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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
what is thrombocytopenia? what causes it?
-decreased platelet count -due to increased destruction or consumption
26
what is IMT? What can cause it? what does it lead to?
-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
how can DIC cause thrombocytopenia and to what degree?
moderate thrombocytopenia due to consumption
28
what production issues can lead to thrombocytopenia?
 (auto)immune  bone marrow disease  myelophthisis  infectious agents  drugs  radiation  cyclic hematopoies
29
does hemorrhage lead to thrombocytopenia?
no, only very rarely in massive blood loss cases. Thrombocytopenia usually the cause for hemorrhage.
30
what is splenic sequestration's relationship with thrombocytopenia?
-platelet mass not actually decreased, usually no clinical signs as platelets can be mobilized if needed
31
what is thrombocytosis and when do we see it?
-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
where are pro-coagulation factors made?
-in the liver; most are enzymes
33
what are the contact pro-coagulation factors?
XI, XII, XIII, prekallikrein
34
what are the vitamin K dependent coagulation factors?
Vitamin K dependent factors – II, VII, IX, X (think 1972)
35
what are the non-enzymatic pro-coagulation factors?
V, VIII, fibrinogen
36
what is the goal of pro-coagulation factors
make thrombin and fibrin
37
what are the Anti-coagulant / Pro-fibrinolytic Factors? what is their goal?
 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
what are the different pathways for coagulation?
-contact (intrinsic) pathway -tissue factor (extrinsic) pathway >these converge at the common pathway
39
what instigates the extrinsic coagulation pathway?
exposure of blood clotting factors to the tissue factor in the extravascular tissue -induced by injuries to blood vessels
40
what instigates the intrinsic coagulation pathway?
-involves only factors within blood vessels -activated by exposed endothelial collagen
41
what factors are involved in the beginning step of contact activation?
PK, XII, HMWK
42
what steps are involved in the contact pathway, before the common pathway takes over?
FXI > aFXI FIX > aFIX FVIII
43
what steps are involved in the extrinsic pathway before the common pathway takes over?
tissue factor FVII
44
what steps are involved in the common pathway?
FX > aFX FV FII (prothrombin) FI (fibrinogen)
45
where does the coagulation cascade occur? How?
◦ On the surface of platelets - platelet plug > Negative charge, receptors for certain coag. factors >Ca++ helps negative platelet interact with negatively charged factors
46
when are citrated tubes used?
APTT, OSPT, fibrinogen
47
what is ACT? What does it test? What is its purpose and when/how does it work?
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
What is APTT? What does it test? How does it work?
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
What diseases can we detect with APTT?
 hemophilias, some vWD cases  DIC  hereditary factor XII or XI deficiency  vitamin K deficiency/antagonism  therapeutic anticoagulation
50
what is caused by FVIII deficiency?
hemophilia A
51
What is OSPT? What does it test for?
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
What diseases can we detect with OSPT? Does thrombocytopenia affect this?
-hereditary factor VII deficiency -DIC -vitamin K deficiency/ antagonism **not affected by thrombocytopenia
53
how do we detect increased fibrinogen
heat precipitation
54
amount of fibrinogen is inversely proportional to?
thrombin clotting time (TCT)
55
what conditions could lead to decreased fibrinogen?
-hereditary hypo or dysfibrinogenemia -**DIC -therapeutic anticoagulation -liver disease
56
how do we test for Fibrin-Fibrinogen Degradation Products (FDPs) and d-dimers
-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
what conditions increase FDPs?
Increased concentrations of FDPs are seen with DIC, hemorrhage into body cavities, and decreased kidney function
58
why are FDPs a problem?
interfere with normal platelet function
59
What is DIC? What happens when it occurs?
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
What do we look for to diagnose DIC?
 Appropriate clinical setting  increased OSPT & APTT  increased FDPs  decreased Fibrinogen  decreased Platelets  RBC fragmentation (schistocytes)
61
what can cause hypercoagulability, besides the causes of DIC?
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
what are some other common coagulation tests, other than ACT, APTT, OSPT
 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
what is TEG tracing?
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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