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Unit 4: Blood and Lymph > Pathoma- 1a hemostasis and bleeding disorders > Flashcards

Pathoma- 1a hemostasis and bleeding disorders Flashcards

1
Q

What is hemostasis?

A

repairing damaged blood vessels

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2
Q

What is a thrombus?

A

a clot

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3
Q

What is the 1st stage of clot formation?

A

1a hemostasis

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4
Q

What is the goal of 1a hemostasis?

A

formation of a weak platelet plug

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5
Q

What is the goal of 2a hemostasis?

A

stabilization of platelet plug

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6
Q

2a hemostasis is mediated by the _____.

A

coagulation cascade

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7
Q

What is the first step of 1a hemostasis?

A

rapid, transient vaso-constriction of the damaged BV (“knee-jerk reaction”)

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8
Q

____ and ____ modulate the first step of 1a hemostasis.

A

Neurostimulation and endothelien (from the endothelial cells)

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9
Q

What is the 2nd step of 1a hemostasis?

A

Von Willebrand factor lines the damaged area by binding to exposed collagen

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10
Q

Why does Von Willebrand factor bind to the damaged vessel?

A

to allow platelets to bind to them via GPIb receptor

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11
Q

Platelets bind to Von Willebrand factor via ____.

A

GPIb

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12
Q

Where does Von Willebrand factor come from?

A
  1. platelets

2. endothelial cells (in the Weible-Palae body)

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13
Q

What do Wible-Pilate bodies contain?

A

P-selectin and Von Willebrand factor

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14
Q

What is the 3rd step of 1a hemostasis?

A

activation of platelets

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15
Q

What are the 2 mediators platelets secrete to activate themselves?

A
  1. ADP

2. thromboxane-A2

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16
Q

Thromboxane-A2 is a derivative of ____.

A

platelet cyclooxygenase

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17
Q

What kind of granule carries ADP?

A

dense

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18
Q

ADP induces the platelets to express the ____ receptor.

A

GP2B3A

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19
Q

What does GPIIb/IIIa do?

A

allows the platelets to aggregate to one another

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20
Q

Thromboxane-A2 (TXA2) does what?

A

signals additional platelets to aggregate

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21
Q

What is aggregation?

A

when all the platelets join together at a particular place where initial platelets have adhered

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22
Q

What is adhesion?

A

platelets binding to subendothelial collagen via Von Willebrand factor

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23
Q

What is the molecule that links platelets to each other?

A

fibrinogen

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24
Q

Adhesion causes a ____ in platelets and _____, which releases multiple mediators.

A

shape change; degranulation

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25
Q

Platelets aggregate at site of injury via ____ using ____ as a linking molecule.

A

GpIIb/IIIa; fibrinogen

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26
Q

What is the result of 1a hemostasis?

A

formation of a platelet plug

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27
Q

Name the 2 types of general disorders of 1a hemostasis.

A
  1. quantitative

2. qualitative

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28
Q

1a disorders of hemostasis are usually due to _____.

A

abnormalities in platelets

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29
Q

When pts have 1a hemostasis platelet disorders, they will classically present with ____ and ____ bleeding.

A

mucosal; skin

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30
Q

What complication can occur with severe thrombocytopenia?

A

intracranial bleeds

31
Q

Name some manifestations in the skin that can occur in 1a hemostasis defects.

A
  1. petechiae (quantitative)
  2. purpura
  3. ecchymoses
  4. easy bruising
32
Q

If you suspect a 1a hemostasis disorder, what labs should you order?

A
  1. platelet count
  2. bleeding time
  3. blood smear
  4. bone marrow biopsy
33
Q

What is the normal platelet count range?

A

150,000-400,000

34
Q

What is a normal bleeding time range?

A

2-7 minutes

35
Q

What are we looking for in a bone marrow biopsy?

A

megakaryocytes present/absent/morphology

36
Q

What does ITP stand for?

A

immune thrombocytopenic purpure

37
Q

What is ITP?

A

autoimmune production of IgG against platelet antigens

38
Q

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

A

ITP

39
Q

Where are ITP antibodies produced?

A

in the spleen

40
Q

Where are antibody-marked platelets consumed?

A

in the spleen macrophages

41
Q

What is the acute form of ITP?

A

in children; weeks after viral infection or immunization; self-limited and resolves w/I a few weeks; support pt if platelet count drops too far

42
Q

What is the chronic form of ITP?

A

usually in adult women of child bearing age; can be 1a or 2a; can cross the placenta to give baby transient thrombocytopenia too

43
Q

2a chronic ITP can be due to ____ disease.

A

SLE

44
Q

What are the common lab findings in ITP?

A
  1. low platelet count (<50)
  2. normal PT/PTT
  3. increased megakaryocytes
45
Q

How is ITP treated?

A
  1. corticosteroids (good in children, only works short term in adults)
  2. IVIG (also short lived effect)
  3. splenectomy
46
Q

Why is splenectomy a good treatment for ITP?

A

bc it removes both the source of the autoantibody and the source of the platelet destruction

47
Q

What is microangiopthic hemolytic anemia?

A

platelet microthrombi in small vessels

48
Q

How does hemolytic anemia occur in microangiopthic hemolytic anemia?

A

microthrombi in the BVs damage RBCs as they pass thru, resulting in schistocytes

49
Q

Platelets are ____ in the formation of microthrombi.

A

consumed

50
Q

What is a schistocyte?

A

a helmet cell (damaged RBC)

51
Q

What does TTP stand for?

A

thrombotic thrombocytopenic purpura

52
Q

What does HUS stand for?

A

hemolytic uremic syndrome

53
Q

What is TPP (thrombotic thrombocytopenic purpura)?

A

microthrombi form bc of decreased ADAMTS13 enzyme, allowing abnormal platelet adhesion

54
Q

What does ADAMTS13 do?

A

cleaves VWF into monomers for degradation, preventing abnormal platelet adhesion

55
Q

What causes decreased ADAMTS13?

A
  1. genetic defect

2. autoantibody to it

56
Q

Who is the classic pt with decreased ADAMTS13?

A

adult females

57
Q

What causes HUS?

A

drugs or infections

58
Q

What pathogen is notorious for leading to HUS?

A

E. coli 0157:H7

59
Q

Where do the platelet microthrombi occur in HUS and TTP?

A

kidneys and brain/CNS

60
Q

How does E. coli 0157:H7 cause platelet microthrombi?

A

it produces an endothelium-damaging verotoxin

61
Q

E. coli 0157:H7 is commonly contracted from exposure to ____, causing _____ disease.

A

undercooked beef ; dysentery

62
Q

What are the common clinical findings in TTP and HUS?

A
  1. skin and mucosal bleeding
  2. microangiopathic hemolytic anemia
  3. fever
  4. renal insufficiency
  5. CNS abnormalities
63
Q

What is the predominant problem in HUS?

A

kidney dysfunction

64
Q

What is the prominent problem in TTP?

A

CNS dysfunction

65
Q

What lab findings are common in TTP/HUS?

A
  1. thrombocytopenia
  2. increased bleeding time
  3. PT/PTT normal
  4. anemia w/ schistocytes
  5. increased megakaryocytes
66
Q

How is TTP treated?

A
  1. plasmapheresis

2. corticosteroids

67
Q

What is Bernard-Soulier Syndrome?

A

a genetic GP1b deficiency causing impaired platelet adhesion

68
Q

What is seen in a blood smear of a pt with Bernard-Soulier syndrome?

A

mild thrombocytopenia with enlarged platelets

69
Q

What is GP1b?

A

an adhesion molecule for VWF to attach to the endothelium

70
Q

Why are the platelets enlarged in Bernard-Soulier syndrome?

A

platelets released from bone marrow are immature

71
Q

What is Glanzman thrombastenia?

A

genetic GIIb/IIIa deficiency causing impaired platelet aggregation

72
Q

What drug irreversibly inactivates COX?

A

aspirin

73
Q

How does inactivating COX prevent platelet aggregation?

A

prevents TXA2 from being produced, and that’s the molecule that binds platelets together

74
Q

What does uremia do?

A

causes adhesion and aggregation impairment

Unit 4: Blood and Lymph (25 decks)

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