OME-Dermatology Flashcards
Describe Atopic Dermatitis (Eczema);
What is the pathology?
What is the meaning of the 3As?
Major symptom?
describe In infants with location and ddx
Describe locations in children
adult chronic atopy. what/why of lichenification?
adult chronic presentation.
dx?
treatment goal and why?
General treatment?
adult intervention and goal
infant intervention
Caveat for steroids
Presentation: dry, red rash=ed or inflamed; excessive dryness and scaling; skin folds of arms or legs; possible vesicles.
Pathology: Type I hypersensitivity = IgE ab binds to mast cell
3As = Asthma, Allergies, and Atopy.
pruritis,
Infat pt: presents as papules, vesicles, and crusts (careful with impetigo-clue is it is scattered on the body)
- cheeks (face)
- diaper line
- extensor surfaces (less common).
Children
- antecubitus fossa
- Popliteal fossa
adult presentation: condition usu more chronic, symmetrical lichenification (longterm inflammation and scarring of skin). induced by a chronic itch-scratch cycle.
- AC fossa
- Popliteal fossa
- hands, face, feet, neck, upper chest, genitals
- Flexural surfaces (inside of the fold)
Dx: clinical - clinical diagnosis:
Treatment goal: break the itch-scratch cycle and allow the skin to heal.
- avoid triggers (crucial)
- limit dryness (soap and water exposure)
- emulsions/heavy moisturizers Topical emollients - reduces the itch and break the itch-scratch cycle. might avoid the need for steroids.
- intermediate potency topical for initial; lowest potency for control & systemic corticosteroids
- oral antihistamines ( hydroxyzine then ceterizine)
- cool wet dressings or burow’s solution
e. Infant triggers: de-escalate food additions and slowly add food back. Avoid food that triggers a reaction.
g. If topical steroids are prescribed, they may be used only for a brief time as they can lead to skin atrophy. The
What are the two forms of contact dermatitis?
What is the Pathology
What are some examples?
Pt presentation
dx
intervention
irritant direct damage to stratum corneum: inflammatory nonimmunologic response.
allergic. Path: Type IV delayed hypersensitivity reaction in response to some allergen.
irritant contact dermatitis: direct toxic effect of a chemical on the skin:
- excessive hand-washing,
- rubbing on leather boots
- some occupation-related chemical.
Allergic contact dermatitis
- metals (Nickel–on clothing or jewelry)
- latex
- plants (poison ivy / oak ).
Pt presentation:
- Itch that spreads to where they touch (poison ivy)
- red rash in the shape of an object (like a glove, bracelet, or shoe strap).
Dx: Clinical
Tx:
- avoid trigger
- work modification
- protective equipment
- topical diphenhydramine or aloe
- corticosteroids creams high-potency but not on face
- systemic corticosteroids
What is Stasis Dermatitis? pathology?
Pt predisposing conditions
What does it look like? (presentation)
How is it diagnosed? Avoid? Treatment?
Clinical misjudgment? associated derm condition?
Skin response to being stretched 2/2 chronic lower extremity edema.
Associated conditions: Chronic kidney disease, HF, liver cirrhosis.
Presentation:
- edema (or conditions that cause edema) THEN
- erythema THEN
- brown discoloration. THEN
- hard “tree-bark” skin changes
- scaling (flaking of the skin )
- symmetrical and bilateral.
dx: clinical diagnosis;
Avoid: biopsy as a non-healing ulcer may develop.
Treatment:
- correcting volume overload (diuretics only when overloaded)
- compression stockings
- leg elevation to facilitate drainage of fluid from the legs.
WATCH OUT: Early stasis dermatitis (swollen and red). Mimics cellulitis, BUT stasis dermatitis is bilateral and symmetrical - not cellulitis.
Venous stasis ulcer (bilateral medial malleolus) can accompany stasis dermatitis.
What is Hand Dermatitis?
Pathology?
Most common patient types?
Dx?
Treatment?
The dermatitis is on the hands only.
Path: Resulting from excessive hand-washing
Pt type: food- industry or health-care worker
Dx: Clinical
Treatment:
- avoid frequent hand washing
- wear protective gloves instead.
- Harsh hand soaps should be avoided.
- Moisturizers should be used frequently.
Impetigo and Bullous impetigo
Pt:
Dx:
What is the non-pharm care?
Tx:
Abx class and examples:
Abx for MRSA:
Sequalae:
Prevention:
Impetigo Path: gram + strep; Strep pyogenes. vesicles are < 5 mm (small blister) or staph
Bullous impetigo ( increasing ↑). Path: Staph aureus of colonized from nasal pathogens.
Pt: Child (2-5 yo) w/ honey-crusted lesions on the face. can be any age.
Dx: clinical
non pharm care: gentle wash 2-3 x per day;
Tx: topical mupirocin (Bactroban) if ≤ 5 lesions.b Systemic for ≥ 5 lesions, scattered areas or not responsive to topicals
Abx: gram + spectrum that is stable in the presence of beta-lactamase (dicloxacillin) or 1st/2nd gen cephalosporin. (cephalexin)
MRSA: trimethoprim-sulfamethoxazole; clindamycin; doxycycline (not in peds < 11 yo)
Sequalae: Impetigo can lead to post-strep glomerulonephritis but NOT rheumatic fever.
deeply ulcerated - ecthyma
Prevention: school age children 24 hrs on abx before returning. check family members
Erysipelas
Pt:
Path:
Presentation:
Dx:
Tx:
Erysipelas
Pt: adults
Path: Strep pyogenes
Presentation: infects the lymphatics; distal start
- dark red
- well-demarcated
- indurated lesion
- outlines the lymphatics
- appearing to “climb up the extremity.”
Dx: Clinical
Tx: Beta lactams against strep (amoxicillin if PN allergy then clindamycin)
escalate if no improvement
Acne Vulgaris: most common derm infx
Path:
etiology:
dx:
tx modalities - MOA/SE. (hint 6)
Tx and definitions:
- mild acne
- moderate acne
- severe
- very severe
Drugs that induce acne:
Acne Vulgaris: most common derm infx
Path: Propionibacterium acnes.
etiology: Acne is a product of increased sebum production ⇒plugging of follicles (follicular hyperkeratinization), colonization by P. acnes⇒ inflammatory response.
dx: clinical diagnosis → open and closed comedomes, cysts and pustules.
tx: The type of acne determines the approach. Use the escalation approach. ladder:
- topical retinoids -
- MOA: antimicrobial; keratolytic; alter androgen metabolism? exp 6 weeks of therapy
- SE: irritation and dryness
- benzoyl peroxide
- MOA/SE: antimicrobial; comedolytic
- topical abx: clinda; erythromycin; tetracycline
- for mild to moderate pustular
- oral antibiotics –doxy, minocycline; clindamycin; erythromycin; azithromycin 3-6 months therapy
- E/SE: antimicrob; for moderate
- hormones: estrogen/progestin
- MOA: decrease sebum
- tretinoin/differin/tazarotene:
- MOA: decreases cohesion, keratolytic, increases skin cell turnover, closed to open comedones.
- SE: sun sensitizing
- isotretinoin - 4-5 months
- MOA: inhibit sebum production
- SE: monitor: Mood disorders and SI
- elevated liver enzymes, cheilitis, conjunctivitis, HyperTG; xerosis, photosensitivity, intercranial HTN
- a teratogen. women must use TWO types of birth control.
- Not bad acne =
mild acne = < 20 comedomes/15 inflamed lesions/ total < 30 = retinoids
- Teen cares about acne
= moderate acne = 20-100 comedones or 15-50 inflammatory lesions = benzoyl + retinoids
- Acne won’t go away
= severe = > 5 nodules;inflammatory lesions > 50/ total lesions ? 125 = doxycycline
- Scarring, nothing else has worked,
very severe = isotretinoin
Drugs that induce acne: phenytoin, lithium
Tinea Infections
description:
Presentation;
Dx:
Tx:
Tinea pedis:
Tinea cruris:
- *Tinea Infections**
description: Tinea corporis is an infection on the body.
Presentation; round expanding plaque with moderate scaling and central clearing.
Dx:
Tx: topical antifungals some
Tinea pedis: infection of the foot. Look for interdigital maceration and scaling between toes.
Tinea cruris: is “jock itch” and is a fungal infection of the groin.
Tinea unguium (onychomycosis)
Presentation:
Dx:
Tx including type of dosing
SE:
P450 3A4 pathway -
P450 2C9 pathway -
Tinea unguium (onychomycosis)
Presentation: nail hypertrophy, brittle nails, dull, pithy
Dx: confirm the diagnosis with a KOH prep; fungal cultures from nail clippings
Tx: oral antifungals. (topicals have limited penetration)
- Terbinafine (Lamisil) is best,
- itraconazole - (Sporanox) inhibits P450 3A4;
- fluconazole: ( Diflucan) inhibits P450 2C9
- nail lacquers: ciclopirox have limited efficacy
SE: all increase hepatic enzymes;
Consider pulse dosing and longer treatment for toes vs fingernails. 400 mg 1 week of month for 2 months
P450 3A4 pathway - 50% of prescription drugs including digoxin, anticoagulants, diazepam, HIV meds
P450 2C9 pathway - carbamazepine, some benzos, and CCBs. MANY drug interactions
Burns
Prevention:
Burn types:
outpatient care exceptions
Bacteria:
What much be done or considered? (5)
Rule of 9’s: palmar surface BSA
Burns
Prevention: burn avoidance for children, elderly adults, smokers; hx of current trauma
Burn types:
1st: erythema, hyperemia; pain; blanches
2nd: erythema, hyperemia; pain; moist raw surface
3rd: minimal pain surrounded by 1st and 2nd degree. surface is white and leathery
outpatient care except (refer to specialty care)
- < 10% of BSA
- Minor (second degree or lower)
- does not include hand, food of cosmetic areas
- genitalia
Bacteria: gram +: staph aureus, strep; enterococci;
gram - : p. aeruginous; e. coli; Klebsiella pneumonia
tx: Silvadene (sulfadiazine) or mafenide (sulfamylon)
Rule of 9’s: the palmar surface is 1% of BSA
Bite
Considerations:
Tx:
Animals w/ possible rabies:
Tx for possible rabies
Cat ABX:
Dog ABX:
Bite
Considerations: not benign; obtain complete hx of events leading to bite; all carry an infection risk
Tx:
- vigorous wound cleaning.
- debridement if warranted.
- Tetanus as warranted
- XR if near a joint
- anti-infectives human bites, high-risk (deep puncture, crush, venous or lymphatic compromise; hands or near joint, face or genitals, immunocompromised hosts, surgical repair, asplenic, advanced liver disease, edema
- amoxicillin 1st line 2nd line: clindamycin plus TMP-SMX or ciprofloxacin
Begin prophylactic therapy within 12 hours based on location and origin.
Animals w/ possible rabies: bats, foxes, woodchucks, squirrels & skunks: strep and staph
- Augmentin or doxycycline
- IgG-rabies
- rabies vaccine
Cat: Pasteurella m, Staph. 80%
- culture and treat empirically
- augmentin OR cefuroxime OR doxycycline
- Pen ???
Dog: Pasteurella canis, Staph; strep. 5%
- augmentin OR clindamycin + fluoroquinolone OR clindamycin + TMP-SMX
Herpes Zoster
Path:
Pt:
Considerations:
dx:
tx:
Symptomatic treatment for pain:
sequela:
Concerns;
Post-herpetic neuralgia definition–
risk factors:
postherpetic neuralgia tx:
Herpes Zoster
Path: activation of varicella-zoster virus in the dorsal root ganglion of a dermatome.
Pt: anyone that has had chickenpox; especially any elderly and immunocompromised.
Presentation painful vesicular unilater eruption with dermatomal distribution: most common is thoraci and lumbar. resolves in 14-21 days. (fever, headache, malaise, low grade fever)
MUST teach patient: live virus will be shed; avoid children, pregnant women and immunocompromised; 4% recurrent
dx: clinical; Tzanck smear shows multinucleated cells
tx: acyclovir, valacyclovir within 72 hours; limits severity and neuralgia; systemic corticosteroids (pain)
Symptomatic treatment for pain:
topical lidocaine gel 5%
burow’s solution with NASID or an opioid
sequela: scarring, neuralgia
Concerns; 2ndary infection; facial/ocular presentation
Post-herpetic neuralgia– pain 1 month after rash has healed
risk factors:
site of involvement: trigeminal highest
severe rash
intense prodromal pain
older age
postherpetic neuralgia tx:
TCA, gabapentin, pregabalin, topical lidocaine patches
Scabies
Path:
How is it transferred?
Presentation:
symptoms?
Tx:
Why avoid lindaine -
Tx of linens/clothes?
Scabies
Path: communicable disease by mite;
close skin-to-skin contact or exposure to infected bedding/clothing
Presentation: burrows with a vesicular or papular form with excoriation from scratching. areas of warmth: finger web, axillary fold, beltline, areolae; scrotum, penis, under breasts,
symptoms: INTENSE itching
Tx:
- Permethrin (Elimite). leave on 8-14 hours then wash off.
- low to med potency corticosteroids.
- oral antihistamines - itch
avoid lindaine - neurotoxicity, lower seizure risk, lower efficacy, no pregnant, children or elderly
Tx of linens/clothes
- wash in hot water
- place in dryer
- bags for 1 week
Psoriasis
Path:
male to female ratio?
Presentation:
Common Locations:
Associated Physical s/sx:
Important DONT MISS:
Tx:
Psoriasis
Path: an autoimmune disease that causes the proliferation of keratinocytes with excessive accumulation of the stratum corneum. perhaps dysregulation of T-Helper cells.
Pt: Male = female
Presentation: symmetric, well-demarcated silvery scales that bleed when picked. (auspitz sign)
Common Locations: scalp, post-auricular, gluteal fold, elbows, and knees. (extensor surfaces)
Associated Physical s/sx: Nail pitting and onycholysis (detachment of the nailbed) auspitz sign = bleeding with removal of plaque.
Considerations: joint pains may indicate psoriatic arthritis (see rheumatology –seronegatives). Possible biopsy to rule out lymphoma. Several forms of psoriasis
Tx:
- UV light (sunlight or artificial exposure) when more than 30% of the body. Associated with cancer risk and photoaging.
- Topical steroids are used in flares. (med to high used until lesions controlled, then lower potency 3-4 times per week.
- Other agents, both topical and systemic, are beyond the scope of a student (anthralin, TFN modulators/Anti-TNF-alpha: etanercept (Enbrel), adalimumab (Humira), ustekinumab (Stelara), methotrexate, calcineurin-inhibitors, Anti-TNF-alpha-can reactivate TB, risk of infection with pt with diabetes or HF or use of immunosuppressive drugs).
Seborrheic Dermatitis (NOT Seborrheic Keratosis)
Path:
Presentation:
where is it usually found
Tx:
what are some associated conditions?
Seborrheic Dermatitis (NOT Seborrheic Keratosis)
Path: Seborrheic Dermatitis is a fungal infection (Malassezia) that causes an inflammatory reaction in areas rich in sebaceous glands.
Presentation: in hair think super-dandruff. Look for a rash on the scalp and eyebrows, nasolabial folds, that spares other areas of the face and ears.
Tx:
- Treat with selenium shampoo.
- Class IV corticosteroid creams
- Ketoconazole topical
- topical immune modulators (tacrolimus)
Consideration: Low-yield test associations include: HIV infection, cradle cap (infants)
chronically ill: Parkinson’s disease; elderly
Skin Cancer
Prevention:
What are likely pt?
What are sun area?
What type of skin as it risk?
Prevention:
MM risk: sunscreen has little benefit; from melanocytes. most common fatal malignancy
Presentation Malignant melanoma:
Melanoma Dx:
Tx:
Presentation basal cell carcinoma (BCC)
BCC Risk:
Path:
Presentation:
Dx:
Tx: face? head?
limb =
squamous cell carcinoma = SCC
SCC pearls:
Path:
Presentation: lower lip hyperpigmentation
Dx: biopsy
Treatment:
BCC/SCC - cryotherapy, electric dessication, focal radiation, topical cancer treatment
Mohs - invasive or aggressive
Actinic keratoses:
Path:
presentation:
Skin Cancer
Prevention: skin exam; self screen
likely pt:
sun jobs: ships and outdoor labor
sun areas: face, hands, back, shoulder
Sun people: fair skin/ fairer hair, bad burns
Prevention: wide brim hats
MM risk: sunscreen has little benefit; from melanocytes. most common fatal malignancy
Presentation Malignant melanoma:
Jet black WITHOUT any hair
- A = asymmetric with nonmatching sides
- B = Borders are irregular
- C= Color is not uniform
- D = Diameter is usu larger than 5 mm (pencil eraser)
- E = evolving lesions, either new or changing
Melanoma Dx: biopsy with large lesion
excisional biopsy;
Tx: No current treatment. just catch it early
Presentation basal cell carcinoma (BCC)
BCC Risk: significant deformity, altered function, long latency, low metastatic risk.
Path: cancer of the basal layer
Presentation:
- P = pearly papule
- U = ulcerating ( non healing/bleeds easily)
- T = telangiectasia
- O = on face, scalp and pinnae (sun exposed)
- N= nodules that are slow growing
Dx: excisional biopsy (incisional bx). Punch is wrong
Tx: face = mohs
limb = excition. CUT IT out
squamous cell carcinoma = SCC
SCC pearls: more rapid growth the BCC. low but significant metastatic risk, in immuno suppressed; regional
Path: keratonocytes. can met and invade
Presentation: lower lip hyperpigmentation
- N = nodular
- O = opaque/red papule
- S = sun exposed areas
- U = ulcerating/nonhealing/ heals and breaksdown
- N = nondistinct borders/well defined
- later stages inclue scale and firm margins
Dx: biopsy
Treatment:
BCC/SCC - cryotherapy, electric dessication, focal radiation, topical cancer treatment
Mohs - invasive or aggressive
Actinic keratoses:
Path: UV induced skin lesions. Can involve into SCC
presentation: small, rough more felt than seen; rub with finger; has sand paper quality
Noncancerouslesions
Actinic keratoses: pre-malignant lesions of kerotincytes.
Path:
What cancer could evolve?
Presentation?
Dx:
Tx:
Mole:
path:
Tx:
Seborrheic Keratosis
path:
Presentation that shows no cancer?
Dx:
new/old:
Tx:
Noncancerous lesions
Actinic keratoses:
Path: UV induced skin lesions. Can evolve into SCC
presentation: small, rough more felt than seen; rub with finger; has sandpaper quality usu erythematous with scale that is yellow to brown. hyperpigmented
Dx: biopsy
Tx: 5-FU Fluorouracil 0.5% cream
cyrosurgery; curettage, electrodessication, phototherapy, chemical peels
Mole:
path: benign melanocytes if hair is in it, no cancer
Consider the ABCDEs when diagnosing.
Seborrheic Keratosis
path: benign keratinocytes
Pt: large, greasy and stuck on
Dx: Long time (don’t worry)
new: do a biopsy
Urticaria
Path:
Other related conditions
Presentation:
Cause:
Dx:
Tx:
Send them to RAST to identify the culprit antigen.
Urticaria
Path: Type I Hypersensitivity Reaction. exposure to an antigen ⇒crosslinks IgE on mast cells ⇒ Histamine released. vasodilation, leaky capillaries, mucous production, tissue swelling.
atopy pearls: includes allergic rhinitis, atopic dermatitis, allergic gastroenteropathy, and allergy-based asthma. strong fam hx.
Presentation: producing an annular, blanching red papule of varying size (wheal).
Cause: antigen can be anything: bee stings, pressure, heat, food, contact dermatitis.
Dx: If there’s no anaphylaxis - (hypotension -angioedema, difficulty breathing anaphylaxis)
a clinical diagnosis
- Tx: use anti-histamines to decrease the rash.
- topical corticosteroids, leukotriene modifiers (montelukast/singulair); systemic corticosteroids
critical to identify the agent and avoid using it again.
Send them to RAST to identify the culprit antigen. Radioallergosorbant test. detects IgE antibodies.
Warts
What virus type is associated with non genital warts? How is it transferred?
- What is the first line treatment and result? when is it most effective? When is this least effective?
- other treatments with SE and infor
Warts-verruca vulgaris
Path: HPV 1, 2, 4. non genital warts via person to person contact
Tx:
- Leave alone usu resolve over 12-24 month period. Treat if interfere with function. Children most effect; immunocompromised and elderly this is the least effective.
- Keratolytic (peeling) agents - apply until lesion resolves.
- example: salacylic acid, imiquimod
- Cryotherapy - Liquid nitrogen - painful; multiple txts
- Duct tape = leave on for 6 days, then filed leave off then put on again. Leave on for 6 cycles.
- electrocautery -
- tretinoin - consistant trt. 4-6 bid
- immunomodulators-
- cimetidine
- quadravalent HPV vaccine has been shown to clear recalcitrant warts.
