Topical Treatment Flashcards

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1
Q

intertriginous areas

A

-inguinal folds
-antecubital space
-maximum absorption-

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2
Q

preserving integrity of skin

A

-barrier
-anything removes water, lipids, proteins, from skin compromises function
-we treat to restore

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3
Q

topical therapies

A

-use of medicine directly on skin or mucosal surface
-stratum corneum is the rate limited barrier to “percutaneous drug delivery”
-drug penetration is inversely proportional to thickness of stratum cornea
-absorption is maximal over mucous membranes (eyelids scrotum intertriginous areas)

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4
Q

factors affecting absorption

A

-drug concentration
-thickness of skin and thickness of vehicle
-surface area
-occlusion
-hair follicles
-cutaneous circulation

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5
Q

composition of vehicles

A

-ointments- water in oil emulsion
-creams (aqueous creams)- oil in water emulsion
-gels- semisolid emulsion in alcohol base
-lotion/solutions- powder in water (some oil water)

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6
Q

topical therapies

A

-anti-microbials- dial soap, antibiotics, bleach baths
-anti-inflammatory agents- steroids and NSAIDs (voltarin)
-cleansers- cetaphil, cerave, dove soap…NOT IVORY SOAP
-moisturizers- cetaphil, lubriderm
-useful when there is need to target treatment area while avoiding systemic side effects

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7
Q

creams, lotion, ointments, and gels and solution

A

-restore water and lipids
-creams are generally thicker than lotions
-ointments are dense and oily
-best applied to damp skin (not wet)
-efficacy not necessarily dictated by cost
-gels are usually more drying and are used when emollients are not necessary
-solutions are best for hairy areas

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8
Q

vehicle: sequence of potency

A

-max -> min
-ointment
-cream
-lotion
-gel
-spray
-foam

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9
Q

ointment advantage

A

-best occlusive
-used in chronic, dry, brittle, lichenified dermatoses
-most potent effect
-fewer preservatives- less water, so micro-organisms cannot grow

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10
Q

ointment disadvantage

A

-difficult to spread and wash
-adherent to skin
-decreased evaporation/heat loss -> never put ointment on burn
-should not be used on weeping (exudates) lesions and intertriginous areas
-sticky and cosmetically unacceptable

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11
Q

lotions

A

-combination of liquids and powders
-less acute dermatoses
-can be drying
-should not be used on exudative lesions

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12
Q

creams

A

-semi solid emulsions containing lipids and water
-falls somewhere between an ointment and a lotion
-most people prefer consistency- less sticky less runny
-most prescribed
-contain preservatives
-if cream made reaction worse- think about allergy to preservatives

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13
Q

gels

A

-thickened lotion
-semi-solid clear base
-jelly like consistency
-tend to dry out when left on skin
-used to treat scalp and other hairy areas
-used on exudative inflammation (PI)
-can use on weeping lesions
-poison ivy

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14
Q

pros and cones of vehicles

A

-ointment- enhances penetration very well BUT greasy and hard to spread
-cream- easier to spread BUT may sting and acutely inflame skin
-solution- easy to use in hair BUT may sting in acutely inflamed skin, runny
-gel- easy to use in hair and mouth and penetration enhancer BUT alcohol base will sting inflamed skin and can dry skin

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15
Q

topical therapies powders

A

-cooling
-prevents friction
-absorbs moisture
-most useful in intertriginous areas
-do not use on oozing skin -> curst formation
-use for jock itch

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16
Q

topical therapies- baths

A

-whole or part of body is immersed in liquid
-widespread exudative leisons
-cleansing baths
-medicated baths
-duration limited to no more than 30 minutes
-temp 95-100 degrees
-use clorox for bad ezcema / infection

17
Q

steroids-inflamatory cascade

A

-immunosuppressive
-anti-inflammatory
-lipocortins- steroid induced inhibitor of arachidonic acid -> mediates anti-inflammatory action of steroids
-stops inflammatory cascade
-anti-proliferative
-factors to consider- disease location, amount and duration of steroid

18
Q

groups of steroids

A

-group 1-7 (weakest)

19
Q

group 1 steroids

A

-group 1- treat difficult inflammatory diseases -> plaque, psoriasis, hand eczema
-BID-TID for 2 weeks -> 1 week rest

20
Q

groups 2-7

A

-BID-TID and limited to 2-6 weeks
-careful when treating areas like face, intertriginous areas, scrotum -> absorption is much higher in these areas
-palms and soles are difficult to treat and require higher potency steroid -> usually 1 or 2

21
Q

occulsion

A

-can be helped to enhance absorption
-sweater through skin and now covering it -> softens stratum corneum
-creates moisture to soften stratum corneum
-children skin is more receptive to steroids and care should be taken to use lower potency creams and lotions
-diapers form occlusion
-only group 6-7 agents should be used in diapers are no more than 10 days
-avoid group 1 in pre pubertal children all together

22
Q

downside of steroids

A

-topical steroids have excellent safety record however some adverse reactions can occur
-potential side effects should be discussed with pt before prescribing:
-burning, itching, irritation, dryness, cause by vehicle
-hypertrichosis of face- hair growth
-hypo/hyper pigmentation
-milia/folliculitis after occlusion
-ocular hypertension/cataracts
-acne induced steroid use

23
Q

steroids continued

A

-rebound phenomenon- once you stop using it comes back
-skin atrophy- thinning
-striae- lines that look like stretch marks, red
-systemic absorption
-tinea incognito- makes fungal infections worse
-skin blanching from acute vasocontriction
-nonhealing leg ulcers (steroids retard the healing process) WHY??? -> steroids stop inflammatory cascade -> slows healing
-YOU CANT use steroids on areas of infection
-steroid rosecea
-perioral dermatitis
-thins skin - can see the vasculature

24
Q

class 1

A

-clobetasol 0.05%
-Cheetahs are Faster Than Humans

25
Q

class 2

A

fluocinonide 0.05%c

26
Q

class 4

A

triamcinolone 0.1%

27
Q

class 7

A

hydrocortisone 2.5%

28
Q

perioral dermatitis

A

-are you using retinae in the last 6 months?
-itchy
-can be caused by steroids
-tx- discontinue irritating agent

29
Q

when do we use steroids

A

-inflammatory and puritic conditions

30
Q

inflammatory cascade- pathogenesis and clinical findings

A

-immunocomplex at the site
-mast cells release histamine -> increase vessel permeability, vasodilation
-pro-inflammatory cytokines release -> chemotaxis (immune cells migrate to injury)
-disrupted endothelial cells release leukocytosis induced factors (b and t cells) -> increase WBC

31
Q

cardinal signs of the inflammatory response

A

-redness (rubor)
-heat (calor)
-pain (dolor)
-swelling (tumor)

32
Q

liquid nitrogen

A

-irritates the area and triggers the cascade
-triggers brain to send WBC to area
-creates inflammatory cascade to heal it
-body clears virus/warts on its own
-never give steroids for this -> blocks the cascade!!!

33
Q

steroids

A

-modify the function of epidermal, dermal cells, and leukocytes that are involved in inflammatory skin diseases
-after passing through cell membrane, they react with receptor proteins within the cell to form steroid receptor complex

34
Q

mechanisms of action for anti-inflammatory steroids

A

-suppress t-cell activation and cytokine production
-suppress mast cell degranulation
-decrease capillary permeability indirectly by inhibiting mast cells and basophils
-reduce expression of cyclooxygenase 2 and prostaglandin synthesis
-reduce prostaglandins, leukotriene and platelet activating factor levels by altering phospholipase A2 activity

35
Q

corticosteroids

A

-decrease number of eosinophil (apoptosis)
-decrease cytokines produced by t lymphocytes
-decrease number of mast cells
-decrease cytokines produced by macrophages
-decrease number of dendritic cells

36
Q

sunscreen

A

-chemical and physical blocker
-chemical sunscreens can be endocrine disrupters
-chemical sunscreens- degrade with heat
-physical- do not degrade