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

25
What type of disorder in Von willebrands factor
Autosomal dominant
26
What type of diesease is haemophilia A,B and C
A - x-linked recessive B- x-linked recessive C- autosomal recessive
27
Where does Von willebrands factor come from
Subendothelium space
28
What is protein C
Protein in the body that would stop the blood from clotting too much
29
What does thrombomodulin
Coagulation inhibitor Cofactor for thrombin-mediated activation of protein C Inhibits the procoagulant functions of thrombin
30
Where does tissue plasminogen activator come from
The endothelial tissue
31
What factor is also effected when have Von willebrands disease
Stabilising factor 13
32
What can a d-dimer test show
Deep vein thrombosis Pulmonary embolism
33
What type of molecule is Von willebrands factor
A glycoprotein
34
What mediates the attachment of the platelets
Fibrinogen (Between the GP11B/111A)
35
What are some natural anticoagulants
Protein s Hepatic - like molecule The thrombomodulin (protein c would be its cofacto)
36
What would the COX 1 enzyme stimulate
The thrmoboxane
37
What is another function of Von willebrands factor
Stabilises factor 8 So no VwF would not have the intrinsic pathway be able to finish
38
Where would tPA be realised from and what would it be controlled by
The endothelium Controlled by thrombin.
39
What is the mechanism of DIC
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
What would be the outcome of an advanced lesion
The fibrosis so full occlusion
41
How can smoking cause Atheroma (think damage)
Increased coagulation Increased platelet aggregation