Thrombus, Embolism And Atherloscerosis Flashcards Preview

Pathological processes > Thrombus, Embolism And Atherloscerosis > Flashcards

Flashcards in Thrombus, Embolism And Atherloscerosis Deck (31)
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What is a thombus?
Why do thrombus occur?

- 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


What do thrombi look like in arteries?

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


What do thrombi look like in veins?

- soft
- gelatinous
- deep red as higher red cell content


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

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


What is an embolism?

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.


What is the consequence of a venous thrombo- emboli?
What is the consequence of an arterial thrombi-emboli?

- 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)


What other substances can cause embolisms?

- 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


What are the risk factors for DVTs?

Post op
Oral contraceptives
Disseminated cancer


How can DVT be treated?

- TED stockings
- 'flowtron boots' which periodically inflate
- oral warfarin (wont lyse thrombus but will prevent growth)
- IV type heparin (again wont lyse)


What is a straddle embolism?

One that straddles the bifurcation of a pulmonary trunk


What are symptoms of major and massive pulmonary embolism?

Massive- 60% of blood flow to lungs occluded, rapid death
Major: short of breath, coughing, blood stained sputum


What is an iatrogenic embolism?

Embolism resulting from treatment
(Air embolism or medical equipment)


What do fat emboli most commonly occcur?

After closed fractures


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

- 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


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

- 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.


What does an atheroma start off as?

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


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

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


Where are atheroma most common?

Any arteries except in arms
- aorta
- coronary arteries
- carotid artery
- cerebral arteries
- leg arteries


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

- proliferation of smooth muscle cells
- extracellular lipid and foam cell accumulation
- 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


What is arteriosclerosis?

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


What is aneurysms and how do they occur?

- abnormal dilitation of a blood vessel wall
- media damage means less tension able to be put on blood vessel meaning it expands


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

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


What is intermittent claudication?

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


List the major risk factors for atherloslcerosis

- 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


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

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


What is the thrombogenic theory for atheroma formation?

-plaques form from repeated thrombi
- the lipid comes from the thrombi
- a fiberous cap forms on top


What in insudation theory"?

Endothelial injury
Leads to inflammation
increases permeability to lipid from plasma


What is the reaction to injury hypothesis?

- 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


What is the monoclonal hypothesis for atheroma formation?

- each plaque is a benign tumour of smooth muscle cell proliferation


Describe the unifying hypothesis for atheroma formation.

- 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