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Y2S1 - SAM I > Final exam - transfusions / immune-mediated disease > Flashcards

Final exam - transfusions / immune-mediated disease Flashcards

1
Q

How quickly do you expect to see regeneration of RBCs?

A

3-5 days

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2
Q

What are the (very) general ddx for anemia?

A

Non-regenerative: various chronic dz processes

Regenerative: loss or lysis (immune-mediated, toxic)

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3
Q

What are the canine blood groups? What is considered the “universal donor”?

A

DEA 1.1, 1.2, 3, 4, 5, 6, 7, 8; DAL-Dal

Universal is DEA 4+, negative for all others (anti-DEA 4 do not cause hemolysis)

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4
Q

What are the feline blood groups? What is the “universal donor”?

A

Type A, B, AB; MIK

NO universal donor

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5
Q

Fill in the blank: NEVER transfuse __ blood to __ cats

A

NEVER transfuse A blood to B cats

Type B cats have HIGH levels of anti-A Ab’s (Brits hate Americans)

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6
Q

What are the 4 broad indications for transfusion?

A
  1. Anemia
  2. Coagulopathies
  3. Hypoalbuminemia - volumes to raise plasma albumin levels are tremendous, don’t use for this reason alone
  4. Thrombocytopenia - may last only minutes to hours, use only in crisis
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7
Q

How are canine blood donors selected?

A

> 25 kg lean body weight
Normal/healthy - routine CBC/chem/UA/fecal
Neg for HW, Lyme, Borrelia, Rickettsial dz
DEA 1.1, 1.2, and 7 negative
Greyhounds - usually universal donors, lean with good veins, PCV often higher

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8
Q

How are feline blood donors selected?

A

> 4.5kg lean body weight
Indoor only and neg for FeLV/FIV, T. gondii, Bardonella
Normal/healthy - routine CBC/chem/UA/fecal
Males preferred

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9
Q

How much blood (based on BW) can be donated?

A

1% of BW (10% of blood volume, BW is 10% blood)

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10
Q

What is in plasma?

A

Everything but RBC (WBC, hemostatic factors, albumin, globulins, etc.)

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11
Q

What is in cryoprecipitate?

A

vWF and factor VII

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12
Q

What is in cryosupernatant?

A

Factors II, VII, IX, XII; albumin, globulins

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13
Q

What supplementation is recommended for blood donors?

A

IV crystalloids while donating

Ferrous sulfate supplements

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14
Q

What does the major crossmatch test?

A

Recipient sera + donor RBC

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15
Q

What does the minor crossmatch test?

A

Donor sera + recipient RBC

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16
Q

When should transfusion be considered? Clinical signs and clin path findings

A
  1. Tachycardia, tachypnea, dyspnea
  2. Depressed from anemia
  3. PCV <12-15% (chronic) or acutely drops
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17
Q

How can you calculate how much blood to transfuse? (Real equation and quick estimation)

A

mL needed = recipient blood vol x [(desired PCV - current PCV) / PCV of donor]
*1mL (FWB) per pound raises the PCV by 1%
10-20 mL/kg FWB is the general indication

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18
Q

What immunologic complications are associated with blood transfusion?

A

Fever
Hemolysis
Acute hypersensitivity
Immunosuppression

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19
Q

What non-immunologic complications are associated with blood transfusion?

A 
Circulatory overload
Bacterial contamination
Transmission of infectious diseases
Citrate toxicity (hypoCa)
Pulmonary microembolism / TRALI
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20
Q

What CS are associated with a transfusion complication?

A

Body temp increases >1ºC
Tachycardia, tachypnea, vomiting develops
Hemoglobinuria
Anaphylaxis: hypotension, urticaria, respiratory distress

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21
Q

How are transfusion complications treated?

A

STOP the transfusion (duh.)
Give crystalloids (or colloids if low BP)
Diphenhydramine for anaphylaxis
Dexamthasone sodium phosphate / epinephrine for shock
Pred acetate for urticaria only

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22
Q

What is oxyglobin? How does it work?

A

Polymerized bovine hemoglobin - no crossmatch needed, long shelf life
Increases free HgB

23
Q

When are hetastarch/vetstarch indicated?

A

Hypotension, hypoproteinemia, hypoalbuminemia (*<1.5 albumin = fluid loss)
Used to maintain fluid within vascular space

24
Q

When is human albumin indicated?

A

OFF LABEL use for hypoalbuminemia and resuscitation

25
Q

What are the etiologies for IMHA?

A

Primary - immune-mediated
Secondary
-Medications (sulfas, etc.), toxins, venom
-Immunologic (SLE, etc.)
-Infectious (FeLV, Babesia, Lepto, etc.)
-Neoplastic (lymphoma, hemangiosarc, etc.)

26
Q

What is the clinical history of a patient with IMHA?

A

Lethargy, weakness, pale mms, +/- hemolysis (pigmenturia and icterus)

27
Q

How is IMHA diagnosed?

A

Anemia (usually regenerative)

  1. autoagglutination
  2. spherocytosis (dogs only)
    • Coombs test (60-80% positive)
28
Q

What additional workup should be done once IMHA is diagnosed?

A
  1. Imaging to look for secondary causes
  2. Coag panel to r/o blood loss and recognize DIC
  3. Arterial blood gas/SAO2 to detect pulmonary thromboembolism
29
Q

What is the cause of death in most cases of IMHA?

A

Hypercoagulability and thromboembolism

30
Q

What is Virchow’s triangle?

A

Describes parameters that predispose thromboembolism

  1. Endothelial damage
  2. Blood stasis/altered flow
  3. Hypercoagulability
31
Q

What is the general treatment strategy for IMHA?

A

Treat secondary cause
Immunosuppression:
-Glucocorticoids (2-4 mg/kg/day)
-Azathioprine

32
Q

What adjunct therapies are used in IMHA cases?

A
  1. Blood products to minimize tissue hypoxia
  2. Gastric protectants
  3. Aspirin/clopidigrel (anti-thrombotics to prevent TE)
33
Q

What is the prognosis for IMHA? What are some NPIs?

A

50% in hospital mortality

NPIs: bilirubin >10mg/dL, autoagglutination

34
Q

What are the main differences in feline IMHA?

A 
Affects male cats
<50% regenerative anemia
Lymphocytosis common
Rarely TE
Lower mortality
35
Q

What are the general ddx for thrombocytopenia?

A
  1. Destruction (immune-mediated, infectious, drugs)
  2. Consumption (DIC, neoplasia, loss d/t bleeding, sequestration)
  3. Decreased production (bone marrow dz, drugs)
36
Q

What are the etiologies of ITP?

A 
Primary
-autoimmune
-idopathic
-genetic?
Secondary
-infection (Anaplasma, E. canis)
-neoplasia
-drugs (sulfas, cephs)
37
Q

What clinical signs are consistent with ITP?

A

Petechia, ecchymosis

Lethargy/anorexia, bruising, anemia

38
Q

How is ITP diagnosed?

A

Presumptive dx by r/o other causes

  • CBC, tick panels, UA
  • coag profile
  • imaging
  • bone marrow
39
Q

How is ITP treated?

A
  1. eliminate underlying risks
  2. minimize bleeding
  3. immunosuppression
    - glucocorticoids (2-4mg/kg/day)
    - azathioprine
  4. Minimize adverse effects
    - GI protectants, pRBCs, O2, etc.
40
Q

What is the prognosis of ITP?

A

Most improve within 7-10 days

Mortality ~30%

41
Q

What clinical signs are consistent with SLE?

A

Polyarthropathy, skin lesions, proteinuria, blood dyscrasias (anemia, thrombocytopenia)

42
Q

How is SLE diagnosed?

A

ANA (not very reliable)

Definitive dx: +ANA and 2 body systems with immune dz

43
Q

How is SLE treated?

A

Immunosuppression
-Prednisone
-Azathioprine / cyclosporin
Levamisole (anti-parasite, immunomodulator)

44
Q

What is the prognosis for SLE cases?

A

Guarded. Relapses common, often require long-term therapy

45
Q

What are the general ddx for polyarthropathies?

A 
Infectious (tick)
Osteoarthritis
Immune-mediated:
-SLE
-Erosive (rheumatoid)
-Non-erosive (infectious, hepatic/GI-associated, neoplasia)
46
Q

What clinical signs are associated with IMPAs

A

Lameness, fever, joint pain

47
Q

What is the general workup for IMPAs?

A 
CBC (non-specific)
Chem (liver up)
U/A (proteinuria)
Joint rads
Tick panel
Arthrocentesis
48
Q

How do arthrocentesis results differ between primary/secondary IMPA and rheumatoid arthritis?

A

Primary/secondary IMPA > non-degenerate neutrophils

Rheumatoid > degenerate neutrophils

49
Q

How is IMPA treated?

A

Prednisone (immunosuppressive)

Azathioprine (careful of hepatotox) / mycophenolate

50
Q

What is the prognosis for primary IMPA?

A

Good!

51
Q

What signalment is associated with erosive (rheumatoid) arthritis?

A

Small/medium breeds

Greyhounds, Shelties

52
Q

What is the pathogenesis of rheumatoid arthritis?

A

RFs and anti-IgG antibodies contribute to immune-complex formation in joints > synovitis and erosive joint changes

53
Q

How is rheumatoid arthritis diagnosed?

A

MDB like IMPA
Rads (early may not show erosions)
Joint tap (degenerate neutrophils)
RF factor positive

54
Q

How is rheumatoid arthritis treated? What is the prognosis?

A

No specific tx - pain management, immunosuppression may slow progression
POOR prognosis

Y2S1 - SAM I (3 decks)

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