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Pathology
Atherosclerosis
Distribution
Atheromatous/Fibrofatty plaques
Complicated lesions
Aorta
Coronary arteries
Carotid and vertebrobasilar arteries
Lower limb arteries
Pulmonary arteries (only in pulmonary
hypertension)
(Not upper limb arteries)
Typically raised white to yellow-white
lesions of 3-15 mm diameter
Intimal thickening
Variable amounts of extracellular lipid
Covered by collagenous cap
containing SM
May be central necrosis
Foam cells, other inflammatory cells,
and granulation tissue may be present
at base
Disruption of internal elastic lamina
In advanced plaques:
Atrophy of tunica media
Calcification
Same as atheromatous/
fibrofatty plaques
Features
Sub-clinical, precursor
lesions
First develop in
childhood, with
increasing numbers in
individuals aged 15-35
years
Do not necessarily
progress further, and
may regress
completely
Intraluminal thrombosis
due to obstruction of
endothelial surface
Haemorrhage into
plaques due to rupturing
of intima, and formation
of haematoma in plaque,
producing plaque
enlargement and luminal
occlusion
Embolism of plaque
content
Aneurysmal dilation of
large vessels due to loss
of vessel elasticity
Progression of
atheromatous/fibrofatty
plaques
Can result in ischeamia
of any involved vascular
bed
Mortality primarily from
myocardial ischaemia
(including infarction),
cerebral infarction, and
aneurysm rupture
Illustration
Progression
Atherosclerotic progression
Matt Schiller
Page 1 of 12
Pathology
Thrombosis
Inhibiting and Predisposing Factors to Thrombosis
Thrombus solid or semi-solid mass formed from constituents of blood within the
vascular system during life (distinct from haemostasis).
Thrombus formation
Factor
Mechanism
Injury to or activation
of endothelium
May be exposure of
sub-endothelial layers
(notably collagen)
May be due to
atherosclerosis,
inflammation
(vasculitis), or trauma
Turbulence / High
shear forces
Stagnation (due to
immobility, heart
failure, or
arrhythmias)
Matt Schiller
Page 2 of 12
Pathology
Thrombosis Types
Origin
Sites
Morphology
Venous
Arterial
Mural
Outcomes (if
not resolved)
Matt Schiller
High flow
Injured
endothelium
(especially due
to
atherosclerosis)
Coronary
circulation
(myocardial
infarction)
Cerebral
circulation
(cerebral
infarction)
Femoral arteries
(lower limb
ischaemia)
Laminated
alternative layers of:
Fibrin and
platelets (white)
Increased
numbers of
erythrocytes
(red)
Occlusion
Systemic
embolism
Following myocardial
infarction (decreased
flow, injured
endothelium, and
pro-coagulant effect
of necrotic tissue)
Atrial fibrillation
Valvular damage
Cardiac chambers
(especially left
ventricle and atrium)
Aorta
Damaged valves
Non-occlusive
Systemic embolism
Page 3 of 12
Pathology
Embolism
Embolism the transportation by the blood of abnormal material and its impaction in a
vessel at a point remote from its entry into the circulation.
Origin
Pulmonary
Arterial/Systemic
Route
Outcome
Possible
clinical
presentations
Venous thrombosis
Majority form in deep veins of
calf
Propagation in direction of flow
(Dependent on site)
Matt Schiller
Page 4 of 12
Pathology
Fat
Cholesterol
Origin/Description
Presentation/Outcome
Amniotic fluid
Septic
Air
Decompression
sickness
Foreign body
Dyspnoea
Coma
Generally presents 1-3 days
following injury
Skin symptoms
Gangrene of extremities
Renal failure
Cardiovascular shock
Excessive bleeding
Disseminated intravascular
coagulation
Chokes (pulmonary
obstruction/haemorrhage)
Page 5 of 12
Pathology
Myocardial Infarction
Ischaemic Heart Disease
Ischaemic heart disease (IHD) group of diseases characterised by an inability of the
coronary arteries to deliver sufficient oxygen to meet the demands of the heart
(usually due to coronary atherosclerosis).
Decreased supply
Increased demand
Anaemia
Carbon monoxide poising and
carboxyhaemoglobin
Myocardial hypertrophy
Tachycardia
Causes of the imbalance between oxygen supply and demand that underlies IHD
Left anterior
descending
branch (LAD)
Right coronary
artery (RCA)
Tissue supplied
Common site
of lesions
Proximal and
distal thirds
Relative frequency
of occlusion
30-40%
Left circumflex
Proximal (first 15-20%
branch (LCX)
2 cm)
Coronary arteries and their associated atherosclerotic lesions
Matt Schiller
Page 6 of 12
Pathology
Syndrome
Pathology
Angina
Unstable Angina
Myocardial infarction
Angina Pectoris
Angina pectoris syndrome of episodic, paroxysmal, substernal or precordial chest
pain due to inability of diseased coronary arteries to provide adequate blood for
myocardial oxygenation.
Description
Seriousness
Stable
Only precipitated by exertion
Less
Unstable Increased frequency with less exertion
More
Variant
Not precipitated by exertion, involving coronary artery spasm Most
Clinical types of angina pectoris
Myocardial Infarction
Transmural
Subendocardial
Description
Commonality
Size and area of
infarct
Most common
Unifocal and large lesion
Distribution of affected
coronary artery
Atheroma and thrombus of
one artery
Possible
Cause
Pericarditis
Not possible (not involving pericardial
(complication)
surface)
Aneurysm
Possible
Not possible (whole wall not damaged)
(complication)
Comparison of transmural and subendocardial types of myocardial infarction
Matt Schiller
Page 7 of 12
Pathology
Microscopic
Matt Schiller
Page 8 of 12
Pathology
Valvular Heart Disease and Congestive Cardiac Failure
Stenosis and Incompetence
Left
Right
Definition
Lesion type
Type of load
on chamber
Effect on
chamber
Cause
Disease associations
Mitral
Aortic
Tricuspid
Stenosis (Obstruction)
Incompetence (Regurgitation)
Narrowing of orifice
Always chronic
Pressure
Concentric hypertrophy,
then dilation
Vegetation formation
Rheumatic
Rheumatic
Calcific
Congenital (bicuspid)
Matt Schiller
Page 9 of 12
Pathology
Rheumatic Fever and Infective Endocarditis
Rheumatic fever
Infective endocarditis
Definition
Microbiology
Pathology
Acute/Chronic
Clinical
features
Friable vegetations
Tissue destruction of leaflets, apparatus,
and/or annulus
Acute or subacute
Fever
New or changing murmur
Embolic phenomena
Event
Consequences
Atrial fibrillation
Embolic phenomena
Pulmonary venous congestion Dyspnoea
Orthopnoea (breathing discomfort when flat)
Paroxysmal nocturnal dyspnoea
Decreased renal perfusion
Activation of renin-angiotensin-aldosterone pathway
Salt and water retention
Peripheral oedema
Right heart failure
Chronic passive congestion of liver
Tender, pulsative hepatomegaly
Cardiac cirrhosis
Matt Schiller
Page 10 of 12
Pathology
Fever
Hyperthermia and Fever
Normal body temperature is 37.2C to 37.5C.
Hyperthemia
Fever
Thermoregulatory
responses
Thermal set-point
Pathogenesis
Altered
Normal
Normal
Overwhelming of
heat loss
mechanisms by
internal and external
heat
Impairment of heat
loss mechanisms by
disease or drugs
Magnitude
Commonality
Harmfulness
Tissue injury and
multiple organ
failure
Elevated
Infection (most commonly)
Exogenous pyrogens stimulate cells
to release pro-inflammatory
cytokines
Cytokines reach anterior
hypothalamus via circulation and
neurones and induce PG-E2
production which elevates thermal
set-point
Efferent responses:
Reduced heat loss
cutaneous vasoconstriction
Increased heat production
piloerection, shivering, rigors
Rarely exceed 41C
More
Less
Not reported
Advantages
Disadvantages
Matt Schiller
Page 11 of 12
Pathology
Features of Fever
Patient experience
Cold
Hot
Wet
Fever
Fever
History
Examination
Investigations
Constitutional
symptoms
Localising symptoms
Epidemiological clues
Temperature
Localising
signs
Matt Schiller
Page 12 of 12