Thrombus, Embolism And Atherloscerosis Flashcards

1
Q

What is a thombus?

Why do thrombus occur?

A
  • Formation of a solid mass of blood within circulatory system.
  • Virchow’s Triad …
  1. Defects of vessel walls
    - atheroma
    - direct injury
    - inflammation
  2. Abnormalities of flow
    - stasis - e.g.: due to narrowing of vessel or low bp
    - turbulent flow - e.g.: due to stenosis
  3. Abnormalities in blood components
    - smokers (hyper coagulable state)
    - after giving birth
    - after operations
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2
Q

What do thrombi look like in arteries?

A
  • pale (less RBCs within)
  • granular
  • lines of zhan (colour depends on composition of blood at that time)
  • lower cell content
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3
Q

What do thrombi look like in veins?

A
  • soft
  • gelatinous
  • deep red as higher red cell content
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4
Q

What can the outcomes of a thrombus be? (4)

A

1) lysis - when thrombi are small, complete dissolution by fibrinolytic system + establishment of blood flow
2) propagation - spread and growth of thrombi, distal in arteries, proximal in veins
3) organisation - repair with granulation like tissue- still obstructs lumen
4) Recanalisation - one or more channels form allowing limited flow through thrombus
5) Embolism

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5
Q

What is an embolism?

A

The blockage of a blood vessel by solid, liquid or gas at a distant site to its origin - when thrombus breaks off and travels through bloodstream.

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6
Q

What is the consequence of a venous thrombo- emboli?

What is the consequence of an arterial thrombi-emboli?

A
  • congestion of veins
  • oedema- fluids cannot be exchanged as easily
  • ischaemia and infarction as blood cannot flow as easily
  • Ischaemia + infarction (depends on site + collateral circulation)
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7
Q

What other substances can cause embolisms?

A
  • air (need 15ml to have effect, makes blood throthy so cant pump as well)
  • amniotic fluid
  • nitrogen (from dissolved N2 becoming gaseous in decompression syndrome)
  • medical equipment
  • tumour cells
  • fat + bone marrow
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8
Q

What are the risk factors for DVTs?

A
Immobility
Post op
Pregnancy
Burns 
Oral contraceptives 
Disseminated cancer
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9
Q

How can DVT be treated?

A
  • TED stockings
  • ‘flowtron boots’ which periodically inflate
  • oral warfarin (wont lyse thrombus but will prevent growth)
  • IV type heparin (again wont lyse)
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10
Q

What is a straddle embolism?

A

One that straddles the bifurcation of a pulmonary trunk

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11
Q

What are symptoms of major and massive pulmonary embolism?

A

Massive- 60% of blood flow to lungs occluded, rapid death

Major: short of breath, coughing, blood stained sputum

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12
Q

What is an iatrogenic embolism?

A

Embolism resulting from treatment

Air embolism or medical equipment

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13
Q

What do fat emboli most commonly occcur?

A

After closed fractures

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14
Q

What are the preventative and treatment options for thrombosis and thromboembolism?

A
  • low molecular weight heparin (SC), mobilise early and TED stockings for prophylaxis in high risk patients.
  • Clot busters, LMW heparin (e.g.: apixaban), oral warfarin
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15
Q

What is atheroma?
What is atherosclerosis?
What is arteriosclerosis?

A
  • The accumulation of intracellular and extracellular lipid in the tunica intima and media of large and medium sized arteries
  • Thickening and hardening of arterial walls as a consequence of atheroma
  • The thickening of arterial walls and arterioles due to hypertension or DM.
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16
Q

What does an atheroma start off as?

A

Starts off as fatty streak
Lipid deposits in intima, looks yellow and slightly raised
Do not always go on to form plaques

17
Q

What is the difference between a simple plaque and complicated plaque?

A
  • Simple is a yellow raised larger area with irregular outline
  • A complicated one is where plaque has complications, eg thrombosis, haemorrhage, calcification, aneurism ect
18
Q

Where are atheroma most common?

A

Any arteries except in arms

  • aorta
  • coronary arteries
  • carotid artery
  • cerebral arteries
  • leg arteries
19
Q

Describe the microscopic changes that occur in the formation of an atherosclerotic plaque?

A
Early:
- proliferation of smooth muscle cells 
- extracellular lipid and foam cell accumulation 
Late: 
- fibrosis 
- necrosis
- cholesterol clefts (holes where extracellular lipids dissolved away)
Even later:
- calcification 
- elastic laminar disruption 
- damage to media due to pressure from plaque 
- ingrown of blood vessels 
- plaque ruptures surface (fissuring)
- thrombus
20
Q

What is arteriosclerosis?

A

Hardening of the media in microvasculature due to hypertension with no fat deposits

21
Q

What is aneurysms and how do they occur?

A
  • abnormal dilitation of a blood vessel wall

- media damage means less tension able to be put on blood vessel meaning it expands

22
Q

Where is mesneteric ischaemia? Where is it most commonly seen?

A

Atherosclerosis of mesenteric artery
Usually seen at splenic flexure where collateral blood supply is worst
Leads to malabsorption ect

23
Q

What is intermittent claudication?

A

Pain in calfs on walking which goes away after rest but will come back after progressively shorter periods of walking. It is a part of peripheral vascular disease

24
Q

List the major risk factors for atherloslcerosis

A
  • Older age
  • Men (women protected till menopause)
  • hyperlipidaemia
  • cigarette smoking
  • hypertension
  • diabetes
  • alcohol (small amounts are protective)
  • infection
  • Genetics
  • lack of exersize
  • obesity
  • soft water
  • oral contraceptives
  • stress
25
Q

What are the signs of a genetic predisposition to atherlosclerosis (familial hyperlipidaemia)?

A
  • arcus (yellow corneum)

- xantheromas (macrophage filled plaques on skin surface- typically over joints)

26
Q

What is the thrombogenic theory for atheroma formation?

A
  • plaques form from repeated thrombi
  • the lipid comes from the thrombi
  • a fiberous cap forms on top
27
Q

What in insudation theory”?

A

Endothelial injury
Leads to inflammation
increases permeability to lipid from plasma

28
Q

What is the reaction to injury hypothesis?

A
  • plaques from as a result of endothelial injury
  • high cholesterol could cause this damage due to oxidation
  • Injury allows high permeability and platelet adhesion
  • monocytes penetrate epithelium
  • smooth muscle cells proliferate and migrate to intima
29
Q

What is the monoclonal hypothesis for atheroma formation?

A
  • each plaque is a benign tumour of smooth muscle cell proliferation
30
Q

Describe the unifying hypothesis for atheroma formation.

A
  • endothelial injury (due to high LDL, toxins, hypertension, haemodynamic stress)
  • This causes platelet adhesion and platelet derived GF release leading to smooth muscle proliferation and migration into the intima
  • and also leads to accumulations of lipids and uptake of these makes foam cells- which release cytokines for further smooth muscle cell proliferation and other inflammatory cells
  • and also to migration of monocytes into intima
  • Smooth muscle cells also stimulated to produce more matrix
31
Q

How can atherosclerosis be prevented?

A
  • decrease smoking
  • decrease fat intake
  • treat hypertension
  • decrease alcohol
  • regular exersize and weight control
  • lipid lowering drugs like statins