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Principles 2018 > Pathology Part 6 > Flashcards

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
Q

Describe thrombosis

A

intravascular.

Trigger of coagulation within a vessel.

Static. Not circulating

26
Q

What would happen if we couldn’t coagulate?

A

Exsanguination

27
Q

Define coagulation

A

End point- aggregate of platelets, abcs and fibrin

28
Q

What is the roll of fibrin?

A

Bind everything together

29
Q

What activates the intrinsic pathway of coagulation?

A

Activation of factor XII

30
Q

What activates the extrinsic pathway of coagulation?

A

Commonest- starts with tissue factor

31
Q

What is the intrinsic pathway measured by?

A

Prothrombin time

32
Q

What is the extrinsic pathway measured by?

A

Activated partial thromboplastin time

33
Q

What is the endpoint of the coagulation cascade?

A

Prothrombin-thrombin

Fibrinogen-Fibrin

34
Q

Where is thrombosis favoured?

A

Sites of endothelial injury

turbulent blood flow

hypercoagulable blood

35
Q

What causes endothelial damage?

A

Increased exposure to tissue factor

Weak vessel walls

Toxins

Infectious agents

Smoking related

Autoimmune
-primary vasculitis

turbulence

36
Q

What does stasis cause?

A

Increased contact of platelets etc.

With vessel walls

No washing out

37
Q

What can cause primary hypercoagulability?

A 
Lots of inherited disorders – 
primary causes
 - factor V Lieden
 - Protein C deficiency
 - Protein S deficiency
 - Antithrombin III deficiency
38
Q

What is a secondary cause of hypercoagulability?

A

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
Q

What are low risk causes of hyper coagulability?

A

The “pill”
Smoking
Renal disease – nephrotic syndrome
Cardiomyopathy

40
Q

Where is most thrombosis?

A

Venous

  • leg
  • iliac veins
  • IVC
  • right atrium
  • right ventricle
41
Q

Define ischaemia

A

Insufficient blood supply

42
Q

Define infarction

A

death of tissue as a result of ischaemia

43
Q

What can be found in an embolus?

A 
Air embolism
Amniotic fluid 
Fat embolism
Tumour emboli
Septic emboli
44
Q

What volume causes an air embolism to be functional?

A

Generally need 100ml

45
Q

Describe the process of an amniotic fluid embolism?

A

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
Q

Describe the process of a fat embolism?

A

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
Q

What are tumour emboli associated with?

A

Some tumours have a propensity for vascular invasion

Tumours are often friable by their nature

Failed metastases?

48
Q

What is the process of a septic emboli?

A

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

Principles 2018 (34 decks)

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