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Pathological Processes (Milly's) > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What are the aims of haemostasis?

A
  • prevents bleeding

- prevents unnecessary coagulation, allow blood to flow

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2
Q

How are the aims of haemostasis reached?

A

Make clot

Control clotting

Break it down (when tissue healing occurs)

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3
Q

What are the essentials for haemostasis?

A
  • Keep blood moving
  • platelets
  • coagulation factors (proteins involved in clotting cascade)
  • anticoagulant factors
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4
Q

Where are platelets produced and what is their life span?

A

Megakaryocytes in bone marrow

They ‘bud’ from cytoplasm

Normal life span 7-10 days (important to note when someone is on platelet inhibiting drugs ie aspirin)

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5
Q

What is the 3 roles and functions of platelets in haemostasis?

A

3 steps:
Platelet adhesion
Platelet Activation
Platelet Aggregation

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6
Q

What is platelet adhesion?

A

First step in primary haemostasis

If there is damage to a vessel wall, there will be exposure of underlying tissues- namely collagen. Platelets adhere to said collagen via the vWF/receptor

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7
Q

What is platelet activation?

A

2nd step in primary haemostasis

Platelets secrete different substances like ADP and thromboxane which auto-activate and activate other platelets.

They’re also involved in the activation of the clotting cascade.

Provide some coagulation factors (factor V) by secretion from internal stores.

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8
Q

What is platelet aggregation?

A

Final step in primary haemostasis

Once activated the platelets will form cross links with other platelet to form a platelet plug (/weak clot)

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9
Q

Name some mediating factors of primary haemostasis (7)

A

Plt receptors (glycoprotein complexes eg GP1b-V-IX, GPIIIa)

Von willebrands factor

Fibrinogen

Collagen

ADP

Thromboxane/arachidonic acid

Thrombin

[Some of these are targets for anticlotting drugs]

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10
Q

What is the main role of thrombin?

A

Converts soluble fibrinogen into insoluble fibrin which will stabilise the clot

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11
Q

Why do we have natural anticoagulants in the blood?

A

Control clotting and prevent further coagulation

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12
Q

What factors are involved in the extrinsic pathway of the clotting cascade?

A

7

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13
Q

What factors are involved in the intrinsic pathways of the clotting cascade?

A

8,9,11,12

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14
Q

What factors are found in the common pathway of the clotting cascade?

A

5, 10, prothrombin, fibrinogen

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15
Q

What is another name for the extrinsic and intrinsic pathways of the clotting cascade?

A

Extrinsic- PT - prothrombin time (measure of this shows extrinsic and common pathway times)

Intrinsic- APPT- activated partial thromboplastin time (measure of this shows the intrinsic and common pathway times)

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16
Q

What is the first factor in the clotting cascade to be released? What does it do?

A

Tissue factor

Activated factor 7 of the extrinsic pathway

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17
Q

If the extrinsic pathway is activated by tissue factors, how is the intrinsic pathway of the clotting cascade activated?

A

The thrombin produced as a result of the extrinsic and common pathways activates other clotting factors

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18
Q

What is the thrombin burst?

A

It is the massive thrombin production caused by the intrinsic clotting pathway. Resulting from the thrombin produced by the extrinsic pathway feeding back and activating other factors

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19
Q

What is Von Willebrand Factor in the clotting cascade?

A

Involved in platelet adhesion to the vessel wall, platelet aggregation and also carries Factor 8

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20
Q

What is the role of the vessel wall in the clotting process?

A
  • vasoconstriction- reduced blood flow to site of injury which will reduce the amount of haemorrhage
  • production of Von Willebrand Factor
  • exposure of collage and tissue factor in the vessel wall which activates the clotting factors (7 of extrinsic pathway)- causes clotting cascade and platelet adhesion
21
Q

What is fibrinolysis?

A

Is it the process of breaking down a clot

22
Q

What is needed for fibrinolysis?

A

Plasmid from plasminogen

23
Q

What is a D-diner in the clotting process?

A

They are fibrin degradation product, a small protein fragment present in the blood after the blood clot is degraded by fibrinolysis.

These can be measured to look at the levels of plasminogen and plasmin within the blood

24
Q

Name some anticoagulants (3)

A

Protein C
Protein S
Antithrombin

If someone is deficient in one of these than they might have an issue with over clotting

25
Q

What causes bleeding disorders?

A

Due to abnormality in vessel walls, platelet or coagulation factors

They can be inherited or acquired

26
Q

Name some coagulation factor diseases and state whether they are congenital (2) or acquired (2)

A

Haemophilia A (factor 8)- congenital

Haemophilia B/christmas disease (factor 9)- congenital

Liver disease - acquired (because coagulation factors are produced in the liver)

Vitamin K deficiency- acquired (needed for the metabolism of factors)

Anticoagulants including warfarin (inhibits Vit K) - acquired

27
Q

List some of the signs and symptoms caused by coagulation factor disorders (6)

A
  • muscle haematomas
  • recurrent haemarthroses (bleeding into joints)
  • joint pain (arthritis) and deformation (swelling etc)
  • prolonged bleeding post dental extraction
  • life threatening post op and post traumatic bleeding
  • intracerebral haemorrhage
28
Q

How is haemophilia A inherited?

A

X-linked recessive

29
Q

What is haemophilia A?

A

Congenital lack of factor 8 in clotting factor (part of intrinsic- appt pathway)

30
Q

At what time is Haemophilia A often diagnosed?

A

Pre-natally or soon after birth if there is a family history/in infancy if new spontaneous mutation has occurred

31
Q

How is Haemophilai A treated?

A

Recombinant factor 8 or DDAVP (also used for Von Willebramd Disease)

32
Q

What is haemophilia B?

A

Simialr presentation to haemophilia A

Congenital reduction in factor 9

Rarer!

33
Q

What is Von Willebrand disease?

A

Autosomal dominant

Causes abnormal platelet adhesion to vessel walls and reduced amounts/activity of factor 8 (because Von willebrand factor carries factor 8 and mediates platelet adhesion to the endothelium)

Often due to a reduced amount of vwf but can sometime be a qualitative defect as opposed to a quantitative defect

34
Q

What are the symptoms of vWD (von Willebrand disease)?

A
  • skin and mucous membrane bleeding: epistaxis (nose bleeds), gum bleeding and bruising (easy)
  • prolonged bleeding after trauma: heavy periods (menorrhagia), post surgery and post dental extraction

Spontaneous joint or muscle bleeds seen in haemophilia are rare

35
Q

What can arise as a result of vessel wall abnormalities?

A
  • Easy bruising
  • Spontaneous bleeding from small vessels
  • Skin mainly
  • Can be mucous membranes
36
Q

Problems with vessel walls in the clotting cascade can be congenital and acquired, give an example of each

A

Congenital- hereditary haemorrhagic telangiectasia (HHT)- autosomal dominant, dilated microvascular swellings increases with time and GI haemorrhage can lead to iron deficiency anaemia/connective tissue disorders-elhers danlos (easy breaks in vessel walls)

Acquired- senile purpura (very common, vessel walls become weak)/ steroid (easy bruising)/ infection (measles/meningitis-non blanching potecheal rash-due to abnormalities in vessel wall) / scurvy (vit C deficiency- no collagen)

37
Q

What is a low platelet count called?

A

Thrombocytopenia

38
Q

What can a low platelet count (thrombocytopenia) be as a result of?

A

Reduced production (in bone marrow)

increased removal- non-immune destruction/ immune destruction/ splenic pooling (removed by spleen)

39
Q

How can you tell the root of the cause for thrombocytopenia?

A

Do a bone marrow biopsy

If many megakaryocytes are seen it suggests that platelets are being made normalling in the bone marrow but are being removed at an increased rate

40
Q

What are the precursors for platelets?

A

Megakaryocytes (large nucleated cell)

41
Q

What is the most common cause of thrombocytopenia?

A

Immune thrombocytopenia purpura (ITP) - antibodies- immune destruction

42
Q

What is immune thrombocytopenia purpura?

A

Most common cause of thrombocytopenia, antibodies are produced that attack the glycoproteins on platelets cell surface

Usually idiopathic, or secondary to viral infection

Can be secondary to autoimmune diseases eg SLE / lymphoproliferative disorder eg lymphoma, CLL

Treated with immunosuppressions

Causes easy bruising, pitecheal rash, severe mucosal bleeding

Platelets transfusion don’t work because the antibodies attack the new platelets

43
Q

Name some causes of thrombocytopenia that is classed as non immune destruction

A

Mircoangiopathic haemolytic states: TTP, DIC, HUS

Eg cardiopulmonary bypass surgery (platelets consumed)

44
Q

What can cause reduced production of platelets?

A

Deficiency in B12 and folate~ failure of building blocks

Infiltration of bone marrow by cancer cells or fibrosis

Drugs- chemotherapy, antibiotics (including chloramphenicol and co-trimoxazole)

Viruses- HIV (often clinical feature of), infective hepatitis, EBV and CMV

45
Q

What are the consequences of sever thrombocytopenia?

A

No symptoms until platelets <30 (normal 150-400)

  • easy bruising
  • petechiae, purpura
  • mucosal bleeding
  • severe bleeding after trauma
  • intracranial haemorrhage
46
Q

Name some anti-platelet drugs

A

Aspirin/NSAIDS/clopidogrel

All effect platelet function not platelet count

47
Q

What is DIC?

A

Disseminated intravascular coagulation - type of microangiopathic haemolytic anaemia

Lots of coagulation leads to lots of microthrombi which leads to consumption of clotting factors and platelets and a haemolytic anaemia because the red cells are damaged when they pass the thrombi (see fragments of RBCs in a blood smear)

At risk of both bleeding and thrombosis

48
Q

What clotting tests results would you get if someone had DIC?

A

Usually raised PT/INR, raise APTT,
Low fibrinogen,
Raised D dimer/fibrin degradation products

49
Q

What causes DIC?

A
  • Malignancy
  • massive tissue injury-burns
  • infections- usually gram negative sepsis
  • massive haemorrhage and transfusion
  • ABO transfusion reaction
  • obstetric causes- placenta abruption, pre-eclampsia, amniotic fluid embolism

Often need to treat underlying causes rather than the DIC itself

Pathological Processes (Milly's) (21 decks)

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