Derm & Musculoskeletal Drugs Flashcards Preview

OSD Drugs > Derm & Musculoskeletal Drugs > Flashcards

Flashcards in Derm & Musculoskeletal Drugs Deck (55):
1

Acetaminophen

Class: Weak COX Inhibitor

-Strong analgesic (non-opioid)

-Antipyretic

-Very weak antiinflammatory activity



Rx:

-Analgesia in children



AE:

-Fatal liver disease if overdose



Note: AM404 is active metabolite, which:

-Agonist at TRPV1 channel

-Agonist Cannabinoid CB1 receptor

-Inhibits endogenous cellular CB uptake

-Inhibits COX-1 and COX-2.

2

Aspirin

Class: Nonselective / COX-1 Inhibitors
-Class 3 NSAID

MOA:
-Irreversible acetylation (inactivation) of COX (non-selective).
-Analgesia, antipyresis, antiinflammation, inhibits thrombosis (post-MI).

AE:
-GI Irritation
-Asthma Exacerbation
-Gestation Prolongation
-Renal Function Inhibition
-Gout Exacerbation

3

Diclofenac

Class: Nonselective / COX-1 Inhibitors

Phase 1: Competitive, time dependent, reversible COX inhibitor.
Phase 2: with time, conformational change with tighter binding. Class 2 NSAID.

AE:
-Increase COX-1 selectivity increases risk of ulcer and GI risks.

4

Etodolac

Class: Nonselective / COX-1 Inhibitors

5

Ibuprofen

Class: Nonselective / COX-1 Inhibitors
-Class 1 NSAID

MOA:
-Competitive, reversible COX inhibitor
-Competes with arachidonic acid for COX active site.

AE:
-Increase COX-1 selectivity increases risk of ulcer and GI risks.

6

Indomethacin

Class: Nonselective / COX-1 Inhibitors
-Class 2 NSAID

MOA:
-Phase 1: Competitive, time dependent, reversible COX inhibitor.
-Phase 2: with time, conformational change with tighter binding.

AE:
-Increase COX-1 selectivity increases risk of ulcer and GI risks.

7

Ketorolac

Class: Nonselective / COX-1 Inhibitors

MOA:
-Effective perenteral opioid alternative, COX-1 selective.
-Analgesia with minimal toxicity, for use IM (slower) or IV (faster)
-Prolonged IM effect allowing longer dosing interval.

AE:
-Not for use >5 days, high GI ulcer risk (25% at 1 week)
-Avoid using pre-surgery (platelet inhibition and delayed healing).

8

Naproxen

Class: Nonselective / COX-1 Inhibitors
-Class 1 NSAID

MOA:
-Competitive, reversible COX inhibitor
-Competes with arachidonic acid for COX active site.

AE:
-Increase COX-1 selectivity increases risk of ulcer and GI risks.

9

Celecoxib

Class: COX-2 Inhibitors

MOA:
-Inhibits COX-2 prostaglandins that mediate inflammation, fever, and pain
-Does not block the GI/renal injuring PGs (COX-1).

AE:
-Increase COX-2 selectivity increases risk of:
-Thrombosis and CV
-CHF
-Hypertension

10

Diclofenac

Class: COX-2 Inhibitors

MOA:
-Inhibits COX-2 prostaglandins that mediate inflammation, fever, and pain
-Does not block the GI/renal injuring PGs (COX-1).

AE:
-Increase COX-2 selectivity increases risk of:
-Thrombosis and CV
-CHF
-Hypertension

11

Etodolac

Class: COX-2 Inhibitors

MOA:
-Inhibits COX-2 prostaglandins that mediate inflammation, fever, and pain
-Does not block the GI/renal injuring PGs (COX-1).

AE:
-Increase COX-2 selectivity increases risk of:
-Thrombosis and CV
-CHF
-Hypertension

12

Hydroxycholorquine

Class: DMARD

MOA:
-Antimalarial
-Unknown mechanism, accumulates in lysosome.
-Decreases neutrophils chemotaxis, phagocytosis and superoxide synthesis.
-Inhibits TLR-9 signaling.

Rx:
-RA
-SLE

AE:
-GI Irritation
-Macular Toxicity (requires annual eye exam)
-Myopathy

13

Leflunomide

Class: DMARD

MOA: Pyrimidine synthesis inhibitor

Rx:
-RA (Not Useful at all)

Note: Useless drug in RA. This is known in France as "Le Fluke-o-mide"

14

Methotrexate

Class: DMARD

MOA:
-Dihydrofalte reductase inhibitor
-Thus, blocks Purine Synthesis

-Very potent antiinflammatory, used with anti-TNFs.
-Decreases Joint pain

Note: If no response alone, can add sulfasalazine and hydrochlorquine, leflunomide, anti-TNF agent, anakinra, abatacept.

Triple therapy = MTX + SSZ + HCQ (not as good as anti-TNF).

Rx:
-RA
-Psoriasis

AE:
-Hepatotoxicity,
-cytopenia
-stomatitis
-GI irritation

Note: Can decrease AE's with folic acid or leucovorin after MTX dose.

15

Sulfasalazine

Class; DMARD
-5-ASA

MOA:
-sulfapyridine and salicylate bound by axo group. Unknown mechanism.

Rx:
-RA
-IBD
-Spolyloarthropathy

AE:
-Hypospermia (from sulfapyridine metabolite)
-GI irritation
-Headache

16

Etanercept

Class: DMARD
-Biologic

MOA:
-TNF-a receptor decoy
-Etanercept Intercepts TNF

Rx:
-RA
-Psoriasis

AE:
-Opportunistic Infection (TB; can't form granulomas)
-Serious Infection (avoid in Chronic Infection; HBV, Immunosuppressed)
-Demyelination (Avoid in MS, Optic Neuritis)
-CHF (Avoid in CHF patients)
-Lupus

17

Anakinra

Class: DMARD
-Biologic

MOA:
-IL-1 receptor antagonist

Rx: RA
-Note Effective for RA

18

Infliximab

Class: DMARD

MOA:
-Neutralizes soluble and cell-bound TNF-a and beta

AE:
-Opportunistic Infection (TB; can't form granulomas)
-Serious Infection (avoid in Chronic Infection; HBV, Immunosuppressed)
-Demyelination (Avoid in MS, Optic Neuritis)
-CHF (Avoid in CHF patients)
-Lupus

19

Allopurinol

Class: Anti-Gout Agent

MOA:
-Xanthine oxidase inhibitor (Hypoxanthine analogue)
-Metabolized to Oxipurinol, which is the clinically effective XO inhibitor.

Note:
-Has short t1/2
-But Oxipurinol has t1/2 = 14-26 hours (prolonged if decreased GFR).
-Max effect in 4-14 days.

Rx:
-Gout
-Not for Acute Gout
-Urate Nephrolithiasis

AE:
-Stevens-Johnson Syndrome
-Hypersensitivity (more common if on diuretics; 25% mortality)
-Myelosuppression
-Hepatotox
-Nephrotox
-Vasculitis

DDIs:
-Azothioprine
-Warfarin
-6MP

20

Colchicine

Class: Anti-Gout agent

Readily bioavailable (<50%) PO following jejunal and ileal uptake.

MOA:
-Binds Tubulin and forms complex; prevents elongation/contraction of Dynamin tubulin Polymers
-Promotes depolymerization (high concentration)
-Blocks cell division, signal transduction, gene expression
-Arrests growth (low concentration)
-Disrupts Phagocytosis by PMN

Rx:
-Actue Gout (within 24-36hrs)
-Prophylaxis of Gout during initiation of Urate lowering drugs


AE:
-Narrow therapeutic-toxicity window
-Avoid use in Hepatic and Renal patients


Note:
-Major elimination via ABCB1 (GI tract)
-Minor elimination by CYP3A4 (enteric and hepatic cytochrome).
-Renal Elimination also

Note: Alkaloid derivative of meadow saffron.

21

Probenecid

Class: Anti-Gout agent
-Uricosuric

MOA:
-Targets URAT-1 urate transporter in proximal tubule.
-Inhibits urate-anion exchange at proximal tubule to block reabsorption

Note:
-Rapid hepatic metabolism and urinary excretion.
-Take with fluids, alkalinize urine
-Monitor urate, CBC, LFTs, creatinine.

AE:
-Pregnancy risk factor B
-Rash
-Nephrotic Syndrome
-Stones
-Aplastic Anemia
-Hemolytic Anemia
-Leukopenia
-Hepatic Necrosis

DDI:
-Salicylates (inhibits uricosuric effect)
-Beta lactams
-NSAIDS
-Increased Methotrexate Tox
-Dapsone
-Acyclovir
-Heparin
-Loop Diuretics
-Quinolones
-Benzodiazapines

22

Febuxostat

Class: Anti-Gout agent

MOA:

-Nonpurine analogue inhibitor of xanthine oxidase
-Can inhibit oxidized and reduced XO forms.

Rx:
-Prophylaxis for Gout
-Used with NSAIDs or Colchicine for up to 6months.

Contraindicated:
-Azathioprine
-6MP
-Monitor LFTs
-CVA

Note:
-Metabolized hepatically
-Activity is not altered in mild to moderate renal insufficiency.

23

Tacrolimus

Class: Calcineurin Inhibitor
-Anti-inflammatory ointment/cream

MOA:
-Binds FK506
-Forms complex that inhibits calcineurin and blocks cytokine production.

Rx:
-Atopic Dermatitis

AE:
-Vitiligo
-Granuloma facialis
-Eye lid and intertrigenous regions of body

24

Pimecrolimus

Class: Calcineurin Inhibitor
-Anti-inflammatory ointment/cream

MOA:
-Binds FK506
-Forms complex that inhibits calcineurin and blocks cytokine production.

Rx:
-Atopic Dermatitis

AE:
-Skin cancer and Lymphoma
-Black box warning - avoid long term use.

25

Methotrexate

Class: RA and Psoriasis agents

MOA:
-Dihydrofalte reductase inhibitor
-Thus, blocks Purine Synthesis

-Very potent antiinflammatory, used with anti-TNFs.
-Decreases Joint pain

Note:
-For RA, if no response alone, can add sulfasalazine and hydrochlorquine, leflunomide, anti-TNF agent, anakinra, abatacept.

Triple therapy = MTX + SSZ + HCQ (not as good as anti-TNF).

Rx:
-RA
-Psoriasis

AE:
-Hepatotoxicity,
-cytopenia
-stomatitis
-GI irritation

Note: Can decrease AE's with folic acid or leucovorin after MTX dose.
AE:
-

26

Methoxsalen

Class: Psoriasis Agent

MOA:
-Photosensitizer (makes cells more susceptible to UV radiation damage)
-Preferentially taken up by epidermal cells and binds DNA

Rx:
-Psoriasis

AE:
-Erythema

27

Etanercept

Class: Psoriasis agent and DMARD
-Biologic

MOA:
-TNF-a receptor decoy
-Etanercept Intercepts TNF

Rx:
-RA
-Psoriasis

AE:
-Opportunistic Infection (TB; can't form granulomas)
-Serious Infection (avoid in Chronic Infection; HBV, Immunosuppressed)
-Demyelination (Avoid in MS, Optic Neuritis)
-CHF (Avoid in CHF patients)
-Lupus

28

Infliximab

Class: Psoriasis and DMARD

MOA:
-Neutralizes soluble and cell-bound TNF-a and beta

AE:
-Opportunistic Infection (TB; can't form granulomas)
-Serious Infection (avoid in Chronic Infection; HBV, Immunosuppressed)
-Demyelination (Avoid in MS, Optic Neuritis)
-CHF (Avoid in CHF patients)
-Lupus

29

Benzoyl Peroxide

Class: Acne drug

MOA:
-bacteriostatic
-combined with erythromycin or clindamycin to prevent development of resistance.

30

Clindamycin

Class: Acne drug

MOA:
-Antibiotic
-Binds 50S ribosome to suppress protein synthesis

AE:
-Increased risk for CDIFF infection

31

Doxycycline

Class: Acne drug

MOA:
-Binds 30S subunit and inhibits protein synthesis

Note:
-Also used in Rx for Ricketsia Rickettsii

32

Metronidazole

Class: Acne drug

MOA:
-Anti-Inflammatory
-Inhibits nucleic acid synthesis by disrupting DNA

Rx:
-ACNE ROSACEA

33

Acitretin

Class: Acne drug
-Retinoid (unstable in sunlight)

MOA:
-Functional vitamin A analogue
-Acts at retinoic acid receptor, retinoid X receptor.
-Alters gene expression by binding nuclear receptor.

Results in:
-Differentiation of epidermis
-Modulates proliferation
-Prevents keratinization and Follicle plugging (=anti-acne),
-Antiinflammatory and Apoptotic

AE:
-Teratogenic
-Drying and Itching
-Photosensitization

34

Adapalene

Class: Acne drug
-Retinoid (unstable in sunlight)

MOA:
-Functional vitamin A analogue
-Acts at retinoic acid receptor, retinoid X receptor.
-Alters gene expression by binding nuclear receptor.

Results in:
-Differentiation of epidermis
-Modulates proliferation
-Prevents keratinization and Follicle plugging (=anti-acne),
-Antiinflammatory and Apoptotic

AE:
-Teratogenic
-Drying and Itching
-Photosensitization

35

Isotretinoin

Class: Acne drug
-Retinoid (unstable in sunlight)

Note: Oral Form of Tretinoin
-ISO for I-SwallO

MOA:
-Functional vitamin A analogue
-Acts at retinoic acid receptor, retinoid X receptor.
-Alters gene expression by binding nuclear receptor.

Results in:
-Differentiation of epidermis
-Modulates proliferation
-Prevents keratinization and Follicle plugging (=anti-acne),
-Antiinflammatory and Apoptotic

AE:
-SERIOUS Teratogenic
-Drying and Itching
-Photosensitization (decreased Keratin)

Baby AE:
-Craniofacial
-CNS
-Cardiac

36

Tretinoin

Class: Acne drug
-Retinoid (unstable in sunlight)

MOA:
-Functional vitamin A analogue
-Acts at retinoic acid receptor, retinoid X receptor.
-Alters gene expression by binding nuclear receptor.

Results in:
-Differentiation of epidermis
-Modulates proliferation
-Prevents keratinization and Follicle plugging (=anti-acne),
-Antiinflammatory and Apoptotic

AE:
-Teratogenic
-Drying and Itching
-Photosensitization (decreased Keratin)

37

Calcipotriene

Class: Anti Psoriasis

MOA:
-Vitamin D analogue
-Inhibits keratinocyte proliferation and promotes differentiation (=slows growth).
-Steroid-alternative.

Rx:
-Psoriasis

AE:
-Calcium and Bone Metabolism (high doses)

38

Ketoconazole

Class: Antifungal

MOA:
-Blocks 14-a-demethylase to block ergosterol synthesis and inhibit cell wall formation

39

Mycostatin

Class: Antifungal

MOA:
-Binds ergosterol in fungal cell wall.
-Same as Nystatin

AE:
-Can bind human Cholesterol at high doses

40

Clotrimazole

Class: Antifungal

MOA:
-Blocks 14-a-demethylase to block ergosterol synthesis and inhibit cell wall formation

41

Econazole

Class: Antifungal

MOA:
-Blocks 14-a-demethylase to block ergosterol synthesis and inhibit cell wall formation

42

Itraconazole

Class: Antifungal

MOA:
-Blocks 14-a-demethylase to block ergosterol synthesis and inhibit cell wall formation

43

Terbinafine

Class: Antifungal

MOA:
-Inhibits squalene epoxidase
-Thus, Reduces ergosterol synthesis and inhibits fungal cell wall formation.

Note: Oral or topical.

44

Acyclovir

Class: Antiviral

MOA:
-Interferes with DNA polymerase to inhibit DNA replication via chain termination.

Rx:
-Herpes

45

Neomycin

Class: Antibiotic

MOA:
-Aminoglycoside
-Binds 30S subunit of ribosome

AE:
-Contact Dermatitis

46

Erythromycin

Class: Antibiotic

MOA:
-Binds 50S ribosome to suppress protein synthesis

47

Bacitracin

Class: Antibiotic

MOA:
-Targets Gram (+)

AE:
-Contact Dermatitis
-Nephrotox when given IM

48

Mupirocin

Class: Antibiotic

MOA:
-Reversibly binds isoleucyl tRNA synthetase.

Note: Ointment; derived from Pseudomonas

49

Cephalexin

Class: Antibiotic
-First generation cephalosporin

MOA:
-Binds penicillin binding proteins to arrest bacterial cell wall synthesis
-Inhibit bacterial replication.

AE:
-Diarrhea

50

Cefazolin

Class: Antibiotic
-First generation cephalosporin

MOA:
-Binds penicillin binding proteins to arrest bacterial cell wall synthesis
-Inhibit bacterial replication.

AE:
-Diarrhea

51

Polymyxin B

Class: Peptide antibiotic

Rx:
-Gram (-)

AE:
-Nephrotoxicity
-Neurotoxicity

52

Imiquimod

Class: Immune Modulator

MOA:
-Binds TLR-7, to induce cytokines (INF-a and TNF-a).
- Antiviral and anti-tumor immune modulator

AE:
-Incites immune response, therefore Flu-like symptoms
-Erythema
-Irritation
-Ulceration

53

Topical 5-fluorouracil

Class: Anti-wart agent & Miscellaneous

MOA:
-Inhibits thymidylate synthetase
-Pyrimidine antimetabolite.

54

Liquid nitrogen

Class: Miscellaneous

MOA:
-Cryotherapy for removal of skin lesions

Rx:
-Warts
-AK

AE:
-Blistering

55

Permethrin

Class: Antiparasitic

MOA:
-Synthetic pyrethroid, <2% absorbed percutaneously.
-Paralyzes mite by sodium channel disruption.

NOTE: Only acts on mite (not eggs), so must give multiple treatments.