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Oncology > Equine Immunology and Hematology I > Flashcards

Equine Immunology and Hematology I Flashcards

1
Q

What are components of Innate immunity?

A 
Nonspecific
Acute phase proteins
-Fibrinogen
Proinflammatory cytokines
-IL-1, IL-6, TNFalpha
Complement system
Lipid mediators
-Prostaglandins, leukotrienes
Granulocytes, monocytes
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2
Q

Components of Adaptive immunity

A 
Specificity and memory
Cellular and humoral (Ab mediated)
B cell lymphocytes
- Memory cells
- Immunoglobulins
T-cell lymphocytes
-CD8, CD4
-MHC
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3
Q

Neutrophilia causes in the horse

A

Chronic/established infection
Abscess
Neoplasia, glucocorticoids

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4
Q

Neutropenia causes in the horse

A

Acute, severe infection (GI)
Septicemia, endotoxemia
- L shift and toxic changes
Endotoxemia is rapid redistribution of N0 to marginal and tissue pools

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5
Q

Lymphopenia causes

A

Acute viral, rickettsial, or severe bacterial infection

Endotoxemia

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6
Q

Eosinophilia causes

A

Parasitic
Hypersensitivity
Neoplasia

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7
Q

Basophilia causes

A

Hypersensitivity

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8
Q

Immunodeficiencies

A 
Primary (rare): genetic
Secondary: altered responses of normal immune system
- Disease (PPD)
- Age
- Pregnancy
- Drugs
- Stressors
- Neoplasia
- Malnutrition, nutrient deficiencies
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9
Q

Clinical features of immunodeficiency

A

Onset at young age
Repeat infections, poorly responsive to treatment
Increased susceptibility to organisms of low pathogenicity
Illness or poor immunologic response to vaccination
Persistent abnormalities in leukocytes

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10
Q

Dx of immunodeficiency

A

Ab mediated immunity: quantitative tests for Ig levels, functional test of response to vax
Cellular immunity: Quantitative CBC, lymphocyte phenotyping, functional test response to vax
Granulocytes, monocytes, M0: quantitative only
Bone marrow: evaluate progenitor cell populations

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11
Q

SCID

A

Lethal, autosomal recessive condition primarily seen in Arabian foals
- Chromosome 9 mutation
- 8-25% Arabians in US are carriers
T and B cell function absent
- Absence of cell mediated and Ab mediated immunity

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12
Q

Other rare immunodeficiencies

A 
Common variable immunodeficiency
- Late onset (6-14yr) no breed or gender disposition
- Recurrent bacterial infections
IgM dificiency
Agammaglobulinemia
Transient hypogammaglobulinemia
Fell pony syndrome
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13
Q

Lymphoproliferative disorders

A

Lymphoma
Leukemia
Myeloma

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14
Q

Equine lymphoma basics

A

Most common neoplasia of the horse

Mean diagnostics 5-10y

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15
Q

CS of equine lymphona

A 
Lymphadenopathy
Lethargy, weight loss, fever
Others dependent
Peripheral lymphadenopathy rare
Hematologic abnormalities are variable
- Anemia, lymphopenia
- Lymphocyte morphology abnormal
- Inflammatory leukogram, hyperglobulinemia
Paraneoplastic syndromes
- Hypercalcemia
- Immune mediated Hemolytic anemia or thrombocytopenia
Occasional suspect association with EHV 5
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16
Q

Equine lymphoma classification

A

Morphologic: small cell, large cell, mixed
Cell lineage: immunohistochemical evaluation, T cell rich, large b cell most common
Anatomic distribution: multicentric, generalized, alimentary/intestinal, thoracic, cutaneous

17
Q

Multicentric lymphoma

A

Multiple lymph nodes

No extra nodal involvement

18
Q

Generalized lymphoma

A 
Metastasis to extra-nodal tissues
Nonlymphoid tissue involved
Spleen most common organ
Very poor prognosis
Severe clinical signs
Leukemia possible
19
Q

Intestinal lymphoma

A

CS: malabsorption, PLE, weight loss, edema, abdominal effusion, colic, diarrhea
Neoplastic lesions: diffuse, segmental thickening, focal masses, scattered ulcerative lesions
Dx: US, biopsy, Abd fluid analysis

MOST common neoplasia of GIT
Lymphadenopathy not typical

20
Q

Thoracic lymphoma

A

Most common thoracic neoplasia; Mediastinal, thymic, or pulmonary T cell predominates
CS nonspecific: Nasal discharge, adventitial lung sounds, pleural effusion*, ventral thoracic and limb edema, lymphadenopathy

21
Q

Cutaneous lymphoma

A

Skin associated lymphoid tissue
Distribution variable; single to multiple firm, SQ, nonpainful masses
Predominantly T cell rich large B cell
Often aggressive - may progress
Often responsive to corticosteroids, sx excision

Best one to get

22
Q

Lymphoma Dx and Tx

A 
Antemortem Dx difficult
Excisional biopsy, fluid analysis
Bone marrow
Other
Tx: Corticosteroids, immunomodulation, antiviral medication, chemo (transient remission possible, recurrence typical)
Long term prognosis poor
23
Q

Equine leukemia basics

A

Primary originats from bone marrow
Secondary is leukemic phase of lymphoma

Myeloid or lymphoid cell lineage
Leukemic: profound leukocytosis
Subleukemic: blast cells, low/normal WBC
Aleukemic: abnormal bone marrow only

Grave prognosis

24
Q

Equine leukemia CS

A 
Weight loss
anorexia
lethargy
Pyrexia
Lymphademopathy if secondary to lymphoma
25
Q

Equine leukemia hematologic changes

A 
Anemia
Thrombocytopenia
Marked leukocytosis
Pancytopenia
- Neutropenia, lymphopenia
Increased blast or atypical cells in blood
Hyperproteinemia
Hyperfibrinogenemia
26
Q

Equine leukemia Dx

A

Bone marrow aspirate
Flow cytometry
IHC, immunophenotyping

27
Q

Equine myeloma

A 
Plasma cell proliferation
Primary: bone marrow
Secondary: extramedullary
- LN, spleen, kidney, liver
Multiple myeloma: bone marrow and tissues
28
Q

Equine myeloma CS

A

Weight loss, fever, lethargy
Pale MM
Limb edema
Recurrent infection

29
Q

Equine myeloma Dx

A

Bone marrow: plasmacytosis
Hematology: anemia, hyperproteinemia (globulins), Pancytopenia (myelopathies), hypercalcemia, monoclonal immunoglobulinemia

Poor prognosis, rapid deterioration

30
Q

Equine erythron

A 
Variable PCV
- ~30% circulating equine RBC in spleen
- Excitement/pain - transient increase in PCV
- alpha 2 agonists - transient decrease in PCV
Rouleau
Peripheral reticulocytes extremely rare
Howell Jolly Bodies
- Basophilic nuclear remnants
31
Q

Clinical evaluation of erythron

A

Coomb’s test: detect Ig or complement on erythrocyte surface
- Agglutination = positive
- Useful with IMHA
RBC fragility
Bone marrow eval: Aspirate or core biopsy, characterize anemia (Regen, nonregen, NO circulating reticulocytes), myeloid:erythroid (

32
Q

Anemia

A

Decreased O2 carrying capacity of blood secondary to RBC loss - hypoxia
Causes: blood loss, hemolysis, impaired RBC production
CS vary: tachycardia, tachypnea, depression, mucosal pallor/icterus, hemoglobinuria, lethargy, weakness

33
Q

Anemia Dx

A 
Hx
PE
CBC
Urinalysis
Bone marrow aspirate
34
Q

Acute blood loss: hemorrhage

A

Causes: trauma, Sx, guttural pouch mycosis, hemorrhage into body cavity, peripartum hemorrhage, coagulopathy, neoplasia
CS: Hypovolemic shock, colic and abd distension, dyspnea, braced stance, epistaxis

35
Q

Acute blood loss Dx

A

PCV/TP decrease over 12-24h, with IMHA TP shouldn’t decrease
Blood lactate increases secondary to tissue hypoxia
US
Abdominocentesis, thoracocentesis

36
Q

Acute blood loss Tx

A 
Stop hemorrhage
Address hypovolemic shock
Judicious use of sedation
Replace blood loss
With internal hemorrhage body can reuse blood components- avoid removal if posiible
37
Q

Blood transfusion basics

A

Transfused RBC last 2-4d in adult horse
Cross match
-Major: donor RBC- recipient serum alloAb
- Minor: dono serum Ab - recipient RBC
If cross match not possible Qa, Aa neg geldings or maiden mares

38
Q

Blood transfudsion strategy

A

Replace 20-40% of total loss
Can safely remove 5-10L from donor
Avoid adverse rxn to transfused RBC (start slow)
CS of adverse rxn: tachycardia, urticaria, dyspnea, pyrexia, colic, diarrhea, anaphylaxis, pulmonary edema, hemolysis, DIC

39
Q

Causes of chronic blood loss

A

GI or urogenital/renal dz: neoplasia, EGUS, RDC, Hemostatic dysfunction
Physiologic adaptation to gradual onset of tissue hypoxia secondary to anemia
Iron stores may become depleted: low serum iron, decreased bone marrow iron stores, increased total iron binding capacity, hypochromic, microcytic anemia

Oncology (3 decks)

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