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PED2007 > thrombosis > Flashcards

thrombosis Flashcards

1
Q

how does thrombosis presents as

A

characterised by the lines of Zahn (platelets and red blood cells held together by fibrin)
and attachment to vessel walls

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2
Q

what are the 3 risk factor of thrombosis called

A

Virchow’s triad

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3
Q

1st point of Virchow’s triad (1) D_ o_ B_ F_

A

Disruption of blood flow
- immobilisation (flight/bedrest)
-cardiac wall dysfunction
-Aneurysm
-atrial fibrillation

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4
Q

2nd of Virchow’s traid (2) E_ C_ D_

A

Endothelial cell damage
-Atheroscelrosis (reptured plaque)
-vasculitis
-high levels of homocysteine (low B12)
-turbulent blood flow of arterial bifurcation
-oxidised LDL
-cigarrette smoke
-cytokines

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5
Q

3rd of Virchow’s traid (3) H_ S_

A

Hypercoaguable states
-due to excessive procoagulant factors /defective anticoagulants
-may be inherited (AT3 deficiency), acquired (DIC)
(classic presentation is recurrent DVT or DVT at early age)

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6
Q

what is the most common cause and site of venous thrombosis

A

Stasis of blood
most common site is deep vein of lower limbs

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7
Q

what is the presentation of DVT

A

Red swollen painful legs with skin discolouration

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8
Q

what can happen if a person has DVT

A

can dislodge to the lungs and cause a pulmonary embolism

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9
Q

Arterial thrombosis is commonly due to what - and what is an rare cause

A

common = endothelial damage related to turbulent blood flow at bifurcation or over atherosclerotic plaque in high velocity vessels
rare = hypercoagulabilty + stasis

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10
Q

Arterial thrombosis causes -(3)

A

myocardial infarctions
small bowel infarction
strokes

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11
Q

what is INR

A

International normalised ratio

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12
Q

what is normal INR

A

1

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13
Q

what is INR used for

A

montiter warfarin therapy

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14
Q

what is INR=2.5

A

treatment of DVT, pulmonary/arterial embolsim, atrial fibrillation, myocardial infraction

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15
Q

what is INR=3.5

A

treatment of recurrent DVT or pulmonary embolism

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16
Q

describe Prothrombin time (PT)

A

-evaluates the extrinsic coagulation system to formation of the fibrin clots
-monitored person taking warfarin + liver synthesis function

17
Q

what is normal PT

A

11-15 second

18
Q

Time is prolonged when clotting factor level is

A

30-40% of normal PT

19
Q

what is a pulmonary embolism

A

An intravascular mass that travels and occludes pulmonary blood vessels
Most common cause is a dislodged thrombus (thromboembolus) – 95%

20
Q

what is used to treat AIS

A

Alteplase
Aspirin (24h after thrombolysis)

21
Q

what is used to treat venous thrombosis

A

Rivaroxaban + Apixaban

22
Q

what is used to treat arterial thrombosis

A

inhibitor of platelets aggregation prevent formation - Aspirin

23
Q

what is thrombin

A

acts on fibrinogen to produce fibrin monomers
activates fibrin stabilising factor 13 (13a)

24
Q

thrombin (extensive mechanims)

A
  • converts these monomers to cross linked fibrin which strengthens blood clots
  • acts on a feedback loop to activates several other coagulation factors and is therefore pivitol in the amplification system
25
Q

what switches off thrombin

A

natural anticoagulant antithrombin 3 - limits clot formation

26
Q

What does plasmin does

A
  • breaks down clots, cleave fibrin & fibronigen into degradation products (fragments known as D-dimers)
  • degrades some clotting factors + blocks platelet aggregation
27
Q

what are the three stages of platelet activation

A

adhesion, release reaction, aggregation

28
Q

platelet undergo shape changes and degranulation which causes -

A

-release mediator ADP (from dense core granules)
-ADP induces the expression of GP2b/3a (GPIIb/IIIa) another essential receptor of aggregation and and fibrinogen which acts as a linker molecule in the developing clot
- production thromboxane A2 (TXA2)(a derivative of platelets cyclooxygenases) its a vasocontrictor that also promotes platelets aggregation
-releases calcium

29
Q

Plaque formation (using LDL and anti-inflammatory systems)

A

-Circulating LDL gains access to subendothelial spaces where their oxidised
-cytokines IL-1 and MCP-1 attract circulating monocytes

30
Q

macrophages phagocytose LDL to form _ in plaque formation

A

foam cells

31
Q

what happens after foam cells formation

A

smooth muscle cells migrate and proliferate under the influence of smooth muscle mitogens

32
Q

A primative plaque is formed of

A

Foam cells, smooth muscle cells, lipids & necrotic cells

33
Q

how does plaques mature

A

the plaque enlarged, develops a fibrous capsule and protrudes in vessel lumen

PED2007 (8 decks)

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