Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophysiology > Primary Hemostasis > Flashcards

Primary Hemostasis Flashcards

1
Q

What are the hallmarks of primary hemostasis?

A

formation of weak platelet plug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the goal of secondary hemostasis?

A

stabilization of platelet plug (mediated by coagulation cascade)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is step one of damaged vessels?

A

transient vasoconstriction (knee jerk reaction to pull away)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What mediates step 1 (vasoconstriction)?

A

1) neural reflex

2) endothelial cells themselves secrete endothelin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is von willebrand’s factor?

A

a factor that will come line the break down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What allows for VWF to bind?

A

exposed collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the function of VWF?

A

to serve as a linker to bind to platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where does VWF come from?

A

1) platelet

2) endothelial cells (most important)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is step 3?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

TXA2 is a derivative of _________________

A

platelet cyclooxygenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is essential for platelet aggregation?

A

GP2b3a (glycoprotein 2b3a)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is essential for the expression of GP2b3a?

A

ADP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the role of TXA2?

A

to further recruit platelets to aggregate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the important linker molecule between Gp2b3a and platelets?

A

fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

platelet aggregation occurs via ________ using ___________ as a linker

A

Gp2b3a

fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Define adhesion

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What receptor do platelets use to bind to VWF?

A

Gp1b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What promotes exposure of GpIIb/IIIa?

A

ADP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
What is a normal platelet count?
150,000-400,000/uL
26
What produces platelets?
megakaryocytes in the bone marrow
27
What is ITP?
autoimmune disorder where you produce IgG against platelet antigens (like GPIIb/IIIa)
28
What is the most common cause of thrombocytopenia?
ITP
29
What produces those autoantibodies in ITP?
plasma cells in the spleen macrophages in the spleen also consume the platelets that are bound to the antibody
30
What do lab results look like in ITP?
1) LOW platelets 2) normal PT/PTT 3) HIGH megakaryocytes
31
Why treat ITP with IVIG?
spleen will start eating IVIG instead of platelets with autoantibody (SHORT LIVED effect) defend platelets for a short period of time
32
What is the most permanent solution to ITP?
splenectomy
33
What is microangiopathic hemolytic anemia?
get abnormal aggregation of platelets forming microthrombus which shears the RBCs that pass by -- called shistocyte (hemolysis)
34
What are complications of microangiopathic hemolytic anemia?
low platelet count (used up in forming microthrombus)
35
What are the 2 classic disorders that lead to microangiopathic hemolytic anemia?
1) TTP (thrombotic thrombocytopenic purpura) | 2) HUS (hemolytic uremic syndrome)
36
Why do platelet thrombii occur in TTP?
decrease in ADAMTS13 enzyme (responsible for cleaving VWF multimers) VWF multimers lead to abnormal platelet adhesion - results in platelets forming microthrombi
37
Why would you ever have a decrease in ADAMTS13?
autoantibody to destroy it (or genetic)
38
What bug causes HUS?
Ecoli O157 H7
39
Wheredo platelet microthrombi occur in HUS?
kidney and brain
40
Who gets Ecoli O157 H7?
children who eat undercooked beef (bug produces verotoxin)
41
What are some of the clinical findings in TTP and HUS?
1) skin and mucosal bleeding (platelets are consumed in microthrombi) 2) microangiopathic hemolytic anemia 3) fever 4) renal insufficiency 5) CNS abnormalities
42
In TTP, the predominant problem is ________________ while in HUS, the predominant problem is _________________
CNS abnormalities (TTP) renal (HUS)
43
True or False: PT/PTT are NORMAL in microangiopathic hemolytic anemia
TRUE (haven't activated coagulation cascade)
44
What is a big example of a qualitative platelet disorder?
Bernard Soulier syndrome (genetic GP1b deficiency)
45
What is the pathology of Bernard Soulier?
GP1b is gone so platelet adhesion is impaired (platelets cannot bind VWF)
46
What does blood smear show for bernard soulier?
1) mild thrombocytopenia (platelets have shorter life span) 2) enlarged platelets (immature) Bernard Soulier get Big Suckers
47
What is Glanzmann thrombasthenia?
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
Why is aspirin a bleeding concern?
COX is irreversibly inactivated so you have decreased TXA2 -- less signal to aggregate platelets cannot aggregate
49
What is uremia?
poor kidney function, build up of nitrogenous waste (adhesion and aggregation are impaired)

Pathophysiology (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions