Coagulation Flashcards
1
Q
What measures platelet function?
A
Bleeding Time
2
Q
most common hereditary bleeding disorder
A
vWF
3
Q
what does vWF stabilize?
A
factor VIII
4
Q
what type of inheritance is vWF
A
autosomal dominant
5
Q
qualitative platelet defects are normally acquired or hereditary?
A
acquired - drugs, renal failure
6
Q
acquired platelet defects don’t normally cause_______ ________ _________
A
serious bleeding disorders
7
Q
What three causes would give you a prolonged BT?
A
- platelet count
- qualitative platelet defect
- vW Disease
8
Q
If vWD is quantitative defect, there will be a decreased amount of vWF and correspondingly, a decreased amount of ___________ that can bind to it
A
factor VIII
9
Q
What is the classic lab finding in vWD?
A
failure of ristocetin to agglutinate platelets
10
Q
How do you treat minor bleeding in vWD?
A
desmopressin (DDAVP), which increases level of vWf and factor VIII
11
Q
How do you treat severe bleeding in vWD?
A
intermediate purity factor VIII concentrate which contains vWF
12
Q
What are the treatments for qualitative platelet defect caused by renal failure?
A
- initiate or increase dialysis
- keep HCT 30 or above
- DDAVP (to release vWF from endothelial cells)
13
Q
What are the most important severe coagulation factor deficiencies?
A
VIII, IX
14
Q
What factor deficiencies do you suspect if you have:
- prolonged PTT
- normal PT
- normal BT
A
VIII, IX, XI
15
Q
Which factor deficiencies have severe bleeding manifestations including hematoma and hemarthroses?
A
VIII, IX
16
Q
What type of transmission is VIII and IX deficiency?
A
X-linked
17
Q
What type of transmission is XI deficiency?
A
autosomal recessive
18
Q
If a 1:1 mixing study corrects a factor VIII deficiency, is the problem the factor deficiency or an Ab to the factor?
A
factor deficiency
19
Q
If a 1:1 mixing study does NOT correct a factor deficiency, what does this mean?
A
the problem is an Ab to the factor
20
Q
Lab testing for IX, VIII, and XI are the same, and 1:1 mixing corrects the prolonged PTT, so what do you need to do to make the final diagnosis?
A
a specific assay to the factor (ex: factor VIII assay)
21
Q
Tx mild to moderate VIII deficiency
A
DDAVP
22
Q
Tx severe VIII deficiency
A
factor VIII replacement
23
Q
Tx factor IX deficiency
A
factor IX replacement
24
Q
Tx XI deficiency
A
FFP (contains all coagulation factors)
25
How does aspirin interfere with coagulation
irreversibly inhibits cyclyoxygenase 1 and 2 preventing platelet aggregation
26
how does Clipidogrel (Plavix) interfere with coagulation?
inhibits ADP activation of platelets
27
how do IIb/IIIa inhibitors interfere with coagulation?
prevent fibrinogen binding to IIB/IIIA receptors on platelets--> prevent platelet aggregation
28
what are three anti platelet agents
- aspirin
- clipidogrel (plavix)
- IIB/IIIA inhibitors
29
Example of fibrinolytic agent
t-PA (tissue plasminogen activator) = alteplase
30
What does the fibrinolytic system do in the vasculature?
protects against excessive clotting (and tissue infarction)
31
How does the fibrinolytic system protect against excessive clotting in the vasculature?
endothelium near clot/thrombus secrets plasminogen activator --> converts plaminogen to plasmin which lyses the clot
32
What do you use acutely for ST segment elevated MIs and strokes to lyse the thrombus and re-establish blood flow?
t-PA (tissue plasminogen activator) = alteplase
33
What are three naturally occurring inhibitors that prevent excessive coagulation?
- Protein C
- Protein S
- Antithrombin
34
What does Protein C do?
inactivates factor Va
35
What does Protein S do?
cofactor for Protein C --> inactivation of factor Va
36
What does antithrombin do?
inactivates thrombin and Xa
37
A hereditary deficiency of Protein C, Protein S, or antithrombin would result in an increased risk of what?
DVT formation and P.E.
38
What is the most common cause of hereditary hypercoagulability?
Activated Protein C resistance (APC resistance)
39
Where is the mutation in APC resistance and what does it do?
mutation in factor V
| -prevents protein C from inactivating factor Va
40
What is the second most common hereditary clotting disorder?
A mutation of prothrombin gene
41
What does a mutation of the prothrombin gene do?
increases synthesis of prothrombin (so causes hypercoagulation)
42
What do you use heparin to treat?
DVT, PE, acute coronary syndrome (ACS)
43
How does heparin work?
binds to antithrombin, which increases its anticoagulant ability
44
Which heparin do you monitor? and what do you monitor it with?
Unfractionated Heparin
| -monitor with PTT
45
What should PTT be when monitoring UFH
| what is the therapeutic range
1.5-2.5x the control (50-70 seconds)
| is the therapeutic range
46
What is the dose of LMWH based on?
weight based dosing
47
How does heparin help with anti coagulation?
it prevents FURTHER clot formation
| does not lyse clots!
48
What is heparin incapable of doing with clots (that the endogenous fibrinolytic system does)?
cannot lyse clots
49
how does coumadin act as an anti-coagulant?
prevents vit K from converting to activating form
| no vit K means the vit K dependent factors inhibited
50
which coagulation factors are vitamin K dependent
II, VII, IX, X
51
how do you monitor coumadin?
PT/INR
52
What does INR do?
standardizes PT values (because labs use different thromboplastins, etc)
53
When can coumadin NOT be used
pregnancy
54
What is coumadin usually used for? (treatment of what?)
DVT, PE, and prevent embolic stroke in atrial fibrilation
55
what should you use if a pt. needs anticoagulation during pregnancy
heparin
56
what is a major complication of all anticoagulants -- which one has the greatest risk?
bleeding
| -greatest risk with fibrinolytic agents because risk of CNS bleed
57
how is heparin induced thrombocytopenia (HIT) diagnosed?
platelet count drop below 120,000 5-14 days after initiating heparin
58
which heparin causes HIT more?
UFH
59
explain HIT/How? i don't know either. just whatever the sentence was under HIT
Ab to heparin-PF4 complex activates platelets and increases risk of thrombosis and acquired hyper coagulability
60
treatment of HIT?
- stop heparin
| - initiate direct thrombin inhibitor therapy (not coumadin initially)
61
Lab results seen in Vitamin K deficiency (PT, etc)
- initially only PT prolonged
- severe: PT & PTT prolonged
- 1:1 mixing study WILL correct PT
62
Treatment of Vit K deficiency
-vit K
-FFP if acute bleeding
(vit K takes up to 24 h, so you would give the FFP regardless)
63
treatment of Vit K deficiency if acute bleeding
FFP
64
treatment of coumadin induced acute bleeding
FFP because it contains all the coagulation factors
65
What does TT (thrombin time test)
quantitative and qualitative for fibrinogen
| -is fibrinogen working and do you have enough
66
What happens in DIC? (disseminated intravascular coagulation)
TF is released into blood so thrombi occur in microcirculation and activation of fibrinolytic system
67
What are labs for DIC?
prolonged PT, prolonged PTT, decreased platelets, decreased fibrinogen, increased fibrin split products, increased D-dimer
68
___is always secondary to something else, such as___________
DIC, secondary to sepsis and OB complications
69
treatment for DIC
address the cause first ( the underlying disease)
- FFP
- platelets
- heparin in special situations
70
When is D-Dimer elevated?
in DIC
71
If D Dimer is not elevated, what can you use this finding to exclude?
exclude dx of DVT in patient with LOW risk
72
What would be the labs of a Coagulation defect secondary to liver disease?
- prolonged PT
- prolonged PTT
- PT more sensitive (because of liver and vit K. dependent factors)
73
What is autoimmune thrombocytopenia?
platelet destruction secondary to autoantibody production
74
What is ITP (idiopathic thrombocytopenia purpura)
type of autoimmune thrombocytopenia
75
ITP in kids vs adults
- self limiting in children
| - adult form is chronic
76
labs suggesting ITP dx
- decreased platelet count
| - normal HCT & WBC
77
If dx of ITP is uncertain, what do you evaluate?
Bone marrow. Should be normal
78
What do you need to rule out when suspecting an ITP dx
-HIV and HEP C because they can both present the same way
79
What does a peripheral smear show you in ITP
-decreased platelet count
(IgG coated platelets destroyed in spleen)
-enlarged platelets
80
physical presentation of ITP
petechia
81
tx ITP
- steroids (1mg/kg prednisone)
- splenectomy
- immunosuppressive therapy
- emergent treatment secondary to acute bleeding--> steroids & IV immunoglobulin
82
List new oral anticoagulants
- Pradaxa (Dabigatran)
- Eliquis (Apixaban)
- Xarelto (Rivaroxaban)
83
What does Dabigatran inhibit?
direct thrombin inhibitor
84
What does Rivaroxaban inhibit
factor Xa
85
What does apixaban inhibit
factor Xa
86
What are indications for the new oral anticoagulants
- acute tx of DVT & PE
- tx of nonvalular A.F. to reduce risk of stroke
- DVT prophylaxis after joint replacement
87
What is the benefit of using the new oral anticoagulants vs coumadin?
- do not require lab monitoring
| - far fewer drug interactions
88
major complication of new oral anticoagulants
bleeding & no antidote to reverse the bleeding
89
What is pancytopenia
- all cell lines below normal
| - leukocytes
90
clinical presentation of aplastic anemia
- fatigue & pallor from anemia
- petechiae, brusing, bleeding
- fever & sx of bacterial infix because of neutropenia
91
tx of aplastic anemia
stem cell transplantation or immunosuppresive therapy
92
What tests measure kidney function
- BUN (blood urea nitrogen)
- Creatinine
- both excreted in urine so decrease in kidney function elevates level in blood
93
Normal Values for BUN
6-20 mg/dl
94
Normal Values for Creatinine
0.6-1.2 mg/dl
95
What happens in Thrombotic Thrombocytopenia Purport (TTP)
deficiency of vWF-cleaving protease so large multimers floating in blood cause platelet agglutination--> diffuse platelet thrombi in microcirculation
96
What two lab values are absolutely necessary for dx of TTP
-microangiopathic hemolytic anemia (blood smear shows SCHISTOCYTES) and thrombocytopenia
97
Other lab values of TTP
- increased LDH level (released in RBC destruction)
- normal PT & PTT
- might evaluate of BUN & Creatinine
98
Other findings in TTP
-neurologic manifestation, renal impairment, & fever
99
tx for TTP:
immediate plasma exchange therapy (remove their plasma with the fucked up multimers and give regular plasma)
100
What is the most common cause of acute renal failure in children
Hemolytic Uremic Syndrome (HUS)
101
Classic presentation of HUS (Hemolytic uremia syndrome)
young children who develop thrombocytopenia with microangiopathic hemolysis (schistocytes), oliguria, proteinuria, and increase in BUN and creatinine
102
What does HUS commonly follow?
bloody diarrheal illness caused by E. coli
103
lab findings in HUS
- microangiopathic hemolytic anemia (schistocytes)
- thrombocytopenia
- increase LDH (lactate dehydrogenase)
- increase BUN/Creatinine
- normal PT & PTT
104
diagnosis of HUS requires what findings
-schistocytes, thrombocytopenia, increase BUN/Creatinine
105
tx for HUS
supportive therapy, dialysis for renal failure (uremia)
106
when i say microangiopathic hemolytic anemia
you say schistocytes
107
What does thrombin time (TT) measure
quantity and quality of fibrinogen
108
what will prolong the TT (thrombin time)
anticoagulants
109
if ristocetin can't agglutinate platelets, what does this tell you?
qualitative problem with vWF
110
normal values for platelets
150k-400k
111
What is considered thrombocytopenia?
112
what causes hemophilia A
deficiency factor VIII
113
what causes hemophilia B
deficiency factor IX
