Derm & Musculoskeletal Drugs Flashcards
These are all of the drugs- except the corticosteroids.
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.
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
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.
Etodolac
Class: Nonselective / COX-1 Inhibitors
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.
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.
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).
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.
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
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
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
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
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”
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.
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
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
Anakinra
Class: DMARD
-Biologic
MOA:
-IL-1 receptor antagonist
Rx: RA
-Note Effective for RA
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
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
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.
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
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.
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
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.
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:
-
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
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
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
Benzoyl Peroxide
Class: Acne drug
MOA:
- bacteriostatic
- combined with erythromycin or clindamycin to prevent development of resistance.
Clindamycin
Class: Acne drug
MOA:
- Antibiotic
- Binds 50S ribosome to suppress protein synthesis
AE:
-Increased risk for CDIFF infection
Doxycycline
Class: Acne drug
MOA:
-Binds 30S subunit and inhibits protein synthesis
Note:
-Also used in Rx for Ricketsia Rickettsii
Metronidazole
Class: Acne drug
MOA:
- Anti-Inflammatory
- Inhibits nucleic acid synthesis by disrupting DNA
Rx:
-ACNE ROSACEA
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
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
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
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)
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)
Ketoconazole
Class: Antifungal
MOA:
-Blocks 14-a-demethylase to block ergosterol synthesis and inhibit cell wall formation
Mycostatin
Class: Antifungal
MOA:
- Binds ergosterol in fungal cell wall.
- Same as Nystatin
AE:
-Can bind human Cholesterol at high doses
Clotrimazole
Class: Antifungal
MOA:
-Blocks 14-a-demethylase to block ergosterol synthesis and inhibit cell wall formation
Econazole
Class: Antifungal
MOA:
-Blocks 14-a-demethylase to block ergosterol synthesis and inhibit cell wall formation
Itraconazole
Class: Antifungal
MOA:
-Blocks 14-a-demethylase to block ergosterol synthesis and inhibit cell wall formation
Terbinafine
Class: Antifungal
MOA:
- Inhibits squalene epoxidase
- Thus, Reduces ergosterol synthesis and inhibits fungal cell wall formation.
Note: Oral or topical.
Acyclovir
Class: Antiviral
MOA:
-Interferes with DNA polymerase to inhibit DNA replication via chain termination.
Rx:
-Herpes
Neomycin
Class: Antibiotic
MOA:
- Aminoglycoside
- Binds 30S subunit of ribosome
AE:
-Contact Dermatitis
Erythromycin
Class: Antibiotic
MOA:
-Binds 50S ribosome to suppress protein synthesis
Bacitracin
Class: Antibiotic
MOA:
-Targets Gram (+)
AE:
- Contact Dermatitis
- Nephrotox when given IM
Mupirocin
Class: Antibiotic
MOA:
-Reversibly binds isoleucyl tRNA synthetase.
Note: Ointment; derived from Pseudomonas
Cephalexin
Class: Antibiotic
-First generation cephalosporin
MOA:
- Binds penicillin binding proteins to arrest bacterial cell wall synthesis
- Inhibit bacterial replication.
AE:
-Diarrhea
Cefazolin
Class: Antibiotic
-First generation cephalosporin
MOA:
- Binds penicillin binding proteins to arrest bacterial cell wall synthesis
- Inhibit bacterial replication.
AE:
-Diarrhea
Polymyxin B
Class: Peptide antibiotic
Rx:
-Gram (-)
AE:
- Nephrotoxicity
- Neurotoxicity
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
Topical 5-fluorouracil
Class: Anti-wart agent & Miscellaneous
MOA:
- Inhibits thymidylate synthetase
- Pyrimidine antimetabolite.
Liquid nitrogen
Class: Miscellaneous
MOA:
-Cryotherapy for removal of skin lesions
Rx:
- Warts
- AK
AE:
-Blistering
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.
