Cumulative Final Flashcards
need a fungal cultures for tinea capitis or unguium because
hard to treat, make sure you have the right organism
atopic triad
Eczema, asthma and hay fever (allergic rhinitis)
lichen simplex chronicus
due to constant itching of atopic dermatitis. scaly, well demarcated, rough plaques with exaggerated skin lines
pityriasis rosea presentation and treatment
herald patch, then 2 weeks–>salmon colored macules in trunk and upper extremities in “christmas tree” pattern. NO TREATMENT NEEDED. its very itchy though so maybe topical steroids, po antihistamines
what causes psoriasis
inflammatory/autoimmune (genetics). keratin hyperplasia (epidermal thickening/dermis is continually turning over) due to T cell activation
what are you going to see for tinea versicolor on diagnostics (which diagnostic too)
KOH: “spaghetti and meatballs” hyphae and spores. ALSO yellow/green on wood’s lamp
treat tinea versicolor
selenium sulfide lotion, oral fluconazole–>dont shower need to sweat it out to get to skin.
seborrheic dermatitis occurs where
high sebaceous oversecretion–>scalp, face, eyebrows, body folds. fungal?
treat psoriasis
-NEVER USE SYSTEMIC CORTICOSTEROID -phototherapy, high potency topical corticosteroid + Vitamin D analogs
oval, fawn/salmon-colored, scaly plaques with collarette scale
Pityriasis Rosea
seborrheic dermatitis treatment
-scalp: zinc pyrithione.selenium shampoo -facial and intertriginous: hydrocortisone
what is this
erythema multiforme: classic target lesion 3 concentric zones of color change, found acrally on hands and feet
benign, pruritic, TENSE blisters in flexural areas
bullous pemphigoid
pruritic, VIOLACEOUS, flat-topped papules with fine white streaks; mucosal lacy lesions of buccal/vaginal mucosa; on flexural surfaces and trunk. starts at the WRIST
lichen planus, can develop into SCC
burning or stinging (CNS); erythematous, dilated vessels on cheeks—telangiectasias; papules/pustules possible
rosacea, mc 30-50. avoid the triggers and treat with topical metronidazole or clindamycin
rosacea vs ance?
neurovascular component of rosacea and comedones are in acne and absent in rosacea
actinic keratosis
- prolonged sun exposure
“sandpaper pink macules/papules”
- Pre-malignant–>SCC
- treat with 5-FU/cryotherapy
–>can also get hypertrophic
Basal cell vs SCC
Basal: pearly/waxy/arborizing vessels/telangestasias. mc, local infiltrating, doesnt met
SCC: more likely to met, often preceded by actinic keratosis
seborrheic keratosis
“stuck on” benign lesion of elderly people with sun exposure–velvety/warty
extensor (elbows and knees) vs flexor (antecubital and knee fossa)
psoriasis–>extensor and nail pitting
atopic dermatitis–>flexor, atopic triad
impetigo causative agents and treatment
s aureus, GAS
mupirocen
erysipelas caused and DOC
group A streptococcus
(edematous hot raised circumscribed red area on *cheeks or leg)
Penicillin! (GAS)
Edematous erythematous warm spreading plaque. chills, fever, malaise, lymphadenopathy
cellulitis. have to have a break in the skin (ex tinea pedis). treat with antibiotics 7-10 days. s aureus GAS common offenders.
treat folliculitis
mupirocin, s aureus mc. its a hair follicle infection
what do folliculitis and furuncle have in common
folliculitis is superficial infection of the hair follicle and furuncle/boil is deeper infection—tender nodule. i&d that shit.
scabies!
start in finger/toe webs/wrist.
intensely itchy
pain increases at night
scrape the skin for dx–see the mites and eggs
cough, coryza (runny nose), and conjunctivitis is the prodromal (pre-rash) of which viral xanthem?
rubeola/measles
koplik spots?
measles/rubeola, its part of the prodromal phase
etological agent of erythema infectiosum (5th’s disease)
parvovirus B19 DNA virus
causative agent of rubella
rubivirus RNA virus
measles causative agent
paramyxoviridae
xanthem that could cause aplastic anemia
erythema infectiosum
cause of roseola
HHV 6
Chronic dacrostenosis presentation
yellow bacterial overgrowth from stagnant tears no other signs of infection. no swelling, redness, tenderness.
what may lead to a chalazion
internal hordeolum–>memobian gland abscess. the chalazion is a chronic internal hordeolum.
two types of anterior blepharitis and differeniating features
staphalococcal and seborrheic (zeis and moll gland inflammation and associated eyelid skin and eyelashes
Staph: ULCERATIONS, burning sensation. bacitracin treat.
Seborreic: white skin flakes.
keep lids clean, warm cloth
posterior blepharitis assoc with which dermatologic condition
mebomian gland infection or dysfunction.
assoc with ROSACEA–telangectasias
if blocking the cornea or involved in the conjunctiva–>antibiotics (tetracyclin) eye drop antis, corticosteroids topical short term
frothy oily tears assoc with
posterior blepharitis!
why do we worry about acute dacrocystitis
it could lead to preseptal or orbital cellulitis–>systemic antibiotics
treat gonoccal conjunctivits
1 g IM ceftriaxone
chemical to the eye what are you worried about and what do you do
IRRIGATION within 5 min! alkaline cpds worse, get through cornea
thickening of conjunctiva with active BV growth
pteryguim and pingecula
white patch on cornea? and s/s
corneal ulcer, from infection, exposure keratitis, etc.
s/s: pain, redness, photophobia, tearing, reduction in vision
mc cause of bacterial keratitis
pseudomonas, water lovin, opaque cornea. treat with cipro drops
defining feature of chronic glaucoma
aka open angle glaucoma
BIALTERAL slow peripheral vision loss, “tunnel vision”
key defining features to postseptal orbital cellulitis–>infection of the fat and ocular mm
decreased vision, pain with moving eyes–>behind the septum and PROPTOSIS
preseptal wont have the vision changes or pain with eye movements
defining feature of dry “non exudative” macular degeneration
drusen bodies, retinal pigment dies, bilateral central vision lost GRADUALLY
Hallmark of wet macular degeneration
neovascularization. its more sudden vision loss.
do the anti-VEGF therapy to prevent the new blood vessel formation
ischemic optic neuropathy assoc with
giant cell arteritis, systemic steriods to save other eye
associated with multiple schlerosis
optic neuritis
s/s of optic neuritis
UNILATERAL vision loss over a few days, color first
central loss—central scotoma
pain with eye movements
relative afferent pupillary defect!
the result of increased intracranial pressure in the eye is called
papilledema: bilateral increase of blindspot
rapid loss of vision in 1 eye with curtain
retinal detachment
central and branch retinal vein occlusions
both sudden vision loss in 1 eye with no pain or redness
difference is the amount of hemorrhage
“flame shaped hemorrhages and cotton wool spots”
hallmark of diabetic retinopathy
macular edema, in proliferative or non proliferative
arteriovenous nicking and copper wiring assoc with
chronic HTN retinopathy
later stage malignant HTN gets the papilledema
manifest vs latent and cominant vs incominant strabismus
manifest: there, cant induce ; latent: cover uncover shows it
cominant: same in all gazes, incominant: can induce with H test
unequal red relfex in a kid could mean
retinoblastoma
strabismus can be tested with
corneal light relfex and cover/uncover