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3. Cat & Dog > Hemostasis Pt. 1 > Flashcards

Hemostasis Pt. 1 Flashcards

1
Q

Components of Normal Hemostasis (3)

A
  1. Blood vessel
  2. Adequate platelet mass & function
  3. Adequate plasma coagulation factor levels & function
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2
Q

Hemostatic tests for intrinsic pathway

A

ACT, PTT

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3
Q

Hemostatic tests for extrinsic pathway

A

PT

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4
Q

What causes hemorrhage?
- blood vessel, platelet, and coagulation factor causes

A

Blood vessels
* Damage (e.g., trauma)
* Inflammation (vasculitis)

Platelets
* Reduced number (<50,000/uL; especially < 20,000)
* Impaired function

Coagulation factors
* Reduced levels
* (Impaired function)

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5
Q

Primary Hemostatic Defect; clinical signs? what are they due to?

A
  • Clinical signs due to lack of platelet plug
  • Widespread cutaneous & mucosal petechiae / ecchymoses:
  • Gingival bleeding
  • Epistaxis
  • Hematuria
  • Hematemesis / melena / hematochezia
  • Hematoma after venipuncture
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6
Q

Secondary Hemostatic Defect; clinical signs?

A
  • Clinical signs:
  • Hemothorax
  • Hemoabdomen
  • Hemarthrosis
  • Epistaxis
  • Hematemesis / melena / hematochezia
  • Large ecchymoses
  • Petechiae typically not observed
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7
Q

what are primary and secondary hemostasis?

A

Hemostasis has two phases: primary and secondary hemostasis. In primary hemostasis, platelets aggregate to form a plug at the site of an injured blood vessel. While these platelets are aggregating, coagulation, or secondary hemostasis starts.

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8
Q

pre-surgery plan for breeds at risk of vWD?

A
  • Pre-anesthetic CBC & mini-chemistry panel (liver/kidneys)
  • Buccal mucosal bleeding time
  • vWf: Ag level
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9
Q

Von Willebrand Disease - what does VWF circulate with, and what does it do? is this a common disorder?

A
  • VWF circulates with factor VIII
  • Promotes platelet-endothelial interaction
  • Most common inherited hemostatic disorder in dogs
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10
Q

types of VWD and definitions

A

Type 1 VWD:
- Most common
- Reduction in all multimers of VWF

Type 2 VWD:
- Reduction in high molecular weight multimers

Type 3 VWD:
- Virtual absence of any VWF

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11
Q

VWD Clinical Signs

A
  • Spontaneous hemorrhage, especially mucosal
  • Severity highly variable
    > Signs might only be seen after trauma
  • Petechial hemorrhage uncommon
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12
Q

Diagnosing VWD - helpful tests and what they mean?

A
  • BMBT not specific for VWD
    > Even when normal can still be at risk for bleeding
  • VWF Antigen Test
    > Reported as a percentage of “normal”
    > Normal range is 70-180%
  • VWF deficient:
    > <50% = VWD carrier or affected
    => <35% = usually affected
    > 50-69% = borderline (VWD carrier or normal)
  • VWF Function (collagen binding assay)
    > Preliminary studies: appears to correlate well with bleeding risk
    > Longer turnaround vs Antigen test
  • DNA test
    > Often used to identify carriers (breeding stock)
    > Does not correlate with risk of bleeding
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13
Q

Peri-Operative Risk management for dog with VWD?

A
  • Pre-operative transfusion options
    > Cryporecipitate plasma transfusion
    : Concentrated source of VWF, Factor VIII (to stabilize existing VWF), fibrinogen
    > Fresh frozen plasma
    : VWF and all coagulation factors
  • DDAVP (Desmopressin)
    > Stimulates VWF release
    > Helps for 2-4 hours in some affected dogs
    > Useful adjunct to plasma
    > 1 microgram/kg SQ, 30 min prior to
    surgery
    > No additional benefit in repeated dosing
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14
Q

VWD Patients: Pre-Surgical Planning
- what do we do for dogs with low VWF titre but no previous bleeding episodes & normal BMBT

A
  • Consider giving only DDAVP pre-op
  • (Might not need plasma but ideal to have it in the clinic just in case)
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15
Q

how can we treat a VWD patient in the case of trauma or other factors causing excessive bleeding?

A
  • DDAVP injection
  • Cryoprecipitate or fresh frozen plasma transfusion
  • +/- RBC replacement if marked hemorrhage
  • Compression and other hemostatic techniques
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16
Q

Prognosis for VWD

A

Mild to moderate cases Type I (majority):
* Good prognosis
* Client education
* Treatment of trauma, pre-surgical care needed

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17
Q

other platelet conditions aside from VWD

A
  • Immune mediated thrombocytopenia
  • Platelet function disorders uncommon
    > Often inherited, breed-related
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18
Q

Top differential diagnosis for petechial hemorrhage, mucosal bleeding

A
  • Immune mediated thrombocytopenia
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19
Q

Types of hereditary Secondary Hemostatic Defects

A
  • Hemophilia A, B
  • Other factor deficiencies
20
Q

Types of acquired Secondary Hemostatic Defects

A
  • Liver dysfunction
  • Toxicity (Vitamin K antagonism)
  • Disseminated intravascular coagulation (DIC)
  • Others
21
Q

mechanism of Anticoagulant Rodenticide Toxicity

A

Inhibits recycling of Vitamin K1 from vitamin K1 epoxide reductase

  • Vitamin K antagonism = lack of production of factors II, VII, IX, X
    > FVII has shortest half-life, affected first
  • Several types of anticoagulant rodenticides exist, variable half-life
    > Warfarin (and Similar 1st generation Anticoagulants): ~7 days
    > Bromadiolone: ~14 days
    > Brodifacoum (& Other “Super Warfarins”): 3-4 weeks
22
Q

Clinical Signs of anticoagulant rodenticide toxicity and timing

A
  • Develop 3-5 days following ingestion
  • Common clinical signs:
  • Dyspnea, coughing
  • Exercise intolerance
  • Hematomas
  • Hematemesis, melena
  • Hematuria
  • Pale MMs
  • Signs secondary to bleeding in other locations
23
Q

Diagnosing Rodenticide Toxicity - common tests and findings

A
  • Prolongation of PT, PTT, ACT
    > PT prolonged first
  • CBC findings:
    > May see anemia, mild thrombocytopenia
    Radiographs
  • Radiographs
    > Thoracic or abdominal effusions
24
Q

Less Common Tests for Rodenticide toxicity

A

PIVKA:
* Proteins induced by vitamin K antagonism
* Levels will be increased
* Not widely available
()
Definitive diagnosis requires serum levels (or tissue levels, stomach contents)
* Rarely performed

25
Q

Initial Treatment for warfarin toxicity

A
  • Vitamin K1
  • Transfusion depends on clinical signs
    > Plasma - replace coagulation factors
    > RBC replacement may be needed
26
Q

Supportive Treatment for warfarin toxicity

A
  • Supportive care as indicated:
  • IV fluids
  • Oxygen supplementation
  • Cage rest
  • Other:
    > Thoracocentesis if effusion interfering with respiration (give plasma first)
27
Q

Ongoing Vitamin K1 therapy for rodenticide toxicity protocol

A
  • 2.5 mg/kg PO q 12 hours
  • Administer with (high fat?) food
  • For 1-4 weeks depending on specific anticoagulant
  • Recheck PT 48 hours after last dose
    > If still elevated, resume treatment for 1 week and recheck again
28
Q

what to do for acute rodenticide ingestion

A

If ingestion witnessed <24 hours ago decontamination indicated:
* Induce emesis
* Activated charcoal
()
* Not effective if clinical signs are present
* Ingestion has occurred days ago

29
Q

how long does it take for PT/PTT to increase after rodenticide ingestion

A
  • Takes several days
30
Q

how do we know if we should start vit K therapy after rodenticide toxicity based on PT/PTT?

A
  • Takes several days for PT/PTT to increase
  • Monitor at baseline, 48, and 72 hours
    > If normal at 72 hours, no additional treatment
  • If PT/PTT increasing, start Vitamin K1
31
Q

Prognosis: Anticoagulant Intoxication

A
  • Good with prompt care
  • Factors that might influence prognosis:
  • Costs associated with care
  • Compliance
  • Possible adverse reactions to plasma transfusions
32
Q

what is hemophilia A and in what species is it reported?
What coagulation test(s) will be abnormal?

A
  • Haemophilia A
  • Deficient in factor VIII
  • Reported in dogs & cats

> intrinsic pathway abnormal - PTT, ACT

33
Q

what is hemophilia B and in what species is it reported? is it common compared to A?
What coagulation test(s) will be abnormal?

A

Haemophilia B
* Deficient in factor IX
* Reported in dogs & cats (less common than A)

> intrinsic pathway will be abnormal - PTT, ACT

34
Q

Factor deficiency secondary to liver failure - what signs will we see?

A
  • Clinical signs of liver failure predominate
  • Prolonged PT/PTT, could see hemorrhage
  • Seen in hepatic lipidosis, chronic severe hepatitis, acute hepatopathy
35
Q

how do we treat factor deficiency secondary to liver failure?

A
  • Treat liver disease
  • Vitamin K +/- plasma
36
Q

what type of coagulation disorder is Disseminated Intravascular Coagulation? often associated with what?

A
  • Mixed coagulation disorder
  • Thrombosis and bleeding
  • Complication of an underlying disorder
  • Often associated with heightened inflammatory response
37
Q

DIC: Common Underlying Conditions

A
  • Neoplasia (e.g. hemangiosarcoma, others)
  • Sepsis, infections
  • Immune mediated disorders (e.g. IMHA)
  • Snake envenomation
  • Heatstroke
  • Gastric dilation & volvulus (GDV)
  • Massive inflammation (e.g. severe pancreatitis)
  • Trauma
38
Q

DIC: Pathophysiology

A
  • Systemic disease causes excessive thrombosis in microcirculation due to one or more of:
    > Endothelial damage (e.g., heatstroke)
    > Activated platelets (e.g., sepsis, IMHA)
    > Procoagulants released into circulation (e.g., trauma, pancreatitis)
  • Excess thrombosis eventually consumes most of the platelets & coagulation factors; fibrinolysis is activated
    > Bleeding can result
39
Q

Diagnosing DIC

A
  1. Evidence of fibrin clot lysis
    *Fibrin degradation products
    * D-dimers
  2. Thrombocytopenia (usually mild to moderate)
  3. Increasing PT/PTT
  4. CBC – schistocytes/RBC fragments
40
Q

Treating DIC

A
  • Treatment of underlying disorder
  • Supportive care
    > Maintain perfusion & oxygenation
  • Treatment of coagulation abnormality depending on phase of DIC
    > (Hyper or hypocoagulability)
41
Q

DIC Prognosis

A
  • Overall a guarded prognosis
  • Can support some patients through the crisis
  • Depends partially on underlying cause
  • Need intensive care
42
Q

most common Thromboembolic Diseases

A
  • Arterial thromboembolism (ATE) in cats with hypertrophic cardiomyopathy
  • Pulmonary thromboembolism (venous) in dogs and cats
43
Q

diseases associated with pulmonary thromboembolism

A
  • neoplasia
  • immune-mediated hemolytic anemia
  • cardiomyopathy
44
Q

Diagnosis of Thromboembolism - clinical signs? required diagnostic method?

A
  • Clinical signs depend on site that is not perfused
    > Lack of arterial perfusion to an area (e.g., cold limb in ATE cat)
    > Lack of venous drainage (e.g., edematous limb, effusion in cavity)
    > Dyspnea with PTE
  • Imaging required to identify the thrombus
45
Q

Treatment of TE

A
  • Direct lysis of clot difficult (referral procedure)
    > High complication rate
    > Streptokinase infusion
  • Provide thromboprophylaxis to prevent new TE formation
    > Often combine anti-platelet and anticoagulant therapy
    > E.g., clopidogrel plus rivaroxaban

3. Cat & Dog (33 decks)

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