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14 Cardiovascular Flashcards

1
Q

Front (Term)

A

Back (Definition)

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2
Q

What are some anticoagulant and antithrombotic molecules produced by endothelial cells?

A

Prostacyclin
Thrombomodulin
Plasminogen activator
Heparin-like molecules

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3
Q

What are some prothrombotic molecules produced by endothelial cells?

A

Von willebrand factor Plasminogen activator inhibitor

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4
Q

What immunomodulatory molecules are produced by endothelial cells?

A

IL1, 6, 8, adhesion molecules, histocompatibilty antigens.

1.Maintenance of permeability barrier controlling transfer of molecules into and out of the vascular system.

  1. 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

  1. Modulation of blood flow and vascular reactivity
    Formation of endothelin, ACE
    Formation of prostacyclin, NO
  2. 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
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5
Q

What activates endothelial sells to produce mediators?

A

Cytokines
Complement products
Advanced glycosylation end products
Lipid products

Bacterial products, Viruses

Haemodynamic forces
Hypoxia
Activated endothelial cells respond by producing mediators listed above

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6
Q

What are the promoters and inhibitors of endothelial cell proliferation/synthesis of growth factors/matrix proteins?

A

Promotors
PDGF FGF IL1

Inhibitors
Heparin NO Gamma interferon

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7
Q

What is the response of endothelial cells to vascular injury?

A

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

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8
Q

Define Atherosclerosis

A

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.

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9
Q

What is the pathogenesis of atherosclerosis?

A

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.

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10
Q

What do atherosclerotic plaques look like morphologically?

A

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

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11
Q

What do atheromas look like under the microscope?

A

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.

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12
Q

What % of hypertension is essential hypertension?

A

Essential hypertension (90-95%)

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13
Q

What are the renal causes of hypertension?

A 
Acute glomerulonephritis 
Chronic renal disease 
Polycystic disease 
Renal artery stenosis 
Renal vasculitis
Renin producing tumours
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14
Q

What is the pathogenesis of essential hypertension?

A

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.

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15
Q

What are the small vessel diseases caused by essential hypertension?

A

Hyaline arteriolosclerosis

Hyperplastic arteriolosclerosis

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16
Q

What is a true aneurism?

A

Bounded by complete but generally attenuated arterial wall components. Blood always remains within the vascular space.

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17
Q

What is a false aneurism?

A

Extravascular haematoma that communicates with the intravascular space.

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18
Q

What is a mycotic aneurism?

A

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

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19
Q

What are the 3 morphological classifications of aneurisms?

A

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.

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20
Q

Define a dissection?

A

Blood enters the wall of an artery and forms a false lumen.

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21
Q

What is the epidemiology of AAA

A

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
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22
Q

Pathogenesis of AAA?

A

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

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23
Q

Most likely location for AAA?

A

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.

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24
Q

Complications of AAA including % risk of rupture of 5 cm?

A

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

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25
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’
26
Epideiology of aortic dissection?
Most common in 40-60 year age group or in younger patients with Marfans
27
Csuse of aortic dissection?
Hypertension (causative factor in 90%) | Connective tissue abnormalities – Marfans Rare complication of pregnancy
28
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.
29
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.
30
What is Virchow's triad?
Endothelial injury Stasis or turbulence of blood flow Blood hypercoagulability
31
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 ```
32
What is the prognosis of CCF?
Common Poor prognosis 50% 5-year mortality The most frequent specific causes are hypertension and IHD
33
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.
34
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
35
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. ```
36
Morphology of right heart failure?
Congestive hepatomegaly Congestive splenomegaly Ascites Renal congestion Pleural and pericardial effusions Peripheral oedema
37
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.
38
What does acute cor pulmonaele look like morphologically?
Marked dilation of the right ventricle without hypertrophy.
39
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.
40
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.
41
Leading cause of death among men and women?
IHD
42
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.
43
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.
44
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.
45
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
46
Define an MI?
‘ischaemic necrosis of the myocardium’
47
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
48
Time to irreversible injury (necrosis in MI)?
20-40 mins
49
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.
50
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.
51
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.
52
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)
53
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
54
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
55
What is rheumatic fever?
Acute immune mediated multisystem inflammatory disease occurring 1-5 weeks after infection by group A beta haemolytic streptococcus.
56
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.
57
Pathogenesis of rheumatic fever?
Antistreptococcal antibodies cross react with tissue glycoproteins in heart, joints and other tissues.
58
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.
59
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.
60
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 1. Migratory large joint polyarthritis – 90% of adults, uncommon in children. 2. Carditis – 50% of children, 35% of adults. 3. Subcutaneous nodules 4. Erythema marginatum – macular lesions with erythematous rim and central clearing, seen in 10-60%. 5. Sydenham chorea - rapid involuntary purposeless movements Minor Fever Arthralgia Elevated acute phase proteins Leukocytosis
61
What are the major jones criteria for RHD?
1. Migratory large joint polyarthritis – 90% of adults, uncommon in children. 2. Carditis – 50% of children, 35% of adults. 3. Subcutaneous nodules 4. Erythema marginatum – macular lesions with erythematous rim and central clearing, seen in 10-60%. 5. Sydenham chorea - rapid involuntary purposeless movements
62
What are the minor jones criteria for RHD?
Fever Arthralgia Elevated acute phase proteins Leukocytosis
63
What is the most common valvular abnormality?
Mitral valve prolapse (myxomatous degeneration of the mitral valve) affects 3% of adults – most common valvular abnormality
64
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
65
Causes of aortic stenosis?
Senile calcific aortic stenosis | Calcification of congenitally abnormal (bicuspid) valve Rheumatic heart disease
66
Causes of aortic regurgitation?
``` Degenerative aortic dilation Rheumatic heart disease Infective endocarditis Syphilitic aortitis Ankylosing spondylitis Rheumatoid arthritis Marfan syndrome ```
67
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.
68
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.
69
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
70
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.
71
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 ```
72
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.
73
Features of subacute infective endocarditis?
Insidious onset malaise, low grade fever, weight loss. | Petechiae, subungal haemorrhages, roth spots may also occur.
74
Define primary cardiomyopathy?
Primary cardiomyopathy is defined as myocardial disease of unknown aetilology
75
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 ```
76
Aetiology of dilated cardiomyopathy?
``` Idiopathic Genetic Alcohol - ?direct toxicity Pregnancy – nutritional deficiency, hypertension, volume overload, metabolic derangements – 50% resolve. Viral myocarditis Haemochromatosis Sarcoid ```
77
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.
78
Causes of restrictive cardiomyopathy?
``` Cardiac amyloid Radiation Endomyocardial fibrosis – found typically in children and young adults in Africa Loeffler’s endocarditis Endocardial fibroelastosis ```
79
Morphology of dilated cardiomyopathy?
``` Characterized by gradual 4-chamber dilatation and cardiomegaly. Poor contraction (systolic dysfunction) and stasis leads to mural thrombi. ```
80
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.
81
Microscopic morphology of HCM?
Septum shows ‘helter skelter myocyte disarray’ and diffuse interstitial fibrosis.
82
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.
83
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.
84
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
85
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.
86
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.
87
Clinical features of myocarditis?
May be entirely asymptomatic. May present with sudden onset of arrythmia or congestive heart failure. May cause sudden death.
88
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 ```
89
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
90
What causes serous periucarditis?
Rheumatic fever SLE Scleroderma Neoplasm Uraemia
91
What causes fibrinous pericarditis?
Rheumatic fever SLE Uraemia MI Dressler syndrome Radiation Trauma
92
What causes haemorrhagic pericardititis?
TB Neoplasm TB also causes caseous

ACEM pathology (4 decks)

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