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28 Cards in this Set

  • Front
  • Back
Immune mediated dz subcategories
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
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
Myasthenia Gravis
immune- mediated dz affecting NMJ
may be assoc. with thymoma, neoplasm, infection and inflammation
Mechanism of MG
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
Focal, Chroinc and Acute fulminate generalized MG
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
MG predispostion
Female > male
akitas, terrier, german shorthair pointer, abyssinians, somalis
<4 yr, >9 yr
MG clinical signs
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)
MG ddx
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
MG therapy- long acting ACh esterase inhibitor
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
MG therapy- immunosuppresion
not a lot of evidence supporting it
megaesophagus w/ MG so can cause aspiration pneumonia with pred, use in case by case bases
MG- supportive care
aspiration pneumonia most common cause of death, need Antibiotics and resp care
MG- nutritional support
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
MG prognosis
guarded (depend on how well response to tx and whether have aspiration pneumonia)
80% go into remission
may have recurrance
Systemic Lupus Erythematosis (SLE)
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
SLE clinical signs: dermatoloigcal
crust, alopecia,ulcers,
1. mucocutanrous junction (mouth, genital, urinary area and rectum)
2. area of poor blood circulation (ear tip, toes)
SLE clinical signs: orthopedic
1. polyarthritis (joint swelling, pain)
2. shifting leg lameness
3. muscle pain, myositis
4. muscle wasting
SLE clinical signs: hematological
1. thrombocytopenia
2. hemolytic anemia
3. leukopenia
Immune system trigger attack on all these elements in body
SLE clinical signs: systemic
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)
Ddx of SLE (positive ANA plus 2 of these criteria)
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
Diagnostic testing of SLE
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
SLE tx
immunosuppresion is key
steroids (pred)- start with this
azathoprine (toxic to cats)
cyclosporin ($$$, fewer side effect of fat, PU/PD)
SLE supportive care
pain meds (skin and joint painful)
prevent/ control infection (2nd infection and renal infetion)
omega 3 FA to modulate inflam
SLE prognosis
guarded (depends on severity of sings and quality of life
Masticatory myositis
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
MM acute signs
fever, muscle swelling, pain, difficulty eating, may be unable to close mouth
MM chroinc signs
atrophy and fibrosis of muscle
difficulty opening mouth
Ddx of MM
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
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