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in acute inflammation, leukocytes aim to:
- 1. destroy bacteria at the site
- 2. direct other cells of inflammatory process to start clean up process by removing dead/dying cells
- 3. pave way for healing process to start
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main leukocyte involved in acute inflammation
- neutrophil initially
- lymphocytes follow in time
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5 cardinal signs of inflammation
- swelling
- redness
- heat
- pain
- loss of function
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degranulate
leukocytes release the contents of their granules to kill bacteria, neutralize toxins, and breakdown dead/dying tissue
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primary conversion of the arachidonic acid
cyclooxygenase
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glucocorticoid
natural steroid in the body
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corticosteroids
group of steroid hormones produced in the adrenal cortex or made synthetically
blocks the action of phospholipase thus abruptly stopping progression of inflammation
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what corticosteroids do?
- inhibit phospholipase
- deposits glycogen in liver
- increase blood glucose levels
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mineralocorticoids
- little or no effect on inflammation
- associated with water&electrolyte balance
(an ex. is Aldosterone)
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zona glomerulosa produces
mineralcorticoids
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zona fasiculata produces
glucocorticoids
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types of corticosteroids (time)
- short acting (less than 12 hrs)
- intermediate acting (12-36)
- long acting (longer than 48)
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example of short acting corticosteroid
hydrocortisone
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example of intermediate acting corticosteroid
prednisone, prednisolone, triamcinolone
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use prednisolone in what species?
cats
(dog: prednisone)
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example of long acting corticosteroid
dexamethasone sodium, betamethasone, flumethasone
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of the 3 liquid forms of corticosteroids which is ultra short acting?
aqueous solution
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aqueous solution
corticosteroids combined with a salt to make them soluble in water (sodium phosphate, sodium succinate)
- uses: shock therapy, CNS trauma
- advantages: can be given IV in large doses
- (ex: Solu-Delta-Cortet)
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suspension
- corticosteroid suspended in a diluent
- long acting
(metacortin)
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autacoids or eicosanoids
prostaglandins, thromboxanes, leukotrienes
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3 things that cause bilateral hair loss
- hyperadrenocortism
- hyperestrogenism
- hypothyroidism
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corticosteroid effects
- reduce inflammation
- reduce capillary permeability
- inhibit fibroblasts
- suppress T-lymphocytes
- catabolic effect on proteins
- abortion
- stress triad
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if stressed, the body is producing
glucocorticoids
(and therefore, stress triad)
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stress triad
- decrease in lymphocytes, eosinophils, monocytes
- increase in platelets and neutrophils
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contraindications for steroid
- systemic or fungal infections
- vaccines
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nickname for hyperadrenocortism
Cushing's Disease
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Hyperadrenocortism
over production of hormones from adrenal gland
symptoms: alopecia, muscle wasting, polyuria, polydipsia, polyphagia, pot belly, thin skin
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nickname for hypoadrenocortism
Addison's Disease
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Hypoadrenocortism
not enough hormones being produced by adrenal gland
usually results from taking animal off steroids after yrs of administration (going from hyper to hypo over night)
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blocks MOTB
Selegiline hydrochloride
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MOTB
Monoamino Oxidase Type B
chemical produced by body with natural aging
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how do most NSAIDs work?
block activity of cyclooxygenase and subsequent production of prostaglandins
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although most NSAIDs do not block formation of leukotrienes, this drug inhibits lipoxygenase preventing production of leukotrienes
Ibuprofen (Advil)
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non-proprietary name for Aspirin
acetylsalicylic acid
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long-term use of aspirin (acetylsalicylic acid)
gastrointestinal toxicity
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1971
J R Vane discovered NSAIDs block production of prostaglandins from arachidonic acid
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1976
- cyclooxygenase identified
- NSAIDs exert their effects by inhibiting production of local tissue cyclooxygenase and its production of prostaglandins
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non-proprietary name for Banamine
flunixin meglumine
(acts for 24 hrs)
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proprietary for piroxicam and meloxicam
- feldene
- metacam V, mobic H
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COX1
role in normal tissue function
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COX2
associated with pain, fever, inflammation
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which COX would we ideally like to eliminate and which would we ideally like to leave alone?
- eliminate COX2
- leave COX1 alone
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Rimadyl is made by
Pfizer
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what should you never to give to animals?
acetaminophen
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phenylbutazone tabs&paste can cause
calcium breakdown in long bones causing osteogenic imperfecta- thin long bones
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coxib
compounds that target inhibition of COX2 only
*want to leave COX1 alone because protects gastric mucosa--older NSAIDs block COX1 along with COX2 which accounts for their commonly seen gastric side effects*
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inhibit COX1 for prolonged periods?
- GI ulceration/erosion
- adverse effects on renal function
- problems with hemostasis (platelet production)
-
required for sodium homeostasis in kidney
Prostaglandin E2
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eating long-chain fatty acids promotes
replacing PGE2 with PGE3=less inflammatory effect
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no inhibition of COX2 at any time
aspirin
always complete COX1 inhibition
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major use in horses with colic and off label use in dogs w/ parvo or other GI pain
Flunixin Meglumine (Banamine)
includes analgesic, antipyrexia, and anti-inflammation
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used mainly as pain relief associated with degenerative joint disease or postoperative pain of soft tissue
Carprofen (Rimadyl)
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why is aspirin not recommended for cats?
they lack glucuronic acid to (phase 2 of biotransformation) so is not excreted and goes through again
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what are chondroprotective agents?
meds designed to slow the process of arthritis in joints by supporting the health of the joint cartilage
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PSGAGs
Polysulfated Glycosaminoglycans
- look and act like normal components of normal joint cartilage.
- these molecules trap water, act as moisturizer for the cartilage preserving its "springy" characteristic and ability to respond to shock
(ex: Adequan)
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Hylauronic Acid
- natural component of synovial fluid
- functions to increase the thickness of the joint fluid and, in doing so, acts as a lubricant for contact between cartilage surfaces
Hyaluronate sodium-acts to reduce inflammation caused by prostaglandins by suppressing its production
(ex: Legend, Hyalovet)
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Glucosamine and Chondroitin sulfate
called Nutraceuticals because used like drugs but are found naturally in the body
presence of both in serum= stimulates production of hyaluronic acid and inhibits destructive enzymes found in diseased cartilage
(ex: Cosequin)
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often grouped with NSAIDs but is not a true member. Why isn't it?
Acetaminophen (Tylenol)
does reduce the perception of pain& has antipyretic properties but does NOT block prostaglandins which cause inflammation
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