Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Board Review 2020 > Coagulation Phys > Flashcards

Coagulation Phys Flashcards

1
Q

What is the difference between the cell based model and the traditional model?

A

Traditional: two pathways operate semi-independent distinct, redunt interactions between factors and cells are limited
Cell based model: Plasma does not clot therefore cells invovled

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

What is the extrinsic pathway of coagulation

A

Tissue Damage —> Tissue factor + Ca –> FVIIa with Ca + Phospholipid –> FXa

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

What is the intrinsic pathway of coagulation

A

Damaged vessel –> FXII —> FXI + Ca —-> FIX w/ FVIII + Ca + plt phospholipid —> FX

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

What are the Vitamin K factors and why is one more likely decreased?

A

Thrombin (II), FVII, IX, X

FVII shortest 1/2 life 4-6 hrs

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

What Coagulation factors are tested in PT

A

Extrinsic and common pathway

Added to TF, phospholipid, and Ca

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

What coagulation factors are tested in PTT

A

Intrinsic and common

Added to contact activator and phospholipid and Ca

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

In the cell based model of coagulation what is the initiation phase:

A

‘Spark’ Tissue factor exposed to endothelium to circulating FVII forms complex with Ca
Extrinsic factor tenase complex activates FXa w/ FV get thrombin formation
Tissue factor inhibitor inhibits Extrinsic factor tenase complex

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

In the cell based model of coagulation what is the amplification phase

A

Thrombin burst: Activation and aggregation of platelets
Thrombin activates FVIII which binds with FIX to make intrinsic factor tenase complex—> FX with Ca
50-100 times more thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

In the cell based model of coagulation what is the propagation phase

A

Dependent on platelets: Leads to fibrin deposition

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

What are the procoagulation effects of thrombin

A

FV, Fibrin, FXI, FXIII, TAFI

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

What are the anticoagulation effects of thrombin

A

Plasmin, Protien C (by binding with thrombomodulin)

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

How does uremeic thrombocytopathy affect coagulation

A

Increased thrombosis, increased fibrin activation of P-selectin, abnormal release of microparticles

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

What is the pathway of fibrinolysis

A

tPA (tissue plasminogen activator) Released from vascular endothelial cells binds and activates plasminogen to plasmin
Plasmin molecules bineds to lysine residues on fibrin

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

What is the difference in FDPs and D-dimers

A

FDPs- are fibrin and cross-linked fibrin

D-Dimers- only cross-linked

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

What are the regulators of fibrinolysis

A

Plasminogen activator inhibitor-1 (PAI-1)
Alpha 2 Antiplasmin
Thrombin-activated Fibrionlysis inhibitor (TAFI)

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

What does Plasminogen activator inhibitor 1 do

A

inhibits tPA and uPa

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

What does alpha 2 antiplasmin do

A

Forms complex with plasmin

Prevents plasminogen into active clot

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

What does Thrombin-activated fibrinolysis inhibitor do

A

Down regulates fibrinolysis prevents palsmin from binding fibrin

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

What is the difference between primary and secondary hyperfibrinolysis

A

Primary: quantitative /qualitative abnormalities in regulation of fibrionlysis
Secondary: hyperactivity of normal fibrinolysis due to other coagulation abnormaliteies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the difference in TEG versus Rotem

A

TEG: Cup moves around stationary pin
ROTEM: Pin moves around stationary cup

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the treatment for low fibrin

A

cyroprecipitate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How is hyperfibrinolysis develop with cavitary effusions

A

Anticoagulant environment, mesothelial cells secrete tPA and uPA, increase local expression of Protien C
Systemic due to reabsorption of hyperfib fluid via thoracic duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does hyperfibrinolysis develop with hepatic failure?

A

decreased hepatic production of alpha 2 atniplasmin

decreased clearance of plasminogen activators and plasmin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the MOA of EACA and TXA

A

Lysine analogues competitively bind c-terminal lysine sties on plasminogen
Plasmin formation is inhibited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are platelets, how long til mature
anucleate cytoplasmic fagments from megakaryocytes | Mature in 3-5 days, life span 5-7 days
26
What are 4 key features of platelets for coagulation
Phospholipd membraned with high density regulated adhesive receptors Cytoskeleton with contractile proteins dense tubular system equest/release Ca Secretory granules
27
What are the types of platelet secretory granules and what is included
Alpha granules: fibrinogen, P-selectin, Factor V, FXI, growth factors, VWF Dense granules: released for mass platelet attraction ADP, Epiniphrine, serotonion, histamine, calcium
28
How does platelet adhesion occur
Subendothelial collagen exposed with vascular injury GPV1 or GP1b-IX-V receptor w/ VWF alpha 2b Beta 2 (GP2B3A) intrigren with VWF
29
Where is VWF produced and stored
Produced by endothelial or megakaryocytes Stored in weibel-palade bodies Also prevents degredation of FVII
30
Which VWF has the higher affinitiy for platelets
Larger
31
What occurs in activation to lead to increased platelet binding
Adhesion triggers intracellular signaling to alpha 2bB3 to high affinity for further adhesioin membrane flipping exposing phosphaltidylserine creating a neg charge (scrambalase) Contractile protein change shape to incrase surface area Dense granules TXA2 Potent platelet agonist stimulated by AA and Cox
32
What occurs in platelet aggregation
Adhesion of activated platelets to each other using receptor bound fibrinogen
33
What are the normal inhibitory mechanism of platelet activation and aggregation
Endothelial cells relase ADPase, prostacyclins: inhibit platelet activation Negatively charged glycocosaminoglycans release nitric oxide to inhibit aggregation
34
What are the three types of VW disease
1: low multimers of all sizes 2: variable concentrations, absence of large size 3: marked reduction/absence of all sizes
35
What are three tests of platelet function
``` PFA-200: adhesion under shear stress Light transmission aggegometry Electrical impedance (muultiplate): ```
36
What is the MOA of coagulapothay with rattle snake envenomation
Local: Metalloprotienases damage extracellular matrix proteins mostly collagen Phospholipase A2, protein C, antithrombin, and FV denaturation Leads to decreased platelets, consumptive coagulatoapthy
37
What is the MOA of uremic bleeding
Primary hemostasis Platelet secretion defects abnormal vessel wall interaction Increase platelet inhibitors, uremic toxins
38
How does anemia result in hypercoagulable viscoelastic testing
Increase of clotting factors per volume of RBCs
39
What is the MOA of Rivaroxabain
Directly inhibits factors Xa | Renal and biliary excretion
40
What is the MOA of Warfarin
Vitamin K antagonist | FII, VII, IX, X
41
What is the MOA of unfractionanted heparin
Increase activity of antithrombin 3 Inhibit Xa and IIa (thrombinogen) Inhibits thrombin formation
42
What is the MOA of LMWH
Binds AT3, Higher impact on Xa vs. IIa
43
What is the MOA of daltparin
Binds AT3, Higher impact on Xa vs. IIa
44
What is the MOA of Enoxaparin
Binds AT3, Higher impact on Xa vs. IIa
45
What is the MOA of protamine
Postive cationic that forms a salt with heparin
46
What is the MOA of clopidogrel
ADP irreversible P2Y12 inhibitor | Platelet activation inhibitior
47
What is the MOA of Aspirin
Irreversible inhibition of TXA2 formation | Inhibits platelet activation
48
What is the MOA of NSAID in coagulation
Reversible inhibition of TXA 2 Formation inhibits platelet activation
49
What is the proposed MOA of Yunnan biayo
enhanced expression of surface glycoprotiens on platelets under condition of stimulation
50
What are the eitologies of aortic thrombosis in dogs
Disregulation mechanisms-- Increase generation of prothombotic elements Inhibition of anticoagulation mechanisms Inhbition of thrombolysis via fibrinolytic system
51
What is virchawos triad in aortic thrombosis in dogs
alterations in flow endothelial damage Hypercoagulable states
52
Name 10 underlying disease process that have been reported with ATE
PLN, PLE, HypoT4, Hypo adrenal, hyperadrenal, Immune mediated disease, DM, neoplasia, steroid administration, endocardiosis, PDA endocarditis, Spiroceria
53
What is the difference between arterial and venous clots
Arterial: high shear, VWF, Platelet rich, Tx with platelet inhibitors Venous: low shear, fibrinogen, RBCs, WBCs, Fibrin, anticogulants
54
How does PLN lead to ATE in dogs
Loss of antithrombin 3 in kidneys
55
How does TRALI occur after blood transfusion
antibiodies in donor plasma agains antigens present in reciepnt leukocytes (why leukoreduction might not help)
56
What are 7 factors that make IMHA patients hypercoagulable
excessive platelet activation TF expression of microparticles Sequestation of nitric oxide Cytokine induce endothelial TF expression Monocyte activation of TF expession TF expressing microparticles derived from monocytes bind to endothelium Phosphatidylserine exposing particles released from platelets
57
How does oxidative hemolysis lead to anemia
denaturation of hemoglobin leads to heinz body formation Methehemoglobinemia Felines more susceptible due to sulfhydroxyl groups
58
How does Zinc lead to anemia
Intravascular hemolysis | Pennies after 1982, bolts, screws, skin products
59
How does endogenous heparin sulfate work and where is it found
On glycocalyx. Works with antithrombin to inhibit II and X
60
What are eicosanoids
Signaling molecules generated following release of arachadonic acid from phospholipid bilayers of cells especially platelets and immune cells
61
What are the canine dog blood types
DEA 1.1, 1.2, 1.3, 3, 4, 5, 7 | Dahl
62
Which blood type is most common and which is most immunogenic in dogs
1.1 most immunogenic | Alloantibiotied against 7 highest
63
What is leukoreduction
Filter the blood to remove WBCs (platelets) prior to storage
64
What is cryopriciptate
Contains FVIII, VWF, Fibrinogen, and FXIII
65
What disease processes if cryopreciptate used for and what is it better than FFP for
VWD and hemophillia | More effective at increasing BMBT in VWD
66
Define Massive transfusion- at least three
1 blood volume in 24 hrs 50% of blood volume in 3 hrs 150% of blood volume regardless of time 1.5 ml/kg/min of blood products for 20 minutes
67
What shock index in dogs is likely to result in transfusion after blunt trauma
SI > 1.43 | 71% resulted in transfusions
68
Define the blood vicious cycle of ATC
bleeding --> resuscitation --> dilutional and hypothermia --> coagulopathy ---> bleeding
69
What are complications of massive transfusions
Transfusion reactions Hypocalcemia (citrate from blood or failure of liver to break down citrate) Hypomagnesemia HyperK (increase K in RBC supernate Hypothermia metabolic alkalosis--- citrate broken down to bicarb Metabolic acidosis--- units have low pH
70
Name immunologic transfusion reactions state if delayed or acute
Hemolytic -acute Fever- acute Uticareia - acute Transfusion realted immunomodulation (TRIM) - delayed
71
Name acute non immunologic transfusion reactions (9)
``` TACO Vomiting ARDS Infectious disease citrate toxicity TRALI Dilutional thrombocytopenia embolism Hemosiderosis (iron overloade ```
72
In hemolytic transfusion reactions what is the mechanism
Type II hypersenstivity | Steroids/antihistamines won't prevent
73
In febrile non hemolytic reactions what is the mechanism
cytokines and WBCs in donor unit | Steroids and antihistamines won't prevent

Board Review 2020 (37 decks)

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