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Tobias ECVS > Ch 7 - Bleeding and Haemostasis > Flashcards

Ch 7 - Bleeding and Haemostasis Flashcards

1
Q

Where are platelets produced and at what rate?

A

In the bone marrow from porgenitor megakaryocytes at a rate of approx 10^11 platelets/day

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2
Q

What are the main substances released from platelet granules to recruit and activate other platelet?

A

TxA2 and ADP

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3
Q

What are the 3 phases of the cell-based model of coagulation?

A
  • Initiation
  • Amplification
  • Propagation
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4
Q

What are the three endothelial inhibitors of platelet reactivity?

A
  • Prostacyclin (PGI2) - limits response to TxA2
  • Ectoadenosine diphosphatase (ecto-ADPase) - metabolises ADP released from platelets, inhibiting recruitment and activation
  • Nitric oxide - decreases Ca influx thereby reducing affinity of fibrinogen binding sites
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5
Q

What are the three natural anticoagulant pathways?

A
  • Antithrombin - inactivates coagulation proteins which escape into the circulation (mostly thrombin and factor X). ALso inhibits neutrophil adherence excerting a potent anti-inflam effect
  • Activated protein C - Inactivates VIIIa and Va and slows thrombin formation. Enhances fibrinolysis
  • Tissue factor pathway inhibitor - Inactivates Xa, and VIIIa-TF
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6
Q

How is fibrin autoregulatory?

A

It acts as both a coenzyme for plasminogen activation (increases its efficacy 1000 fold) and is also a substrate for plasmin. I.e Fibrin stimulates the production of plasmin which then degrades fibrin

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7
Q

How can you estimate platelet count?

A

Multiply average number of platelets per HPF by 15,000

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8
Q

What are the normal BMBT in dogs and sedated cats?

A
  • Dogs - less than 3 min
  • Sedated cat - 34 -105 seconds

Elevated with thrombocytopaenia, thrombocytopathis or vasculopathy

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9
Q

Which pathways do PT and APPT test?

A

PT - extrinsic and common
APPT - intrinsic and common

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10
Q

How much does a single factor need to be reduced by before you will see an increase in the PT or APPT?

A

less than 25-30% of normal concentration

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11
Q

Which factor is effected first with VitK deficiency and which pathway/test will be prolonged?

A

Factor VII due to its short half-life. Causes an increased PT (extrinsic pathway)

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12
Q

What pathways does ACT test?

A

Intrinsic and common - significantly less sensitive then APPT

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13
Q

What casuse elevated fibrin split products? In which conditions can it be elevated?

A

Formed when plasmin lyses fibrinogen or fibrin.
Commonly seen with DIC. Also with thromboembolism, neoplasia, IMHA, hepatic failure, sepsis, SIRS, heat stroke, trauma, GDV etc

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14
Q

What are d-Dimers?

A

Specific degradation products of cross-linked fibrin. Specific for concurrent active coagulation and fibrinolysis

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15
Q

What are the three hypotheses to explain acute traumatic coagulopathy?

A
  • DIC with hyperfibrinolytic phenotype
  • Enhanced thrombomodulin-thrombin protein C pathway
  • Catecholamine-induced endothelial damage
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16
Q

How does acidaemia effect coagulation?

A
  • Increased fibrinogen degradation
  • Impairs coagulation protein activity (fXa-Va)
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17
Q

How does hypothermia effect coagulation?

A
  • Platelets are extremely temperature sensitive
  • Decreases vWF-mediated platelt adhesion
  • Decreased activity of fVIIa-TF
18
Q

What is considered a “massive transfusion” contributing to a dilutional coagulopathy?

A
  • Transfusion volume greater than the patients blood volume over 24 hours
  • OR transfusion of half the blood volume over 3 hours
19
Q

What are the goals of hypotensive resuscitation?

A
  • Systolic BP 90mmHg
  • MAP 60mmHg
20
Q

What coagulation factors are in frozen plasma

A

VIII, VI, X, II

21
Q

What factors does cryoprecipitate contain?

A

VIII, vWF, fibrinogen, fibronectin (cold insoluble factors)

22
Q

What is the action of desmopression?

A

Binds to V2 receptors causing the release od subendothelial vWF stores. Also stimulates the release of VIII and plasminogen

Not effective for type 2 or 3 vWF disease

23
Q

What are the 2 main anti-fibrinolytics? How do they work?

A
  • Epsilon-aminocaproic acid
  • Tranexamic acid

Block the binding and activation of plasminogen

Greyhounds undergoing amputation were 5.7x more likely to experience post-op bleeding without aminocaproic acid and with elective goanadectomy, 33% without experiences bleeding, compared to 10% with

24
Q

What breed has nonpathologic thrombocytopaenia?

A

CKCS

25
Q

What is the most common bleeding disorder of dogs?
What are the three types of this disorder?

A

von Willebrand disease
- Type 1 - Presence of all multipers but in reduced concentrations. Spontanelous bleeding if less than 20%. Dobermans, Standard Poodles, Shelties, GSD, Airedale Terriers
- Type 2 - Disproportionate loss of high molecular weight multimers. Uncommon and results in severe bleeding. GSD, German Wirehaired Pointers
- Type 3 - Almost complete absence of vWF (less than 0.1%). Shelties, Scottish Terriers, Chesapeake Retrievers, Dutch Kooikers.

26
Q

What are the treatment options for vWF-associated haemorrhage?

A
  • Cryoprecipitate
  • FFP
  • Desmopression (type 1)
27
Q

What factors are VitK dependant?

A

II, VII, IX, X

28
Q

How much functional hepatic mass needs to be lost before you will see a coagulopathy?

A

More than 70%

29
Q

What is Virchow’s triad?

A

The three main risk factors for a thrombotic tendancy
- Abnormalities of the vessel wall
- Abnormalities of the blood flow
- Abnormalities of the bloos constituents that promote haemostasis

30
Q

What are the radiographic signs of PTE?

A
  • Pulmonary infiltrates (usually alveolar)
  • Westermark sign (regional oligemia) - best seen on VD/DV, areas of increased radiolucency representing hypovascular lung regions
  • Enlargement of main pulmonary artery
  • Attenuation of lobar artery or vein
31
Q

What may be seen on arterial blood gas analysis in a patient with a PTE?

A
  • Increased A-a gradient
  • Hypoxaemia
  • Hypocapnia
  • Decreased oxygen responsiveness (extreme V/Q mismatch)
32
Q

What lab test has the only proven clinical utility in the diagnosis of PTE?

A

d-Dimers
A strong positive response in the absense of intercavitary haemorrhage is strongly suggestive of PTE

33
Q

What are some definitive imaging tests for the diagnosis of PTE?

A
  • Selective pulmonary angiography
  • Pulmonary scintigraphy
  • Helical CT pulmonary angiographt
34
Q

List anticoagulant options

A
  • Unfractionated heparin - potientiates the activity of antithrombin
  • Low-molecular-weight heparin - inhibits factor X and thrombin (moreso X)
  • Warfarin - VitK antagonist (II, VII, IX, X)
  • Rivaroxaban - direct Xa inhibitor
  • Dabigatran - irreversible thrombin inhibitor
35
Q

What are the 2 main anti-platelet drugs?

A
  • Aspirin - inactivates COX-1 thereby suppressing synthesis of TxA2
  • Clopridogrel - Irreversibly block ADP. Takes 3-5 days to reach steady serum state, can give IV loasking dose for effect within24hr
36
Q

List the contraindications to anticoagulant therapy

A
  • Active internal bleeding
  • Surgery or organ biopsy within the last 2-3 weeks
  • GI ulceration
37
Q

Define DIC

A

The systemic activation of coagulation, leading to widespread microvascular thrombosis that compromise organ perfusion and can contribute to organ failure

38
Q

What are the reported mortality rates of DIC in dogs and cats?

A
  • Dogs - 50-77%
  • Cats - 93%
39
Q

How are leucocytes a major initiator of DIC?

A

They release TNFa, IL-1 and IL-6 which are all initiators of DIC
- Amplify thrombin generation
- Depress natural anticoagulants (antithrombin, protein C etc)
- Inhibits fibrinolysis

Leads to a loss of localisation of haemostasis and widespread microvascular thrombosis

40
Q

How is DIC generally diagnosed?

A

The presence of an underlying condition that could trigger DIC, together with 3+ of the following:
- Thrombocytopaenia
- PT and/or APPT prolongation
- Elevated fibrin split products or d-dimers
- hypofibrinogenaemia
- reduced antithrombin activity
- red blood cell fragmentation

41
Q

Whar are some of the major components of managing DIC?

A
  • Early aggressive treatment of the underlying condition
  • Maintain adequate perfusion
  • Close monitoring of renal function
  • O2 supplementation if required (pulmonary compromise) +/- mechanical ventilation
  • Early enteral nutrition
  • Transfusion (if active bleeding or undergoing an invasive procedure)
  • FFP transfusions do not achieve clinically relevant elevations of antithrombin
  • Heparin? - Evidence suggests ineffective

Tobias ECVS (110 decks)

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