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Pathoma LAH > Blood: 4.1: 1a hemostatsis and bleeding > Flashcards

Blood: 4.1: 1a hemostatsis and bleeding 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 goal of 1a hemostasis?

A

formation of a weak platelet plug

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4
Q

What is the goal of 2a hemostasis?

A

stabilization of platelet plug

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5
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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6
Q

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

A
  • Neurostimulation
  • endothelien- from the endothelial cells
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7
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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8
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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9
Q

Platelets bind to Von Willebrand factor via ____.

A

GPIb

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10
Q

Where does Von Willebrand factor come from?

A
  1. platelets
  2. endothelial cells (in the Weible-Palae body)
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11
Q

What do Wible-Pilate bodies contain?

A
  • P-selectin
  • Von Willebrand factor
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12
Q

What is the 3rd step of 1a hemostasis?

A

activation of platelets

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13
Q

What are the 2 mediators platelets secrete to activate themselves?

A
  1. ADP
  2. thromboxane-A2
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14
Q

Thromboxane-A2 is a derivative of ____.

A

platelet cyclooxygenase

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15
Q

What kind of granule carries ADP?

A

dense

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16
Q

ADP induces the platelets to express the ____ receptor.

A

GP2B3A

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17
Q

What does GPIIb/IIIa do?

A

allows the platelets to aggregate to one another

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18
Q

Thromboxane-A2 (TXA2) does what?

A

signals additional platelets to aggregate

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19
Q

What is aggregation?

A

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

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20
Q

What is adhesion?

A

platelets binding to subendothelial collagen via Von Willebrand factor

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21
Q

What is the molecule that links platelets to each other?

A

fibrinogen

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22
Q

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

A

shape change; degranulation

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23
Q

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

A

GpIIb/IIIa; fibrinogen

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24
Q

What is the result of 1a hemostasis?

A

formation of a platelet plug

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25
Q

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

A
  1. quantitative
  2. qualitative
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26
Q

1a disorders of hemostasis are usually due to _____.

A

abnormalities in platelets

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27
Q

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

A

mucosal and skin

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28
Q

What complication can occur with severe thrombocytopenia?

A

intracranial bleeding

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29
Q

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

A
  1. petechiae
  2. purpura
  3. ecchymoses
  4. easy bruising
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30
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
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31
Q

What is the normal platelet count range?

A

150,000-400,000

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32
Q

What is a normal bleeding time range?

A

2-7 minutes

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33
Q

What are we looking for in a bone marrow biopsy?

A
  • megakaryocytes
    • present/absent/morphology
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34
Q

What does ITP stand for?

A

immune thrombocytopenic purpura

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35
Q

What is ITP?

A

autoimmune production of IgG against platelet antigens (GPIIb/IIIa)

36
Q

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

A

ITP

37
Q

Where are ITP antibodies produced?

A

plasma cells in the spleen

38
Q

Where are antibody-marked platelets consumed? What is the result?

A
  • the spleen macrophages
  • thrombocytopenia
39
Q

Who gets the acute form of ITP? When? What is the tx?

A
  • in children
  • weeks after viral infection or immunization
  • self-limited- resolves w/i a few weeks; support pt if platelet count drops too far
40
Q

Who gets the chronic form of ITP? What does it cause in pregnant women?

A
  • adult women of child bearing age
  • can cross the placenta to give baby transient thrombocytopenia too
41
Q

What are the common lab findings in ITP?

A
  1. low platelet count (less than 50,000)
  2. normal PT/PTT
  3. increased megakaryocytes on bone marrow biopsy
42
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
43
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

44
Q

What is microangiopthic hemolytic anemia?

A

pathologic formation of platelet microthrombi in small vessels

45
Q

How does hemolytic anemia occur in microangiopthic hemolytic anemia? What is the result to the RBC?

A
  • microthrombi in the BVs damage RBCs as they pass thru, resulting in:
  • schistocytes
46
Q

Platelets are ____ in the formation of microthrombi.

A

consumed

47
Q

What is a schistocyte? When are they seen?

A
  • a helmet cell (damaged RBC)
  • microangiopathic hemolytic anemia, aortic stenosis
48
Q

What does TTP stand for?

A

thrombotic thrombocytopenic purpura

49
Q

What does HUS stand for?

A

hemolytic uremic syndrome

50
Q

What is formed in TPP (thrombotic thrombocytopenic purpura)? Why does this occur?

A
  • microthrombi form, allowing abnormal platelet adhesion
  • decreased ADAMTS13 enzyme
51
Q

What does ADAMTS13 do?

A

cleaves VWF into monomers for degradation, preventing abnormal platelet adhesion

52
Q

What causes decreased ADAMTS13? What is the most common reason?

A
  1. genetic defects
  2. autoantibodies** most common
53
Q

Who is the classic pt with decreased ADAMTS13?

A

adult females

54
Q

What causes HUS?

A

drugs or infections

55
Q

What pathogen is notorious for leading to HUS?

A

E. coli 0157:H7

56
Q

Where do the platelet microthrombi occur in HUS and TTP?

A
  • kidneys
  • brain/CNS
57
Q

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

A

it produces an endothelium-damaging verotoxin

58
Q

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

A

undercooked beef ; dysentery

59
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
60
Q

What is the predominant problem in HUS?

A

kidney dysfunction

61
Q

What is the prominent problem in TTP?

A

CNS dysfunction

62
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
63
Q

How is TTP treated?

A
  1. plasmapheresis
  2. corticosteroids
64
Q

What is Bernard-Soulier Syndrome? What causes it?

A
  • impaired platelet adhesion
  • a genetic GP1b deficiency causing
65
Q

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

A
  • mild thrombocytopenia
  • enlarged platelets
66
Q

What is GP1b?

A

an adhesion molecule for VWF to attach to the endothelium

67
Q

Why are the platelets enlarged in Bernard-Soulier syndrome?

A

platelets released from bone marrow are immature

68
Q

What is Glanzman thrombastenia? What causes it?

A
  • impaired platelet aggregation
  • genetic GIIb/IIIa deficiency
69
Q

What drug irreversibly inactivates COX?

A

aspirin

70
Q

How does inactivating COX prevent platelet aggregation?

A
  • prevents TXA2 from being produced (the molecule that binds platelets together)
71
Q

What does uremia do?

A

causes platelet adhesion and aggregation impairment

72
Q

What causes the “knee jerk” vasoconstriction to start coagulation?

A

endothelien

73
Q

What are the s/s of mucosal bleeding in 1a hemostatis disorders?

A
  • epistaxis
  • hemoptysis
  • GI bleeding
  • hematuria
  • menorrhagia
74
Q

Petechiae are a sign of ______.

A

thrombocytopenia

75
Q

______ binds exposed subendothelial collagen.

A

Von Willebrand factor (vWF)

76
Q

Von Willebrand factor (vWF) binds ______.

A

exposed subendothelial collagen

77
Q

Platelets bind _____ using the GPlb receptor.

A

von Willebrand Factor (vWF)

78
Q

Platelets bind vWF using the _____ receptor.

A

GPlb

79
Q

Platelets aggregate at the site of injury via _____ using fibrinogen as a linking molecule.

A

GPIIb/IIla

80
Q

Platelets aggregate at the site of injury via GPIIb/IIla using _____ as a linking molecule.

A

fibrinogen

81
Q

What is GPIIb/IIIa?

A

receptor used to cross-link platelets via fibrinogen

82
Q

Name a disease associated with chronic ITP.

A

SLE

83
Q

Why is IVIG a treatment for ITP?

A

it’s a distraction- the spleen starts consuming the IVIG instead of the platelets for a while

84
Q

What does a schistocyte look like?

A
  • an RBC with two pointy ends- a “helmet cell”
85
Q

What is uremia?

A

a build up of urea and other nitrogenous wastes in the blood

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