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Pathology > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is ischaemia?

A

result of impaired blood flow or perfusion of tissues depriving it of oxygen and nutrients

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2
Q

What are the effects of ischaemia?

A

reversible
dependent of duration of ischaemia
dependent on tissue metabolic demands

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3
Q

What is infarction?

A

death (necrosis) of tissue as a result of ischaemia

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4
Q

What are the effects of infarction?

A

irreversible

tissues vary in ability to repair and regenerate

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5
Q

What do infarctions illicit?

A

inflammatory response

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6
Q

What determines whether ischaemia or infarction develops?

A

nature of blood supply (single or biphasic)
duration of occlusion
vulnerability of tissue to hypoxia
oxygen content of blood

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7
Q

What are red infarcts?

A

venous occlusions

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8
Q

Where do red infarcts occur?

A

loose tissues (like lung)
tissues with dual circulation
tissues which have been congested before and have referfusion damage

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9
Q

Where do pale infarcts occur?

A

solid organs

single blood supply

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10
Q

What causes ischaemia and infarction?

A 
thrombosis
embolism
spasm
atheroma
compression
vasculitis
steal
hyperviscosity
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11
Q

What 3 areas cause ischaemia or infarction?

A

things in lumen
things in wall
things outside wall

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12
Q

What 3 factors cause thrombosis?

A 
Virchow's triad:
changes in
1. intimal surface of vessel
2. pattern of blood flow
3. blood constituents
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13
Q

Explain how a thrombus forms on an atheromatous plaque

A

turbulent blood flow around plaque (changes to flow)
changes in surface overlying atheromatous plaque (changes to intimal wall)
platelet activation due to these changes
activation of clotting cascade
deposition of thrombus

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14
Q

What is propgation?

A

growth of thrombus in direction of flow

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15
Q

What are the clinical effects of arterial thrombosis?

A 
distal tissues become:
oale
cold
painful
infarcted
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16
Q

What are the clinical effects of venous thrombosis?

A 
usually happens in leg
distal tissues become:
red
swollen
tender
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17
Q

What are the 4 fates of a thrombus?

A
  1. lysis and resolution
  2. organisation
  3. recanalisation
  4. embolism
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18
Q

What is recanalisation?

A

blood flow restored with multiple small vessels but leaves behind scar and residual thrombus

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19
Q

What is an embolism?

A

mass of material that can move within vascular system and become lodged in a vessel blocking its lumen

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20
Q

What are emboli usually derived from?

A

thrombus

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21
Q

What is the most common type of embolism?

A

thromboembolism

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22
Q

What other types of embolus are there?

A 
atheromatous emboli
amniotic fluid (parturition)
gas
fat
tumour (metastasis)
foreign material
infective agents
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23
Q

Describe the structure of a normal artery from outside in

A 
adventitiae
external elastic lamina
media
internal elastic intima
endothelium
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24
Q

What is an atheroma?

A

deposition of tissue within intimal layers

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25
Q

What is deposited in atheromas?

A

fat macrophages
inflamatory cells
fibrovascular connective tissue

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26
Q

What do atheromas cause?

A

luminal narrowing and vascular insufficiency

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27
Q

What are the major risk factors for atheromas?

A 
age
sex
hyperlipidaemia
smoking
hypertension
diabetes mellitus
sedentary lifestyle
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28
Q

What are the 3 types of atheromatous lesions?

A

fatty streak
fibrolipid plaque
comlicated lesion

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29
Q

WHat is a fatty streak?

A

linear elevations of lipid laden macrophages

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30
Q

What is a fibrolipid plaque?

A

bigger lesion that a fatty streak
fat
fibrosis
fibroblasts present

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31
Q

What is a complicated lesion?

A

narrowing
endothelial erosion with thrombosis
plaque rupture and fissuring
aneurysm formation

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32
Q

What sites are typically affected by atheroma?

A 
high pressure vessels
lower abdominal arota/iliac
coronary
popliteal
descending thoracic aorta
internal carotid and circle of willis
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33
Q

What vesselsWhat are complications of an atheroma?

A

narrowing of vessel
thrombus on plaque
fissuring and cracking (bleeding onto plaque)
aneurysm

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34
Q

What is the s[ectrum of ischaemic heart disease?

A

angina
myocardial infarction
sudden death

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35
Q

What is the main cause of ischaemic heart disease?

A

atheroma

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36
Q

What are teh risk factors for ischaemic heart disease?

A 
family Hx
smoking +++
diet
lifestyle
race (blackF)
obesity
diabetes mellitus
hypertension
hyperlipidaemia
stress
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37
Q

What is the pathogenesis of ischaemic heart disease?

A

when blood supply becomes inefficient through:
reduction in blood supply (atheroma)
increased demand (muscle hypertrophy)
reduced oxygen carriage (anaemia)

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37
Q

What is the pathogenesis of ischaemic heart disease?

A

when blood supply becomes inefficient through:
reduction in blood supply (atheroma)
increased demand (muscle hypertrophy)
reduced oxygen carriage (anaemia)

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38
Q

What does angina present with?

A

reversible chest pain

can be stable (exertion related) or unstable (unpredictable)

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39
Q

What does MI present with?

A

central crushing chest pain

left arm and neck radiation

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40
Q

What are the 3 commonest arteries to be affected in MI?

A

LAD
RCA
LCX

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41
Q

What happens the ventricles in acute MI?

A

necrosis of left ventricle
inflammatory infiltration
fibrous repair
necrotic muscle releases enzymes (troponin)

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42
Q

Explain the ECG changes depending on where the MI occurs?

A

LAD “artery of sudden death”
infarction of anterior aspect of myocardium
ECG changes in anterior chest leads

LCA
lateral infarction
ECG changes I, AVL, lateral chest leads

RCX
ECG changes II, III and AVF (inferior leads)

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43
Q

What changes within the first 24 hours of MI?

A

nothing to be seen

within first 6 hours swollen mitochrondria microscopically

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44
Q

What can be seen 24 hours after MI?

A

infarction pale
inflammatory reaction
myocytes lose typical striations

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45
Q

What can be seen days to weeks after MI?

A

dead myocytes removed by macrophages
healing by repair, organisation and progressive fibrosis
formation of fibrous scar

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46
Q

WHat can be seen months after MI?

A

akinetic segment

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47
Q

What are the complications of MIs?

A 
sudden death
arrhythmias
angina
cardiac failure
mitral incompetence
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48
Q

What causes sudden death in MI?

A

VF

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49
Q

What causes arrhythmias in MI?

A

damage to conducting system in first few days

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50
Q

What causes angina?

A

ischaemia

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51
Q

What causes cardiac failure?

A

muscle necrosis/arrhythmia

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52
Q

What causes mitral incompetence?

A

papillary muscle damage

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53
Q

What causes pericarditis to be a complication of MI and when does it occur?

A

transmural infarct with pericardial inflammation

2-4 days

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54
Q

What causes cardiac rupture in MI and when does it occur?

A

wall weakening following muscle necrosis and acute inflammation
3-5 days

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55
Q

Wjat causes mural thromosis in MI? When does it occur?

A

ischaemia and endothelial damage

7+ dyas

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56
Q

What causes ventricular aneurysm in MI?

A

muscle necrosis/arrhythmia

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57
Q

What causes Dressler’s syndrome in MI?

A

autoimmune

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58
Q

What does Dressler’s syndrome present with?

A

chest pain
fever
effusions

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59
Q

Compare and contrast myocardial rupture and ventricular aneurysm

A
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60
Q

What is arterial blood pressure?

A

measure of the force exerted on arterial walls by circulating blood

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61
Q

What is the diagnostic threshold of systolic and diastolic blood pressure?

A

systolic 140mmHg

diastolic 90mmHg

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62
Q

What is hypertension a major risk factor for?

A 
stroke
MI
HF
CKD
cognitive decline
premature death
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63
Q

What are risk factors for primary/essential hypertension?

A 
age
FHx
african/caribbean origin
high salt
lack of excercise
overweight
smoking
alcohol
stress
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64
Q

What are 5 areas that can cause secondary hypertension?

A 
renal
endocrine
coarctation of aorta
medications
pregnancy
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65
Q

What endocrine causes for hypertension are there?

A

pheochromocytoma
Cushing’s
hyperaldosteronism

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66
Q

What medications can cause hypertension?

A

NSAIDs
oral contraceptive
steroids

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67
Q

What are renal parenchymal diseases?

A 
diabetic nephropathy
chronic glomerulonephritis
polycystic kidney disease
chronic tubulointerstitial nephritis
hypertensive renal disease
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68
Q

What is renal artery stenosis?

A

decrease in blood flow through one/both main renal arteries or branches

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69
Q

What causes renal stenosis?

A 
atherosclerosis
fibromuscular dysplasia (FMD)
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70
Q

How is renal stenosis diagnosed?

A

CT
angiography
MRI

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71
Q

What is FMD?

A

fibromuscular dysplasia

pathogenic thickening of arterial wall

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72
Q

Who does FMD commonly affect?

A

younger adults

mainly females 20-50s

73
Q

What is produced in the adrenal cortex?

A

aldosterone
cortisol
testosterone precursor

74
Q

What is produced in the adrenal edulla?

A

adrenaline

noradrenaline

75
Q

What is produced in the adrenal medulla?

A

adrenaline

noradrenaline

76
Q

What can cause elevated aldosterone?

A

aldosteronoma

77
Q

What can cause elevated noradrenaline and adrenaline?

A

phaeochromocytoma

78
Q

What can cause Cushing’s syndrome/hypercortisolism?

A

ectopic ACTH due to lung cancer
pituitary adenoma
adrenal adenoma
corticosteroids

79
Q

How does coarctation of the aorta cause hypertension?

A

reduced blood flow in lower half of body and lower BP

higher BP in arms and upper body

80
Q

What are the clinical manifestations of hypertension/what organs are affected?

A

cardiovascular system
kidneys
retina

81
Q

What happens to the heart in hypertension?

A

left ventricular hypertrophy

82
Q

What is hypertrophic cardiomyopathy?

A

asymmetrical left ventricular hypertrophy
often involves IV septum
genetic disease
can cause sudden death in young adults

83
Q

What is the difference between atherosclerosis and arteriolosclerosis?

A

ATHERO - asymmetrical narrowing of lumen of LARGER vessels by LIPID accumulation within INTIMA

ARTERIOLO - symmetrical narrowing of lumen of SMALLER vessels by deposition of PROTEIN within the wall of blood vessels

84
Q

What is haemorrhagic stroke?

A

rupture of small cerebral micro-aneurysms

85
Q

What is hypertensive nephrosclerosis?

A

progressive renal impairment caused by chronic poorly controlled hypertension

86
Q

What can results from hypertensive arteriolar nephrosclerosis?

A

CKD

87
Q

What is hypertensive retinopathy?

A

thickened blood vessel walls reduces blood flow
causes ischaemia and infarction
damage to blood vessels then causes bleeding and loss of vision

88
Q

Who is typically affected by rheumatic fever?

A

children with Group A haemolytic streptococci throat infection

89
Q

When do symptoms of rheumatic fever generally present after Group A haemolytic streptococcal throat infections?

A

2-6 weeks

90
Q

How is rheumatic fever diagnosed?

A

2 major or 1 major and 2 minor criteria and evidence of previous streptococcal infection

91
Q

What is evidence of previous streptococcal infection?

A

rising antistreptolysin O titre

92
Q

What are major criteria for rheumatic fever?

A 
carditis
polyarthritis
erythema marginatum
Sydenham's chorea
subcutaneous nodules
93
Q

What is erythema marginatum?

A

skin rash over trunk and limbs

round, pale-pink centre surrounded by slightly raised red outline

94
Q

What is Sydenham’s chorea?

A

rare neurological disorder
sudden onset chorea
random-appearing, continuous, involuntary movements
often includes the face and tongue

95
Q

What are the minor criteria for rheumatic fever?

A 
fever
arthralgia
raised CRP (lab abnormalities)
ECG abnormalities (prolonged PR interval)
evidence of streptococcal infection
96
Q

What is the hallmark of rheumatic fever?

A

pancarditis

97
Q

What can patients present with in rheumatic fever?

A

pleural effusion and fibrinous pericarditis
man
manifests as audible rub

98
Q

What is an Aschoff body?

A

when pericarditis develops into myocarditis and endocarditis
valves are swollen and infiltrated with inflammatory cells
small vegetations on valve leaflets

99
Q

What causes the architectural disruption to the vales and the long term complications of rheumatic fever?

A

fibrotic healing response

100
Q

What does an Aschoff body consist of and what is it surrounded by?

A

central core of collagen

small Aschoff giant cells

101
Q

What is seen by the arrow?

A

Anitschkow cells

long bar of central chromatin

102
Q

What are the 2 overarching areas causing valvular heart disease?

A

stenosis

incompetence

103
Q

What is stenosis of valves?

A

thickened and/or calcified causing obstruction to flow

104
Q

What is incompetence of heart valves?

A

regurgitataion or insufficiency

lose normal function and leak

105
Q

What are causes of valve disease?

A 
age - calcification
functional changes
rheumatic fever
floppy valves
congenital defects
infective endocarditis
106
Q

What are 2 causes of aortic stenosis?

A

calcific degeneration

rheumatic fever

107
Q

What are complications of aortic stenosis?

A 
left ventricular hypertrophy
angina
syncope
left ventricular failure
sudden death
108
Q

What are causes of aortic incompetence?

A

aortic root dilatation

rheumatic valve disease

109
Q

What is the pathophysiology of left ventricular hypertrophy in aortic stenosis?

A

left ventricular chamber becomes pressure loaded

compensatory hypertrophy

110
Q

What is seen in the picture?

A

calcific aortic valve stenosis

111
Q

What is seen in the picture?

A

congenital bicuspic aortic valve stenosis

112
Q

What is seen in the picture?

A

aortic valve regurgitation due to dilatation of aortic root

113
Q

What causes mitral stenosis?

A

rheumatic fever

114
Q

What are the complications of mitral stenosis?

A

pulmonary hypertension
left atrial hypertrophy
right ventricular hypertrophy

115
Q

What causes mitral incompetence?

A

floppy valves
rheumatic fever
dilated mitral valve annulus
papillary muscle dysfunction

116
Q

What can be seen in the picture?

A

mitral valve leaflet expanded

projecting back into left atrium

117
Q

What is infective endocarditis

A

acute/chronic disease resulting from infection of focal area of endocardium (usually over valve)

118
Q

What does infective endocarditis look like?

A

vegetations

friable masses containing organisms, platelets, fibrin and inflammatory cells

119
Q

What are predisposing factors to infective endocarditis?

A

structural cardiac abnormalities
prostheses and catheters
bacteraemias
altered immunity

120
Q

What are local complications of infective endocarditis?

A

chordae/ cusp rupture
valvular incompetence
myocarditis

121
Q

What are systemic complications of infective endocarditis?

A

fever
weight loss
malaise

122
Q

What are systemic complications of infective endocarditis?

A

fever
weight loss
malaise

123
Q

What is heart failure?

A

clinical syndrome characterised by typical symptoms accompanied by signs caused by structural/functional cardiac abnormality resulting in reduced cardiac output and/or elevated intracardiac pressures at rest or exertion

124
Q

What is the equation for ejection fraction?

A

sttroke volume/ end diastolic volume

125
Q

What is reduced LVEF?

A

<40%

126
Q

How many classes are there in heart failure?

A

4
1 is no limitation
2 mild limitation - rest normal but exertion causes fatigue, dyspnoea or palpitations
3 marked limitation - comfortable at rest but gentle exertion is symptomatic
4 HF symptoms occur at rest and are exacerbated by exertion

127
Q

What causes heart failure?

A

myocardial abnormality

128
Q

What are the 3 Frank-Starling mechanisms in heart failure?

A

myocardial adaptations
endothelial function
antidiuretic hormone

129
Q

What myocardial adaptations occur in heart failure?

A 
myocyte hypertrophy
fibrosis
apoptosis
abnormal calcium homeostasis
gene expression
130
Q

What happens to circulating levels of endothelin in heart failure?

A

increase

131
Q

What happens sodium levels in HF?

A

decrease due to high levels of antidiuretic hormone

132
Q

What happens the activity of NO in HF?

A

blunted

133
Q

What are the 3 neurohumoral systems activated in heart failure?

A
  1. RAAS
  2. sympathetic nervous system
  3. natriuretic peptides
134
Q

How is the RAAS system activated in HF?

A

↓ cardiac output
↓ renal perfusion
RAAS activated

135
Q

What does RAAS do?

A

salt and water retention
↑ venous pressure
toxic effects of myocardial cells

136
Q

What medications are used if HF specifically for RAAS?

A

ACE inhibitors and ARBs

137
Q

Why does the sympathetic nervous system get activated in HF?

A

CO = SV x HR
↓ SV due to myocardial impairment
↑ compensatory HR

138
Q

What are ANP and BNP and what do they do?

A

natriuretic peptides
counter RAAS
reduces blood volume, arterial pressure and central venous pressure

139
Q

What happens to lead to left-sided heart failure?

A

pulmonary congestion and oedema
pleural effusions
blood pools in the pulmonary circulation

140
Q

What is the consequence of LSHF?

A

blood stasis in left chambers

inadequate perfusion of downstream tissues

141
Q

What increases in risk with left atrial dilatation?

A

atrial fibrilation and thrombus

142
Q

What can be seen in the alveoli in LSHF?

A

haemosiderin-laden macrophages

143
Q

Why can pulmonary effusions arise from LSHF?

A

elevated capillary pressure

144
Q

What are the clinical symptoms of LSHF?

A

dyspnoea
orthopnoea
PND

145
Q

What happens to the kidney in severe hypoperfusion?

A

impaired excretion of nitrogenous

pre-renal azotaemia

146
Q

What happens the brain in advanced heart failure?

A

hypoxic-ischaemic encephalopathy
irritability
progress to come

147
Q

How does right sided heart failure commonly arise?

A

as a result of LSHF

148
Q

What can also cause RSHF?

A

pulmonary hypertension
right ventricular infarction
right ventricular cardiomyopathy
adult congenital heart disease

149
Q

In RSHF what is congested?

A

systemic and portal veins

NOT lungs

150
Q

What is the pathology of congestion of vessels in RSHF?

A

hepatomegaly (nutmeg liver)
splenomegaly (platelet sequestration)
congestion and oedema of bowel wall

151
Q

What happens in systemic congestion in RSHF?

A

fluid accumulation in pleural, pericardial or peritoneal spaces
ankle and pre-tibial oedema
pre-sacral oedema
anasarca (generalised massive oedema)

152
Q

What is an aneurysm?

A

localised, permanent abnormal dilatation of blood vessel

153
Q

What is a false aneurysm?

A

haematoma which lies alongside vessel often enveloped by thin rim of adventitial tissue
communicates with vascular lumen via narrown defect in media

154
Q

What is a true aneurysm?

A

weakness in vessel wall composed of intima, media and adventitia

155
Q

What is the underlying pathology for false aneurysm and where is it normally found?

A

trauma

femoral artery

156
Q

What is the underlying pathology for saccular and diffuse aneurysm and where is it normally found?

A

atherosclerosis
abdominal aorta
thoracic aorta
cerebral artery

157
Q

What is the underlying pathology for dissecting aneurysm and where is it normally found?

A

Marfan’s (non-inflammatory medial disease)

aorta and main branches

158
Q

What is the underlying pathology for capillary micro aneurysm and where is it normally found?

A

hypertension
pericyte loss in diabetes
cerebral caps
retinal caps

159
Q

What is the underlying pathology for myocytic aneurysm and where is it normally found?

A

infection and septic emboli

any vessel

160
Q

What are the consequences of aneurysms?

A 
may be asymptomatic
can rupture causing life-threatening haemorrhage
compression of adjacent structures
tissue/organ ischaemia
thrombosis/embolism
161
Q

What is seen on the picture?

A

atheromatous aneurysm in abdominal aorta

162
Q

What is seen in the picture?

A

berry aneurysm in circle of willis

163
Q

What is seen in the picture?

A

ruptured abdominal aortic aneurysm

dark, porridge material lining aneurysm is thrombus

164
Q

What is myocarditis?

A

inflammation of the myocardium

165
Q

What are the 5 main causes of myocarditis?

A 
viral
bacterial
parasitic
ionising radiation (inc therapy)
drugs
166
Q

What viral causes are there for myocarditis?

A

caxsackie
ECHO
adenoviruses

167
Q

What bacterial causes are there for myocarditis?

A

diphtheria

meningococcus

168
Q

What parasites cause myocarditis?

A

trypanosomiasis

Chagas’ disease

169
Q

What drug can cause myocarditis?

A

adriamycin

170
Q

What is pericarditis?

A

inflammatory reaction in visceral and/or parietal layers of pericardium

171
Q

What are the causes of pericarditis?

A 
viral
bacterial
TB
post MI
post surgery
Dressler's syndrome
carcinomatous
uraemic
172
Q

What classifies a serous pericarditis?

A

clear, straw-coloured
high specific gravity
high protein content

173
Q

What classifies a serofibrinous pericarditis?

A

clumps of fibrin mixed in fluid

174
Q

What is a purulent or supprative pericarditis?

A

frank pus

175
Q

What is a blood-stained pericarditis suspicious of?

A

mlignancy

176
Q

What is caseous pericarditis?

A

fungal/mycobacterial infection

177
Q

What can happen when a caseous pericarditis is healing?

A

fibrotic obliteration of pericardial space (constrictive pericarditis)

178
Q

What must happen with any pericarditis?

A

aspirate submitted to cytological lab

179
Q

What are end results of shock?

A

hypotension
impaired tissue perfusion
cellular hypoxia

180
Q

What are the 3 categories of shock?

A

cardiogenic
hypovolaemic
septic

181
Q

What happens the brain, heart, kidneys, lungs, liver and GI tract in shock?

A
  1. neuronal damage
  2. focal/widespread necrosis (sub-endocardial region)
  3. acute tubular necrosis
  4. diffuse alveolar damage
  5. fatty change, zone 3 necrosis
  6. haemorrhagic enteropathy

Pathology (5 decks)

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