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Pathoma > Chapter 4 - Hemostatsis and Related Disorders > Flashcards

Chapter 4 - Hemostatsis and Related Disorders Flashcards

1
Q

What 2 important substances come from Weibel-Palade Bodies?

A
  1. P-Selectin
  2. von Willebrand’s Factor
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2
Q

What is Primary Hemostasis?

A

Platelet Plug Formation

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3
Q

What is Secondary Hemostatis?

A

Stabilization of the Platelet Plug

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4
Q

What are the 4 steps of Primary Hemostasis?

A
  1. Vasoconstriction
  2. Platelet Adhesion
  3. Platelet Degranulation
  4. Platelet Aggregation
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5
Q

What is the mechanism of Vasoconstrition in Primary Hemostasis?

A
  1. Neural Stimulation

2. Endothelin Release (from endothelial cells)

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6
Q

What is the mechanism of Platelet Adhesion?

A
  1. Von Willebrand Factor (vWF) binds exposed subendothelial collagen
  2. Platelets bind vWF via the GP1b receptor
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7
Q

Where is vWF found?

A
  1. Weible-Palade Bodeis
  2. α-granules of platelets
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8
Q

What causes platelet degranulation?

A

the shape change induced by Adhesion

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9
Q

What 2 things are released upon platelet degranulation?

A

ADP

(promotes exposure of GPIIb/IIa receptor on platelets)

TXA2

(promotes platelet aggregation)

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10
Q

Where is TXA2 synthesized?

A

In Platelets by COX

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11
Q

What is the mehanism of Platelet aggregation?

A

the link to fibrinogen using GPIIb/IIa

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12
Q

What are the 2 main clinical features of disorders of Primary Hemostasis?

A

Mucosal Bleeding

Skin Bleeding

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13
Q

Order the folling from smallest to largest:

Eccyumoses

Petechiae

Purpura

A

Petechiae = 1-2 mm

3 mm < Pupura < 1 cm

1 cm < Ecchymoses

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14
Q

What 4 tests would be used to diagnose a disorder of Primary Hemostasis?

A
  1. Platelet count
  2. Bleeding Time
  3. Blood Smear
  4. Bone Marrow Biopsy
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15
Q

Is bleeding time prolonged with quantitative or qualititaive platelet disorders?

A

Both

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16
Q

What does a blood smear assess?

A

Platelet Count

Platelet Size

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17
Q

What does a bone marrow biopsy assess (in relation to platelet disorders)?

A

Megakaryocytes

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18
Q

What is the most common cause of thrombocytopenia in children and adults?

A

Immune Thrombocytopenic Purpura

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19
Q

What is Immune Thrombocytopenic Purpura (ITP)?

A

Autoimmune production of IgG against paltelet antigens (e.g. GPIIb/IIa)

20
Q

In ITP, what happens to the Platelets bound by IgG?

A

consumed by Splenic Macrophages

21
Q

What is the demographic of Acute ITP and how long does it last?

A

Children (who have recently had a viral infection or an immunization)

Lasts for a few weeks

22
Q

What is the demographic of Chronic ITP?

A

Women of Childbearing age

(IgG can cross placenta to cause short-lived thrombocytopenia in fetus)

It can be primary or secondary

23
Q

What are the 3 main lab findings for ITP?

A

↓ Platelet Count

Normal PT/PTT

↑ Megakaryocytes

24
Q

what are the 3 treatments for ITP?

A
  1. Corticosteroids (works better for children
  2. IVIG (Intravenous IgG)
  3. Splenectomy (removes the source of the antibodies and the site of platelet destruction)
25
Q

What is Microangiopathic Hemolytic Anemia?

A

the pathologic formation of Platelet Microthrombi in small vessels

26
Q

What are Schistocytes?

A

RBCs that are “sheared” as they cross the microthrombi

27
Q

What are two disorders where Microangiopathic Hemolytic Anemia is found?

A
  1. Thrombotic Thrombocytopenic Purpura (TTP)
  2. Hemolytic Uremic Syndrome (HUS)
28
Q

What is the cause of TTP?

A

Decreased ADAMTS13

29
Q

What is the function of ADAMTS13?

A

Cleaves vWF multimers into smaller monomers

30
Q

What causesa decrease in ADAMTS13?

A

Acquited autoantibody

(most commonly in adult females)

31
Q

What is the cause of HUS?

(Adults and Children)

A

Endothelial damage by drugs of infection

(Children = E Coli O157;H7)

(Adults = E Coli Verotoxin damage)

32
Q

What are the 5 clinical findings of HUS and TTP?

A
  1. Skin and mucosal bleeding
  2. Microangiopathic Hemolytic Anemia
  3. Fever
  4. Renal Insufficiency (more common in HUS)

(Thrombi involve vessels of the kidney)

  1. CNS Abnormalities (more common in TTP)

(Thrombi involve vessels of the CNS

33
Q

What are the 4 Lab findings of TPP and HUS?

A
  1. Thrombocytopenia with ↑ bleeding time
  2. Normal PT/PTT (coagulation cascade isn’t activated)
  3. Anemia with Shistocytes
  4. ↑ megakaryocytes on bone marrow biopsy
34
Q

What is the treatment for TPP and HUS?

A

Plasmapheresis

Corticosteroids

35
Q

What are the 4 Qualitative Platelet Disorders?

A
  1. Bernard-Soulier Syndrome
  2. Glanzmann Thrombasthenia
  3. Aspirin inactivatoin of COX
  4. Uremia
36
Q

What is Bernard-Soulier Syndrome?

(What does this cause?)

A

Genetic GP1B deiciency

(Impaired Platelet Adhesion)

37
Q

What does a blood smear show if you have Bernard-Soulier Syndrome?

A

mild thrombocytopenia with enlarged platelets

38
Q

What is Glanzmann Thrombasthenia?

(what does it cause?)

A

A genetic GPIIb/GPIIIa deficiency

(platelet aggregation is impaired)

39
Q

How does Aspirin affect platelets?

A

irreversibly inactivates COX

(lack of TXA2 impairs aggergation)

40
Q

How does Uremia affect platelets?

A

disrupts adhesion and aggregation

41
Q

What is the purpose of Secondary Hemostasis?

A

Stabilize the platelet plug

(via the coagulation cascade)

42
Q

What are the three steps that stabilize the weak platelet plug?

A
  1. Coagulation Cascade produces Thrombin
  2. Thrombin converts fibinogen (in the plug) to fibrin

3. Fibrin is cross-linked

43
Q

What 3 things does activation of the coagulation cascade require?

A
  1. Exposure to an activating substance
  2. Phospholipid surface of platelets
  3. Calcium
44
Q

What is the activating substance for the extrinsic pathway?

A

Tissue Thromboplastin

(Activates Factor VII)

45
Q

What is the activating substance for the intrinsic pathway?

A

Subendothelial Collagen

(Activates Factor XII)

Pathoma (4 decks)

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