Coagulation and Lab Evaluation Flashcards

1
Q

Primary hemostasis

A

Vessel/platelets/vWF interactions

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

Secondary hemostasis

A

Coagulation and anticoagulant factors, cross links the platelet plug to strengthen it

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

Fibrinolysis

A

Plasmin activation and fibrin and dissolution

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

Coagulation cascade enzymatic reactions 3

and 2 requirements

A

1) formation of thrombin
2) conversion of fibrinogen into fibrin
3) clot stabilization/formation

Phospholipid surface (platelets) and Ca2+

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

Production center of coagulation factors

A

Liver

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

Liver function/dz

A

removes activated coagulation factors.

If diseased can result in the hypocoagulation

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

Vitamin K dependent factors Canada

A

II, VII, IX, X 1972

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

3 likes that merge for coagulation cascade

A

Intrinsic, extrinsic, common

occur simultaneously

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

coagulation is primarily activated through…

A

extrinsic

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

Intrinsic components

A

not 12…. but 11.98

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

extrinsic components

A

III (TF)

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

PT

A

Extrinsic system - Play Tennis (outside - Extrinsic)

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

PTT

A

Intrinsic system - Play Table Tennis (inside - intrinsic)

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

Common pathway factors

A

10,5,2,1

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

Intrinsic pathway initiation

A

factor 12 in contact with a negatively charged surface

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

Factor XII deficiency

A

Common in Cats.

prolonged clotting time even though not clinically bleeding

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

Factor VIII and IX deficiency

A

sex-linked
Hemophilia A: VIII
Hemophilia B: IX

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

Extrinsic pathway initiation

A
Factor III  (tissue factor) exposure at site of tissue injury activates X and IX (crosses over to intrinsic)
can be activated during traumatic venipuncture (clotted sample)
19
Q

Factor VII

A

Produced in liver, vit. K dependent
shortest half life of Vit. K dependent factors
first factor to deplete in early rodenticide toxicity
USE TEST PT for vit K antagonist

20
Q

Common Pathway initiation

A

Thrombin responsible for amplification of hemostasis (PT/PTT tests used in combo to test this)
Promote platelet aggregation and activation

21
Q

Antithrombin

A

inhibitor of coagulation
lost in protein-losing nephropathies/enteropathies
Consumed in DIC
Directly inhibits thrombin and indirectly inhibits thrombin formation

22
Q

anticoagulant Proteins other from Liver

A

Proteins C and S

Fibrin(ogen) degradation products

23
Q

Fibrinolytic proteins (break down clots)

A

Plasmin degrades fibrinogen, fibrin monomers/polymers, and cross-linked Fibrin
leads to FDPs and D-Dimers

24
Q

FDP vs. D-Dimers

A

formed from degradation of fibrinogen, fibrin and cross-linked fibrin (ANY PART OF THE MESH WORK)
D-dimers are formed only from degradation of cross-linked fibrin SPECIFICALLY FOR CROSS LINKED

25
Q

Activated Clotting Time (ACT)

A

Intrinsic and common pathway.
Severe thrombocytopenia (,10,000/uL) may prolong clot time
requires significant depletion of a factor to be abnormal

26
Q

Samples collected for coagulation

A
trisodium citrate (Blue Top) for PTT, PT, TT
avoid traumatic venipuncture
27
Q

PTT

A
Partial Thromboplastin Time
intrinsic and common
Prolonged when at least one factor of these pathways are decreased to 30% of normal
NOT affected by thrombocytopenia
NOT an indicator of hypercoaguloability
28
Q

PT

A
Prothrombin Time 
Extrinsic and common pathways
Prolonged when at least one factor is decreased by 30% 
NOT affected by thrombocytopenia
NOT indicator of hypercoagulability
29
Q

Fibrinogen concentration 2

A

Heat precipitation - (point of care) only detects large differences. Better at determining INCREASED concentrations with inflammatory disease
low concentration is indicative of decreased production or increased consumption (DIC)
Clauss method - (laboratory use) assess thrombin conversion to fibrinogen and fibrin, time to clot is measured
Prolonged suggests low or absent FIBRINOGEN

30
Q

FDP

A
detect increased fibrin(ogen)olysis
increased concentration seen with: Thrombosis/thromboembolism
DIC
Internal hemorrhage
Surgery
Liver Dz (lack antithrombin 3)
Kidney Dz (same as liver)
31
Q

D- Dimers

A

increase in only fibrinolysis

thromboembolic dz or DIC (detects an antigen when fibrin is cross-linked)

32
Q

Antithrombin III

A

reported as a percent of normal
Lower than 70% increased risk for thrombosis
decrease: decreased production (increased consumption or loss):
Liver dz (production
Protein losing enteropathy/colic (loss)
Protein losing neuropathy (loss)
DIC (consumption)

33
Q

Evaluate the bleeding pattern of bleeding patient (3)

A

Primary hemostatic defect
Secondary hemostatic defect
Mixed

34
Q

Primary Hemostatic defect

A
defects in platelets or vessels: 
Petechia
Ecchymoses
spontaneous bleeding from MM
Prolonged bleeding from injections site
35
Q

Primary Hemostatic defect evaluation

A

Platelet count

Buccal Mucosal Bleeding Time (BMBT)

36
Q

Secondary Hemostatic defects

A

acquired disorders or congenital cause leading to:
Hematomas
bleeding into joints, m., body cavity
Injection site initially clots and bleeding reoccurs later (clot not stable)

37
Q

Secondary Hemostasis defect evaluation

A

ACT, PTT, PT, TT

38
Q

congenital causes

A

RARE:
factor XII deficiency
Hemophilia A and B (Factors VII and IX)

39
Q

Acquired causes

A

More COMMON:
Vit. K antagonism/malabsorption
Markedly impaired liver function

40
Q

Vitamin K Antagonism

A

Rodenticides: inhibit recycling of Vitamin K1
Moldy sweet clover
ACT, PTT, PT prolonged
IF EARLY ONLY INCREASE IN PT
Deficiency (not able to absorb Vit. K): biliary obstruction or severe enteric dz

41
Q

Coagulopathy associated with liver dz

A

Decreased production of coagulation factors!
Decreased clearance!
ACT, PTT, PT prolonged increase FDPs
can progress to DIC

42
Q

Mixed hemostatic defect

A

Clinical and laboratory tests that indicate a defect in both primary and secondary

DIC IS THE BIG ONE!
disseminated intravascular coagulopathy (Death Is Coming)
really the only one

widespread thrombus formation and hemorrhage
ALWAYS secondary to another process

43
Q

Common Causes of DIC

A

Sepsis, neoplasia, severe trauma, heat stroke

44
Q

Evaluation for DIC

A

platelet numbers are classically mild to moderate

1) thrombocytopenia combined with prolongations of the PT and/or PTT
2) decrease in ATIII or fibrinogen due to consumption
3) Increased FDPs or D-dimers
4) Fragmented erythrocytes (small animal)