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Pathophysiology > Primary Hemostasis > Flashcards

Primary Hemostasis Flashcards

1
Q

What are the hallmarks of primary hemostasis?

A

formation of weak platelet plug

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2
Q

What is the goal of secondary hemostasis?

A

stabilization of platelet plug (mediated by coagulation cascade)

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3
Q

What is step one of damaged vessels?

A

transient vasoconstriction (knee jerk reaction to pull away)

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4
Q

What mediates step 1 (vasoconstriction)?

A

1) neural reflex

2) endothelial cells themselves secrete endothelin

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5
Q

What is von willebrand’s factor?

A

a factor that will come line the break down

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6
Q

What allows for VWF to bind?

A

exposed collagen

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7
Q

What is the function of VWF?

A

to serve as a linker to bind to platelets

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8
Q

Where does VWF come from?

A

1) platelet

2) endothelial cells (most important)

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9
Q

What holds VWF in the endothelial cell?

A

Wiebold pilate body

WP - P reminds that most important is P selectin and W reminds of VWF

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10
Q

What is step 3?

A

shape change in platelets that allows for dumping of mediators (ADP and thromboxane A2 TXA2)

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11
Q

TXA2 is a derivative of _________________

A

platelet cyclooxygenase

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12
Q

What is essential for platelet aggregation?

A

GP2b3a (glycoprotein 2b3a)

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13
Q

What is essential for the expression of GP2b3a?

A

ADP

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14
Q

What is the role of TXA2?

A

to further recruit platelets to aggregate

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15
Q

What is the important linker molecule between Gp2b3a and platelets?

A

fibrinogen

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16
Q

platelet aggregation occurs via ________ using ___________ as a linker

A

Gp2b3a

fibrinogen

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17
Q

Define adhesion

A

binding of VWF to exposed collagen (and then platelets bind to VWF)

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18
Q

What receptor do platelets use to bind to VWF?

A

Gp1b

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19
Q

What promotes exposure of GpIIb/IIIa?

A

ADP

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20
Q

What are the classical signs and symptoms of primary hemostasis disorders?

A

mucosal or skin bleeding

21
Q

What are examples of mucosal bleeding?

A

epistaxis (nose bleeding)

hemoptysis (coughing up blood)

22
Q

What is the feared complication of a low platelet count?

A

intracranial bleeding

23
Q

What are examples of skin bleeding?

A

petechiae
purpura
ecchymoses
easy bruising

24
Q

Petechiae are a sign of ______________

A

thrombocytopenia (few platelets not a qualitative problem)

25
Q

What is a normal platelet count?

A

150,000-400,000/uL

26
Q

What produces platelets?

A

megakaryocytes in the bone marrow

27
Q

What is ITP?

A

autoimmune disorder where you produce IgG against platelet antigens (like GPIIb/IIIa)

28
Q

What is the most common cause of thrombocytopenia?

A

ITP

29
Q

What produces those autoantibodies in ITP?

A

plasma cells in the spleen

macrophages in the spleen also consume the platelets that are bound to the antibody

30
Q

What do lab results look like in ITP?

A

1) LOW platelets
2) normal PT/PTT
3) HIGH megakaryocytes

31
Q

Why treat ITP with IVIG?

A

spleen will start eating IVIG instead of platelets with autoantibody (SHORT LIVED effect)

defend platelets for a short period of time

32
Q

What is the most permanent solution to ITP?

A

splenectomy

33
Q

What is microangiopathic hemolytic anemia?

A

get abnormal aggregation of platelets forming microthrombus which shears the RBCs that pass by – called shistocyte (hemolysis)

34
Q

What are complications of microangiopathic hemolytic anemia?

A

low platelet count (used up in forming microthrombus)

35
Q

What are the 2 classic disorders that lead to microangiopathic hemolytic anemia?

A

1) TTP (thrombotic thrombocytopenic purpura)

2) HUS (hemolytic uremic syndrome)

36
Q

Why do platelet thrombii occur in TTP?

A

decrease in ADAMTS13 enzyme (responsible for cleaving VWF multimers)

VWF multimers lead to abnormal platelet adhesion - results in platelets forming microthrombi

37
Q

Why would you ever have a decrease in ADAMTS13?

A

autoantibody to destroy it (or genetic)

38
Q

What bug causes HUS?

A

Ecoli O157 H7

39
Q

Wheredo platelet microthrombi occur in HUS?

A

kidney and brain

40
Q

Who gets Ecoli O157 H7?

A

children who eat undercooked beef (bug produces verotoxin)

41
Q

What are some of the clinical findings in TTP and HUS?

A

1) skin and mucosal bleeding (platelets are consumed in microthrombi)
2) microangiopathic hemolytic anemia
3) fever
4) renal insufficiency
5) CNS abnormalities

42
Q

In TTP, the predominant problem is ________________ while in HUS, the predominant problem is _________________

A

CNS abnormalities (TTP)

renal (HUS)

43
Q

True or False: PT/PTT are NORMAL in microangiopathic hemolytic anemia

A

TRUE (haven’t activated coagulation cascade)

44
Q

What is a big example of a qualitative platelet disorder?

A

Bernard Soulier syndrome (genetic GP1b deficiency)

45
Q

What is the pathology of Bernard Soulier?

A

GP1b is gone so platelet adhesion is impaired (platelets cannot bind VWF)

46
Q

What does blood smear show for bernard soulier?

A

1) mild thrombocytopenia (platelets have shorter life span)
2) enlarged platelets (immature)

Bernard Soulier get Big Suckers

47
Q

What is Glanzmann thrombasthenia?

A

genetic GIIb/IIIa deficiency

platelets can still bind Gp1b to VWF and release ADP/TXA2 so GPIIb/IIIa will be expressed to recruit more platelets —- dont have GPIIb/IIIa, this part of the cascade cannot happen

48
Q

Why is aspirin a bleeding concern?

A

COX is irreversibly inactivated so you have decreased TXA2 – less signal to aggregate

platelets cannot aggregate

49
Q

What is uremia?

A

poor kidney function, build up of nitrogenous waste (adhesion and aggregation are impaired)

Pathophysiology (26 decks)

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