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Tp2. Pathological Processes > Haemostais > Flashcards

Haemostais Flashcards

1
Q

What is primary Haemostasis

A

The formation of the initial platelet flot

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2
Q

What are the steps in primary Haemostasis

A

Initial vasoconstriction
Thromboxane stimulation (attracts the platelets)
Granules come (ADP, PAF, fibrinogen)
Stimulation of Gbllb/lla (by ADP) allowing platelet adhesion
Platelets swell and change shape to cover a larger area

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3
Q

What is secondary Haemostasis

A

The clotting cascade
Involving the intrinsic and the extrinsic pathways

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4
Q

What is the extrinsic pathway

A

Pathway that would occur from external damage

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5
Q

What is the intrinsic pathway

A

The pathway hat would occur when would have the exposure of collagen

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6
Q

What is Von Willebrand factor

A

Stimulates platelet adhesion
Platelets would expose the GPBl receptor (glycoprotein binding 1)
Would allow then to stick together
(Comes from the subendothelium space)

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7
Q

What would happen in the intrinsic pathway

A

Factor 12 - activates factor 11- activates factor 9 - would bind with calcium and factor 8 and would then stimulate factor 10 (goes to the common pathway)

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8
Q

What happens in the extrinsic pathway

A

Tissue factor (TF) would activate factor 7
Would activate factor 10
Would go to the common pathway

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9
Q

What happens in the common pathway

A

Factor 10 would bind to factor 5 and Calcium
This would then form a promthormobinase complex
This would then convert prothrombin to thrombin (factor 2)
Thrombin would then convert fibrinogen to fibrin (factor 1)

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10
Q

What occurs in fibrolysis

A

Plasminogen goes to plasmin (via tissue plasminogen activator)
Plasmin would then cleave the insoluble fibrin to a soluble product
(Release of d-dimer as a by product)

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11
Q

What is d-dimer

A

Degradation protein of fibrolysis

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12
Q

What is Von willebrand disease

A

Autosomal dominant
Deficiency of Von willebrands factor (from the sub endothelium space)
There would be no binding of the platelets

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13
Q

What factors would he deficient in the haemophilias

A

A- 8 (x linked recessive)
B- 9 (x linked recessive)
C- 11 (autosomal recessive)

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14
Q

What are the dense granules

A

ADP (would stimulate the GDllb/lla)
Calcium
Serotonin

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15
Q

What are the alpha granules

A

Fibrinogen
Von willebrands factor
Platelet factor 3
Platelet activating factor (PAF)

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16
Q

What else does thrombin do

A

Activates factor 13 (a stabilising factor)
Cleaves fibrinogen to fibrin

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17
Q

What are the typical symptoms of the bleeding disorders

A

Excessive bleeding
Excessive nose bleeds
Bleeding in joints
Easy bruising

18
Q

What other things can lead to aquired bleeding disorders

A

Liver disease (produces the tPA)
Vitamin k (deficiency in factors 2, 7, 9 and 10)
Warfarin (vitamin k antagonists - anticoagulant)

19
Q

What occurs in disseminated intravascular coagulapathy

A

Over-coagulation and excessive bleeding
Occurs in sepsis, cancers, pregnancy

20
Q

What are the forms of lab testing

A

D-dimer
Blood time
Platelet count
Prothrombin time (vitamin K factors 2,7,9,10)
Acquired partial thromboplastin time (factors 12,11,9,8)

21
Q

What factors does the prothrombin test test for

A

Vitamin k dependent factors 2, 7, 9, 10

22
Q

What factors does activated partial thromboplastin time test for

A

Factors from the intrinsic pathway
12, 11, 9, 8
Would be for the haeomphillacs

23
Q

What does d-dimer test for

A

Would be a degradation product of fibrolysis
Correct function detected

24
Q

What is the normal platelet count

A

150/400

25
Q

What type of disorder in Von willebrands factor

A

Autosomal dominant

26
Q

What type of diesease is haemophilia A,B and C

A

A - x-linked recessive
B- x-linked recessive
C- autosomal recessive

27
Q

Where does Von willebrands factor come from

A

Subendothelium space

28
Q

What is protein C

A

Protein in the body that would stop the blood from clotting too much

29
Q

What does thrombomodulin

A

Coagulation inhibitor
Cofactor for thrombin-mediated activation of protein C
Inhibits the procoagulant functions of thrombin

30
Q

Where does tissue plasminogen activator come from

A

The endothelial tissue

31
Q

What factor is also effected when have Von willebrands disease

A

Stabilising factor 13

32
Q

What can a d-dimer test show

A

Deep vein thrombosis
Pulmonary embolism

33
Q

What type of molecule is Von willebrands factor

A

A glycoprotein

34
Q

What mediates the attachment of the platelets

A

Fibrinogen
(Between the GP11B/111A)

35
Q

What are some natural anticoagulants

A

Protein s
Hepatic - like molecule
The thrombomodulin (protein c would be its cofacto)

36
Q

What would the COX 1 enzyme stimulate

A

The thrmoboxane

37
Q

What is another function of Von willebrands factor

A

Stabilises factor 8
So no VwF would not have the intrinsic pathway be able to finish

38
Q

Where would tPA be realised from and what would it be controlled by

A

The endothelium
Controlled by thrombin.

39
Q

What is the mechanism of DIC

A

Endothelium damage
The platelet aggregation
But would have the down regulation of the anticoagulant factors, so would lead to wide clotting and soon thrombus formation
Would have ischaemia in many areas
But since no clotting factors, would soon have the HAEMORRHAGE

40
Q

What would be the outcome of an advanced lesion

A

The fibrosis so full occlusion

41
Q

How can smoking cause Atheroma (think damage)

A

Increased coagulation
Increased platelet aggregation

Tp2. Pathological Processes (9 decks)

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