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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
Q

What is the most common inherited immune deficiencies of horses

A

-SCID (severe combined immune deficiency)
-IgM defiency

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26
Q

What is the most common inherited immune deficiency in cows

A

BLAD (Bovine leukocyte adhesion deficency)

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27
Q

What are the typical signs of inherited immune deficiencies

A

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)

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28
Q

Of all the inherited immune disorders, what is the most common

A

B cell dysfunction and decreased antibody

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29
Q

Are inherited or acquired immune deficiencies more common

A

acquired

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30
Q

How might immune deficiencies be acquired in dogs

A

1) Steroid and T cell targeted therapy (Doxy)
2) Cushing’s disease
3) Diabetes mellitus
4) Cancer
5) CKD
6) Cachexia

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31
Q

How might immune deficiencies be acquired in cats

A

Viral infections (FIV, FeLV, FIP)
Diabetes
CKD
Cachexia

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32
Q

How might immune deficiencies be acquired in horses

A

-Failure of passive transfer
-EIAV infection

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33
Q

How might immune deficiencies be acquired in cattle

A

failure of passive transfer
BVD infection

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34
Q

What drugs lead to acquired defects in immune responses

A

Corticosteroids
Oclactinib
Doxycycline

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35
Q

Diseases that lead to acquired defects in immune responses

A

Cushings
Diabetes mellitus
Chronic kidney disease
Weight loss, cachexia
Obesity, chronic inflammation

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36
Q

How can I use info from the CBC and SADP to assess immune function

A

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)

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37
Q

What might be an example of iatrogenic immune deficiencies

A

a dog being treated with cyclosporine might have a reoccurrence of papillovirus

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38
Q

After checking the CBC, what is the next set of diagnostic tests for a patient with suspected immune deficiency?

A

a. Measure serum immunoglobulin concentrations (IgG, IgA, IgM)
b. Quantitate number of circulating T cells and B cells (flow cytometry)

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39
Q

What are examples of more advanced immune function testing

A

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

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40
Q

What should you do for a complement deficiency

A

administer fresh or fresh frozen plasma transfusion

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41
Q

What should you do for CD4 T cell deficiency

A

administer non-specific immune stimulants to induce IFN-y production

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42
Q

What should you do for CD8 T cell deficiency

A

administer immune stimulants to boost NK cell function (can substitute for CD8 T cells)

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43
Q

What should you do for Humoral immune deficiency (CVID, B cell deficiency)

A
  • 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
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44
Q

What are the 4 major immune mediated diseases of dogs and cats

A

IMHA
IMTP
IMP
SLE

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45
Q

autoantibodies directed against RBC surface antigens

A

autoimmune hemolytic anemia (IMHA)

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46
Q

autoantibodies directed against platelet antigens

A

immune mediated thrombocytopenia (IMTP)

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47
Q

autoantibodies or cross-reactive antibodies against poorly defined antigens present in the synovium

A

immune mediated polyarthritis

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48
Q

autoantibodies directed against nuclear antigens (DNA, RNA, histones)

A

systemic lupus erythematosis (SLE)

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49
Q

immune mediated destruction of islet cells

A

Diabetes mellitus

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50
Q

immune mediated destruction of thyroglobin producing cells

A

hypothyroidism

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51
Q

immune mediated destruction of parathyroid gland cells

A

hypoparathyroidism

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52
Q

immune mediated destruction of adrenal cortical cells (some or all layers)

A

Addisons disease

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53
Q

immune mediated injury to iris, posterior chamber seen in equines

A

Equine periodic ophthalmia

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54
Q

immune mediated injury to small joints

A

Rheumatoid arthritis

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55
Q

immune mediated injury to epithelial cells and tight junctions

A

Blistering skin diseases (BP, PVU, DL)

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56
Q

How is the immune response an important mediator in the pathology of septic shock

A

cytokine responses to bacterial infection or tissue damage, all species

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57
Q

Diseases where the immune response an important mediator in the pathology

A

-Septic shock
-Viral or bacterial meningitis and encephalitis
-Osteoarthritis
-Chronic inflammatory hepatitis
-Inflammatory bowel disease
-Allergic airway disease
-Atopy and flea allergy

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58
Q

How do we diagnose IMHA

A

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

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59
Q

What RBC morphology is seen with IMHA

A

spherocytes

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60
Q

What is the history that is concurrent with IMHA

A

relatively acute onset, young to middle aged dog

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61
Q

What are the lab findings seen with IMHA

A

Regenerative anemia* with spherocytes and auto-agglutination

High WBC, mature neutrophilia, often concurrent thrombocytopenia

Hyperbilirubinemia*, hypoalbuminemia, elevated BUN

Agglutination

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62
Q

What does the Coomb’s test measure

A

measures the presence of OgG on surface of patient RBC, using microagglutination assay
-flow cytometry can better measure and quantify RBC IgG

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63
Q

What is the preferred extra diagnostic test for IMHA

A

Flow cytometry

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64
Q

Direct antiglobulin test (DAT) is the

A

Coomb’s test

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65
Q

What are the 6 major negative prognostic findings in dogs with IMHA

A

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

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66
Q

How reliable is a positive Coomb’s test?

A

relatively sensitive but not very specific
-alone doesnt mean iMHA, look at other facts in the picture

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67
Q

What is the typical signalment of an animal with IMTP?

A

young to middle aged female animal

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68
Q

What is a test you can do for test for blood loss

A

fecal occult blood test

69
Q

T/F: degree of anemia is prognostic of IMHA

A

False

70
Q

How do you acutely manage IMHA, IMTP cases

A

-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
Q

What anticoagulation drugs can you use for IMHA acute management

A

clopidogrel, heparin

72
Q

What drugs can you use to initiate T cell target in acute IMHA management

A

Cyclosprine or Mycophenolate

73
Q

How do you chronically manage IMHA, IMTP

A

-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
Q

How do patients with IMTP typically present

A

-Presence of petechia
-Unexplained hematuria or epistaxis or hematochezia
-Unexplained regenerative anemia

75
Q

T/F: magnitude of thrombocytopenia predicts whether IMTP or other causes of platelet comsumption or destruction

A

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
Q

What are other causes of thrombocytopenia that you need to rule out before diagnosing IMTP

A

Rickettsial infection
Platelet consumption (thromboembolic disease)
DIC
Blood clots
Drug history
Estrogens - bone marrow toxicity
Occult neoplasia
Rodenticide
Myelophthisis

77
Q

T/F: bone marrow examination is helpful in IMTP diagnosis

A

False- only occassionally helpful

78
Q

What is the key diagnostic for IMTP

A

Flow cytometry for anti-platelet antibodies

should be used in the workup of any animal with unexplained thrombocytopenia

79
Q

What platelet amount do you start worrying about thrombocytopenia

A

50,000

80
Q

What would be a primary differential for thrombocytopenia that is due to consumption

A

thromboembolic disease

81
Q

What test is used to diagnose IMTP

A

APA test: Anti-platelet antibodies (APA)

82
Q

in thrombocytopenia cases, what can you do as advanced imaging for clot detection

A

AUS, CT

83
Q

How do you treat IMTP

A

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
Q

With IMTP, what drug might stimulate platelet release

A

Vincristine - microtubule inhibitor

85
Q

blocks macrophages from taking up platelets, used in IMTP cases

A

Immune globulins (IVIG)

86
Q

Why might you take the spleen out for primary IMTP cases

A

allows so that platelets cant be destroyed by the macrophages
allows so the patient doesnt have to be on steroids

87
Q

Why do we use Methylprednisolone (Solu-Medrol)

A

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
Q

What are key diagnostics in thrombocytopenia cases

A

CBC
anti-platelet antibody test
4DX panel

89
Q

What are the typical signs of immune mediated polyarthritis (IMPA)

A

-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
Q

How is immune mediated polyarthritis (IMPA) diagnosed

A

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
Q

What is a typical history for an animal with SLE?

A

chronic illness, young to middle aged
many different manifestations: skin lesions, polyarthritis, myopathy, CNS signs
fever often present intermittently

92
Q

How does SLE typically manifest as

A

many different manifestations: skin lesions, polyarthritis, myopathy, CNS signs

93
Q

What lab abnormalities is often found in SLE patients

A

-Regenerative or nonregenerative anemia
Mild thrombocytopenia
Neutropenia
Elevated liver enzymes
Proteinuria
Elevated globulins

94
Q

Why do we do a splenectomy for autoimmune disease (IMHA, IMTP) ?

A

to eliminate phagocytic macrophages immediately

95
Q

What do diseases make you consider splenectomy

A

IMHA, IMTP

96
Q

What are the downsides to doing a splenectomy?

A

Increased risk of infection

97
Q

How do you diagnose primary IMTP

A

APA test

98
Q

Primary rule outs for severe thrombocytopenia

A

primary IMTP
thromboembolic disease

99
Q

What is the most common immune deficiency in dogs

A

antibody deficiency

100
Q

How should you work up an immune deficiency

A

CBC
antibody concentrations*
flow cytometry*
specialized function tests

101
Q

How is SLE diagnosed

A

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
Q

What does a negative antinuclear antibody test for SLE mean?

A

does not rule out SLE

103
Q

How is rheumatoid arthritis diagnosed

A

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
Q

What are the radiographic signs of rhematoid arthrtis

A

erosive joint disease, small distal joints

105
Q

Serology for rheumatoid arthritis detects

A

citrullinated proteins (CCP)

106
Q

joint taps cannot distinguish rheumatoid arthritis from

A

polyarthritis

107
Q

What immunosuppressive drugs are considered broadly active and non-specific

A

1) Corticosteroids
2) Oclacitnib (Apoquel)
3) IV immune globulins
4) Tetracyclines at high doses

108
Q

What 5 immunosuppressive drugs primarily target T lymphocytes

A

Mycophenolate
Cyclosporine
Tacrolimus
Leflunomide
Azathioprine

109
Q

What is the function of IVIG

A

immune suppression by suppressing macrophage function

also broad immune suprresion

110
Q

What is the function of cyclosporine

A

immune suppression by blocking T cell cytokine production

111
Q

What method of immune suppression eliminates macrophages

A

splenectomy

112
Q

What is the function of mycophenolate

A

immune suppression by blocking lymphocyte division

113
Q

What is the function of oclactinib

A

broad immune suppression by blocking cytokine signaling

114
Q

What is the function of tacrolimus

A

immune suppression by blocking T cell cytokine production

115
Q

What is the function of leflunomide

A

immune suppression by blocking lymphocyte division

116
Q

What is the function of azathioprine

A

immune suppression by blocking lymphocyte division

117
Q

What are the broad immune suppression options

A

Corticosteroids*
Oclacitinib
IVIG

118
Q

What drugs block lymphocyte division

A

Mycophenolate
Leflunomide
Azathioprine

119
Q

What drugs block T cell cytokine production

A

Cyclosporine
Tacrolimus
Sirolimus

120
Q

What is the function of sirolimus

A

immune suppression by blocking sirolimus

121
Q

What drug blocks cytokine signaling

A

Oclacitinib

122
Q

What are repurposed anti-inflammatory drugs used for immune suppression

A

Doxycycline
Azithromycin

123
Q

What immunosuppressive drugs primarily target T lymphocytes

A

Block lymphcyte division or production
a) Mycophenolate (div)
b) Cyclosporine (prod)
c) Tacrolimus (prod)
d) Leflunomide (div)
e) Azathioprine (div)

124
Q

What are the side effects of corticosteroids

A

-PU/PD
-panting
-hyperexia
-muscle and skin atrophy
-behavioral changes
-bladder infection

125
Q

How do corticosteroids suppress the immune system?

A

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
Q

What are the side effects of Oclacitinib

A

-GI effects
-Bladder infection

127
Q

What are the side effects of cyclosporine

A

GI side effects (vomiting, diarrhea)

128
Q

What are the side effects of mycophenolate

A

GI side effects (can be severe)
Vomiting and Diarrhea

129
Q

What is the side effect of Azathioprine

A

idosyncratic hepatic necrosis

130
Q

What is the side effect of IVIG

A

anaphylaxis (human proteins)

131
Q

What is the side effect of tacrolimus and sirolimus when given topically

A

local irritation
local hairloss

132
Q

What does a physiological dose of prednisone do

A

replaces the daily cortisol output from the adrenal cortex

0.025-0.05 mg/kg day

133
Q

What is the physiological dose of prednisone

A

0.05-0.1 mg/kg day

134
Q

What is the anti-inflammatory dose of prednisone

A

0.25 to 0.5 mg/kg day

suppresses inflammation without significant immunosuppression, but this can still induce severe side-effects

135
Q

What is an immunosuppressive dose of prednisone

A

1 to 2mg/kg day

significant impairement of the immune system

136
Q

Is dexamethasone or prednisone more potent

A

Dexamethasone
0.75mg equals 100mg of cortisol while 5mg of prednisone equals 100mg

137
Q

Does dexamethasone or prednisone have more mineralo-corticoid potency?

A

Prednisone has some activity and can be used in addisonian dog

138
Q

Is dexamethasone or prednisone used for an addisionian dog

A

Prednisone - has mineralocorticoid potency

139
Q

Does dexamethasone or prednisone have a longer half-life?

A

Dexamethasone 36-54 hours while

prednisone (18-36 hours)

140
Q

Rank the different steroids by potency

A

Least potent to most
1) hydrocortisone
2) prednisone, prednisolone
3) dexamethasone (8X prednisone potency)
4) Topicals (very potent: triamcinolone, betamethasone, fluticasone, budesonide

141
Q

If a dog is on physiological prednisone for Addisons, how much should you increase it before a stressful event (ie surgery)

A

2-3x the dose before surgery

142
Q

What is the general approach to immune suppression for severe immune mediated disorders

A

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
Q

What is the extra-nuclear effects of corticosteroids when <1mg/kg

A

primary effect of corticosteroids is mediated by binding to the glucocorticoid receptor, which in turn alters cytokine gene transcription (genomic activity)

144
Q

What is the extra-nuclear effects of corticosteroids when >1mg/kg and given IV

A

steroids insert into cell membrane and alter cell signaling and ion permeability (extragenomic activity)

145
Q

Do you taper T cell targeted drugs or steroids first

A

Steroids

146
Q

Why do we often combine immunosuppressive drugs

A

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
Q

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

A

1000

148
Q

What is the target of oclactinib (Apoquel)

A

JAK kinase inhibitor- targets 3 major kinases (JAK1,2,3), nonselective kinase inhibitor

broad suppression of cytokine signaling

149
Q

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

A

Oclactinib (Apoquel)

150
Q

What T cell targeted drug is more potent and rapidly acting than azathioprine, can be administered IV

A

Mycophenolate

151
Q

What is the mechanism of Mycophenolate

A

Suppresses lymphocyte division by inhibiting purine synthesis

152
Q

Mycophenolate is often used for

A

severe or refractory IMHA, IMTP, SLE

153
Q

What is the onset of cyclosporine

A

days to weeks

154
Q

What is the mechanism of Cyclosporine

A

inhibits cytokine production (IL-2, IFN-g) by CD4+ T cells

155
Q

What is cyclosporine used for

A

-Maintenance therapy for refractory IMHA, IBD, IMTP, polyarthritis
-Steroid alternative for atopy
-Topical for KCS in dogs
-Perianal fistulas in dogs

156
Q

Drug that blocks lymphocyte division by inhibiting mitochondral enzyme required for uridine synthesis

A

Leflunomide

157
Q

Drugs that suppresses lymphocyte division by inhibiting purine synthesis

A

Mycophenolate
Azathioprine

158
Q

What is the major side effect of Lefluonomide

A

Gi: vomiting and diarrhea

159
Q

What can Leflunomide be used for

A

management of refractory IMHA or IMTP patients

160
Q

What should you do before starting Azathioprine treatment

A

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
Q

How do mesenchymal stem cells suppress immune responses

A

-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
Q

How do you diagnose immune-mediated neutropenia and thrombocytopenia

A

CBC
Bone marrow cytology

163
Q

How do you manage immune-mediated neutropenia and thrombocytopenia

A

immune suppression with prednisone with taper over 30-60 days

164
Q

How do you diagnose Precursor targeted immune mediated anemia (PIMA)

A

bone marrow cytology
clotting times
CBC

can measure serum erythropoietin or estrogen

165
Q

In a dog with Precursor targeted immune mediated anemia (PIMA) what would the bone marrow cytology show you

A

Erythroid hyperplasia
all erythroid lineages present until reticulocytes, which are largely absent
Erythrophagocytos is observed by bone marrow macrophages

166
Q

How do you treat Precursor targeted immune mediated anemia (PIMA)

A

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
Q

Any dog with non-regenerative anemia when bleeding is ruled out should

A

should be trial treated with steroids if full workup is not possible

168
Q

Non-regenerative anemia should get

A

steroid trials

CLIN SCI 4 EX2 (5 decks)

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