Mon Test Week 5 Day 2 Anti-inflam pharma

Question 1

2 ways the immune “malfunctions”?

Answer 1

Deficiency or Over Responsiveness

Question 2

2 types of immune deficiencies?

Answer 2

Primary which is genetic and congenital and Secondary which is developed later in life due to disease, mutations or drugs

Question 3

2 types of immune system over responsiveness?

Answer 3

Autoimmunity- self tolerance fails and body attacks itself\

Hypersensitivity- body over reacts to stimulus, usual an exogenous antigen

Question 4

List innate system components (9)?

Answer 4

1. Dendritic Cell
2. Eosinophils
3. Basophils
4. Neutrophils
5. Monocytes
6. Macrophages
7. Complement Proteins
8. Mast Cells
9. NK cells

Question 5

List of Adaptive immune components? And the Common pathway cells?

Answer 5

T-cells which include CD4 and CD8
Cytokines
B-cells
Antibodies

Common Pathway
NK T cells
Gamma T-cells

Question 6

Which side of the immune system innate or adaptive goes wrong with autoimmune diseases?

Answer 6

The adaptive

Question 7

Do we always want to use anti-inflammatories?

Answer 7

No, inflammation is complex and a part of the human process of healing and defense. By suppressing it we can suppress and delay healing.

Question 8

2 types of anti-inflammatory drugs and the major difference between them?

Answer 8

NSAIDs and Corticosteroids

NSAIDs inhibit a one pathway COX or cyclooxygenase and Corticosteroids inhibit a pathway above it- the conversion of phospholipids to arachidonic acid so they inhibit a lot more
Details on next few cards

Question 9

What do NSAIDs inhibit and what do they not affect?

Answer 9

Inhibit inflammation due to mediators such as
prostaglandin, prostacyclin and thromboxane production.

Do not affect leukotriene, tumor necrosis factor (TNF), or interleukin
production.

Question 10

What do corticosteroids inhibit?

Answer 10

Inhibit prostaglandin, prostacyclin, thromboxane, plus leukotriene, and
interleukin production

A lot more including 10-20% of protein making of a cell. mRNAs don’t get translated.

Question 11

2 major types of NSAIDs and which of the 3 she asked us to know are which kind? A major difference in what they inhibit?

Answer 11

Non-Selective COX1 and COX2 Inhibitors- Ibuprofen and Naproxen

Selective COX2 Inhibitor- Celecoxib

Non-selective inhibit prostaglandin productuction- COX1 makes prostaglandin in the GI tract, kidneys and platelets. Prostaglandin protects the gi tract lining

Question 12

Non selective inhibitor (Ibuprofen and Naproxen) adverse drug reactions?

Answer 12

epigastric pain, heartburn, nausea—avoid use in patients with known or history of gastroesophageal reflux disease (GERD) or peptic ulcer due to risk of GI bleed; can worsen pre-existing edema; tinnitus rare; increases risk of adverse cardiovascular event in patients with pre-existing heart disease (unstable angina, heart failure, prior MI)

Question 13

Non selective inhibitor (Ibuprofen and Naproxen) drug interactions?

Answer 13

Many. Can prolong bleeding time in patients on oral antiplatelet or anticoagulant agents. Can also affect kidney function—use carefully in patients taking ACE inhibitors and thiazide diuretics as incautious use can lead to acute kidney injury

Question 14

Ibuprofen dosing and comments?

Answer 14

Product options. OTC 200 mg tablet, 200 mg/5 mL oral liquid, 100 mg/mL oral liquid; 100 mg chewable tablet; Rx 400 mg, 600 mg, 800 mg tablets; 10% cream (topical)

Typical dosing. adults, for pain: 400 mg three or four times daily; doses for dysmenorrhea or arthritis are typically higher, e.g., 600-800 mg three or four times daily

Comments. Has antipyretic, analgesic properties as well as anti-inflammatory properties

Question 15

Naproxen dosing and comments?

Answer 15

Product options. OTC naproxen 220 mg capsule, 125 mg/5 mL liquid; Rx 250 mg, 375 mg, 500 mg, 550 mg; also comes in delayed/extended-release formulas; 10% cream (topical)

Typical dosing. adults, for pain: 400 mg two or three times daily; doses for dysmenorrhea or arthritis are typically higher

Comments. Available as a base and sodium salt. 200 mg naproxen base = 220 mg naproxen sodium. Has antipyretic, analgesic properties as well as anti-inflammatory properties

Question 16

Celecoxib adverse drug reactions?

Answer 16

Diarrhea, dyspepsia, upper respiratory tract infection;

may increase risk of adverse cardiovascular event in patients with pre-existing heart disease (unstable angina, heart failure, prior MI), but evidence points to risk among the lowest of all NSAIDs

Question 17

Celecoxib drug interactions?

Answer 17

Moderate CYP 2C9 substrate, weak 3A4 substrate. Weak 2D6 inhibitor. Many, but hard to distinguish from non-selective NSAIDs

Question 18

Celecoxib dosing and comments?

Answer 18

Product options- Rx only 50 mg, 100 mg, 200 mg, 400 mg capsules, 120 mg/4.8 mL oral solution

Typical dosing- 100 mg twice daily or 200 mg once daily; can be dosed at 200 mg twice daily for short term intense pain; max daily dose 400 mg

Comments- Probably a better candidate for patients with a history of GERD or peptic ulcer than non-selective NSAID

Question 19

What is diclofenac?

Answer 19

An NSAID that in the 3% gel form may be effective for treating aphthous ulcers aka canker sores.

In ingestible form there are many serious potential reactions and interactions.

Question 20

3 corticosteroids and their slightly different modes of action?

Answer 20

All- Blocks protein synthesis of interleukins (late phase inflammation) and the arachidonic acid pathway so blocks production prostaglandins and leukotrienes;

Prednisone- some mineralocorticoid activity

Dexamethasone- no mineralocorticoid activity

Triamcinolone- minimal mineralocorticoid activity

Question 21

Prednisone and Dexamethasone adverse drug reactions?

Answer 21

Short-term: glucose intolerance, hypertension, dysphoria (dose related), GI toxicity, fluid retention, weight gain.

Long-term: cataracts, glaucoma, osteopenia/osteoporosis, impaired wound healing, skin thinning, striae (particularly with topical use), moon face, edema, buffalo hump and other abnormal fat deposits, anemia

Question 22

Prednisone and Dexamethasone drug interactions?

Answer 22

Many. Major CYP 3A4 substrate, so any inducer will decrease serum concentrations of prednisone.

Concomitant administration will enhance GI toxicity of NSAIDs. May enhance immune suppression effect of other immunotherapies.

Question 23

Triamcinolone oral paste adverse reactions and drug interactions?

Answer 23

Adverse drug reactions. Less than with prednisone because topical or intra-articular administration

Drug interactions. Minimal

Question 24

Prednisone dosing and comments?

Answer 24

Product options- 1 mg, 2.5 mg, 5 mg, 10 mg 20 mg 50 mg tablets; 1 mg/mL and 5 mg/mL oral solutions; 1 mg, 2 mg, 5 mg delayed release tablets

Typical dosing- Dose depends on what is being treated. Long-term dosing at more than 5 mg daily is avoided whenever possible. Short-term treatment for immune hypersensitivity or another acute inflammatory condition can involve doses of 20 mg or more daily. If on longer than 2 weeks, will need to taper therapy. Patients on more than 5 mg/day may need extra stress dose on day of oral surgery.

Comments- 5 mg daily equals physiologic cortisol production

Question 25

Dexamethasone dosing and comments?

Answer 25

Product options- 0.5 mg, 0.75 mg, 1 mg, 2 mg, 4 mg, 6 mg, 20 mg tablets; taper kits for many different options (e.g., 1 week, 10 days, 12 days); 0.5 mg/5 mL oral liquid; 4 mg/mL, 10 mg/mL prefilled injection; other intravenous products

Typical dosing- dose depends on what is being treated.

Comments- Preferred when no mineralocorticoid activity is desired.

Question 26

Triamcinolone dosing and comments?

Answer 26

Product options- 0.1% oral paste; intra-articular suspension 10 mg/mL, 20 mg/mL, 40 mg/mL

Typical dosing- aphthous stomatitis: apply small amount to lesion 2-4 times daily, do not rinse, avoid eating or drinking for 30 minutes after application

Comments- Triamcinolone acetonide is a moderate potency corticosteroid that is widely used as a topical agent for many inflammatory dermatologic conditions.

Question 27

4 general classes of immunosuppressants?

Answer 27

> Anti-inflammatory agents
– Suppress inflammatory processes all over the body
> Disease-modifying drugs
– Slow or arrest the tissue-damaging process (e.g., impair cell division)
> Direct immunosuppressants
– Have several effects on a smaller part of the immune process
> Biological response modifiers
– Target a specific step in the immune process

Question 28

Biological response modifiers, what are they?

Answer 28

Know what is in bold- just the basics

– Target a specific step in the immune process e.g., specific IL receptor
or T-cell (e.g, CD28) or immune modulator or cell signaling pathway

– Monoclonal antibodies (mabs): block, flag, or deliver (chemo)

– Small molecule kinase inhibitors (nibs): target enzymes that affect
cell signaling, metabolism, growth, or survival

– Biosimilars are biologic agents that do the same thing as a

• *previously-introduced biological agent but are not quite the**
• *same exact molecule**

Question 29

3 types of Immunosuppressant Agents on one pager?

Answer 29

> Disease-modifying anti-rheumatic drugs (DMARDs)
– Conventional synthetic DMARDs
– Biological DMARDs
– Targeted synthetic DMARDs
> Immunosuppressants used to prevent organ rejection
– Calcineurin inhibitors
– mTOR kinase inhibitors
– Other immunosuppressants
> Immunosuppressants used for immune-related cancers
and other immune conditions

Question 30

4 common and 1 uncommon oral health effects of Immunosuppressants?

Answer 30

Very Common- aphthous stomatitis, herpes reactivation, oral candidiasis,

Somewhat common- DIGO aka drug induced gingival overgrowth- caused by a few organ rejection agents- cyclosporine, tacrolimus and mycophenolate

Uncommon- Tongue edema- caused by organ rejection agent- glatiramer