CM-Derm Flashcards
what are the 3 layers of the skin and? what is contained in each?
1. epidermis
- stratified squamous epithelium
- melanocytes, langerhans cells, merkels cells
2. dermis
.3-3.0 mm
-papillary layer
3. subcutaneous layer
what is the function of the skin and nails? (5)
- physical barrier- prevents toxins, organisms, trauma
- temp regulation
- protection against UV radiation
- synthesis of Vitamin D
- sensation
what are the four types of hair?
- lanugo- fine, covers fetus
- vellus- peach fuz
- intermediate- vellus and terminal hair
- terminal-scalp, beard, axilla, pubic area influenced by hormones
what are the 3 phases of hair growth?
- anagen-growth phase, 3 years
- catagen- degenerative stage, weeks
- telogen-resting phase, varies by body site
what are the four functions of hair?
- protection
- regulation of temp
- evaporation of perspiration
- sensation
what is really important thing to do when examining the patient?
UNDRESS THEM
oh la la..NOT!..be professional
what are some things you want to take note of when looking at lesion? (6)
- how many are there?!
- type
- size
- color
- palpation (consistency, mobility, temp, and moisture)
- margination
when there are multiple lesions, what are the three things you want to take note of?
- arrangement/configuration
- confluence
- distribution/location
Macule lesion
explain
A macule is a flat, distinct, discolored area of skin less than 1 cm wide that does not involve any change in the thickness or texture of the skin.
papule
explain
A well-circumscribed, elevated, solid lesion, less than 1 cm. Usually dome shaped.
plaque
explaination
A well-circumscribed, elevated, superficial, solid lesion, greater than 1 cm in diameter. Usually “plateau-like” with a flat top.
bullae explaination
A raised, circumscribed lesion (> 0.5 cm) containing serous fluid above the dermis.
crust explaination
Varying colors of liquid debris (serum or pus) that has dried on the surface of the skin.
pustule explaination
A small (< 1 cm in diameter), circumscribed superficial elevation of the skin that is filled with purulent material.
wheel explaination
Transient, circumscribed, elevated papules or plaques, often with erythematous borders and pale centers. These lesions are due to dermal edema and usually resolve within twenty-four hours
ulcer explaination
A lesion with greater than 50% surface area ulceration.
what are four examples of shapes you can use to describe the skin lesions?
- round
- oval
- annular
- serpiginous
atrophy explaination
Thinning or depression of skin due to reduction of underlying tissue.
what are four patterns you can use to describe the distribution of lesions?
- symmetrical
- exposed areas
- sites of pressure
- random
what is vitiligo
loss of pigmentation
explain what grouped lesions for disseminated would look like?
explain the locations that are common for…:
- acne vulgaris
explain the location of atopic dermatitis
explain the site for photosensitive eruptions?
where is the rash for pityriasis rosea?
where do you see the rash for psoriasis?
where is the rash for seborrheic dermatitis?
what type of test is this?
woods lamp
what type of test is this?
punch test
what do you use Tzank smear for?
HERPES SIMPLEX
what are 5 general categories you can use for skin treatment?
- topical
- systemic
- cyrosurgery
- electrocautery
- excisions
what are 3 key things to remember about sunscreen use?
- at least 30 SPF
- UVA and UVB protection
- alive every two horus
what is the percent increase in risk if you go tanning for melanoma?
75% so don’t go tanning….
….just to look good!
what are four general bacterial sources that can cause bacterial infections?
- coagulase-negative staph
- staph aureus and group A, B, and G strep
- break in stratum cornium method of infection
- MRSA
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 does this come from? what are the three stages and what is characteristic of the rashes at each?
allergic reaction
acute: pruritis, redness, vesicle formation, oozing, crusting
subacute: pruritis, redness, parched, or scaled
chronic: pruritis, skin thickening, hyperpigmentation, excoriation, fissuring
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
according to the green pance book, what can the rash from atopic dermatitis look like?
papules and plaques
with or without scales
can have edema, erosions, or crusts
goodluck.
if someone has atopic dermatitis what do you worry about?
since so itchy, they scratch a lot and can lead to secondary infection from s. aureus! watch out for this!!
for atopic dermatitis….what can you do to figure out what is causing it?
PATCH TESTING!!!
what are 6 things that can contribute to atopic dermatitis exacerbation?
- milk
- eggs
- fish
- skin hydration
- time of year
- stress/clothing
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
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)
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
lichen simplex chronicus
what happens to the skin and what is that cause from? what is this a long term manifestation of? what do you see as a manifestation on the skin? what are the 6 areas on the body this is common in? what does a biopsy show?
development of epidermal hyperplasia 2nd to physical trauma of scratching and rubbing
long term manifestation of atopic dermatitis from ALL THAT ITCHING
skin becomes extremely sensitive to touch including trauma, touch, rubbing or scratching leads to skin thickening from the increased rubbing and scratching
well circumscribed thick, firm, plaques that are highly puritic even light touch causes this patients to itch a ton!
most common areas: nuchal area, scalp, ankles, lower legs, upper thighs, and exterior forearms
DX: KOH to rule out fungal infection, BIOPSY SHOWS HYPERPLASIA AND HYPERKERATOSIS!!
lichen simplex chronicus
what are the four treatment options?
interupt the scratch itch cycle
- topical steroids
- intralesional triamcinolone
- antihistamines (ESP AT NIGHT!!)
- occusive dressing with out without tar prep/steroids
how does lichen simplex chronicus appeare on black skin?
follicular pattern of smaller papules…not plaques like on white skin
SO TRICKY!
nummular dermatitis
when does this occur? who is it most common in? what do the rash look like and where is it most common? what are the four treatment options?
puritic inflammatory disorder in young adults (white males) and elderly in fall and winter but exact cause unknown
grouped vesicles that coalesce to form coin shaped plaques with erythematous base with clearly demarkated boarders most common on extremities
TX:
moisterizers & topical steroids for class I and II
tar baths or UVB phototheryapy
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
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**
autosensitisation dermatitis
“ID REACTION”
what is this? what causes this? what are the two presentations of the rash? what is the treatment?
dermatitis occuring at a site distant from primary dermatitis
caused by the release of cytokines from sensitization at primary site
rash: maculopapular/papulovesicular
Tx: corticosteroids
asteatotic dermatitis
when is this common and who is it common in? where are the three places it shows up? what should you avoid and what should you do? what is last resort treatment?
pruritic dermatitis occuring in the WINTER, COMMON IN ELDERLY
legs/arms/trunks
avoid hot showers!!! take some baths with oils and skin lub….god that sounded dirty.
Tx: corticosteroids if lesions are inflammed
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
faruncles
what organism causes this most often? what does it present as? what do you want to culture it for? what are the two treatment options?
abcess formation from STAPH AUREUS
deeper hair infection of the hair folicle than folliculitis, tender nodule with 1 central plug
raised tender warm and fluculent
want to culture it for MRSA
Tx: incision and drainages! antibiotics
carbuncles
what organism is the most common cause of this? what is the presentation? how do you differentiat it from a farbuncle? what are the two treatment options?
abcess formation caused by STAPH AUREUS!!
raised tender warm and flutulant
larger and deeper than farbuncle, more painful, “interlocking farbuncles with multiple openings!”
TX: incision and drainage and antibiotics
infectious intertrigo
what three organisms can cause this? tx and dx?
strep group A, B, or G
Staph
pseudomonas
dx: culture and treat with specific antibiotics
erythrasma
what bacteria causes this? what does the rash look like? what is the interesting thing you use to diagnose this? what are the two treatment options?
corynebacterium minutissimum
lesions in intertriginal areas, tan or pink, sharply demarcated
DX: coral red fluorescnece on woods lamp
Tx: benxyl peroixide and topical antibiotics
necrotizing fascitis
when does this occur? what is necrotized? what is the most common cause of this?
occurts after minor trauma
extensive necrosis of subcutaneous tissue
group A strep
condyloma accuminatum
what virus strains cause this? what are the four descriptions used to describe these lesions? what is the treatment?
“genital wart” from HPV 6 and 11
lesion type:
1. papular
2. cauliflower
3. keratotic
4. flat topped
Tx: no cure but can be removed, tough it a lot of them
herpes simplex
what is a hint that an outbreak is going to occur? what is the important description of these? what are the two different types; where are they found and what percent of the population has them? how do you dx it and what do you see? what are the four treatment options?
prodromal phases: 24 hours before outbreak, get burning and tingling
“painful grouped vesicles on erythmatous base!”
HSV1: oral lesions 85% population infected; transmitted via saliva, outbreak triggered by random things
HSV2: genital herpes (more common and detrimental in women! more likely to have complications like ulcers and necrotic tissue), 25% population infected
DX: tzank smear, geimsa stain shows GIANT MULTINUCLEATED CELLS, can also check for antibodies for this
TX: supportive therapy
suppressive therapy foscarnet
Acyclovir, valacyclovir, famcyclovir
acute hepetic gingivostomatits
what virus causes this? where does this tend to effect? how often are the outbreaks and who are they common in? what are three things you might find in this patient? explain the maturation of the vesicles?
HSV-1-trigeminal nerve predilection, eruptions 2x a year
common in 6 months-5 years CHILDREN
abrupt onset fever, anorexia, red mucosa
vesicles appear on gums, lip, tongue
vesicles colase to form ulcers or plaques
acute herpetic pharyngotonsillitis
what virus causes this? who is it the most common in? what are four symptoms you see with this? what do the lesions look like?
more common in HSV1 than HSV2
primarily in ADULTS
fever, malaise, headache, sore throat
vesicles on posterior pharynx and tonsils that RUPTURE to form ulcers (may have grayish exudate)
Herpes Simplex-2
what does this cause? what percent of the population is infected with this? where does this typically have predilection for? what do the lesions start and finish as? what percent of people will have reactivation in the first 12 months? how many reactivations will they have in their lifetime?
causes genital lesions
25% of the population infected with this
asymptomatic shedding and painful eruptions can occur
sacral root ganglion predilection
VESICLES rupture to form ULCERS
reactivation in 90% occur in the first 12 months!!
30% have 6 episodes in their lifetime!!
where does Herpes simplex virus tend to hide?
dorsal root ganglion
this is why it reactivates
what are the 5 complications you worry about from herpes simplex virus?
1. herpetic withlow (vesicles on the fingers)
2. herpes gladiatorum (disseminated cutaneous infections common ing wrestlers)
3. keratoconjunctivitis (dendritic corneal ulcers)
4. HSV or CNS ENCEPHALOPATHY!! YIKES!! causes change in mental status and headache
5. infection during pregnancy can infect the child
what is herpetic whithlow?
herpes lesion on the FINGERS
molluscum contagiosum
what virus causes this? describe what they look like with the FOUR key descriptors? what two populations is this common in? what are the 5 most common areas? what is the treatment 7 options?
poxviridae virus “pox virus”
“dome shaped” flesh colored with waxy appearence with central umbilication 2-6mm
in children and sexuallly active adults HIGHLY CONTAGIOUS!
viral disease of skin and mucosal membranes
face, trunk, _abdomen_, thighs, _genitals_
Tx: usually self limiting and lasts 3-6 months
if therapy needed, lesions have to be destroyed individually
1. DOC curettage
2. cryrotherapy
3. electrodessication
4. acid, Retin A, Kerolytic pain, Imiquimod cream
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
how long can the post herpetic neuraligia with shingles last? what is a thing you worry about if eldery?
>3 months…so give these people some pain meds
occurence likelyhood is greater if over 60!
what is the treatment options for varicella zoster virus? (4)
- acyclovir, valacyclovir
- pain management for post therapeutic neuralgia
- tricyclate antidepressants
- corticosteroids
what can you do to prevent varicella-zoster virus? (2 options)
VACCINATION!!
child: vaccinated 1-2 years old for varicella
adult: Zostavax single dose >60yrs…basically literally a booster of varicella, becuase it is the same virus, just marketed differently to apeal to elder adults!
**can’t give if allergic to gellatin, neomycin, pregnant, or immunocomprimised!**
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
verrucae
what are the 6 treatment options??
- spontaneous regression common
- salicyclic acid plasters, cyrosurgery, electrocautery
- imiquimod
- intralesional interferon
- surgical excision
- ketolytic agent
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!”
what is the most common fungal infection?
SUPERFICIAL fungal infections
irritant dermatitis
what causes this? what things can cause this?
Results from contact by irritating substance
Direct Toxic effect on skin
Occurs in anyone exposed to causative agent
Common Agents- Abrasives, cleaning agents, caustic agents
Rash
Acute–erythema-Vesicles-Erosion-Crusting
Chronic–Papules-Plaques-Crusts
what are the three most common mucocutaneous fungal infections?
- candida species: require warm humid environment
- malassezia species: humid environment with lipids for growth
- dermatophytes: infect keratinized epithelium, hair follicles, and nail apparatus
what are the 6 dermaphytes that infect the epidermis?
Tinea corporis
Tinea cruris
Tinea pedis
Tinea manuum
Tinea facialis
Tinea incognito
what are the two dermaphytes that infect the hair and hair follicles?
Tinea capitis
Tinea barbae
what dermaphyte infects the nail appartus?
Tinea unguium (aka onychomycosis)
what is the most common dermaphyte?
trichophyton rubrum
most common, although 10 species
what percent of people experience at least 1 yeast infection and which one is most common?
70% have 1 infection
tinea pedis is usually the most common “athletes foot”
how are dermaphytes usually spread?
from one person to another, usually from fomites
this means that it touches an object then another person touches it and then you get it from the contact with the fomite
for hair and nail infections…what type of treatment is required?
for hair and nails, need to use SYSTEMIC treatment!!!! topical won’t work for these!!
explain what allows the dermaphytes to live?
they metbolize and live on KERATIN!!!
the fungus attacks the skin, nails and hair where keratin is the major structual protien, leads to infection!
what are RF for dermophyte infection? (5)
- atopic diathesis/dermtitis (cell mediated immune deficiency for T. rubrum)
- topical immunosuppression from topical corticosteroid ( tinea incognito)
- systemic immunosuppresion
- sweating
- high hummidity
if you suspect a dermaphyte infection, how do you identify it? 3 options, explain what you would see on the first
if its scaly, scrape it!!!
1.KOH most common method
multiple septated, tubelike structures (hyphae or mycelia) and spore formation
- culture
- biopsy if KOH and cultures are negative
what are the four of the 9 classes of arthropods that can cause skin reactions?
Arachnida (4 pairs of legs) – mites, ticks, spiders, scorpions)
Chilopoda (centipedes)
Diplopoda (millipedes)
Insecta (3 pairs of legs) – lice, bedbugs, ants, bees, wasps, hornets, catepillars, butterflies, moths, fleas)
what is a dermaphyte?
a superficial fungal infection that can affect the hair, nails, and skin
what are the three most common dermophytes in the world?
what is the most common one in the industerial world?
trichophyton, microsporum, and epidermophyton
trichophyton rubrum is the most common one in the industerial world
explain how a fungal infection (dermatophytosis) is named?
what are the names of the body for the different infections? (8)
tinea means fungal infection…so thats the first part
the second is the area of the body:
pedis: foot
cruris: groin
corporis: trunk, legs, arms and neck
barbae: beard
unguinum: nails
manuum: hand
facialis: face
capitis: head
what are 6 drugs that can cause drug induced alopecia?
- thallium
- vitamin A
- retenoids
- antimitotic agents
- anticoagulants
- OCP
why is psoriasis a primary care disorder?
because there are so many comorbidities, and we manage those
Psoriatic Arthritis
Obesity
Metabolic syndrome
Vascular disease (CVD, CeVD, PVD)
Malignancy
Autoimmune disease
Nonalcoholic Fatty Liver Disease (NAFLD)
COPD
OSA (Obstructive Sleep Apnea)
Parkinsonism
Psychiatric Disorders
Alcohol abuse
what are the give drugs that can exacerbate psoriasis?
- ETOH
- beta blockers
- lithium carbonate
- antimalarials
- interferon
explain the theory behind biologics used for psoriasis?
The newly developing psoriasis lesion is precipitated by an autoimmune reaction where there is a genetic defect inherent in the interaction between keratinocytes, macrophages and T-lymphocytes
For reasons that are poorly understood, the macrophages appear in the epidermis and proceed to identify the keratinocytes as foreign antigens.
These antigens are then presented to T-lymphocytes which form large populations which then incite the inflammation of psoriasis. (Large populations of activated T-Cells are found in bases of Psoriasis plaques.)
Psoriasis is a TH1-Cell mediated disease
“Biologic” Psoriasis drugs target and disable particular steps along the pathway of T-Cell activation in target tissues (skin keratinocytes) which ultimately results in clinical disease improvement in most patients
what are the five biologics that can be used to treat psoriasis?
- etanercept
- alefacept
- adalimumab
- infliximab
- efalizumab
what can the suffix of biologics tell you?
- ximab
- zumab
- umab
- cept
- ximab: chimeric monoclonal antibody
- zumab: humanized monoclonal antibody
- umab: human monoclonal antibody
- cept: receptor-antibody fusion protein
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!
what are the drugs that can cause steven johnson syndrome or toxic epidermal necrolysis?
sulfonamides, anticonvulsants, aninopenicillins, quinolones, cephalosporins, tetracyclines, phenobarbital, phenytoin, allopurinol, corticosteroids
what percent of pts with SJS have mucosal ulcers?
90% have mucosal ulcers anywhere from the mouth to the anus and are painful!!
what are five things that SJS can cause that you worry about?
- infections
- fluid loss
- electrolyte imbalance
- tubular necrosis
- erosion in lung and gut
how long does skin regrowth take for SJS?
3 weeks!!
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
necrotizing fascitis
what are the 3 bacteria common for causing this? what three populations is it most common in? what are 6 characteristics of the pt? what is the triad? what is a important thing to monitor? what are the two treatment options?
polymicrobial or group A strep or clostridial
salterwater necrotizing fascititis: virbrio
DIABETICS, ALCOHOLICS, IV DRUG USERS
rapidly progressing erythema, tissue crepitus, HIGH TEMP, tachycardia, hypotension, altered mental status
triad: elevated WBC, elevated BUN, hyponatremia (not present in all but heighten suspicion)
****MONITOR RENAL FUNCTION BECAUSE THIS IS A HALLMARK OF THE DISEASE****
TX:
1. aggressive surgical debridement-do US, CT, MRI to determine the amount that needs to be taken out
2. aba to cover ALL pathogens- carbapenem of b-lactam/b-lactamase inhibitor with clindaymycin and one against MRSA like vancomycin
diabetics account for what percent of necrotizing facititis cases?
20-30%
what is the mortality rate for necrotizing facititis?
25-70%
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)
open comedone
what is it? how does it happen?
“blackhead”
forms when the pore wall is able to dilate in response to the increased pressure created by trapped sebum, creating a non-inflammed lesion
closed comedone
what causes it? what is it?
“whitehead”
a semi-ferm dome shaped papule which is also non inflammed
forms when trapped sebum pushes up against the non-dilated opening of the pore
pomade acne
what does this come from? what parts of the body are effected? how long does it take to clear once the instigator is stopped?
unique form of acne
secondary to chronic use of oily hair mousses, gels, tonics by susceptible individuals
always distributed on upper forehead/hairline/anterior scalp with fairly clear border, lower face unaffected
stop use of hair product, acne clears in 2-6 weeks
what percent of fair skinned indiviausl does roceasea occur in?
10%
what is facial flushing and what disease is it commonly assocaited with? (3 characterists of facial flush)
ROSACEA
- greater baseline blood flow
- larger more numerous blood vessels
- vessels more superficial
Cutaneous candidal infection
- candidal intertrigo
- diaper dermatitis
what is the characterists of these? where are the places you would find these? what are the two TX options?
patches and pustules on a ERYTHEM MATOUS BASE beefy red the erode and confluent with “SATELITE LESIONS“ painful with puritis
Candidal intertrigo: axillae, groin, intergluteal, cleft
diaper dermatitis: irrritabiltiy with urination, defication, changing diapers, genital region, inner aspect of thights and butt
TX: keep dry, antifungals nystatin, imidazole powder
oropharyngeal candidiasis
what does this look like and what in what population can this look completely different? what is the key characteristic of this? what are the 2 treatment options?
thrush, white curd like plaques that can be scraped off
what to find the percipitating cause and treat that, then treat with oral antifungals
*****KEEP IN MIND, PEOPLE IN DENTURES CAN APPEARE BIRGHT RED INSTEAD OF WHITE CURD LIKE****
Tx: nystatin oral fluconazole or itraconazole suspension, swish and spit or swallow
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**
angular chelitis
what are four RF for this? what do you see? what are the two causes you need to differentiate between and who are they most common in?
associated with increase moisture and saliva at the commisures
RF: thumb sucking, sagging face, lip lickers, dentures
erythema and masceration at the commissures
KOH for _candidiasis (_seen in older person) and culture staph aureus (seen in atopic dermatitis)
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
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
lichen planus
what is this? where are the 5 most common locations of this? what is the pneumonic to remember this? what does this rash look like? where are they most common? what can you see on the nails ? what happens if you itch?
acute or chronic inflammatory dermatitis in adults
UNKNOWN CAUSE MOST MOST COMMONLY FOUND ON THE WRIST!!!!
5 P’S
PURITIC
PLANAR
POLYGONAL
PURPLE
PAPULES
Flat topped shiny lesions, lacy papules with fine white lines on surface called wickman striae
**lacy lesions of the oral mucosa most common and can have longitudal splintering of the glands, lesions in hair can cause alopecia**
KOEBBNER PNENOMENON PRESENT (itch, the more it itches)
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
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
inverse psoriasis
goes in areas other than the ones excpect….
…can find on the penis and groin area
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
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
acanthosis nigricans
what type of disorder is this? what are three things it is assocaited with? how does it appear and what does it eventually look like? what is the treatment?
hyperpigmentation disorder, acquired or hereditary
commonly associated with obescity, endocrine disorders (insulin resistance), and paraneoplastic syndroms
develops insidiously initially darkens and appears dirty but becomes thick, velvety with accentuated lines
Tx: None you gotta fix the underlying condition!
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!!
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***
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
cysts
epidermal inclusion secondary to traumatic implantation of the epidermis into the dermis
epidermis grows in the dermis with accululation of keratin within the cyst cavity
“dermal node” and most common on palms, soles, and fingers!!!
this is firm and immobile so it is differnt then a Lipoma cause Lipoma’s are soft and very mobile.
Tx: excise that bad boy
melasma
what does this cause? what two locations is it most common, what are 3 things that can cause it and one specific mediation? who is this most common in? what are 3 treatment options?
“black spot” acquired hyperpigmentation of sun exposed areas and can be associated with OCP, pregnancy, meds diphenyludantoin or idiopathic
most common: MALAR and FRONTAL FACE
viewing with a woods lamp accentuates hyperpigmented macules
**90% FEMALES**
Tx:
3% hydroquinone/trentoin gel
hydroquinone
glycolic acid in cream
pilonidal disease
what is this? where does it occure? what are 2 RF? what is the treatment?
piliodonal cysts in an abcess in the sacroccygeal cleft assocaited with subsequent sinus tract formation
**painful fluctulant area of the sacrococcygeal cleft**
MALES
RF: obese, hirsute
Tx: surgical drainage and follicle removal may be required with unroofing of the sinuses
diabetic ulcers
what do these look like and where do you find them? do they feel them? what are the three treatment options and what is the benefits of option #3?
deep punched out lesions over malleoli and plantar surfaces of feet or toes
**painless because of neuropathies**
Tx:
- lifestyle changes
- wet to dry dressings or hydrogels because wounds heal better if kept wet
3. hydrocolloids and enzymatic preps
- maintain moisture
- promote debridement
- improve rates of epithelization
stasis ulcers
what does this occur from? what preceeds it? what does it look like? what makes the pain better? what are the two treatment optons?
occur from chronic venous flow stasis
preceeded with stasis dermatitis
wide but not deep with irregular, undulating edges **elevation of the leg relieves pain**
Tx:
- elevation and compression stockings to promote venous return
- whirlpool limb and unna boot
arterial ulcers
what is something you might see on exam with this? what are 3 treatment options?
painful
**pulses are diminised or absent and distal area is cold**
Tx:
1. lifestyle changes
- wet to dry dressings or hydrogels because wounds heal better if kept wet
3. hydrocolloids and enzymatic preps
- maintain moisture
- promote debridement
- improve rates of epithelization
explain the four stages for decubitis ulcers?
stage 1: nonblanching erythema of the skin
step 2: necrosis, superficial or partial thickness involving the epidermis and or dermis forming a shallow ulcer
dermis, blister, or abrasion
stage 3: deep necrosis, crater ulcer with full thickness skin, can extend down to the fascia subcutaneous layer
stage 4: full thickness ulceration with necrosis to muscle, tendon, or bone
urticaria
what are the most common causes of this? what percent of the population experience this? the release of what 3 things cause this? what does the rash look like? what are the diffrence between acute and chronic?
most commonly from: food, drugs, heat, cold, stress, or infection
15-20% of the population
blancheable hives or wheals on skin caused by release of histamines, bradykinin, and kallikrein from mast or basophils
**the release of these cause the capillaries to get leaky and the fluid causes the swelling**
acute: mins to hours IgE mediatd, treat with H1 antihistmaine, diphenhydramine, or fexofenadine, EPI FOR ACUTE!
chronic: >6 weeks, lesions that wax and wayne, idiopathic cause probs stress TX: H2 first, then H1 if no response
Can differentiate from other because they:
A) have dermatographism! hives can form after firmly stroking or scratching the skin. you can literally write the person’s name on their arm
B) hives will BLANCH; perform diascopy: if you press the center, it will turn white
darrier’s sign
what is this and what causes it?
localized urticaria appearing where the skin is rubbed
HISTAMINE INDUCED
systemic scleroderma
what is this? what are the 5 common presentations? what is the #1 think you worry about in this? what test do you do in the lab? what are the treatments?
thickening and harderning of the skin via collagen deposition
- raynauds (75%)
- vascular changes in nail bed
- GI dysmotility “watermelon stomache”
- puffy hands
- fixed face
*****WORRY ABOUT PULMONARY FIBROSIS AND ACUTE RENAL FAILURE*******
DX: ANA-SPECKLED
Tx: treat system effected
renal-ACE inhibitors
raynauds-calcium channel blockers
Gi: promotility
lungs: cyclophosphamide
CREST Syndrome
what is the pneumonic to remember the symptoms and what do you need to monitor annually in these patients?
LIMITED SCLERODERMA
C- calcinosis of joints leading to puffy hands
R- raynauds
E-Esophageal dysmotility
S-sclerodactyly of MCPs
T: telangiectasis
**complication=pulmonary hypertension so need to get annual PFT/DLCO to make sure no lung fibrosis**
Tx: symptoms
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
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
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!!!
bed bugs
what organism causes this? where are they? how do they attack you? what is the treatment?
cimex lectularius
HIDE IN THE CREVICES OF WALL AND MATTRES, COME OUT AND BITE YOU THEN RUN BACK
pupular urticaria, bites appeare on skin exposued while sleeping!!
Tx: apply bug reppelant to skin and permethrin spray to clothing ***must treat bedding since this is where they hide***
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
cherry angiomas
benign vascular neoplasm
most >30 have them
electrocauter, laser surery, cryrosurgery
what are the ABCDE’s of moles?
A-asymetry
B-Border
C-color
D-diameter >6mm
E-evlolving/changing
epidermoid (sebaceous) cyst
or called Epithelial Inclusion cyst
where does this cure? how large can it grow? what three places is it located?
same as Pilar cysts but where do you see these?
epithelial lining of the hair follicle
assymptomatic
may grow to max of 3 cm
usually face, neck, upper trunk
Pilar cysts on SCALP
make sure if removing.. remove capsule as well!
dermatofibroma
what does it look like? cancerous? what does it do with palpation?
pink, dome shaped
BENIGN
pucker with paplpation
no tx need
she seemed to like this one….so know it!!!
skin tags
begign? what can it look like?
begign growths
can have many
may be flat or pedunculatted
cutaneous horn
what does it look like? what is it made of? who is it more common in?
hard conical shaped
compacted keratin
more common in fair skinned people
related to sun exposure
base may be benign or malignant
aquired nevomelanocytic nevi
what types of cells are this in? how large are they usually? whar are the three types of nevi?
benign skin tumors from melanocytes derived nevus cells
acquired macules, papules, or nodules
onset: childhood, adolescense, symetrical, macules, papules, nodules, several or many
Stops enlarging in ADOLESCENCE!
usually
Junctional: located in dermal/epidermal junction, macules or slightly raised
compound: in pappilary dermis, raised lesions
dermal: fibrotic, dermal
indications for removal of nevi
(5) things
1. site: scalp, mucous membranes, anogenital area
2. growth: rapid change in size
3. color: varigated
4. border: if irregular border
5. erosions
6. symptoms: itching, hurt, or bleed
dyplastic nevi
what is characteristic of these? what do they look like? what is this a possible precursor for?
moles that continue to develop later in life unlike acquired nevomelanocytic nevi
early adolescent onset, irregular, assymetric, continued but limited growth in adulthood, maculopapular
pigmented, curcumscribed
irregular borders, maculopapular and can have distinct or indistinct borders
possible precursor for superficial spreading melanoma (SSM)
hypertropic scars
what are these? what can you treat with? what do you need to be really careful about?
pigmented darker skinned individuals and pink in lighter skinned
intralesional steroids
be carefule when removing it because it can come back as a full blown keyloid!!!
venous malformation
wat do they look like? what are they classfied by? how do they grow?
appear at birth as flat, irregular, red to purple patches
classified by vessel type
***grow in proportion to the patient***
keratocanthoma
what is this a variant of? what does it look like?
variant of squamous cell carcinoma, rapidly growing epithelia lesions
DOME SHAPED NODULE WITH CENTRAL CRATER!!!
bullous pemphigoid
(vesicular bullae)
what typ of rxn is this? whater is it most comon? what type of hypersensitivity is this? what does it attack an what does it cause? what forms? what do you treat with?
autoimmune blistering of the skin
most common in axillae, thighs, groin, abdomen
Type II HSN on the basement membrane of the skin causing subepidermal blistering
prodrome: urticarial papular lesions
then gets BULLAE containing serous or hemorrhagic fluid, collapses and crusts
tx: topical steroids, systemic prednisone, azathioprine
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
nodule formation/cystic acne
what is this marked with? what happens under the skin? what are 3 things you can see with nodules?
marked inflammation with scarring
nodular: follicular walls of papules/pustules rupture, spills into the surrounding tissue
****nodules increase scarring, can become infected, and form communications of “sinus tracts”…which is so disgusting it makes me want to puke****
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
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
difference bewteen solar lentigo and seborrheic keratosis?
the difference: solar lentigo is a subcategory of seborrheic keratosis
and solar lentigo is the browning part and seborrheic keratosis is the stuck on part
so here you can see the brown patch=solar lentigo
and stuck on part seborrheic keratosis
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**
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***
NAIL AND GENITAL MELNOMA
LENTIGO MALIGNA
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,
squamous cell carcinoma account for what percent of skin cancers?
20 %
WHAT KIND OF SQUAMOUS CELL’S ARE THESE?
Solar Keratotic Squamous Cell Carcinoma
hemangioma
what is this and who is it in? growth pattern? where do you see this?
30% have this at birth
vascular tumor, benign
predilection for head and neck
growth for 6-12 months then dreases 10% a year after that
bowen’s disease
what does this develop into? what does it look like? what is the treatment?
develops into squamous cell carcinoma
slightly raised pink patch with scaling
Tx: cyrosurgery, curettage, 5-florouricil
kaposi sarcoma
who is this most common in? local/systemic? what cells does it effecT? what virus is it associated with? where do you see most symptoms? what are 3 thearpy choices?
What are the two different types? Who are these types in? what does it look like in each type? and what is the treatment for each type?
most common in HIV/Immunosuppresed patients
multfocal systemic tumor of endothelial cell origin
connective tissue cancer associated with
HHV-8(human herpes virus 8)
**Get mainly GI symptoms**
can pretty much take any visual form
TX: HAART therapy, chemo/radiation
- 2 types, who does it present in, how does it present, tx:*
1) Classic KS: elderly men of Mediterranean origin without AIDS. Purple plaques or nodules on the lower limbs. Treatment is by cryotherapy, electrocoagulation, or radiotherapy.
2) AIDS-related form: is the most aggressive form, with widely disseminated purple papules or plaques on the skin, mucous membranes, and viscera. Treatment is by chemotherapy.
***Kaposi Sarcoma is a cancerous disease that affects the lungs, intestines, and mouth & these skin lesions should clue you into perhaps a bigger process going on inside the body
lyme disease
what bacteria causes this and in what type of tick? what does the rash look like in the first stage? what about second stage? what two test do you use to diangose? what med for treatment? WHAT ARE 3 OTHER SYMPTOMS YOU CAN SEE WITH THIS?
borellia burgdoferi, IXODES TICK!!!!
Stage 1: erythma migrans, erythematous plaque at bite site in 70-80% of people, “bullseye lesion” but can just be traveling erythema without rings within 30 days of bite, if on scalp won’t always get the bullseye, may just get 1 linear streak, FEVER AND FLU LIKE SYMPTOMS!!
stage 2: secondary lesions
**neurological, muskuloskeletal, and cardiac symptoms**
DX: ELIZA and western blot
Tx: Doxycycline
Rocky mountain spotted fever
what bacteria causes this? which 3 states is it most common in? where does the rash start and where does it travel to? what is it made up of and what do we worry about? what is the tx?
Rickettsia ricketsi
this leads to disseminated erythematous and hemmoragic macules and papules typically appear on ankes or wrists before becoming systemic!
**the hemmoragic leads to necorsis in extremeities because tissues aren’t getting blood. since rash happens at wrist and ankles first, see necrosis here first**
Carolinas, tennesse, Oklahoma
Tx: doxycycline
