Thrombosis Flashcards

1
Q

arterial thrombosis

A

inappropriate activation of platelets and clot formation in ciruclation

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2
Q

common cause of arterial thrombosis

A

atherosclerosis

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3
Q

myocardial infarction MI

A

blockage of arteries due to atheroscloeritc plaque

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4
Q

angina

A

narrowing of coronary arties due to plaque or vasospams

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5
Q

signs and symptoms of MI

A

central chest pain radiating out
sweating, nausea short breath
tachycardia
ECG

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6
Q

what is elevated in a Mi

A

troponin levels, creaine kinase

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7
Q

blockage stroke

A

thrombosis

ischeamic stroke

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8
Q

bleed stroke

A

heamorrhage stroke

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9
Q

TIA

A

transient ischaemic stroke, tetmporary clots

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10
Q

venous thrombosis

A

DVT

caused by inapproriate activation of coagulation

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11
Q

virchows triad

A

stasis of blood, increased coagulation

vessel wall injury

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12
Q

what will increase the risk of a venous thrombosis DVT

A

virchows triad

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13
Q

signs and symptoms of DVT

A

unilateral

  • pain
  • swelling, redness, heat
  • fever, malaise
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14
Q

diagnosis of DVT

A

venogram, X ray with contrast dye

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15
Q

what will increase the risk of a venous thrombosis

A

thrombophillia

can be inherited or acquired

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16
Q

inhereited causes of venous thrombosis

A

hyercaogulability or deficiencies in the inhibitors of caogulation

17
Q

what are natural inhibitors of coagulation

A
  • anti-thrombin III
  • protein C and protein S
  • thrombomodulin
  • plasminogen
18
Q

actions of protein C and S

A

serine protease and cofactor
- thrombin binds thromobmodulin
- protein C and S bind forming a complex
this deactivates the factors in negative regulation

19
Q

types of inherited thrombophillia

A
antithrombin III deficiency
protein C defieciency
protein S defieicncy
factor V leiden
prothombin allele
dysfinrinogenaemia
may-thurner syndrome
20
Q

antithromin 3 deficiency

A

inherited thrombophillia
unable to degrade thrombin and clotting factors
autosomal
- quanititiative form: low levels of antithrombin
- qualitative form: normal amount but it doesnt work well

21
Q

protein C deficiency

A

inhereited thrombophillia

  • quanititiative form: low levels of protein C
  • qualitative form: normal amount but it doesnt work well
22
Q

protein S deficiency

A
inherited thrombophillia
- quanititative
-qualitative
- free protein S reduced but total amount normal
high risk of DVT
women at risk
23
Q

fctor V/5 leiden

A

inherited thrombophilia
mutation to factor 5 cant be inhibited by protein C
very common cause of thrombophillia

24
Q

prothrombin G20210A allele

A

inherited thrombophillia

genetic mutated verios of prothrombin elevating levels making thrombosis risk higher

25
dysfinrinigenaemia
dysfunctional fibrinogen which can cause thrombosis or haemohare pretty rare
26
may-thurner syndrome
congenital anatomic variation predisposing to DVT in the left leg compression of the left common iliac vein by the right common iliac artery causis stasis
27
causes of acquire thrombophilia
``` Previous thrombosis Age Immobilisation Surgery Malignancy Oral contraceptives Hormone replacement therapy Antiphospholipid syndrome Essential thrombocytosis Polycythaemia vera Paroxysmal nocturnal haemaglobinuria ```
28
how can malignancy lead to a higher DVT risk
tumour cells might express tissue factors which are needed for the extrinsic cascade occult (unknown) cancers should be invetigated in these cases
29
what is anti-phospholipid antibody syndrome
lupud anticoagulat/stick blood sydrome not fully understood Ab made against phospholipid which are needed for surface for coagulaton messes things up!
30
essential thrombocytosis or thrombocythaemia
acquired thrombphillia raised plateler count causing thrombosis or bleeding it is a myeloproliferative neoplasma
31
myeloproliferative neoplasm
excess production of myeoid blood ccells | eg essential thrombocytosis or thrombocytheaemia
32
what is polycythaemia Rubra vera
another myeloproliferative neoplama excess RBC raised Hct and HGB thickening of blood slows the flow of blood causing stasis increasing risk of thrombosis
33
what is paraxysmal nocturnal haemaglobinuria
lysis of RBC leadsing to Hb in urine that accumulates overnight loss of GIP anchors on the surface of RBC, proteins missing leads to: haemolyic anaemia and venous thrombosis