Pathology Part 6 Flashcards

1
Q

What are the symonyms for artheroma?

A

Atherosclerosis
Hardening of the arteries
Coronary artery disease
Ischaemic heart disses

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2
Q

What is atheroma a derivative of?

A

Greek for gruel

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3
Q

Describe the aetiology of atheroma

A
Cigarette smoking
Hypertension
Hyperlipidaemia 
Diabetes
Age 
Sex (male)
Genetics
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4
Q

What is the underlying pathogenesis of atheroma?

A

Endothelial injury

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5
Q

What can cause endothelial cell injury?

A

Cigarettes
Viral, infection
Homocysteine

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6
Q

Where does haemodynamic injury occur?

A

Sites of turbulent flow

Branching site

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7
Q

What is the pathology of diabetes?

A

> Increase cholesterol levels

> Advanced Glycation End Products (AGE)

> Abnormal cross linking in vessel walls

> Loss of elasticity – more rigid and increased endothelial injury

> Trap cholesterol - LDL

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8
Q

What genetic changes can alter risk of atheroma?

A
  1. cholesterol metabolism
  2. inflammatory response
  3. control of BP
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9
Q

Describe the outline of plaque formation

A

Primary endothelial injury

Accumulation of lipids and macrophages

Migration of smooth muscle cells

Increase in size

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10
Q

What is the role of fat in atheroma?

A
Macrophages gobble up cholesterol
Initially the volume of cholesterol is low and remains with the cell
Traps cell
LDL is deposited
HDL “shuttles” back to the liver
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11
Q

What is the role of smooth muscle in atheroma?

A

Smooth muscle migrates from the media into the intima

Gets stuck and takes on cholesterol

Produce extracellular matrix – collagen etc,

Change lesion from fatty streak to fibrofatty plaque

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12
Q

Describe the progression of plaque formation?

A

More cholesterol

More macrophages

More smooth muscle and collagen etc

Eventually too much cholesterol and a pool of extracellular cholesterol forms the centre of the plaque

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13
Q

How can a plaque produce critical disease?

A

It is the only artery supplying an organ or tissue (i.e. There is no collateral circulation)

The artery diameter is small (e.g coronary artery versus common iliac artery)

Overall blood flow is reduced (i.e. cardiac failure)

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14
Q

What are the complications of atheroma?

A

Stenosis

Aneurysm

Dissection

Thrombosis and embolism

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15
Q

What is caused by arterial stenosis?

A

NARROWING OF THE ARTERIAL LUMEN

REDUCED ELASTICITY

REDUCED FLOW IN SYSTOLE

TISSUE ISCHAEMIA

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16
Q

What are the clinical effects of cardiac ischaemia?

A

REDUCED EXERCISE TOLERANCE

ANGINA

UNSTABLE ANGINA

MYOCARDIAL INFARCTION

CARDIAC FAILURE

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17
Q

Describe cardiac fibrosis?

A

LOSS OF CARDIAC MYOCYTES

REPLACEMENT BY FIBROUS TISSUE

LOSS OF CONTRACTILITY

REDUCED ELASTICITY & FILLING

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18
Q

What can arterial stenosis of the carotid arteries cause?

A

TIA, STROKE & VASCULAR DEMENTIA

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19
Q

What can arterial stenosis of the renal arteries cause?

A

HYPERTENSION AND RENAL FAILURE

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20
Q

What can arterial stenosis of the peripheral arteries cause?

A

CLAUDICATION AND FOOT/LEG ISCHAEMIA

21
Q

Define aneurysm?

A

Abnormal and persistent dilatation of an artery due to a weakness in its wall

22
Q

What are the different types of aneurysm?

A
Mycotic
atherosclerotic dissecting
congenital
arteriovenous
traumatic
syphillitic
23
Q

Complications of aneurysm?

A
Rupture
Thrombosis 
Embolism
Pressure erosion of adjacent structures
Infection
24
Q

Describe a blood clot

A

Extravascular

RBCs, fibrin, platelets,

Bruising, coughed up

25
Describe thrombosis
intravascular. Trigger of coagulation within a vessel. Static. Not circulating
26
What would happen if we couldn't coagulate?
Exsanguination
27
Define coagulation
End point- aggregate of platelets, abcs and fibrin
28
What is the roll of fibrin?
Bind everything together
29
What activates the intrinsic pathway of coagulation?
Activation of factor XII
30
What activates the extrinsic pathway of coagulation?
Commonest- starts with tissue factor
31
What is the intrinsic pathway measured by?
Prothrombin time
32
What is the extrinsic pathway measured by?
Activated partial thromboplastin time
33
What is the endpoint of the coagulation cascade?
Prothrombin-thrombin Fibrinogen-Fibrin
34
Where is thrombosis favoured?
Sites of endothelial injury turbulent blood flow hypercoagulable blood
35
What causes endothelial damage?
Increased exposure to tissue factor Weak vessel walls Toxins Infectious agents Smoking related Autoimmune -primary vasculitis turbulence
36
What does stasis cause?
Increased contact of platelets etc. With vessel walls No washing out
37
What can cause primary hypercoagulability?
``` Lots of inherited disorders – primary causes - factor V Lieden - Protein C deficiency - Protein S deficiency - Antithrombin III deficiency ```
38
What is a secondary cause of hypercoagulability?
Prolonged immobility Significant tissue injury – burns, RTA Antiphospholipid syndrome – autoimmune Myocardial infarction Atrial fibrillation (irregular cardiac rhythm) Cancer Activate coagulation cascade through tumour produced TF, mucin, inflammatory cytokines Therapy – many chemotherapeutic agents injure endothelium and increase risk of thrombosis Marantic endocarditis – aseptic thrombotic endocarditis
39
What are low risk causes of hyper coagulability?
The “pill” Smoking Renal disease – nephrotic syndrome Cardiomyopathy
40
Where is most thrombosis?
Venous - leg - iliac veins - IVC - right atrium - right ventricle
41
Define ischaemia
Insufficient blood supply
42
Define infarction
death of tissue as a result of ischaemia
43
What can be found in an embolus?
``` Air embolism Amniotic fluid Fat embolism Tumour emboli Septic emboli ```
44
What volume causes an air embolism to be functional?
Generally need 100ml
45
Describe the process of an amniotic fluid embolism?
5th most common cause of maternal mortality Tear in placenta or uterine vessels with secondary infusion of amniotic fluid or fetal material Identify fetal skin (squamous cells) and hair etc in pulmonary vessels
46
Describe the process of a fat embolism?
After large skeletal injuries where marrow contents are embolised – marrow is mainly fat after 30s Occurs in 90% of sig injuries but only 10% symptomatic Delayed onset – 1 to 3 days after injury with a distinct clinical syndrome
47
What are tumour emboli associated with?
Some tumours have a propensity for vascular invasion Tumours are often friable by their nature Failed metastases?
48
What is the process of a septic emboli?
Specific intravascular infections Thrombus forms in association with an infectious agent Abnormal cardiac valves Mycotic aneurysm In the heart – infective endocarditis Symptoms from numerous septic emboli