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NMSKI > Thrombosis > Flashcards

Thrombosis Flashcards

1
Q

normal haemostasis

A

Well-regulated process that maintains blood in a fluid, clot free state in normal vessels and induces the rapid formation of a localised haemostatic plug at the site of vascular injury

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2
Q

Haemostasis and thrombosis are dependent on what three components

A
  • Vessel wall
  • Platelets
  • Coagulation cascade
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3
Q

thrombosis

A

the inappropriate activation of blood clotting in an uninjured vessel/minimally injured vessel leading to the formation of a blood clot (thrombus) within the vascular system, which can obstruct the flow of blood

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4
Q

thrombus

A

an aggregate of coagulated blood containing platelets, fibrin and entrapped cellular elements.

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5
Q

virchows triad

A

change in surface - endothelial injury
change in flow - stasis and turbulence
change its constituents - hypercoagulability

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6
Q

where in the endothelial surface does thrombosis commonly occur and why

A

atheromatous plaques
Injury occurs due to HTN(Hypertension), turbulent
flow, radiation
results from -exposure of stroma, increased platelet adhesion

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7
Q

how does turbulent blood flow cause or influence thrombosis

A

Disrupted flow brings platelets into contact with
the endothelium
Prevent dilution of activated clotting factors by flowing blood

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8
Q

hypercoagulability

A

alteration of the coagulation pathways

-> predisposes to thrombosis

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9
Q

heritable hypercoagulability

A

Factor V leiden, protein c/protein s deficiencies,

prothrombin mutations

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10
Q

examples of Acquired Hypercoagulability

A

Oral contraceptives, pregnancy, malignancy,

nephrotic syndrome

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11
Q

sites of venous thrombus formation

A

– most commonly due to stasis in capillaries and heart

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12
Q

sites of arterial thrombus formation

A

most commonly superimposed on atheroma

capillaries and heart

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13
Q

causes of arterial thrombosis

A

Atheromatous plaque
Smokers
High cholesterol

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14
Q

causes of venous thrombosis

A

Blood pressure lower – atheroma does not occur
Most begin at valves – turbulence, stasis, occlusion
Venous return from the legs relies on calf muscle
contraction and relaxation
Any fall in blood pressure (e.g. during surgery) can
precipitate development

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15
Q

risk factors for venous thrombosis

A 
Immobility
Smoking
Cancer
Pregnancy
Oestrogen therapy
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16
Q

Clinical effects of a arterial thrombus

A

Loss of pulse
Pale, cold
Painful
Death & gangrene of the affected limb/site

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17
Q

Clinical effects of a venous thrombus

A
  • 95% occur in leg veins
  • Tender
  • Swollen
  • Reddened
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18
Q

fate of a thrombus

A 
Lysis and resolution 
Organisation - scar tissue
Recanalization
Propagation
Embolization
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19
Q

Recanalization

A

– ingrowth of new vessel which eventually

join up to restore blood flow, at least partially

20
Q

Propagation

A

enlarges leading to vessel obstruction

21
Q

Embolization

A

dislodges, travelling to a different site

22
Q

embolism

A

 An embolus is a detached intravascular physical mass,
which is carried in the circulation until it reaches a vessel
too small to permit its further passage when occlusion
occurs

23
Q

embolism that arise from a thrombus

A

thromboembolism

24
Q

types of embolism

A 
Fat
Air or gas
Thrombus
Bacteria emboli
Amniotic fluid
Tumour fragments
25
Q

pulmonary embolism

A

Venous thrombi in the leg veins can travel to the lungs

Small emboli may cause no effects

26
Q

larger emboli in pulmonary embolisms can cause

A 
• Chest pain
• Shortness of breath
• Infarction
• Sudden death
o Saddle embolus
27
Q

systemic embolism

A

Arise in the arterial system
Arise in the heart or from atheromatous plaques
May travel to various sites and cause

28
Q

examples of systemic embolism

A
  • Brain – TIA, stroke
  • Renal – infarction
  • Bowel – ischaemic bowel
  • Limbs – ischaemia and gangrene
29
Q

low blood supply

A

• Imbalance between perfusion and demand of

oxygenated blood to a tissue

30
Q

ischaemia

A

Deficient supply of blood

31
Q

how is ischaemia characterised

A

insufficiency of O2
lack of nutrient substrates and inadequate removal of
metabolites (perfusion)

32
Q

Susceptibility of tissues to ischaemia

A

 Blood supply and collateral circulation – may compensate

for reduced perfusion

33
Q

tissues with what kind of metabolism rate are highly susceptible ischaemia

A

Organs with high metabolic rate and aerobic metabolism –

susceptible (heart)

34
Q

tissues of what kind are lowly susceptible to ischaemia

A

Supporting tissues (fibrous, bone) – less susceptible

35
Q

infarction

A

Area of ischaemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue

36
Q

what embolic events cause infarction

A

 Torsion: testicular/bowel
 Extrinsic compression
 Traumatic rupture

37
Q

clinical examples of infarction

A 
 Myocardial infarction
 Cerebrovascular accident (infarct)
 Pulmonary infarction
 Bowel infarction
 Ischaemic necrosis of the extremities
38
Q

causes of iscaemia

A

THROMBOSIS
EMBOLUS
Local vasospasm
Extrinsic compression of vessel

39
Q

macrscopic appearances of infarct

A

Wedge shaped (occluded vessel at apex

40
Q

early macrscopic appearances of infarct

A

• Poorly defined, irregular • Narrow rim of hyperaemia at edge due to inflammation

41
Q

late signs of macroscopic appearances of infarct on solid organ

A

few RBC lysed  some
haemosiderin pigment.
Pale and sharply
defined

42
Q

late signs of macroscopic appearances of infarct on spongy organ

A

Firm and brown

Haemosiderin pigment

43
Q

Microscopic features of infarcts

A

first 12 - 18hrs
→Necrotic tissue stimulates inflammatory response at
edge (1-2days)
→Phagocytosis of cellular debris and dead tissue
→Reparative phase with scar formation

44
Q

exception to microscopic features of infarcts

A

Brain exception – liquefactive necrosis

45
Q

examples of vulnerable tissue

A

‘Watershed’ areas (especially during shock/hypotension)
o Splenic flexure of the colon
o Brain
o Deep myocardium

46
Q

low flow infarction

A

Impaired blood flow rather than absolute cessation

47
Q

susceptibility of infarcts

A

low flow

vulnerable tissue

NMSKI (38 decks)

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