Hematology Flashcards

1
Q

What type of clinical presentation do animals with acute, severe hemorrhage show?

A
  • SHOCK
    • low BP, tachycardia, tachypnea
    • pale MM & prolonged CT
    • poor peripheral pulses & cool extremities
    • trembling, weakness, depression
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2
Q

With acute blood loss, how long does it take for anemia to become clinically important?

A

12-24 hours

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3
Q

What clinical signs are associated with anemia?

A
  • pale MM
  • tachycardia/tachypnea
  • weakness/exercise intolerance
  • anorexia/depression
  • physiological heart murmur
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4
Q

What is a good indicator of regeneration in the horse?

A

MCV > 60 fl

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5
Q

Common causes of hemorrhage in the horse

A
  • uterine rupture (pregnant mares, late gestation)
  • NSAID toxicity
    • renal medullary necrosis
    • GI bleeding
  • exercise-induced pulmonary hemorrhage
  • guttural pouch mycosis (internal carotid rupture)
  • trauma (internal or external hemorrhage)
  • coagulopathy
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6
Q

When do TP & PCV changes occur after an acute blood loss event?

A
  • TP-4-6 hours after
    *may not drop significantly if internal bleeding
  • PCV-12-18 hours after
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7
Q

What bloodwork findings are evidence of acute blood loss anemia?

A

regenerative anemia & hypoproteinemia without evidence of hemolysis

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8
Q

Appropriate diagnostic steps if hemorrhage suspected but not evident externally

A
  • peritoneal or abdominocentesis
  • thoracic or abdominal US
  • rectal examination
  • endoscopy
  • fecal occult blood
  • urinalysis
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9
Q

Hemorrhage is what kind of fluid loss?

A

isotonic

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10
Q

Why should acepromazine be avoided in horses with acute blood loss?

A

Don’t use in hypotensive animals because it reduces peripheral vasoconstrictive response

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11
Q

What is one potential reason to avoid colloids in a hemorrhage situation?

A

colloids can inhibit coagulation, so be careful using unless positive that bleeding is controlled

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12
Q

Fluid support for horse that suffered hemorrhage and is in shock

A
  • Hypertonic fluids first (5% NaCl)
  • follow with isotonic fluids (LRS)
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13
Q

When is a blood transfusion warranted in hemorrhage situations?

A
  • PCV<15 if acute
  • PCV<8-10 if chronic
  • HR>90 een after circulatory support
  • PCV decreases to <20% in 12 hours
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14
Q

Describe the ideal universal blood donor

A
  • non-thoroughbred
  • gelding
  • Aa, Qa, and Ca-negative
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15
Q

What is the lifespan of transfused RBCs?

A

2-5 days

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16
Q

After treating an acute hemorrage, horses should rest until PCV is ______

A

>20%

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17
Q

What causes clinical signs seen with chronic hemorrhage?

A

poor oxygen delivery

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18
Q

What findings provide evidence of iron deficiency?

A
  • non-regenerative anemia
  • LOW serum iron concentration
  • LOW serum transferrin saturation
  • HIGH iron-binding capacity ‘
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19
Q

What is the pathophysiology of chronic hemorrhage?

A
  • bone marrow suppression d/t underlying disease
  • bone marrow failure
  • iron deficiency anemia may be factor
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20
Q

What is the focus of treatment for chronic hemorrhage?

A

treat the underlying cause

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21
Q

What is the dominant clinical picture of chronic hemorrhage?

A

Anemia

  • pale MM
  • tachycardia/tachypnea
  • weakness/exercise intolerance
  • anorexia/depression
  • physiological heart murmur
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22
Q

Differentials for chronic anemia

A
  • chronic blood loss (iron deficiency)
  • underlying disease (anemia of chronic disease or inflammation)
  • EPO administration
  • aplastic anemia
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23
Q

Oral iron should not be given to what age horses?

A

neonates (2-3 weeks)-Hepatotoxic

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24
Q

What findings are used to diagnose hemolytic diseases?

A
  • anemia with normal plasma protein, hyperbilirubinemia, hemoglobinemia, and/or hemoglobinuria
  • altered RBC morphology (spherocytes, eccentrocytes, Heinze bodies, etc.)
25
Q

What are other rule-outs for hemolytic diseases?

A
  • liver disease
  • anorexia
26
Q

What are some main differences between EV and IV hemolysis?

A

MCHC

  • Normal w/ extravascular hemolysis
  • High w/ intravascular hemolysis

Hemoglobinemia & hemoglobinuria-intravascular

Splenomegaly-extravascular

27
Q

Infectious causes of hemolytic disease in horses

A
  • Anaplasma phagocytophila
  • EIA
  • Babesiosis/Piroplasmosis
28
Q

Possible immune-mediated causes for hemolytic disease

A
  • Drugs (Penicillin)
  • Infection (S. equi)
  • Neoplasia
  • Neonatal isoerythrolysis
29
Q

Toxic causes of hemolytic diseases

A
  • Red maple
  • onions
  • phenothiazine
  • rattlesnake venom
30
Q

What type of virus is EIA?

A

Retrovirus

31
Q

How is EIA transmitted?

A

hematophagous arthropods or contaminated instruments

32
Q

What is the mechanism of anemia with EIA?

A

likely from BM suppresion AND hemolysis

33
Q

Typical lab findings with EIA

A
  • PCV 10-20%
  • normal TP (to possibly marginally high)
  • possible thrombocytopenia
  • hyperbilirubinemia
34
Q

Acute EIA clinical signs

A
  • icterus
  • depression
  • fever
  • edema
  • petechia
35
Q

Chronic EIA clinical signs

A
  • intermittent fever
  • icterus
  • weight loss
  • lethargy
  • pale MM

*episodic

36
Q

What is the vector for Anaplasma phagocytophila?

A

Ixodes spp.

37
Q

What cells does A. phagocytophila infect?

A

neutrophils

38
Q

Anemia due to A. phagocytophila is probably by what mechanism?

A

immune-mediated

39
Q

What pathologies result from A. phagocytophila?

A
  • systemic inflammation
  • reduced granulocyte & platelet production/increased clearance
  • vasculitis
40
Q

What clinical signs are seen first with A. phagocytophila infection?

A

fever & depression

41
Q

A. phagocytophila causes what clinical signs?

A
  • fever (104-105) & depression first
  • after 2-3 days:
    • icterus
    • petechia
    • edema
    • ataxia
    • reluctance to move
42
Q

Lab findings associated with A. phagocytophila

A
  • anemia
  • thrombocytopenia
  • neutropenia with left shift
  • hyperbilirubinemia
43
Q

Treatment for A. phagocytophila

A
  • Oxytetracycline IV SID slowly for 7 days
  • Doxycycline PO BID for 2 weeks
  • Supportive care
  • Anti-inflammatory (flunixin meglumine IV 3 d)
44
Q

A. phagocytophila diagnostic tests

A
  • neutrophil inclusions on peripheral blood smear (during first few days of disease then become harder to find)
  • serology (not helpful acutely)
  • PCR-buffy coat-very sensitive
45
Q

What type of hemolysis is most common with IMHA?

A

extravascular

46
Q

Pathophysiology of IMHA

A
  • immune-complex mediated RBC destruction
    • direct (IV) or phagocyte-mediated(EV)
  • tissue hypoxia
  • organ dysfunction
  • systemic inflammation/shock
47
Q

Clinical signs of IMHA

A
  • fever
  • icterus
  • lethargy
  • tachycardia & tachypnea if anemia severe
  • pale MM
  • splenomegaly
  • may also develop thrombocytopenia or DIC
  • rarely hemoglbinemia or hemoglobinuria-if IV
48
Q

IMHA diagnostics

A
  • autoagglutination maybe evident (dilute whole blood in saline)
  • Coombs-direct or indirect
  • higher red cell fragility than normal
  • flow cytomoetery for RBC bound IgG
49
Q

What are some therapies for IMHA?

A

Dexamethasone

Prednisolone

Cyclophosphamide (if refractory)

Plasmapheresis (if refractory)

50
Q

What is the purpose of using diuretics as part of treatment for IMHA?

A

help reduce the nephrotoxicity from pigmenturia-especially important with methemoglobin

51
Q

Major components of Red Maple pathophysiology

A
  • oxidative damage to hemoglobin causing methemoglobinemia
  • oxidative damage to RBC membranes -> hemolysis
  • systemic inflammation
52
Q

Clinical signs of red maple toxicity

A
  • icterus
  • weakness, ataxia
  • yellow-brown membranes
  • brown urine
  • brown serum
  • tachypnea/tachycardia
  • colic (especially prone; painful colic)
  • oliguria or anuria
  • DIC/acute death
53
Q

Treatment for Red Maple toxicity

A
  • remove source-activated charcoal via NGT
  • fluids for circulatory support & diuresis
  • blood transfusions-based on clinical signs since PCV/Hb may be inaccurate
  • diuretics (furosemide)
    • dopamine CRI if remain oliguric
  • anti-oxidants-Vitamin C (?) - can’t hurt, not sure if works
54
Q

What drugs should be avoided in animals with Red Maple toxicity?

A

corticosteroids

55
Q

Causes of relative polycythemia

A
  • hemoconcentration
    • dehydration, endotoxemia
  • splenic contraction
    • excitement, shock
    • drug-induced
56
Q

Clinical signs of polycythemia

A
  • bright red, congested membrane color-relative
  • muddy red membrane color-absolute
  • CS of dehydration/endotoxemia if cause
  • tissue hypoxia signs if absolute
  • thrombosis if absolute
57
Q

What organism is sometimes a cause of thrombophlebitis?

A

Staphylococcus aureus

58
Q

Treatment plan for thrombophlebitis

A
  • early aggressive treatment of underlying disease
  • aspirin for thrombosis
  • antibiotics if septic
  • drainage if infected