Med classes- Skin Quiz 2 Flashcards

1
Q

What are the 2 layers of the skin and what do they do?

A
  1. Epidermis: is the protective layer—its outer most surface (the stratum
    corneum) contains lipids & keratin
  2. Dermis: lies between the epidermis and SQ fat layer—it is composed of
    connective tissue and contains sweat glands, sebaceous glands, hair follicles and vessels
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2
Q

Key factors in a skin exam

A

-Perform in well-lit room
-Use hand-held light for illumination
-Wood’s lamp helpful for fluorescing certain types of lesions
-Skin scrapings may be needed
-KOH (potassium hydroxide) and/or 5% acetic acid prep may be needed for certain pathogens
-Assess appearance of patient and VS
-With ANY suspicious lesion, skin cancer must be ruled out

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3
Q

What to know about steroids on the face

A

-Use lowest strength possible,
starting with a potency that is less than the standard dosage

-NO fluorinated steroids on the face or perineum—can cause striae and
permanent thinning of the tissue

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4
Q

Why does the “vehicle” choice matter in terms of skincare?

A

-Therapeutic effect can depend on whether the vehicle is water or oil based

-The efficacy of the topical agent can depend on the thickness of the stratum corneum, drug concentration and permeability, and frequency of application

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5
Q

What does the sun do to our skin?

A

-Maintains the body’s supply of Vitamin D (positive effect)

-The photoreceptors on the skin [forearms/legs], when uncovered and without sunscreen absorb Vitamin D2 from the sun rays
-This form of Vitamin D is converted to Vitamin D3 in the kidney and then to its active form in a second renal
conversion

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6
Q

What are the two main types of UV radiation?

A
  1. UVB [bad]: are the rays that burn us, cause wrinkling and skin cancers
  2. UVA can cause some wrinkling and with many decades of “lead time” may manifest itself as BCC later in life

-NOTE: Small amounts of UV exposure daily can help maintain our bone and teeth stability

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7
Q

Derm Terms to know

A
  1. MED—minimal erythemal dose—minimum amount of UV radiation that produces evident erythema
    after one exposure
  2. SPF—describes the amount of UVB protection (i.e., protection against sunburn) that a sunscreen provides. SPF values are not related to time but rather to the amount of UV exposure [MED on protected skin ÷ MED on unprotected skin]; gives direction for how long one will be protected before burning
  3. Broad Spectrum—effective against both UVA & UVB radiation; these protect against sunburn, skin cancer
    and photoaging
  4. Water Resistant—sunscreen is effective for 40-80 minutes while a person is swimming [or is sweating]
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8
Q

Sunblock

A

Sunblock:
-Usually contains Zinc oxide/Titanium dioxide
-Block ALL sun rays, not just protect from sun’s burning rays

Per chat:
-Works by reflecting/ scattering rays
-Works as physical blocker
-Thicker, may have a white cast
-Better for use on sensitive/ reactive skin

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9
Q

Sunscreen
Need to double check what she’s looking for for SPF

A

-Per chat:
-Contains chemical ingredients like avobenzone, oxybenzone, octisalate, and homosalate.
-Absorbs UV rays chemically
-Works by chemical filter
-Usually lightweight/ transparent and can be used for all skin types

-Use of sunscreens with SPFs of >16 for 5 years will decrease malignant melanoma risk by 50%

-Educate your patient about what an SPF of a 2, 20, 15, 30 would mean…for a person who burns in 1 minute in the sun without sunscreen??????

-Recommended Use: 3 tablespoons [to cover all BSA] every 120 minutes

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10
Q

Special considerations for sunscreen

A

-Apply sunscreen, then wait 30 minutes to apply insect repellant

-Use a broad-spectrum sunscreen with an SPF of at least 15 (per FDA) or 30 (per the American Academy of Dermatology and Health Canada)

-Limit time in the sun, especially between 10AM and 2PM when the sun’s rays are the strongest

-Apply sunscreen 15 minutes before sun exposure for best effectiveness

-Reapply sunscreen at least every two hours, as well as right after sweating or swimming

-Use a lip balm with SPF 30 or higher to protect the lips

-For infants less than 6 months—use small amounts of SPF 15 or less sparingly

-Sunscreen expires 36 months after date manufactured date

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11
Q

Damage from sun exposure

A

-Photoaging (refers to damage done to skin from prolonged exposure to UV radiation throughout one’s life)

-Normal skin changes of aging are exacerbated by sun exposure

-Photoaging includes—dark spots, wrinkles, droopy skin, yellowish tint to the skin, blood vessels that are
fragile and break easily, leathery skin, skin cancers

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12
Q

Skin phototype

A

Type 1: Porcelain Pale white skin,
blue/hazel eyes; blonde/ red hair
Always burns; does not tan

Type 2: Fair skin with blue eyes Burns easily, tans rarely

Type 3: Darker white skin Tans after an initial burn

Type 4: Light brown skin Burns minimally; tans easily

Type 5: Brown skin Rarely burns; tans darkly with ease

Type 6: Dark brown or black skin Never burns; tans darkly

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13
Q

Glucocorticoids: How they work on the skin

A

-Steroids work via intracellular receptors; they initiate several transcriptions—inhibition of
arachidonic acid cascade, decrease production of many cytokines and inflammatory cells

-Potency is based on vasoconstriction—most potent [VII] to least potent [I]

-Occlusive dressings can significantly increase absorption and may also increase side effects

-Applying topical steroids to wet skin may improve effectiveness

-Total dose for very high potency steroids should generally not exceed 50 grams per week because of the potential for adrenal suppression

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14
Q

Glucocorticoides: ADE

A

-Acneiform eruptions, dermatitis, local infections, hypopigmentation

-In children, applying potent steroids to large BSA can cause systemic toxicity—depression of HPA axis and growth retardation

-Skin changes such as atrophy (thinning), telangiectasias (red or purple clusters on the skin from dilated capillaries), and striae (discolored ridge or groove like a stretch mark)

-Though mild atrophy usually resolves after stopping the steroid, telangiectasia and striae are less likely to resolve with discontinuation.

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15
Q

Acne Vulgaris

A

Patho: Excess sebum, Comedones, Propionibacterium acnes overgrowth, Inflammation

-How its classified:
-Comedones, pustular/papular and nodular

-Disease further subdivided as→

-Mild—comedonal, pustular/papular
-Moderate—pustular/papular, small nodules [up to 1 cm]
-Severe—nodular, cystic/pustular [also called acne conglobate]

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16
Q

Retinoids

A

-Derivatives of Vitamin A

-Influence cell proliferation, immune function, inflammation & sebum production

-These agents are comedolytic and anti-inflammatory

MOA: mediated through nucleic
retinoic acid receptors

ADE’s: irritation, dryness, skin peeling, photosensitivity, dry MM &
eyes

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17
Q

Tretinoin (Prototype drug for retinoids) vs other retinoids

A

-Tretinoin: 1 st generation agent

-Other agents:

-Isotretinoin—1 st generation
agent—category X agent (must be prescribed by licensed providers—I Pledge Program)
-Oral agent
-Used in scarring acne and in
severe disease

-Adapalene / Tazorac—3rd
generation agent—less irritating
-1st line for comedonal and
inflammatory acne

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18
Q

Benzoyl Peroxide fo Acne

A

-1 st line for mild to moderate acne with NO inflammation

-MOA: antiseptic against P acnes and opens pores

ADE’s:—dry skin, peeling, irritation, eyebrow discoloration

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19
Q

Salicylic Acid for acne

A

-Is a Beta hydroxy acid, penetrates pilosebaceous unit

MOA: exfoliates to clear comedones; mild antiinflammatory activity and is keratolytic at high concentrations

-Usually for mild disease

-ADE’s: peeling, dryness, local irritation

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20
Q

Azelaic Acid for acne

A

-Antibacterial against P acnes and it has antiinflammatory actioins

-Normalizes keratinization and its anticomedogenic

-Used in mild to moderate inflammatory acne

-ADE: skin irritation

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21
Q

Antibiotics for acne

A

-P acnes is a gram + rod associated

-For moderate to severe acne with inflammatory lesions, topical or oral antibiotics can inhibit this bacteria’s
growth (Erythromycin and Clindamycin are available and used)

-Topical antibiotics best when combined with Benzoyl peroxide or
retinoids

-Topical Dapsone [a sulfonamide] is available (MOA is unknown)
ADE: methylhemaglobinemia (PERMANENT DONT GIVE)

-Moderate to severe acne requires ORAL antibiotics— Doxycycline [preferred] or Minocycline

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22
Q

How to know which acne treatment to use

A

For mild acne:
-If mainly comedones—treatment of
choice is topical retinoid

-If mainly is papular/pustular—treatment of choice is topical retinoid + benzoyl peroxide [BPO] OR topical retinoid + BPO/antibiotic combination

For moderate acne:
-For papular/pustular disease—topical retinoid + oral antibiotic & BPO (or OCP)

-For nodular disease— topical retinoid + oral antibiotic & BPO [or
BPO/antibiotic]
-Alternative—Isotretinoin orally

For severe disease:
-For nodular—oral antibiotic and topical retinoid + BPO (can add
OCP)

-For cystic/pustular—oral
Isotretinoin [Accutane]

-Alternative is high dose
oral antibiotic and topical
retinoid + BPO (& OCP)

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23
Q

Isotrentinoin important warnings

A

-Requires prescribers be trained and registered— have a federal ID number [based on your NPI and
completion of training]

-Category X pregnancy

-The iPLEDGE program is a mandatory, FDA-regulated initiative for isotretinoin prescribing to prevent fetal exposure. Key components include:
-Monthly doctor visits for pregnancy tests and counseling.
-Strict rules for contraception (two forms of birth control or abstinence).
Limited prescription fills (usually for 30 days).

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24
Q

Rosacea

A

-Chronic acne-like inflammation of central area of face, yet no comedones are present

-Etiology:
-Cutaneous vascular disorder of capillaries

» Increased reaction to heat causes “flushing”
» Ocular symptoms may include blepharitis, conjunctivitis

-Incidence/Demographics:
-Common in fair skinned, middle aged to elderly people

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25
Q

Rhinophyma

A

-Severe form of rosacea seen almost exclusively in men >40 years

-Irreversible hypertrophy of
the nose– is a result of chronic
inflammation

26
Q

What meds do we give for rosacea

A

-Sodium Sulfacetamide with Sulfur
(Usually prescribed as a daily wash)

-Topical Metronidazole (This agent is considered DOC and is safe in pregancy)

-Azelaic acid ( Effective for papules,
pustules, erythema but does not
deter telangiectasias, Safe in pregnancy)

-Oral Doxycycline (Can give erythro)

27
Q

What is Actinic Keratosis?

A

-Discrete, dry, scaly lesions occurring on sun exposed skin of susceptible adults

-Precursor to squamous cell carcinoma [SCC]

-Etiology: Recurrent or prolonged sun-exposure in skin photo types I, II and III

-Common in elders from photoaging of skin (More common in males)

-Lesions begin as single or multiple discrete adherent hyperkeratotic scaly lesions; near 1 cm in size—
round/oval in shape; color ranges from light tan to brown with or without reddish tinge

28
Q

How do you treat actinic keratosis?

A

Topical Therapies:

-Cryotherapy, curettage, photodynamic therapy, facial resurfacing, medium depth chemical peels

5 Flourouracil (Efudex)
-MOA—inhibits DNA & RNA synthesis
-Side effects—redness, crusting, intense stinging

-Imiquimod (Aldara)
[MOA is unknown—immune
modulator]
-Side effects—redness, crusting, intense stinging

29
Q

Atopic dermatitis

A

Global term that may be referring to atopic dermatitis [eczema] or allergic contact dermatitis

-Inflammation of epidermis and dermis that causes profound pruritus—often termed “the itch that rashes”

-Chronic disorder; genetic linked—made worse by stress, hormonal variation

-These individuals often have marked allergies to food, medications, pollens and the like

-Lesions often appear in first year of life

30
Q

How to treat atopic dermatitis?

A

-Treated with a regimen of emollients, topical steroids [ointment preparations] +/- topical immune
modulators [such as tacrolimus]

-Topical steroids

-Calcineurin Inhibitors

  • Tacrolimus ointment [Protopic]
    -Pimecrolimus cream [Elidel]
    -BOTH Used as steroid sparing agents in chronic eczema
    -Both have BLACK BOX WARNINGS for skin malignancies and lymphoma

-Neither to be used in children under the age of 3 years

31
Q

Verruca (warts) Defined

A

-Small, usually painless growths on the skin caused by [HPV]; generally harmless—they can itch or hurt
if on plantar aspect of the feet

-Different types of warts:
-common warts: are usually on hands, but can appear anywhere

-Flat warts—often found on face and
forehead; common, in children, rare in adults

-Genital warts (also known as condyloma):seen on genitals, in pubic area, and in between the thighs, but can appear inside vagina & anal canal

-Subungual and periungual warts: appear around the fingernails and toenails

-Plantar warts: are found on soles of feet

32
Q

Treatment of warts

A

-OTC wart removal products: patients should try and file wart down after bathing before applying the agent

-Salicylic acid topically: many OTC formulations

-Other prescription agents—Podophyllin [MOA is
unknown; inhibits cell mitosis] or Imiquimod [Aldara] [MOA is
unknown—immunomodulator]

-Other treatments—surgical removal, cryotherapy, electrocautery or laser

33
Q

Alopecia

A

-Trichogenic agents are used
to treat androgenic alopecia
[male pattern baldness]

-Minoxidil (PROTOYPE) originally used as an antihypertensive—used to
halt hair loss in both men & women
-MOA unknown; thought to act by shortening the rest phase of the hair cycle; must be used continuously

-Finasteride—5 alpha reductase
inhibitor that blocks conversion of
testosterone to 5 alpha
dihydrotestosterone [DHT]
-High levels of DHT cause the
hair follicle to atrophy; this
agent lowers scalp and serum
DHT levels
-Adverse effects—decreased
libido, decreased ejaculation, ED

-Approved for men, should not
be used or handled in pregnancy as it can cause hypospadius in male fetus

34
Q

Hypo vs hyperpigmentation of the skin

A
  1. Hypopigmentation: Vitiligo
  2. Hyperpigmentation: Freckles and melasma
35
Q

Hydroquinone (PROTOTPYE)

A

-Topical skin whitening agent (inhibits the tyrosinase enzyme
required for melanin synthesis)

-Used to reduce pigmentation—along with topical retinoids
- 4% preparation is best agent

-2-3% may be available in your area as OTC products

-Adverse effects—local skin
irritation

NOTE Rebound Hyperpigmentation may occur if it is used without breaks, the skin may develop resistance, and pigmentation can return more intensely after discontinuation.

36
Q

Monobenzone (benzyl ether of hydroquinone

A

-This agent can be used to even out the skin discoloration of vitiligo

-Methoxsalen—photoactive
substance that stimulates
melanocytes; used as a
repigmentation agent for vitiligo

-Must be activated by UVA
radiation [PUVA]

-This agent inhibits cell proliferation
& promotes cell differentiation of
epithelial cells; topical may be
used for small patches of vitiligo;
oral used for widespread disease

-Adverse effects—aging of the skin
and increased risk of skin cancer

37
Q

What to know about skin infections

A

-Acute infection of dermis and
subcutaneous tissues

-Common Etiologies:
-MSSA and MRSA strains
-Streptococcus pyogenes
-Gram negative—E. coli, Pseudomonas aeruginosa, Clostridium spp.

-Can cause folliculitis, abscesses,
fasciitis, cellulitis, impetigo

38
Q

Treating GRAM POSITIVE skin infections Topically

A

-Bacitracin: used most often for prevention of skin disease after burns and scrapes (small area)

-Mupirocin—protein synthesis inhibitor; Useful for treating impetigo and other serious gram +

-Retapamulin—newer protein synthesis inhibitor approved for the treatment of impetigo

39
Q

Treating GRAM NEGATIVE skin infections Topically

A

-Polymyxin B—cyclic hydrophobic peptide that disrupts the bacterial cell membrane of gram - pathogens
-Commonly combined with Neomycin** & Bacitracin in
triple antibiotic [TAO] products

-Gentamycin

**Allergic dermatitis and other sensitivities common with Neomycin

40
Q

Treating skin infections systemically

A

-Augmentin [or high dose Amoxicillin]

-Cephalexin

-Doxycycline

If MRSA suspected—Trimethoprim/Sulfa or Doxycycline

-Clindamycin or Rifampin if infection severe

-Fluoroquinolones might be an option—depending on your
geographical area—Levofloxacin or Moxifloxacin

41
Q

Ectoparasitic infections of the skin

A

-Parasites that live on animal skin [where they obtain their nutrition] and can jump “species” and infect humans

-Pediculosis—lice

-Scabies—mite

Agents we use in these infections—Lindane, Permethrin, Synergized pyrethrins with piperonyl butoxide

42
Q

Antiparasitic agents

A

-Lindane—cyclohexane derivative
-Available as cream or shampoo; kills lice & scabies

-Permethrin—synthetic pyrethroid that is neurotoxic to lice [1%
OTC] [Nix] and scabies [5% prescription] [Elimite]
(Preferred over Lindane, as Lindane can cause neurotoxicity)

-Ivermectin—given orally, is an alternative therapy for lice and
scabies (Stromectal)

-Synergized pyrethrins with piperonyl butoxide—OTC product used to treat head and pubic lice [Rid]

-Pyrethrins are pesticides

-Low risk of toxicity; DOC for pediculosis

43
Q

Fungal infections of the skin

A

-These are infections that are limited to the hair follicle and epidermal layer of the skin and nails

-Dermatophytosis: Do not invade dermis because of keratin dependency (aka ringworm)

-Candidiasis: More common in patients with comorbidities—obesity, diabetes, recent antibiotics
-Also affects the mucous membranes and can cause systemic
disease in the immunosuppressed

44
Q

Treating fungal infections

A

-Yeast infections—candida species

-Non-yeast fungal infections—dermatophytes [tinea]
 Most common—Trichophyton, Microsporum, Epidermophyton, Malassezia

-Tinea is classified by area of body it affects—tinea pedis [tinea on feet]

-Tinea appears as rings or round red patches with clear centers (often called “ringworm”)

45
Q

Candidiasis

A

-Characterized by pruritic, bright red, macerated plaques with surrounding ‘satellite’ vesiculopustules

-Loves skin folds—axillary, inframammary, genitocrural

46
Q

How do we treat fungal infections?

A

-Squalene Epoxidase Inhibitors

-These agents block the biosynthesis of ergosterol— which is needed in the fungal cell membrane

Other Agents in Class:
- Naftifine [Naftin] (Used to treat tinea corporis, cruris, and pedis)

  • Butenafine [Lotrimin Ultra]
47
Q

Terbinafine [Lamisil] PROTOTYPE DRUG

A

-Active against most all strains of dermatophytes
[including Scopulariopsis—a fungus responsible for deep fungal infections in the immunosuppressed] & near 50% of candida infections

-Comes in oral, cream, gel and solution

–Oral form is DOC for onychomycosis (topicals don’t work)

-Topical [cream usually] treats tinea
pedis, corporis, cruris

-Highly protein bound; concentrates in breast milk

  • ½ life in tissues is 200-400 hours
  • Metabolized in liver and excreted in
    liver

-Avoid in patients with liver dysfunction

-ADE’s:—diarrhea, dyspepsia,
nausea, headache, elevated LFTs

48
Q

Griseofulvin

A

-Antifungal

-This agent disrupts the mitotic spindle and inhibits fungal mitosis

-Older agent (has been replaced for the most part by Terbinafine, but still used for dermatophytes of scalp
and hair)

-Agent is fungostatic—so duration of treatment is long—500 mg po daily 6 to 12 months for nails

-Absorbed from GI tract, enhanced by high fat meal

-It increases the metabolism of anticoagulants

-Contraindicated in pregnancy and patients with porphyria

49
Q

Nyststatin

A

-This agent is a polyene antifungal

-MOA: involves binding to ergosterol, a key component of the fungal cell membrane.

-Used for treatment of cutaneous and oral Candida infections

-Negligibly absorbed from GI tract; not used systemically because causes toxicity

-For oral-pharyngeal infection—it is given as a swish & swallow regimen; used topical for cutaneous infections; intravaginally for vulvovaginal infections

-NOTE* Treats candida not tinea

50
Q

Imidazoles

A

-“Azole’s”

Azole derivatives that have a wide
range of activity against the 4 most
common dermatophytes and Candida species

-These agents are given for tinea
corporis, cruris and pedis; oral/pharyngeal & vaginal Candida

-Prolonged topical use can cause
contact dermatitis, vulvovaginal
irritation/edema

-Clotrimazole and Miconazole both
come in a troche/buccal forms

-The only AZOLE that covers Candida glabrata is terconazole [Terazol]

-Examples: Butoconazole, Clotrimazole, Econazole,, Ketoconazole, Miconazole,
Oxiconazole, Sertaconazole, Sulconazole, Terconazole—Terazol [vaginal] Tioconazole—Monistat [vaginal], Fluconazole—Diflucan (oral)

51
Q

Ciclopirox

A

-Agent inhibits transport of essential elements that allow DNA, RNA and protein synthesis

-Only topical antifungal active against ALL dermatophytes and all strains of Candida

-Used for tinea pedis, corporis & cruris, cutaneous candidiasis and tinea versicolor

-Available in shampoo [1%] for seborrhea dermatitis; cream, gel suspension, or topical for nails

-Not used for vaginal candidiasis

52
Q

Tolnaftate

A

-This agent distorts the hyphae and stuns mycelial growth

-NOT effective for Trichophyton or
Candida

-Used to treat tinea pedis, cruris & corporis

-1% solution, cream, powder

-EX: Tinactin; Lamisil AF Defense

53
Q

New, promising antifungals

A

-Within last year, 2 topicals with reasonable efficacy have come to market

-Boric acid key component of both!!
- Efinaconazole—1-2 gtts to each affected nail for 48 weeks
-Tavaborole— penetrates nail/plate and polis, paint on nail and under tip at HS for 48 weeks

54
Q

Psoriasis

A

-Chronic, scaling papules and plaques

-Characteristic distribution is knees, elbows, scalp

-Skin lesions occur insidiously [on occasion may be acute +/-
pruritus; may be associated with acute systemic illness w fever and malaise (strep)

-Etiology: Alteration in cell kinetics of keratinocytes with shortening of cell
turnover rate, resulting in increased production of epidermal cells

  • Silvery-white scaling with pinpoint
    bleeding when scale removed (Auspitz sign)
  • Assess quality of life—ask about
    pain

-Important nondrug therapies—avoid
rubbing/scratching; advise patient
to eat a healthful diet, exercise and
lose weight, stop smoking

55
Q

How to treat psoriasis

A

-Patients with mild to moderate disease [<5% of BSA and not involving palms or soles] can be
managed with topicals—retinoids, Vitamin D analogues, keratolytics, topical steroids

-For more severe disease, systemic therapies—
Methotrexate, Cyclosporine, immune modulators

-If patient not a candidate for the aforementioned—
phototherapy [Methoxsalen + UVA [PUVA] OR UVB alone]

56
Q

Retinoids used in psoriasis

A

-Tazarotene [Tazorac]—topical retinoid for plaque psoriasis

-Acitretin [Soriatane]—2nd generation retinoid; given
PO for pustular psoriasis
-½ life of 120 days; ETOH contraindicated as it increases potency and prolongs ½ life

-Teratogenic and women must avoid pregnancy for at least 3 years after using Acitretin

-ADE: cheiliitis (cracking lip cornners) pruritus, peeling skin, hyperlipidemia

57
Q

Vitamin D Analogues

A

-These agents inhibit growth of keratinocytes

-Calcipotriene & Calcitriol

-Synthetic Vitamin D3 derivatives used topically to treat plaque psoriasis
-Can cause hypercalcemia

ADE: itching, dryness, burning irritation and erythema

58
Q

Keratolytic agents

A

-Coal tar—inhibits excessive skin cell proliferation

-Salicylic acid: Both used on scalp to remove scale and improve steroid penetration

-These agents have largely been replaced in psoriatic care by the newer topical agents

59
Q

Other agents used for psoriasis

A

-Corticosteroids and immune
modulators (suppress the
dysregulated immune response)
-High potency topical steroids
for 2-3 weeks; then, use in pulse
fashion for 2 d/week
-Intralesional steroids
-Avoid ORAL steroids which can cause
rebound flares
-Long term use of topical corticosteroids is limited by
cutaneous atrophy

-Calcineurin Inhibitors:
-Tacrolimus [Protopic]
-Pimecrolimus [Elidel]
-These agents inhibit T-cell activation/ proliferation by blocking calcineurin phosphatase. This leads to the suppression of these cells and reduced production of pro-inflammatory cytokines, including TNF-α, IFN-γ, and IL-2, which are key players in an amplified T-cell response

-Steroid sparing agents; used
in flexural and facial psoriasis

60
Q

Systemic therapies for psoriasis

A

-If unresponsive to topicals or BSA >5%:
-Apremilast [Otezla]
-Methotrexate (With Folic acid)
-Cyclosporine

-TNF Alpha Blockers
-Adalimumab [Humira]
-Etanercept [Enbrel]
-Infliximab [Remicade]

-Interleukin IL-12 & IL 23 Blocker:
-Ustekinumab

-Interleukin IL-17A Blocker
-Secukinumab [Cosentyx]

-Phototherapy (Can be used with topicals) (can get basal cells down the road)

-PUVA [Psoralen with UVA light]

-Narrow band UVB therapy