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Haematology > Platelets > Flashcards

Platelets Flashcards

1
Q

how are platelets formed?

A

produced in the bone marrow from fragments of megakaryocytes

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2
Q

What regulates platelet production?

A

thrombopoietin produced by the liver

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3
Q

what is the lifespan of a platelet?

A

7-10 days

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4
Q

what organ removes platelets from the blood?

A

the spleen

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5
Q

name some surface proteins on platelets

A

ABO
HPA
HLA Class I (not class II)
Glycoproteins e.g. GP1a

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6
Q

how are platelets activated?

A

a) Adhesion to collagen via GPIa

b) Adhesion to vWF via GPIb and IIb/IIIa

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7
Q

what does activation of platelets lead to?

A

release of substances from alpha and dense granules

membrane phospholipids activate clotting factors

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8
Q

what substance cross-links activated platelets?

A

fibrin

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9
Q

what substances can bind to the activated platelet surface and what does this lead to?

A

coagulation factors - this enhances the clotting cascade

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10
Q

Name some substances released by platelet granules

A 
ADP
thrombin
calcium
PDGF
fibrinogen
vWF
PF4
serotonin
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11
Q

How can we investigate platelet problems?

A

a) number- FBC
b) appearance - blood film
c) function: bleeding time and PFA - platelet function analyser
d) surface proteins- flow cytometry

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12
Q

what are the clinical features of platelet dysfunction?

A

a) mucosal bleeding eg epistaxis, gum bleeding and menorrhagia
b) easy bruising
c) petechiae, purpura
d) traumatic haematomas eg subdural haematoma

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13
Q

What are the categories of causes of low platelet count?

A

production failure
increased removal
(artifact)

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14
Q

What are the causes of low platelet production?

A

congenital

acquired: Drugs, Marrow suppression, Marrow failure, Marrow replacement

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15
Q

What are the causes of increased removal of platelets?

A

immune
consumption
splenomegaly

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16
Q

what are the causes of impaired platelet FUNCTION?

A

congenital: storage pool disorders, Glanzmann, Bernard Soulier, von Willebrand disease
acquired: uraemia, drugs

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17
Q

What are the causes of thrombocytopenia that are due to decreased production of platelets?

A
  1. congenital thrombocytopenia
  2. infiltration of the bone marrow
  3. reduced platelet production by the bone marrow
  4. dysfunctional production of platelets in the bone marrow
18
Q

What happens in congenital thrombocytopenia?

A

absent/ reduced or malfunctioning megakaryocytes in BM

19
Q

Give examples of conditions where there is an infiltration of the BM

A 
leukaemia 
metastatic malignancy 
lymphoma 
myeloma
myelofibrosis
20
Q

What are some reasons why the BM would produce less platelets apart from infiltration?

A 
Low B12 / folate
Reduced TPO (e.g. liver disease)
Medication: Methotrexate, chemotherapy 
Toxins: e.g. Alcohol
Infections: e.g. viral (e.g. HIV) TB 
Aplastic anaemia (auto immune)
21
Q

What are the causes of thrombocytopenia due to increased destruction of platelets?

A 
autoimmune - immune thrombocytopenic purpura 
post transfusion purpura
sequestration
massive transfusion
hypersplenism 
drug-related immune destruction
DIC
thrombotic thrombocytopenic purpura 
HUS 
haemolysis with elevated liver enzymes and low platelets - HELLP
major haemorrhage
22
Q

Name an autoimmune condition that results in thrombocytopenia due to increased destruction of platelets

A

immune thrombocytopenia

ITP

23
Q

Name some targets of medication in the platelet

A

P2Y12
Gp IIbIIIa
COX1

24
Q

If a pt presents with easy bruising after a viral infection, what is the most likely diagnosis and by what mechanism does the platelet count decrease?

A

immune thrombocytopenia - increased destruction

25
Q

What is the pathophysiology of immune thrombocytopenia?

A

IgG antibodies form to platelet and megakaryocyte surface glycoproteins
these opsonised platelets are removed by the RES

26
Q

What are the triggers for primary immune thrombocytopenia?

A

following viral infection

following immunisation

27
Q

What are the secondary causes of immune thrombocytopenia?

A

malignancy eg CLL

infections HIV, Hep C

28
Q

What are the treatments available for immune thrombocytopenia?

A
  1. immunosuppression eg steroids
  2. IV immunoglobulin
  3. treat the underlying cause
  4. if bleeding, give platelets
  5. Tranexamic acid - inhibits the breakdown of fibrin
29
Q

What is done to investigate immune thrombocytopenia?

A

try and find an underlying cause

30
Q

If a 3 year old presents with easy bruising and gum bleeding, with low platelets and small cervical lymph nodes palpable with a widened mediastinum on X-ray, what is the likely diagnosis?

A

ALL - acute lymphoblastic leukaemmia

31
Q

Why does ALL cause thrombocytopenia?

A

due to bone marrow infiltration

32
Q

If a diabetic has gram negative sepsis and low platelets with very raised CRP, raised WBCs, raised PT, low fibrin and the blood film shows toxic neutrophils, what is the diagnosis? Why is the platelet count reduced?

A

DIC - due to increased consumption of platelets

33
Q

What is the pathophysiology of DIC?

A

production of cytokines in SIRS causes systemic activation of the clotting cascade, consumption of platelets and clotting factors, causing bleeding but also microvascular thrombosis which causes organ failure

34
Q

What are the investigations done for DIC?

A 
blood test to check for: 
thrombocytopenia
prolonged PT and APTT
low fibrinogen 
high D dimers

evidence for organ failure
find out what the underlying cause is

35
Q

What conditions can cause SIRS?

A 
sepsis 
malignancy 
obstetric emergency
pancreatitis 
trauma
36
Q

What are the treatments for DIC?

A

a) platelets
b) fresh frozen plasma - which contain clotting factors
d) cryoprecipitate - which contains fibrinogen and some clotting factors
e) treat the underlying cause

37
Q

What platelet condition does a pt who has fever, dysarthria and left sided weakness have?
They are found to have an infarct in the MCA - middle cerebral artery. What is the mechanism whereby the platelet count reduces?

A

Thrombotic thrombocytopenic purpura

increased consumption of platelets

38
Q

what is the pathophysiology of TTP?

A

antibodies are produced against ADAMTS13 which is a metalloprotease that is responsible for cleaving large multimers of vWF into smaller units. This means there is an increase in circulating multimers of vWF, which increases platelet adhesion to areas ofendothelialinjury. This means small thrombi form, decreasing the overall number of circulating platelets
this increases the risk of life-threatening bleeds

red blood cells passing the microscopic clots are damaged and form schistocytes (like shredding the RBCs)

39
Q

What are the treatments of TTP?

A

urgent plasma exchange to replace ADAMTS 13 and remove Ab produced by the body
immunosuppression to reduce the Ab level - methylprednisolone

40
Q

What should you NOT give to sb with TTP?

A

platelets

41
Q

what is the function of platelets?

A

primary haemostasis

Haematology (9 decks)

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