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VET433: ECC & Toxicology > Bleeding & Hemostasis > Flashcards

Bleeding & Hemostasis Flashcards

1
Q

components of the hemostatic system

A
  • circulating blood (contains platelets and coagulation factors)
  • endothelium
  • subendothelial matrices
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2
Q

how is hemostasis regulated

A

balance of pro and antithrombotic properties
- prevents inappropriate thrombosis
- allows rapid hemostasis if injured

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3
Q

steps of hemostasis

A
  1. vasoconstriction
  2. primary hemostasis
  3. secondary hemostasis
  4. fibrinolysis
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4
Q

primary hemostasis

A

formation of a platelet plug

involves:
- platelets
- vWF
- endothelium

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5
Q

resting endothelial cell properties

A
  • inactive
  • have an ANTIcoagulant surface to prevent platelet adherence
  • no expression of tissue factor or exposure of collagen
  • normal vWF levels
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6
Q

anticoagulant endothelial cell membrane

A

when inactive - endothelium has a neutral outer phospholipid membrane and a procoagulant inner membrane (negatively charged)

maintained by flippase and floppase enzymes

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7
Q

how does endothelium change when vascular injury occurs

A
  • activated
  • scramblase enzyme flips the phospholipids so that the outer membrane becomes procoagulant
  • facilitates adhesion of circulating platelets
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8
Q

platelets

A

anuclear, discoid shaped fragments of megakaryocytes

primary effectors of hemostasis - secretes granules that facilitate hemostasis

SHORT lifespan (7-10 days)

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9
Q

steps of platelet activation

A
  1. initiation (adhesion)
  2. extension (activation)
  3. stabilization (aggregation)
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10
Q

platelet initiation/adhesion

A
  1. vascular injury causes exposure of collagen + vWF
  2. circulating platelets tether to vWF and collagen
  3. platelets roll along endothelium
  4. adhesion of a platelet monolayer over injured endothelium –> forms platelet plug
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11
Q

platelet extension/activation

A
  1. additional platelets adhere to platelet plug
  2. platelets get activated by adhesion and soluble agonists
  3. changes platelet from low to high affinity state

high affinity platelets
- increased granule release
- procoagulant membrane formation
- integrin activation (aIIbB3)

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12
Q

platelet stabilization/aggregation

A
  1. aIIbB binds to fibrinogen to initiate aggregation
  2. allows fibrinogen, fibrin, and vWF to bind to aIIbB3
  3. initiates outside-in signaling leading to:
    - clustering of integrins
    - actin remodeling
    - clot retraction
  4. stabilizes platelet plug
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13
Q

secondary hemostasis

A

formation of a stable fibrin clot

involves:
- coagulation factors

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14
Q

coagulation factors

A

factors that circulate as inactive zymogens

requires activation via coagulation cascade

some may require activation by vitamin K

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15
Q

what is used as the docking site for the assembly of coagulation complexes

A

pro-coagulant phospholipid membrane on cell surface

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16
Q

coagulation cascade

A

series of zymogen cleavage into active clotting factors

allows for signal amplification and multiple points of regulation

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17
Q

extrinsic pathway

A

initiated by endothelial injury

  1. injury exposes tissue factor (III)
  2. tissue factor binds to factor VII
  3. factor VII activates factor X
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18
Q

intrinsic pathway

A
  1. factor XII activates factor XI
  2. factor XI activates factor IX
  3. factor IX activates factor VIII
  4. factor VIII activates factor X
19
Q

common pathway

A
  1. activated factor X (from intrinsic and extrinsic), V, and C cleave prothrombin (factor II) into thrombin
  2. thrombin cleaves fibrinogen (factor I) into fibrin
  3. thrombin activates factor XIII
  4. factor XIII binds active C to create fibrin cross links that stabilize the clot
20
Q

how does coagulation in vivo typically work

A

mostly via the extrinsic pathway

tissue factor (III) + factor VII are the main initiators of clotting in vivo

21
Q

thrombin

A

pro-inflammatory:
- activates platelets
- activates TF V, IX, XI, XIII
- cleaves fibrinogen into fibrin
- crosslinks fibrin

has some anticoagulant and fibrinolytic properties

22
Q

fibrinolysis

A

breakdown and removal of clot

goal is to reestablish blood flow after vascular healing

HIGHLY regulated balance of proteolytic and inhibitory proteins

23
Q

plasminogen/plasmin

A
  1. plasminogen gets cleaved into plasmin by activators
  2. plasmin cleaves fibrin to form fibrin degradation products (FDPs) and D-dimers
24
Q

FDPs vs D-dimers

A

FDPs: breakdown product of all fibrin
D-dimers: breakdown product of cross-linked fibrin only

25
Q

what are primary hemostatic disorders

A

abnormalities in PLATELET number or function

can also be caused by vWF or endothelial abnormalities

26
Q

what are secondary hemostatic disorders

A

abnormalities in COAGULATION FACTORS

can be acquired or congenital

27
Q

hyperfibrinolysis

A

RARE

excessive or rapid clot breakdown

28
Q

clinical signs of primary hemostatic disorders

A

SMALL body bleeds

  • petechiae/ecchymosis
  • epistaxis
  • gingival bleeding
  • hyphema
  • hematuria
  • melena
  • CNS/pulmonary hemorrhage
29
Q

clinical signs of secondary hemostatic disorders

A

LARGE body bleeds

  • hemoabdomen
  • hemothorax
  • hemoptysis
  • hemarthrosis
  • hematoma
  • SQ/IM bleeding
  • CNS/pulmonary hemorrhage
30
Q

causes of primary hemostatic disease

A
  1. thrombocytopenia
  2. von willebrand’s disease
31
Q

causes of thrombocytopenia

A
  1. destruction of platelets - IMTP
  2. decreased production
  3. increased consumption
  4. sequestration

diagnosed on platelet count

32
Q

von willebrand’s disease

A

inherited vWF disorder

type 1: decreased vWF
type 2: decreased & abnormal vWF
type 3: marked reduced or absent vWF

diagnosed on vWF assay

33
Q

causes of acquired secondary hemostatic disease

A
  • anticoagulant rodenticide toxicity
  • liver failure
  • heat stroke
  • DIC
  • shock
  • severe hypothermia
  • hemodilution
  • acidemia
  • drug ingestion
34
Q

causes of congenital secondary hemostatic disease

A

hemophilia A: factor 8 deficiency (males only, GSDs)

hemophilia B: factor 9 deficiency

hageman factor deficiency: factor 12 deficiency (NO clinical bleeding but has prolonged aPTT)

35
Q

primary hemostatic disorder diagnostics

A
  1. platelet count - CBC + manual slide review
  2. vWF assay
  3. buccal mucosal bleeding time
  4. platelet function testing
36
Q

secondary hemostatic disorder diagnostics

A
  1. PT/aPTT
  2. ACT
  3. viscoelastic testing
  4. single factor analysis/assay
37
Q

hyperfibrinolysis diagnostics

A
  1. viscoelastic testing
  2. FDPs or D-dimers
38
Q

platelet count

A

CBC + manual review

check for clumping - causes artificially low platelet count on CBC

count on high power (100x) with oil immersion

1 platelet per high power field = 15,000 platelets

39
Q

vWF assay

A

measures concentration and function of vWF

antigen assay - type 1 vs type 3
collagen binding - type 2

40
Q

buccal mucosal bleeding time (BMBT)

A

highly subjective test of primary hemostatic disorder

dogs: 3-4 min
cats: <2 min

only do once thrombocytopenia has been ruled out

41
Q

PT

A

prothrombin time

tests extrinsic & common pathways

42
Q

aPTT

A

partial thromboplastin time

tests intrinsic & common pathways

43
Q

ACT

A

activated clotting time

tests intrinsic & common pathways

less sensitive than aPTT

44
Q

viscoelastic testing (TEG)

A

visual representation of hemostasis

measures:
1. time to form initial fibrin clot
2. time to reach certain clot firmness
3. rate of fibrin accumulation and cross linking
4. clot strength
5. rate of fibrinolysis

VET433: ECC & Toxicology (9 decks)

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