Derm Flashcards
explain the location of atopic dermatitis
atopic dermatitis
what age group is this found it? what are the three characteristics in a patient that make them higher risk for this? what are three things you might see on this patient? what type of hypersensitivity is this? where is this most commonly found (2) places and 4 others? what must you differentiate from? what is the diagnosis made from?
chronic relapsing skin disoder that starts in children and goes through adulthood
ALLERGY, ALLERGIC RHINNITIS, ASTHMA, PERIORAL PALOR, DENNIE MORGAN LINES, ALLERGIC SHINERS
type 1 IgE mediated hypersensitivity
-dry skin, puritis with “itch scratch cycle” flexor creases (antecubital and popliteal) most common
neck, eyelids, forehead, face, and dorsum of hands and feet, dermatographism characteristic
can be either atopic or contact (touching something you’re allergic to)
*make sure to culture for S. aureus and make sure not secondary infection and HSV in crusted lesions*
DX: IgE serum levels
atopic dermatitis
what are 6 possible treatment options for this?
1. avoid irritants
- skin lubrication/emollients (moistureizers)
3. topical corticosteroids
4. antihistamines
- calcineurin inhibitors (tacrolimbus + pimecrolmus)
- UVB phototherapy is effective
for atopic dermatitis….what can you do to figure out what is causing it?
PATCH TESTING!!!
contact dermatitis: allergic
what cells initiati this? what are 5 common causes? what is the difference between the acute and chronic skin presentations?
t-cell mediated, occurs in those that have become sensitized
- common causes: medication, jelwrey, rubber, disinfectants, cosmetics, plants*
acute: erythema, vesicles, eroisions, crusting
chronic: papules, plaques, crusts
**can do patch testing after dermatitis to figure out the cause**
contact dermatitis: non allergic
what is this caused by? (3)
what do the acute and chronic skin presentations look like?
comes from contact with an irritating substance
direct toxin on the skin
common causes: abrasive, cleaning agents, caustic agents
Acute: erythema, vesicles, erosions, crusting
chronic: papules, plaques, crusts
where is the rash for seborrheic dermatitis?
seborrheic dermatitis
what does this occur in? what are the four most common places? what is the most common agent? what does this cause in infants and what does this cause in adults? what do the infected areas look like? what are the 7 treatment options for this?
subacute/chronic inflammation of the areas with increased SEBACEOUS GLANDS
body folds, face, scalp, genitalia
caustitive agent: pityrosporum ovale (yeast)
“cradle cap” in infants, “dandruff” in adults
scattered yellow gray scaly macules and papules with GREASY LOOK!!!
sticky crusts with fissures found behind the ears!!!
Tx:
- OTC dandruff shampoo
- cold tar shampoo
- Ketoconazole
- cradle cap: olive oil compresses, shampoo with sulfur, or ketoconazole shampoo
- UV radiation
6. shampoos with selenium sulfide
7. topical steroids hydrocorisone
stasis dermatitis
what causes this? what two populations of people is it worse in? the incompetency leads to what 5 things? what does the pt complain of? what 3 things do you see before the skin changes? what are two ways to make the DX and what do you see?
chronic rash on lower legs secondary to venous insufficiency
worse in pregnancy and women
see papules, scales and crusts
valvular incompetency leads to edema, dermatitis, brown stippled hyperpigmentation, fibrosis, ulceration (30%)
pt complain of aching in legs that is worse with standing, relieved by walking
typically see caricose veins, superficial phlebitis, and venous thrombus before skin changes
DX:
- doppler studies, sonography or venography will confirm chronic insufficiency
- biospy-show dilated tortuous veins, edema, and fibrin deposition
dyshidrosis
what type of dermatitis is this and where does it occur? what age group? what is it commonly associated with? what is the funny food it is associated with looking like and what other characteristic is common? what are four triggers? what does it transform in to in late disease (5)? what two things are used to diagnose it?
acute/chronic puritic vesicular dermatitis on palms and soles
purititc, clusters of small vesicles in clusters “tapioca like appearence” on palms/soles
triggers: sweating, emotional stress, warm/humid weather, metals
Late disease: papules, scaling, lichenification, erosions ruptured from vesicles, painful fissures
DX: culture and KOH to rule out dermatophytosis
dyshridrosis
what are the 5 treatment options?
- burrows solution and antihistamines (control itch)
2. topical high steroids
- systemic steroids if severe
4. intralesional triamcinolone
- fissures treated with: collodoin
what are the treatment options for stasis dermatitis?
(6)
1. manage edema
2. topical corticosteroids
3. wet compress for oozing and crusting (caution with ulcers)
- compression stockings
- sclerosis of varicose veins to prevent dermatitis
- vascular bypass, endothelial thermal ablation or stenting (these are only mildy effective)
explain the locations that are common for…:
- acne vulgaris
acne vulgaris
what are the four causes?
1. increased sebum production seen with puberty and increased androgens
2. clogged sebaceous glands
3. propionibacterium acne overgrowth
- anaerobic bacteria that is part of normal flora in the PS unit
- digeste the sebum, but when large plug stimulates baterial for form lipase, this breaks down sebum in to fatty acids which spart inflammation process causing neutrophil attach to follcular wall
4. inflammatory response
Acne Vulgaris
what are the three general types?
- comedomes
2. inflammatory pustules/papules
3. nodular or cystic acne
acne vulgaris
comedomes
what are the two types? explain what causes each.
- open “blackheads”
- infundibulum: hyperkeratosis, comecyte cohesiveness
- androgen stimulations and sebum secretion
2. closed “whiteheads” - accumulation of shed keratin and sebum
- formation whorled lamellar concentrations
what are the ratings for acne severity? (3)
what are the meds associated with each?
mild: comedones +/- small amounts of pustules retinoids, azelaic acids, salicyclic acid
moderate: comedones larger amounts of pustules and papules topical trentoin, erythromycin, clindamycin
severe: nodular or cystic oral minocycline, tetracycline, doxy, Isotrentoin
erythmatotelangiectatic rosacea
what is it
facial flushing with telangiectasis, central face edema, SPARES PERIORBITAL AREAS
papulopustular rosacea (PPR)
central face erythema with papules and pustules, less often stinging
SPARES THE PERIORBITAL AREA
Phymatous rosacea
what is it and where does it occur?
follicular orficies thicken!!!! get nodularities that are disfiguring!
more common in men
get a rubery thickening of skin of the nose, chin, forehead, eyelids, or ears
what are the treatment options for acne vulgaris? (6) options
- benzyl peroxide
- topical antibiotics (clindamycin, erythromycin, dapsone)
- azeleic acid-unique plant derived compound that has anti-bacterial and anti-comedogenic properties
- salycyclic and glycolic acids gels and washes
- topical retenoids-adapalenes (differin), tretoin, and tazarotene
- oral antibiotics minocycline, tetracycline, doxy! these are different than the topical abx!!
- isotretinoin-drastically attentuates acivitt of sebaceous glands and rate of keratinization in epi ONLY DERM CAN DO THIS HIGHLY TETRAGENIC!!!!
*****notice there is a difference between oral and topical antibiotics*******
rosacea
what is this caused from? who is this most common in? what can be triggers for this? what are 4 unique presentations to this? what distinguishes this from acne? what are the 5 treatment options?
conrtoversy if cause is from inflammation or infectious
most common in fair skinned individuals
triggers: hot/cold,, HOT DRINKS, hot baths, spicy foods, ETOH, emotions
flushing and telangiectasis are key features of disease!!! causes phyma (enlargement of random area of the body), symmetrical presentation can have facial burning or stining, dry appearance, occular manifestifestations
***absense of comedones, distinguishes it from acne***
TX:
- topical metronidazole sodium, sulfacetamide, sulfur, erythromycin
- systemic abx: minocycline, doxy, metronidazole
- isotrentinoin
- ivermectin (anihelminthic)
- surgery for phyma
cellulitis
where does this infection occur? what are the 3 organisms most likely to cause this in adults? what are the 3 organisms likely in kids? what are the 5 symptoms the patient will experience? what is the strange animal you can get this from? what do you do to DX this?
acute, spreading inflammation of the dermis and subcuteous tissues, occurs from breaks in the skin
adults: s. aureus, group A strep can get it from cat bite pasturella mulicida
children: hae. influenzae (periorbital), strep pneumoniae, s. aureus
expanding, red, swollen and tender, FEVER!! HEAD!! LYMPAHDENOPHATHY!! EDEMA!! NOT sharply demarkated…pt feels ILL
DX: culturing and drainage of discharge by needle aspiration
cellulitis
what are the four treatment options? and what is really important to do when treating a cellulitis patient?
- rest/heat
- begin treatment ASAP with abx that cover haemophilis influenzae, strep and staph!
- dicloxacillin or cephalosporin, if allergic to penicillin use erythromycin
- if severe give first generation cephalo IV!!
really important to mark the boarders so you can tell if it is improving or not!! may need surgery if necrotizing infection develops
erysipelas
what aged people is this common in? what are the two places this commonly appeares? what is the #1 causing organism? what does the rash look like and what is it characterized yet? when does it disappeare? what is the DX and TX?
variant of cellulitis in ELDERLY on FACE AND EXTREMITIES
group A beta strep
painful macular rash with well defined margins, vessicles, FEVER, rapid onsetand progression“fiery red face“
- rash desquamates in 5-10 days*
- DX:* bacterial culture
TX: treat with antibiotics depending on organism!
impetigo contagiosa
what two age groups is this common in? what two environmental things is it common with? where do you typically see this and is there a family hx? what key description of the lesions? what are the 3 organisms that commonly cause this? what are the three tx options?
common in INFANTS AND CHILDREN!!
higher rates with poor hygiene and malnuitrition
HIGHLY CONTRAGIOUS!!! COMMONLY ON FACE!!! usually have family history of this!
THICK CRUSTED “HONEY” colored macules and papules! starts as one, and spreads
#1- staph aureus
#2-GABHS
#3-streptococcus pyoderma
TX:
- bactroban
- cephalexin or dicloxacillin if severe and need systemic
bullous impetigo
what organism causes this? who is it most common in? what three places do you see this rash most commonly present? what do you worry about as a SEVERE COMPLICATION?
Staph group II, staphlococcus with endotoxin
STAPH AUREUS
- most common in children/infants* overall not common
- face, neck, and extremities*
erythema that progresses to epidermal sloughing, worry about progression to scalded skin syndrome!!!
TX:
- bactroban
- cephalexin or dicloxacillin if systemic needed
folliculitis
what organism is most common for causing this? what is the second most common? what three areas does this most commonly effect? what are the two types of presentations you see? what are the two treatments?
staph aureus infection of the hair follicles!
commonly seen on butt, thighs and beard!
“superficial hair”
can be pseudomonas
PAPULES AND PUSTULES
Tx:
antiseptic cleaners
mupirocin
hidradentitis suppurativa
occurs in areas with apocrine glands like axilla, angiogenital, and scalp leading to potential scarring and fibrosis
females: axilla more common
men: angiogenital more common
TENDER INFLAMMATORY NODULES OR ABCESSES, open comedomes and sinus tracts may drain purlulent fluid
TX:
- trimcinoloine
- drainage of the abscess and excision of the sinus tracts
- antibiotics until lesions resolve
**should consider psychological support for anogenital because it can be stressful***
basal cell carcinoma
how does this cancer most commonly present? fast or slow? why does the pt ususally seek help? where is it most common? what is the treatment?
MOST COMMON SKIN CANCER
pearly boarder (most common presentation), smooth nodule with telangectasis!!! KNOW THIS
spreads SLOW, easily treated they can itch or bleed and this is why pt seeks help because it won’t heal!!
ear, face, neck most common!!!
Can come in these 3 other presentations, but not as important:
Flat scaly lesions
Flesh colored or Brown
Morpheaform-scar like
Tx: complete eradication
- excise
- curettage
- cryrotherapy
- surgery
- mohs
more pics of basal cell carcinoma
Melanoma
how aggressive? what is it most commonly associated with? metastasis? what colors can it be? what abou borders? how does the pigment spread? what about lesion type? what is the treatment?
VERRYYYYY AGRESSIVE!!!!
80% ASSOCIATED WITH UV RADIATION!!!! (can be in eye and anus)
HIGH METASTASIZEEEEEEE RATE!!!!!
BLACK OR DARK BROWN, SOMETIMES BLUE WITH MULTIPLE COLORS
IRREGULAR BORDERS
OUTWARD SPREADING PIGMENT
CAN BE MACULAR TO NODULAR OR FLAT
Tx:
*****MUST EXCISE ALLL OF IT THROUGH MOHS OR FULL THICKNESS EXCISIONAL BIOPSY!!!*****
what are the four types of melanoma and who/where would you find them?
1. Superficial spreading malignant melanoma
****MOST COMMON***
single melanoma
upper back and legs
mostly adults
plaque irregular
GREAT IRREGULARITY
always growing
2. lentigo maligna melanoma
in eldery
3. nodular malignant melanoma
4. acral lentiginous melanomas
***In palms, soles, nail beds***
squamous cell carcinoma
what happens in this? why do patients often seek help? metastasis? what are two things that commonly preced it? what are the treatments?
2nd most common type of skin cancer
originates in the keratinocytes of the mucosa and skin KERATINIZATION
patients often seek help because they bleed or itch and they don’t seem to heel (same as basal)
red firm nodules, scaly with crust, sometimes bleed METASTASIZES
often preceeded by actinic keratosis or HPV
Tx:
excision, curettage, cyrotherapy, radiation, mohs,
what is the most common melanoma type?
superficial spreading melanoma
where are the 5 places melanoma likes to metastasize?
- lymph nodes
- skin
- liver
- lungs
- brain
NAIL AND GENITAL MELNOMA
LENTIGO MALIGNA
what determines the prognostic factor for melanoma mets? what are four regional places with worse prognosis?
the depth of the cancer=breslow’s depth
**deeper=worse prognosis**
worse prognosis if on upper back, upper arm, neck, or scalp
what is key in melanoma?
early detection!!!
alopecia
what percent have family history? what happens in this? what does the hair look like? and what about new hairs? what are the two categories of alopecia? what are the two treatment options
cause unknown can be assocaited with autoimmune like SLE
10-20% have family hx, usually toung
disruption of normal hair cycle where hair follicles prematurely enter inactive phase
exclaimation mark point hair pulls out easily from head, new hairs often gray or white
1. androgenic alopecia: male pattern baldness, TX: minoxidil or finasteride
2. alopecia arata: exclaimation pointhairs, alopecial totalis or universalis
TX:
1. intralesional triamcinolone for small lesions
2. systemia corticosteroids for large regions
what are four RF for onchomycosis?
- exzema
- DM
- immunosuppresion
- occusive footwear
onychomycosis
(tinea unguium)
what fungus causes this? where is it most common? what does the look like? what MUST you do to dx this? what is the treatment for this? what percent are cured vs. clinical improvement?
trchophyton rubrum
most common in urban areas
infection of 1 or more fingernails or toe nails
opaque, thickened, discolored nails with subungual keratinzation, cracking nail
all dx must be confirmed with lab, NEVER DO on just clinical alone!! KOH
This is because you must do SYSTEMIC TREATMENT for 12 weeks terbinafine
*****only cured in 30-50% but 75% improve clinically*****
paronychia
what is this? what is the difference in the acute/chronic pathogen causes? what might this form that is a medical emergenct? what is the TX for mild, mod and severe?
acute infection of lateral or proximal nail fold, pain my extend into the proximal nail fold and eponychium
acute: staph aureus
chronic: candidia
may form a felon soft tissue infection of the pulp space, it can rupture and cause osteitis or osteomyelitis so MUST DRAIN THIS!!!!! THIS IS AN EMERGENCY!!!!!!
TX:
mild: local wound care, warm soaks
mod: topical antibiotics like bacitracin +/- topical corticosteroids
severe: oral antibiotics with or without excision/drainage with finger web block
alopecia totalis
alopecia universalis
what do these mean?
alopecia totalis=entire scalp
alopecia universalis=entire body
actinic kerratosis
“solar keratosis”
what does this have the potential to develop into? what type of condition is this? what causes this? who is it more common in? what does it feel like and what cells are increasing? what are the 3 treatment options?
potential to develop ino squamous cell carinoma
thickening of the horny layer of the epidermis, premelignant condition caused by sun exposure
-more common in fair skinned individiuals. can also develop into cutaneous horn!!!
rough dry “sandpaper” appearence from hyperkeratinization** and **plaques
TX: topical 5-fluorouricil, cryrosurgery, laser
seborrheic keratosis
who is this most common in? is this cancerous? what causes this? what are the 3 key buzz workds for this? what are the 4 possible treatment options?
MC in fair skinned and ELDERY from sun exposure
BENIGN
thickening of the keratin (keratinozation) of the horny layer of the epidermis
“velvety wart apperance” “greasy” “stuck on appearence” benign plaque beige-brown-black
TX: since begnin don’t need to do anything but if bother the patient can…
- cryrosurgery
- electrodessication
- 5-fluorocil
- ecurettage
where do you see the rash for psoriasis?
psoriasis leading to psoratic arthritis…what are the characteristics of this?
occurs in 5-10% of patients
Labs: elevated ESR, UA, decreased iron
“sausage digits” with pencil in cup deformity, stiffness relieved after 30 mins activity
**LEADS TO HEART DISEASE***
chronic stable plaque psorisis
where are the three areas this is most common? what is it called when person get its it from repetitive trauma? what is a worry with this?
most common subtype of psoriasis
trunk, scalp, and extremities of extensor surfaces
“koebner pnenomenon”- occurs in areas with repetitive trauma, tile setter etc.
ITS REALLY UNPREDICABLE, CAN BE STABLE AND THEN ALL THE STUDDEN GET A LOST WORSE INTO 20-30% BSA WITHOUT REASON (life/stress)
relatively fixed, and stable pink erythematous scaling plaque
palmoplantar pustular psoriasis (PPP)
is this serious? what does it look like and where is it? what can cause it in the pt? what are the three treatment options and which one is the most important?
abrupt and LIFE THREATENING condition characterized by widespread pustules that coalasce to form lakes of pus, accompanied with fever and malaise
DEBILITATING chron eruption of PALMS AND SOLES
painful and deeply seeded
**can lead to depression in pt**
TX:
- GO TO STRONGEST TOPICAL STEROID WITH OCCULSIVE DRESSING AND PLASTIC WRAP
- retinoids and UV light
guttate psoriasis
acute or chronic? what preceeds this and what do the lesions look like? what do you want to make sure you test a patient with this for?
acute/ SUDDEN papulosquamous eruption
strep or viral URI, “rain drop/red paint splatter” appearance
brightly erythematous round scaling disseminated papaules
often persons first experience with their psoriasis, want to do throat culture for strep and lymphatic and treat with empiric abx
lipomas
what are these a tumor of? what are there 4 characteristiscs? what are a subset of these you do worry about and what do you need to do about them? what is a treatment option? what can cause this from long term use?
benign adipose subcutaneous tumors
neoplasm of mature fat cells no harm to the patient
SOFT, NONTENDER, LOBULATED, MOVEABLE MASSES under the skin, can be only one or a whole bunch of them and can be up to 6 cm!
angiolipomas: have vascular component, should be excised, these are tender in cold temp and with compression
Tx: lipomas are fine and only should be removed in irritating area or for cosmetic reasons. if soft and not connected to connective tissue can do LIPOSUCTION!!
-angiolipomas with vacular component need to be removed
chronic steroids can cause uneven and abnormal fat distributions= lipomas
general dermaphyte infections
“ringworm…but not a worm”
what does the rash look like? where might you see other symptoms? what are the treatments? what is important to insure successful treatment? what do you need to monitor? and what can’t you do?
erythematous ANNULAR patch with distinct boarders and central clearing, usually fine scale covers patch
itching, stining maceration or peeling fissures are common between the digits, nail discoloration and onchyologys of the nail bed and plate
Tx: keep area dry with powder, topical antifungals and then systemic if don’t work compliance and monitor is very important with these!! NEED TO MONITOR LIVER FUNCTION AND CANT DRINK WITH GRISEOFULVIN
kerion
boggy inflammatory plaque studded with pustules
can appear in any of the dermaphyte infections but most common in tinea capitis
tinea corporis (dermaphyte)
what population of people do you worry about in this? what do you see on the hair? what does the rash look like? what do you treat with and for how long? how long should the treatment continue?
worry about this in wrestlers**, **broken hair shafts seen as black dots SEEN ON BODY!!!
scaling, sharp, annular ring shaped plaques with central hair clearing with scales
Tx: topical antifungals, usually responds within 4 weeks
****continue treatment 1-2 weeks after clinical clearning***
tinea capitits (dermatophyte)
who is it most common in? what two things will you see? what is the treatment?
most common fungal infection in children
causes ALOPECIA, can have presence of KERION
TX: oral griseofulvin
Tinea pedis (dermatophyte)
what is this called? where are the two most common presentations? what does the lesion look like? how long can it last? how can ou prevent it?
“Athletes foot”, most common 20-50s
two most common presentations:
- in between the twos
2. mocasin presentations with sole and heels
erythema, scaling, maceration or bullae formation with burning or stinging
***can last months to years to lifetime***
Prevention: shower shoes, keep it dry antifungal powder for tx
tinea versicolor
aka
pityriasis versicolor
what organism causes this? what does it look like on the person? what does it look like under the microscope? what color does it fluoress? what type of yeast is this? when do people usually notice this? where is it most common? what are the 3 treatmetion options and how long does it last?
malassezia furfur
“velvety” hyopigmented macules 4-5 mm
“spaghetti and meatballs” on KOH hyphae and spores, green/yellow flurescence on woods lamp,
THIS IS A YEAST!!! lipophilic yeast that lives in te keratin of skin and hair follicles but can overgrow, NOT CONTAGIOUS
people usually get this in the summer when they go in the sun and get tan but get blotchy areas that don’t tan
most common on upper trunk and shoulders
Tx: ketoconazole shampoo, selenium sulfide, oral ketoconozole in extreme cases **dyspigmentation persists months after successful treatment**
tinea cruris (dermaphyte)
what is this? where is it common and what does it spare? what is it always associated with? what does lesion look like? what do you tx with?
“JOCK ITCH’
dermaphyte infection in upper thigh, groin and extend to butt
scrotom and penis rarely involved!
always associated with tinea pedis, weird!!
large scaling with well demarked plaques with central clearning
Tx: antifungal
exanthematous/mobilform rash
when can this happen? what does it show up as? what are the 5 most common drug causes? what do you treat with?
most commmon skin eruption following drug admin
generalized bright red macules and papuples that colasce to form plaques
abx, NASAIDS, allopurinol, thaizide, diuretics
TX: oral histamines
where is the rash for pityriasis rosea?
pityriasis rosea
what might this be caused by? what are two things that preceed the systemic rash? what does it look like and what pattern does the rash take? what is the treatment
unknown, thought herpes virus 7, fall/spring, teenagers and young adults, URI prodrome first 1-2 weeks prior that leads to the herald patch
herald patch, salmon colored (solitary round salmon plaque with scales on trunk) which preceeds a widespread symmetrical papular eruption by 1 week
this new rash is salmon colored and follows the the natural skin folds making a christmas tree distribution
Tx: self limiting 6-8 weeks, UVB may be helpful if first week
varicella-zoster virus
explain the differences seen between the primary and secondary eroptios of this virus? how are they descirbed? what sign do you watch out for? what is the order of the lesion developement? where does it begin and where does it spread to?
VARICELLA-ZOSTER virus
varicella (chicken pox): 1st exsposure vesicles on a erythematous base “DEW DROPS ON A ROSE PETAL” describe the different stages
macules->papules->vesicles “dew drops on a rose petal”->pustules->crusts **appeare in crops!**
BEGIN ON FACE AND TRUNK AND SPREADS TO EXTREMITIES
Herpes zoster (shingles): VZV reactivation along a Dermatone in THORACIC OR LUMBAR REGIONS, reactivation from ganglionic satelite cells!
-Hutchinson’s sign:lesions on the nose mean lesions in the eye sincetrigeminal nerve involvement CN #5
what are the two complications you worry about with herpes zoster virus reactivation (shingles)?
- eye involement herpes zoster opthalmicus: look for hutchinson’s sign which is lesions at the end of the nose, if seen here likely it is already in the eye since it follows along the trigeminal nerve or CN 5
- ear involvement herpes zoster oticus: look for ramsay hunt syndrome if lesions are seen on the ear, likely in the canal since it follows facial nerve or CN 7
verrucae
what are they caused by? what is the most common? what are the 5 types of warts that can present? what are the three things that help you diagnose this?
caused by 100+ serotypes of HPV!
verrucae vulgaris mos common!
firm papules, skin colored, _vegitation_s, red brow spots
1. skin warts: flat/superficial verrucae vulgaris
2. plantar warts: deep, “tiny heads of colliflower”
3. oral cavity warts or in pharynx: can be life threatening if block the airway
4. angiogenital warts: squamous epithelium of external genitalia CONDYLOMATA
5. cervical warts: HPV 16 and 18 cause dysplasia
Dx: microscope: hyperplasia, hyperkeratosis,
koiliocytic squamous cells present!
immunofluorescence->see HPV
erythema infectiosum
human parvovirus B19
fifth disease, red face”slapped cheek”, arthropathy
pink lacey rash with slapped face appearence, arthropathy is common in older children and adults
infectious disease associated with arthropathy! spreads by respiratory droplets!
***CAUTION!!…this can cause an aplastic crisis in sickle cell patients***
roseola infantum
what virus causes this? what unique thing does the fever correlate with and how long does it last? what is interesting about the rash location and progession? who is this common in?
herpes virus 6 or 7
fever for 4 days, this resolves before you get the pink macular rash!!** during this time though the child still appeares well, doens’t seem sick!
children
only childhood exanthem that starts on the trunk and migrates to the face!!
measles
what virus causes this? what type of rash? what are the 3 things you should relate to this? what can you see in the mouth and what do they look like? where does the rash start? what is the treatment?
paramyxovirus=maculopapular rash
URI prodrome with 3 C’s:
COUGH, CORYZA, CONJUNCTIVITIS
FEVER, COUGH, ANOREXIA
KOPLIK SPOTS IN THE MOUTH: small red spots in the buccal mucosa with blue/white paler center
Brick red rash on skin begining at the hairline!!
Tx: supportive and antiinflammatories!!
rubella (german measles)
what virus is this caused by? how long does the rash last? what is the important thing to consider if the woman is pregnant and what 3 things can it cause? what do you see for lymphadenopathy? what is the buzz word rash?
togavirus
rash lasts 3 days!! pink maculopapular rash head to toe TERATOGENIC!
can see lymphadenopathy posterior cervical and posterior auricular
can see transient joint pain and photosensitivity in young women
TERATOGENIC IN 1ST SEMESTER: congenital syndrome, sensineural deafness, “BLUEBERRY MUFFIN RASH!”
peduculosis capitis
how many legs does this have? who is it most common in? what do the eggs look like? can this cause infectious disease? what are the 4 treatment options and WHAT MUST YOU REMEMEBER TO DO??
“Head Lice” 6 legs 1-2 mm common in overcrowding or poor hygiene, children!
lice lay white oval egges at base of hair follicle, only survive few hours off scalp
CANT CAUSE INFECTIOUS DISEASE THANK GOD
TX:
- permerthrin DOC
- lindane/ivermectin (oral) DOC
- special combes and petroleum jelly
- wash all bedding and clothes, and put the in the dryer, or put them in a bag for 14 days
*******KEY: MUST REAPPLY IN 7-10 DAYS TO KILL ANY NEWLY HATCHED EGGS AND LICE*****
pediculosis corporis
where doe these live? can these transmit disease? what do you need to do? treatment?
live in the seams of the clothing, NOT THE BODY!!
THEY DO TRANSMIT INFECTIOUS DISEASE
dispose of infected clothing and bedding!! puritis!!
Tx: permethrin
pediculosis pubis
what is this? what does it look like? what is the treatment? who else must you treat?
“CRAB LICE/PUBIC LICE”
brownish gray specks, with puritis for months
TX: permethrin cream MUST TREAT SEXUAL PARTNER!!!
scabies
what is the parasite that causes this? how many legs? where is this a major concern? where is the itching characteristic? what do you see on the skin? what is pathoneumonic if you see on the skin? what are the four treatment options and what must you do??????
sarcoptes scabei 8 legged mites, MAJOR COCERN IN LESS DEVELOPED COUNTRIES
webbed spaces between fingers and toes, wrists, around belt line or at edges of socks, EXTREMELY PURITIC
burrows, papules or nodules on scrotom glands or penile shaft are indicative, brown dots visible microscopically…thats the poop
TX:
1. 1% lidane, 5% permetherin lotion
- ivermectin (oral)
2. antihistamies for itching
- topical corticosteroids for itching
******MUST TREAT EVERYONE AROUND THEM REGARDLESS OF SYMPTOMS!!!******
black widow spider bite
what spider species is this? what does this cause? what does the lesion look like with which key thing? what are the four treatment options?
latrodectus mactans
neurological overstimulization (muscle aches, spasms, rigitity), OUTSIDE THE HOUSE, target lesions with diaphoresis around effected site
Tx:
- muscles spasms: diazapam
- pain: opoids
- ridgity: calcium gluconate
4: antivenom (requires horse serum senstivity testing first and reserved for elderly or infants!)
brown recluse spider bite
what species of spider causes this? where are they most likely found? when does the pain start? what are 3 things/apparences the lesions takes? what symptoms does the patient get? WHAT DOES THIS LEAD TO? what are two treatment options?
loxosceles reclusa
most bites happen in the morning when somone puts on their clothes that have been lying on the ground MOSTLY INSIDE THE HOME
pain 3 horus after bite:
1. infarct on skin with rapid blood coagulation
2. “sinking” macule pale grey in color and eroded in the center with halo appearance (pance)
3. “red halo” hemmoragic bullae that undergoes eschar formation (pearls)
fever, headache, malasie and arthralgia leading to NECROSIS
Tx: oral corticosteroids with consideration of early excision at bite site
stevens johnson’s syndrome
what is this thought to be a sever form of? what percent of the BSA? what does it look like? what are the two most common drugs that cause this? what are the 3 complications you worry about? what does the patient present with and then what do they look like 4 days later? what is the treatment? what is the special sign?
thought to be a severe form of erythema multiforme but unknown cause
mucotaneous blistering reactions most often caused by drug rxn sloughing especially sulfanamides and anti convulsants
worry bout complications!! infections, fluid loss, and electrolyte imbalance
pt presents with:
fever, photophobia, sore throat with mucosal inflammation and cutaneous lesions on trunk
4 days later:
diffuse erythema, necrotic epidermis, wrinkled surfaces, sheet like loss of epidermis, raised flaccid blisters nikolsky sign
tx: send them to the burn unit for care, fluid care and electrolyte imbalance!! treat it like a severe burn!
Toxic epidermal necrolysis (TEN)
what is this a severe form of? what is the difference between this and SJS? what are the presentations? what percent of sloughing? what are three things you worry about? how do you tx?
severe form of SJS, unknown cause but immune mediate
***Only difference, HIGHER TEMP AND MORE SLOUGHING***
life threatening
diffuse erythema, necrotic epidermis, wrinkled surfaces, sheet like loss of epidermis, raised flaccid blisters nikolsky sign
sloughing >30% BSA, mucotaneous blistering reactions most often caused by drug rxn
worry about infections, fluid loss, and electrolyte imbalance
TX: send to burn unit and treat like severe burns!!!
what are two keys lab keys a patient with SJS or TEN will have?
anemia and lymphopenia
erythema multiforme
what type of hypersensitivity is this? what two other things can it effect? what are the three main causes?
5
2
1
explain the characteristic rash appearance for this? what also accompanies this? what are the 3 treatments?
type IV hypersensitivity rxn (delayed cell mediated),
***can effect lungs and eyes***
causes:
- drugs-sulfonamides, phenytoin, barbituates, penicillin, allopurinol
- infections: HERPES SIMPLEX (#1), mycoplasma
- idiopathic
Rash: macular->papular then vesicles and bullae form in the center of the papules get target or iris lesions “dusty violet” red, with mucosal lesions that erode and are painful
TX:
- avoid trigger
- control herpes outbreak: acyclovir
- systemic corticoids if severe
what are the two different types of erythema multiforme?
erythema multiforme minor: target lesions distributed acrally, no mucosal membrane lesions
erythema multiform major: target lesions that involve >1 mucous membrane, NO EPIDERMAL DETACHMENT!! (oral, genital, ocular mucosa)
urticaria and angiodema
drug rxn
what type of hypersenstivity is this? when does it develope? what four causes are this? what are the two treatment options?
Type I IgE mediated
2nd most common type, occurs within miniutes to hours
drugs: abx, NSAIDS, optiates, and radiocontrast
Tx: systemic corticosteroids and anithistamines depending
1st degree burn
what is damages and what does it look like?
minor damages to epidermis
erythema, tenderness, absence of blisters!!
2nd degree burn
what are the two types? what do they extend to? what characteristics do they have?
1. superficial partial thickness burn
- goes to papillary dermis
- thinned walled blisters, most blanche with pressure, painful
2. deep superficial burns
- extend to reticular dermis
- thicker walled blisters which may rupture, mixture of erythema and pallor, painful with pressure application
3rd degree burn
what does this destroy, what does the skin look like, what does this person lack
destroys the epidermis and dermis including dermal appendages
skin appears white and leathery or charred
dry without presence of sensation
4th degree burns
what does this involve? pain?
destroy skin subcutaneous tissue, fascia, muscle or bone
significant charring, with exposure of muscle fascia or bone
EXTENSIVE DAMAGE TO NERVES resulting in little to NO PAIN!!
vitiligo
what type of condition is this and what is destroyed? what are two things this can be associated with? what does the condition present as? what are the 3 treatment options? what do you want to be aware of in these patients?
AUTOIMMUNE destruction of the melanocytes
associations: thyroid disease, pernicios anemia
30% have family hx
macules of hypopigmentation that can occur focally, generalized pattern etc
tx:
1. SUNSCREEN
2. costmetic coverup
- repigmentation by DERM
**caution can cause depression in patients ebcause it effects them socially**
erythema infectiosum
human parvovirus B19
fifth disease, red face”slapped cheek”, arthropathy
pink lacey rash with slapped face appearence, arthropathy is common in older children and adults
infectious disease associated with arthropathy! spreads by respiratory droplets!
***CAUTION!!…this can cause an aplastic crisis in sickle cell patients***
roseola infantum
what virus causes this? what unique thing does the fever correlate with and how long does it last? what is interesting about the rash location and progession? who is this common in?
herpes virus 6 or 7
fever for 4 days, this resolves before you get the pink macular rash!!** during this time though the child still appeares well, doens’t seem sick!
children
only childhood exanthem that starts on the trunk and migrates to the face!!
Molluscum Contagiosum
what cuases this?
4 descriptive words?
tx?
POXVIRUS
skin and mucous membranes in children
groin and lower abdomen in adults
- flesh colored waxy dome shaped umbilicated papules over face trunk and extremities
- expell white material
TX: self limited
