Immunopharm Flashcards
Basic inflammatory response
Inflammatory challenges, inflammatory mediators, inflammatory responses, outcome of inflammatory responses
Acetaminophen has similar mechanism of action as aspirin, but not classified as an NSAid. Why
Acetaminophen has no anti-inflammatory properties. Doesn’t have antiplatelet properties so no risk of bleeding in Tylenol. Tylenol is also antipyretic
Mechanism of action of NSAIDS
Cyclooxygenase (COX) inhibitors
COX1 has a broad tissue distribution COX2 has more narrow tissue distribution and a strongly activated during an inflammatory response
Enteric coated aspirin provides excellent protection against risk for G.I. bleeding, true or false
True aspirin has coating that lets it pass through the stomach and then release into the duodenum
Why do cox2 inhibitors get recalled?
Increase risk of thrombogenictiy, myocardial infarction and stroke
Pharma toxicology of NSAIDS
Aspirin can induce Reyes syndrome in children(which is acute hepatic, encephalopathy) hypoglycemia, development of hepatic and renal fatty deposits and cerebral edema
Ototoxic pregnancy category c, d
Glucocorticoids block, the action of what?
Arachidonic acid which blocks cox and lox and in turn prostoglandins and leukotrienes
Why is the side effect of glucocorticoids increase in white blood cell count?
They prevent leukocyte immigration, so white blood cells stay in the bloodstream as opposed to leaking out into the cells
When glucocorticoid side effects appear is it a good medical practice to immediately withdrawal treatment to avoid the development of more serious side effects
If it’s short term steroids, that’s OK
If it’s long-term steroid use you need to wean . The HPA ( hypothalamic-pituitary-adrenal ) axis gets suppressed. and you need to get it restarted
Diphenhydramine mechanism of action
Antihistamine, A1 histamine receptor antagonist
ZILEUTON mechanism of action
Lipooxygenase inhibitor that blocks the synthesis of Leukotrienes
Therapeutic effects- inhibits leukotriene induced bronco, construction and mucus production associated with asthma
Infliximab (remicade) MOA
Antibody against TNF
Therapeutic use - treatment of rheumatoid arthritis, Crohn’s disease and psoriasis
Anakinra
Antibody against il1
Therapeutic use - treatment of rheumatoid arthritis, Crohn’s disease and psoriasis
Tofacitinib
Janus kinase (JAK) inhibitor
Therapeutic use - treatment of rheumatoid arthritis, Crohn’s disease and psoriasis
Young children less then 2 years of age and elderly adults the _______ and _______ effects of antihistamines can be exaggerated
Sedating and anticholinergic
Anticholinergic symptoms are mydrasis, dry eyes, dry mouth, and urinary retention
The ________ ________ caused by first generation antihistamines can predisposed the elderly patients to _____, ______, and _____.
Alpha-adrenergic blockade
Hypotension, syncope, and falls
What happens on Janus kinase Stat pathway
Interleukin binds to the interleukin receptor, Janus kinase enzyme is attracted to the receptors and phosphorylates the receptors. the STAT molecules stick to phosphorylated part of receptor and move into the nucleus to activate different genes to produce inflammation
What is cytokine storm
Activation cascade that leads to an autoamplifying cytokine cycle.
Cytokine release that attracts other cells and they release other cytokines and becomes sepsis.
How do NSAIDS drugs reduce inflammatory states like rheumatoid arthritis
The inflammatory challenge is an auto immune response, then forms arachidonic acid, which gets converted by cox2 to prostaglandins and causes inflammation.
NSAIDS ARE BLOCKING COX2 SO NO PROSTAGLANDINS AND NO INFLAMMATION
How do NSAIDS drugs produce antipyretic effects
Inflammatory challenge is infectious, produces interleukins, then formation of arachidonic acid in hypothalamus converts to prostaglandins by cox and activates the hypothalamic therm control center, activates thermogenjc responses like shivering.
NSAIDS BLOCK COX SO NO PROSTAGLANDINS, DECREASING ACTIVATION IF THERMOGENIC CONTROL CENTER reducing fever
Inflammatory trigger for injury
Injury or inflammation causes cell lysis. Cell lysis releases arachidonic acid (as any cellular injury does). Make prostaglandins through COX and they sensitize nocicoreceptors to autocoids, activate pain impulse transmission to higher brain centers producing pain
NSAIDS STOP COX DECREASE PROSTAGLANDINS AND DECREASE SENSITIVITY IN NOCICORECEPTORS
Vascular injury and calcified plaque
Activate platelets, then forms arachidonic acid forms thromboxane through Cox. Thromboxanes induce platelet aggregation and form clot formation
NSAIDS BLOCK COX, DECREASED THROMBOXANES, REDUCED PLT AGGREGATION AND CLOT FORMATION
Treatment of dysmenorrhea
Decrease in progesterone production by corpus luteum initiation of menstruation results in endometrial necrosis, which leads to cell death and release of arachidonic acid, prostaglandins or form through Cox, which causes induction of myometrial contractions, and the development of menstrual cramping
NSA IDS block Cox and decrease symptoms of dysmenorrhea
Why do selective cox2 inhibitors have an increased rate of mis and strokes?
In platelets, arachidonic acid makes thromboxane through Cox 1 and in endothelial cells arachidonic acid makes prostacyclin through Cox one and two that form counter regulation of plt aggregation. If you inhibit Cox 2 you don’t get the prostacyclin and you don’t get balance regulation of clot formation.
Short intermediate and long acting steroid anti-inflammatory drugs
Hydrocortisone and Cortizone are short acting. Prednisone is intermediate acting, and dexamethasone as long acting.
Mechanism of action of steroid anti-inflammatory drugs
Cortisol receptor agonist that high doses, mimic the natural hormone cortisol and suppresses genes that regulate inflammatory response
Pharma toxicology steroids
Gastric and intestinal irritation ulcer formation, clotting, and spontaneous hemorrhage, induction of hyperglycemia can result in development of non-insulin dependent diabetes, moon face, bufalo hump
