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Hematological Emergencies > Hemotological ECC > Flashcards

Hemotological ECC Flashcards

1
Q

Metabolism of RBC’s

A

Primarily through anaerobic glycolysis and hexose monophosphate shunt

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2
Q

Feline RBC’s

A
  • more susceptible to oxidation injury and Heinz body formation than canines
  • contains high percentage of sulfur-containing amino acids
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3
Q

What factors affect the amount of RBC’s circulating at any given time?

A
  • Plasma volume
  • Splenic contraction
  • Erythropoietin (EPO)
  • Rate of production from bone marrow
  • Rate of destruction or loss
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4
Q

What hormones play a part in maintaining the RBC numbers?

A
  • pituitary
  • thyroid
  • adrenal cortex
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5
Q

What is a normal PCV for canine?

A

37-55%

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6
Q

Normal PCV for felines?

A

35-45%

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7
Q

What is the term used for total increase in RBC count or PCV?

A

Polycythemia

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8
Q

When does a relative polycythemia occur?

A

In cases of severe dehydration. The TP will also be elevated

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9
Q

How is Hemoglobin usually calculated?

A

It is usually 1/3 of the PCV in g/dL

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10
Q

What terms do you use to determine the types of anaemia?

A

Mean corpuscular volume (MCV)
Mean corpuscular hemoglobin (MCH)
Mean corpuscular hemoglobin concentration (MCHC)

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11
Q

Mean corpuscular volume (MCV)

A

*Mean volume of a group of erythrocytes by diving PCV by RBC count and multiply by 10
*Canine: 60-77
*Feline: 39-55
*Normocytic: RBCs normal sized
Macrocytic: RBCs larger than normal
Microcytic: RBC smaller than normal = usually indicate iron deficiency

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12
Q

Mean corpuscular hemoglobin (MCH)

A

Mean weight of hemoglobin contained in the average RBC
*divide hemoglobin concentration by RBC count and multiplying by 10
*Normal canine: 19-23
Feline: 13-17
*Not as accurate as MCV measurements

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13
Q

Mean corpuscular hemoglobin concentration (MCHC)

A
  • Concentration of hemoglobin in the average erythrocyte
  • Cal by divining hemoglobin concentration by PCV and multiplying by 100
  • Normal MCHC = normochromic anaemia
  • Low MCHC = hypochromic state of anaemia, also likely due to low iron levels
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14
Q

Primary hemostasis

A
  • Is a complex interaction between platelets, blood vessels and coagulation cascade
  • Goal is to form a clot
  • Effective primary hemostasis depends on adequate platelets, adequate platelet function, vessel wall integrity and von Willebrand factor (vWf)
  • Vessels: initial reaction to injury is vasoconstriction
  • Blood exposed to subendothelial layer activates platelets to adhere to the site
  • Interaction is mediated by vWf
  • Platelets are activated by releasing substances that recruit platelets to form a plug and maintain vasoconstriction
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15
Q

Coagulation cascade

A
  • Coagulation factors are enzymes, cofactors, or substrates synthesized by the liver
  • Calcium (factor IV) = required for most coagulation factors
  • Vitamin K is essential for functional synthesis of factors II, VII, IX(9) and X
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16
Q

Extrinsic pathway

A
  • initiated when tissue wall is damaged
  • extravascular process because thromboplastin is not usually found in blood
  • Tissue factor (thromboplastin), then binds with factor VII in plasma
  • The combination activates factors IX and X initiating the common pathway
  • End product is thrombin
  • Thormbin
  • initiates activity of other cofactors within the intrinsic pathway
  • most potent platelet aggregation agent
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17
Q

Intrinsic pathway

A
  • intrinsic factors found within vascular space
  • Platelets release phospholipids allowing coagulation factors to activate each other
  • Final product is fibrin - stabilises the temporary plug
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18
Q

Fibrinolysis

A
  • Final stage of hemostasis
  • once vessel is healed, plasminogen is activated
  • plasmin breaks down the fibrin clot - which produces fibrin degradation products (FDP) and forms D-dimers
  • FDP act as anticoagulants - inhibits the function of the platelets
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19
Q

Bleeding disorders of primary hemostasis

A
  • related to platelets or vessels
  • Vasculopathies results in: excessive fragility, or abnormally interactions with platelets
  • Platelet disorders: quantitative (thrombocytopenia) or qualitative (thrombopathia)
20
Q

What are the clinical signs of bleeding disorders of primary hemostasis?

A
  • epistaxis
  • petechiation
  • ecchymosis
  • gastrointestinal bleeding
  • or prolonged bleeding from vessel or surgical site
  • hematuria
  • intraocular hemorrhage
21
Q

Bleeding disorders of Secondary hemostasis

A
  • Related to problems with coagulation cascade
  • Acquired disorders: vit K antagonist rodenticide intoxication, drug side effects (heparin, colloids, Coumadin), DIC and liver disease
  • Hereditary disorders: hemophilia and multiple factor deficiencies
22
Q

Clinical signs of secondary hemolysis

A
  • hematomas
  • Hemoabdomen
  • hemothorax
  • hemoarthrosis
23
Q

What diagnostic test would you use to detect primary hemostatic disorders?

A
  1. Platelet estimate (blood smear) and count (auto or manual)
  2. Buccal mucosal bleeding time (BMBT)
  3. Bone marrow evaluation
  4. Von Wilebrand factor assay
24
Q

Platelet estimate and count

A
  • blood smear and count manual or auto
  • primary hemostasis test
  • 1 platelet per oil immersion = 20,000 platelets
  • 11-25 per high powered field normal
  • large platelet indicates regenerative process
  • machines can’t accurately count cat platelets due to size - use manual
  • blood needs to be stored in EDTA
  • assay should be done within 12 hours of sample collection
25
Q

Buccal mucosal bleeding time (BMBT)

A
  • detects primary hemostasis problem
  • accurate with platelet counts of 50,000 - 100, 000uL as thrombocytopenia can cause a prolonged bleeding time
  • if BMBT is prolonged with a normal platelet count = platelet dysfunction or a thrombocytopathia
  • large margin of error - user dependent
26
Q

Bone marrow evaluation

A
  • assess megakaryocyte (platelet originates here) numbers

* Normal should have 3-5 megakaryocytes per HPF

27
Q

Von Wilebrand factor assay

A
  • performed by reference laboratories

* measures and reports amount of functional von Wilebrand factor

28
Q

Diagnostic tests to detect secondary hemostatic disorders

A
  1. PCV and Total solids
  2. Observe clotting time in red top tube
  3. Coagulation panel, D-diners
  4. Intrinsic and Common pathways
    a. Activated clotting times (ACT)
    b. Activated partial thromboplastin time (aPTT)
    5.Extrinsic and common pathways
    A. Prothrombin Time (PT)
    B. Protein induced by Vitamin K Antagonism or Absence (PIVKA)
29
Q

At what age would you identify inherited coagulation defects?

A

At 6months of age or younger for severe cases.

Less severe cases become more apparent when they undergo their first surgical procedure.

30
Q

What are the common ailments that should prompt you to consider hemostatic monitoring?

A
  • Liver disease
  • Biliary disease
  • Neoplasia
  • Significant trauma
  • Certain toxin ingestion
  • Patients with risk for disseminated intravascular coagulation
31
Q

Thrombocytopenia

A
  • most common primary hemostatic defect
  • result from: decrease production, increased destruction, or increased consumption or sequestration
  • significant thrombocytopenia (<40,000 uL): will start to show clinical signs of hemorrhage
  • must rule out secondary hemostasis (DIC etc) first
32
Q

Common causes of consumption or sequestration thrombocytopenia

A

DIC, sepsis, vasculitis, splenic torsion

33
Q

What would you use to evaluate platelet production or rule in or out neoplasia, infectious, and immune mediated processes?

A

A bone marrow aspirate

34
Q

Collecting blood sample for both coagulation and von Willebrand’s factor analysis

A
  • Ensure blood comes into contact with citrate as soon as possible
  • Jugular venipuncture using the vacutainer method is preferred
  • don’t use this method if concern with coagulopathy
  • central line and then other veins
  • avoid traumatic venipuncture or incomplete blood draw
  • may activate, deplete or dilute factors
  • If plasma contains visible clots or is grossly hemolyzed - do not use sample
  • These tubes should NOT be used for a coagulation panel or a von Willebrand factor assay:
  • EDTA, heparin, serum separator, and clot activator
  • Sample should be collected prior to giving plasma or cyroprecipitate therapy
  • if not possible, collect sample no sooner than 48 hours post plasma or cryotherapy
  • Blood MUST be centrifuged, separated, and frozen (if shipping) within 1/2 hour of being drawn
  • if sample cannot be run immediately, separate plasma from RBCs and freeze plasma in separate clean plastic tube
  • do not freeze whole blood
35
Q

Buccal mucosal bleeding time procedure

A
  • Restraint, sedate or anesthesia
  • SQ recommended due to the possibility of impaired hemostasis
  • Patient in lateral recumbency
  • upper lip folded upwards and held in place with roll gauze which is tight enough to result in vessel congestion
  • Standard incision made in the buccal mucosa with Simplate II device
  • select an area without visible blood vessels
  • start timing when trigger has been depressed
  • remove device one second after triggering
  • Blot the flow of blood at 5 second intervals with filter paper
  • careful not to touch the edge of the wound
  • record time to cessation of bleeding
  • BMBT is the mean bleeding time for the two incisions
  • if bleeding continues for >20mins, remove bandage and timing stopped
  • Normal time to cessation of bleeding in dogs 1.7-4.2 mins with a mean of 2.6 minutes and cats 1.4-2.4minutes
36
Q

What is the BMBT for dogs?

A

1.7-4.2 mins with a mean of 2.6mins

37
Q

When should you remove the bandage for a BMBT procedure?

A

20 minutes

38
Q

What is the BMBT for cats?

A

1.4-2.4mins

39
Q

Immune mediated thrombocytopenia

A
  • Common cause of decreased platelets is dogs
  • affects middle age female dogs
  • toy and old English sheep dogs overrepresented
40
Q

What are the other causes of thrombocytopenia (non-immune mediated)?

A

Tick-borne disease, neoplasia, and heartworm disease

41
Q

Definition of Thrombocytopathia

A

Dysfunctional platelets

42
Q

Clinical signs of thrombocytopathia

A
  • Primary hemostatic disorder
  • Petechia (tiny spots)
  • ecchymosis (bruises)

BUT platelets numbers are normal
*Confirmed with a prolonged BMBT

43
Q

How is thrombocytopathia acquired?

A
  • Frequently drug induced
  • commonly seen in NSAIDs use
  • Disease can precipitate platelet dysfunction
  • pancreatitis
  • hepatic disorders
  • uremia
  • various neoplasia condition
44
Q

von Willebrand Disease (vWD)

A

*Inherited bleeding disorder seen in over 50 dog breeds
*Lack functional vW factor (vWf)
-necessary adhesive protein that promotes platelet adhesion and aggregation after vascular injury
*3 types:
TYPE ONE:
-seen in most other dogs
-Doberman Pinscher: low amount of vWf but protein itself has a normal structure
TYPE TWO:
-Most commonly seen in German shorthair pointers
-Low amount of vWf and an abnormal protein structure
-more severe
TYPE THREE:
-Most devastating form
-Scottish Terriers, Chesapeake Bay Retrievers, Shetland Sheep dogs
-circulating vWf is very low or absent!

  • Low factor VIII
  • binds to vWf to protect the Factor VIII from rapid breakdown in the bloodstream
45
Q

What Factor is vWD patients deficient in?

A

Factor VIII

-binds to vWf for protection from rapid breakdown in the bloodstream

46
Q

AT III

A

Inactivates thrombin with the goal to inhibit clot formation downstream from an injury

Hematological Emergencies (3 decks)

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