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Cardiovascular pathology Flashcards

1
Q

What is cardiomyopathy?

A

Any disease f the cardiac muscle often resulting in changes in the size of the heart chambers and thickness of the heart wall

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2
Q

What is dilated cardiomyopathy?

A

A large weak and flabby heart. 2-3 times the normal size but the normal weight.
Non speific histological features

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3
Q

What are teh causes of dilated cardiomyopathy?

A

50% genetic effecting genes which code for heart muscle proteins eg. Desmin or dystrophin. X linked or mitochondrail
Toxins- alcohol (direct toxic effect of ethanol on myocardium. Doxorubicin- chemotherapy that is cardiotoxic used in lymphomas
Rarely: Cardiac infection or pregnancy

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4
Q

What are the clinical features of dilated cardiomyopathy?

A

General picture of heart failure: SOB, oedema, poor exercise tollerance and cardiac output

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5
Q

What is hypertrophic cardiomyopathy?

A

Big solid, muscle bound heart with heavy and strong contraction. Esp large septum
Diastolic dysfunction as the heart cannot relax and fill eventually leading to outflow obstruction and sudden death in atheletes

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6
Q

What are the causes of Hypertrophic cardiomyopathy?

A

Majority are genetic- any of teh genes which code for muscle tissue
Beta myosin heavy chain, Myosin binding protein C, alpha tropomyosin

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7
Q

What is seen at autopsy in hypertrophic cardiomyopathy (often clinically silent)?

A

Large interventricualr septum
Assymetrical heart with outflow tract obstruction and left ventricular luminal reduction
Large heart supplied by the same coronary arteries => ischemia

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8
Q

What can been seen in the histology in hypertrophic cardiomyopathy?

A

Disorganised myofibril/swirls which do not contract regularly

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9
Q

What is restrictive cardiomyopathy?

A

A stiff heart which causes a lack of compliance (complience is the relaxation of the heart during diastole)
Little elastic tissue => incomplete filling and diastolic dysfunction
Heart looks normal- you may see bilateral atrail dilation due to back pressure.
Do not necessarily have thick walls

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10
Q

What are the causes of restrictive cardiomyopathy?

A

Deposition of something in the myocardium
Metabolic byproducts like iron
Amyloid
Sarcoidosis- multisystem granulomatous disorder
Tumours of the heart or fibrosis (possibly following radiation)

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11
Q

What is amyloid disease?

A

Abnormal deposition of abnormal proteins

Many different types of proteins which form beta pleated sheets and the body cannot get rid of them

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12
Q

Amyloid is divided into 5 classes. What is the AA classification?

A

Related to chronic diseases like rheumatoid

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13
Q

Amyloid is divided into 5 classes. What is the AL classification?

A

Related to abnormal light chains in abnormal immunoglobulin

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14
Q

Amyloid is divided into 5 classes. What is the haemodialysis associated classification?

A

Beta 2 mycroglobulin

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15
Q

Amyloid is divided into 5 classes. What is the familial classification?

A

Transthyretin and other inherited forms

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16
Q

Amyloid is divided into 5 classes. What is the diabetes or alzhimers disease classification?

A

Amyloid associated with diabetes or alzhimers

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17
Q

Amyloid affects the heart. Can it affect anywhere else?

A

Some can. Some are isolated to the heart like senile cardiac amyloidosis

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18
Q

What is seen in histology of amyloid?

A

Heavy heart
Waxy pink material which stains positively for congo red and exhibits apple green birefringence. These are the diagnostic tests

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19
Q

What happens when amyloid proteins enter the SA/AV node?

A

Arrhythmias and death

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20
Q

What is arrhythmogenic right ventricular dysplasia?

A

Genetic autosomal dominant with low penitrance

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21
Q

What are the signs of arrhythmogenic right ventricular dysplasia?

A

Syncope and funny turns

Arrhythmias and occasionally sudden death in young, fit males

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22
Q

How is arrhythmogenic right ventricular dysplasia diagnosed?

A

Hard to diagnose

Right ventricle is largely replaced by adipose tissue which is big, floppy and non contractile => arrythmias

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23
Q

What is myocarditis?

A

inflammation of the heart

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24
Q

What are the causes of myocarditis?

A

Infectious (most common) and non infectious causes:
Viral (coxackie A+B, echovirus) bacterial, fungal, protozoal, helminth
Changa’s disease in S America
Lyme’s disease Borrelia burgdorferi
HIV virus

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25
Q

What is the pathology if myocarditis?

A

Thickened beefy myocardium
Infectious = inflammatory infiltration of the heart
Non infectious = immune mediated hypersensitivity

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26
Q

Which hypersensitivity reactions can cause non infectious myocarditis?

A

Hypersensitivity to infection - rheumatic fever post strep throat
Hypersensitivity to drugs- Eosinophilic myocarditis
Systemic Lupus Erythematosus (SLE)

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27
Q

What is rheumatic fever?

A

A hypersensitivity disease caused by a cross reaction following strep throat infection

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28
Q

What are the signs of rheumatic fever?

A

Mitral stenosis with thickening and fusion of valve leaflets
Short thick chordae tendonae and inflamed myocardium
=> Fibrosis of heart valves

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29
Q

What are the histological signs of rheumatic fever?

A

Deposition of aschoff bodies and granuloma

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30
Q

What is pericarditis?

A

inflammation of the pericardial layers

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31
Q

What are the causes of pericarditis?

A

Infection, immune mediated (rheumatic fever), idiopathic, uraemic (renal failure), post MI (dresslers syndrome), SLE

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32
Q

What are the causes specifically of infectious endocarditis?

A

Virues esp ECHOvirus
Bacterial tend to be extenetion from elsewhere eg lungs => purulent effusion
Fungi in immunosuppressed (post transplant) +>purulent effusions
Tuberculin infections causes effusions and constrictive pericarditis

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33
Q

What colour is the effusion produced by ECHO virus in pericarditis?

A

Straw coloured

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34
Q

What is Dressler’s Syndrome?

A

Pericarditis post MI.
Usually occurs weeks later and throught to be immune mediated. Damaged heart muscle encounters previously unencountered material =>immune response

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35
Q

What are the complications of pericarditis?

A

Pericardial effusion => cardiac tamponade, constrictive pericarditis, cardiac failure and death

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36
Q

What are the causes of cardiac tamponade?

A

Post MI
Pericarditis
Aortic dissection

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37
Q

What is endocarditis?

A

Inflammation of the lining of the heart (usually valves)

Can be infectious or non infectious

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38
Q

Which patient groups are at high risk of infective endocarditis?

A

PWID, Septic patients and people with abnormal heart valves (prosthetic valves, congenital bicuspid aortic valve, Mitral valve prolapse or calcific disease)

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39
Q

What is a mitral valve prolapse?

A

Where the 2 valve cusps do not close evenly

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40
Q

Usually infective endocarditis requires a virulent bacteria or fungi but if you are at high risk you can get endocarditis from organisms which live in the mouth. What should happen if you need dental work?

A

Prophylactic antibiotic coverage

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41
Q

What are the HACEK organisms?

A

Gram negatives causing endocarditis

Haemophylus, Actinobaccillus, cardiobacteria, Einkenella, Kingella

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42
Q

If you have a prosthetic valve, which organism is most likely causing your endocarditis?

A

Staph epidermidis

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43
Q

If you are a PWID, which organism is likely to be causing your endocarditis?

A

Staph aureus or Candida

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44
Q

What is the pathology of infective endocarditis?

A

1) Aggregates of organisms on heartvalves called vegitiations
2) Bacteria excite acute inflamation+ bacterial and inflammatory cell products digest valve leaflets
3) Causes swing fevers and loud murmurs
4) Emboli can be produced => systemic infection
5) Even when treated valvular failure for rest of life

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45
Q

What are the cardiac complications of infective endocarditis?

A

Acute valvular incompetence, high output cardic failure, abscesses, fistulas and pericarditis

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46
Q

What are the systemic signs of infective endocarditis?

A 
Osler's nodes
Janeway lesions
Roth spots
Finger clubbing 
Splinter hemorrhages
Septic emboli in brain and kidney
Mycotic aneurysm
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47
Q

What are the causes of non infective endocarditis?

A

Rheumatic fever, SLE, Non bacterial thrombotic endocarditis NBTE, carcinoid heart disease

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48
Q

What is non bacterial thrombolic endocarditis?

A

Non invasive and dozen’t destroy the valves
Small and multiple vegetations
Can cause embolic disease and is associated with cancer (mucinous adenocarcinomas
Hypercoaguable state

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49
Q

What type of endocarditis dos SLE cause and what is it?

A

Libman-Sack’s Endocarditis
Small sterile emboli on the undersurfaces of valves or on chordae
Small asymptomatic deposits or significant valvulitis

50
Q

What is carcinoid heart disease?

A

Carcinoid tumours are neoplasms of neuroendocrine cells (common in GI tract and lung mucosa)
They relaease hormones

51
Q

When does carcinoid syndrome happen?

A

When the tumour has spread to the liver

52
Q

What is carcinoid syndrome and what symptoms does this lead to?

A

Excess 5HIAA, seratonin, histamine, bradykinin produced by the tumour
Flushing of skin, nausea, vomiting and diarrhoea
Right sided cardiac valve disease with tricuspid and pulmonary valve insufficiency

53
Q

Why are primary cardiac tumours rare in the heart?

A

Cardiac myocytes are end differentiated

54
Q

What is the most common type of primary cardiac tumour and where does it occur

A

Atrial myxoma- benign and 90% of time occurs in left atrium

55
Q

What are the symptoms of atrail myxoma?

A

Systemic fever and malaise. Releases IL 6

Causes valve obstruction, tumour emboli and endocarditis

56
Q

What are the most common secondary cancers in the heart?

A 
Malignant melanoma (met)
Carcinoma of lung or oesophagus (direct invasion)
57
Q

What is labile hypertension?

A

Hypertension which is borderline and fluctuates between normal and high

58
Q

WHat is hypertension a risk factor for?

A

Cerebral haemorrhage, atheroma, renal failure, sudden cardiac death (heart >400g in weight

59
Q

Which global population groups are at high and low risk of hypertension?

A

High risk = black population

Low risk = south pacific

60
Q

What is primary hypertension?

A

Hypertension with no known cause

Environment/genetics

61
Q

What is secondary hypertension?

A

Hypertension with a known cause

62
Q

What mediator cause vaoconstriction and which cause vasodilation?

A 
Vasoconstriction = Endothelin, Angiotensin 2, catercholamines 
Vasodilation = nitric oxide, prostaglandins
63
Q

Renal blood flow is an important determinant of systemic BP. Why?

A

Because of the RAAS system

64
Q

What is salt sensitive hypertension and when is it most common?

A

Hypertension which can be reduced by reducing salt intake..
Influenced by polymorphisms but usually in renal disease, secondary hypertension is salt sensitive and most primary hypertension is salt sensitive

65
Q

What are the more frequent causes of secondary hypertension?

A

Renal disease = infection, cancer, surgery (=> reduced flow => increased BP)
Endocrine disease = excess hormones produced from the cortex => increased BP
Aortic disease = coarctation or dissection
Renal artery stenosis = narrowing of artery. Reduced flow => increased BP
Drug therapy = steroid consumption => hypertension

66
Q

Which renal diseases can cause hypertension?

A

Any.
Acute/chronic glomerulonephritis, renal artery stenosis, chronis pyclonephritis, cystic diseases, interstitial nephritis, chronic thyroid nephritis
=> Decreased renal blood flow => increase renin release => increased salt and water retention

67
Q

How does Conn’s syndrome cause hypertension?

A

Excess aldosterone from adrenal gland => increased salt and water retention

68
Q

How does Cushing’s syndrome cause hypertension?

A

Excess corticosteriod production

69
Q

How does phaechromocytoma cause hypertension ?

A

Excess noradrenaline => increased sympathetic to the heart

70
Q

What is coarctation of the aorta and how does this lead to hypertension?

A

Congenital narrowing ot the aorta beyond the great vessels

=> hypertension in head and neck and upper limbs and hypotention in lower limbs

71
Q

What is benign hypertension?

A

Usually asymptomatic and an incidental finding at a health check
Due to increase is SVR and afterload

72
Q

What are the consequences of benign hypertension if left untreated?

A 
Left ventricular hypertrophy
Congestive cardiac failure
Increased atheroma
Increased aneurysm rupture (aortic dissections and berry aneurysms)
Renal disease
73
Q

What is hypertensive heart disease and what characterises it?

A

Left ventricular hypertrophy. No hyperplasia. DUe to increased after load

1) Larger myocytes have a greater demand for oxygen and nutrients but are supplied by the same coronary arteries => poor cardiac perfusion => development of arrhythmias
2) Interstitial fibrosis- stiffening of muscle due to calcification. Cells speed out and excitation doesn’t spread well
3) Diastolic dysfunction because the ventricle is unable to relax and fill

74
Q

Hypertension contributes to atheroma due to increased andothilial injury. How does complicated atheromas increase hypertension?

A

They stiffen artery walls due to calcification and they cannot relax during systole => hypertension

75
Q

How do aortic dissections lead to hypertension?

A

narrow the lumen of arteries

76
Q

What is a berry aneurysm and where is it most commonly found?

A

Small aneurysm which classically occurs where cerebral arteries depart from the circle of Willis at the base of the brain => subarachnoid haemorrhage

77
Q

What is Hyaline arteriosclerosis?

A

Blood vessel changes in small arteries and arterioles- commonly in the retina and kidney
Thickening of the media as plasma proteins enter the vessel wall. => narrowing of the lumen, reducing blood flow and increasing renin release and BP
Hypertensive retinopathy

78
Q

What is malignant hypertension?

A

Diastolic pressure >130-140mmHg. Life threatening and serious. Most common in secondary hypertension but can be primary. Requires urgent treatment

79
Q

WHat are the signs of malignant hypertension? (straight to hospital)

A

Cerebral oedema =>papilloedema (swelling of optic discs)
Acute renal failure (onion skinning of vessel wall with fibrin
Acute heart failure
Headache and cerebral haemorrhage
Blood vessels show fibrinoid necrosis and endarteries proliferans of their wall

80
Q

How common is pregnancy induced hypertension?

A

10%
Increases maternal and foetal morbidity and mortality
Hypertension may be secondary to silent renal or systemic disease

81
Q

What is Pre-eclampsia?

A

Hypertension and proteinurea

Develops around 20 weeks and resolves following birth

82
Q

WHat is Eclampsia?

A

Onset of seizures in women with pre-eclamsia

Obstetric emergency- baby must be delivered to save mother

83
Q

What is thrombosis?

A

Formation of a blood clot inside a blood vessel obstructing the flow through the vessel

84
Q

what is embolism?

A

The lodging of an embolus, a gas, liquid or solid phase particle in a blood vessel causing occlusion

85
Q

What is a blood clot?

A

Formation of a blood clot outside a blood vessel (bleeding into soft tissue) => bruise. Passive process

86
Q

Where is thrombus formation most likely?

A

Virchows triad!

Endothilial injury, Turbulent/static blood flow, Hypercoaguable blood

87
Q

Intravascular coagulation is an active process. What 2 things are required for this to happen?

A

1) Platelet activation

2) Fibrin production via coagulation cascade

88
Q

What is platelet activation and how does it occur?

A

Primary haemostasis

1) Endothilium is damaged which exposes underlying collagen
2) Collagen releases glycoproteins 1a and 2b and von Willebrands factor. Platelets have receptors for these molecules so bind to the site of injury => platelet plug
3) Activated platelets release granules to attract other platelets (vWF, PAF (platelet activating factor), Thromboxane A2 and ADP)
4) Glycoproteins A and B later bind fibrinogen

89
Q

What is secondary haemostasis and how does it occur?

A

Secondary haemostasis

1) One factor activates another- the sequence provides lots of steps which can be inhibited to ensure control
2) Phospholipid (platelets) are negatively charges and release Ca++ ions
3) The tissue factors are negatively charged so are attracted to the platlets

90
Q

What is the extrinsic pathway within the coagulation cascade?

A

Due to tissue injury and the subsequent release of tissue factor and factor 7 which is activated to 7a
This then joins the common pathway

91
Q

How is the extrinsic pathway measured?

A

Activated partial thromboplastin time APTT

92
Q

WHat is the intrinsic pathway within the coagulation cascade?

A

Begins with the Hageman factor and kalikrien and follows a number of steps to the common pathway

93
Q

How is the intrinsic pathway measured?

A

Prothrombin time PT

94
Q

What is the common pathway within the coagulation cascade?

A

Begins when thrombin is formed from prothrombin, stimulated by factor 5 and factor 10a. Ca++ and energy dependent
Throbin causes fibrinogen to turn to fibrin

95
Q

What forms the amplification loop for the coagulation cascade?

A

Factor 8 and 9

96
Q

Which factors require vitamin K (a fat soluble vitamin)to form?

A

Factor 7, 9 and 10

97
Q

Where is vitamin K stored?

A

In the liver => liver disease can effect the coagulation cascade

98
Q

What does warfrin do?

A

Prevents production of factor 7, 9, 10 and thrombin

99
Q

WHat causes endothilial injury?

A 
Hypertension
Toxins
Infectious agents (virus')
Autoimmune disease (primary vasculitis)
Turbulence
100
Q

Why does thrombosis not usually occur in the arteries?

A

High flow so procoagulant material is swept along without attaching to the vessel wall. Thrombosis can occur when there is underlying atherosclerosis

101
Q

Why does stasis lead to increased thrombosis?

A

Coagulation due to cell margination.
Increase contact of platelets with the vessel wall and no washing out.
Common in the venous system due to faulty valves and venous insufficiency => DVT

102
Q

What are the primary causes of hypercoagulbility?

A

Dehydration, polycythemia (increased cells) and leukemias

103
Q

How does fibrinolysis take place?

A

Tissue plasminogen activaor combines with plasminogen to form plasmin which breaks down fibrin into fibrin degredation products

104
Q

What are the naturally occurring anticoagulants?

A

Antithrombin is a protein which switches off thrombin

Protein S and C switch of factor 5 and 8 => no amplification loop

105
Q

How are protein C and S activated?

A

Thrombin chages to thrombomodulin

106
Q

What is factor V Lieden?

A

Mutation in factor 5 targeted by prtein C and S => blood remains coagulated.
Inherited disorder

107
Q

Deficiency in Protein C, S or antithrmbin causes what?

A

Hypercoaguable blood

108
Q

What are the secondary causes of hypercoaguable blood?

A

High risk: Prolonged immobility, Significant tissue injured, antiphospholipid syndrome (autoimmune), myocardial infarction, AF, Cancer, Chemotherapy (injures epithilium), Marantic endocarditis (aseptic thrombotic endocarditis)
Low risk: The pill. renal disease, cardiomyopathy, smoking

109
Q

What are the common sites for thrombi?

A

Coronary vessels, above the bifurcation of the aorta

Origin and division of carotid arteries, Renal arteries, superior mesenteric artery

110
Q

Which organs are therefore susceptible to embolism and infarction?

A

Heart, brain, small bowel, kidneys

111
Q

What is a saddle emboli?

A

Large emboli which gets stuck at the bifurcation of the pulmonary trunk which prevents blood flow to both lungs => no oxygenated blood to the heart

112
Q

Why can small emboli in the pulmonary artery be assymptomatic?

A

Because the bronchial arteries also supply the lungs

113
Q

Can many small emboli be the cause of pulmonary hypertension?

A

Yes

114
Q

What are the other other types of emboli?

A

Air, Septic, Amniotic fluid, umour, Fat

115
Q

When do you get fat emboli?

A

Post RTA or major trauma released from bone marrow

116
Q

When do you get Amniotic fluid emboli?

A

After difficult births and you find keritinised skin calls in the mothers lung

117
Q

Which tumours embolis most commonly?

A

Renal cell and liver carcinoma

118
Q

What are the signs of air emboli?

A

Frothy blood which prevents the heart from contracting

119
Q

What is ischemia?

A

Insufficient blood supply

120
Q

What is infarction?

A

Death of a tissue due to ischemia

121
Q

What is found with an athoromatous plaque?

A

Lots of tissue factor

Cardiovascular (24 decks)

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