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Haematology > Bleeding Disorders > Flashcards

Bleeding Disorders Flashcards

1
Q

what is primary haemostasis

A

formation of a platelet plug

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2
Q

what is secondary haemostasis

A

formation of a fibrin clot

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3
Q

failure of what aspects of haemostasis usually cause bleeding disorders

A

primary and secondary haemostasis

problems with fibrinolysis and anticoag defences less likely

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4
Q

what can cause platelet plug formation failure

A

vascular (collagen loss, hereditary, acquired)
platelets:
- reduced number (thrombocytopenia- marrow problem, ITP)
-reduced function (drugs e.g. aspirin, anti-inflammatories)
von willebrand factor (hereditary deficiency)

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5
Q

what is thrombocytopenia

A

reduced platelets

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6
Q

what inheritance is VWF deficiency

A

AD

affects men and women equally

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7
Q

why does collagen loss cause failure of primary haemostasis

A

vessel less efficient, more leaky

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8
Q

what hereditary conditions can cause vascular abnormalities

A

hereditary deficiencies in collagen: marfans, disorders of hyperflexibilty

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9
Q

what are the acquired causes of vascular abnormalities causing failure of primary haemostasis

A

vasculitis: inflammation of vessel, makes it more leaky
e. g. HSP

scurvy (vit c needed to make collagen)

age- senile purpura

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10
Q

what are the features of henoch schonlein purpura

A

seen in children
triggered by viral infection
Antibodies to virus stick to vessel wall and make them leaky
mucosal bleeding- purpura on lower limbs
supportive Tx, usually self limiting, occasionally need transfusion

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11
Q

where is purpura most commonly seen

A

on lower limbs (gravity effect)
can be seen on chest if have cough
fundi on ophthalmoscope
blood blisters in mouth

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12
Q

is hereditary or acquired thombocytopenia more common

A

acquired

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13
Q

what are the causes of acquired thrombocytopenia

A

reduced production:
-marrow problem (viral infection, aplastic anaemia, malignancy (mets or blood), chemo, alcohol) (will also have anaemia and low wbc)

increased destruction (most common cause)

  • usually autoimmune (ITP)
  • coagulopathy (DIC)
  • hyperplenism
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14
Q

what is the normal lifespan of a platelet

A 
7 days 
(in increase peripheral destruction will last couple of hours)
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15
Q

what is seen on blood film in increased peripheral destruction of platelets

A

large platelets (immature forms)

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16
Q

what is usually the Tx for thrombocytopenia caused by increased peripheral destruction

A

(treat cause)
usually self limiting problem
Tx in children is to observe
Tx can involve steroids in adults

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17
Q

what causes DIC

A

(disseminated intravascular coagulation)
trigger (trauma, RTA, sepsis, incompatible transfusion, cancer) that results in tissue damage activates both primary and secondary haemostasis
this uses up clotting factors (prolonged PT and APTT)
blood clots block small blood vessels causing hypoxia which triggers more clots
body recognises this and activated fibrinolysis but this only causes more tissue damage and destroys clotting factors

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18
Q

how does hypersplenism affect platelets

A

caused by e.g. liver disease, cancer
blood cant get into liver due to cirrhosis and spleen engorges
this then increases transit time of blood through spleen, increasing destruction of platelets

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19
Q

what are the causes of platelet functional defects

A

hereditary (VWF def)

acquired

  • drugs; aspirin, NSAIDs
  • renal failure
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20
Q

are NSAIDs antiplatelets or anticoagulants

A

anti platelets

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21
Q

why does renal failure affect platelets function

A

due to build up of urea and in blood

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22
Q

what are the causes of VWF deficiency

A

acquired (autoimmune, antibody to VWF (rare))

hereditary (common, AD, variable severity- generally mild)

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23
Q

what does hereditary VWF def tend to cause

A

primary haemostatic problems: nose bleeds, gum bleeds, menorrhagia, bleeding after surgery/ dental extraction
(all these mucosal bleeds)

24
Q

what is the commonest cause of primary haemostatic failure

A

thrombocytopenia

this is usually acquiredL marrow failure (pancytopenia), peripheral destruction (ITP)

25
Q

what is the treatment for thrombocytopenia

A

transfusion (unless caused by increased peripheral destruction)

26
Q

what is ITP

A

immune thrombocytopneic purpura
autoimmune disorder with increased platelet destruction and reduced prodcution (can be idiopathic or due to another AI condition, viral infections, H. pylori infections, medications and lymphproliferative disorders)
can occur in adults and children

27
Q

what can cause a failure in fibrin clot formation

A

multiple clotting deficiencies (usually acquired e.g. DIC (destroyed), liver failure (not produced))

single clotting factor deficiency (generally hereditary - Heamophilia A and B)

28
Q

what can cause multiple clotting factor deficiencies

A 
liver failure 
vit K deficiency/ warfarin therapy
complex coagulaopathy (DIC)
29
Q

how do you measure liver production

A

albumin

30
Q

what is the role of vit K

A

allow carboxylase to make clotting factors negative so they can stick to +ve platelets

31
Q

WHAT CLOTTING FACTORS ARE MADE WITH VIT K IN EXAMS LEARN THIS

A

2,7,9 and 10

32
Q

what antagonises vit k

A

warfarin

33
Q

what clotting tests are affected in a multiple factor deficiency

A

both PT and APTT increased

34
Q

where are all coagluation factors synthesised

A

in hepatocytes (reduced in liver failure)

35
Q

what clotting factors are carboxylated by vit K IN EXAMS

A

2,7,9,10

36
Q

what are the sources of vit K

A 
diet 
intestinal synthesis (made by bacterial in bowl)
37
Q

where is vit K absorbed and what is needed

A

in upper intestine

need bile salts to absorb it

38
Q

why do babies get haemorrhagic disease of the new born

A

as deficient in vit k- none in breast milk and very little bowel bacterial to make any

39
Q

what are all babies given at birth

A

vit k injection

40
Q

what can cause decreased vit k absorption

A 
bowel disease 
obstructive jaundice (gallstones)
41
Q

what are the causes of vit k deficiency

A 
poor diet 
malabsorption 
obstructive jaundice 
vit K antagonists (warfarin) 
haemorrhagic disease of the new born
42
Q

what are the dietary sources of vit K

A

leafy green veg

43
Q

what causes the clinical features of DIC

A

excessive and inappropriate activation of haemostasis (primary, secondary and fibrinolysis)

microvascular thrombus formation = end organ failure

clotting factor and platelet consumption= bruising, purpura and generalised bleeding

44
Q

what are the screening tests for fibrin clot formation

A

if CF deficiency (multiple- DIC, liver disease, warfarin) then PT and APTT will both be affected

fibrin degredation products (e.g. D-dimers)

45
Q

what clotting factors are affected by warfarin

A

2,7,9 and 10

46
Q

which clotting test is most sensitive

A

PT and measures CF & which has the shortest half life

47
Q

what can cause DIC

A

sepsis (tissue damage due to infection or later shock)
obstetric emergencies (placenta v rich in phospholipid and tissue factor, things like abruption can cause placenta to die causing coagulation)
cancer
hypovolaemic shock

48
Q

what is the treatment of DIC

A

treat underlying cause (sepsis 6, fluids)
replacement therapy:
-platelet transfusions
-plasma transfusions (TTP to replace clotting factors)
-fibrinogen replacement (cryoprecipitate)

49
Q

what is haemophilia

A

X linked hereditary disorder that causes loss of amplification (CF 8 and 9) process in haemostasis
abnormally prolonged bleeding recurs episodically at one/ few sites on each occasions

50
Q

does haemophilia affect males or females

A

males (females can be carriers)

51
Q

what are the types of haemophilia

A

A- factor 8 deficiency (most common)

B- factor 9 deficiency

52
Q

how does haemophilia present

A

no abnormality of primary haemostasis (fine with small cuts)
mucosal bleeding less common
bleeding will be from medium to large vessels
get target joints- bleeding into ankle, knee and elbow joints causes synovitis which then causes neovascularisation in synovium which are friable and also bleed

53
Q

what are the severities of haemophilia

A

mild (>5% CF, only issues after trauma)
mod 2-5% CF
severe <2% CF

54
Q

what screening tests for haemophilias

A

APTT will be affected (v prolonged)

looks at CF 8 and 9

55
Q

what are the clinical features of haemophilia

A

recurrent haemarthoses
recurrent soft tissue bleeds (bruising in toddlers)
prolonged bleeding after dental extractions/ invasive procedures
(usually FHx, 1/3rd new mutation)

56
Q

what Tx for haemophilia

A

prophylactic CF injections every 2nd day

may need joint replacements

Haematology (27 decks)

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