Exam 3 Material Flashcards

1
Q

atopic dermatitis

A

chronic skin disease characterized by itchy, inflamed skin
more common in males, white, higher socioecon class, and urban areas
strong genetic link

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2
Q

signs and symptoms of atopic dermatitis

A

red to brownish-gray colored patches that look like chapping
pruritus
small, raised vesicles which may leak fluid and crust over
thickened, cracked or scaly skin
raw, sensitive skin from scratching
secondary bacterial infections are common
Adults: hands/feet
Children: face/scalp

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3
Q

exacerbating factors of atopic dermatitis

A

exposure to allergens
long, hot baths or showers (dries skin out)
dry skin
stress
sweating
rapid changes in temp or low humidity
solvents, cleaners, soaps, or detergents
wool

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4
Q

pathophysiology of atopic dermatitis

A

genetic component:
1) genes encoding for epidermal or other epithelial structural proteins
2) genes encoding for the major elements of the immune system

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5
Q

FLG atopic dermatitis

A

encodes for profilaggrin->degrades to filaggrins-terminal differentiation of epidermis and formation of the skin barrier; natural moisturizers

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6
Q

FLG variants/deficiency

A

results in permeability barrier dysfunction: penetration of high MW allergens in pollens, microbes, food, etc
have more persistent disease, higher incidence of eczema herpeticum, greater risk of multiple allergies
-not exactly a pure correlation btwn FLG deficiency and eczema

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7
Q

genes for cytokines (AD)

A

TH1-suppress IgE
TH2-increase IgE->causes blood eosinophilia, increased total serum IgE, and increased growth and development of mast cells

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8
Q

features of AD pathophysiology

A

skin barrier dysfunction
immune deviation toward TH2
subsequent increased IgE

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9
Q

medication classes for treating AD

A

corticosteroids
calcineurin inhibitors
PDE-4 inhibitors
IL-4ra antagonist

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10
Q

psoriasis

A

chronic disease with recurrent exacerbations/remissions of thickened, red, scaly plaques
keratinocyte hyperproliferation and incomplete differentiation caused by cytokines released from infiltrating activated T cells

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11
Q

pathophysiology of psoriasis

A

T cell mediated systemic inflammatory disease
interaction btwn genetics and environmental influences
comorbidities are consequence of chronic inflammation
defects in epidermal cell cycle
genetic predisposition
immunologic disorder

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12
Q

psoriasis defects in epidermal cell cycle

A

normal: 13 days to divide skin cells and 26 to mature
Psoriasis: 1.5 days to divide and 4 days to mature
T cells contribute to the hyperproliferation of the epidermis
altered maturation of the epidermis occurs

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13
Q

immunologic disorder psoriasis pathophysio

A

keratinocytes encounter an antigen or undergo trauma
inflammatory triggers results in recruitment of T cells to site
histocompatibility complex->release of T cell cytokines->vasodilation and new capillary formation
T cell cytokines also cause further inflammation

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14
Q

contributing factors of psoriasis

A

climate
stress
infections
trauma
-koebner response
medications: lithium, Beta blockers

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15
Q

koebner response

A

lesions begin at previous clear sites on skin as a result of trauma
trauma=friction, venipuncture, bites, surgery, or pressure

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16
Q

medication classes for treating psoriasis

A

corticosteroids
calcineurin inhibitors
cytotoxic agents
T cell and cytokine suppressors
monoclonal antibodies: T cell inhibitor, TNFa inhibitor, IL-12/IL-13 inhibitor, IL-23 inhibitor, IL-17A inhibitor, JAK inhibitor
retinoids
Vit D analogs
PDE-4 inhibitor
phototherapy

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17
Q

pathophys of acne

A

increased androgen production both sexes (puberty)->follicular hyperkeratinization, increased sebum production, proliferation of P. acnes

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18
Q

follicular hyperkeratinization

A

causes skin cells to stick together

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19
Q

sebum production

A

sebaceous gland size/# and sebum production increases with an androgen surge at puberty

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20
Q

P. acnes

A

produces lipase->glyceride from sebum into free fatty acids, which irritate follicular walls
have an antigenic effect

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21
Q

formation of acne

A

skin cells stick together and are NOT shed
channel is plugged by a combo of skin cells and sebum
normal flow of sebum is blocked

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22
Q

exacerbating factors of acne

A

environmental and physical factors:
-high humidity or sweating
-acne mechanica
-occupational acne
-acne cosmetica
stress/emotions
hormones
acne medica mentosa
genetics
high glycemic index diet

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23
Q

acne mechanica

A

anything the occludes the skin or irritates it

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24
Q

occupational acne

A

excessive dirt, vaporized cooking oil, exposure to some industrial chemicals

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25
acne cosmetica
mild form of acne to comediogenic oils in cosmetics
26
medication classes for treating acne
keratolytics antibiotics retinoids
27
topical corticosteroids
treats psoriasis and AD low potency for face and long duration maintenance therapy medium potency for body and short term management
28
topical corticosteroids side effects
local skin reactions hypothalamic-pituitary adrenal axis suppression, infections, hyperglycemia, cataracts, glaucoma, and growth inhibition
29
retinoids MOA
drug binds to RAR (in the RAR-RXR complex), which then binds to RARE in the nucleus to activate gene transcription
30
retinoids pharmacodynamic effects
decreases proliferation, promotes differentiation, increases the turnover, reduces the cohesiveness anti-inflammatory and anti-proliferative reduces the thickness of the stratum corneum treats acne and psoriasis
31
tretinoin
acid form of Vit A (all-trans retinoic acid or ATRA) topical acne: more comedones during first 4-6 weeks and then optimal improvement in 8-12 weeks apply to dry skin
32
tretinoin side effects
blistering, peeling, crusting, burning, edema erythema and dryness tumorigenic potential of UV radiation->minimize sun exposure teratogenicity
33
adapalene
derivative of naphthoic acid topical retinoid more comedones during first 4-6 weeks and then optimal improvement in 8-12 weeks
34
adapalene side effects
erythema, scaling, dryness, pruritus, and burning
35
tazarotene
derivative of naphthoic acid topical psoriasis retinoid
36
tazarotene side effects
erythema, scaling, dryness, pruritus, and burning photosensitive no known systemic SEs
37
isotretinoin
PO for severe acne
38
isotretinoin pharm effect
decreases sebaceous gland size decreases sebum production reduces inflammation reduces keratinization
39
isotretinoin dermatological side effects
inflammation of the lips, epistaxis, itching skin rash, peeling, photosensitization
40
isotretinoin systemic side effects
arthralgia persistent headache: pseudotumor cerebri CNS: lethargy and fatigue; depression, suicidal ideation ophthalmic blood lipids TERATOGENIC
41
acitretin
PO and topical retinoid t1/2=49 hrs drug is still detectable in blood 1-3 years after discontinuation
42
acitretin pharm effect
reduces proliferation and enhances differentiation of keratinocytes does NOT suppress sebum production
43
acitretin side effects
dermatological ophthalmic pseudotumor cerebri TERATOGENIC
44
acitretin warnings
do NOT drink alcohol with this drug do NOT use any of the retinoids in patients with AD
45
calcipotriene MOA
exerts its effect through VDR->drug-RXRa complex->increases expression of genes, which improves psoriatic plaques
46
calcipotriene pharm effect
inhibits proliferation and promotes keratinocyte differentiation decreases inflammation by decreasing inflammatory cytokine release
47
calcipotriene side effects
topical: burning, itching, erythema, mild photosensitivity systemic: hypercalcemia and hypercalciuria
48
calcineurin inhibitors
used to treat AD and psoriasis reduce extent and severity of symptoms inhibit activation of T cells and mast cells, blocking the production of proinflammatory cytokines and mediators->immunosuppressants
49
calcineurin inhibitors MOA
inhibit the production of IL-2 needed for T cell proliferation by inhibiting normal calcineurin activity
50
topical calcineurin inhibitors pharmacodynamics
pimecrolimus and tacrolimus
51
topical calcineurin inhibitors pharmacodynamics
inhibit the activation of key cells involved in AD, including T cells and mast cells, blocking the production of proinflammatory cytokines and mediators relieves pruritus tacro: decreases # and costimulatory ability of epidermal dendritic cells pime: distribute to the skin as opposed to the systemic circulation
52
topical calcineurin inhibitors side effects
transient discomfort at application site potential for local skin carcinogenesis->rec sun protection potential for systemic effects if high blood levels are reached
53
oral calcineurin inhibitor
cyclosporine (treats psoriasis)
54
oral/topical calcineurin inhibitors BBW
increased risk of lymphoma and other malignancies increased susceptibility to bacterial, viral, fungal, and protozoal infections
55
cyclosporine and tacrolimus side effects
nephrotoxicity, HTN, upper resp tract infections, cough and headache
56
cyclosporine only side effect
gingival hyperplasia
57
tacrolimus only side effect
neuropathes
58
cyclosporine drug interactions
with drugs metabolized by CYP3A4
59
PDE-4 inhibitors MOA
nonsteroidal, anti-inflammatory cAMP is increased, get relaxation of smooth muscle and inhibition of inflammatory cells
60
PDE-4 inhibitors
crisaborole apremilast
61
crisaborole
mild to moderate AD
62
crisaborole adverse effects
application site pain hypersensitivity
63
apremilast
treats psoriasis PO
64
apremilast side effects
diarrhea, nausea, and headache use cautiously in depressed patients weight loss do NOT use with strong CYP3A4 inducers
65
keratolytics
benzoyl peroxide sulfur salicylic acid
66
benzoyl peroxide MOA
keratolytic antimicrobial activity against P. acnes peeling and comedolytic effects penetrates stratum corneum or follicular openings then metabolized to benzoic acid
67
benzoyl peroxide pharm effect
loosens keratinocytes increases turnover rate prevents closure antibacterial activity against P. acnes
68
benzoyl peroxide side effects
skin irritation potent contact sensitizer
69
benzoyl peroxide cautions
AVOID contact with the eyes and mucous membranes oxidant->bleaches hair or colored fabrics
70
sulfur MOA
mild keratolytic bacteriostatic properties
71
sulfur pharm effect
sulfur is reduced to H2S inside the keratinocytes causes inflammation which promotes peeling and unblocking of plugs
72
sulfur side effects
redness, skin irritation, peeling, comedogenic sulfur odor
73
salicylic acid MOA
may solubilize cell surface proteins that keep the stratum corneum intact, thereby resulting in desquamation of keratotic debris
74
salicylic acid pharm effect
promote the shedding of the stratum corneum range from peeling to desquamation
75
salicylic acid concentration
3-6% skin conditions: dandruff, acne, and psoriasis 6%-may cause skin damage up to 40%: wart and corn removal
76
salicylic acid side effects
irritation and inflammation of normal skin ulceration with high conc urticaria, anaphylaxis, erythema during allergic rxn salicylism->salicylate poisoning
77
salicylic acid caution
must be careful when use on extremities of diabetes or patients with peripheral vascular disease
78
tetracyclines class
sarecycline minocycline doxycycline tetracycline
79
tetracyclines class MOA
inhibit protein synthesis by irreversible binding to 30S subunit of bacterial ribosome, blocking aminocyl-tRNA binding to acceptor site on mRNA ribosome complex enter microorganisms by passive diffusion and active transport
80
tetracyclines class pharm effect
broad-spectrum bacteriostatic antibiotics
81
tetracycline side effects
GI: N/V/D pseudomembranous colitis bones and teeth are discolored and growth is impaired in young photosensitivity increased incidence of superinfections
82
clindamycin MOA
inhibits bacterial protein synthesis by attaching to the 50S subunit of the bacterial ribosome
83
clindamycin pharm effects
bacteriostatic
84
clindamycin PO side effects
pseudomembranous colitis N/V/D impaired liver function neutropenia-rare
85
clindamycin topical side effects
still has a risk of pseudomembranous colitis water based: well tolerated and less likely to cause irritation hydroalcoholic vehicle: drying and irritation resistance is now a problem
86
erythromycin and azithromycin MOA
macrolide antibiotic that attaches to the 50S ribosomal unit and prevents translocation
87
erythromycin and azithromycin pharm effect
bacterostatic
88
erythromycin and azithromycin PO side effects
N/V/D and epigastric pain has MANY DIs
89
erythromycin and azithromycin topical side effects
burning and drying (esp with benzoyl peroxide) resistance is a problem
90
trimethoprim MOA
inhibits bacterial production of tetrahydrofolic acid from dihydrofolic acid by reversibly inhibiting dihydrofolate reductase
91
sulfamethoxazole MOA
inhibits bacterial synthesis of dihydrofolic acid by competing with PABA
92
dapsone
antimicrobial treats leprosy and acne
93
dapsone MOA acne
anti-inflammatory activity neutrophils and neutrophil products may be a site of action for dapsone in reducing inflammation
94
metronidazole MOA
is unknown, but it may relate to the inhibitory effects on Demodex brevis (rosacea) or the drug may act as an anti-inflammatory agent by direct effect on neutrophil cellular function (acne)
95
metronidazole side effects
water based: dry skin, redness, watering of eyes cream and lotion may be better tolerated
96
cytotoxic agents
coal tar anthralin shale tar selenium sulfide and zinc pyrithione
97
Coal tar MOA
antiproliferative and anti-inflammatory crosslinks with DNA to inhibit cell division for antimitotic action
98
Coal tar pharm effects
may be anti-inflammatory and antipruritic affect may be due to placebo effect
99
Coal tar side effects
irritation, stinging, and burning folliculitis contact dermatitis photosensitizing carcinogenic systemic side effects do NOT occur will stain light skin and hair unpleasant odor
100
Coal tar caution
not studied in preg, breastfeeding, children AVOID products in AD with vesiculation and oozing
101
anthralin MOA
exact MOA not known may have a direct antiproliferative effect on epidermal keratinocytes by affecting mitochondria reducing mitotic activity prevents T cell activation
102
anthralin pharm effect
suppresses hyperplastic keratinocyte cell growth
103
anthralin side effects
local irritation erythema on normal skin around lesions severe conjunctivitis with eye contact systemic SEs do NOT occur will stain skin, hair, clothes
104
anthralin use
SCAT: applied to thick plaques for < 2 hr and then wiped off; zinc oxide applied to normal skin severe skin irritation possibility on face and intertriginous
105
shale tar
cytotoxic but MOA is unknown gives symptomatic relief less irritating and has NO photosensitizing activity treats AD, rosacea, and acute otitis externa
106
selenium sulfide and zinc purithione
cytostatic and antifungal activity MOA not known
107
t cell suppressor meds
methotrexate mycophenolate
108
methotrexate MOA
inhibits dihydrofolate reductase (DHFR)->causes cell death direct anti-inflammatory benefits, and a lot of other things
109
methotrexate pharm effect
reduces keratinocyte hyperproliferation-plaque formations reduces the # of T cells
110
methotrexate side effects
cumulative liver toxicity abortifacient and teratogenic
111
mycophenolate MOA
inhibitor of T and B cell activation through inhibition of IMPDH, thereby reducing GMP synthesis preferentially inhibits type II
112
mycophenolate pharm effect
reduces the # of B and T cells anti-inflammatory
113
mycophenolate side effects
bone marrow suppression, GI upset, flu-like symptoms
114
monoclonals and small molecule inhibitors drugs
abatacept dupilumab secukinumab ixekizumab broadalumab ustekinumab guselkumab tildrakizumab-asmn rsankizumab etanercept infliximab adalimumab golimumab certolizumab pegol tofacitinib ruxolitinib upadacitinib
115
abatacept MOA
blocks 2nd signal needed for T cell activation inhibits T cell activation by binding to CD80/86 on APCs; CD28 on T cells therefore cannot bnd and stimulate the T cell
116
dupilumab MOA
binds to IL-4ra->inhibits IL-4 and 13 to decrease IgE synthesis
117
dupilumab
moderate to severe AD SQ
118
dupilumab adverse effects
generally mild nasopharygnitis and headache injection site rxns, conjunctivitis, blepharitis, PO herpes, keratitis, eye pruritus, and dry eye
119
IL-17 stimulation
increases keratinocyte expression of inflammatory cytokines plaque psoriasis
120
IL-17 inhibitors
secukinumab ixekizumab brodalumab
121
secukinumab MOA
IgG1 antibody that binds the IL-17A cytokine, inhibiting its interaction with the IL-17A receptor
122
secukinumab pharm effect
reduces the # and size of plaques
123
secukinumab side effects
risk for infection evaluated for TB nasopharyngitis may exacerbate Crohn's
124
ixekizumab MOA
humanized IgG4 antibody against IL-17A cytokine
125
brodalumab MOA
IgG2 antibody that blocks the release of proinflammatory cytokines and chemokines by selectively binding to IL-17ra
126
ustekinumab MOA
IL-12 and IL-23 antagonist; suppresses formation of proinflammatory TH1 and TH17 cells
127
ustekinumab pharm effect
reduces the # and size of the plaques
128
ustekinumab side effects
upper resp tract infections serious allergic rxns serious infections DO NOT give live vaccines malignancy
129
guselkumab MOA
IgG1lambda antibody inhibits release of proinflammatory cytokines and chemokines through binding IL-23, which inhibits the interaction of the subunit with IL-23 receptor
130
tildrakizumab-asmn MOA
IgG1/k antibody inhibits release of proinflammatory cytokines and chemokines through binding IL-23, which inhibits the interaction of the subunit with IL-23 receptor
131
IL-23 inhibitor
guselkumab tldraizumab-asmn risankizumab
132
risankizumab MOA
humanized IgG1 antibody inhibits release of proinflammatory cytokines and chemokines through binding IL-23, which inhibits the interaction of the subunit with IL-23-proinflammatory effect
133
risankizumab
SQ and IV moderate to severe plaque psoriasis
134
risankizumab side effects
fatigue, nasopharyngitis, headache, skin rashes, and local injection rxns severe infections, reactivation of TB, and skin cancer
135
TNFa inhibitors MOA
bind to TNFa, preventing it from interacting with TNF receptors on inflammatory cells reduces the # and size of the plaques
136
TNFa inhibitors BBW
increased risk for developing serious infections that may lead to hospitalization or death->lymphoma, malignancies
137
TNFa inhibitors drugs
etanercept infliximab adalimumab golimumab certolizumab pegol
138
etanercept
TNFa inhibitor fusion protein; binds to TNF, making it inactive and preventing it from interacting with the cell-surface TNF receptors that would lead to cell activation
139
etanercept side effects
rare local injection site reactions pancytopenia and neurologic demyelinating syndromes
140
infliximab
chimeric antibody IgG1 binds to TNF and prevents its interaction with TNF receptors on inflammatory cells TNFa inhibitor
141
infliximab side effects
antibodies develop risk of infusion rxns antibodies against drug may reduce efficacy increased risk of infection possible autoantibodies and lupus-like syndrome
142
adalimumab
human IgG1 antibody to TNF SQ TNFa inhibitor
143
adalimumab side effects
less antigenic local injection site rxns increased risk for infections
144
golimumab
humanized antibody to TNFa
145
certolizumab pegol
recombinant Fab fragment of humanized anti-TNF-a antibody TNFa inhibitor
146
certolizumab pegol side effects
upper resp, rash, and UTIs
147
JAK inhibitors MOA
inhibits the production of inflammatory cytokines through the inhibition of JAK
148
JAK inhibitors drugs
tofacitinib ruxolitinib upadacitinib
149
tofacitinib MOA
inhibits the production of inflammatory cytokines through JAK inhibition
150
tofacitinib BBW
severe infection, lymphoma, and malignancies; caution in patients who are at high risk for G perforation
151
ruxolitinib MOA
JAK1 and JAK2 inhibitor
152
upadacitinib MOA
we don't know what selectivity of this drug for JAK inhibitors
153
methoxsalen MOA
PUVA combine UVA light intercalate into the DNA strand stimulate melanocytes and induce antiproliferative, immunosuppressive, and anti-inflammatory effects
154
methoxsalen pharm effect
normalizes # and arrangement of keratinocytes reorganizes cutaneous blood vessels cytotoxic to T cells increases melanin pigmentation
155
methoxsalen side effects
pruritus, nausea, erythema and blistering, hyperpigmentation, increased skin aging, increased risk of skin cancer, cataracts
156
UVB
280-320 nm can cause sunburn, skin carcinoma, and premature aging of skin produces vitamin D3 in the skin
157
UVA
320-400 nm able to penetrate further into dermis than UVB radiation no erythema, but still has a role in skin cancer and causes aging
158
factors that affect tanning
time, clouds, reflection (snow, water, sand), location, clothing, thickness of the epidermis and stratum corneum, pigmentation of the skin
159
immediate pigmentation
pigment darkening starts 5-10 min after exposure lasts 24-48 hrs
160
delayed pigmentation
takes about 48-72 hrs to develop after exposure peaks at 7-10 days and lasts weeks to months
161
sunburn
histamine, cytokines, and prostaglandins are released symptoms: mild erythema, tenderness, and edema severe sun burns: 2nd degree burn with blisters; fever, chills, weakness, and shock
162
minimal erythemal dose (MED)
minimal single dose of UV radiation that produces clearly marginated erythema in the irrradiated site
163
sun protection factor (SPF)
personal time to get 1 MED measure of UVB protection and does NOT provide info regarding UVA coverage
164
the higher the SPF
less likely to burn longer time that can be spent in the sun
165
broad spectrum
both UVB and UVA
166
substantivity
how well does product stick to skin
167
best substantivity
waterproof, water-resistant products, sweat-resistant
168
sunblocks MOA
inorganic particulates that scatter or reflect visible, UV, and infrared radiation
169
sunblocks uses
prominently exposed areas like nose and ears used when cannot or control sun exposure
170
sunblocks products
zinc oxide and titanium oxide; broad spectrum
171
sunblocks side effects
may occlude pores causing milaria, folliculitis, or acne may stain clothing
172
sunblocks other facts
not easily removed with water, but melts in hot sun protection decreases after 2 hrs of direct sun
173
sunscreens MOA
organic agents (chemical blockers) that absorb UV radiation n the UVB or UVA ranges, then convert it to heat energy may be combo of products
174
hydroxy acids
keratolytics glycolic acid (GA) salicylic acid (SA)
175
glycolic acid (GA) chem
an a-hydroxy acid hydrophilic acid higher conc for deeper skin peels
176
salicylic acid (SA) chem
increase hydration-low pH causes lower skin layers to swell, soften and desquamate more lipophilic than glycolic acid
177
hydroxy acids SARs
COOH group(s) most possess OH on alpha-C R-mostly alkyl
178
sulfur chem
monotherapy or mixtures S reacts with cysteine to produce H2S which degrades keratin
179
benzoyl peroxide
pH lowering and free radicals is absorbed by skin and forms benzoic acid via ester hydrolysis
180
retinoids actions
anti-inflammatory, antiproliferative, decrease sebum production, teratogenic
181
1st gen retinoids
non-aromatics tretinoin isoterinoin
182
tretinoin chem
1st retinoid (non-aromatics) for acne all-trans retinoic acid
183
isotretinoin chem
13-cis retinoic acid geometric isomer of tretinoin 1st gen retinoids (non-aromatics)
184
acitretin chem
2nd gen retinoid (mono-aromatics) active form of etretinate via ester hydrolysis
185
3rd gen retinoids
poly-aromatics adapalene trifarotene tazarotene lipophilic low systemic absorption
186
azelaic acid chem
C9 bi-carboxylic acid anti-inflammatory agent
187
clindamycin chem
lincomycin topical
188
erythromycin chem
macrolide-macrocyclic lactone poor PO absorpton unstable @ pH 4 or lower structural modifications (acid salts and esters) -increases H2O and lipid solublities
189
tetracycline chem
broad spectrum chealation: metals, insoluble salts absorption affected by food t1/2=8.5 hrs
190
doxycycline and minocycline chem
food does NOT affect absorption are lipophilic and longer acting -doxy t1/2=11-13 hrs -mino t/12=14-22 hrs cross reactivities due to structure similarity
191
emollients chem
mostly H2O emulsions (prevents skin H2O loss)->decrease scaling petrolatum lanolin dimethicone cyclomethicone
192
coal tar chem
mixture of organic molecules may be used with YVB is photosensitizing
193
shale tars and wood tars chem
non-photosensitizer
194
anthralin or dithranol chem
hydroxyanthrone Lassar's paste antiproliferative autooxidation to produce anthrayl radicals and super oxide anion
195
psoralens chem
furanocourmarins + UVA=PUVA crosslinking of base pairs (intercalation) and decreases DNA synthesis
196
glucocorticoid potency rankings
chem structure delivery vehicle % conc n formulation
197
calcineurin inhibitors chem
decrease release of inflammatory cytokines from mast cells pimecrolimus-higher skin protein binding tacrolimus-able to reach systemic circulation macrocyclic lactones
198
methotrexate chem
antiproliferative-competitvely inhibits DHFR->decreases DNA/RNA synthesis bc decrease n THF immunosuppressant and anti-inflammatory
199
Methotrexate SAR
pteridine ring (should remain aromatic) PABA glutamic acid aromatic N-alkylation decreases activity N-CH3-essential for activity
200
cyclosporin chem
11 aa cyclic peptide prodrug immunosuppressant activated by complexation with cyclophilin receptor inhibits calcineurin phosphatase and T cell signaling highly inactivated by CYP3A4
201
mycophenolate chem
prodrug immunosuppressant-rapidly forms MPA after PO or IV inhibitor of IMPDH inhibits T and B cells proliferation activated by ester hydrolysis to MPA inactivated by phenolic glucuronidation to MPAG
202
crisaborole chem
benzoxaborole soft drug PDE-4 inhibitor (higher cAMP and decreases inflammatory cytokines) rapid metabolism limits systemic exposure to crisaborole
203
ruxolitinib chem
pyrrolopyrmidine JAK inhibitors
204
upadacitinib chem
imidazopyrrolopyridine JAK inhibitors
205
hydroquinone chem
topically for whitening or depigmentation of aged spots inhibits melanin biosynthesis via tyrosinase inhibition protect drug from light and O2
206
a-OHs acids (AHAs)
promote dead skin cells removal and stimulate collagen production glycolic, lactic, tartaric, malic, citric acids
207
hyaluronic acid (HA)
endogenous mucopolysaccharides non-antigenic and non-immunogenic forms a viscoelastic film that maintains skin moisture hygroscopic MW influences skin penetration to re-est HA content -high MW: increase time stayed on skin
208
scalp FTU
3
209
face and neck FTU
2.5
210
one hand (front and back) including fingers FTU
1
211
one arm including entire hand FTU
4
212
elbows FTU
1
213
both soles FTU
1.5
214
one foot including toes FTU
2
215
one leg including foot FTU
8
216
buttocks FTU
4
217
knees FTU
1
218
trunk both sides FTU
14 (7 FTU each side)
219
atopic dermatitis risk factors
personal or fam history of AD -atopic triad -atopic march loss of function mutation in FLG gene living in an urban an environment smaller fam size higher level of parental edu
220
atopic triad
allergic rhinitis asthma AD
221
atopic march
dry skin->eczema->food allergies->rhinitis/nasal allergies->asthma
222
atopic dermatitis triggers
irritants allergens environment personal factors
223
irritants AD triggers
airborne-tobacco smoke, air pollution cosmetics, fragrance, astringents irritating soaps/scrubs/detergents dyes/preservatives
224
allergens AD triggers
food clothing aeroallergens
225
environment AD triggers
extreme temps low humidity
226
personal factors AD triggers
stress excessive skin washing and sanitizing
227
AD clinical presentation infants (0-2 years)
erythematous, popular rash that tends to ooze face, scalp, trunk, arms, and legs onset: 3-6 months, majority by 1
228
AD clinical presentation childhood (2-puberty)
dry, flaky, rough, cracked skin, crusting, lichenification face, creases of the neck, elbows, wrists, knees, ankles majority by 5
229
AD clinical presentation adulthood
more diffuse with underlying erythema, dry, scaly skin, lichenification less common on face; more common on the hands, neck, inner elbows, back of knees, and ankles may have resolution of disease
230
mild SCORAD score and characteristics
< 25 areas of dry skin, infrequent itching (with or without small areas of redness); little impact on everyday activities, sleep, and psychosocial wellbeing
231
moderate SCORAD score and characteristics
25-50 mild characteristics with frequent itching, moderate impact on everyday activities, sleep
232
severe SCORAD score and characteristics
> 50 widespread areas of dry skin, incessant itching, redness, thickening, bleeding, oozing, severe limitation to activities, and nightly loss of sleep
233
acute AD
acutely inflamed papules, vesicles, exudate, and crusts
234
subacute AD
dry, inflamed papules, patches, or plaques
235
chronic AD
lichenified papules or plaques, fine scale, hypo/hyperpigmentation
236
AD complications
sleep disturbances impact quality and family's quality of life skin infections -S. aureus -prone to infections with HSV depression
237
nonpharm treatments of AD
bathing practices gentle cleansers wet wrap soft cotton clothing avoid known triggers decrease stress
238
AD bathing practices
suggest 10 min lukewarm (tepid) bath, use gentle cleansers, gentle towel dry pat -may add oatmeal or baking soda -may add bleach to prevent bacterial infections occlusive moisturizers
239
OTC moisturizers for AD
petroleum containing ceramide containing urea containing emollients
240
petroleum containing moisturizers
occlusive, can be greasy, uncomfortable aquaphor eucerin lubriderm
241
ceramide containing moisturzers
creams, provides barrier cerave aveeno eczema therapy
242
urea containing moisturizer
humectant carmol, lac-hydrin side effects: burning, stinging, irritation on broken skin
243
emollients moisturizers
less effective apply 3x a day or more, after bathing/washing cetaphil lotion, keri original, neutrogena lotion
244
AD OTC self-care follow up
if does not improve or worsens after 2-3 days of self-treatment, refer to a physician if atrophy occurs, discontinue and refer
245
pharm treatments of AD
topical corticosteroids topical calcineurin inhibitor topical PDE-4 inhibitor monoclonal (IL-4) antagonist injection systemic immunosuppressants
246
mild AD pharm treatment
basic management -skin care -antiseptic measure->antibiotics, if needed -trigger avoidance
247
moderate AD pharm treatment
basic management + topical anti-inflammatory medication -maintenance TCS -maintenance TCI (pimecrolimus, tacrolimus) -crisaborole
248
severe AD pharm treatment
basic management + referral to AD specialist -phototherapy -dupiblumab -systemic immunosuppressants -consider acute treatment
249
topical corticosteroids max duration
max 3-7 days or until flare up is cleared, but not apply for longer than 2 weeks
250
potencies of topical corticosteroids
ointment>creams>lotions>solutions>gels>sprays
251
topical calcineurin inhibitors counseling points
apply to clean and dry area apply a thin layer and rub in gently until med vanishes do not bathe, shower, or swim right after application store in cool, dry, room temp location do NOT use in children < 2 years response in weeks, continue to apply (1-8 weeks)
252
topical corticosteroids counseling points
apply to clean and dry area apply a thin layer and rub in gently until med vanishes store in cool, dry, room temp location do not apply for longer than 2 weeks
253
pimecrolimus (elidel)
mild-moderate eczema >2 years reduces incidence of flares apply 2x daily
254
tacrolimus (protopic)
moderate-severe eczema > 2 years apply 2x daily to affected skin
255
PDE-4 inhibitor crisaborole (eucrisa)
apply to clean and dry area apply a thin layer and rub in gently until med vanishes do not bathe, shower, or swim right after application store in cool, dry, room temp location
256
crisaborole (eucrisa)
apply a thin layer 2x daily for mild to moderate eczema treat flares > 3 months only when a steroid not appropriate or as an adjunct therapy
257
monoclonal antibody IL-4 antagonist
dupilumab (dupixent)
258
dupilumab (dupixent) counseling points
clean and dry admin site area inject at a 90 deg angle into thigh or lower abdomen, may administer in upper arm rotate injection sites store in fridge, allow solution to reach room temp for 30-45 min before admin
259
dupilumab (dupixent) dosing
adult: 600 mg LD, followed by 300 mg every other week children (6-17): weight based dosing
260
tralokinumab
IL-13 inhibitor moderate to severe AD not controlled with or unable to use topical therapy alternative to dupilumab (dupixent) adverse events: ocular adverse events, upper resp tract infections, injection site rxns
261
JAK inhibitors for AD
moderate-severe abrocitinib, upadactinib, ruxolitinib
262
JAK inhibitors BBW
serious infections, mortality, malignancies, MACE, thrombosis
263
diaper rash prevention-infants
diaper changing freq disposable diapers cleaning with every change barrier cream application breastfeeding
264
diaper dermatitis signs and symptoms
red in patches, red to bright red, shiny, wet-looking patches and lesions
265
incontinence associated dermatitis prevention-adults
cleansing routine skin hydration barrier cream application pressure sore prevention good nutrition
266
diaper/incontinence dermatitis prevention and nonpharm treatment
ABCDE air barrier cleansing diaper education
267
diaper/incontinence dermatitis prevention and pharm treatment
apply skin protectants -provides physical barrier and lubrication to skin -apply liberally to skin in diaper/perineal area->cover red areas with product -can continue to use after rash heals to prevent recurrence
268
skin protectant examples
zinc oxide 1-40% petrolatum 30-100% combo examples
269
diaper dermatitis cautions
diaper area is a significant portion of baby's BSA->may topical products lead to systemic side effects DO NOT USE: -topical antifungals, topical antibacterials, topical anesthetics, hydrocortisone or other topical corticosteroid
270
diaper dermatitis follow up
if improved but not healed, after 7 days: continue treatment until healed if not healed, improved, or worsened after 7 days: refer to a physician
271
exclusions for self care of diaper dermatitis
lesions for > 7 days secondary infection broken skin oozing, bleeding, pus behavioral changes comorbidities
272
non-inflammatory acne lesions
normal follicle blackhead whitehead
273
inflammatory acne lesions
papule pustule nodule/cysts
274
type 1 mildly clear acne
rare noninflammatory lesions with no more than 1 small lesion
275
type 2 mild acne
some noninflammatory lesions no more than a few inflammatory lesions (papules and pustules only, no nodules) minimal scarring
276
type 3 moderate acne
many noninflammatory lesions some inflammatory lesions no more than 1 nodules mild scarring possible
277
type 4 severe acne
many noninflammatory and inflammatory lesions no more than a few nodular lesions moderate to extensive scarring
278
acne risk factors
age: 12-20 years old cosmetics family history hydration: humidity and sweating irritation: local skin friction medications
279
causative medications for acne
hormones neuropsych drugs vitamins cytostatic agents immunomodulating agents anti-tuberculin drugs halogens
280
acne complications
anxiety depression scarring
281
considerations for acne management
grade and classify acne lesions presence of scarring patient age family history adherence potential treatment preferences skin type cost response to previous therapy psychologic effects
282
acne exclusions for self-treatment
severe acne possible rosacea exacerbating factors: comedogenic drugs
283
nonpharm treatment for acne
cleanse skin w/ mild soap or non-soap cleanser 2x a day extraction strips or professional extraction UV light/laser therapy diet changes stay well hydrated
284
diet changes for acne
encourage low glycemic index foods limit dairy products potential benefit: fish oil, probiotics, oral zinc mediterranean diet
285
mildly clear acne 1st line treatment
+/- BP alone or essential oils
286
mild acne 1st line treatment
topical single treatment -BP or top retinoid -or top combo treatment (BP + top antibiotic OR BP + top retinoid OR BP + top retinoid + top antibiotics)
287
mild acne 2nd line treatment
may add (if not on): top retinoid or BP or consider alternate retinoid or consider top dapsone
288
moderate acne 1st line treatment
top combo treatment: BP + top retinoid or BP + top antibiotics or BP + top retinoid + top antibiotics OR oral antibiotics + top retinoid + BP or oral antibiotics + top retinoid + BP + top antibiotics
289
moderate acne 2nd line treatment
consider alternate combo treatment OR consider change in oral antibiotics or add oral contraceptive or oral spironolactone (females only) or consider oral isotretinoin
290
severe acne 1st line treatment
oral antibiotic + top combo treatment: oral antibiotic + BP + top retinoid OR oral antibiotic + BP + top antibiotic OR BP + top retinoid + top antibiotic OR oral isotretinoin
291
severe acne 2nd line treatment
consider change in oral antibiotics or add combined oral contraceptive or oral spironolactone (females only) or consider oral isotretinoin
292
benzoyl peroxide
used alone (mild-moderate) or in combo with oral/topical antibiotics (moderate-severe) efficacy as soon as 5 days, lesion severity and # SE: skin irritation and will stabilize within 1-2 weeks
293
retinoids
efficacy as soon as 5 days SE: skin irritation and will stabilize within 1-2 weeks apply at night after washing face or other affected areas DO NOT USE with sulfur, resorcinol, salicylic acid, or vitamin C products separate use from BP > 12 years to use use with moisturizer/sunscreen
294
alpha hydroxy acids
glycolic, lactic, citric acids exfoliate non-inflammatory lesions -can be used as a chem peel to reduce acne scarring wait 2-4 weeks btwn peels use sunscreen
295
beta hydroxy acid-salicylic acid
SE: drying, photosensitivity apply 1-2x daily as a cleanser or top gel max effectiveness and duration of use for 4-6 weeks use sunscreen
296
complementary therapy for acne
tea tree therapy frankincense oil provide anti-inflammatory benefits
297
oral antibiotics for acne
minocycline/doxycycline sarecycline clindamycin sulfamethoxazole/trimethoprim erythromycin/azithromycin NEED TO USE WITH BP, NOT MONOTHERAPY FOR ACNE
298
minocycline/doxycycline
tetracycline eradicate P. acnes photosensitivity, fetal harm (avoid during preg), may cause permanent discoloration to teeth if used < 12
299
sarecycline
tetracycline derivative nonkodular moderate to severe acne
300
erythromycin/azithromycin
macrolide less commonly used due to resistance: topical or oral
301
oral antibiotic use not
use for the shortest possible duration to minimize development of bacterial resistance; re-evaluate at 3-4 months
302
combo oral contraceptives
for women who also want contraception should be > 14 years old or over 2 years since period starts should be non-smoker < 35 years
303
combo oral contraceptives benefits
contraception decreased hyper androgen symptoms decrease risk of colorectal, ovarian, and endometrial cancers
304
combo oral contraceptives increased risks
venous thrombotic events (clots) myocardial infarction breast or cervical cancer osteoporosis/decreased bone mass
305
isotretinoin treats
severe refractory nodular acne acne causing significant physiological/psychological scarring
306
isotretinoin BBW
birth defects, must not be used by women who are preg or may become preg
307
isotretinoin side effects
dry nose, eyes, mouth, inflammation of lips musculoskeletal, ophthalmic effects, headache, CNS effects mood disorders, depression, suicidal ideation
308
efficacy and monitoring for acne
patient: daily pharm: every 4-8 weeks on therapy