Diseases of the Cardiovascular System Flashcards

1
Q

What is ischaemic heart disease

A

inadequate blood supply to the myocardium

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2
Q

Incidence of CHD

A

10% in women, 16% in men

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3
Q

Causes of Ischaemic Heart Disease

A

Almost always atheroma +/- thrombosis
Myocardial hypertrophy - usually occurs in conjunction
Vasculitis or amyloid deposition

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4
Q

When does auto regulation of coronary blood flow break down

A

Over 70% occlusion

If over 90% occlusion insufficient at rest

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5
Q

Which area of the heart has the lowest perfusion levels

A

Sub-endocardial

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6
Q

3 types of angina

A

Stable/typical - predicatable
unstable/crescendo - unpredictable - coronary artery spasms treat with calcium channel blockers
Variant/Prizemental - RED FLAG SYMTPOM, getting worse often due to plaque disruption

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7
Q

What is acute coronary syndrome

A

Actue MI and crescendo angina

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8
Q

What usually causes sudden cardiac death

A

Arrhythmias

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9
Q

What does chronic ischaemic heart disease cause

A

Hypertrophied heart

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10
Q

What is acute ischaemia

A

atheroma + acute thrombosis/haemorrhage
Get transmural MI
Usually due to atheroma plays rupturing

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11
Q

Describe the MI Morphology stages

A

1)

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12
Q

When can a subendocardial MI occur

A

Can infarct without any coronary artery occlusion if:
Stable atheromatous occlusion of coronary artery
Acute hypotensive episode

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13
Q

5 Markers of cardiac myocyte damage

A
Troponin
CKMB
LDH1
Aspartate Transaminases
Myoglobin
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14
Q

Troponin in MI’s

A

Peaks 12/24 hours
Detectable for 7 days
Also raised post PE, heart failure and my carditis

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15
Q

CKMB in MIs

A

Peaks 10-24 hours
Detectable for 3 days
3 types of CK, CKMM, CKBB, CKMB

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16
Q

LDH1

A

Peaks at 3 days

Detectable for 14 days

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17
Q

Myoglobin

A

Peaks at 2 hours

Also detecable in skeletal muscle damage

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18
Q

Aspartate transaminases

A

Also present in liver so less useful

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19
Q

MI Complications

A

Mural thrombosis/emboli can cause stroke (due to altered flow)
Autoimmune pericarditis (dressler;s syndrome)
LV Failure
Ischaemic pain
Arrythmias
Myocardial rupture –> tamponade

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20
Q

How is familial hypercholesterolaemia inherited

A

mutation in LDL receptor gene or apolipoprotein B

Autosomal dominant

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21
Q

What do heterozygotes for familiar hypercholesterolaemia get

A

Early atherosclerosis
Tendon Xanthoma
Corneus Arcus

Treat with statinsQ

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22
Q

What are statins

A

Hydroxymethylglutamyl Co A Reductase inhibitos

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23
Q

What is abnormal bp

A

140/90

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24
Q

Secondary hypertension causes

A

Renal, endocrine, CV, neurological

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25
Q

All inherited and acquired hypertension share

A

Increased net salt balance

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26
Q

Primary hypertension causes

A
cardiac baroreceptors
RAS
Kenin-kallikrein defeciency
naturetic peptides
adrenergic receptros
ANS
autrocrine factors released by blood vessels
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27
Q

Where is renin synthesised and stored

A

in the juxtaglomerular apparatus in the afferent arteriole of the kidney

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28
Q

What does angiotensinogen II do

A

short half life
causes vasoconstriction
Causes renal cortex to secrete aldoesterone

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29
Q

What secretes aldosterone

A

the zone glomerulosa cells of the adrenal cortex

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30
Q

What can cause increased aldosterone production

A

Renal artery stenosis

Coarctation of the aorta

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31
Q

How do we detect coarctation of the aorta

A

differences in leg/arm bp

characteristic chest x-ray

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32
Q

What is conn’s syndrome

A

Excessive aldosterone production but low renin

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33
Q

Causes of conn’s syndrome

A

Mostly due to adrenocortical adenoma

Some due to nodular hyperplasia

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34
Q

Effects of Conns Syndrome

A

High bp due to aldosterone

Potassium loss - muscle weakness, cardiac arrythmias, paraesthesis, metabolic alkalosis

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35
Q

Diagnosing conns syndrome

A

CT of adrenas

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36
Q

What is phaemochromacytoma

A

Tumour of the adrenal medulla -> causes an increased secretion of catecholamines (adrenaline/noradrenaline)

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37
Q

Presentation of phaemochromacytoma

A

Pallor, headaches, nervous, hypertension

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38
Q

Diagnosis of phaemochromacytoma

A

24 hours urine collection

Surgery to treat

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39
Q

What is cushing disease

A

Overproduction of cortisol

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40
Q

What produces cortisol

A

The zone fasiculata cells of the adrenal cortex

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41
Q

Causes of cushing’s disease

A
Pituitary adenoma (80%)
Paraeoplastic effects of other cancers --> particularly small cell lung cancer as it secretes adrenocorticotrophic horome
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42
Q

Effects of Cushings

A

Aldosterone like effect on kidney

Increased sympathetic nervous system activation

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43
Q

Hypertension effects

A

Hypertensive heart disease
Renal
Cerebrovascular

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44
Q

What is hypertensive heart disease

A

Systemic heart disease causes LV hypertrophy –> Initially without dilation
Later get dilation and LV failure
Cause of Sudden cardiac death

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45
Q

Renal effects of hypertension

A

Vascular changes:
Hyaline arteriosclerosis
Arterial intimal fibroelastosis

Gradual decline in renal function causing chronic renal failure

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46
Q

Cerebrovascular effects of hypertension

A

Hypertensive encephalopathy

Increased risk of rupture: Atheromatous (intracranial haemorrhage), circle of willis (SAH)

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47
Q

What is a hypertensive crisis

A

bp 180/120
Hypertensive encephalopathy
Retinal haemorrhage
Renal failure

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48
Q

What is hypertensive encephalopathy

A

Confusion, vomiting, convulsions, coma and death

Diffuse cerebral dysfunction

Rapidly treat to reduce raised ICP

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49
Q

Risk assessment of CVD

A

Framinghams, SCORE and QRISK

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50
Q

Cardiac disease in low risk individuals

A

Coronary atheromas due to familial hypercholesterolaemias
Cardiomyopathyies e.g. hypertrophic heart
Channel-opathies causing cardiac arryhytmias e.g. Long-QT and Brugada syndrome

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51
Q

Causes of pulmonary hypertension

A

Loss of pulmonary vasculature
Secondary to LVF
Systemic to pulm. artery shunting
Primary/idiopathic

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52
Q

What does RV failure cause

A

systemic oedema

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53
Q

what is heart failure

A

an insufficiency of cardiac output to meet metabolic demand

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54
Q

What are the main causes of heart failure

A

1) MI
2) Hypertension
3) Valvular

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55
Q

Describe what happens in heart failure

A

Increased cardiac work, increased wall stretch, increased cell stretch, hypertrophy, dilation, cardiac failure

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56
Q

Is preload proportional to contractile power?

A

Yes - but if volume overload causes disruption in blood flow patterns –> regurgitation and decreased contraction etc.

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57
Q

Causes of Left sided heart failure? (congestion)

A

Pre-renal azotemia

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58
Q

What is pre-renal azotemia?

A

Poor perfusion to kidneys causes high urea in blood
Kidneys secrete renin - activates RAS
Naturietc peptides secreted
Causes salt and water retention

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59
Q

Where are naturetic peptides produced?

A

Produced by the atrium when its dilated to cause salt and water retention

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60
Q

Features of pulmonary congestion

A
Oedema and heart failure
Blood tingled sputum
Dyspnoae, paraoxysmal nocturnal dyspnoea
Cyanosis
Elevated WEDGE pressure
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61
Q

Main cause of RH Failure

A

Pulmonary hypertension - usually secondary to left sided heart failure

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62
Q

Signs of Rh Failure

A

Liver/Spleen Enlargement: Due to passive congestion and NUTMEG LIVER
Kidneys effected
Pericardial and pleural effusion
Systemic Oedema

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63
Q

Autopsy of findings in congestive heart failure

A

Box Car Nuclei
Cardiomegaly
Dilated chambers
Hypertrophy of myocardial fibres

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64
Q

What causes valvular heart disease

A

Due to opening problems (stenosis) or regurgitation (closing problems)

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65
Q

Causes of aortic stenosis

A

Rheumatic fever

Calcification of valve

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66
Q

Cause of mitral valve stenosis

A

Rheumatic Fever

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67
Q

Why does rheumatic fever cause valve problems?

A

Group A Streptcoccci haemolytic infection
Antibodies produced against
Cross reacts with tissue glycoproteins
Can occur in heart –> causes vegetations

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68
Q

acute features of rheumatic fever

A

Inflammation
Aschoff Bodies
Atischkow bodies - macrophages in the cell
Pancarditis
Vegetations –> on the chordae tendinae and leaflet junctions

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69
Q

chronic features of rheumatic fever

A

Thickened valves
Commissural fusion
Thick, short chordae tendinae

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70
Q

Aortic stenosis

A

Left ventricular hypertrophy but no hypertension

Get ischaemia, cardiac decompression, angina and CHF

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71
Q

What is mitral annular calcification

A

Calcification of the mitral skeleton

Usually get regurgitation but stenosis possible

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72
Q

Who is mitral annular calcification more common in

A

women

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73
Q

Causes of aortic regurgitation

A

Rheumatic Fever
Infection
Aortic dilation - syphilis, rheumatoid arthritis and Marfans

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74
Q

Causes of mitral regurgitations

A

Mitral valve prolapse

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75
Q

Causes of mitral valve prolapse - degeneration of the mitral valve

A

Infection
Fen-Phen (reaction to anti-obesity drug)
Chrodae tendinae and papillary muscle problems
Calcification of the mitral ring (annulus)

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76
Q

What is mitral valve prolapse associated with?

A

Connective tissue disorders

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77
Q

Consequences of mitral valve prolapse

A

Usually asymptomatic
But get floppy valve - prone to infective endocarditis
Get a mid-systolic ‘click’ - holosystolic murmur if regurgitation present
Can get occasional chest pain and dyspnoea

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78
Q

What causes congenital heart diseases

A

Problems in embryogenesis in weeks 3-8

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79
Q

what % of congenital heart diseases are due to gene abnormalities?

A

10%

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80
Q

What genes are usually involved in congenital heart disease

A

12, 15, 18, 21 and XO

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81
Q

Mutations in which gene cause congenital heart problems?

A

TBX5 - ASD, VSD
NKX2.5 - VSD

These genes code for transcription factors

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82
Q

Which chromosome is important for heart development?

A

Chromosome 22

Deletions cause conotrucus!

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83
Q

Is rubella a teratogen for heart disease?

A

Yes

84
Q

What is patent foramen ovale

A

where the septum primum and secundum don’t fuse

occurs in 1 in 4

85
Q

Symptoms of PFO

A

Usually asymptomatic

UNLESS increased pressure on the R side such as pulmonary hypertension

86
Q

Describe the developmet of the aorticopulmonary septum

A

Septum divides the bulbis cords and truncus and aorta and pulmonary artery
Spirals

87
Q

When does the ductus arteriosus close

A

Usually at birth due to increase in oxygen and decrease in prostaglandins

88
Q

What happens in patent ductus arteriosus

A

Oxygenated blood flows back to the heart
Pulmonary hypertension
Ventricular hypertrophy
Heart failure

89
Q

How to treat PDA

A

Prostaglandin inhibitors

90
Q

3 types of Congential heart Disease2

A

R->L shunts
L–>R Shunts
Obstructions - of aorta or pulmonary artery

91
Q

What causes L–>R Shunts

A

1) Atrial Septal Defects
2) Ventricular Septal Defects
3) Patent Ductus Arteriosus
4) Atrioventricular Septal Defect

92
Q

What causes R–>L Shunts

A

1) Tetralogy of Fallots
2) Transposition of the great vessels
3) Truncus Arteriosus
4) Total anomalous pulmonary venous connection
5) Tricuspid atresia

93
Q

What causes ASD’s

A

90% due to problem in septum secundum
5% due to problem in septum primum
5% due to sinus venosus –> abnormal pulmonary veins draining into the SVC or RA

94
Q

Problems with ASD

A

Usually asymptomatic until adulthood

95
Q

What causes VSD

A

90% involve problems in the membranous septum

If muscular septum involved often get multiple holes –> small ones can fix themselves larger ones need surgery

96
Q

Most common congenital heart defect

A

VSD - 30% occur alone but lots occur with tetralogy of ballots

Can cause pulmonary hypertension

97
Q

What causes atrioventricular septal defects (AVSD)

A

Defection AV vavles

Can be partial or complete with all 4 chambers freely communicating

98
Q

What do a 1/3 of people AVSD also have

A

Downs Syndrome

99
Q

Direction of shunt in PDA

A

Initially L–>R

Then R–> L when it reaches systemic pressure

100
Q

Symptoms of PDA

A

No cyanosis
Pulmonary hypertension
Significant pulmonary hypertension –> irreversible

101
Q

What is tetralogy of fallots

A

VSD
Overriding aorta
Pulmonary Stenosis
RV Hypertrophy

102
Q

What causes PINK tetralogy of fallots

A

if the pulmonic obstruction is small

103
Q

What causes transposition of the great vessels

A

Abnormal formation of the conotruncal septum –> does not spiral

104
Q

What do you need to survive in the transposition of the great vessels

A

PDA or PFO

VSD can occur

105
Q

Which ventricle is thicker in transposition of the great vessels

A

Right Ventricle

Fatal in first few months without surgical switching

106
Q

What causes truncus arteriosus

A

Developmental failure of seperation of the truncus arteriosus CONOTRUNCAL SEPTUM DOESNT FORM –> pulmonary artery and aorta are not separated

107
Q

What problems are associated with truncus arteriosus

A

VSD - as the conotruncal septum doesn’t form it can’t fuse with inter ventricular septum so you get a VSD

108
Q

What does truncus arterioles causes

A

Systemic cyanosis with increased pulmonary blood flow

109
Q

What is total anomalous venous connection

A

Pulmonary veins drain into the left innominate vein or the coronary sinus

110
Q

What happens if you get a total anomalous venous connection

A

Get a hypo plastic left atrium

Need a PFO or an ASD otherwise a fatal condition due to lack of perfusion to the organs!

111
Q

What happens if you get tricuspid atresia

A

Hypoplastic RV

112
Q

What do you need to survive if you have a tricuspid atresia

A

PDA or ASD defect needed to fill the Left atrium with blood
VSD needed to pump blood into the pulmonary arteries

Left ventricle supplies both the aorta and pulmonary artery! Heart unable to pump oxygenated blood properly

113
Q

Who is coarctation of the aorta more common in

A

Males and XO’s

114
Q

Which form of aorta coarctation happens in infants that is serious

A

Proximal to the PDA

115
Q

What occurs with coarctation of the aorta 50% of the time

A

Bicuspid aortic valve

116
Q

What happens with 100% artretic pulmonary stenosis

A

Hypoplastic RV with ASD

117
Q

What happens if you get severe aortic stenosis/vavlular

A

If severe can cause hypo plastic LV which is fatal

118
Q

3 types of aortic stenosis

A

Valvular
Sub-valvular
Supra-valvular

119
Q

What is endocarditis

A

inflammation of the endocardium of the heart

120
Q

What are the 2 main forms of endocarditis?

A

1) Infective

2) Non-infective: e.g. NonBacterial Thrombotic Endocarditis (NBTE) or endocarditis of SLE (Libman Sacks)

121
Q

What is the main cause of infective endocarditis

A

Bacteria, then fungi then virus

122
Q

What are the vegetations in infective endocarditis

A

Mixture of thrombotic debris and organism –> destroyed the underlying cardiac tissue

123
Q

Describe acute infective endocarditis

A

Infects normal heart valves
Highly virulent organisms
Necrotizing, ulcerative, destructive lesions
Difficult to cure with antibiotics and usually require surgery
Death frequent

124
Q

Describe sub-acute infective endocarditis

A

Less virulent organisms
Usually infects formed valves
Wax and wane of flu like symptoms
Cured by antibiotics

125
Q

Risk factors for endocarditis

A

Cardiac/valvular abnormalities i.e. rheumatic fever
Dental wrok
Structural abnormalities of the heart

126
Q

Bacteria causing endocarditis from mouth

A

Strep viridans

127
Q

Bacteria causing endocarditis from skin

A

Staph aureus, especially in IVDU

128
Q

Bacteria causing endocarditis that indicates bowel cancer

A

Strep. bovis

129
Q

What bacteria commonly infects prosthetic heart valves

A

Coagulase negative staphylococci e.g. S. Epidermidis

130
Q

What are the vegetation of acute infective endocarditis like

A

Bulky, friable, potentially destructive
Can cause abscesses
Emboli contain large numbers of virulent organsisms

Usually affects AV, MV and right hear (especially in IVDU)

131
Q

Clinical features of infective endocarditis

A

Fever, flu-like symptoms, weight loss, murmurs (in 90% of those with left sided infective endocarditis)

132
Q

Clinical Signs of Infective Endocarditis

A
F-fever
R-Roth spots (retinal haemorrhages)
O-Oslers Nodes (subcutaneous lesions in the pulp of digits)
M-Murmur
J-Janeway lesion
A-Anaemia
N-Nail (splinter) haemorrhages
E-Emboli (septic)
133
Q

Complication of infective endocarditis

A

Immunological mediated conditions e.g. glomerulonephritis

134
Q

Who does NBTE infect

A

Often debilitated patients often with hypercoaguble state
e.g. DVT, PE, Cancer, pro-coagulant effect of tumour-derived mucin or tissue factor

Can occur part of trousseau syndrome of migratory thrombophlebitis

135
Q

What predisposes you to NBTE

A

endocardial trauma and indwelling catheter

136
Q

What is NBTE (Libman Sacks) associated with

A

SLE

usually asymptomatic apart from the SLE symptoms

137
Q

What are the vegetations in Libamn Sacks like

A

AV vealves affects

Small, pink, sterile, and warty

138
Q

What are aschoff bodies

A

Distinctive in cardiac lesions i.e. rheumatic fever

Foci of T cell, plasma cell and macrophages

139
Q

What does rheumatic fever cause

A

Pancarditis

Vegetations are called verucae

140
Q

what are antibodies directed against in Rheumatic fever

A

Against the M proteins of the streptococci infection

141
Q

How does rheumatic fever damage heart tissue

A

CD4+ T cells specific for streptococcal peptides react with streptococcal peptides that read with self-proteins in heart, produce cytokines that activate macrophages

Diagnose with Jones Criteria

142
Q

Causes of Pericarditis

A

Infection - viruses, Coxsackie B
Immunological processes: RHeumatic Fever, SLE, Dresslers etc
Post MI, surgery, neoplasia, trauma etc

143
Q

Describe types acute pericarditis

A

Serous/serofibrinous/fibrinous
Purulent/supparative
Haemorrhagic
Caseous

144
Q

Describe chronic pericarditis

A

ADHESIVE, can cause constrictive peridcarditis

145
Q

Causes of serous pericarditis

A

Generally non-infective –> usually due to inflammation of adjacent structure or sometimes viral (coxsackie or echovirus)

146
Q

Type of inflammation in serous pericarditis

A

clear, serous fluid accumulation

147
Q

Most common form of pericarditis

A

Serofibrinous/fibrinous

148
Q

Cause of fibrinous/serofibrinous pericarditis

A
Post MI
Dresslers
Uraemia
Radiation
Rheumatic fever, SLE, 
Trauma and surgery
149
Q

Type of inflammation in fibrinous/serofibrinous

A

Fibrous –> without fluid, dry and granular surface with more intense inflammatory response
Serious fluid and or fibrinous exudate in the pericardial sac

150
Q

Purulent/supurative pericarditis cause

A

Infection

151
Q

Type of inflammation in purulent/supparative pericaditis

A

Red, granular exudate upto 500ml
Can cause restrictive pericarditis
Inflammation can extend causing media-stino pericarditis

152
Q

Haemorrhagic pericarditis inflammation type

A

Caseous (Cheesy) pericarditis e.g. TB or fungal

153
Q

Causes of hemorrhagic pericarditis

A

Neoplasic
Infection e.g. TB
Following surgery

154
Q

Clinical features of pericarditis

A

Sharp central chest pain: worse on inhalation and movement, better on sitting forward
Pericardial friction rub - loudest over diaphragm in left sternal edge
Fever, leucocytosis, lymphocytosis
Can get pericardial effusion/tamponade

155
Q

Types of chronic pericarditis

A

Adhesive - obliterates pericardial cavity
Adhesive mediastinopericarditis –> follow infections, surgery or radiation. Obliterated pericardial cavity extending to surrounding structures. Causes hypertrophy/dilation
Constrictive pericarditis

156
Q

How to treat constrictive pericarditis

A

Surgery

157
Q

what is cardiomyopathy

A

Disorder of the myocardium

158
Q

What are the 4 main of types of cardiomyopathy

A

1) Dilated
2) Hypertrophic
3) Restrictive
4) Arrythmogenic Right Ventricular

159
Q

What is dilated cardiomyopathy

A

Progressive dilation
Causes contractile dysfunction and systolic failures
Heart gets enlarged, flabby and heavy

160
Q

Causes of dilated cardiomyopathy

A

20-50% Genetic - AD Mutations in cytoskeleton Proteins

Rest due to alcohol and toxins e.g. chemo

161
Q

Signs of dilated cardiomyopathy

A

Congestive heart failure, SOB, dyspnoea, poor exertional acapcity

162
Q

Treatment of dilated cardiomyopathy

A

Transplant or long-term ventricular assist

163
Q

What is hypertrophic cardiomyopathy

A

Hypertrophy and poorly compliant left ventricular myocardium
Diastole dysfunction but systolic function preserved –> can’t dilate in diastole due to poorly compliant/stiff walls

Main cause of Left Ventricular Hypertrophy

164
Q

Causes of hypertrophic cardiomyopathy

A

100% genetic - problems in the sarcomeric proteins

165
Q

Signs of hypertrophic cardiomyopathy

A

Reduced stroke volume and obstruction to LV outflow –> this causes a systolic ejection murmur

Exertional dyspnoea

The anterior mitral leaflet moves towards the inter ventricular septum in systole

166
Q

Main cause of sudden death in young athletes

A

hypertrophic cardiomyopathy

167
Q

What can hypertrophic cardiomyopathy lead to?

A
Arrythmias
Mural thrombosis
Cardiac Failures
AF
Sudde Death
168
Q

What is restrictive cardiomyopathy

A

Primary decrease in ventricular compliance –> reduces ventricular filling during diastole

169
Q

Causes of restrictive cardiomyopathy

A
Fibrosis
Amyloidosis
Sarcoidosis
Metastatic tumours
Deposition of metabolites
170
Q

Size of ventricles in restrictive cardiomyopathy

A

Normal/slightly enlarged.

Myocardium is stiff and non-compliant

171
Q

What is arrythmogenic right ventricular cardiomyopathy

A

Right ventricular dilation and myocardial thinning

172
Q

Cause of arrythmogenic right ventricular cardiomyopathy

A

Genetic Disease - autosomal dominant
Problem with desmosomes (for cell-cell adhesion)
cells fall off and die during exercise
Replacement of RV with fibrofatty cells

173
Q

Signs of arrythmogenic right ventricular cardiomyopathy

A

Can be silent, syncope, cardiac death in the young

174
Q

Causes of myocarditis

A

Mostly infective: Cocsackie A/B Virus

Chaga’s Disease (Trypanosome cruzi protozoa) –> endemic in S. AMerica

175
Q

Symptoms of Myocarditis

A

Asyomptomatic/heart failures/arrythmias/sudden death
Non-specific symptoms: fatigue, palpitation, precordial deiscomfort, fever

Can mimic an acute MI

176
Q

What can develop from myocarrditis

A

Dilated cardiomyopathy

177
Q

What do we use to name vasculitis

A

Chapel Hill Nomenclature

178
Q

What is the most common form of vasculitis

A

Giant Cell Arteritis (GCA)

179
Q

What arteries does GCA affect?

A

Large/medium sized

Arteries in head i.e. temporal
Also ophthalmic and vertebral

180
Q

Consequence of GCA in the ophthalmic artery

A

Can cause permanent blindness –> medical emergency

181
Q

Morphology of GCA

A

Intimal thickening –> narrows the lumen
Chronic granulomatous inflammaton –> elastic lamina configuration
Multinucleated cells

182
Q

Clinical features of GCA

A

Facial pain or headache –> particularly superficial temporal artery and jaw claudication
Vague symptoms e.g. fever/weight loss
Rare in under 50s

183
Q

Treatment of GCA

A

corticosteroids and anti-TNF

184
Q

Diagnosis of GCA

A

biopsy - take 2-3cm of artery as it is a segmental disease

185
Q

What are aneurysms

A

localised, permanent dilations of a blood vessel

186
Q

Types of aneursyms

A
atherosclerotic
dissecting
berry
micro
syphilitic
Mycocytic
False
187
Q

Most common aneurysm

A

Atherosclerotic aneurysm –> commonly affects AAA

188
Q

Risk of AAA rupture

A

less than 4cm no risk
4-5cm = 1%
5-6cm = 11%
over 6 cm = 25%

189
Q

How to detect AAA

A

Ultrasound and then have endovascular repair

190
Q

What is dissecting aneursym

A

Tear in the vessel wall and blood goes between the intimal and medial layers

191
Q

Where do dissecting aneurysms usually occur

A

Usually in the thoracic artery secondary to systemic hypertension

192
Q

Signs of thoracic aorta

A

Tearing pain in chest radiating upper left shoulder
Progressive vascular occlusion and haemopericardium
High mortality if not treated

193
Q

What are berry aneurysms

A

Secular lesions in the circle of willis –> commonly at medial weakness of arterial bifurcaions

194
Q

Who berry aneurysms usually occur in

A

Young hypertensive patients

195
Q

Cause of micro aneursyms

A

Charcot-Bouchard syndrome –> aneurysms in small cerebral capillaries in hypertensive disease –> causes intracerebral haemorrhages

Also retinal aneurysms in diabetes can causes diabetic retinopathy

196
Q

Cause of syphilitc aneurusms

A

Tertiary syphilis can cause aneurysms in the ascending aorta

197
Q

What is a mycotic aneurysms

A

Weakening of the arterial wall secondary to bacterial/fungal infections

198
Q

How to organisms enter in mycotic aneurysms

A

Enter the media via the vasa vasorum

199
Q

Most common underlying infection in mycotic aneursysms

A

Sub-acute endocarditis

200
Q

Where do mycotic aneurysms commonly occur

A

The cerebral arteries

If it infects the AAA there is a risk of rupture

201
Q

What are false aneurysms

A

Blood filled spaces around a vessel following traumatic rupture of perforating injury

Adventitial fibrous tissue contains the haematoma

202
Q

When are false aneurysms classically seen

A

Femoral artery puncture during angioplasty/angiography

203
Q

What do we give to treat acute coronary artery occlusion

A

Oxygen, ACEi, GTN, Beta blcokers, Pain relief, Statins

204
Q

Why might you collapse and die after an MI

A

Likely an arrhythmia

205
Q

What could a systolic murmur indicate

A

Aortic stenosis

206
Q

How can COPD affect the heart

A

Causes pulmonary hypertension can cause RH failure

207
Q

When is BNP raised

A

Raised in myocardial stress