Anemia Flashcards

1
Q

What does PCV depend on in the horse?

A

Age, breed, and level of fitness

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2
Q

What percentage of the red cell mass can be stored in the spleen?

A

30%

Splenocontraction an increase PCV by up to 50%

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3
Q

What is the PCV in the spleen?

A

~80%

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4
Q

What kind of horses typically have higher PCVs?

A

Thoroughbreds (hot-blooded)

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5
Q

What happens to neonatal PCV in horses?

A

Born with near adult values but it rrapidly decreases then returns to normal at around 18months

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6
Q

T/F: More athletic animals have higher PCVs.

A

True

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7
Q

What is a common finding in horse blood slides that may be pathologic in other animals?

A

Rouleaux formation

Do not confuse with agglutination

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8
Q

T/F: Howel Jolly bodies are a normal finding in the horse.

A

True- 1-2% of RBCs

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9
Q

What can be done to help “unstick” RBCs to differentiate agglutination and rouleaux?

A

Drop of saline on the slide

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10
Q

T/F: Horses do not release reticulocytes into circulation

A

True- cannot accurately assess regenerative anemia

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11
Q

What do you have to do to assess regeneration in the horse?

A

Bone marrow aspirates

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12
Q

What are the two most antigenic blood systems in the horse?

A

Aa and Qa

No universal donor

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13
Q

What are the clinical signs of anemia dependent on?

A

Rate and severity

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14
Q

What will subtle anemia typically manifest with?

A

Exercise intolerance and poor performance due to decreased oxygen carrying capacity

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15
Q

What will chronic anemia typically manifest with?

A

Some degree of regeneration and adaptation for low PCV

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16
Q

T/F: Slowly developing anemia can get significantly lower than acute without development of clinical signs.

A

True

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17
Q

What are the clinical signs of acute anemia?

A
o Poor performance
o Lethargy/depression 
o Weakenss, tachycardia, tachypnea
o Pale MM
o Red-tinged, serum, red-tinged urine
o Poor perfusion, shock syndrome 
o Collapse, seizures, death
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18
Q

What are the clinical signs of chronic anemia?

A

Similar to acute but less severe due to adaptation to reduced PCV

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19
Q

What can systolic murmurs be due to in anemia cases?

A

Decreased blood viscosity and increased turbulence

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20
Q

Why do some cases of anemia present with fever?

A

If anemia is due to an infectious process

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21
Q

What are the three general things that will lead to decreased PCV?

A
  1. Inadequate production
  2. Increased destruction
  3. RBC loss eg hemorrhage
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22
Q

What is the most common cause of anemia in large animals?

A

Depression of RBC production due to chronic disease

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23
Q

What are three things can can result in depression anemia?

A
  1. Vitamin/mineral deficiency
  2. Chronic/systemic disease
  3. Processes that damage bone marrow components (typically mild to moderate anemia)
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24
Q

What is the most common cause of iron deficiency anemia in the horse?

A

Blood loss

Equine diets typically are very rich in iron and absorption issues are rare

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25
Q

What are three common causes of chronic blood loss leading to IDA?

A
  1. Parasitism
  2. Bleeding GIT lesions
  3. Hemostatic defects
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26
Q

What is functional iron deficiency caused by?

A

Anemia of inflammatory or chronic disease

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27
Q

What is the pathogenesis of functional iron deficiency?

A
  • Inhibition of iron release
  • Defective marrow response to EPO
  • Decreased RBC life span
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28
Q

What is the typical PCV range of a horse with functional iron deficiency?

A

Never less than 18-19%

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29
Q

Where is most of the iron in horses stored?

A

2/3 in the circulating RBC pool

The rest is in the liver, spleen, and bone marrow

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30
Q

What is the most common cause of anemia in the horse?

A

Anemia of inflammatory disease

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31
Q

How is the anemia characterized in anemia of inflammatory disease?

A

Mild to moderate non-responsive anemia with decreased serum iron and TIBC

PCV typically in the low 20s but can get down to 19%

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32
Q

What protein is responsible for transporting iron in the body?

A

Transferrin

Measured by evaluation of TIB

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33
Q

What is TIBC a measure of?

A

Derived from iron content of serum after total saturation of carrier protein

Gives an idea of the ability of the body to more iron

34
Q

What does a decreased TIBC value tell you?

A

Proteins are unable to take up more iron aka decreased iron binding capacity

35
Q

What is the treatment for true iron deficiency?

A

Iron supplementation

36
Q

What is the only parenteral iron supplementation you can give in a horse?

A

Iron cacodylate

37
Q

Why is iron dextran contraindicated in horses?

A

Possible anaphylaxis

38
Q

T/F: Anemia of inflammation/chronic disease will not respond to clinical treatment.

A

True- iron supplementation has no effect

Must treat underlying disease not the anemia

39
Q

How is anemia secondary to organ dysfunction characterized?

A

Mild to moderate nonresponsive anemia

40
Q

What kind of organ/system dysfunction leads to anemia?

A

Chronic endocrine, renal, hepatic, or GIT disease

41
Q

What is the typical pathogenesis of organ dysfunction anemia?

A

Bone marrow supression

Decrease in essential components, presence of toxic compounds, interference of normal EPO action/production

42
Q

T/F: It is more important to treat anemia directly in organ dysfunction than the underlying cause since it can lead to severe anemia.

A

No. Never true. Always treat underlying cause.

Dummy.

43
Q

What are two ways that EPO issues can mess with RBC production?

A

EPO deficiency due to renal disease/damage

Recombinant EPO dosing

44
Q

What are the issues with EPO doping in horses?

A

Development of antibodies against the recombinant EPO that cross-react with the horses own EPO leading to life-threatening non-regenerative anemia that can only be treated with corticosteroids and transfusions

aka don’t do this to your horse, it will die

45
Q

What are the clinical signs of equine prioplasmosis/babesiosis?

A

 Fever (102-107.6C)
 Hemolytic anemia
 Icterus, hemoglobinuria
 Death
 Generalized signs- depression, weakness, anorexia, incoordination, lacrimation, mucous nasal discharge, swelling of the eyelids
 Greater incidence of hemoglobinuria and death with T. equi

46
Q

What is anemia associated with in equine prioplasmosis/babesiosis?

A

Increased RBC destruction

47
Q

How do you diagnose equine prioplasmosis/babesiosis?

A

Visualization of parasites on blood smear or detection of antibodies (within 14 days of infection)

48
Q

How does the treatment for equine prioplasmosis/babesiosis differ from endemic to non-endemic areas?

A

Endemic- suppress clinical signs without eliminating organism from the animal

Non-endemic- completely eradicate organism from circulation

49
Q

What drug is used to eradicate equine prioplasmosis/babesiosis and what are it’s issues?

A

Iminocarb (cholinesterase inhibitor)

Side effects are colic and diarrhea

Can be fatal in donkeys

50
Q

T/F: EIA is reportable.

A

True

aka Swamp fever

51
Q

What is the epidemiology of EIA?

A

Lentivirus of the retroviridae familiy

Infects macrophages and integrates into host genome causing indirect destruction of RBCs

Vectors: Large biting flies, iatrogenic via needles and instruments; milk/semen possible but very rare

52
Q

What are the clinical signs of EIA?

A

Anemia
Weight loss
Chronic illness

53
Q

How do you diagnose EIA?

A

Gold standard: Coggins test- needed for USDA/APHIS international/interstate travel

ELISA: used to verify coggins test (false positives possible so recommended to use together)

54
Q

How do you treat EIA?

A

You can’t

55
Q

What is the recommendation for horses infected with EIA?

A

Euthanasia and donation for research

Bodies must be marked with an A on the shoulder or neck

56
Q

What can you do if the owner is unwilling to euthanize a horse infected with EIA?

A

Isolation 200yd away from other horses at all times

Double screened stalls

57
Q

What is anemia associated with IMHA caused by?

A

Production of autologous antibodies against the animals own RBCS and hemolysis

58
Q

T/F: IMHA can be either a primary or secondary process but is most commonly secondary due to an underlying primary disease process.

A

True

59
Q

T/F: IMHA is often associated with destruction of thrombocytes as well.

A

True- not always accompanied but isn’t a surprising finding

60
Q

What are some primary diseases/conditions that can lead to IMHA?

A
  • Virus – EIA
  • Bacteria – C. perfringens
  • Protozoa – Equine ehrlichiosis/Babesiosis
  • Neoplasia – lymphosarcoma
  • Drugs – penicillin, sulphas, phenylbutazone
  • Immune mediated disease – purpura hemorrhagica or systemic lupus erythematosus
61
Q

What are some initiating factors of IMHA?

A

Alteration of RBC membrane proteins

Alterations to the immune system that will result in cross-reative antibodies

62
Q

Is IMHA typically more associated with intravascular or extravascular hemolysis?

A

Extravascular hemolysis since complement activation is typically not strong enough to result in intravascular cell lysis

63
Q

What is a hallmark RBC change of IMHA? Is it useful in the horse?

A

Spherocytes

Not useful in the horse since they don’t have central depressions in their RBCs

64
Q

What are the clinical signs of IMHA in the horse?

A

Variable degrees on anemia based on the primary process

Typically signs of extravascular hemolysis

PCV typically around 10-20%

65
Q

How do you treat IMHA?

A

Treat primary process

If IMHA IS the primary process- corticosteroids only effective treatment (dexamethasone followed by prednisolone)

66
Q

What are the three major causes of anemia due to blood loss?

A

Trauma, coagulopathies, infections

67
Q

What are some specific causes of blood loss in the horse?

A

o Respiratory: guttural pouch, ethmoid hematoma
o Gastrointestinal: GI ulcers, parasitism, gastric squamous cell carcinoma
o Genitourinary: lacerations of vessels, middle uterine artery rupture, cystic calculi
o MSQ/cutaneous: trauma
o Coagulopathies: warfarin, liver disease, thrombocytopenia, congenital (hemophilia)
o Iatrogenic – post surgery: ethmoid hematoma, castrations

68
Q

What are clinical signs of blood loss typically associate with?

A

Hypovolemia and diminished oxygen carrying capacity

69
Q

What are some specific clinical signs associated with blood loss?

(Other than maybe finding a puddle of blood)

A
 Pale MM
 Lethargy, exercise intolerance, poor performance 
 Tachycardia
 Tachypnea
 Systolic heart murmur
70
Q

What are clinical signs associated with blood loss due to thrombocytopenia?

A

Petechia, prolonged bleeding times, epistaxis

71
Q

What are some things associated with clotting factor deficiency?

A
  • Ecchymoses, hemarthrosis, hematoma
  • Warfarin and sweet clover toxicity
  • Liver failure
  • Inherited coagulation deficiencies
72
Q

T/F: DIC is never a primary disorder.

A

True- triggered by something else

73
Q

T/F: In early stages of blood loss there is little to no change in PCV and TP.

A

True- makes it difficult to evaluate extent of hemorrhage

74
Q

How does splenocontraction change presentation of blood loss anemia?

A

Will increase TP within 4-6 hours of contracion

Increase in PCV until about 12-24 hours when there will be an obvious reduction and will bottom out at 48hr

75
Q

How often do you want to recheck PCV/TP in an bleeding horse?

A

Every 4 hours

76
Q

How do you treat a bleeding horse?

A
  • Fluid replacement with crystalloids

- Transfusions

77
Q

When is it appropriate to transfuse a horse with acute and chronic anemia?

A

Acute = PCV

78
Q

Why do you wait longer to transfuse a horse with chronic anemia?

A

Because the horse will have adapted to the lower PCV and not be in as much trouble as the acutely bleeding horse

79
Q

What do you need to be concerned about correcting in a horse with anemia?

A
  1. Perfusion (circulating volume correction)
  2. Maintenance of colume within vascular space
  3. O2 carrying capacity
80
Q

How long do transfused RBCs stay in circulating volume?

A

Avery of 5 days with a half life of 2 days