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Year 2 > Platelets + Disorders > Flashcards

Platelets + Disorders Flashcards

1
Q

How are platelets formed

A

Formed by fragmentation of megakaryocytic cytoplasm in bone marrow

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2
Q

Advantage of platelets having a disc shape

A

Allows them to flow close to the endothelium

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3
Q

Lifespan of platelets

A

7-10 days

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4
Q

How are platelets broken down

A

Phagocytksed by splenic macrophages in red pulp

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5
Q

Where is thrombopoietin produced

A

Liver

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6
Q

How does liver damage effect platelets

A

Reduced thrombopoietin = decreased platelets

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7
Q

Compensatory mechanism for decreased TPO

A

More TPO able to bind to MK = increased platelet production

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8
Q

What precursor molecule is Thromboxane A2 made from

A

Arachidonic acid via COX-1

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9
Q

Role of Thromboxane A2

A

Induces platelet aggregation + vasoconstriction

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10
Q

What molecule activates P2Y12

A

ADP

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11
Q

Role of P2Y12

A

Amplifies activation of platelets + helps activate glycoprotein IIb/IIIa

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12
Q

Role of IIb/IIIa

A

Receptor for fibrinogen and vWF

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13
Q

What is vWF

A

clotting factor needed for platelets to adhere to damaged blood vessels

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14
Q

Role of IIb/IIIa

A

Aids platelet adherence and aggregation

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15
Q

What is vWF disease

A

reduced vWF activity = platelets are unable to bind to damaged blood vessels resulting in platelet dysfunction + muco-cutaneous bleeding

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16
Q

What is thrombocytopenia

A

Deficiency of platelets in th blood

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17
Q

What is congenital thrombocytopenia

A
  1. Malfunctioning megakaryocytes in bone marrow
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18
Q

What causes thrombocytopenia

A
  1. Infiltration of bone marrow (leukaemia, metastatic malignancy, lymphoma, myeloma, myelofibrosis)
  2. Reduced platelet production by bone marrow
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19
Q

What can result in reduced platelet production by bone marrow = thrombcytopenia

A
  1. Low B12/folate
  2. Reduced TPO
  3. Medication
  4. Toxins
  5. Infections
  6. Aplastic anaemia
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20
Q

What medication causes thrombocytopenia

A
  1. Methotrexate

2. Chemotherapy

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21
Q

4 ways increased DESTRUCTION of platelets = thrombocytopenia

A
  1. Autoimmune (ITP)
  2. Hypersplenism (portal hypertension + splenomegaly)
    Drug-related immune destruction (heparin induced thrombocytopenia)
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22
Q

What disorders cause consumption of platelets

A
  1. DIC

2. TTP

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23
Q

How is ITP caused

A

Immune destruction by platelets

Antibody-coated platelets are removed following binding to Fc receptors on macrophages

IgG antibodies form to platelets and megakaryocytes

24
Q

Where is primary ITP more common

25
Q

What age group does ITP mainly cause

26
Q

Onset of ITP

A

Acute with much-cutaneous bleeding + history or recent viral infection (inc. chickenpox or measles)

Self-limiting Purport (red spots on skin due to bleeding underneath)

27
Q

Is life-threatening haemorrhage common in ITP

28
Q

When does Secondary ITP occur (chronic)

29
Q

Gender does 2ndary ITP occur

30
Q

What autoimmune conditions is Secondary ITP associated with

A
  1. SLE
  2. Thyroid disease
  3. Autoimmune haemolytic anaemia
  4. CLL
31
Q

Clinical presentation of ITP

A
  1. Easy bruising
  2. Epistaxis
  3. Menorrhagia
  4. Purpura
  5. Gum bleeding
  6. Major haemorrhage is rare
  7. Splenomegaly is rare
32
Q

How is ITP diagnosed

A
  1. Bone marrow examination (increased megakaryocytes in marrow - thrombocytopenia)
  2. Platlet autoantibodies (not used for final diagnosis)
33
Q

How is secondary ITP treated

A
  1. Corticosteroids

2. IV immunoglobulin (IgG)

34
Q

Name a corticosteroid used to treat ITP

A

PREDNISOLONE

35
Q

Why is IV IgG given

A

Raises platelet count more rapidly than steroids

36
Q

Second line treatment for ITp

A

Splenectomy

If splenectomy fails - immunosuppression

37
Q

What immunosuppression is given to ITP

A

ORAL AZATHIOPRINE

38
Q

How is TTP (Thrombotic Thrombocytopenia Purport caused)

A

Widespread adhesion + aggregation of platelets leads to microvascular thrombosis + consumption of platelets = profound thrombocytopenia

Reduction in ADAMTS-13 (attacked by immune system)

Large multimers of vWF form resulting in platelets aggregation + fibrin deposition in small vessels = micro thrombi

39
Q

Role of ADAMTS-13

A

Degradation of vWF

40
Q

Causes of TTp

A

1, Idiopathic

  1. Autoimmune
  2. Cancer
  3. Pregnancy
  4. Drug-associated
41
Q

Clinical presentation of TTP

A
  1. Purpura
  2. Fever
  3. Fluctuating cerebral dysfunction
  4. Haemolytic anaemia with red cell fragmentation accompanied by acute kidney injury
42
Q

How is TTP treated

A

Plasma exchange to remove antibody to ADAMTS-13 as well as provide a source of ADAMTS-13

  1. IV METHYLPREDNISOLONE
  2. V RITUXIMAB
43
Q

Does DIC occur in isolation

44
Q

Why does DIC arise

A

Systemic activation of coagulation either by release of procoagulant material (e.g. tissue factor) or via cytokine pathways as part of the inflammatory response

Activation leads to widespread generation of fibrin and depositing in blood vessels = thrombosis + multi organ failure)

Also increases consumption of platelets + clotting factors and increased risk of bleeding

45
Q

Causes of DIC

A
  1. Massive activation of coagulation cascade
  2. Initiating factors (extensive damage to vascular endothelium thereby exposing tissue factor + enhance expression of tissue factor by monocytes in response to cytokines)
  3. Sepsis
  4. Major trauma + tissue destruction
  5. Advanced cancer
  6. Obstetric complications
46
Q

Clinical presentation of DIC

A
  1. Patient is acutely ill

2. Bleeding occurs from mouth, nose and venipuncture sites + widespread ecchymoses

47
Q

What is ecchymoses

A

Discolouration of skin due to bleeding caused by bruising

Confusion

Bruising

Thrombotic events

48
Q

Why does thrombotic events occur in DIC

A
  1. Vessel occlusion by fibrin and platelets - any organ may be involved but skin, brian and kidneys are most affected
49
Q

How is DIC diagnosed

A
  1. Severe thrombocytopenia
  2. Diagnosis can be suggested from history
  3. Decreased fibrinogen
  4. Elevated FDPs (fibrin degradation products) - D-dimer
  5. PT, APTT, TT
50
Q

What would blood films show in DIC

A

Fragmented RBCs

51
Q

How is DIC treated

A

Treat underlying condition
Replace platlets via transfusion
FFP (fresh frozen plasma) to replace coagulation factors
Cryoprecipitate to replace fibrinogen + some coagulation factors
Red cell transfusion in patients who are bleeding

52
Q

How does Heparin induce thrombocytopenia

A
  1. Heparin binds to a protein in th blood called PF4 (platelet factor IV) - forming Factor IV/Heparin

IgG binds to this complex forming IgG/PF4/Heparin which binds and activates platelets

Platelet consumption = thrombocytopenia/necoriss/thrombosis

53
Q

Who are most at risk of heparin-induced thrombocytopenia

A

Cardiac Bypass surgery + unfractioned heparin treatment

54
Q

How is Heprain-indcued thrombocytopenia diagnosed

A

Seen as a SHARP fall in platelets 5-19 days after Heparin treatment

55
Q

How is Heparin-Induced thrombi treated

A

Immediatelyy stop heparin + start alternative anticoagulants

NEVER RE-EXPOSE to heparin

Year 2 (155 decks)

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