Pharm: Module 7 Inflammation Flashcards
chemical mediators of inflammation
histamine, prostaglandins, bradykinin
these cause pain
bradykinin
these cause pain and fever
prostaglandins
these cause mast cells and vasodilation
histamine
what are the stages of the inflammatory response
1)vascular response 2) cellular response and phagocytosis 3) tissue repair
these convert arachidonic acid into prostaglandins
COX enzyme
protects stomach lining and regulates platelets
COX1
triggers inflammation and pain
COX2
natural mediators of inflammation
can increase intensity and duration of pain
induce signs of inflammation
prostaglandins
reproductive related to prostaglandins
used to terminate pregnancy
may play a role in male infertility
what are the cardinal sings of inflammation
redness, warm, pain, swelling, loss of function
what do NSAIDs do
inhibit biosynthesis of prostaglandins inhibit platelet aggregation mimic corticosteroids inhibit COX enzyme analgesic and antipyretic effects
first generation NSAIDs
salicylates, phenylacetic acids, fenamates
second generation NSAIDs
selective COX 2 inhibitors
describe salicylates
NSAID
ASPIRIN
blood thinner
anti-inflammatory, antiplatelet, antipyretic
levels of salicylates
therapeutic: 15-30 mg/dL
mild toxicity: >30 mg/dL
severe toxicity: > 50 mg/dL
interactions with salicylates
increased bleeding with anticoagulants and NSAIDs
risk for hypoglycemia with oral antidiabetics
increased gastric ulcer risk with glucocorticoids
decreased with ACE inhibitors, loop diuretics
labs to monitor with salicylates
increased PT, bleeding time, INR, uric acid
decreased cholesterol, T3 and T4 levels
what food contain salicylates
prunes, raisons, licorice, curry, paprika
cautions with salicylates
do not take with other NSAIDS
avoid last trimester of pregnancy
do not give to children (Reye syndrome)
side effects of salicylates
GI distress, bleeding, ulceration
nursing interventions for salicylates
monitor serum salicylate levels
observe for bleeding
do not take with warfarin or alcohol
discontinue 7 days prior to surgery
COX1 and COX2 inhibition
prostaglandin synthesis inhibitor
indoles
side effects of indoles
GI distress, headache, vertigo, hepatotoxicity, nephrotoxicity
what is a synergist with indoles
warfarin (increases bleeding)
drug interactions with indoles
increased GI distress risk with aspirin
prolonged 1/2 life with digoxin
decreases effects of antihypertensives
drug name of phenylacetic acid
ketorolac
what is phenylacetic acid used for
short term pain management for arthritis
what does phenylacetic acid inhibit
prostaglandin synthesis
side effects of phenylacetic acid
dizziness, headache, weakness, GI distress/bleeding, hypertension, sodium and water retention
what is propionic acid
ibuprofen (Advil and Motrin)
what is the most widely used NSAID
propionic acid
what is the action and use of propionic acid
inhibits prostaglandin synthesis
used for pain and arthritis
side effects of ibuprofen
drowsiness, confusion, insomnia, GI distress/bleeding, tinnitus, dysrhythmias, nephrotoxicity
interactions with ibuprofen
increased bleeding with warfarin
increased effects with phenytoin and sulfonamides
decreased effect with aspirin
interventions associated with ibuprofen
bleeding gums, petechiae, ecchymosis, black tarry stools, GI discomfort, AVOID with other NSAIDs and alcohol
main selective COX 2 inhibitor
celecoxib
side effects of COX2 inhibitors
STROKE RISK, dizziness, headache, GI distress/ulceration, hypertension, renal dysfunction
action and use of corticosteroids
control inflammation and used for arthritis
naturally occurring produced by adrenal gland
how do you discontinue corticosteroids
taper off over 5-10 days
what are the glucocorticoids
hydrocortisone, prednisone, dexamethasone
what is the mineralocorticoid
fludrocortisone
anti inflammatory
inhibition of immune response (decrease of histamine)
bronchodilation
glucocorticoids
side effects of Cushing’s syndrome
gluconeogenesis, osteoporosis, acne, hirsutism, fragile skin, sodium retention, increase in gastric activity, decrease in resistance to infection, dependency
interventions for glucocorticoids
monitor glucose, electrolyte, skin and mucus, GI status
do not discontinue abruptly
take with food
weight daily
diet increase of protein, Ca and K (low in fat)
selective drugs
inhibit only COX 2
nonselective drugs
inhibit BOTH COX 1 and 2
who CANNOT be given celecoxib
patients who have undergone CABG
what is Cushing’s syndrome
making too much steroid
shock, become skinny and pale
increase in potassium
dependent on steroid (cannot stop abruptly)
Addisonian crisis
