Dermatology Flashcards
Basal cell carcinoma? Hx & PE? Dx? Tx?
MC form of skin cancer
Hx PE = waxy lesion pearly appearance
Dx = shave biopsy
Tx = 1. cryosurgery for superficial lesion
2. topical imiquimod if < 2cm
3. topical furacil if multiple to decrease lesions in the neck & head
- can use Mohs surgery
Squamous Cell carcinoma of skin? RF? Hx & PE? Dx? Criteria? Tx?
SCC - atypical transformed kertinocytes in
keritinocytes in skin w/ malgn behavior
in situ (confined to outer layer of skin =
Bowen disease), MC found on lips
RF - smokers, organ transplant secondary to long term immunosuppressant drugs,
Hx & PE - ulcer that doesn’t heal, erythema
scaly indurated papule/plaque
Dx - biopsy
Criteria - differentiated/TMN/invasion
Tx - local remove - cryotherapy,
Mohn procedure <2 cm facial area
What is malgn melanoma? Etio? RF? Dx? Tx? Criteria?
malignant tumor arising from melanocytes
Epi - 6th MC cancer, increased rate of incidence
Etio - arise from melanocytes due to genetic & environment
RF’s - family Hx of melanoma, Hx of sunburns as child, increase # benign melanocytes nevi, XP
Hx & PE= A: asymmetry B: border irregularity
C: color irregularities D: diameter greater than 6 millimeters E: evolution (changing in appearance over time)
Dx - clinically - confirm full thickness biopsy
Tx - surgical excision - if shallow invasion w/o mets excision w/ 1cm
Criteria - determining level of invasion (TMN), complication includes mets to brain, local reoccurrence
What is Mohs surgery?
Removal of skin cancer under a dissecting microscope with immediate fro- zen section is one of the most precise methods of treating skin cancer. Mohs allows removal of the skin cancer with the loss of only the smallest amount of normal tissue.
- stop resecting once its margin cancer free - don’t need wide margins
Karposi sarcoma? Etio? RF? Hx & PE? Dx? Tx?
most common cause now is AIDS. KS is from human herpes virus 8, which is oncogenic.
Hx & PE = lesion is more reddish/purplish because it is more vascular than other forms of skin cancer, KS is also found in the GI tract and in the lung
Dx = HIV test, confirm w biopsy
Tx = Treat the AIDS with antiretrovirals and the majority ofKS will disappear as the CD4 count improves.
What is actinic keratosis? Etio? epi? RFs? Dx? Tx?
Etio - chronic exposure to UV rays
Epi - increased w older pts >80yo, genetic
RFs - chronic exp/light skin/ freckling
albinism/ >40yrs
Hx & PE = yellow skin color scaly hyperkeratotic lesion plaque or papule in sun exposed area
Dx = clinically
Tx - curettage, liquid nitrogen, cryotherapy
laser, complication - 1-2% SCC risk
What is seborrheic keratoses? another name for SK?
aka pityrasis ovale
they are found in elderly, characterized as hyperpigmented lesions that look stuck on
- no premalgn potential
- removed for cosmetic reasons via cryotherapy, surgery or laser
- tx w steriods if there is pruritis
Describe atopic dermatitis? epi? etio? Hx & PE? criteria? Dx? Tx?
Epi - presents in childhood, family hx of
asthma, allergic rhinitis
Etio - due to overactivity of mast cells &
immune system, rare after 30 yrs
Hx & PE - pruritis/xerosis (dry skin), skin
lesion leads to thickened skin —>lichenified
leads to superficial infection by s. aureus
Criteria - hx of dry skin in last year,
dermatitis of flexor surface (adults), face
extensors (inflants) fam hx of asthma
<2 yrs old
Tx - staying moisturized, avoid bathing/dry
soaps, topical steriods can be used,
calcineurin inhibitors - tacrolimus/ pimecrolimus
antihistamine - nonsedating fexofenadine, loratadine
antibiotic w/ impetigo - cephalexin, mupirocin,
What organism causes atopic dermatitis?
Staph
What is psoriasis? RF? Hx & PE? Dx? Tx?
scaly plaques on elbows, knee,
extensor limb, scalp, fluctuating disease
RFs - genetic/infection/local trauma
Dx - clinical
- severe disease assoc w depression
- rarely comes w arthritis
Tx - local
Topical high-potency steroids: fluocinonide, triamcinolone, betametha- sone, clobetasol
extensive disease - Antitumor necrosis factor (TNF) inhibitors (etanercept, adalimumab,
inflixirnab). or MTX
What are the side effects of TNF inhibitors?
reactivation of latent TB, do PPD test 1st
What labs do you have to do when give MTX?
monitor LFTs
What is stasis dermatitis? How do you treat?
Stastis Dermatitis - build up of hemosiderin
due to venous insufficiency resulting
purpura, irreversible
Tx - elevate legs, stockings hose
What is pityriasis rosea? epi? etio? Hx & PE? Dx? Tx?
transient dermatitis starts with single lesion (herald patch), spares palms & soles
Epi - b/t 10-35yo, female > men
Etio - unclear
Hx & PE - red oral plaque w central scale, spares palms and soles, occurs in trunk prox lesion
Dx -clinical
Tx - self-limited in 2-3months; tx w steroids & UV light
Seborrheic dermatitis - epi? etio? Dx? Tx?
aka dandruff - inflam skin manifests as erythema & scaling of scalp, nasolabial folds, anterior chest, worsens w stress
Epi - usually w/in 3m of life, decreases by
age 4, pityrasis capitis is craddle cap in kids
Etio - pityrasis ovale, pityrasis sica (dandru)
Tx - ketoconazole + selenium sulfide (1st)
nonscalp disease - topical steriods (hydro)
and antifungal (ketoconazole)
What population do you see seborrheic dermatitis?
AIDS
Parkinson
Pemphigus Vulgaris? epi? etio? RFs? Hx & PE? Dx? Tx?
PV - autoimmune blistering disease involves
epidermal surface of skin/mucosa/both
Epi - 50-60yo
Etio - autoimmune, blistering skin condition,
antibody mediating
RFs - HLA-DR4, underlying malgn
Hx & PE - bullae easily ruptures, mouth involved
+ Nikolsky’s sign, IgG deposits against desmosomes (epidermis) anti-glidan Abs
Dx - most accurate - biopsy
Tx - steriods, azathioprine or mycophenolate to wean off steriods or
rituximab (anti-CD20 Abs)
What drugs assoc w Pemphigus vulgaris?
- ACE inhibitors
- Penicillamine
- Phenobarbital
- Penicillin
Describe dermatitis hermpetiformis? Tx?
Dermatitis Herpetiformis - bullae dermatitis
IgA against dermal layers, neutrophils are
present
Tx - gluten free diet
Bullous pemphigoid? Hx & PE? Dx? Tx?
Bullae stay intact and there is less loss of fluid and infection, Mouth involvement is uncommon.
Dx - biopsy most accurate
Tx - best initial therapy is prednisone
mild bullous pemphigoid - responds to erythromycin, dapsone, and nicotinamide
Porphyria Cutanea Tarda? Etio? Hx & PE? Dx? Tx?
a blistering skin disease of sun-exposed areas in those with a history of:
• Liver disease (hepatitis C, alcoholism)
• Estrogen use
• Iron overload (hemochromatosis)
Dx = The most accurate diagnostic test is increased uroporphyrins in a 24-hour urine collection.
Tx =Correct the underly- ing cause (stop alcohol, stop estrogens) and remove iron with phlebotomy or deforaxamine
Describe Lichen Planus? assoc w?
6 P’s?
Lichen Planus - flexor surfaces of skin, polygonal violet
papules - wrists, ankle, mucous membranes
rarely assoc w Hep C
- think of 6 Ps purple, puritic, polygonal, peripheral, papules, penis, TX - steriods
Impetigo? Etio? Hx & PE? Dx? Tx?
- Staphylococcus and Streptococcus i
- invade the epidermis, resulting in weeping, crusting, oozing, and draining of the skin.
- found in warm, humid climate and poverty children
Dx - clinical
Tx - mild treat w mupirocin (topical 2%)
severe can give IV dicloxacillin & cephalexin
MRSA - give doxy or clindamycin or TMP-SMZ
Erysipelas? Etio? Hx & PE? Dx? Tx?
Erysipelas described as painful lesion on face, deep erythema raised margins well demarcated warm to touch
- more severe disease than impetigo because it occurs at a deeper level in the skin.
- more common cause is strep vs staph
- invades dermal lymphatics and causes bacteremia, leukocytosis, fever, and chills.
Dx - clinical, confirm by culture
Tx - if confirmed strep then give Pen G or ampillicin other treat for both unless cultures come back
What meds do you use for cellulitis, folliculitis, furuncles & carbuncles?
Mild disease: Use oral medications:
• Dicloxacillin, cephalexin, cefadroxyl
• Penicillin allergic: erythromycin, clarithromycin, or clindamycin
• MRSA: doxycycline, dindamycin, trimethoprim/sulfamethoxazole
Severe disease (fever present): Use intravenous medications:
• Oxacillin, nafcillin, cefazolin
• Penicillin allergic: clindamycin,vancomycin
• MRSA: vancomycin, linezolid, daptomycin, tigecycline, ceftaroline
What is cellulitis?
occurs below the dermal - epidermal junction
infection of soft tissue
- affects the lower legs, skin is warm, red, swollen, and tender
- unilateral erythematous plaque that poorly demarcated
- more commonly caused by staph
- Dx - clinical, most accurate is inject saline into skin and aspirate for culture
How would you treat cellulitis?
oxacillin, naficillin, cefazolin are best empiric therapy
- remember topical antibiotics will not work
What happens when hair follicles get infected?
staph infection of the hair bulb
furuncle develop into a small abscess –> collection of furuncles are called carbuncles
folliculitis –> furuncle –> carbuncles
How do you treat folliculitis, furuncles and carbuncles?
Can be treated w warm compress w/o antibiotics - if not then use mupirocin is best choice
for folliculitis and furuncles and carbuncles are treated w anti-staph antibiotics, IV for
carbuncles
What is necrotizing fascitiis? Hx & PE? Dx? Tx?
Necrotizing fasciitis - extremely severe, life threatening skin infection
MC polymicrobial, DM are at increased risk
Hx & PE - bullae and palpable crepitus, high fever
Dx - lab evid - increased CPK, imaging shows air in tissue or necrosis
confirm w surgical debridement
Tx - surgery, best empiric is ampicillin/sulbactam, if strep pyo tx w clindamycin + pen
What is paranychia? Difference btw chronic and acute?
Paranychia - loculation under skin, surrounding nail - tx - small incision & drainage w antistaph antibiotics
Chronic - nail not intact, can lose cuticle, affects women
Acute - nail is intact, yellow discoloration
MRSA infect - clinda oral
What antibiotics cover staph infections but aren’t specific skin infection?
Second generation cephalosporins (cefoxitin,cefotetan,cefuroxime)
• Beta-lactam/beta-lactamase combinations
Amoxicillin/clavulanate -
Ampicillin/sulbactam
Ticarcillin/clavulanate
Piperacillin/tazobactam
• Carbapenems (imipenem, meropenem)
superficial fungal infections are called - tinea
tinea coporis
tinea manus
tinea pedis
tinea cruris
Fungal infection - tinea & oncomycosis
Dx - initially clinical, confirmed w KOH prep
KOH dissolves skin & nail but not fungus which
shows fungal hyphae and yeast (balls & spagetti), if KOH + then no culture needed most accurate dx is culture
Tx oncomycosis (nail infection) or tinea
captis (hair) are treated with either
terbinafine (12wk for toenails & 6 wk fingernail) or itraconazole; must check LFT w terbinafine
other infections can be treated w ketoconazole
clotrimazole, econazole, terbinafine,
miconazole
What are the DDx for tinea?
DDx - Pitraysis vesicolor (hyperpig & hypopig lesion) = Wood light - yellow to white fluroscence
DDx erythesma = bacterial infection looks like fungal Wood light = coral red caused coryn
What is Ciclopirox?
antifungal
What antifungal is antiandrogenic?
oral ketoconazole causes gynecomastia
What are some of the drugs that cause hypersensitivity reactions?
- Penicillins
- Sulfa drugs (including thiazides, furosemide, and sulfonylureas)
- Allopurinol
- Phenytoin
- Lamotrigine
- NSAIDs
What is a fixed drug reaction? MC? Hx & PE?
Tx?
Fixed drug reaction - localized allergic rxn that
occurs within the same anatomical site on skin
with repeated drug exposure
MC - due aspirin, NSAID, tetracy, barb
Hx & PE - shar demarcated lesion leaving
hyperpigmentation spot after resolution
Tx - d/c drug & treat w topical sterioids
What is the morbilliform rash? Tx?
Skin stays intact without mucous mem- brane1involvement. No specific therapy.
Erythema multiforme? Hx & PE? Dx? Tx?
widespread, small “target” lesions; most are on the trunk. occurs in 7 days of infection No mucous membrane involvement. May also be from herpes or mycoplasma.
Hx & PE = erythema w central vesicles palms and soles, involves lips & buccal mucosal
Tx - antihistamine
Steven Johnson Syndrome? Hx & PE? Dx? Tx?
involves the mucous membranes. Sloughs off respiratory epithelium and may lead to respiratory failure.
<10-15% of total body surface area, usually involves face & body,
Tx - withdraw offending agent, supportive care & mechanical ventilation Steroids not clearly beneficial. Use intravenous immunoglobulins (IVIG)
Toxic Epidermal Necrolysis (TEN)? Hx & PE? Dx? Tx?
> 40-50%, more serious and severe, drug induced, Dx - biopsy reveals epidermal necrosisSepsis is MCC of death, prophylactic antibiotic systemic antibiotics
- rash with mucous membrane involvement and adds Nikolsky sign. Steroids definitely do not help. Treat with IVIG.
Toxic Shock Syndrome? RF? Hx & PE? Criteria? Dx? Tx?
TEN - exotoxin mediated illness caused by
either Group A strep or s. aureus
RFs = DM, alcohol, single tampon use,
surgery
Hx & PE = fever, hypotension, diffuse rash
Criteria = fever >38.9, diffuse macular
erythroderma - desquamation 1-2 wk after
rash, hypotension >3 organs involved
Dx - clinically
Tx - clindamycin + ticarillin/clavulanate or
pipercillin/tazobactam (IV)
if staph - clinda + vanco
Staphylococcal Scalded Skin syndrome?
+ Nikolsky sign
treatment w supportive care and anti-staphy (oxacillin or nafcillin)
- drugs don’t reverse the disease but kill staph
What are decubitus ulcers? Hx & PE? Dx? Tx?
Decubitus Ulcers - chronic sores occuring in the pressure areas of body where bone is closer to skin, pts who are bedridden Hx & PE - nonblanchable reddness —> destruction of superificial epidermis —> destruc all the way to bone Dx - surgical debridement Tx - relieve pressure if still there then antibiotics
What is erythema nodosum? Hx & PE? Dx? Tx?
Erythema Nodosum - localized inflammatory condition of skin secondary to recent infection
assoc w pregnancy, strep infection, coccidiomycosis, histoplasmosis, sarcoidosis, IBD, syphillus or hepatits
Hx & PE - multiple painful red raised nodules on anterior surface of lower ext, lasting 6 wks
Dx - ASLO titers show recent strep infection if no etiology in hx
Tx - treat underlining condition & analgesics - NSAIDS and potassium iodide solution respond to treatment
What is alopecia acreata?
Alopecia Acreata - autoimmune disease - Ab’s attack hair follicles and destroy hair production
Tx - resolves spont; immediate therapy is steroid injection
Rosacea? Hx & PE? Etio? RF? Hx & PE? Dx? Tx?
Rosacea - chronic inflam condition that causes flushing w burning sensation
most common manifestations are flushing, dilated prominent telangiectases
(primarily on the face), persistent facial erythema
Etio = exaggerated vasodilatory response to increased temperature, and redness
can be easily exacerbated by hot drinks and hot baths or showers
RF = lighter skin, hot showers, extreme climate
Hx & PE = flushing, nontransient erythema, dome shaped red papules & pustules
phyma - distinct swelling caused by lymphedema and hypertrophy of subcut skin
Dx - clinically
Tx - avoid topical steriods, telangiectasia tx w ablation
oral tetracycline/topical metro/oral erythromycin
What is the patho of pemphigus vulgaris? Etio?
Pemphigus vulgaris is an autoimmune disease of unclear etiology in which the body essentially becomes allergic to its own skin. Antibodies are produced against antigens in the intercellular spaces of the epidermal cells.
Etio - Pemphigus vulgaris is most often idiopathic, but ACE inhibitors or penicillamine can occasionally cause it.
What is the clinical presentation?
Vulgaris occurs in patients age 30s and 40s
Pemphigus vulgaris is a much more serious and potentially life- threatening disease than pemphigoid. Vulgaris occurs prominently in the mouth and often starts there. The oral lesions are erosions, not bullae.
The bullae are very thin and flaccid and break easily. This leads to the loss of large volumes of skin surface area, so it acts like a burn.
pemphigus vulgaris are painful, not pruritic.
What is Nikolsky sign? What diseases have it?
The presence of the Nikolsky sign (the easy removal of skin by just a little pressure from the examiner’s finger, pulling the skin off like a sheet)
pemphigus vulgaris, staphylococcal scalded skin syndrome, and toxic epidermal necrolysis.
How do you Dx PVulgaris?
The most accurate diagnostic test is to biopsy the skin and to use immunofluorescent
stains. These stains will detect intercellular deposits of IgG and C3 in the epidermis.
Treatment of PVulgaris?
Treatment is with systemic glucocorticoids, such as prednisone.
For those in whom steroids are ineffective or not tolerated, you can use azathioprine, mycophenolate, or cyclophosphamide. Rituximab and IVIG are also effective.
What is the patho of bullous pemphigoid?
Pemphigoid is 2× as common as pemphigus vulgaris and occurs in elderly persons age 70s and 80s. It can also be drug induced with sulfa drugs, including furosemide, penicilla- mine, and others.
How does Bullous pemphigoid present?
The defect occurs at the dermo-epidermal junction, so the layer of skin that separates off is much thicker.
Hence, there is much less fluid loss, and infection is much less likely as compared with pemphigus vulgaris. less mortality
How do you Dx bullous pemphigoid?
The most accurate diagnostic test is a biopsy with immunofluorescent antibodies at the dermo-epidermal junction (basement membrane).
What is the treatment of bullous pemphigoid?
Systemic steroids, such as prednisone, are the standard means of treatment. Tetracycline or erythromycin combined with nicotinamide is the alternative to steroids. Use topical steroids only if no oral lesions are present.
What is the patho of porphyria cutanea tarda?
Porphyria cutanea tarda is a disorder of porphyrin metabolism. Deficiency of the enzyme uroporphyrinogen decarboxylase results in an abnormally high accumulation of porphyrins, which then leads to a photosensitivity reaction.
- The test question should give a history of HIV, alcoholism, liver disease, chronic hepatitis C, or a woman taking oral contraceptives.
- porphyria cutanea tarda is associated with increased liver iron stores
- Diabetes is found in 25% of patients.
What is the presentation of porphyria cutanea tarda?
Fragile, nonhealing blisters are seen on the sun-exposed parts of the body, such as the backs of the hands and the face. This leads to hyperpigmentation of the skin in general and hypertrichosis of the face.
How is porphyria cutanea tarda Dx?
The diagnostic test is a level of urinary uroporphyrins. Uroporphyrins are elevated 2–5× above the coproporphyrins in this disease.
What is the treatment of porphyria cutanea tarda?
The best initial step in management is to stop drinking alcohol (although it is unlikely to be effective) and to discontinue all estrogen use
- Combine treatment with barrier sun protection, such as clothing, because most sunscreens do not seem to block the wavelength of light causing the dermal reaction.
- The most effective therapy to use if this is insufficient is phlebotomy to remove iron.
- Deferoxamine is used to remove iron if phlebotomy is not possible
- antimalarial drug chloroquine increases the excretion of porphyrins.
What is the patho of urticaria?
Acute urticaria is a hypersensitivity reaction most often mediated by IgE and mast cell activation, resulting in evanescent wheals and hives. It is a type of localized, cutaneous anaphylaxis, but without the hypotension and hemodynamic instability.
- The most common causes of acute urticaria are allergic reactions to medications, insect bites, and foods, and occasionally, the result of emotions.
- The most common medications are aspirin, NSAIDs, morphine, codeine, penicillins, phenytoin, and quinolones. ACE inhibitors are also associated with urticaria, as well as angioedema
- most common foods are peanuts, shellfish, tomatoes, and strawberries. Contact with latex in any form can also cause urticaria.
What is the clinical presentation of acute and chronic urticaria?
Acute urticaria lasts 6 weeks in duration and is associated with pressure on the skin, cold, or vibration. In patients with chronic urticaria lasting >6 weeks, you should investigate the etiology.
Treatment of urticaria?
Urticaria is treated with H1 antihistamines. Severe, acute urticaria is treated with older medications, such as diphenhydramine (Benadryl), hydroxyzine (Atarax), or cypro- heptadine. If it is life-threatening, use H2 antihistamines when H1 antihistamines fail and add systemic steroids.
- Chronic therapy is with newer, nonsedating antihistamines, such loratadine, desloratadine, fexofenadine, or cetirizine
- Astemizole and terfenadine should never be used and are no longer marketed;
