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CLIN SCI 4 EX2 > Immune Diseases > Flashcards

Immune Diseases Flashcards

1
Q

First line of defense against infection using cytokines, phagocytosis, antimicrobial peptides, reactive oxygen and nitrogen

A

Innate immunity

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2
Q

response slower to develop

A

adaptive immunity

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3
Q

responds to infections and vaccines by making cytokines and antibodies and more lymphocytes

A

adaptive immunity

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4
Q

rapid response to infection, tissue injury

A

innate immunity

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5
Q

consists of neutrophils, monocytes, macrophages, NK cells, and dendritic cells

A

innate immunity

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6
Q

consists of lymphocytes (B and t cells)

A

adaptive immunity

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7
Q

What happens when the innate immune system (first line) doesnt work

A

-Recurrent bacterial infections: diarrhea, pneumonia, skin and UTI
-Commensal (non-pathogenic) bacteria infections
-Spontaneous septic arthritic and osteomyelitis
-Chronic, recurrent fungal infections

typically in younger patients

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8
Q

What are the top differentials for young animals with recurrent infections

A

-Decreased or absent antibody production
-T cell dysfunction
-Neutrophil function defects
-Monocyte function defects
-Complement deficiency
-Ciliary dyskinesia
-Infections with highly resistant bacteria

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9
Q

11 mo Irish setter male with chronic bacterial infections and pneumonia.
CBC: Marked leukocytosis (126,500) with 4% bands
Culture and cytology from lungs: tracheal wash sample grew Bordetella and E. Coli cytology, revealed few PMN, many bacteria
What are some plausible differentials?
What are two tip-offs this dog may have an immune deficiency disorder?
How was diagnosis confirmed?

A

-Systemic bacteria infection or Highly drug resistant organism?
Lots of neutrophils in the blood stream and not in the lungs is the key observation

Diagnosis: Inherited leukocyte adhesion molecule deficiency (neutrophils and monocytes) - very rare
Do flow cytometry on blood sample to confirm deficiency
Prognosis: guarded; judicious antimicrobial therapt, consider microbiome transplants to reduce colonization with pathobionts

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10
Q

What is the prognosis and treatment of inherited leukocyte adhesion molecule (CD18) deficiency

A

judicious antimicrobial therapy, consider microbiome transplants to reduce colonization with pathobionts

guarded prognosis

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11
Q

How do you diagnose inherited leukocyte adhesion molecule (CD18) deficiency

A

flow cytometry - CD18 to see if neutrophils can enter into the site of infection

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12
Q

What happens when the 3 major components (neutrophils, monocyte/macrophages, complement) of
the innate immune system either don’t work properly or are deficient?

A

a. Neutrophil dysfunction (deficiency extremely rare): Recurrent, extracellular bacterial
infections of skin, lungs, GI tract, and urinary tract
b. Monocyte/macrophage dysfunction (deficiency extremely rare): Development of systemic
fungal infections, intracellular bacterial infections, chronic viral infections
c. Complement deficiency: Recurrent, extracellular bacterial infections of skin, lungs, GI tract,
urinary tract

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13
Q

What happens when the 3 major components (B cells, CD4 + T cells, CD8+ T cells) of the adaptive
immune system don’t work properly, due to either dysfunction or decreased numbers of cells?

A

a. CD4+ T cell deficiency or dysfunction: Recurrent and/or disseminated infections with
protozoa, fungi, viruses, and intracellular bacteria (eg, Mycobacteria)

b. CD8+ T cell deficiency or dysfunction: Recurrent and/or disseminated viral, protozoal, and
intracellular bacterial infections (eg, Listeria, Mycobacteria)

c. B cell deficiency or dysfunction: Recurrent, extracellular bacterial infections of skin, lungs, GI
tract, urinary tract

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14
Q

What happens when the adaptive immune system doesn’t work

A

-Chronic recurrent bacterial infections (Staph, Strepto)
-Chronic viral infections (herpes, papillomavirus)
-Chronic fungal infections (eg Cryptococcus)
-Chronic intracellular bacterial infections (Mycobacteria, Listeria)
-Increased incidence of virally-induced cancers

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15
Q

What virus infections are chronic with adaptive immune suppression

A

herpes, papillomavirus

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16
Q

a 3yo CM Basset Hound with chronic recurring bronchopneumonia whole life
very antibiotic responsive
Why would we suspect possible immune deficiency

A

-Recurrence and age of onset (started at 6 months of age)

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17
Q

What is the sequence of diagnostic tests for assessing adaptive immune function in patients with suspected immune deficiency *

A

1) CBC, biochem, UA
2) Immunoglobulin quantitation (IgG, IgA, IgM)
3) T and B cells using flow cytometry numbers
4) Specialized function test (neutrophil killing, phagocytosis, T cell proliferation and cytokine release, complement assays)

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18
Q

First wave for assessing adaptive immune function in patients with suspected immune deficiency

A

CBC, biochem, UA

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19
Q

a 3yo CM Basset Hound with chronic recurring bronchopneumonia whole life
very antibiotic responsive
CBC: mature neutrophilia, mild anemia
Very low IgG, IgM, and IgA concentrations
T cells normal, low normal B cells
What is going on?

A

very low immunoglobin levels (B cell dysfunction or low number)
but there are plenty of B cells
therefore it is B cell dysfunction - likely cause of receptor

key diagnostics was immunoglobulin quantitation and flow cytometry

tx: plasma or high titered parvo serum q3-6 mos; judicious antimicrobial therapy

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20
Q

What is the most common inherited immune deficiency in dogs (although rare)

A

Common Variable Immune Deficiency (CVID)
IgA deficiency: German Shepard dogs
leukocyte adhesion defiency (irish setters)

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21
Q

Leukocyte adhesion deficiency is common in

A

Irish Setters

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22
Q

IgA deficiency is common in

A

German Shepard

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23
Q

T/F: its uncommon to see neutrophils in lymph nodes

A

true

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24
Q

What is the most common inherited immune deficiencies in cats

A

-Pelger-Huet
-Chediak Higashi syndrome

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25
What is the most common inherited immune deficiencies of horses
-SCID (severe combined immune deficiency) -IgM defiency
26
What is the most common inherited immune deficiency in cows
BLAD (Bovine leukocyte adhesion deficency)
27
What are the typical signs of inherited immune deficiencies
a) Early age of onset (before one year) b) Recurrent or chronic bacterial infections c) Infections that don't respond to standard therapy d) Unusual infections (atypical mycobacteria, disseminated Toxoplasma)
28
Of all the inherited immune disorders, what is the most common
B cell dysfunction and decreased antibody
29
Are inherited or acquired immune deficiencies more common
acquired
30
How might immune deficiencies be acquired in dogs
1) Steroid and T cell targeted therapy (Doxy) 2) Cushing's disease 3) Diabetes mellitus 4) Cancer 5) CKD 6) Cachexia
31
How might immune deficiencies be acquired in cats
Viral infections (FIV, FeLV, FIP) Diabetes CKD Cachexia
32
How might immune deficiencies be acquired in horses
-Failure of passive transfer -EIAV infection
33
How might immune deficiencies be acquired in cattle
failure of passive transfer BVD infection
34
What drugs lead to acquired defects in immune responses
Corticosteroids Oclactinib Doxycycline
35
Diseases that lead to acquired defects in immune responses
Cushings Diabetes mellitus Chronic kidney disease Weight loss, cachexia Obesity, chronic inflammation
36
How can I use info from the CBC and SADP to assess immune function
1) Check number of neutrophils and lymphocytes (both high and low values are significant) 2) Check cytologic appearance of lymphocutes and neutrophils (activated; granules) 3) Check the number of monocytes (high values are significant) 4) Check the globulin concentrations (most of this is comprised of IgG immunoglobulins)
37
What might be an example of iatrogenic immune deficiencies
a dog being treated with cyclosporine might have a reoccurrence of papillovirus
38
After checking the CBC, what is the next set of diagnostic tests for a patient with suspected immune deficiency?
a. Measure serum immunoglobulin concentrations (IgG, IgA, IgM) b. Quantitate number of circulating T cells and B cells (flow cytometry)
39
What are examples of more advanced immune function testing
a. Measure complement concentrations b. Assess neutrophil and monocyte respiratory burst and phagocytosis c. Assess lymphocyte cytokine production and proliferation d. Assess neutrophil and monocyte chemotaxis
40
What should you do for a complement deficiency
administer fresh or fresh frozen plasma transfusion
41
What should you do for CD4 T cell deficiency
administer non-specific immune stimulants to induce IFN-y production
42
What should you do for CD8 T cell deficiency
administer immune stimulants to boost NK cell function (can substitute for CD8 T cells)
43
What should you do for Humoral immune deficiency (CVID, B cell deficiency)
- administer periodic plasma or whole blood transfusions - administer hyperimmune globulins (eg, high-titered parvovirus serum) - aggressive, but short-term rotating program of antimicrobial therapy - use probiotics or fecal transfer to displace pathogenic bacteria in the gut
44
What are the 4 major immune mediated diseases of dogs and cats
IMHA IMTP IMP SLE
45
autoantibodies directed against RBC surface antigens
autoimmune hemolytic anemia (IMHA)
46
autoantibodies directed against platelet antigens
immune mediated thrombocytopenia (IMTP)
47
autoantibodies or cross-reactive antibodies against poorly defined antigens present in the synovium
immune mediated polyarthritis
48
autoantibodies directed against nuclear antigens (DNA, RNA, histones)
systemic lupus erythematosis (SLE)
49
immune mediated destruction of islet cells
Diabetes mellitus
50
immune mediated destruction of thyroglobin producing cells
hypothyroidism
51
immune mediated destruction of parathyroid gland cells
hypoparathyroidism
52
immune mediated destruction of adrenal cortical cells (some or all layers)
Addisons disease
53
immune mediated injury to iris, posterior chamber seen in equines
Equine periodic ophthalmia
54
immune mediated injury to small joints
Rheumatoid arthritis
55
immune mediated injury to epithelial cells and tight junctions
Blistering skin diseases (BP, PVU, DL)
56
How is the immune response an important mediator in the pathology of septic shock
cytokine responses to bacterial infection or tissue damage, all species
57
Diseases where the immune response an important mediator in the pathology
-Septic shock -Viral or bacterial meningitis and encephalitis -Osteoarthritis -Chronic inflammatory hepatitis -Inflammatory bowel disease -Allergic airway disease -Atopy and flea allergy
58
How do we diagnose IMHA
History: relatively acute onset, young to middle aged dog Regenerative anemia with spherocytes and auto-agglutination High WBC, mature neutrophilia, often concurrent thrombocytopenia Hyperbilirubinemia, hypoalbuminemia, elevated BUN
59
What RBC morphology is seen with IMHA
spherocytes
60
What is the history that is concurrent with IMHA
relatively acute onset, young to middle aged dog
61
What are the lab findings seen with IMHA
Regenerative anemia* with spherocytes and auto-agglutination High WBC, mature neutrophilia, often concurrent thrombocytopenia Hyperbilirubinemia*, hypoalbuminemia, elevated BUN Agglutination
62
What does the Coomb's test measure
measures the presence of OgG on surface of patient RBC, using microagglutination assay -flow cytometry can better measure and quantify RBC IgG
63
What is the preferred extra diagnostic test for IMHA
Flow cytometry
64
Direct antiglobulin test (DAT) is the
Coomb's test
65
What are the 6 major negative prognostic findings in dogs with IMHA
1) Concurrent thrombocytopenia 2) Hyperbilirubinemia 3) Elevated WBC and neutrophilia with increased bands 4) Increased BUN 5) Decreased serum albumin 6) Monocytosis PCV is not prognostic
66
How reliable is a positive Coomb's test?
relatively sensitive but not very specific -alone doesnt mean iMHA, look at other facts in the picture
67
What is the typical signalment of an animal with IMTP?
young to middle aged female animal
68
What is a test you can do for test for blood loss
fecal occult blood test
69
T/F: degree of anemia is prognostic of IMHA
False
70
How do you acutely manage IMHA, IMTP cases
-High dose steroids, IV for first few doses -Clopidogrel, heparin (Anticoagulation) -Initiate T cell target drug (cyclosporine or Mycophenolate) -Induce full disease remission (anemia or thrombocytopenia)
71
What anticoagulation drugs can you use for IMHA acute management
clopidogrel, heparin
72
What drugs can you use to initiate T cell target in acute IMHA management
Cyclosprine or Mycophenolate
73
How do you chronically manage IMHA, IMTP
-Maintain remission for 1-2months before starting taper -Taper steroids first, keep T cell targeted drugs at full close -50% steroid dose reduction, re-evaluate monthly (CBC) -Further reduction by 50% then go to EOD dosing -If in remission, stop steroids, begin taper of T cell drug (50% then DC) -Whole process can take 6 months or longer
74
How do patients with IMTP typically present
-Presence of petechia -Unexplained hematuria or epistaxis or hematochezia -Unexplained regenerative anemia
75
T/F: magnitude of thrombocytopenia predicts whether IMTP or other causes of platelet comsumption or destruction
False- a very low platelet count can occur in animals with platelet destruction due to causes other than anti-platelet antibodies (eg/ consumptions due to blood clots) plus patients with IMTP can also haveo nly midly decreased platelet counts
76
What are other causes of thrombocytopenia that you need to rule out before diagnosing IMTP
Rickettsial infection Platelet consumption (thromboembolic disease) DIC Blood clots Drug history Estrogens - bone marrow toxicity Occult neoplasia Rodenticide Myelophthisis
77
T/F: bone marrow examination is helpful in IMTP diagnosis
False- only occassionally helpful
78
What is the key diagnostic for IMTP
Flow cytometry for anti-platelet antibodies should be used in the workup of any animal with unexplained thrombocytopenia
79
What platelet amount do you start worrying about thrombocytopenia
50,000
80
What would be a primary differential for thrombocytopenia that is due to consumption
thromboembolic disease
81
What test is used to diagnose IMTP
APA test: Anti-platelet antibodies (APA)
82
in thrombocytopenia cases, what can you do as advanced imaging for clot detection
AUS, CT
83
How do you treat IMTP
1) Initial high dose IV* steroids: Dexamethasone or Methylprednisolone follow with oral prednisolone (1-2mg/kg/day) other options 2) Add mycophenolate or cyclosporine 3) Add vincristine to stimulate platelet release 4) Add immune globulins (IVIG) - blocks macrophages from taking up platelets 5) Nuclear option (splenectomy)- consider because reducing the spleen reduces the ability of platelets to be destroyed
84
With IMTP, what drug might stimulate platelet release
Vincristine - microtubule inhibitor
85
blocks macrophages from taking up platelets, used in IMTP cases
Immune globulins (IVIG)
86
Why might you take the spleen out for primary IMTP cases
allows so that platelets cant be destroyed by the macrophages allows so the patient doesnt have to be on steroids
87
Why do we use Methylprednisolone (Solu-Medrol)
steroid to ramp up steroid immune suppression with rapid high dose induction (extragenomic steroid mechanism) gets really high plasma levels 10-30mg/kg IV bolus
88
What are key diagnostics in thrombocytopenia cases
CBC anti-platelet antibody test 4DX panel
89
What are the typical signs of immune mediated polyarthritis (IMPA)
-young animal, acute to subacute onset -Intermittent fever common -Shifting leg lameness -General malaise, inappetence, lack of activity -joint effusion (often cannot be palpated reliably)
90
How is immune mediated polyarthritis (IMPA) diagnosed
Rule out infectious causes with serology Joint tap and cytology: typical findings are increased numbers of non-degenerate neutrophils with variable numbers of lymphocytes and macrophages; high protein content of fluid, background staining on slides Joint fluid cultures nearly always negative
91
What is a typical history for an animal with SLE?
chronic illness, young to middle aged many different manifestations: skin lesions, polyarthritis, myopathy, CNS signs fever often present intermittently
92
How does SLE typically manifest as
many different manifestations: skin lesions, polyarthritis, myopathy, CNS signs
93
What lab abnormalities is often found in SLE patients
-Regenerative or nonregenerative anemia Mild thrombocytopenia Neutropenia Elevated liver enzymes Proteinuria Elevated globulins
94
Why do we do a splenectomy for autoimmune disease (IMHA, IMTP) ?
to eliminate phagocytic macrophages immediately
95
What do diseases make you consider splenectomy
IMHA, IMTP
96
What are the downsides to doing a splenectomy?
Increased risk of infection
97
How do you diagnose primary IMTP
APA test
98
Primary rule outs for severe thrombocytopenia
primary IMTP thromboembolic disease
99
What is the most common immune deficiency in dogs
antibody deficiency
100
How should you work up an immune deficiency
CBC antibody concentrations* flow cytometry* specialized function tests
101
How is SLE diagnosed
1) Combination of 4 or more clinical or lab abnormalities -Regenerative or nonregenerative anemia -Mild thrombocytopenia -Neutropenia -Elevated liver enzymes -Proteinuria -Elevated globulins 2) ANA (antinuclear antibody test) helpful if positive but negative ANA does not rule SLE
102
What does a negative antinuclear antibody test for SLE mean?
does not rule out SLE
103
How is rheumatoid arthritis diagnosed
1) Typical radiographic findings: erosive joint disease, small distal joints 2) RA test: measures IgM antibodies directed against Fc portion of IgG antibody 3)*Serology for detection of antibodies to citrullinated proteins (CCP) Joint taps: cannot be used to distinguish RA from polyarthritis
104
What are the radiographic signs of rhematoid arthrtis
erosive joint disease, small distal joints
105
Serology for rheumatoid arthritis detects
citrullinated proteins (CCP)
106
joint taps cannot distinguish rheumatoid arthritis from
polyarthritis
107
What immunosuppressive drugs are considered broadly active and non-specific
1) Corticosteroids 2) Oclacitnib (Apoquel) 3) IV immune globulins 4) Tetracyclines at high doses
108
What 5 immunosuppressive drugs primarily target T lymphocytes
Mycophenolate Cyclosporine Tacrolimus Leflunomide Azathioprine
109
What is the function of IVIG
immune suppression by suppressing macrophage function also broad immune suprresion
110
What is the function of cyclosporine
immune suppression by blocking T cell cytokine production
111
What method of immune suppression eliminates macrophages
splenectomy
112
What is the function of mycophenolate
immune suppression by blocking lymphocyte division
113
What is the function of oclactinib
broad immune suppression by blocking cytokine signaling
114
What is the function of tacrolimus
immune suppression by blocking T cell cytokine production
115
What is the function of leflunomide
immune suppression by blocking lymphocyte division
116
What is the function of azathioprine
immune suppression by blocking lymphocyte division
117
What are the broad immune suppression options
Corticosteroids* Oclacitinib IVIG
118
What drugs block lymphocyte division
Mycophenolate Leflunomide Azathioprine
119
What drugs block T cell cytokine production
Cyclosporine Tacrolimus Sirolimus
120
What is the function of sirolimus
immune suppression by blocking sirolimus
121
What drug blocks cytokine signaling
Oclacitinib
122
What are repurposed anti-inflammatory drugs used for immune suppression
Doxycycline Azithromycin
123
What immunosuppressive drugs primarily target T lymphocytes
Block lymphcyte division or production a) Mycophenolate (div) b) Cyclosporine (prod) c) Tacrolimus (prod) d) Leflunomide (div) e) Azathioprine (div)
124
What are the side effects of corticosteroids
-PU/PD -panting -hyperexia -muscle and skin atrophy -behavioral changes -bladder infection
125
How do corticosteroids suppress the immune system?
1) Suppress cytokine production by activated macrophages, monocytes, and neutrophils 2) Suppress neutrophil and macrophage phagocytosis 3) Suppress neutrophil migration into tissues 4) Suppress T cell cytokine production 5) Induce T cell apoptosis
126
What are the side effects of Oclacitinib
-GI effects -Bladder infection
127
What are the side effects of cyclosporine
GI side effects (vomiting, diarrhea)
128
What are the side effects of mycophenolate
GI side effects (can be severe) Vomiting and Diarrhea
129
What is the side effect of Azathioprine
idosyncratic hepatic necrosis
130
What is the side effect of IVIG
anaphylaxis (human proteins)
131
What is the side effect of tacrolimus and sirolimus when given topically
local irritation local hairloss
132
What does a physiological dose of prednisone do
replaces the daily cortisol output from the adrenal cortex 0.025-0.05 mg/kg day
133
What is the physiological dose of prednisone
0.05-0.1 mg/kg day
134
What is the anti-inflammatory dose of prednisone
0.25 to 0.5 mg/kg day suppresses inflammation without significant immunosuppression, but this can still induce severe side-effects
135
What is an immunosuppressive dose of prednisone
1 to 2mg/kg day significant impairement of the immune system
136
Is dexamethasone or prednisone more potent
Dexamethasone 0.75mg equals 100mg of cortisol while 5mg of prednisone equals 100mg
137
Does dexamethasone or prednisone have more mineralo-corticoid potency?
Prednisone has some activity and can be used in addisonian dog
138
Is dexamethasone or prednisone used for an addisionian dog
Prednisone - has mineralocorticoid potency
139
Does dexamethasone or prednisone have a longer half-life?
Dexamethasone 36-54 hours while prednisone (18-36 hours)
140
Rank the different steroids by potency
Least potent to most 1) hydrocortisone 2) prednisone, prednisolone 3) dexamethasone (8X prednisone potency) 4) Topicals (very potent: triamcinolone, betamethasone, fluticasone, budesonide
141
If a dog is on physiological prednisone for Addisons, how much should you increase it before a stressful event (ie surgery)
2-3x the dose before surgery
142
What is the general approach to immune suppression for severe immune mediated disorders
1) Initial high-dose corticosteroids (IV to start) 2) Add a second drug to augment immune suppression (T cell targeted drugs - cyclosporine and mycophenolate) 3) Treat until disease in clinical remission: maintain 1-2 months 4) Taper steroids first (reduce side effects) 5) Taper slowly to avoid triggering disease release 6) Monitor disease activity clinically and with specific tests
143
What is the extra-nuclear effects of corticosteroids when <1mg/kg
primary effect of corticosteroids is mediated by binding to the glucocorticoid receptor, which in turn alters cytokine gene transcription (genomic activity)
144
What is the extra-nuclear effects of corticosteroids when >1mg/kg and given IV
steroids insert into cell membrane and alter cell signaling and ion permeability (extragenomic activity)
145
Do you taper T cell targeted drugs or steroids first
Steroids
146
Why do we often combine immunosuppressive drugs
a) Reduce dose of steroids to minimize steroid side effects b) Greater potency from combined therapy c) Greater specificity for certain populations of immune effector cells (eg T cells)
147
When your neutrophil count drops below _________ youre in the danger zone because there isnt enough neutrophils for the bacterial showers that enter the blood stream
1000
148
What is the target of oclactinib (Apoquel)
JAK kinase inhibitor- targets 3 major kinases (JAK1,2,3), nonselective kinase inhibitor broad suppression of cytokine signaling
149
Approved for treatment of atopy in dogs; being used now for immune suppressive therapy of immune mediated diseases in dogs including IBD and chronic rhinitis
Oclactinib (Apoquel)
150
What T cell targeted drug is more potent and rapidly acting than azathioprine, can be administered IV
Mycophenolate
151
What is the mechanism of Mycophenolate
Suppresses lymphocyte division by inhibiting purine synthesis
152
Mycophenolate is often used for
severe or refractory IMHA, IMTP, SLE
153
What is the onset of cyclosporine
days to weeks
154
What is the mechanism of Cyclosporine
inhibits cytokine production (IL-2, IFN-g) by CD4+ T cells
155
What is cyclosporine used for
-Maintenance therapy for refractory IMHA, IBD, IMTP, polyarthritis -Steroid alternative for atopy -Topical for KCS in dogs -Perianal fistulas in dogs
156
Drug that blocks lymphocyte division by inhibiting mitochondral enzyme required for uridine synthesis
Leflunomide
157
Drugs that suppresses lymphocyte division by inhibiting purine synthesis
Mycophenolate Azathioprine
158
What is the major side effect of Lefluonomide
Gi: vomiting and diarrhea
159
What can Leflunomide be used for
management of refractory IMHA or IMTP patients
160
What should you do before starting Azathioprine treatment
Since this drug causes fatal hepatic necrosis, which is reversible if detected detected early, you should check liver enzymes (esp ALT) before treatment and then again at 2 weeks and 4 weeks Discontinue drugs if ALT increases
161
How do mesenchymal stem cells suppress immune responses
-Produce immunosuppressive factors- PGE2, TGF-b, adenosine, IL-10 -Suppress lymphocyte proliferation, cytokine production and DC and macrophage function -Both local and systemic immune suppressive effects are induced -Broad immune suppression
162
How do you diagnose immune-mediated neutropenia and thrombocytopenia
CBC Bone marrow cytology
163
How do you manage immune-mediated neutropenia and thrombocytopenia
immune suppression with prednisone with taper over 30-60 days
164
How do you diagnose Precursor targeted immune mediated anemia (PIMA)
bone marrow cytology clotting times CBC can measure serum erythropoietin or estrogen
165
In a dog with Precursor targeted immune mediated anemia (PIMA) what would the bone marrow cytology show you
Erythroid hyperplasia all erythroid lineages present until reticulocytes, which are largely absent Erythrophagocytos is observed by bone marrow macrophages
166
How do you treat Precursor targeted immune mediated anemia (PIMA)
immune suppression with corticosteroids (prednisolone, 2mg/kg/day) plus cyclosporine (5mg/kg/day) monitor: CBC in 2 week intervals add additional immune suppression if partial response
167
Any dog with non-regenerative anemia when bleeding is ruled out should
should be trial treated with steroids if full workup is not possible
168
Non-regenerative anemia should get
steroid trials

CLIN SCI 4 EX2 (5 decks)

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