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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
Name the 2 types of general disorders of 1a hemostasis.
1. quantitative 2. qualitative
26
1a disorders of hemostasis are usually due to \_\_\_\_\_.
abnormalities in platelets
27
When pts have 1a hemostasis platelet disorders, they will classically present with ____ and ____ bleeding.
mucosal and skin
28
What complication can occur with severe thrombocytopenia?
intracranial bleeding
29
Name some skin manifestations that can occur in 1a hemostasis defects.
1. petechiae 2. purpura 3. ecchymoses 4. easy bruising
30
If you suspect a 1a hemostasis disorder, what labs should you order?
1. platelet count 2. bleeding time 3. blood smear 4. bone marrow biopsy
31
What is the normal platelet count range?
150,000-400,000
32
What is a normal bleeding time range?
2-7 minutes
33
What are we looking for in a bone marrow biopsy?
* megakaryocytes * present/absent/morphology
34
What does ITP stand for?
immune thrombocytopenic purpura
35
What is ITP?
autoimmune production of IgG against platelet antigens (GPIIb/IIIa)
36
What is the most common cause of thrombocytopenia in children and adults?
ITP
37
Where are ITP antibodies produced?
plasma cells in the spleen
38
Where are antibody-marked platelets consumed? What is the result?
* the spleen macrophages * thrombocytopenia
39
Who gets the acute form of ITP? When? What is the tx?
* 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
Who gets the chronic form of ITP? What does it cause in pregnant women?
* adult women of child bearing age * can cross the placenta to give baby transient thrombocytopenia too
41
What are the common lab findings in ITP?
1. low platelet count (less than 50,000) 2. normal PT/PTT 3. increased megakaryocytes on bone marrow biopsy
42
How is ITP treated?
1. corticosteroids (good in children, only works short-term in adults) 2. IVIG (also short-lived effect) 3. splenectomy
43
Why is splenectomy a good treatment for ITP?
bc it removes both the source of the autoantibody and the source of the platelet destruction
44
What is microangiopthic hemolytic anemia?
pathologic formation of platelet microthrombi in small vessels
45
How does hemolytic anemia occur in microangiopthic hemolytic anemia? What is the result to the RBC?
* microthrombi in the BVs damage RBCs as they pass thru, resulting in: * schistocytes
46
Platelets are ____ in the formation of microthrombi.
consumed
47
What is a schistocyte? When are they seen?
* a helmet cell (damaged RBC) * microangiopathic hemolytic anemia, aortic stenosis
48
What does TTP stand for?
thrombotic thrombocytopenic purpura
49
What does HUS stand for?
hemolytic uremic syndrome
50
What is formed in TPP (thrombotic thrombocytopenic purpura)? Why does this occur?
* microthrombi form, allowing abnormal platelet adhesion * decreased ADAMTS13 enzyme
51
What does ADAMTS13 do?
cleaves VWF into monomers for degradation, preventing abnormal platelet adhesion
52
What causes decreased ADAMTS13? What is the most common reason?
1. genetic defects 2. autoantibodies\*\* most common
53
Who is the classic pt with decreased ADAMTS13?
adult females
54
What causes HUS?
drugs or infections
55
What pathogen is notorious for leading to HUS?
E. coli 0157:H7
56
Where do the platelet microthrombi occur in HUS and TTP?
* kidneys * brain/CNS
57
How does E. coli 0157:H7 cause platelet microthrombi?
it produces an endothelium-damaging verotoxin
58
E. coli 0157:H7 is commonly contracted from exposure to \_\_\_\_, causing \_\_\_\_\_.
undercooked beef ; dysentery
59
What are the common clinical findings in TTP and HUS?
1. skin and mucosal bleeding 2. microangiopathic hemolytic anemia 3. fever 4. renal insufficiency 5. CNS abnormalities
60
What is the predominant problem in HUS?
kidney dysfunction
61
What is the prominent problem in TTP?
CNS dysfunction
62
What lab findings are common in TTP/HUS?
1. thrombocytopenia 2. increased bleeding time 3. PT/PTT normal 4. anemia w/ schistocytes 5. increased megakaryocytes
63
How is TTP treated?
1. plasmapheresis 2. corticosteroids
64
What is Bernard-Soulier Syndrome? What causes it?
* impaired platelet adhesion * a genetic GP1b deficiency causing
65
What is seen in a blood smear of a pt with Bernard-Soulier syndrome?
* mild thrombocytopenia * enlarged platelets
66
What is GP1b?
an adhesion molecule for VWF to attach to the endothelium
67
Why are the platelets enlarged in Bernard-Soulier syndrome?
platelets released from bone marrow are immature
68
What is Glanzman thrombastenia? What causes it?
* impaired platelet aggregation * genetic GIIb/IIIa deficiency
69
What drug irreversibly inactivates COX?
aspirin
70
How does inactivating COX prevent platelet aggregation?
* prevents TXA2 from being produced (the molecule that binds platelets together)
71
What does uremia do?
causes platelet adhesion and aggregation impairment
72
What causes the "knee jerk" vasoconstriction to start coagulation?
endothelien
73
What are the s/s of mucosal bleeding in 1a hemostatis disorders?
* epistaxis * hemoptysis * GI bleeding * hematuria * menorrhagia
74
Petechiae are a sign of \_\_\_\_\_\_.
thrombocytopenia
75
\_\_\_\_\_\_ binds exposed subendothelial collagen.
Von Willebrand factor (vWF)
76
Von Willebrand factor (vWF) binds \_\_\_\_\_\_.
exposed subendothelial collagen
77
Platelets bind _____ using the GPlb receptor.
von Willebrand Factor (vWF)
78
Platelets bind vWF using the _____ receptor.
GPlb
79
Platelets aggregate at the site of injury via _____ using fibrinogen as a linking molecule.
GPIIb/IIla
80
Platelets aggregate at the site of injury via GPIIb/IIla using _____ as a linking molecule.
fibrinogen
81
What is GPIIb/IIIa?
receptor used to cross-link platelets via fibrinogen
82
Name a disease associated with chronic ITP.
SLE
83
Why is IVIG a treatment for ITP?
it's a distraction- the spleen starts consuming the IVIG instead of the platelets for a while
84
What does a schistocyte look like?
* an RBC with two pointy ends- a "helmet cell"
85
What is uremia?
a build up of urea and other nitrogenous wastes in the blood

Pathoma LAH (77 decks)

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