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RUSVM LAM I > E2: Anemia > Flashcards

E2: Anemia Flashcards

1
Q

Anemia is defined as a reduction in ____ and/or the amount of ______.

A

RBC number

hemoglobin

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2
Q

The spleen has a reserve of up to ___% of the red cell mass.

A

30

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3
Q

What drug class can cause red cell sequestration and a reduced PCV? Why/how?

A

Promazine tranquilizers

Splenic relaxation

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4
Q

Hot-blooded horses, such as TBs, typically have a ______(higher/lower) PCV than cold-blooded horses, such as Drafts.

A

Higher

(35-53% vs 24-44%)

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5
Q

How many blood group systems do horses have? Which one is the universal donor?

A

8

There is no universal donor in horses

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6
Q

Why should donkey blood not be used for horse transfusions?

A

Donkey factor makes donkey blood incompatible with horses

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7
Q

T/F: Clinical signs associated with chronic anemia are less severe than those for acute anemia.

A

False, acute more severe

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8
Q

T/F: It is not possible to assess RBC regeneration on a peripheral blood smear of the horse.

A

True

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9
Q

Which is normal in horses, agglutination or rouleaux?

A

Rouleaux

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10
Q

What is the best way to evaluate response to anemia in horses? What type of tube do you put your sample in?

A

Bone marrow aspiration

LTT/EDTA (purple top)

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11
Q

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

A

Chronic Disease

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12
Q

Splenic contraction can increase measured PCV by up to ___%. The PCV in the spleen is usually around ___%.

A

50

80

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13
Q

Why are MCV and MCH not very helpful when evaluating anemia in horses?

A

Macrocytosis and polychromasia do not occur in horses

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14
Q

What is shown in this picture (overall and black arrowhead)?

A

Rouleaux

Howel Jolly Bodies (arrowhead)

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15
Q

What is a normal RDW in a horse? What can this measurement allow you to infer?

A

19

Regeneration if RDW > 19

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16
Q

What is the normal range for PCV (generally) for horses?

A

29-53%

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17
Q

In horses, what is typically the cause of iron deficiency?

A

Chronic blood loss (parasites, bleeding, hemostatic defects)

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18
Q

Horses with functional iron deficiency anemia typically have PCV less than ______%.

A

18-19

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19
Q

Where is most of the total reserves of iron in a horse? Where else is it stored?

A

Ciruclating RBCs (2/3 of total)

Liver, Spleen, Bone marrow

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20
Q

What is the carrier protein responsible for iron transport and distribution in the body? How can it be measured?

A

Transferrin

Measured by evaluating TIBC (total iron binding capacity)

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21
Q

What is the only safe parenteral preparation for iron supplementation in the horse?

A

Iron cacodylate

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22
Q

T/F: PCV varies with breed and age.

A

True

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23
Q

What patholgy and drug can cause agglutination in horses?

A

IMHA

Heparin

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24
Q

How can you evaluate regeneration in a horse, aside from interpreting RDW? What indicates regeneration?

A

Bone marrow aspirate for Myeloid-Erythroid Ratio

M:E < 0.5 = regeneration

>5% reticulocutes in bone marrow= regeneration

25
Q

What factors affect the CS and their severity in an anemic horse?

A

Severity of anemia

Duration

Rapidity of anemia (if slowly progressive body can compensate)

26
Q

What 3 basic pathophysiologic processes cause anemia?

A

Inadequate production

Increased destruction

Blood loss

27
Q

What findings do you expect in a horse with anemia of chronic disease?

A

Concurrent disease

Increased fibrinogen (severity and chronicity)

Increased WBCs

PCV >18-19%

28
Q

How is fibrinogen usually measured in horses? When does it increase due to inflammation?

A

Indirectly (heat precipitation)

>48 hours

29
Q

What value indicates iron binding capacity?

A

TIBC

30
Q

In horses with anemia of chronic disease (i.e. functional iron deficiency), the available iron pool (TIBC, serum iron) are _______ while iron storage (serum ferritin, marrow iron stores) are _______.

In horses with a true iron deficiency the opposite occurs.

Decreased or Increased?

A

(normal to) Decreased

(normal to) Increased

31
Q

How can you treat anemia caused by EPO administration?

A

Corticoteroids +/- Transfusion

However, may not be treatable and thus fatal

32
Q

What causes increased red cell destruciton in horses?

A

Most important: Infectious diseases

Immunologic causes

Toxins (e.g. wilted Red maple leaves)

33
Q

In areas where babesiosis or piroplasmosis are endemic, why would you be concerned if an older horse develops fever, icterus and anemia following a stressful event?

A

May have been a carrier of these diseases and not shown CS until a stressor caused it to emerge

34
Q

What is the more severe form of babesiosis caused by? What does it cause that the less severe form does not? What does this cause?

A

Babesia equi

Causes intravascular hemolysis (as well as extravascular, which is caused by both this and B. cabali)

Hemoglobinemia and hemoglobinuria (with B. equi but not B. cabali)

35
Q

What is the preferred/most commonly used test for babesiosis? Why is it better than analyzing a blood smear?

A

Compliment Fixation Test (CFT)

It can identify carriers

36
Q

Do you expect to see parasites on a blood smear if a horse is presenting with clinical signs of babesiosis? What clinical signs are these?

A

Yes

Fever, Tachycardia, Tachypnea, Weakness

37
Q

Why does the treatment goal for babesiosis vary depending on whether it is endemic in that area or not?

A

In endemic areas, you do not want to clear the organism completely because maintaining a low level confers a certain level of immunity against the disease. So the goal is to minimize the severity of the disease and clinical symptoms.

In non-endemic areas the goal is to become seronegative for the disease

38
Q

What is the treatment protocol for Babesiosis?

A

Imidocarb dipropionate (cholinesterase inhibitor)

Prevent diarrhea/colic by spacing out the dose (give 1/2 now and the rest 1 hour later) or by pre-treating with glycopyrrolate (or atropine, but it can cause GI issues)

+/- Buparvaquone for acute B. equi

39
Q

What is “Swamp Fever”?

A

Equine Infectious Anemia

40
Q

What vectors are associated with EIA?

A

Deer and Horse flies

+/- mosquitoes

41
Q

How can EIA be transmitted iatrogenically?

A

Most common: Dental equiptment

Needles, NG tubes, gloves

42
Q

What type of virus is EIA?

A

Retrovirus- Lentivirus

43
Q

What cells does EIA affect? How does it cause anemia?

A

Macrophages

Immunological pathophysiology: Antigen-Antibody complex deposition -> INDIRECT destruction of RBCs -> Immune-mediated EXTRAVASCULAR hemolysis

44
Q

What causes the recurrent episodic hemolytic crises in horses with EIA?

A

Antigenic drift/shift (Mutation) occuring in a sequential predetermined pattern

45
Q

What is the recommended and USDA-accepted test for EIA? What can you use to verify this test?

A

Coggins Test

ELISA test

46
Q

How long does it take for a horse post-EIA infection for a positive AGID test result? Which test can be used for earlier cases?

A

(Coggins is an AGID test)

45 days

ELISA

47
Q

What are the general requirements for isolation/quarantine?

A

Double screening insect control in barns

Minimum of 200 yards away from closest horse, separated by double fencing pasture (due to vector behavior)

Disinfection of all instruments used on affected horses

If leave facility, must be marked with “A” on neck or shoulder

48
Q

What is one example of each of the common secondary causes of IMHA: Viurs, Bacteria, Neoplasia, Drugs, Immune-Mediated disease?

A

Virus: EIA

Bacteria: Clostridium perfingens

Protozoa: Ehrlichia, Babesia

Neoplasia: LSA

Drugs: Penicillin, Sulfas, Phenylbutazone

Immune-mediated: Purpura hemorrhagica, SLE

49
Q

What can trigger an antibody response leading to IMHA?

A

Alteration of the RBC membrane (direct or indirect damage)

Alertations in the immune system

Alterations in the immune system stimulation

50
Q

What causes Equine Granulocytic Ehrlichoisis? What cells are infected?

A

Anaplasia phagocytophilia

Neutrophils and Eosinophils

51
Q

What are the compensatory mechanisms when hemorrhage occurs?

A

Cardiac (first mechanism)- heart rate

Vascular: vasoconstriction, plasma volume increase - autotransfusion (fluid absorption from 3rd space, increase in glucose (fluid shift))

Hormonal: Vasopressin/ADH release

52
Q

Why is it difficult to evaluate the extent of hemorrhage in horses?

A

Splenocontraction

53
Q

When will a horse bottom out due to hemorrhage?

A

2 days

54
Q

What are the criteria used to determine the need for a blood transfusion?

A

Absolute PCV number

+

Severity of loss: rapidity of decreasing PCV

+

Time: Acute vs Chronic

+

Clinical signs

+

Determining the problem: Volume/perfusion or O2 carrying capacity

55
Q

How long do RBCs from a transfusion last?

A

2-4 days

56
Q

When can you use crystalloids to replace blood lost through hemorrhage?

A

If the problem is VOLUME not O2 carrying capacity

When the blood volume loss is 15-30%

57
Q

When can you use colloids to replace blood lost through hemorrhage?

A

Blood loss >25% causing a concern for RETAINING the fluids in the vasculature due to LOW PROTEIN

Can give Plasma +/- Hetastarch (Hetastarch is more cost-effective)

58
Q

When can you use a blood transfusion to replace blood lost through hemorrhage?

A

Blood loss >50%

PCV <10-12% (especially if acute)

For O2 carrying capacity issues

RUSVM LAM I (19 decks)

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