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PP > L9 - haemostasis > Flashcards

L9 - haemostasis Flashcards

1
Q

define haemostasis

A

A multifactoral process in which bloodflow is stopped as a result of injury to prevent haemorrhage

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2
Q

Haemostasis is a three step process. The first step is vasoconstriction - this reduces the blood pressure downstream of the insult, what are the following two steps

A

2) The primary haemostatic response - Formation of a primary haemostatic plug from activated platelets that stick to both the vessel and the underlying connective tissue - weak (second to minutes)
3) The secondary haemostatic response - Formation of the secondary haemostatic plug (Fibrin haemostatic plug, 30 mins)

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3
Q

There are three steps in platelet activation - adhesion, activation and aggregation. Briefly describe each

A

Adhesion - Platelet adheres to subendothelial layer at site of insult via von willebrand factor binding its receptor
Activation - Contact with collagen in the underlying layer activates the platelets, platelets now release ADP which amplifies the response
Aggregation - Platelets change shape and cross link to form a plug

NOTE - Von willebrand factor is in the blood, receptor is sub-endothelial and receptor ligand complex allows contact with collagen

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4
Q

Thrombocytopenia is a low platelet count in the blood, will the PT or APTT be raised?

A

No neither will be raised, it is the function of the platelets not the clotting cascade which is impaired

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5
Q

Give two potential causes and the symptoms of thrombocytopenia

A

Causes - decreased platelets due to drugs/malignancies
Increased consumption of platelets due to infection/splenomegaly/DIC

Symtpoms - Petechia in the skin due to bleeding from small peripheral vessels

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6
Q

How is fibrin activated, only the key components at the end of the clotting cascade need be discussed

A

Thrombin is the end product of the clotting cascade, it cleaves circulating fibrinogen to fibrin which then forms the secondary haemostatic plug

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7
Q

Which pathway requires tissue factor released from damaged cells

A

Extrinsic pathway

Note - the intrinsic pathway doesn’t require vessel damage to occur

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8
Q

Give an example of natural anticoagulants released as clotting is started

A

antithrombin/ protein C

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9
Q

What plasma protein is responsible for fibrinolysis - a process which is activated immediately alongside clot formation?

A

plasmin which is the cleaved and activated form of plasminogen. Plasminogen is the circulating inactive form of plasmin

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10
Q

which test assesses the extrinsic pathway PT or APTT?

A

PT - utilises tissue factor in a test tube to look at how long it takes a clot to form (tests common pathway too)

APTT looks at intrinsic and common pathway

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11
Q

How are coagulation factor disorders treated

A

With recombinant forms of the deficient factor

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12
Q

Give some symptoms of haemophilias A and B

A

Easy brusing/massive haemorrhage after surgery/joint deformities

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13
Q

What would the results be to the following tests in a haemophiliac:
platelet count
PT
APTT

A

platelet counut - normal
PT - normal
APTT - prolonged
Intrinsic pathway is compromised

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14
Q

Which factor is deficient in each haemophilia?

A

A - F VIII

B - F IX

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15
Q

Give some common symptoms of vWB disease

A

Easy bruising/ spontaneous bleeds from mucous membranes/ prolonged bleeding after trauma

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16
Q

What do we see clinically in vWB disease i.e. at factor level?

A

Reduced platelet adhesion to wall/
Reduced vWB and F VIII as vWB carries and protects this factor/
Raised bleeding time and APTT

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17
Q

What levels are raised in DIC?

A

PT, APTT and raised D dimers

18
Q

What is DIC ?

A

A clotting activator gets into the blood from tissue damage causing bodywide microthrombi, it is a secondary complication causing excessive consumption of platelets and clotting factors as well as fibrinolysis

19
Q

What are DIC patients at high risk of and what is the treatment?

A

Great risk of bleeding and thrombosis due to excessive clotting - bleeding becasue of using up factors

Treat - heparin and possible platelet transufsion as they are used up AND TREAT THE UNDERLYING CAUSE

20
Q

Give an example of a condition that predisposes to DIC

A

severe trauma/ sepsis/ malignancy/ snake bite/ extensive burns

21
Q

What are thrombophilias ?

A

A set of conditions which predispose to thrombosis

22
Q

Other than ADP what else is released by platelets to amplify the activation response?

A

thromboxane A2

23
Q

How does aspirin work?

A

It inactivates an enzyme responsible for the production of thromboxane A2 and thus downregulates the clotting response

24
Q

How do the elements of the clotting cascade activate each other concurrently?

A

Proteolytic cleavage

25
Q

What does plasmin degrade fibrin too? When do we clinically measure this?

A

Many things but mainly D dimers

Thus we measure D dimers in patients with a suspected deep vein thrombosis, raised D dimers suggest a likely DVT/PE

26
Q

Therapeutically we take advantage of plasmin to break down clots, what plasminogen activator do we use clinically for this?

A

Streptokinase

27
Q

What inheritance pattern do we see in haemophilia?

A

X-linked recessive (need to look at first semester again to go over inheritance patterns)

28
Q

Describe the symptoms of haemophilia

A

Bleeding into muscles and joints/regular mucous membrane bleeds/easy bruising etc.

29
Q

What would coagulation tests show in haemophilia?

A

Prolonged APTT/deficient in the particular factor/normal platelet count, PT and bleeding time

30
Q

What is the inheritance pattern of vWB disease?

A

autosomal dominant

31
Q

Give an example of an inherited thrombophilia

A

Anticoagulant e.g. antithrombin deficiency

32
Q

What would you give to a patient who had overdosed on warfarin (note this is easy to do very narrow therapeutic range)?

A

Vitamin K - Warfarin is a vitamin K antagonist, there are many vitamin K dependent factors in the clotting cascade

33
Q

How does heparin work?

A

Binds to antithrombin to improve its ability in inactivating thrombin

34
Q

Give some symptoms of DIC

A

confusion/gangrene/renal failure/respiratory distress (end organ damage doe to poor blood flow from microthrombi

35
Q

Calcium is an important co-factor required for clotting

A

T

36
Q

Prothrombin requires Vitamin K for its synthesis

A

T

37
Q

What is INR and what is it used for?

A

Calculated from PT, gives an indication of how well anticoagulant therapy is working

38
Q

What is trousseaus syndrome?

A

an acquired thrombophilia due to disseminated cancer - cancer causes hypercoagulability and endothelial damage. Two important prongs of virchow’s triad for thrombosis.

39
Q

Give symptoms of a DVT

A
  • pain and tenderness in one of your legs (usually your calf)
  • swelling
    • a heavy ache in the affected area.
    • warm skin in the area of the clot.
    • red skin, particularly at the back of your leg below the knee.
40
Q

How does a DVT form?

A

Immobility or whatever causes stasis of blood -> increased risk of thrombosis -> formation of a thrombus

41
Q

What are some risk factors for DVT?

A

the combined contraceptive pill/surgery/pregnancy/immobility/dehydration

PP (19 decks)

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