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2a- Cardiology > Cardiovascular pathology > Flashcards

Cardiovascular pathology Flashcards

1
Q

What is the normal weight of the heart?

A
  • 0.45% body mass (male)
    • 280-340 g male
  • 0.4% body mass (female)
    • 230-280 g female
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2
Q

Describe contraction in the heart basically

A
  • Two stage electrical generated contraction
  • Sarcomere proteins
  • Contraction initiated by depolarisation and changes to calcium concentration
  • Protein conformational change – contraction
  • Removal of calcium (energy dependent) for relaxation to occur
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3
Q

What are the 2 types of cardiac myocyte?

A
  1. Atrio-ventricular conduction system – slightly faster conduction
  2. General cardiac myocyte
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4
Q

What is the normal systolic ejection fraction?

A

60-60%

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5
Q

What is cardiac failure?

A

Failure to transport blood out of heart

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6
Q

What is severe failure?

A

Cardiogenic shock

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7
Q

When can myocardial hypertrophy be adaptive/physiology?

A

Athletes and pregnancy

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8
Q

What happens if you exceed stretch capability of sarcomeres?

A

cardiac contraction force diminishes

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9
Q

What is the hypertrophic response triggered by?

A
  • Angiotensin 2
  • ET-1 and insulin-like growth factor 1
  • TGF-beta
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10
Q

Describe left sided cardiac failure

A
  • Pulmonary congestion
  • Heart is not able to pump efficiently so blood backs up in the veins that take blood through the lungs
  • Pressure in these vessels increases and fluid is pushed into the alveoli and then overload of right side
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11
Q

Describe right sided cardiac failure

A
  • Venous hypertension
  • High pressure in the veins of the legs, caused by venous insufficiency where blood leaks downwards due to the effect of gravity through leaky valves
  • And congestion
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12
Q

Describe diastolic cardiac failure

A
  • Stiffer heart (left ventricle)
  • A stiffer heart means the left ventricle cannot fill properly with blood during the diastolic phase, reducing the amount of blood pumped out to the body
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13
Q

Describe foetal embryogenesis

A
  • Up until 5th week of gestation the heart is a single chamber, divided by the intra-ventricular
    and intra-atrial septa from endocardial cushions
  • The muscular intra-ventricular septum grows upwards from the apex of the heart, producing the four chambers and allowing valve development to occur
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14
Q

What is congenital heart disease?

A

A general term for a range of birth defects that affect the normal way the heart works

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15
Q

What does congenital heart disease result from?

A
  • Results from faulty embryonic development
    • misplaced structures or arrest of the progression of normal structure development
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16
Q

What are the 4 most common congenital heart disease?

A
  1. VSD (ventricular septal defect) 25-30%
  2. ASD (atrial septal defect) 10-15%
  3. PDA (persistent/patent ductus arteriosus) 10-20%
  4. Fallots 4-10%
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17
Q

What is multifactorial inheritance?

A

One child with the defect increases the probability of second child with another defect

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18
Q

What are some disorders where single genes are affected?

A

trisomy 21, Turner Syndrome (XO)

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19
Q

How can infections cause congenital heart disease?

A

e.g. rubella – causes congenital heart disease in baby if pregnant mother develops rubella

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20
Q

What is a cardiac shunt?

A

A pattern of blood flow in the heart that deviates from the normal circuit of the circulatory system

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21
Q

What are reasons left-right shunts occur?

A
  • Ventricular septal defect
  • Atrial septal defect
  • Persistent ductus arteriosus
  • Truncus arteriosus (a single blood vessel comes out of the right and left ventricles
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22
Q

What is anomalous pulmonary venous drainage?

A

blood flow from a few of the pulmonary veins return to the right atrium instead of the left atrium – some pulmonary venous flow enters the systemic venous circulation

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23
Q

What is hypoplastic left heart syndrome?

A

left side of the heart does not form correctly – underdeveloped left ventricle

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24
Q

What are reasons right-left shunts occur?

A
  • Tetralogy of Fallot
  • Tricuspid atresia – absence of tricuspid valve, underdeveloped right ventricle
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25
Q

What are defects that result in no shunt?

A
  • Complete transposition of great vessels
  • Coarctation
  • Pulmonary stenosis
  • Aortic stenosis
  • Coronary artery origin from pulmonary artery
  • Ebstein malformation/anomaly
  • Endocardial fibroelastosis
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26
Q

What is complete transposition of great vessels?

A

an abnormal spatial arrangement of any of the great vessels

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27
Q

What is coarctation?

A

congenital narrowing of a short section of the aorta

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28
Q

What is pulmonary stenosis?

A

narrowing at a point from the right ventricle to the pulmonary artery causing obstruction of blood flow

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29
Q

What is aortic stenosis?

A

narrowing of the aortic valve opening restricting blood flow from the left ventricle to the aorta

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30
Q

What is Ebstein malformation/anomaly?

A

faulty tricuspid valve

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31
Q

What is endocardial fibroelastosis?

A

thickening within the muscular lining of the heart chambers due to an increase in the amount of supporting connective tissue, leading to cardiac hypertrophy

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32
Q

Describe Eisenmenger’s complex progression?

A
  • Initially left-right shunt
  • Then right-left shunting
  • Associated with right side cardiac failure and right side cardiac
    hypertrophy
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33
Q

What is patent foramen ovale?

A

A condition that occurs when the foramen ovale present before birth fails to close

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34
Q

What does patent foramen ovale eventually lead to?

A
  • It eventually produces cardiac arrhythmias, pulmonary hypertension, right ventricular hypertrophy and cardiac failure
  • There is also a risk of infective endocarditis
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35
Q

What is patent ductus arteriosus?

A
  • The ductus arteriosus is a blood vessel connecting the pulmonary artery to the proximal descending aorta before birth
    • It should usually occlude once the baby starts breathing
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36
Q

What is the consequence of ductus arteriosis?

A
  • Left-right shunt eventually overloads the lung circulation with pulmonary hypertension and then right side cardiac failure
  • There is also risk of infecting endocarditis
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37
Q

How can you close a patent ductus arteriosis?

A

It can be closed surgically, by catheters or by prostaglandin inhibitors

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38
Q

What are the 4 main features of tetralogy of fallot?

A
  1. Pulmonary stenosis
  2. Ventricular septal defect
  3. Dextroposition/ over-riding aorta (aorta straddles the VSD)
  4. Right ventricle hypertrophy
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39
Q

What does tetralogy of fallot lead to?

A

The right ventricle blood is shunted into the left heart, producing cyanosis from birth

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40
Q

How do you treat tetralogy of fallot?

A

Surgical correction usually required during first two years of life, as progressive cardiac debility and risk of cerebral thrombosis increases

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41
Q

What is cyanosis?

A

a bluish colour of the skin and the mucous membranes due to insufficient oxygen in the blood

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42
Q

What is ischaemic heart disease?

A
  • Disease characterised by reduced blood supply to the heart
  • The coronary arteries supply blood to the heart so a blockage reduces the supply of blood to the heart muscle
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43
Q

What can ischaemic heart disease cause?

A
  • Angina (standard, unstable, accelerated)
  • Myocardial infarction
  • Chronic congestive cardiac failure
  • Sudden death
44
Q

What are the main risk factors for IHD?

A
  • Systemic hypertension
  • Cigarette smoking
  • Diabetes mellitus
  • Elevated cholesterol
45
Q

What are other risk factors for IHD?

A
  • Obesity
  • Increasing age
  • Male sex
  • Family history
  • Oral contraceptive pill
  • Sedentary lifestyle
46
Q

What are the main reasons for a reduced blood supply to the heart?

A
  • Atherosclerosis
  • Thrombosis
  • Thromboembolism
  • Coronary artery spasm
  • Collateral blood vessels
  • Blood pressure/ cardiac output/ heart rate
  • Arteritis
47
Q

What is thromboembolism?

A

formation of a clot in a blood vessel that breaks loose, is carried by the blood and plugs another blood vessel

48
Q

What is coronary artery spasm?

A

a sudden tightening of the muscles within the arteries of the heart

49
Q

What are collateral blood vessels?

A

abnormal blood vessels that connect the aorta with the pulmonary arteries

50
Q

What is arteritis?

A

inflammation of the walls of arteries

51
Q

What are other reasons for reduced blood supply to the heart?

A

anaemia, increased demand from hypertension, hyperthyroidism and
fever

52
Q

What are conditions that limit coronary flow?

A
  • Coronary arteritis
  • Dissecting aneurysm of aorta
  • Syphilitic aortitis
  • Myocardial bridge
53
Q

What is a dissecting aneurysm of aorta?

A

an aneurysm, outward bulging due to a weakened blood vessel, in which the wall of the coronary artery rips longitudinally

54
Q

What is syphilitic aortitis?

A

congenital abnormality of coronary artery origin

55
Q

What is myocardial bridge?

A

a band of heart muscle that lies on top of a coronary artery, the artery dips into underneath and then comes back out

56
Q

What are the 2 types of myocardial infarction?

A
  • Subendocardial/ patchy infarction
  • Transmural infarction
57
Q

What is a subendocardial/ patchy infarction?

A
  • involves the innermost layer and some middle parts of the myocardium, but not the epicardium
  • NSTEMI
58
Q

What is a transmural infarction?

A

full thickness of the myocardium

59
Q

What is reperfusion?

A

restoring the flow of blood to an organ/tissue (typically after heart attack/stroke)

60
Q

What can reperfusion after following clot-busting agents and angioplasty techniques of completely infarcted tissue cause?

A
  • can produce significant haemorrhage
  • It can lead to contraction band necrosis – a type of uncontrolled cell death unique to cardiac myocytes that arises in reperfusion from hypercontraction
61
Q

What are pathological complications of ischaemic damage?

A
  • Arrhythmias
  • Left ventricular failure – cardiogenic shock
  • Extension of infarction, rupture of myocardium (into pericardial space, between chambers, across papillary muscle insertion)
62
Q

What is pericarditis (Dressler syndrome)?

A
  • Inflammation of the pericardium, the protective sac that surrounds your heart
  • The pericardium can become inflamed if blood/fluid leaks between the two layers of the pericardium
63
Q

What are treatment methods of pericarditis?

A
  • Thrombolytic enzymes
  • Percutaneous transluminal coronary angioplasty (PTCA)
  • Coronary bypass grafting
  • Stents
  • Transplants
64
Q

What is the WHO classification of hypertension?

A

> 140/90mmHg

65
Q

What are hypertensive heart diseases?

A

heart failure, ischaemic heart disease and left ventricular
hypertrophy

66
Q

What is the definition of Cor pulmonale?

A

right ventricular hypertrophy and dilatation due to pulmonary hypertension

67
Q

What can Cor pulmonale be caused by?

A
  • Embolization of material into the pulmonary circuit
  • Chronic bronchitis and emphysema
  • Pulmonary fibrosis
  • Cystic fibrosis
  • Recurrent emboli
  • Primary pulmonary hypertension
68
Q

What is infective endocarditis?

A

An infective process involving the cardiac valves

69
Q

What is the most common cause for infective endocarditis in children?

A

congenital heart disease

70
Q

What is the most common cause for infective endocarditis in adults?

A

rheumatic valvular heart, mitral valve prolapse, IV drug abuse, prosthetic valves, and diabetes

71
Q

What are the characteristic organisms causing infection in infective endocarditis?

A

streptococci and staphylococci

72
Q

What are the consequences of infective endocarditis?

A
  • Infection produces rapidly increasing cardiac valve distortion and disruption with acute cardiac dysfunction
  • There can also be other consequences including; fever, anorexia, fatigue, neurological dysfunction due to mitotic emboli and aneurysms
73
Q

What is calcific aortic stenosis?

A

Nodular calcific deposits in cusps with progressive distortion of valves opening/closure

74
Q

What is calcific aortic stenosis accelerated in?

A

bicuspid aortic valves

75
Q

What is calcific aortic stenosis associated with?

A

coronary artery disease

76
Q

What does calcific aortic stenosis lead to?

A

Obstruction to left ventricle outflow produces pressure overload and cardiac hypertrophy

77
Q

What is there a risk of in calcific aortic stenosis?

A
  • Risk of sudden cardiac death
  • Myocardial infarction risk
78
Q

What is mitral valve prolapse?

A
  • Degeneration of the mitral valves such that the inner fibrosa layer becomes more loose and fragmentary with accumulation of mucopolysaccharide material
  • Valve cusps bow upwards and may not close adequately producing regurgitation
79
Q

What is the risk of mitral valve prolapse?

A
  • Association with sudden cardiac death
  • Risk of infective endocarditis
80
Q

What is mitral valve prolapse associated with?

A

underlying connective tissue disorders, Marfan’s syndrome and myotonic dystrophy

81
Q

What symptoms does calcification of the mitral valve annulus produce?

A

usually asymptomatic and of no significance

82
Q

What is myocarditis?

A

Inflammation of the myocardium – usually associated with muscle cell necrosis and degeneration

83
Q

What are causes of myocarditis?

A
  • Viruses e.g. influenza. Viral myocarditis is most common aetiology
  • Rickettsia – typhus
  • Bacteria e.g. staphylococcal, streptococcal
  • Fungi and protozoa parasites
  • Metazoa
84
Q

What are non-infectious causes of myocarditis?

A
  • Hypersensitivity/ immune related diseases
  • Radiation
  • Miscellaneous – sarcoid, uraemia
85
Q

What do drug reactions often cause?

A
  • an inflammatory infiltrate particularly around blood vessels
    within the myocardium
  • There may be a predominance of eosinophils
86
Q

What is giant cell myocarditis?

A
  • a very rare, highly aggressive form of cardiac disease with areas of muscle cells death due to macrophage giant cells
    • Often fatal
87
Q

What is cardiomyopathy?

A
  • Primary cardiac disease with contractile dysfunction and atypical morphology
  • The heart doesn’t pump as well as it should
88
Q

Describe features of dilated cardiomyopathy (DCM)

A
  • Most autosomal dominant, but some recessive and X-linked
  • Mutations in several genes are recognised – dystrophin, troponin T
  • Poorly generated contractile force leads to progressive dilation of heart with some diffuse interstitial tissue
89
Q

What is the clinical progression of dilated cardiomyopathy (DCM)?

A

slowly deteriorating cardiac failure, dysrhythmias and ultimately death

90
Q

What are causes of secondary dilated cardiomyopathy (SDC)?

A
  • Alcohol
  • Male bias
  • Cobalt toxicity
  • Catecholamines
  • Cocaine
  • Pregnancy
91
Q

Describe features of Hypertrophic cardiomyopathy (HCM)

A
  • Many mutations recognised involving beta-myosin binding protein C, troponin T, titin etc
  • HCM is related to defects in force degeneration/ energy usage allowing progressive sarcomeric dysfunction
  • Compensatory hypertrophy often occurs
92
Q

What are clinical features of HCM?

A
  • Mutation in beta-myosin = cardiac hypertrophic and dysrhythmia
  • Elevated Troponin T = risk of sudden death
93
Q

What are problems seen in HCM?

A
  • Increased fibrosis in tissues
  • Ventricular outflow distortion
  • Myocyte disarray
  • Variation in small artery substructure
  • Many patients have positive family history with cardiac failure and sudden death
  • Some present with classic ischaemic heart disease symptoms
94
Q

What is ARVC?

A

Arrhythmogenic right ventricular cardiomyopathy

95
Q

What is Arrhythmogenic right ventricular cardiomyopathy (ARVC)?

A

a degenerative condition with progressive dilatation of the right ventricle with fibrosis, lymphoid infiltrate and fatty tissue replacement

96
Q

What is restrictive cardiomyopathy?

A

a group of disease in which poor dilation of the heart restricts the eventual ability of the heart to take on blood and pass it to the rest of the body

97
Q

What are channelopathies?

A

Gating currents for Na, K with association to long QT syndrome, Brugada syndrome etc.

98
Q

What is cardiac myxoma?

A

rather jelly like proliferation of myxoid cells with abundant endothelial vascular

99
Q

What is a rhabdomyoma?

A

paediatric tumour with similarity to foetal cardiac cells

100
Q

What can cardiac sarcomas be?

A

can show differentiation towards vascular, fibrous and muscle phenotypes

101
Q

What are all the pericardial diseases?

A
  • Serous pericardial effusion
  • Sero-sanguinous effusion
  • Haemopericardium
  • Cardiac tamponade
  • Acute pericarditis
102
Q

Describe Serous pericardial effusion

A

low protein content with few cellular elements

103
Q

Describe Sero-sanguinous effusion

A

following trauma, surgery or resuscitation

104
Q

Describe Haemopericardium

A

direct bleeding from the vasculature wall through the ventricular wall following MI

105
Q

Describe Cardiac tamponade

A

compression of the heart leading to acute cardiac failure following bleeding in to the pericardial space

106
Q

Describe acute pericarditis

A

often follows viral infection with acute/ chronic inflammation of the pericardial surface

2a- Cardiology (7 decks)

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