-
insulin aspartate
- rapid acting insulin analog
- B28 proline replaced by aspartic acid
- injected 30 min. before a meal
-
insulin glargine
- long acting insulin analog
- 2 arginine residues added to the B-chain C-terminus and an asparagine residue replaces glycine at A21
-
Humulin
- recombinant human regular insulin
- insulin monomers associated in hexameric aggregates
-
insulin glulysine
- rapid acting analog
- B29 lysine replaced by glutamic acid and B23 asparagine replaced by lysine
- shortest duration of action: 1-2.5 hours
- clear - no Zn, buffer, or protein added
-
insulin lispro
- rapid acting insulin analog
- B28 (Pro) and B29 (Lys) have been reversed, impairs hexamer formation for faster action
- injected 30 min before a meal
-
NPH insulin
- neutral protamine Hagedorn (isophane)
- intermediate acting insulin
-
tolbutamide
- 1st gen; short acting sulfonylurea
- Stimulates insulin release from b-islet cells, binds SUR1 receptor
- For Type 2 DM
-
Rosiglitazone
- Insulin sensitizer, PPAR-gamma (peroxisome proliferator activated receptor) agonist
- Nuclear TF, regulates carb and lipid metabolism
- requires insulin for its action
- ADR: liver toxicity, edema, weight gain
-
Pioglitazone
- Insulin sensitizer, PPAR-gamma agonist
- Nuclear TF, regulates carb and lipid metabolism
- requires insulin for its action
- ADR: liver toxicity, edema, weight gain
-
chlorpropramide
- 1st generation sulfonylurea; long acting
- Stimulates insulin release from b-islet cells, binds SUR1 receptor
- For Type 2 DM
-
troglitazone
- insulin sensitizer, binds PPAR-gamma
- d/c because of liver toxicity
-
glyburide
- 2nd generation sulfonylurea; short acting
- Stimulates insulin release from b-islet cells, binds SUR1 receptor
- For Type 2 DM
- ADR: hypoglycemia
-
glipizide
- 2nd generation sulfonylurea; long acting
- Stimulates insulin release from b-islet cells, binds SUR1 receptor
- For Type 2 DM
- ADR: hypoglycemia
-
Acarbose
- Alpha-glucosidase inhibitor for Type 2 DM
- Reduces intestinal absorption of starch, dextrin, disacch.
- reduces post-prandial glucose spike
- does NOT produce hypoglycemia
-
miglitol
- Alpha-glucosidase inhibitor for type 2 DM
- Reduces intestinal absorption of starch, dextrin, disacch.
- reduces post-prandial glucose spike
- does NOT produce hypoglycemia
-
repaglinide
- meglitinide secretagogue
- short acting
- block ATP/K channels, prevent postprandial glucose spike
-
nateglinide
- Phenylalanine secretagogue
- short acting
- block ATP/K channels, prevent postprandial glucose spike
-
exendin-4
- incretin for type 2 DM, BID injection
- GLP-1 (glucagon like peptide) receptor (Gs) agonist, increase GLUT2 expression which increases insulin release
- proconvertase convertes proglucan to GLP-1, degraded by dipeptidyl peptidase IV
-
aminoguanide
agent used successfully in trials to prevent oxidation of nonenzymatic glycosylated proteins (which can undergo oxidation and cause cell damage)
-
liraglutide
- incretin for type 2 DM, QD injection
- GLP-1 (glucagon like peptide) receptor agonist (Gs), increases GLUT2 expression which increases insulin release
- proconvertase convertes proglucan to GLP-1, degraded by dipeptidyl peptidase IV
- More effective than exendin-4
-
metformin
- oral biguanide for type 2 DM
- activates AMP- activated protein kinase
- decreases hepatic glucose production, enhances insulin action in muscle and adipose, reduces TGs
- does NOT produce hypoglycemia
-
phenformin
- d/c, biguanide similar to metformin
- activates AMPK
- produced too much lactic acidosis
-
tretinoin
- 1st generation retinoid (Retin-A)
- Reduces hyperkeratinization/acne vulgaris
- Used with anthracycline for APL (acute promyelocytic leukemia)
-
Isotretinoin
- AKA accutane
- 1st generation retinoid
- Normalizes keratinization, reduces P. acnes
- For nodulocystic acne vulgaris
-
Alitretinoin
- 1st generation retinoid, binds all RAR and RXRs
- For Kaposi's sarcoma
-
Acitretin
- 2nd generation retinoid
- For plaque psoriasis
- T1/2= 2-3 days, stored in fat
-
Bexarotene
- 3rd generation retinoid
- Selectively binds RXR
- For Tcell lymphoma
- ADR: hypothyroidism
-
Adapalene
- Similar to tretinoin, naphthoic acid derivative, retinoid-like (3rd generation)
- More anti-inflammatory, more stable to sunlight
-
Calcipotriene (dermatologic)
- Vitamin D analog
- Binds VDR which then associates with RXR-alpha
- Enhances differentiation
- For mild/moderate psoriasis
-
Methotrexate (dermatologic)
- Decreases expression of CLA positive T-cells and endothelial E-selectin
- 3 doses once a week
- For moderate/severe psoriasis
- ADR: hepatic fibrosis
-
Mycophenolate Mofetil (dermatologic)
- Inhibits IMPDH (type 2) in B and T cells
- For moderate/severe psoriasis
-
Alefacept (dermatologic)
- anti-CD2 - recombinant fusion protein (LFA3 + IgG1 Fc domain)
- blocks memory T-cell costimulation
- ADR: reduction in CD4+ cells
- For moderate/severe psoriasis
-
Tacrolimus (dermatologic)
- Calcineurin inhibitor ,binds FK506-BP12
- stops NFAT from initiating IL-2 production in T-cells
- Also binds langerhans cells, mast cells, keratinocytes
- ADR: HTN and renal dysfunction, NO epidermal thinning
- For moderate/severe psoriasis, also rosacia
-
Cyclosporine (dermatologic)
- Calcineurin inhibitor, which stops NFAT from initiating IL-2 production in T-cells
- Also binds langerhans cells, mast cells, keratinocytes
- ADR: HTN and renal dysfunction
- For moderate/severe psoriasis
-
Etanercept (dermatologic)
- Recombinant anti-TNF-?
- Fusion protein (TNF binding domain + IgG1 fc domain)
- ADR: increased risk of infection
-
Betamethasone (dermatologic)
- Fluorinated topical GC, most potent
- For psoriasis, not for face or genitals
- ADR: skin atrophy (GCs)
-
Hydrocortisone (dermatologic)
- Least potent topical GC
- For mild/moderate psoriasis
- ADR: skin atrophy
-
Prednisone (dermatologic)
- Systemic GC for severe psoriasis
- Extensive ADRs, pustular flares if rapidly tapered
-
Infliximab (derm.)
- anti-TNF-alpha (bound and unbound) - complement dependent
- ADR: reactivate TB, exacerbate CHF
- For moderate/severe psoriasis
-
efalizumab (dermatologic)
- anti-CD11a of LFA1, blocks binding to ICAM-1 on APCs
- For moderate/severe psoriasis
-
8-methoxypsoralen
- photosensitizer used in combo with UVA for severe psoriasis
- type 1 rxn O2 independent, type 2 rxn O2 dependent
- Better GI absorption than 4,5,8 TMP
-
Aminolevulinic acid (ALA)
- Photosensitizer, used in combo with PDT
- Converted to protoporphyrin
- For actinic keratoses and non-melanoma cancer
-
Avobenzone, Oxybenzone, titanium oxide, zinc oxide
UVA sunscreen, reduce deeply penetrating light
-
4,5,8-trimethylpsoralen
- photosensitizer used in combo with UVA for severe psoriasis
- type 1 rxn O2 independent, type 2 (melanogenesis) rxn O2 dependent
- Less GI absorption than 8-MOP
-
Methoxsalen
- Photosensitizer used in combo with UVA
- For psoriasis, vitiligo, atopic dermatitis, cutaneous lymphoma
- ADR: blistering, erythema. Chronic= actinic keratoses
-
PABA esters, cinnamates, salicylates
UVB sunscreen agents
-
minoxidil
- originally for HTN, opens K+ channels, hyperpolarizes, relaxation
- for alopecia, enhances follicle size
-
Finasteride
- Inhibits type 2 5-alpha-reductase, decreases DHT
- for alopecia for men
- ADR: ED, decrease libido
-
Timolol
- nonselective beta antagonist
- decreases aqueous humor production
- 1st line OAG
-
apraclonidine
- selective alpha-2 agonist for OAG
- decreases aqueous humor production, maybe more meshwork outflow
-
pilocarpine
- M3 agonist,2nd/3rd line OAG
- Increases trabecular outflow
-
levobunolol
- nonselective beta antagonist for OAG
- decreases aqueous humor production
-
Clonidine
- alpha-2 agonist for OAG
- decreases aqueous humor production, maybe more meshwork outflow
-
carbachol
- M3 agonist, 2nd/3rd line OAG
- Increases trabecular outflow
-
metipranolol
- nonselective beta antagonist 1st line OAG
- decreases aqueous humor production
-
brimonidine
- selective alpha-2 agonist for OAG
- decreases aqueous humor production
- preferred over apraclonidine
-
echothiophate
- AchE-I, 2nd/3rd line OAG
- Increases trabecular outflow
-
carteolol
- nonselective beta antagonist
- decreases aqueous humor production
- 1st line for OAG
-
betaxolol
- Beta antagonist (Beta-1-selective), not as effective in OAG
- Decreases aqueous humor production
-
dorzalamide
- topical carbonic anhydrase-I for OAG
- decreases aqueous humor production
-
brinzolamide
- topical carbonic anhydrase-I for OAG
- decreases aqueous humor production
-
latanoprost
- PG analog, 1st line OAG
- Increases uveoscleral outflow
-
Acetazolamide
- oral carbonic anhydrase-I for OAG
- decreases aqueous humor production
-
travoprost
- PG analog, for OAG
- Increases uveoscleral outflow
- 2nd line, ADR: pigmentation, CV effects
-
Methazolamide
- oral carbonic anhydrase-I for OAG
- decreases aqueous humor production
-
bimatoprost
- PG analog, 1st line OAG
- Increases uveoscleral outflow
-
Tafluprost
- PG analog, 1st line OAG
- Increases uveoscleral outflow
- Ester prodrug, no preservative
-
Dipivefrin
- Epinephrine prodrug converted by esterases in cornea
- Stimulates alpha-2, increases outflow for OAG
-
3 classes of drugs used for CAG
- Ach agonist
- Hyperosmotic
- Beta blocker
-
verteporfin
- Deposits in new vessels, used with photodynamic therapy
- Produces ROS to damage and occlude new vessels
- For exudative (neovascular) AMD
-
Pegaptanib
- PEG anti-VEGF aptamer
- Single mRNA strand that binds VEGF
-
vit-E, vit-C, vit-B2, ZnO, CuO
supplements recommended for those at risk for AMD
-
Ranibizumab
- rh monoclonal igG1 - binds VEGF-A
- for neovascular AMD
-
bevacizumab (for AMD)
- murine-mAb against VEGF-A
- most widely used for neovascular AMD(low cost), off-label
-
lutein
caratenoid, antioxidant for AMD
-
zeaxanthin
caratenoid, antioxidant for AMD
-
lycopene
caratenoid, powerful antioxidant
-
aflibercept
- fusion protein (VEGFR-1/2 + IgG1 Fc)
- binds VEGF-A
- for neovascular AMD
-
restasis
- topical cyclosporin
- increases tear production, decreases inflammation
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