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28 Cards in this Set
- Front
- Back
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Immune mediated dz subcategories
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alloimmmune- Ab from another member of same species wth Ag on affected individual's cell
Primary= Ab against self- Ag 2nd= Ab against absorbed Ag on cells e.g. antibiotics, red cell parasite |
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Autoimmunity
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Specific recognition of SELF Ag by:
1. breakdown of self tolerance: genetic prdisposition, allow survival of self reactive T- cells (should be removed during development) 2. breakdown of peripheral tolerance: self Ag exposed by inflam, breaks sequestration 3. molecular mimcry: foreign Ag loks enough like self Ag that trigger rxn to self Ag 4. Dysregulation: failure of regulatory cells 5. infectious trigger: overcome cytokines deviation |
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Myasthenia Gravis
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immune- mediated dz affecting NMJ
may be assoc. with thymoma, neoplasm, infection and inflammation |
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Mechanism of MG
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normally ACh bind to post synaptic ACh receptor and removed by ACh esterase
now Ab block ACh receptor in post synaptic membrane causing muscle weakness (take away stimulating effect of ACh) use anticholinesterase drug so Ach stick around longer |
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Focal, Chroinc and Acute fulminate generalized MG
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Focal- facial, laryngeal, esophagus (most common)
Chroinc generalized- develop over several wks acute fulminate generalized- develop over hours, animal become very weak, affect resp muscle thus affect breathing, often time dir |
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MG predispostion
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Female > male
akitas, terrier, german shorthair pointer, abyssinians, somalis <4 yr, >9 yr |
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MG clinical signs
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regurgitation- esophageal dysfunction, megaesophagus
dysphagia (dicciculty swallowing) weakness, w/ exercise- rest a little, get up, walk a few step, collaspe again cause so few receptors, wait a few seconds and more receptors come back dyspena- shortness of breath (2nd to aspiration pneumonia or resp muscle weakness) |
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MG ddx
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Ach receptor AB titer (best, 15% sero -ve, 2 wks for result)
Tensilon test- short acting ACh esterase inhibitor (dont' just affect NMJ but other sites, will have difficulty breathing, have atropine on hand). Neg result does not rule out dz cause not all response to it. If focal MG, can't asses area accurately |
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MG therapy- long acting ACh esterase inhibitor
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long acting anticholinesterase
Mesthinon- start @ low dose and gradually incr, take long time to response so start while waiting for test result Nostigmine- if pt w/ acute distress |
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MG therapy- immunosuppresion
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not a lot of evidence supporting it
megaesophagus w/ MG so can cause aspiration pneumonia with pred, use in case by case bases |
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MG- supportive care
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aspiration pneumonia most common cause of death, need Antibiotics and resp care
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MG- nutritional support
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elevated feeding (use gravity to slide food down esophagus)
high quality diet some do better with kibble, some do better with can, usually meat ball or canned food |
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MG prognosis
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guarded (depend on how well response to tx and whether have aspiration pneumonia)
80% go into remission may have recurrance |
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Systemic Lupus Erythematosis (SLE)
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loss of control of B- cell
lots of auto Ab produced, lots of circulating complexes Ihumoral immmunity) complement activation, phagocytosis (cell- mediated immunity) Type III hypersensitivity most likely genetics |
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SLE clinical signs: dermatoloigcal
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crust, alopecia,ulcers,
1. mucocutanrous junction (mouth, genital, urinary area and rectum) 2. area of poor blood circulation (ear tip, toes) |
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SLE clinical signs: orthopedic
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1. polyarthritis (joint swelling, pain)
2. shifting leg lameness 3. muscle pain, myositis 4. muscle wasting |
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SLE clinical signs: hematological
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1. thrombocytopenia
2. hemolytic anemia 3. leukopenia Immune system trigger attack on all these elements in body |
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SLE clinical signs: systemic
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1. Glomerular dz(most common): proteinuria (immune complex lodge in glomerula, cause damage, may progress to renal dz and become fatal despite tx
2. Vasculitis (lodge in blood vessels) 3. myocarditis 4. pul thromboembolism (clots in lung cause immune complex lodge in aveoli) |
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Ddx of SLE (positive ANA plus 2 of these criteria)
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immune mediated polyarthriti
imune mediatd skin dz immune compex glomerulonephritis AIHA (hemolytic anemia) ITP ( Idiopathic thrombocytopenic purpura, immune system attacking platelets) seroal inflam neurological dz polymyositis (inflam of skeletal muscle) endocrine dz coagulopathy pneumonitis |
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Diagnostic testing of SLE
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1. antinuclear Ag- detect Ab vs. DNA, histones, nonhistone nuclear protein
2. LE cells 3.histopathology- immunofluorescence against immune complex to see where complexes are |
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SLE tx
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immunosuppresion is key
steroids (pred)- start with this azathoprine (toxic to cats) cyclosporin ($$$, fewer side effect of fat, PU/PD) |
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SLE supportive care
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pain meds (skin and joint painful)
prevent/ control infection (2nd infection and renal infetion) omega 3 FA to modulate inflam |
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SLE prognosis
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guarded (depends on severity of sings and quality of life
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Masticatory myositis
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severe inflam (swollen head) followed by significant scarring (nercrosis, fibrosis and scarring), caved in looking head
type 2M fiber affected, distinct type of myosin affects all breed and age (german shepard predisposed |
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MM acute signs
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fever, muscle swelling, pain, difficulty eating, may be unable to close mouth
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MM chroinc signs
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atrophy and fibrosis of muscle
difficulty opening mouth |
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Ddx of MM
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increased AST and CPK
type 2M antibody titer muscle biopsy (see necrosis and phagocytosis of 2M fiber) EMG- spontanoues muscle activity, put needle in muscle, normally silent, now sound like pop corn |
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MM Tx
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may be successful if ddx early, unsuccessful if fibrosis and can't open mouth and have to put feeding tube in for rest of animal's life
immunosuppresive dose of steroids, may beed long term or repeat if relaspe |
