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ENDO, NUT, INF > Immune Diseases > Flashcards

Immune Diseases Flashcards

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1
Q

T/F: IMHA is almost always secondary to another disease

A

False - it is almost always a primary disorder

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2
Q

What are the 4 classic labratory findings of IMHA

A

-Regenerative anemia
-Spherocytosis
-RBC autoagglutination
-Hyperbilirubinemia

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3
Q

What onset is IMHA typically

A

Subacute onset: depression, weakness, inappetance, icterus

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4
Q

What are the primary differentials for dogs with severe regenerative anemia

A
  • Blood loss (>3d duration)
    -RBC destruction, IMHA
    -RBC destruction, infectious (Babesia)
    -RBC lysis, toxin (Zn, low P)
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5
Q

What infectious agent can cause RBC destruction

A

Babesia

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6
Q

What is not an important prognostic factor of IMHA
-Concurrent thrombocytopenia
-Severity of anemia
-Severity of leukocytosis
-Elevated BUN
-Hyperbilirubinemia
-Monocytosis

A

-Severity of anemia

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7
Q

Anemia from IMHA is typically regenerative or non-regenerative

A

Regenerative

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8
Q

What are differentials for anemia

A

-Anemia of chronic disease
-Bone marrow infiltrative disease
-Iron deficiency anemia
-Chronic blood loss anemia
-Pure red cell aplasia
-Immune destruction of red blood cell precursors (PIMA)

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9
Q

What diagnostic tests do we consider for patients presenting for non-regenerative anemia

A

-Serology for tickborne infections
-Coombs test or RBC flow cytometry
-Bone marrow aspirate or biopsy
-Fecal occult blood test
-GI barium series (to look for ulcers if occult blood positive)

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10
Q

immune attack target at RBC precursors in bone marrow
mature cells never leave marrow
non-regenerative because reticulocytes killed off

A

Precursor-targeted immune mediated anemia (PIMA)

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11
Q

PIMA usually responds to

A

long-term immune suppressive therapy with steroids and JAK inhibitors

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12
Q

Why do we consider IMHA two diseases in one

A

Most dogs with IMHA develop concurrent thromboembolic disease

clinical thromboembolism reflected by thrombocytopenia, leukocytosis, abnormal coagulation test

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13
Q

What is the primary cause of death in most dogs with IMHA

A

Thromboembolism

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14
Q

What is the two-fold treatment approach for patients with IMHA

A

1) Immunosuppression: stop RBC destruction by inactivating macrophages and lymphocytes

2) Anticoagulation: Reduce risk of thromboembolic disease

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15
Q

Why do dogs with IMHA typically develop thromboembolic disease

A

likely do to excessive plately activation or monocyte activation and tissue factor release

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16
Q

What is a major prognosis factor of IMHA

A

hyperbilirubinemia

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17
Q

Treating IMTP requires

A

quick decisions bc diagnostically difficult and life-threatening

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18
Q

What are ranked differentials for thrombocytopenia

A

-Immune mediated thrombocytopenia (primary)
-Platelet consumption (secondary to thromboembolic disease)
-Drug reaction
-Bone marrow toxicity or myelophthisis
-Chronic ehrlichiosis
-Disseminated intravascular coagulation (DIC)

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19
Q

Primary IMTP mediated in most cases by

A

anti-platelet antibodies

in some patients, platelet destruction is independent of antibodies (APA-negative)

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20
Q

Immune destruction of platelets or _____ can cause thrombocytopenia

A

megakaryocyte

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21
Q

What is a second major differential for severe thrombocytopenia, after IMTP

A

thromboembolic disease

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22
Q

How do you diagnose IMTP

A

-Typical clinical findings
-Detection of anti-platelet antibodies (APA) can work in some patients but some IMTP patients are APA negative
-Platelet size (MPV) distribution may be helpful
-Bone marrow examination indicated if APA-negative and other immune causes of thrombocytopenia is ruled out

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23
Q

What is indicated if APA-negative and other immune causes of thrombocytopenia is ruled out

A

Bone marrow examination

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24
Q

How do we treat IMTP if sure of diagnosis

A

-Intial high doses of prednisone (1-2mg/kg/day)
-Consider high-dose IV methylprednisolone for life-threatening IMTP
-Often add mycophenolate or cyclosporine
-Single IV treatment with purified immune globulins (IVIG)

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25
What are possible differentials for a dog with fever, anorexia, and reluctance to walk
Immune: IMPA, SLE, drug reaction Infectious: Rickettsial infection Neoplastic: occult lymphoma, myeloma, histiocytic sarcoma Orthopedic: Septic arthritis /polyarthritis
26
What is your diagnostic approach to a patient with suspected IMPA
Screening labwork Joint taps and cytology Rickettsial titers maybe: joint culture, rads, Bartonella serology/culture
27
What will you see on joint fluid analysis of a dog with IMPA
typically large numbers of non-degenerate neutrophils high protein background
28
What are your treatment options for a patient with IMPA
-Initial anti-inflammatory or midly immune suppressive dose of prednisone 0.5-1 mg/kg/day typically 1/3 does great, 1/3 little tougher if no response: increase pred dose; add T cell target drugs (cyclosporine, mycophenolate) -maybe synergy with anti-inflammatory antibiotics (doxycycline)
29
Whats the typical history of dogs with SLE
vague signs, anorexia occasional fever often treated for other diseases major signs: polyarthritis, hemolytic anemia, leukopenia, thrombocytopenia, skin lesions, proteinuria, positive ANA minor signs: fever of unknown origin, CNS signs, lymphadenopathy, serositis
30
How do you treat SLE
Immune suppression with corticosteroids for 2-4 weeks then taper may want to add other immune suppressive agents -Mycophenolate if proteinuria is present -Monitor proteinuria for disease actvity -Monitor renal function*, eyes, joints, CBC -Monitor ANA status if positive
31
What are the broadly active immune suppressive drugs
Corticosteroids Oclacitinib Ilunocitinib
32
What immune suppressive drugs block lymphocyte division
Mycophenolate Leflunomide
33
What immune suppressive drugs suppress T cell cytokine production
Cyclosporine Sirolimus Tacrolimus Corticosteroids
34
What immune suppressive drugs suppress cytokine signaling
Oclactinib, ilunocitinib
35
What immune suppressive drugs suppress macrophage function
IV immune globulin steroids
36
Broadly acting drugs that suppress cytokine signaling
Oclactinib, ilunocitinib
37
At what prednisone dose is 100% of the glucocorticoid receptors saturated
>1.5 mg/kg
38
Does hydrocortisone, prednisone, or dexamethasone have a higher anti-inflammatory potency
Dexamethasone: 20-30 Pred: 4 Hydrocortisone: 1
39
Why combine drugs for immunosuppressive therapy
1) Use drugs with synergistic mechanisms of action 2) Control disease while reducing steroid doses and side-effects 3) Increase speed of immune suppression
40
What is the typical protocol for management of acute IMHA
1) Induction with high-dose IV or oral steroid (1-2mg/kg/day) 2) Frequently combine with mycophenolate or cyclosporine at outset of treatment 3) Treat until clinical remission 4) Taper over 3-6 months problems: mortality in first week still up to 50% massive side effects
41
is mycophenolate or azathioprine more potent
mycophenolate - also more rapidly acting
42
What is the mechanism of action of mycophenolate
inhibits purine biosynthesis
43
Why is mycophenolate safer than azathioprine
No liver toxicity
44
What are the side effects of mycophenolate
Vomiting Diarrhea (can be severe)
45
What is the mechanism of cyclosporine
Blocks IL-2 and IFN-g production Inhibits lymphocyte proliferation
46
What are the side effects of cyclosporine
GI toxicity Inappetence Lethargy
47
What are the indications for cyclosporine
-Longterm management of IMHA, IMTP, SLE, IBD -Topical for KCS and perianal fistulas -Systemic for atopic dogs
48
Azathioprine toxicity causes
idiosyncratic hepatic toxicity can be ftal if not detected early
49
converted to active metabolite (6-mercaptopurine) in vivo; inhibits purien biosynthesis onset of action is slow days; proliferating T and B cell affected can cause idiosyncratic hepatic toxicity
Azathioprine
50
suppresses lymphocyte proliferation by pyrimidine synthesis inhibition potentially fewer side effects than mycophenolate
Leflunomide
51
What drugs cause borad suppression of T cell immunity through cytokine signaling inhibition (JAK1,2,3)
Oclacitinib (Apoquel) Ilunocitinib (Zenrelia)
52
What is the mechanism of IVIG ***
delivers potent immune suppressive signal to macrophages in spleen and liver rapid onset of action blocks clearance of opsonized RBC and platelets used in dogs with refractory IMHA, IMTP
53
If disease is in remission, how do you taper prednisone
Taper prednisone from 1-2mg/kg to 0.5 to 0.25 mg/kg within 2-4 weeks dose of drug #2 (cyclosporine, mycophenolate) kept constant if stable at 0.25mg/lg prednisone dose for 3-4 weeks, go to alternate day therapy for 30 days if stable, reduce pred to 0.1 to 0.2mg/kg EOD for 30d if stable, stop prednisone, continue drug #2 for another 1-3 months
54
autoantibodies directed against nuclear antigens (DNA, RNA, histones) which are present in all cells of the body autoantibodies also against non-nucleated cells included RBC and platelets
Systemic lupus erythematosis (SLE)
55
antibodies that thought to be cross-reactive against poorly defined antigens present in synovium antibodies may be induced by prior infection (viral, rickettsial) or drug rxns
Immune mediated polyarthritis (IMPA)
56
What are the major negative prognostic findings in dogs with IMHA
1) Hyperbilirubinemia (most important) 2) Concurrent thrombocytopenia (Evan's syndrome) 3) Leukocytosis and neutrophilia 4) Monocytosis 5) Azotemia 6) Hypoalbuminemia
57
For IMPA, why do we always tap multiple joint
if seen in multiple joints, meets criteria for polyarthritis
58
What is a typical history for an animal with IMPA
young animal, acute to sub-acute onset fever often present shifting leg lameness, can be clinically vague General malaise obvious joint effusion not present or detectable
59
What does the joint tap cytology for typical IMPA patient look like
Markedly cellular samples High proteinaceous background Most often non-degenerate PMN, with some macrophages
60
What does the Coombs test measure
direct antiglobulin test (DAT) -measures the presence of IgG on surface of patient RBC, using microagglutination assay -IgG binding to RBC can be measured and quantitiated more precisely using flow cytometry
61
What is typical histroy for animal with IMTP
young to middle aged female dog petechiation, multiple sites (skin, gums, eyes) hematuria, epistaxis, hematachezia unexplained regenerative anemia (occult blood loss)
62
IMTP has severe thrombocytopenia that is typically
<50,000 platelets/ul
63
If you have a mild to moderate thrombocytopenia (50-150,000/ul) then you should consider
rickettsial infection drug reaction estrogens occult neoplasia IMTP is severe <50,000 platelets/ul
64
How do you culture joints
Aerobic +mycoplasma testing
65
What is the single best diagnostic test for IMTP
flow cytometry for anti-platelet antibodies (APA) can help differentiate IMTP from thromboembolism some IMTP are APA negatives (do bone marrow examination)
66
Why might your joint culture be negative
bacteria in biofilm in synovium that take long to reproduce often trigger and negative culture
67
How is IMPA diagnosed
Labratory evlauation: serology to screen for infectious etiology (esp rickettsial infection) Joint tap and fluid cytology: high numbers of non-degenerate neutrophils with variable numbers of lymphocytes and macrophages; high protein concentration and proteinaceous background Joint fluid cultures nearly always negative (not an infectious process) beware of skin contaminants if you get a positive joint culture
68
What is the typical history for an animal with SLE
chronic illness, young to middle aged animal, more often female many different manifestations: skin lesions, polyarthritis, myopahty, cytopenias, proteinuria fever often present intermittently
69
What lab abnormalities are typically found in SLE
Regenerative or non-regenerative anemia Mild thrombocytopenia Neutropenia Elevated liver enzymes Proteinuria Elevated globulins
70
How is SLE diagnosed
Combination of 4 or more major abnormalities 1) Cytopenias 2) Fever 3) Polyarthritis 4) Skin lesions 5) ANA + postive (negative doesnt rule out SLE)
71
How is rheumatoid arthritis diagnosed
Radiographic findings: erosive joint disease, involving distal joints (phalanges) Conventional RA test: detect IgM antibodies directed against Fc portion of IgG antibodies Newer RA test: detect antibodies against citrinullated proteins (serology) Joint taps: cannot be used to distinguish RA from immune (non-erosive) polyarthritis
72
What is the relative potency of different steroids
Least potent: hydrocortisone Intermediate: prednisone, prednisolone More potent: dexamethasone (8x pred potency) Very potent (topical steroids; nasal, GI): triamcinolone, betamethasone, fluticasone, budesonide
73
Antimicrobials should be administered only if
1) A clinically significant bacterial infection is diagnosed or strongly susepcted 2) There is an established indication for short-term antimicrobial prophylaxis
74
What is best way to see thromboembolic disease
CT - clots can be anywhere
75
How do you manage IMTP
1) Initial high dose of dexamethasone IV (0.3mg/kg/day) or 2) Rapid IV steroid induction: high dose (10-30mg/kg) methylprednisolone (Solu-Medrol) IV once daily x 3-5 days often follow these with oral prednisolone as maintenance 1mg/kg/day often add mycophenolate or cyclosporine single IV treatment withIVIG
76
Why is Vincristine used to manage IMTP
microtubule inhibitor - megakaryocytes increase platelet count not too good clinically
77
If IMTP management is difficult, what might be indicated for a patient
splenectomy
78
What is the mechanism of IVIG **
shutting down macrophage phagocytosis
79
What are the classic findings of IMHA *
Regenerative anemia Bilirubinemia Spherocytes Autoagglutination *These are sufficient to make the diagnosis
80
When do you know to give a patient a blood transfusion
PCV: <20% acutely
81
Severe neutropenia can be
Immune mediated Neoplastic Marrow intrinsic problem
82
What is the diagnostic test for immune mediated neutropenia
bone marrow cytology
83
How do you treat immune mediated neutropenia
immune suppressive doses of steroids

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