Anti Inflammatories

Question 1

Why are NSAIDs used in Rheumatoid Conditions?

Answer 1

• reduce associated pain
• improve mobility
• slow or arrest tissue-damage, not curative though

**aspirin is no longer the initial drug of choice in treating articular and musculoskeletal disorders

Question 2

What is the adverse result of reduction in PGE2 levels caused by NSAIDs?

Answer 2

-decreased gastric mucosal acid secretion

Question 3

What is the adverse result of reduction in PGI2 levels caused by NSAIDs?

Answer 3

-decreased vasodilatory actions reducing cytoprotective properties

Question 4

What is the beneficial result of reduciton in PGE2 levels caused by NSAIDs?

Answer 4

-decreased erythema, edema, pain, local heat, and systemic fever

Question 5

What is the beneficial result of reduction in PGI2 levels caused by NSAIDs?

Answer 5

-Decreased erythema, pain, local heat, and systemic fever

Question 6

What is erythema?

Answer 6

-redness of the skin or mucosa

Question 7

Why is inhibition of COX-1 bad?

Answer 7

• it results in most of the unwanted side effects of NSAIDs

- particularly gastric ulcers

Question 8

Why is inhibition of COX-2 good?

Answer 8

Inhibition of COX-2 is thought to mediate,at least in part, the antipyretic (antifever), analgesic and anti-inflammatory actions of NSAIDs

Question 9

What are the most common GI side effects of NSAIDs? Mechanism?

Answer 9

• Gastric or intestinal ulceration

- Caused by inhibition of PGI2 and PGE2

Question 10

What are the most common Hemostatic effects of NSAIDs? Mechanism?

Answer 10

• disturbances in platelet function

- Inhibition of Thromboxane A2

Question 11

What kind of patient is more susceptible to Stevens-Johnson Syndrome caused by NSAIDS?

Answer 11

-patients with Lupus or HIV

Question 12

What is Stevens-Johnson syndrome?

Answer 12

-A diffuse, severe, mucocutaneous eruption involving 2 or more mucosal surfaces

+/- visceral involvement

Question 13

What is the most common use of Aspirin?

Answer 13

-inhibition of platelet aggregation

Question 14

How does aspirin affect warfarin levels? Why?

Answer 14

• Increases plasma warfarin levels

- displaces warfarin from plasma protein binding sites

Question 15

How do we manage aspirin overdose?

Answer 15

• Patient will be acidemic
• cardiovascular and respiratory support followed by administration of sodium bicarbonate to correct acid-base abnormalities

Question 16

Is acetaminophen a NSAID?

Answer 16

• maybe
• it is an effective alternative to aspirin, used as an analgesic-antipyretic, but lacks the anti-inflammatory and anti platelet effects
• It is a weak inhibitor of peripheral COX

Question 17

What is the antidote for acetaminophen overdose?

Answer 17

• activated charcoal
• N-acetyl-cysteine (Mucomyst), a replacement for glutathione
• consider liver transplant for pts with fulminant hepatic failure

Question 18

What is Indomethacin used for?

Answer 18

• NSAID
• Anti-inflammatory in treatment of gouty arthritis and ankylosing spondylitis
• Also promotes closure of patent ductus arteriosus in newborns

**not for simple analgesia

Question 19

Ketorolac is a potent analgesic, when is it used?

Answer 19

• One of the few NSAIDs approved for parenteral administration
• Use for post-op pain when pt cannot swallow, and you don’t want to give a narcotic

Question 20

What are COXIBs?

Answer 20

-NSAIDs that have been designed to selectively target COX-2 over COX-1 to minimize stomach ulcer risk

Question 21

Do NSAIDS affect leukotriene synthesis?

Answer 21

-no

Question 22

Why don’t we give aspirin to children? What can we give instead?

Answer 22

• there is an epidemiological association of Reye’s Syndrome in children (ages 2 to 16) with administration of aspirin for the treatment of febrile viral illnessess (influenza B > A) -> FUO
• can give acetaminophen

Question 23

What does Reye’s syndrome involve?

Answer 23

-swelling of the liver and edema of the brain

Question 24

What should Grammy do if she decides to take aspirin/NSAIDs while taking warfarin?

Answer 24

-Have her prothrombin time checked

Question 25

What are the higher strength fluorinated glucocorticoids?

Answer 25

• dexamethasone

- triamcinolone

Question 26

Glucocorticoids bind to Hormone Responsive Elements (HREs) which cause induction of ________.

Answer 26

Lipocortins

Question 27

What do lipocortins do?

Answer 27

• suppress phospholipase A2

- decrease release of arachidonic acid & production of proinflammatory eicosanoids

Question 28

What are the adverse effects of long term corticosteroids?

Answer 28

• perforations
• ulcerations
• bleeds
• immunodeficiency
• hyperglycemia/diabetes
• osteoporosis/osteonecrosis
• cateracts
• adrenal atrophy

Question 29

How do corticosteroids work on the cellular level?

Answer 29

block cellular recruitment to a site of inflammation by inhibiting chemotactic factors

Question 30

How do corticosteroids function on connective tissue?

Answer 30

• promote tissue repair

- synthesis of new tissue & repair damaged tissue

Question 31

What does 11B-HSD II do?

Answer 31

• degrades glucocorticoids

* chemists want to decrease affinity of synthetic steroids for this enzyme, so they last longer

Question 32

Addison’s disease

Answer 32

• don’t make enough cortisol

- treat with hydrocortisone with a mineralocorticoid

Question 33

Are steroids a good treatment for meningitis?

Answer 33

-yeh

Question 34

Cushing’s Syndrome

Answer 34

• too much ACTH

- caused by pituitary or ectopic ACTH overproduction

Question 35

What are the adverse effects of withdrawal from glucocorticoid therapy?

Answer 35

• Most frequent: flare up of the disease
• Most severe: acute adrenal insufficiency

**if changing route of administration, keep in mind the systemic effects, might need to taper dose