Anti-inflammatory 1

false. inflammation is part of the normal healing process

• increases blood supply to the affected area - dilute and immobilizes the cause of inflammation
• draws WBC's to the area - segs and macrophages (phagocytes) and lymphocytes (part of the immune system).

• pain (dolor)
• heat (calor)
• redness (rubor)
• swelling (tumor)
• loss of function

• when it is inappropriate or excessive, causes pain and tissue damage
• arthritis, allergies, autoimmune disease

heat inactivation of invading microorganisms, can also speed up chemical reactions in the patient's body.

a substance that can cause a fever in a patient.

• exogenus - from outside the patient's body
• endogenus - from inside the body

NSAIDs

block perception of pain and decrease tissue damage due to inflammation by blocking part of the inflammatory pathway.

glucocorticoids and NSAIDs - non-steroidal anti-inflammatory drugs

when the patient's tissue is damaged in some way - trauma, burns, radiation, infection, etc - cell structures are exposed and acted on by enzymes, and broke down into compounds which cause inflammation

• phospholipids cell membranes are disrupted by tissue damage, so that the phosopolipase enzymes can "get at" the phospholipids and break them down - one of the compounds formed is arachidonic acid.
• arachidonic acid can be either broken down or COX (cyclooxygenase) - to form prostaglandins and thromboxanes, or by LOX (lipoxygenase) to form leukotrienes

eicosanoids

• prostaglandins
• thromboxanes
• leukotrienes

no - there are others, such as histamine

cause inflammation (musculo-skeletal system)

are protective - cause increased fluid secretion into stomach, increased mucus production, decreased HCl production in stomach

cause lysis of CL - corpus luteum

renal COX 1 prostaglandins counteract vasoconstriction, allow vasodialtion of the renal blood supply - protective.

beneficial - help to maintain bronchodilation

• COX 1 in the GI system forms "good" protective GI prostaglandins
• COX 2 forms "bad" inflammatory prostaglandins

by blocking phospholipase (and some depression of cyclooxygenase) to prevent or reduce the formation of eicosanoids - prostaglandins, thromboxanes, and leukotrienes

by blocking COX - cyclooxygenase to prevent or reduce the formation of prostaglandins and thromboxanes. some NSAIDs also block LOX - lipoxygenase and thuse prevent or reduce formation of leukotrienes also.

no

lipid soluble

steroid compounds formed in the adrenal cortex

• glucocorticoids
• mineralocorticoids
• gonadal steroids

aldosterone

Addison's disease - hypoadrenocorticism, high K, low Na.

desoxycorticosterone - Percorten - V

• estrogens
• androgens (testosterone)
• progesterone

glucocorticoids are the "anti-inflammatory steroids" that happen to be named after their influence on glucose metabolism.

• hypothalamus detects low blood levels of glucocorticoids.
• hypothalamus releases CRF - corticotrophin releasing factor - which causes the pituitary to release ACTH (adrenocorticotropic hormone) - ACTH travels to adrenal cortex, causes it to produce glucocorticoids (cortisol) - glucocoritcoid blood levels rise - hypothalamus detects this, stops releasing CRF

yes - stress can cause CRF release by the hypothalamus

• anti-inflammatory
• anti-pruritic
• inhibit fibroblasts
• glucose metabolism
• catabolic
• Na and water retention
• PU/PD
• polyphagia and weight gain
• induce parturition
• immunosuppressive
• inhibits "good" GI prostaglandins
• stress leukogram

yes

may make it much worse by breaking down the protein exposed in the cornea. may cause perforation

can be harmful - glucocorticoids cause the patient to retain sodium and water, which can make pulmonary edema worse

• allergies
• musculoskeletal inflammation
• shock/toxemia
• laminitis
• Addison's disease
• autoimmune disease
• lymphocytic neoplasms

hyperadrenocorticism - by giving too much glucocorticoids for too long. usually overdoing "allergy shots"

hypoadrenocorticism - by giving steriods long enough to trigger long-term negative feedback - the hypothalamus detects plenty of glucocoritcoids, stops sending out CRF, so the pituitary stops releasing ACTH, so the adrenal cortex is not stimulated to produce glucocorticoids, so the adrenal cortex atrophies. then, we abruptly stop giving glucocorticoids, the patient cannot make any, and he has an Addisonian crisis and may die

wean off gradually - to prevent the above scenario

• short-acting (less than 12 hours)
• intermediate-acting (12-36 hours)
• long-acting (over 48 hours)

• hydrocortisone, cortisone.
• hydrocortisone is used the most - it is the active form
• cortisone is not active, and has to be converted by the liver to hydrocortisone to be active

• the 4 "preds"
• prednisone
• prednisolone-Solu-Delta-Cortef
• methylprednisolone
• isoflupredone
• triamcinolone-Vetalog

prednisolone (liver converts prenisone to prednisolone)

• "the methasones"
• dexamethasone - Azium, Tresaderm
• betamethasone
• flumethasone
• paramethasone

• aqueous solution
• alcohol solutions
• suspensions

• clear
• no shaking
• yes - IV

can give IV - large amounts rapidly - for emergency purposes

• sodium phosphate
• sodium succinate

• dexamethasone Na phosphate - Azium
• prednisolone Na succinate - Solu-Delta-Cortef

no

• opaque
• yes shaking
• no IV

• acetate
• diacetate
• privalate
• acetonide
• valerate

the drug is in a crystal form, given IM, takes time for the crystal to dissolve and be absorbed

the actetate crystal suspension form is long-acting

avoid extreme temperatures - this causes larger crystals to be formed, which are more irritating when injected IM, and take longer to dissolve and be absorbed

cats

prevent iatrogenic Cushing's disease

• avoid if possible
• use smallest dose possible
• reduce dose as patient improves
• use alternate-day dosing
• avoid frequent use of repository form
• wean patient off of glucocorticoids gradually