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Equine Med Final (Old Material) > Hematopoietic Disease > Flashcards

Hematopoietic Disease Flashcards

1
Q

What do dark mucous membranes suggest?

A
  • Increased PCV
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2
Q

Clinical signs of a horse with anemia

A
  • Pale mucous membranes
  • Tachycardia
  • Tachypnea
  • Systolic heart murmur
  • Lethargy
  • Exercise intolerance
  • Pale slera
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3
Q

Severity of anemia

A
  • Mild: 30-33%
  • Moderate: 20-29%
  • Severe: 13-19%
  • Very severe: <13%
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4
Q

What is the limit for anemia of chronic disease severity?

A

20%

Should not be lower than 20%

If it is, it’s something else

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5
Q

1st step to assessing anemia

A
  • Regenerative vs non-regenerative
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6
Q

What is unique about horse blood that makes it hard to assess regeneration?

A
  • Lack reticulocytes
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7
Q

Regenerative disorders

A
  • Hemorrhage and hemolysis
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8
Q

Non-regenerative disorders

A
  • Anemia of chronic disease, neoplasia, chronic renal disease, bone marrow issues, chronic inflammation
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9
Q

Hemorrhage signs

A
  • If external, hopefully fairly obvious
  • Not as obvious if internal hemorrhage
  • Look with ultrasound or tap
  • Might not see if there is a big hematoma
  • Can have blood loss into the GIT, but not as common
  • Not as obvious in the feces
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10
Q

What are the three general principles of hemorrhage control?

A
  1. Stop the hemorrhage
  2. Volume replacement (balance with hemodilution)
  3. Maintain oxygen carrying capacity
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11
Q

Common cause of internal hemorrhage/hemoabdomen in brood mares

A
  • Uterine artery hemorrhage
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12
Q

Treatment for hemoabdomen in broodmares

A
  • Keep relaxed
  • Can give acepromazine to decrease blood pressure and decrease anxiety
  • Can nasal canula oxygen
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13
Q

What do you want to give if sending to a referral hospital?

A
  • Hypertonic saline
  • Increase osmolarity of blood and will suck volume in
  • Lasts about 3-4 hours
  • Give a couple of liters
  • Make sure you’ve stopped the hemorrhage first
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14
Q

Signs of acute internal hemorrhage

A
  • Sweating
  • muscle fasciculations
  • Tachycardia
  • Tachypnea
  • Pale mucous membranes
  • Cool extremities
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15
Q

What are the three causes of dark red urine?

A
  • Myoglobin, hemoglobin, and whole red blood cells
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16
Q

Signs of intravascular hemolysis

A
  • Hemoglobinuria
  • Hemoglobinemia
  • Increased indirect (unconjugated) bilirubin

Red blood cell is destroyed and is filtered through kidney

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17
Q

Signs of extravascular hemolysis

A
  • Only increased unconjugated (indirect)

- Surface of RBC is destroyed and goes to bone marrow, liver, or spleen

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18
Q

Which is more common in horses: intravascular or extravascular hemolysis?

A
  • Extravascular by far
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19
Q

Causes of hemolysis

A
  • Immune mediated (most common out here)
  • Oxidative hemolysis
  • Infectious diseases (equine piroplasmosis and equine infectious anemia)
  • Toxins (Clostridium, oak, DMSO)
  • Iatrogenic (hypotonic or hypertonic fluids)
  • Miscellaneous (liver disease, DIC)
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20
Q

What are two tests used to diagnosis immune mediated hemolysis?

A
  • Autoagglutination

- Coombs test

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21
Q

How do you differentiate autoagglutination from rouleaux?

A
  • Mix 1 part blood with 4 parts saline to allow rouleaux to disperse
  • Autoagglutination stays clumped together
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22
Q

Significance of positive autoagglutination?

A
  • IMHA
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23
Q

What to do if autoagglutination is negative but you still suspect IMHA?

A
  • Coombs test
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24
Q

Important aspects of IMHA pathology

A
  • Look for an underlying cause
  • Usually secondary to something
  • Other concurrent immune-mediated abnormalities are possible
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25
Q

Treatment for immune-mediated hemolysis

A
  1. Discontinue current medications
  2. Diurese (VERY important in intravascular hemolysis as the free hemoglobin can cause tubular disease)
  3. Corticosteroids (can be helpful if immune mediated especially)
  4. Maintain oxygen carrying capacity (consider transfusion if showing clinical signs)
  5. Treat underlying problems
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26
Q

Differentials for oxidative hemolysis and which is most common?

A
  • Red maple leaf toxicity (Acer rubrum)** (most common by far)
  • Wild onion (need a lot)
  • Phenothiazine (rarely used anthelminthic)
  • nitrate (rare in horses)
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27
Q

Red Maple Leaf toxicity Diagnosis general

A
  • History

- Clinical signs

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28
Q

What specific bloodwork changes would suggest red maple leaf toxicity?

A
  • Blood methemoglobin levels

- Heinz bodies

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29
Q

How do you visualize Heinz bodies?

A
  • Stain a blood smear with new methylene blue
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30
Q

Treatment for red maple leaf toxicity (3 aspects)

A
  1. Maintain oxygenation of tissues (transfusion ideally if needed; caution as they can get profound reperfusion injuries)
  2. Diurese to protect kidneys
  3. Decontaminate (activated charcoal and pass a stomach tube; mix in water with these guys)
  4. Make sure you treat other horses that were possibly exposed
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31
Q

Equine Infectious anemia overview

A
  • Retrovirus

- Lentivirus

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32
Q

Infected cell type in Equine Infectious anemia

A
  • Tissue macrophages and dendritic cells
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33
Q

How long does EIA last?

A
  • Lifelong
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34
Q

How does EIA result in anemia?

A
  • Likely stimulates an antibody response
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35
Q

What do most horses look like with EIA?

A
  • super healthy

- They can still have sufficient virus to act as reservoirs

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36
Q

Horses with chronic EIA?

A
  • Pitting edema
  • Weight loss
  • Recurring fevers
  • Thrombocytopenia and anemia
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37
Q

How is EIA transmitted?

A
  • Biting flies (Tabanids, Chrysops)
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38
Q

What type of vector are biting flies for EIA?

A
  • Mechanical vectors

- Spread the virus by getting blood on their mouthparts

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39
Q

How far can tabanids fly for EIA?

A
  • 200 yards

- If test positive and owners elect to quarantine, rule is they must be 200 yards from another horse

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40
Q

Diagnosis of EIA (screening and confirmatory test)

A
  • Screening test: Agar gel immunodiffusion (AGID or Coggins)
  • Confirmatory test: ELISA assays
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41
Q

Coggins test

A
  • Positive antigen protein in central well
  • Samples from the horses
  • If the horse has ANTIBODY circulating to EIA, then it meets the antigen and creates a line of precipitation
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42
Q

ELISA assays for EIA

A
  • More sensitive
  • Less specific
  • Confirm results
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43
Q

Who can do the Coggins test?

A
  • Official test at approved labs only
44
Q

What happens to reactors for EIA?

A
  • Reactors officially identified
  • Positive horses may not move interstate
  • Exceptions are movement to farm of origin, slaughter, research
  • Quarantine laws vary by state
45
Q

Vaccine for EIA

A
  • NONE AVAILABLE!!!!
46
Q

Recommendations for control of EIA

A
  1. ) Require a negative test for prepurchase
  2. ) Require a negative test for new horses
  3. ) Require a negative test for horse events
  4. ) Test all horses on the farm at least yearly
  5. ) Disinfect instruments
  6. ) One needle, one horse
  7. ) Vector control
47
Q

Agents of Equine Piroplasmosis

A
  • Babesia caballi
  • Theileria equi
  • Both are protozoa
48
Q

Which agent of equine piroplasmosis is biggest in the US?

A
  • Theileria equi
49
Q

Where is equine piroplasmosis enzootic?

A
  • Florida and Texas
50
Q

What are the vectors of equine piroplasmosis

A
  • Ixodid ticks
51
Q

Signs of equine piroplasmosis

A
  • Anemia, fever, icterus
52
Q

Diagnosis of equine piroplasmosis

A
  • Visualize organisms in the RBCs

- Serologic tests too (ELISA)

53
Q

Treatment of equine piroplasmosis

A
  • Imidocarb
54
Q

Example history of a horse with anemia of chronic disease

A
  • CAN BE VARIABLE, but this is an example
  • 2y/o QH running around that impaled himself
  • DId great and was treated well
  • Had a chronic infection
55
Q

What is the most common cause of anemia in horses?

A
  • Anemia of chronic disease
56
Q

Pathogenesis of the anemia of chronic disease

A
  • Sequestration of iron due to influence of cytokines
57
Q

Characteristics of anemia of chronic disease

A
  • Normocytic, normochromic, nonregenerative

- RARELY BELOW 20% FOR ANEMIA

58
Q

Treating anemia of chronic disease

A
  • Treat the underlying cause

- no iron supplementation is required

59
Q

Causes of nonregenerative anemia in horses

A
  • Iron deficiency
  • Anemia of chronic disease
  • Bone marrow failure (drugs, neoplasia, toxins, myeloproliferative disease)
60
Q

Chronic signs of iron deficiency on CBC

A
  • Macrocytic, hypochromic anemia
61
Q

When do you see iron deficiency anemias in horses most often?

A
  • If a young foal is very sick and kept in an artificial environment with concrete floors and no access to mother’s milk or dirt
  • Less commonly from adult horses with a chronic GI bleed, but in general, adult horses have very good iron stores
62
Q

Life span of neutrophils, platelets, and RBCs

A
  • Neutrophils (1 day)
  • Platelets (6-10 days)
  • RBCs (140-150 days)
63
Q

What are the most common causes of bone marrow failure?

A
  • Neoplasia and myeloproliferative disease I guess
64
Q

Where is the best place to get a bone marrow sample?

A
  • Sternum
65
Q

4 causes of thrombocytopenia

A
  1. Decreased production
  2. Increased utilization
  3. Increased destruction
  4. Sequestration
66
Q

Causes of thrombocytopenia due to increased destruction

A
  • Immune-mediated (primary and secondary)
  • Infectious causes (Anaplasma phagocytophilum, Equine Infectious Anemia)
  • Drugs or toxins
  • Snake bite
67
Q

How do you diagnose immune-mediated thrombocytopenia?

A
  • It’s a disease of exclusion
  • You cannot do a Coombs test for this
  • Blood smear to tell if you have adequate platelts
68
Q

How do you treat immune mediated thrombocytopenia?

A
  1. Discontinue medications
  2. Treat the underlying cause
  3. Corticosteroids possibly because they work well (not in all cases, e.g. ITP secondary to Rhodococcus pneumonia)
69
Q

What is the level for platelets to become so low that you worry about spontaneous bleeding?

A
  • Below 10,000 super worried

- 10,000-20,000 evaluate clinical signs

70
Q

Agent of Equine Granulocytic Ehrlichiosis

A
  • Anaplasma phagocytophilum
71
Q

Vector of Equine Granulocytic Ehrlichiosis

A
  • Ixodes species
72
Q

Infected cell type in Equine Granulocytic Ehrlichiosis

A
  • Eosinophils, neutrophils, basophils
73
Q

Clinical signs of Equine Granulocytic Ehrlichiosis

A
  • Fever, icterus, ataxia***
  • Ventral edema
  • More severe in older horses
  • Petechial hemorrhage
74
Q

CBC changes for EGE

A
  • Thrombocytopenia, anemia, leukopenia
75
Q

What is a unique signs with EGE that helps distinguish it from similar diseases?

A
  • Ataxia
76
Q

Diagnosis of EGE

A
  • Clinical signs, lab findings
  • Visualize morulae in granulocytes
  • Indirect fluorescent antibody test (paired titers)
  • PCR (helpful in early and late stages)***
77
Q

Treatment of EGE

A
  • Oxytetracycline for 5-7 days
  • Untreated is self-limiting
  • Supportive care
78
Q

Causes of increased utilization of platelets

A
  • Trauma or hemorrhage, transiently
  • Thrombosis
  • Disseminated intravascular coagulation (most common)
79
Q

What is the category of thrombocytopenia cause that is most common in the referral hospital?

A
  • Increased utilization
80
Q

DIC definition

A
  • Pathologic activation of coagulation and fibrinolytic systems
  • Something is going wrong to trigger blood to clot when it normally shouldn’t
  • Consumption of platelets and increased fibrinolytic
81
Q

Initiating factors of DIC

A
  • SIRS/endotoxemia (far and away the most common)
  • Hemolysis, bacteremia, viremia, neoplasia, burns, hepatic/renal disease, severe dystocia, fetal death, immune complex disorders
82
Q

Clinical signs of DIC

A
  • Initially hypercoagulable (draw blood and then later there is a thrombus or catheter stops working due to a giant clot)
  • Renal dysfunction can occur
  • Later, prolonged bleeding (petechia, ecchymoses, bleeding)
  • Organ dysfunction
  • Frank blood from nostrils, rectum, etc.
  • Very rare, and end stage DIC
83
Q

Diagnosis of DIC

A
  • Multiple hemostatic abnormalities and thrombotic/hemorrhagic tendencies
  • Can run coag panels (PT/PTT, FDP, platelet count)
84
Q

Treatment of DIC

A
  • TREAT THE UNDERLYING CONDITION
  • Super important
  • Critical care principals
85
Q

Prognosis of DIC

A
  • Poor if cannot resolve underlying condition or overt hemorrhage develops
  • If a surgery would correct the underlying cause, then you need to go to surgery
86
Q

Fairly common cause of thrombocytopenia

A
  • Lab error
87
Q

If you suspect thrombocytopenia secondary to a lab error, then what steps would you take?

A
  • Sensitive to EDTA

- Re-draw into a sodium citrate anticoagulant tube to get a more accurate count

88
Q

Lymphosarcoma breed/sex predilection

A
  • None
89
Q

Age predilection for lymphosarcoma

A
  • Common in YOUNG and middle-aged horses
90
Q

Clinical signs of lymphosarcoma that are most common

A
  • Nonspecific :P
91
Q

Four classic forms of LSA

A
  • Cutaneous
  • Multicentric
  • Alimentary
  • Mediastinal
92
Q

Multicentric LSA location

A
  • Spinal cord lymphoma, spleen, hepatic
93
Q

Alimentary LSA

A
  • Chronic weight loss, often young

- May have abdominal fluid (won’t be able to get neoplastic cells from that fluid)

94
Q

Mediastinal LSA

A
  • Majority have excess fluid
  • May have edema in the cranial half of the body
  • Muffled lung sounds in ventral thorax
  • Mild tachycardia, tachypnea
95
Q

Clinical signs of LSA

A
  • Dependent on type
  • Depression
  • Anorexia
  • Lymphadenopathy (firm, non-painful)
  • Ventral edema
  • Fever
  • Respiratory distress
  • Colic, diarrhea
  • Pallor
  • mass on rectal exam
96
Q

Clinical pathology of LSA

A
  • Anemia (chronic disease, IMHA, bone marrow involvement)
  • Increased fibrinogen
  • IMHA, IMTP
  • Polyclonal gammopathy (T cell usually)
  • Increased liver enzyme activities
  • Hypercalcemia uncommon
  • IgM deficiency uncommon
  • Lymphocytic leukemia
  • Serum thymidine kinase (sTK) activity
97
Q

Diagnosis of LSA

A
  • Biopsy (NOT FNA)
  • Difficult to find
  • Possible serum thymidine kinase activity
98
Q

Treatment of LSA

A
  • Usually none
  • Some chemotherapy regimens
  • Can be transiently responsive to steroids
99
Q

Cutaneous lymphosarcoma

A
  • Often slowly progressive, may wax and wane
  • May show improvement when mares become pregnant
  • May be related to estrogen
  • At least one case resolved after surgical removal of granulosa thecal cell tumor
100
Q

Pigeon breast etiology

A
  • Corynebacterium pseudotuberculosis
  • In the rest of the world, more commonly ulcerative lymphangitis
  • In the US, most commonly manifests as internal abscesses
101
Q

Transmission of C. pseudotuberculosis

A
  • Organisms from soil gain access through possible breaks in the skin
  • May be associated with ventral midline dermatitis
  • Stable flies most likely
102
Q

C. pseudotuberculosis time of year

A
  • Late summer
103
Q

Signs of C. pseudotuberculosis

A
  • Edema, abscess (pectoral, inguinal, internal)
  • Fever, anorexia, weight loss
  • Lameness (acute onset non-weight bearing lameness)
104
Q

Diagnosis of C. pseudotuberculosis***

A
  • Culture of an aspirate

- Serology (single sample high titer)

105
Q

Treatment of C. pseudotuberculosis

A
  • Drain
  • Antibiotics
  • NSAIDs
  • TMS and rifampin usually
106
Q

Prognosis of C. pseudotuberculosis

A
  • Usually good

- May recur

107
Q

Four causes of edema

A
  1. Increased hydrostatic pressure (non-painful, cool edema) like secondary to right heart failure
  2. Decreased oncotic pressure (non-painful, cool edema due to decreased albumin)
  3. Increased vascular permeability (warm, painful edema)
  4. Decreased lymphatic drainage (can be warm, painful edema, or cool); often localized

Equine Med Final (Old Material) (11 decks)

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