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Hemostasis and Coagulation Flashcards

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1
Q

aPTT

A

activated partial thromboblastin time

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2
Q

aPTT ingredients

A

1 part citrated plasma 1 part

silica contact activator plus phospholipid- incubate at 37 degrees for 5 minutes and then 1 part add calcium ions

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3
Q

PT

A

prothrombin time

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4
Q

PT ingredients

A
  1. citrated plasma to 2 parts calcium, phospholipid and tissue factor
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5
Q

what does aPTT test for?

A

2, 8, 9, 10, 11. Heparin therapy, lupus anticoagulant, hereditary or acquired deficiency, severe liver disease.

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6
Q

what does PT test for

A

2, 5, 7, 10. Warfarin therapy, vitamin K deficiency, liver disease, factors or assay inhibitors

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7
Q

Vitamin K dependent factors

A

2-7-9-10

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8
Q

Cortifact

A

drug for factor XIII deficiency

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9
Q

Factor VIII deficiency treatment

A

recombinant factor VIII or virus inactivated monoclonal antibody purified plasma derived factor VIII products.

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10
Q

GP1b

A

binds to vWF on exposed collagen - primary hemostasis

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11
Q

GPIIb/IIIa

A

binds to fibrinogen to form bridge between other platelets (complex: Gp2b/3a-fibrinogen-Gp2b/3a)

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12
Q

vwbF- what it is and what it does, where is is

A

von willebrand factor mediates platelet adherence to injured vessel wall by binging collagen and platelet receptor complex (Gp1b/V/IX) binding causes platelets to degranulate and attract more platelets. Von Willebrand factor is synthesized in the walls of the blood vessels and circulates freely in the blood in a folded form. When it encounters damage to the wall of a blood vessel, particularly in situations of high velocity blood flow, it binds to the collagen beneath the damaged endothelium and uncoils into its active form.

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13
Q

ADAMTS13

A

cleaves ULvwF multimers- if not cleaved, promotes platelet aggregation-microthrombi

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14
Q

List the Intrinsic pathway for coagulation

A

12 activates 11-(with ca)11a, which activates 9-(with ca)9a, 8+9= activation of 10a(with PS and Ca), 10+5=2-2a(with PS and Ca)- activates fibrinogen to soluble fibrin. 13 crosslinks fibrin

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15
Q

List extrinsic (trauma) coagulation cascade

A

Vascular injury- exposed Tissue Factor- activates VII-VIIa, this complex TF-VIIa activates 10- 10 and 5 make 2(with PS and Ca), activates prothrombin-thrombin and fibrinogen to fibrin, XIII- crosslinks fibrin

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16
Q

Heyde’s syndrome

A

aortic stenosis, the stenotic aortic valve becomes narrowed. Blood flow rate is increased to make up for the narrowing, the combination of narrowing and increased flow rate causes sheer stress which causes vWF to unravel like it does when it senses capillary vessel trauma, cleaved by ADAMTS13, the amount of (inactivated) vWF in the blood decreases and therefore bleeding increases. due to angiodysplasia- causes GI bleeds

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17
Q

angiodysplasia

A

small vascular malformation in the gut

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18
Q

Primary hemostasis

A

formation of the platelet plug due to platelet binding and aggregation

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19
Q

Secondary hemostasis

A

coagulation cascade- ending in crosslinking and stabilization of fibrin. Triggered by Tissue Factor released from epithelial cells with vascular trauma.

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20
Q

Tertiary hemostais

A

Fibrinolysis

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21
Q

Which part of primary hemostasis effects secondary hemostasis

A

Primary hemostasis creates Phospholipid which is used in some of the steps within the coagulation cascade.

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22
Q

gla

A

Gamma carboxyl glutamate residues on 2,7,9,10, these residues are formed by vitamin K dependent enzymes and facilitate calcium dependent complex binding to phospholipid membranes

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23
Q

which coagulation factor has the shortest half-life

A

VII, 5-8 hours, this is why FFP needs to be frozen in 8 hours. more than 8 hours, half the VII is left.

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24
Q

PCC

A

prothrombin complex concentration, factor 9 complex, medication 2,9, 10. some version contain factor 7 as well.

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25
Hemophilia B
factor 9 deficiency"christmas disease"- joint bleeding,
26
Treatment for hemophilia B
PCC, recombinant factor IX- recombinant- animal derived.
27
Choice for material replacement: Fibrinogen
Cryo, FFP, fibrinogen concentrate
28
Choice for meterial replacement : Prothrombin
PCC, FFp
29
Factor 5 choice for material replacement
FFP
30
Factor7 choice for material replacement
FVIIa, FFP PCC (if it contains factor VII)
31
Factor 8 choice for material replacement (secondary name for Factor 8)
antihemolytic factor=factor 8, choice for material replacement= Factor VIII concentrate, rFVIII (recombinant factor VIII= drug of choice)
32
Factor 9 alternate name and choice for material replacement
Christmas factor and Factor 9 concentrate, rFIX, PCC
33
Factor 10 alternate name and choice for material replacement
Stuart factor, PCC, FFP
34
XII alternate name and choice for material replacement
Hageman factor and not necessary for replacement, no history of bleeding with this factor deficiency, will show a prolonged aPTT but invivo functionality is normal without this factor.
35
Non correction with plasma mixing studies
denotes an inhibitor, factor deficiency corrects, and stays corrected
36
Immediate correction with plasma mixing studies
Due to factor deficiency
37
Slow correction
Could be due to time sensitive inhibition.
38
Factor XIII alternate name and choice for material replacement
fibrin stabilizing factor, cryoprecipiate and FFP
39
vWF choice of replacement
Cryo, humate-P
40
humate P
used in treatment of vWF deficiency, combination of antihemolytic factor(VIII) and vWF complex, purified from pooled human plasma
41
HMWK
high molecular weight kininogen
42
Tissue Factor deficiency
Factor III, this is a trick question there is no such thing as TF deficiency- no known examples causing the industry to imagine that if this were a possible deficiency it is probably incompatible with life and this is why we don't see it.
43
Plasmin
the active form (plasminogen is the inactive form) o
44
INR
international normalized ratio. used to standardize PT between different labs. INR= (PTpatient/PTcontrol)^ISI
45
ISI
international sensitivity index- varies between different PT reagents
46
Thrombin Time what does it measure
Time to fibrin clot formation, this bypasses clotting cascade
47
Thrombin Time what is involved in the testing
Bovine thrombin added to patient plasma
48
Elevated TT: what does it tell you
Heparin, Low or dysfunctional fibrinogen, DIC due to high D Dimer consumption
49
Reptilase time
Like thrombin time but uses snake venom, this is insensitive to heparin.
50
Half life of Factor VII
shortest half time (5-8 hours) requirement for plasma to be frozen within 8 hours.
51
Half life of Factor VIII
8-12 hours
52
plasminogen
inactive form of plasmin, is produced by the liver
53
TPA
Tissue plasminogen activator, along with urokinase converts plasminogen to active form Plasmin
54
Where does TPA come from
TPA is released slowly into blood from damaged blood vessels, so that once bleeding has stopped it's able to activate plasminogen and break down clots
55
Plasminogen in clot
plasminogen gets stuck inside of the clot so when it's activated to plasmin it is able to breakdown fibrin mesh
56
D-Dimer
fibrin degradation product
57
PAI
plasminogen activator inhibitor- inhibits TPA
58
D-Dimer or TT which is more specific
more specific that TT
59
Mixing studies
Mixes 1:1 with patient plasma and normal plasma, should allow a minimum of 50% factor activity, need approximately 30% to have normal PT/PTT
60
At what points (time) do you asess the PT and PTT during mixing studies
0 minutes and 90 minutes
61
Correction at 0 minutes and 90 minutes
indicates factor deficiency
62
Correction at 0 minutes but not 90 minutes
indicated time/temperature dependent inhibitor
63
No correction at 0 minutes or 90 minutes
Inhibitor (hepain, lupus anticoagulant)
64
Unfractionated heparin
Binds antithrombin and accelerates it's action against factor II (thrombin)
65
What tests does unfractionated heparin prolong
PTT and TT
66
unfractionated heparin is reversed with
protamine
67
LMWH
low molecular weight heparin (Enoxaparin example) binds antithrombin and preferentially inactivates factor Xa. small amount binds to thrombin
68
LMWH effect on PTT
usually does not affect PTT, needs to be montitored with anti-Xa levels
69
Warfarin (Coumadin)
Prevents vitamin K dependent factors from being synthesized (2, 7, 9 10, protein C and S)
70
Reversal of warfarin
Reversal with FFP, vitamin K and PCCs ( prothrombin complex concentration)
71
Direct thrombin inhibitors
Directly binds to thrombin and inhibit it's interaction with fibrin IV(bivalirudin, argatroban) oral (dabigatran)
72
Monitoring direct thrombin inhibitors
PTT. thromin time is too sensitive, only necessary for IV not oral, dilute thrombin time.
73
Reversal agent for direct thrombin inhibitors (oral)
Idarucizumab- FDA recently approved first reversal agent for Dabigatran
74
Direct Factor Xa inhibitors
inhibits both free and bound Xa (Rivaroxaban, apixaban, edoxaban)
75
Monitoring direct factor Xa inhibitors
anti-Xa if necessary, "heparin assay"
76
Reversal agent for direct factor Xa inhibitor
no reversal agent yet.
77
Hemophelia A
Factor VIII deficiency, x-linked recessive, most common severe hereditary bleeding disorder
78
Classification of severity based on factor levels
<1% severe 1-5% moderate >5% mild
79
Risk of providing factor replacement products
patient may develop antibodies against infused factors.
80
Recombinant Factor VIII or IX
recombinant products are safer tahn concentrates. PCC (for IX) FFP and CRYO, both are acceptable but no longer used due to better alternatives
81
Novo7
recombinant factor VII, for high titer inhibitor
82
vWF where is it made
synthesized in endothelial cells and megakaryocytes
83
vWF what it does
carrier for factor VIII, essential for interaction of platelets with damaged endothelium, binds to GP1b on surface of platelet
84
vWF levels based off blood type
AB>B>A>O
85
bleeding risk when vWF is at what level?
<40%
86
Lab tests for quantity of vWF
platelet function analysis (PFA100), Ristocetin cofactor activity, vWF antigen and activity levels (diagnose disease) and vWF multermer analysis (type)
87
vWF disease
congential or acquired, classification 3 types 1) Partial quanitative deficiency 2) Qualitative deficiency 3) severe quantitative deficiency
88
Therapy fro vWF disease
DDAVP (desmopressin) causes release of vwf from endothelial cells and platelets. Cryo- contains vwf Humate P- Factor VIII concentrate and vwf
89
BiG differences in vwd and hemophelia A (VIII)
vwf- abnormal PFA100 and RIPA where factor VIII is normal. aPTT is increased in VIII deficiency but normal in vw disease. Decreased vwf:Ag in vw disease
90
DIC
Disseminated intravascular coagulation, continual activation of the clotting and fibrinolytic cascades: Fibrin formation=Clotting, consumptive coagulopathy=bleeding
91
Lab results of DIC
prolonged PT and PTT, decreased fibrinogen, increased D-Dimer, low platelet count, schistocytes
92
D-Dimer
crosslinked fibrin molecule fragment
93
Clinical associations with DIC
sepsis, tissue injury (trauma, surgery, burn), obstetric complication (eclampsia, placental abruption) Malignancy-leukemia, intravascular hemolysis (HTRN) cardiovascular (aortic aneurysm), miscellaneious- snake bite, heat stroke, liver disease, severe anorexia, severe acidosis.
94
Treatment of DIC
treat underlying cause: plasma, cryo, heparin(clotting more than bleeding), anti-fibrinolytics (amicar)
95
anti-fibrinolytics
Amicar (bleeding more than clotting in DIC)
96
Cause of Elevated D-dimer
DIC, infection, active bleeding, thrombosis, tissue injury/surger, liver dysfunction, neoplasia
97
Thrombotic Thrombocytopenic purpura symptoms
Fever, thrombocytopenia, microangiopathic, hemolytic anemia (schistocytes, increased reticulocyte count, increased LDH and bilirubin, low haptoglobin) Neurologic symptoms-altered mental status, renal insufficiency
98
Cause of TTP
deficiency or inhibitor of ADAMTS-13 congenital or acquired
99
Treatment of TTP
plasma exchange or transfusion, steroids, rituximab, platelet transfusion IS CONTRAINDICATED!! will cause thrombosis
100
HIT
heparin induced thrombocytopenia- decreaesd platelet count after exposure to heparin count usually 50-60 K/mL or 50% of baseline. More common with unfractionated heparin but can also occur with low molecular weight heparin (enoxaparin)
101
cause of HIT
Antibody against heparin+ PF4
102
risks associated of HIT
high risk of thrombosis- arterial or venous
103
Treatment
discontinue all heparin, direct thrombin inhibitors (bivalirudin, argatroban), platelets are containdicated!!!
104
ITP
immune thromboctyopenic purpura- severely decreased platelet counts- usually <10K/mm3.
105
Antibody involved in ITP
usually anti- GPIIB/IIIA, unclear etiology
106
Treatment for ITP
Steroids, IVIG, Splenoctomy, platelet transfusion- risk is for bleeding not thrombosis (as in HIT and TTP)
107
PFA-100
platelet function assay, pushes patient blood through reusable cartridge coated with Collagen and ADP- causes clot formation and aperture to close. People with VW disease have abnormal PFA-100
108
RIPA
ristocetin induced platelet aggregation. uses patients live endogenous platelets- detect interaction between vWF and GP1B/V/IX. abnormal in patients with vWF
109
DIC abnormal lab values
increased D dimers, Decreased platelets decreased fibrinogen. Prolonged PT and aPTT, schistocytes present. All is due to the continuous activation of clotting and fibrinolytic cascades
110
MAHA
microangiopathic hemolytic anemia: schistocytes, increased retic count, increased LDH and bilirubin and low haptoglobin
111
Lupus anticoagulant
anti-phospholipid antibody found in lupus patients
112
Danaparoid
mixture of naturally occuring heparan sulfate, dermatan, chondoitin, alternative anticoagulant to HIT
113
aRGATROBAN
anticoagulant, inhibitor of thromibin, given as alternative to HIT
114
Fondapainux
anticoagulant amnagement of HIT
115
bivalrudin
anticoagulant management of HIT
116
what drugs can be given instead of heparin in HIT
Danaparoid, argatroban, fondapainux, bivalrudin
117
HIT causation, why clot?
upon receiving heparin, can form antibodies against heparin and PF4- platelet factor 4, this causes antibodies to bind to platelets and activate them releasing procoagulatory particles that cause thrombosis (specifically bind to FcjRIIIa on platelets)
118
What has a high association with HIT?
cardiac surgery patients.
119
Cryo reduced plasma
after cyro is made, this is for TTP exchange fluid use
120
When patient with Liver disease what coag factors are decreased
all except factor 8
121
When patient has DIC which factors are decreased?
all factors are decreased

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