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POD > hemostasis > Flashcards

hemostasis Flashcards

1
Q

what interacts to maintain hemostasis?

A

interaction of blood vessels, platelets, and soluble coagulation factors

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2
Q

what does coagulation refer to?

A

the soluble components of plasma that ultimately lead to the conversion of fibrinogen to fibrin and stabilization of the fibrin clot

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3
Q

what limits the size of a blood clot?

A

As quickly as fibrin clots are formed, the fibrinolytic system becomes activated (plasminogen to plasmin) to limit the size of the clot.

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4
Q

what are the functions of platelets?

A

> Form platelet plugs
- seal defects in damaged vessels
Participate in inflammation
Adhere to subendothelial collagen
-Adherence mediated by vWF

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5
Q

what is vWF

A

adhesive glycoprotein that is important for platelet-platelet and platelet-vessel hemostatic interactions

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6
Q

what are shift platelets?

A

younger, larger platelets that are larger than a red cell

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7
Q

broadly, what do platelet granules contain? What types are there?

A

a variety of substances important for hemostasis. there are alpha granules, dense bodies, and lysosomes.

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8
Q

what do platelet alpha granules contain?

A

beta-thromboglobulin
factor VIII-related antigen (FVIII-RA or vWF)
platelet factor 4
fibrinogen

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9
Q

what do platelet dense bodies contain?

A

ADP, histamine, and serotonin

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10
Q

what do platelet lysosomes contain?

A

variety of proteolytic enzymes

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11
Q

what hormone controls platelet production? How does it work?

A

thrombopoeitein
-binds to the surface of platelets
-concentration proportional to platelet mass (number x volume)
-smaller platelet mass means more free thrombopoietin > more is free to stimulate production in the bone marrow

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12
Q

where can 1/3 of platelets be found? What can change this?

A

splenic pool
–more will be here with splenic congestion
-less with excitement, splenic contraction (= more in the blood)

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13
Q

what allows for the adherence of platelets? what mediates this?

A

Disruption of endothelium and exposure of subendothelial collagen
-adhesion mediated by von willebrand factor, present in endothelial cells and megakaryocytes

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14
Q

how is a platelet plug formed?

A

-platelet associates with subendothelial collagen > adheres via vWF
-shape change, exposure of surface receptors for fibrinogen
-aggregation
-platelet granule release, ADP enhances aggregation
-arachadonic acid production
-chemical reactions, platelets form gel like mass

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15
Q

how to quantify platelets. Not reliable in which animal and why? Difficult in which other animals and why?

A

-EDTA-anticoagulated blood
-less than 8 hours from sampling
-cat platelets overlap in size with RBCs so machines are tricked
-small RBCs in small ruminants can look like platelets
-cattle have tiny platelets, can go undetected

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16
Q

what is BMBT and what does it measure? When should we use this test and why? what factors can effect this test?

A

buccal mucosal bleeding time
-evaluates platelet function and/or number
- A small, standardized incision is made in the oral mucosa and the time to cessation of bleeding is measured
-can have normal numbers but abnormal function
-don’t do if hemorrhage related to low platelet count
-standard incision on mucous membrane
-may be increased in vWD
-drug treatments
-increase with DIC, uremia, myeloma
-unaltered by coagulation factor deficiencies

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17
Q

how will iron deficiency effect platelets?

A

makes them small

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18
Q

platelet concentration changes due to:

A
  1. increased destruction or consumption e.g. DIC, ITP
  2. decreased production in bone marrow
    e.g. myelophthisis due to neoplasia, drug-induced
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19
Q

what is von Willebrand disease? What are the signs?

A

-inherited disease, common in dobermans
-3 types
clinical signs:
>petechial hemorrhages not usually present
>bleeding from mucous membranes
>prolonged bleeding after trauma, surgery, venipuncture

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20
Q

what does von willebrand factor do, specifically?

A

-allows platelet adhesion to subendothelium, other platelets, stabilizes FVIII

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21
Q

how do we diagnose vWD?

A

-clinical signs, breed
- +/- BMBT, APTT
- vWF antigen, ELISA
- genetic test for breed, collagen binding assay, multimer analysis

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22
Q

platelet function defect common in basset hounds

A

thrombopathy

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23
Q

what platelet issues do otterhounds, fox hounds, and scottish terriers have?

A

thrombasthenic thrombopathia

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24
Q

what platelet issues do semmintals have?

A

epistaxis

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25
Q

what is thrombocytopenia? what causes it?

A

-decreased platelet count
-due to increased destruction or consumption

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26
Q

what is IMT? What can cause it? what does it lead to?

A

-A common cause of decreased platelet count is immune-mediated thrombocytopenia (IMT)
-can be autoimmune or related to foreign antigens bound to platelets
-drugs, rickettsia, bacteria, viruses, mod live vaccines can cause
-leads to marked thrombocytopenia

27
Q

how can DIC cause thrombocytopenia and to what degree?

A

moderate thrombocytopenia due to consumption

28
Q

what production issues can lead to thrombocytopenia?

A

 (auto)immune
 bone marrow disease
 myelophthisis
 infectious agents
 drugs
 radiation
 cyclic hematopoies

29
Q

does hemorrhage lead to thrombocytopenia?

A

no, only very rarely in massive blood loss cases. Thrombocytopenia usually the cause for hemorrhage.

30
Q

what is splenic sequestration’s relationship with thrombocytopenia?

A

-platelet mass not actually decreased, usually no clinical signs as platelets can be mobilized if needed

31
Q

what is thrombocytosis and when do we see it?

A

-increased platelet count due to:
-rebound
-inflammatory disease
-splenectomy, splenic contraction
-hemorrhage, blood-sucking parasites
-paraneoplasia
-iron deficiency
-non-neoplastic FeLV-associated disease
-myeloproliferative disease (MPD)
>primary thrombocythemia
>megakaryoblastic leukemia

32
Q

where are pro-coagulation factors made?

A

-in the liver; most are enzymes

33
Q

what are the contact pro-coagulation factors?

A

XI, XII, XIII, prekallikrein

34
Q

what are the vitamin K dependent coagulation factors?

A

Vitamin K dependent factors – II, VII, IX, X (think 1972)

35
Q

what are the non-enzymatic pro-coagulation factors?

A

V, VIII, fibrinogen

36
Q

what is the goal of pro-coagulation factors

A

make thrombin and fibrin

37
Q

what are the Anti-coagulant / Pro-fibrinolytic Factors? what is their goal?

A

 Antithrombin III (w/ heparin)
 Protein C (also Vitamin K dependent)
 Tissue factor pathway inhibitor (TFPI)
Plasminogen > Plasmin (degrades fibrin clots)

Goal - localize and minimize clot

38
Q

what are the different pathways for coagulation?

A

-contact (intrinsic) pathway
-tissue factor (extrinsic) pathway
>these converge at the common pathway

39
Q

what instigates the extrinsic coagulation pathway?

A

exposure of blood clotting factors to the tissue factor in the extravascular tissue
-induced by injuries to blood vessels

40
Q

what instigates the intrinsic coagulation pathway?

A

-involves only factors within blood vessels
-activated by exposed endothelial collagen

41
Q

what factors are involved in the beginning step of contact activation?

A

PK, XII, HMWK

42
Q

what steps are involved in the contact pathway, before the common pathway takes over?

A

FXI > aFXI
FIX > aFIX
FVIII

43
Q

what steps are involved in the extrinsic pathway before the common pathway takes over?

A

tissue factor
FVII

44
Q

what steps are involved in the common pathway?

A

FX > aFX
FV
FII (prothrombin)
FI (fibrinogen)

45
Q

where does the coagulation cascade occur? How?

A

◦ On the surface of platelets - platelet plug
> Negative charge, receptors for certain coag. factors
>Ca++ helps negative platelet interact with negatively charged factors

46
Q

when are citrated tubes used?

A

APTT, OSPT, fibrinogen

47
Q

what is ACT? What does it test? What is its purpose and when/how does it work?

A

Activated Clotting Time
 Contact (intrinsic) & common pathway defects
 special tube, 37 C incubation
 factor deficiency detected if < 5% of normal
 less sensitive than APTT
 marked decrease in platelets will result in prolongation; ideally do when platelet count is normal
Advantage – Inexpensive, can do in practice

48
Q

What is APTT? What does it test? How does it work?

A

Activated Partial Thromboplastin Time (aka PTT)
 contact (intrinsic) & common pathway defects
 citrated sample, 9:1
 separate plasma quickly
 few hours 4 C, > 4 hours freeze
 factor deficiency detected if < 30% of normal
** Not affected by thrombocytopenia

49
Q

What diseases can we detect with APTT?

A

 hemophilias, some vWD cases
 DIC
 hereditary factor XII or XI deficiency
 vitamin K deficiency/antagonism
 therapeutic anticoagulation

50
Q

what is caused by FVIII deficiency?

A

hemophilia A

51
Q

What is OSPT? What does it test for?

A

One-Stage Prothrombin Time (OSPT or PT)
-Deficiencies in the tissue factor (extrinsic) and common pathways in which a factor is present at 30% or less

52
Q

What diseases can we detect with OSPT? Does thrombocytopenia affect this?

A

-hereditary factor VII deficiency
-DIC
-vitamin K deficiency/ antagonism
**not affected by thrombocytopenia

53
Q

how do we detect increased fibrinogen

A

heat precipitation

54
Q

amount of fibrinogen is inversely proportional to?

A

thrombin clotting time (TCT)

55
Q

what conditions could lead to decreased fibrinogen?

A

-hereditary hypo or dysfibrinogenemia
-**DIC
-therapeutic anticoagulation
-liver disease

56
Q

how do we test for Fibrin-Fibrinogen Degradation Products (FDPs) and d-dimers

A

-blood collected in citrated tubes
-The plasma is collected and a latex agglutination test is used to determine the concentration of FDPs
-can also test urine

57
Q

what conditions increase FDPs?

A

Increased concentrations of FDPs are seen with DIC, hemorrhage into body cavities, and decreased kidney function

58
Q

why are FDPs a problem?

A

interfere with normal platelet function

59
Q

What is DIC? What happens when it occurs?

A

Disseminated Intravascular Coagulation (DIC)
-common result of many disease processes
-Initially in DIC there is excessive coagulation exhausting the nonenzymatic coagulation factors due to systemic exposure to tissue factor
-The fibrinolytic mechanism is activated. Subsequently hemorrhage develops as a result of the depletion of coagulation factors and enhanced fibrinolysis.
=>consumption coaguopathy, microangiopathic
=>hemolytic anemia

60
Q

What do we look for to diagnose DIC?

A

 Appropriate clinical setting
 increased OSPT & APTT
 increased FDPs
 decreased Fibrinogen
 decreased Platelets
 RBC fragmentation (schistocytes)

61
Q

what can cause hypercoagulability, besides the causes of DIC?

A

in addition to the causes of DIC:
 hypoalbuminemia
 loss of antithrombin III
 polycythemia
 hyperviscosity, proteins/cells
 shock
 drugs, platelet agonists
 snake bites, other toxins

62
Q

what are some other common coagulation tests, other than ACT, APTT, OSPT

A

 Individual factor assays
o Coagulation based assay vs. chromogenic assay
o FII, FV, FVII, FVIII, FIX, FX, FXI, FXII
 Antithrombin
 D-dimer assays – alternative to FDPs
 Thromboelastography

63
Q

what is TEG tracing?

A

Thromboelastography (TEG) is a viscoelastic hemostatic assay that measures the global viscoelastic properties of whole blood clot formation under low shear stress
-tests clot strength (platelet function), clotting time (clotting factors), clot kinetics, and clot stability/clot breakdown

POD (21 decks)

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