Immunopharm

Question 1

Basic inflammatory response

Answer 1

Inflammatory challenges, inflammatory mediators, inflammatory responses, outcome of inflammatory responses

Question 2

Acetaminophen has similar mechanism of action as aspirin, but not classified as an NSAid. Why

Answer 2

Acetaminophen has no anti-inflammatory properties. Doesn’t have antiplatelet properties so no risk of bleeding in Tylenol. Tylenol is also antipyretic

Question 3

Mechanism of action of NSAIDS

Answer 3

Cyclooxygenase (COX) inhibitors

COX1 has a broad tissue distribution COX2 has more narrow tissue distribution and a strongly activated during an inflammatory response

Question 4

Enteric coated aspirin provides excellent protection against risk for G.I. bleeding, true or false

Answer 4

True aspirin has coating that lets it pass through the stomach and then release into the duodenum

Question 5

Why do cox2 inhibitors get recalled?

Answer 5

Increase risk of thrombogenictiy, myocardial infarction and stroke

Question 6

Pharma toxicology of NSAIDS

Answer 6

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

Question 7

Glucocorticoids block, the action of what?

Answer 7

Arachidonic acid which blocks cox and lox and in turn prostoglandins and leukotrienes

Question 8

Why is the side effect of glucocorticoids increase in white blood cell count?

Answer 8

They prevent leukocyte immigration, so white blood cells stay in the bloodstream as opposed to leaking out into the cells

Question 9

When glucocorticoid side effects appear is it a good medical practice to immediately withdrawal treatment to avoid the development of more serious side effects

Answer 9

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

Question 10

Diphenhydramine mechanism of action

Answer 10

Antihistamine, A1 histamine receptor antagonist

Question 11

ZILEUTON mechanism of action

Answer 11

Lipooxygenase inhibitor that blocks the synthesis of Leukotrienes

Therapeutic effects- inhibits leukotriene induced bronco, construction and mucus production associated with asthma

Question 12

Infliximab (remicade) MOA

Answer 12

Antibody against TNF

Therapeutic use - treatment of rheumatoid arthritis, Crohn’s disease and psoriasis

Question 13

Anakinra

Answer 13

Antibody against il1

Therapeutic use - treatment of rheumatoid arthritis, Crohn’s disease and psoriasis

Question 14

Tofacitinib

Answer 14

Janus kinase (JAK) inhibitor

Therapeutic use - treatment of rheumatoid arthritis, Crohn’s disease and psoriasis

Question 15

Young children less then 2 years of age and elderly adults the _______ and _______ effects of antihistamines can be exaggerated

Answer 15

Sedating and anticholinergic

Anticholinergic symptoms are mydrasis, dry eyes, dry mouth, and urinary retention

Question 16

The ________ ________ caused by first generation antihistamines can predisposed the elderly patients to _____, ______, and _____.

Answer 16

Alpha-adrenergic blockade

Hypotension, syncope, and falls

Question 17

What happens on Janus kinase Stat pathway

Answer 17

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

Question 18

What is cytokine storm

Answer 18

Activation cascade that leads to an autoamplifying cytokine cycle.

Cytokine release that attracts other cells and they release other cytokines and becomes sepsis.

Question 19

How do NSAIDS drugs reduce inflammatory states like rheumatoid arthritis

Answer 19

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

Question 20

How do NSAIDS drugs produce antipyretic effects

Answer 20

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

Question 21

Inflammatory trigger for injury

Answer 21

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

Question 22

Vascular injury and calcified plaque

Answer 22

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

Question 23

Treatment of dysmenorrhea

Answer 23

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

Question 24

Why do selective cox2 inhibitors have an increased rate of mis and strokes?

Answer 24

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.

Question 25

Short intermediate and long acting steroid anti-inflammatory drugs

Answer 25

Hydrocortisone and Cortizone are short acting. Prednisone is intermediate acting, and dexamethasone as long acting.

Question 26

Mechanism of action of steroid anti-inflammatory drugs

Answer 26

Cortisol receptor agonist that high doses, mimic the natural hormone cortisol and suppresses genes that regulate inflammatory response

Question 27

Pharma toxicology steroids

Answer 27

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