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NMF: Haematology > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is primary haemostasis?

A
  1. endothelial damage
  2. platelets adhere
  3. platelets aggregate
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2
Q

What allows platelet adhesion?

A

Exposed collagen and Von Willebrand factor

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3
Q

What allows platelets to aggregate?

A

Activated platelets release granules (containing ADP, thrombin and thromboxane A2) that activate coagulation and recruit other platelets

These other platelets aggregate via membrane glycoproteins

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4
Q

Causes of failed primary haemostasis

A
  1. problem with platelets: thrombocytopenia or reduced function
  2. vascular causes
  3. problems with VWF
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5
Q

What is secondary haemostasis?

A

a coagulation cascade involving clotting factors to strengthen the platelet clot with a fibrin mesh

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6
Q

How do healthy cells prevent adhesion of platelets?

A

they secrete nitric oxide and prostaglandins

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7
Q

Describe initiation of secondary haemostasis

A

Breakage of the endothelium exposes tissue factor which forms a complex with factor VIIa. This complex catalyses the formation of Xa and IXa and forms a small amount of thrombin. Thrombin then activates factors V and VIII.

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8
Q

Describe amplification of secondary haemostasis

A

With factors VIII and IXa now activated, they form a complex which amplifies the cascade by activating factor Xa

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9
Q

Describe propagation of secondary haemostasis

A

Factors V and Xa form a complex which activates prothrombin to thrombin. Thrombin cleaves fibrinogen into soluble fibrin monomers.

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10
Q

What does thrombin do other than cleave fibrin?

A

activate platelets

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11
Q

natural anticoagulants

A

protein C is converted to activated protein C by a thrombin-thrombomodulin complex located on the surface of endothelial cells.

Activated protein C in association with its cofactor protein S cleaves and inactivates the cofactors FV and FVIII.

The primary target of the anticoagulant protein antithrombin is thrombin, although it can also inactivate other coagulation proteases in the cascade, including FIXa, FXa, FXIa, and FXIIa.

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12
Q

How is fibrin broken down into FDPs?

A

tissue plasminogen activator (tPA) cleaves plasminogen into plasmin which breaks down fibrin

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13
Q

VWF is involved in primary haemostasis. So how does it cause a prolonged APTT when VWF is deficient?

A

VWF carries factor 8 so it causes indirect deficiency

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14
Q

is warfarin immediately anti-coagulant?

A

no initially it is pro-thrombotic due to its action on protein C and S

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15
Q

What effect does heparin enhance?

A

unfractioned: potentiates anti-thrombin

LMWH: anti-thrombin binds to factor 10

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16
Q

Give some vascular causes of failed primary haemostasis

A

age, steroids, henoch-schonlein, scurvy, inherited collagen disorders

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17
Q

What is henoch schonlein purpura?

A

an autoimmune vasculitis seen in children after a viral infection where there are IgA deposits on blood vessels

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18
Q

How does henoch schonlein purpura present?

A

rash (legs)
abdominal pain
arthritis/arthralgia
glomerulonephritis.

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19
Q

What causes thrombocytopenia?

A

reduced production when there is a bone marrow problem

increased destruction in DIC, ITP and hypersplenism (eg liver disease)

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20
Q

What is immune thrombocytopenic purpura (ITP)?

A

autoimmune condition of unknown cause that presents as a purpuric rash and increased tendency to bleed.

seen acutely in children (after virus) and chronically in adults

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21
Q

What factors will reduce platelet function?

A

drugs like aspirin and NSAIDS

renal failure

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22
Q

Is VwF deficiency usually acquired or inherited?

A

inherited

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23
Q

What is Von Willebrand disease?

A

an AD condition that results in low levels of VwF. Generally mild ie. menorrhagia, epistaxis…

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24
Q

Are single or multiple clotting factor deficiencies usually acquired?

A

single = inherited

multiple = aquired

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25
Q

What are the causes of multiple clotting factor deficiency?

A

complex coagulopathy eg DIC
liver disease
vitamin K deficiency

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26
Q

What is disseminated intravascular coagulation (DIC)?

A

Excessive and inappropriate activation of the haemostatic system when you have had massive tissue damage with loads of tissue factor produced activating clotting factors. This means thrombus form and get stuck in small vessels causing organ failure

27
Q

When do you see DIC?

A 
crush injuries
RTA
ABO mismatch
end-organ failure in sepsis
obstetric emergency
malignancy
hypovolaemic shop
28
Q

Why does liver disease affect secondary haemostasis?

A

all the clotting factors are produced in the liver

29
Q

Which clotting factors require vitamin K for carboxylation?

A

2 7 9 and 10

30
Q

Give 2 sources of vitamin K

A

green leafy veg

gut flora

31
Q

Causes of vitamin K deficiency

A
  • poor dietary intake
  • malabsorption in small intestine (eg. Crohns)
  • obstructive jaundice stopping bile salts
  • HDN
  • warfarin therapy
32
Q

What is haemophilia?

A

An x-linked condition characterized by problems with blood clotting due to deficiency in either coagulation factor VIII (haemophilia A which is 5x more common) or factor IX (haemophilia B).

33
Q

Where does haemophilia affect?

A

joints (knee and ankle) and muscles (quad)

34
Q

What is a target joint?

A

bleeding into joints means iron sitting in the joint irritates the synovium and stimulates neovascularisation. These fragile vessels are more likely to bleed again.

35
Q

How would haemophilia present in a coagulation screen?

A

APTT would be prolonged with normal PT as it affects the intrinsic pathway.

36
Q

If both APTT and PT are prolonged what is the problem?

A

multiple clotting factor deficiency

then check d-dimers (high in DIC, not in liver disease)

37
Q

What is the problem is only the prothrombin time is abnormal?

A

factor 7 deficiency due to liver disease (rare to be inherited)

38
Q

What is a venous thrombosis?

A

a fibrin-rich clot in a low pressure system that occurs due to the coagulation cascade

39
Q

What is the MOA of heparin?

A

has an immediate effect

unfractioned: potentiates antithrombin (monitor with APTT)

LMW: affects factor Xa

40
Q

What increases the risk of venous thromboses?

A

Virchow’s triad: stasis, hypercoagulability and vessel wall (valve)

41
Q

What is the MOA of warfarin?

A

Vitamin K antagonist

- blocks the ability of vitamin K to carboxylate the dependent clotting factors and reducing their coagulant activity.

42
Q

Name an

a) oral direct thrombin inhibitor
b) oral Xa inhibitor

A

a) dabigatran

b) rivaroxaban

43
Q

What is an arterial thromboses?

A

a platelet-rich clot in a high-pressure system triggered by epithelial rupture due to atherosclerosis

44
Q

What is the MOA of aspirin?

A

inhibits cyclo-oxygenase which is necessary to produce thromboxane A2 (platelet agonist).

45
Q

What are some side-effects of aspirin?

A

bleeding, block prostaglandin production, GI ulceration, bronchospasm

46
Q

What is the MOA of clopidogrel?

A

ADP receptor antagonists

47
Q

What is the MOA of dypridamole?

A

phosphodiesterase inhibitor so reduces cAMP (activates platelets)

48
Q

How long do anti-platelets need to be stopped before elective operations?

A

7 days prior

49
Q

What is microangiopathic haemolytic anaemia (MAHA)?

A

a group of diseases that cause damage to small blood vessels resulting in intravascular haemolysis. red cell fragments are seen on blood film

50
Q

Causes of MAHA

A

DIC, TTP, HELLP syndrome, APS, malignancy, cardiac valve, lupus, paroxysmal nocturnal haematuria

51
Q

What is paroxysmal noctural haemoglobinuria?

A

an acquired disease where there is a defect on the surface of red blood cells (because one stem cell develops a mutation) and the blood cells are destroyed by the complement system

52
Q

Which test differentiates immune from acquired haemolytic anaemia?

A

coomb’s (direct antibody)

53
Q

Which NOAC is used in patients with impaired renal function?

A

apixaban

54
Q

When do you need to monitor LMWH?

A

pregnancy and renal impairment

55
Q

How do you monitor

a) unfractioned heparin?
b) LMWH?
c) warfarin?

A

a) APTT
b) anti-Xa assay
c) INR

56
Q

Do NOACs need to be monitored?

A

no

57
Q

A 17 year old woman presents to the emergency department with a 2 day history of diarrhoea. On examination, she looks unwell and has purpura. Her full blood count shows haemaglobin 9.8g/dL (normal range 12-16.0), white cell count 14.4x109/L (normal range 4-11.0), platelet 46x109/L (normal range 150-400), and her creatinine is 587umol/L (normal range 44-80). A blood film shows marked red blood cell fragmentation and polychromasia.

A

Haemolytic uraemic syndrome due to e. coli 0157

58
Q

Warfarin treatment for a
a) patient with one DVT
b) patient with +1 DVT
should last how long? with what target?

A

a) 3 months, INR at 2.5

b) life-long, INR at 3.5

59
Q

What happens to platelet count in DIC?

A

it is low

60
Q

A woman is known to carry a mutation in the factor VIII gene that causes X-linked haemophilia. She has experienced haemorrhage following surgery. Why?

A

normal X inactivation

50% of the patients liver cells will have the mutant X chromosome as the only active one. She has, therefore reduced capacity for making factor VIII.

61
Q

When can blood transfusion be given?

A

when Hb is less than 8

62
Q

Does warfarin or heparin act on the intrinsic pathway?

A

heparin

lowers APTT

63
Q

Will heparin or warfarin cause prolonged PT?

A

warfarin

NMF: Haematology (8 decks)

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