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PATH 402 > Disorders of Primary Haemostasis > Flashcards

Disorders of Primary Haemostasis Flashcards

1
Q

What is the source of platelets?

A

Megakaryocyte

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2
Q

What are the characteristics of platelets?

A
  1. platelet count → 1.5 - 4x10^(11)/L
  2. New platelets are larger and have a higher density than old platelets
  3. Circulation life span is 7-12 days
  4. Platelet survival is determine by peripheral platelet count of radiaoactively labelled platelets
  5. Removal of platelets is mainly by spleen > liver > BM = lymph nodes
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3
Q

What do the alpha granules of the platelet contain?

A

Coagulation proteins
1. Clotting factor V
2. Protein S
3. Plasminogen activatior inhibitor (PAI)
4. Series of adhesive plasma proteins: fibrinogen, fibronectin, VWF, vitronectin and thrombospondin

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4
Q

What do the delta granules of the platelet contain?

A
  1. Serotonin
  2. ADP
  3. ATP
  4. Phosphate
  5. Calcium
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5
Q

What is the difference between the shapes of a resting platelet vs an activated platelet?

A

Restign platelets are smooth and disc shaped, activated platelets have an irregular shape with many protruding pseudopodia

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6
Q

What is the function of platelet receptors?

A
  1. Hemostasis
  2. Inflammation
  3. Antimicrobial host defense
  4. Tumor growth
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7
Q

What are some examples of platelet receptors?

A
  1. Integrins
  2. Thrombin receptor
  3. ADP receptor
  4. Prostaglandin receptor
  5. Lipid and chemokine receptor
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8
Q

What are the receptors for collagen?

A

GPIa-IIa
GPIIb-IIIa
GPIV

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9
Q

What are the receptors for vWF?

A

GPIb-IX-V
GPIIb-IIIa

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10
Q

What are the receptors for fibrinogen?

A

GPIIb-IIIa

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11
Q

What are the receptors for fibronectin?

A

GPIc-IIa
GPIIb-IIIa

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12
Q

What are the receptors for thrombospondin?

A

Vitronectin receptor
GPIV

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13
Q

What happens after a signal on GPIb-IX-V?

A

Signal on GPIb-IX
- Transferred to the cytoplasm
- Activates GPIIb-IIIa
- Fibrinogen binding

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14
Q

What does fibrinogen depend on?

A

Calcium

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15
Q

What is atherothrombosis?

A

Characterized by sudden atherosclerotic plaque disruption (rupture/erosion) leading to platelet activation and thrombus formation.

Plaque rupture -> embolization -> microvascular obstruction

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16
Q

What is the link between thrombosis and inflammation?

A

Platelets modulate leukocyte adhesion at sites of inflammation by
1. Inducing a pro-inflammatory, pro-adhesive state in endothelial cells and leukocytes
2. Providing a bridge between the endothelium and leukocytes

17
Q

What is are examples of acquired causes of platelet function defects?

A
  1. Uremia
  2. Myeloproliferative disorder
  3. Acute leukemia
  4. Antiplatelet Ab
  5. Liver disease
18
Q

What are examples of inherited causes of platelet function defects?

A
  1. Platelet adhesion (BSS)
  2. Agonist receptors
  3. Signaling pathways
  4. Secretion
  5. Aggregation (Glanzmann)
  6. Platelet-coagulant protein interaction
19
Q

What are the causes of thrombocytopenia? (EXAM)

A
  1. Reduced production
  2. Increased removal
20
Q

What are the disorders of platelet secretion?

A
  1. Alpha granule storage disease (Gray Platelet Syndrome)
    - rare congenital bleeding disorder caused by a reduction/absence of the platelet a-granules in blood platelets or of the proteins contained in these granules
    - under microscopic analysis standard stain, no a-granules in platelets
  2. Hermansky Pudlak syndrome
    - dense granule deficiency in platelets
    - decreased aggregation and secretion with multiple agonists
    - defective pigmentation (albinism)
21
Q

What is the treatment for Hermansky Pudlak syndrome?

A
  • no cure, treatment for chronic hemorrhages only
  • therapy with vit E and antidiretic Demopressin
  • lifelong UV protection
  • avoid anticoagulants like aspirin
22
Q

What are the different quantitative platelet disorders?

A
  1. Idiopathic Thrombocytopenic Purpura (ITP)
  2. Disseminated Intravascualar Coagulation (DIC)
  3. Thrombotic Thrombocytopenic Purpura (TTP)
  4. Hemolytic Uremic Syndrome (HUS)
23
Q

What is idiopathic thrombocytopenic purpura and what causes it?

A

Autoimmune disease where blood doesn’t clot normally and is caused by Ab against platelets

24
Q

What is Disseminated Intravascualar Coagulation (DIC) triggered by? What are the clinical manifestations?

A
  • triggered by inflammation, infection or cancer
  • blood clots throughout body blocks small BV
  • low platelet count, low fibrinogen level, high D-dimers (FGB degradation products)
  • prolonged aPTT and PT
25
Q

What is Thrombotic Thrombocytopenic Purpura (TTP) caused by? What is the pathophysiology? What is the treatment?

A

Caused by infections such as HIV

  • extensive microscopic clots which can cause kidney, heart and brain damage
  • lack of ADAMTS13 enzyme leads to OVERACTIVE BLOOD CLOTTING

Treatment:
- plasma transfusion to replace ADAMTS13
- NO PLATELET TRANSFUSION

26
Q

What is Hemolytic Uremic Syndrome (HUS) caused by? What is the pathophysiology? clinical manifestations? What is the treatment?

A

Caused by infection such as E.coli species tht produces toxic substances (Shiga toxin)

acute kidney failure due to damage to the very small blood vessels of the kidney → destruction of RBC

Low RBC count (anemia), Low platelet count (thrombocytopenia)

Treatment: RBC & PLT transfusion

27
Q

What are drugs that affect platelet function?

A
  1. Clopidogrel (ADP receptor agonist)
    - Leads to an irreversible blockage of the ADP receptor on the platelet membrane
  2. Aspirin (cyclooxygenase inhibitor)
    - Anti-clotting effect and is used long term
    - low doses to prevent MI, strokes, and blood clot
    - low doses may be given immediately after MI to reduce the risk of another MI or death of cardiac tissue
  3. Eptifibatide (GPII/III antagonist)
    - antiplatelet drug tht selectivelyblocks the platelet GP-IIbIIIa receptor

PATH 402 (7 decks)

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