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Derm and Steroids
Pharmacology: Dermatologic Agents and Corticosteroids
| Term | Definition |
|---|---|
| Why use topical agents? | Extensive region for application and absorption. If a skin disorder covers less than 30% of the body, use topicals. |
| Considerations for cutaneous drug admin | age of patient, area of body, pathologic changes in skin, hydration, vascular supply, vehicle. |
| Gels/Jellies | semisolids consisting of dispersions of small/large mollecules in aqueous liquid. Provide cooling sensation when applied to skin. |
| Paste | semisolid suspension containing large proportion of solids in a fatty vehicle stiffer than ointment (Larger proportion of solid materials than ointments). Absorbed slowly but well forming protective layer |
| Lotion | liquid emulsion containing >50% volatile compounds that evaporate rapidly w/cooling sensation. Takes a while to dry. |
| Ointment | semisolid emulsion that is greasy and contains less than 20% volatiles. Slow to evaporate and absorb. Uses: protective barrier, vehicle to incorporate meds, emolliments make skin more pliable. |
| Cream | Formed to be absorbed quickly with little evaporation. Hydrophilic/lipophilic |
| Cold cream | In place of soap. Water evaporates so drug is higher concentrated on skin, and leaves a protective film. Cooling effect. |
| Occlusion on skin | Keeps skin hydrated and warm for maximal absorption. |
| 3 best vehicles for oily skin? | Creams, lotions, gels |
| 2 best vehicle for dry skin? | Ointments, pastes |
| Best vehicle for weeping? | Lotions |
| Topical agents that whitens skin by removing pigment | Hydroquinone, Mequinol. |
| Kills melanocytes resulting in permanent depigmentation | Monobenzone |
| Psoralens used for repigmentation of depigmented macules of vitiligo (or loss of melanocytes). Can cause cataracts or skin cancer. | Trioxsalen, Methoxsalen. |
| Acid form of Vitamin A. Decreases cohesion btwn epidermal cells -> increases turnover -> closed comedones to open comedones -> resulting in expulsion of open comedones. Also promotes collagen synthesis, & thickening of the epidermis (diminishes wrinkles) | Retinoids (retinoic acid and derivatives) |
| Penetrates stratum corneum or follicurlar openings. Has antimicrobial activity, causes peeling/comedolytic effects and bleaching. Often combined w/ erythro or clinda | Benzoyl Peroxide |
| Plant derived primarily for antimicrobial activity. Slows down turnover/pigmentation of skin by reducing production of keratin/melanin. | Azelaic acid |
| 10% systemically absorbed (a lot) leading to possibility of pseudomembranous colitis (USUALLY occurs with widespread application). Complaints of burning and stinging with irritation of skin. Broad spectrum including anaerobes. | Topical Clindamycin |
| Effective treatment of rosacea. Unknown mechanism. Adverse of gel: stinging, dryness, burning esp mucous membranes; cream/lotion better tolerated. Inhibitory effects on Demodex brevis | Metronidazole |
| Wide spectrum esp against coinhibators of acne (staph etc). Possible complication is ABX resistant strains. Adverse: burning, drying, irritation. Combo with benzoyl, but not retinoic acid. | Erythromycin |
| solubilizes cell surface proteins resulting in desquamation of keratotic debris (removes dead cells and debris of acne) Adverse: urticaria, anaphylactic and erythema multiforme reactions, irritation, inflammation, and ulceration. | Salicylic acid |
| Vehicle for organic compounds. Develops osmotic gradient increasing hydration of outer layers of skin. Keratolytic and destructive agent. | Propylene Glycol |
| Humectant activity (softening and moisturizing on stratum corneum. Decreases oily feel. Low risk of dermatitis | Urea |
| Causes death of skin cells, good for precancerous cells. Interferes w/ DNA/RNA synthesis. Use: multiple actinic keratosis. Also an anti-cancer drug | Fluoruracil |
| Keratolytic/destructive agent that is a NSAID | Diclofenac |
| Used in actinic keratosis. After exposure to light, produces cytotoxic superoxide and hydroxyl radicals | Aminolevulinic acid |
| Longwave radiation. Responsible for a slow natural tan and most drug-induced photosensitivity rxns. | UVA |
| Middlewave radiation. Produces new pigment formation, sunburn, Vitamin D synthesis (why we need this radiation), DNA damage; induces skin cancer | UVB |
| Shortwave/germicidal radiation. Does not reach surface of earth so created w/ artificial ultraviolet sources to sterilize hospital rooms (like those hosting TB infx). | UVC |
| A sunshade made of opaque materials that reflect UV radiation. $$. Incorporated into suncreens | Titanium dioxide |
| Factors influencing effectiveness of SPFs | Skin type, thickness of application, time of day, altitude (each 1,000 ft increase adds 4% intensity [Charlotte->Denver +5,000 =20% more likely to get burn]), environment (snow reflects 70+%, water reflects 100% when sun overhead), vehicle. |
| What SPF to select? | above 15 SPF doesn't matter...not multiplied effect you would expect. |
| Very effective against UVB, does NOT prevent drug/chemical photosensitivity. Contact dermatitis possible. Not good for swimming and may stain clothing | PABA (Para-aminobenzoic acid) |
| Very effective against UVB, penetrate less than PABA, less staining, must reapply often. | PABA esters |
| Effective against UVA&UVB. Combined with PABA or PABA ester improves penetration and is superior to both. Beneficial in preventing drug/chemical photosensitivity rxns! | Benzophenones |
| "Extra" protection against burn; absorbs UVA; minimally effective. | Anthranilates |
| minimally effective, absorbs UVB spectrum. Used in combo with others. | Cinnamates and Salicylates |
| Describe main points of steroid biosynthesis cycle | When cortisol is decreased -> ACTH is increased -> ACTH released as peptide and triggers cholesterol synthesis -> ultimately creates aldosterone, cortisol, estradiol |
| T/F: steroids work immediately | F: Steroid effects build over time and work extremely well. Necessary to bridge gap upon starting steroid. Benedryl example of bridge drug. |
| Where are most steroids made? Where are others? | Adrenal cortex. Gonads. |
| Describe diurnal secretory pattern of Cortisol | Cortisol increases and peaks around 9 am, bottoms out around 10 pm. ACTH increases from 3 am on until you stimulated to get up again in the morning. |
| Describe steroid impact upon carbohydrates, protein, and lipid metabolism. | Increases gluconeogenesis, decreases peripheral utilization of glucose. (makes more glucose but turns down receptors) ->hyperglycemia. Promotes adipokinetic agent activity, mobilizes and redistributes fat ->atherogenesis |
| Describe steroid impact on electrolyte/water balance. What disease can be caused? | Aldosterone (mineralocorticoid effect): acts on kidney to increase sodium reabsorption. Addison's disease: autoimmune- Na+ loss, skin darkening, hypotension, hyponatremia, weight loss, shock. |
| Describe glucocorticoid CV system effects. | Prevent leaky capillaries bye restriction of permeability. Increases/maintains tone of arterioles, These small vessels support diastolic BP, so steroids will increase BP |
| Describe glucocorticoid CNS actions | Euphoric or depressive mood fluctuation, esp in elderly or children. Can be psychotic in nature. In spinal cord injury, high dose reduces damage but have inflammatory effects with injury of brain. Thus used in spinal cord injury but not brain injury. |
| Describe glucocorticoid anti-inflammatory effects | Increases lipcortins: prevent initial steps of forming prostaglandins, prostacyclins, thromboxane. |
| Describe glucocorticoid immunosuppressive and anti-allergic actions | suppresses all hypersensitivity and allergic rxns. Strong impact on immune response including transplant rejection. |
| Describe corticosteroid effects on growth and structure. | inhibit DNA synthesis and cell division. Retards growth of children, healing, impairs bone stability (activates osteoclasts, increased Ca2+ excretion/decreased absorption of Ca2+ in GI; risk of osteoporosis) |
| Describe corticosteroid effects on respiratory system | lifesaving in immune and pulmonary system. Single course improves postnatal lung function w/o deleterious consequences but will suppress their growth. NOT bronchodialtors (reduce inflammation, don't cause muscles to relax; foundation therapy for asthma) |
| Potency of Short acting glucocorticoids | Anti-inflammatory/salt retention: 1/1 |
| Potency of Intermediate acting glucocorticoids | Anti-inflammatory/salt retention 5/.1; more potent for anti-inflammatory but NO salt retaining: use for someone with HYPERTENSION |
| Potency of Long acting glucocorticoids | Anti-inflammatory/salt retention: 25/almost 0 AND dosing can be spread out. |
| Potency of mineralcorticoids | Anti-inflammatory/salt retention: .3/3,000 (aldosterone) THEREFORE if you turn off aldosterone, massive effect on salt retention. |
| Mineralcorticoid vs Glucocorticoid | ***Mineralcorticoid retains salt. Glucocorticoid is anti-inflammatory, minimal effect on salt retention*** |
| Basic guidelines for topical glucocorticoids | Penetration differs at different sites (high: thin skin- axilla, face; medium: limbs,trunk; low: palm, sole, elbow, knee. Occlusive dressings enhance absorption 10x. |
| Topical vehicles of choice | Lotions & creams: for exudative lesions Lotions, sprays & gels: for hairy regions Ointments: for chronic scaly lesions |
| Incidence of side effects of steroids are generally related to: | duration of therapy |
| Abrupt cessation of prolonged high dose can | lead to acute adrenal insufficiency (life threatening) ACTH will drop so much there will be deficit with cessation. Must taper doses down. |
| Why would you use a high dose steroid? Low dose? | H: life threatening condition. L: relieve pain or Sx |
| Describe Pulse therapy | Higher dose glucocorticoid for short time, then off, then back on. |
| Longer duration of therapy: | slower the withdrawal |
| Withdrawal guidelines 1) Short term burst 2) Weeks or more 3) Weeks to months | 1) don't need to taper 2) taper over a few days 3) taper gradually*** --can also become hyponatremic (low sodium) (another weakened response) |
| 4 indications for ongoing replacement therapies in Endocrine Disorders | 1) Acute adrenal insufficiency 2) Adrenocortical insufficiency 3) Adrenal insufficiency secondary to anterior pituitary disease 4) congenital adreanall hypoplasia |
| Intra-articular injection of steroids best for | arthritis |
| Steroidal benefits for renal disease | decrease capillary leakage |
| Steroidal benefits for Rheumatic carditis | in addition to salicylates, decrease valve inflammation |
| Steroidal uses in Collagen diseases | Lupus, pemphigus vulgaris, polyarteritis nodosa |
| Steroidal uses in Allergic diseases | Anaphylactic shock, blood transfusion reaction, hay fever |
| Steroidal uses in Bronchial asthma | Not routinely used acutely except in status asthmaticus. IV corticosteroids then oral dosing. For maintenance, inhaled steroids are preferred (Minimal HPA suppression) |
| Steroidal use in Ocular diseases | Outer eye & anterior segment - local application. Posterior segment - systemic use. Always consider immune suppression in cases of bacterial, viral, & fungal conjunctivitis. Check for herpatic eye lesion. |
| Steroidal use in Dermatological conditions | Pemphigus – The life saving therapy is steroids. Eczema, dermatitis & psoriasis respond well |
| Steroidal use in Diseases of intestinal tract | In ulcerative colitis, a hydrocortisone retention enema often provides control when other methods fail (not quite as well for Crohn’s…still used for exacerbations) |
| Steroidal use in cerebral edema | INCREASES RISK OF DEATH in TBI, helpful with neoplasm and parasites |
| Steroidal use in malignancy | Part of multi-drug regimens for acute lymphatic leukemia (children), chronic lymphatic leukemia (adult) |
| Steroidal use in liver diseases | Improves survival rates in active hepatitis ad hepatic necrosis. Reserved in alcoholic hepatitis until severe. Helpful in cirrhosis if no ascites. |
| Steroidal use in acute infectious diseases | Used in gram negative septicemia (can return BP ^), endotoxic shock (TSS), Tubercular meningitis, miliary tuberculosis, and all types (bacterial, viral, fungal, rickettsial, toxic) of encephalitis. Must be accompanied by definitive anti-microbial agents |
| Steroidal use in traumatic shock | Seem helpful, but no convincing experimental evidence |
| Diagnostic uses of Dexamethasone suppression test | Cushing's Syndrome. Locating ectopic sources of androgen production. Dexamethasone suppresses androgen from the adrenal cortex from ectopic sources such as tumors. |
| ACTH undetectable or low | Cortisol: not suppressed. Interpretation: Hypothalamus and pituitary turned off, but cortisol still being produced. |
| ACTH normal | Cortisol: not suppressed. Interpretation: Ectopic ACTH syndrome. Extensive evaluation warranted to detect a non-adrenal tumor (lung) secreting ACTH. |
| ACTH elevated | Cortisol: may be suppressed by high doses. Interpretation: Pituitary (tumor) Cushing syndrome probable (pituitary hyperplasia w/ ACTH secretion) |
| Possible adverse rxns for all steroids | Iatrogenic Cushings, hyperglycemia, myopathy, osteoporosis, retardation of growth, hypertension, CHF, superinfection, "moon face", "buffalo hump", euphoria, avascular necrosis of femoral head |
| Relative CONTRAs with steroids | Infxs, HTN, CHF, psychosis, peptic ulcer, DM, osteoporosis, glaucoma, pregnancy (prednisone MOSTLY safe [cleft lip]) |
Created by:
crward88
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