestive cardiac failure, embolisation of mural thrombi, fatal arrythmias.
Hypertrophic:
Symptoms occur in young adulthood – syncope, dyspnoea, angina, and congestive heart failure.
Risk of sudden death. Atrial fibrillation common.
Restrictive:
Symptoms similar to HOCM.
Aetiology of myocarditis?
Virtually any microbiological agent is potentially causative.
Infections
Viruses
Coxsackie, echo, influenza, HIV, CMV
Chlamydiae
Chlamydia psittaci
Rickettsiae
Bacteria
Corynebacterium diphtheriae, neisseria meningitides, borrelia
Fungi Candida Protozoa Trypanosoma cruzii Helminths Trichinosis
Immune mediated
Post viral Poststreptococcal SLE Drug hypersensitivity Methydopa, sulfonamides
Transplant rejection
Drugs
Doxorubicin Catecholamines – phaechromocytoma , cocaine use
Miscellaneous
Amyloid, Sarcoid
Macroscopic features of myocarditis?
Flabby ventricular myocardium with four chamber dilatation and diffuse haemorrhagic mottling.
Mural thrombi in dilated chambers. Endocardium and valves are unaffected.
Microscopic features of myocarditis?
Focal lesions, sometimes not seen on biopsy. Viral myocarditis produces isolated myofibre necrosis with interstitial oedema and mononuclear infiltrate. Bacteria produce neutrophilic infiltrate, abscesses, granulomas.
Clinical features of myocarditis?
May be entirely asymptomatic. May present with sudden onset of arrythmia or congestive heart failure.
May cause sudden death.
Causes of pericarditis?
Infection Viruses Pyogenic bacteria (direct spread, haematogenous, surgical) TB Fungi
Immune mediated
Rheumatic fever
SLE Scleroderma
Dressler syndrome (2 weeks post MI) Drug hypersensitivity
Miscellaneous MI Uraemia Post surgery Neoplasia Trauma Radiation
What are the results of hearing pericarditis?
Plaque like thickenings – Soldier’s plaque Adhesive pericarditis
Adhesive mediastinopericarditis:
May follow suppurative infection, surgery, irradiation
Pericardial sac is obliterated and adhered to surrounding structures# Results in increased myocardial work
Constrictive pericarditis
Heart encased in dense, fibrous, fibrocalcific scar that limits diastolic expansion and restricts cardiac output
What causes serous periucarditis?
Rheumatic fever SLE Scleroderma Neoplasm Uraemia
What causes fibrinous pericarditis?
Rheumatic fever SLE
Uraemia
MI Dressler syndrome Radiation Trauma
What causes haemorrhagic pericardititis?
TB Neoplasm
TB also causes caseous
