Skin Path Buzzin Flashcards
excoriation
Traumatic lesion breaking the epidermis and causing a raw linear area (i.e., deep scratch); often self-induced
lichenification
Thickened and rough skin (similar to lichen on a rock); usually the result of repeated rubbing
macule/patch
Circumscribed flat lesion distinguished from surrounding skin by color.
Macule 5 mm (or >1 cm in some texts)
Onycholysis
speration of nail plate from nail bed
Papule/
Nodule
Elevated dome-shaped or flat-topped lesion.
Papule < 5 mm
Nodule >5 mm
plaque
Elevated flat-topped lesion, usually greater than 5 mm across (may be caused by coalescent papules
scale
Dry, horny, platelike excrescence; usually the result of imperfect cornification
blisters?
Blister = Any fluid-filled raised lesion
Vesicle 5 mm
wheal
itchy, , transient, elevated lesion with variable blanching and erythema formed as the result of dermal edema
acantholysis
Loss of intercellular cohesion between keratinocytes = SC falling off and floating around
acanthosis
Diffuse epidermal hyperplasia = thickening of epidermis
dyskeratosis
Abnormal, premature keratinization within cells below the stratum granulosum = see keratin layer doesn’t lose nucleus at the surface
exocytosis
Infiltration of the epidermis by inflammatory cells
hydropic swelling
Intracellular edema of keratinocytes, often seen in viral infections = swelling of the cell
hypergranulosis
Hyperplasia of the stratum granulosum, often due to intense rubbing
hyperkaratosis
Thickening of the stratum corneum, often associated with a qualitative abnormality of the keratin
lentiginous
A linear pattern of melanocyte proliferation within the epidermal basal cell layer
papillomatosis
Surface elevation caused by hyperplasia and enlargement of contiguous dermal papillae = lots of little bumps
parakeratosis
Keratinization with retained nuclei in the stratum corneum. On mucous membranes, parakeratosis is normal
spongiosis
intercellular edema of epidermis - b/w cells
ulceration
Discontinuity of the skin showing complete loss of the epidermis revealing dermis or subcutis
vacuolization
Formation of vacuoles within or adjacent to cells; often refers to basal cell-basement membrane zone area = space inside of cell that’s clear
Fibroepithelial Polyp (FEP):
skin tags, squamous papilloma
- Occur in individuals usually age 30 or greater and particularly in obese individuals
- Associated with areas of rubbing by clothing; collar of neck or groin
epithelial inclusion cyst
• Also known as:
– epithelial cyst
– follicular cyst
– wen
– Common
• Caused by obstruction of hair follicle above infundibulum near where hair shaft extends beyond skin surface
• Filled with keratinous debris (i.e., not a sebaceous cyst) and lined by squamous epithelium with a granular cell layer
• If ruptured (trauma), provoke a chronic inflammatory reaction with granuloma elicited by the extravasated keratin (foreign body giant cell reaction) – can be very smelly!
seborrheic keratosis
proliferation of epidermal basal cells
“postage stamp”
FGFR3
round, flat and elevated
clinically appear as “pore like ostea filled with keratin”
acanthosis nigricans
hyperpigmentation at flexural regions
epidermal hyperplasia of stratum spinosum
20% occur d/t underlying ADCA
adnexal neoplasms
• Arise from the ductal and glandular epithelial cells of the three major adnexal groups (sweat glands & ducts; hair-bulb germinal epithelium and sebaceous glands; apocrine glands and ducts)
• Benign adnexal tumors are: – Symmetrical – Small (less than 1 cm) – Superficial – Vertical in orientation
cowden syndrome
multiple thicoepithelioma (hair follicle) w/ dominant inheritance
PTEN mutation
see benign follicular appendage tumors; hamartomatous colon polyps, internal ADCA, cerebellar gangliocytoma
Muire-torre syndrome
sebaceous adenomas with association colorectal malignancy
MSH2/MLH1 mutation
sebaveous adenoma, sebaceous carcinoma, visceral malignancy
Turban tumor
massive confluent cylindromas around forehead and scalp
benign fibrous histiocytoma
= dermatofibroma
- Tan-brown papules which are usually small (less than 1.0 cm) and may occasionally be tender
- More common name is dermatofibroma
- histologically see fibrous lesions w/ prominent collagen bundles and fibroblastic cells
suntan
increased melanin production in epidermis d/t increased melanosomes
melasma
“mask of pregnancy”
• Occurs: increased pigmentation d/t hyperestrogenism
– During pregnancy
– In women taking oral contraceptives
– At menopause
solar lentigo
as opposed to suntan, see actual small increase in melanocytes and also increased melanin production
= “sun spots”
benign, but “lentigo maligna” is term used for things arising in sun exposed areas
vitiligo
skin depigmentation thats transient
associated with: diabetes, hyperTH, melanoma, industrial chemicals
Also associated with Addison’s, alopecia, PA, IBD, and polyendocrine syndrome – CD 8 T cells.
Always look for adrenal and thyroid disease!!!
melanocytic nevi
NRAS and BRAF mutations
benign
= normal mole
junctional: small flat lesion, dermoepidermal junction
compound: raised dome, intraepidermal nests + dermal cells
intradermal: smooth raised dome/ d/t overlying dermis being stretched - just found in dermal layer
dysplastic nevus syndrome
sporadic change in a nevus - one is very little problem, but multiple nevi can develop into melanoma more likely
see dark spots/moles all over back
see nests at tips of rete ridges that are “bridged” and have “fibroplasia”
lentigo maligna
malig. melanoma from sun exposed areas
malignant melanoma
superficial spread = horizontal
nodular spread = vertical phase
usually arise as an isolated lesion, but 10% arise from melanocytic nevus
mets early: LNs, liver, lungs, brain
risks:
- fair skin
- peeling before age 20
mutations:
- nevus have NRAS and BRAF
- to become melanoma, se p16 or CDK4/6 mutation
survival based on mets, and also on thickness 92% survival <1mm
solar elastosis
(“Sailor “ or “Farmer” skin):
Permanent, incremental damage to reticular collagen (elastosis) with loss of texture (leathery skin) and wrinkling
actinic (solar) keratosis
- Actinic keratosis is a precancerous skin condition- feels like “sandpaper”
- Present on common sun-exposed areas of skin such as scalp, face and dorsum of forearms and hands.
1/1000 continue to SCC
• Appear as erythematous, reddish-brown macules or minimally elevated papules with overlying scales.
located in the epidermis, if you get rid of the epidermal layer, get rid of the tumor
can develop” cutaneous horn”
Progression to full-thickness nuclear atypia, with or without the presence of superficial epidermal maturation, heralds the development of squamous cell carcinoma in situ. (note see that there are nuclei in the keratin layer)
Squamous cell carcinoma
malignant proliferation of epidermal keratinocytes which has the potential for metastasis to regional nodes or distant sites, if not sun related. The malignant keratinocyte proliferation has penetrated the dermal-epidermal junction basement membrane and entered the dermis.
– Bowen disease = SCC in situ
long term sun exposure = increased risk of SCC
Major Clinical Characteristics of SCC
• Areas of greatest cumulative sun exposure
• Early invasive SCC is usually a small, firm, skin-colored or erythematous nodule with indistinct margins.
• The surface may be granular, and bleed easily.
• The surface may be smooth, verrucous or papillomatous.
• Older SCCs are larger, invasive, and central area of the tumor on the skin surface may be ulcerated.
• Mortality quite low for SCC of skin
keratocanthoma
- Rapidly growing (days-weeks) neoplasm; occurs on sun-exposed areas (face, hands) of older adults (men more than women)
- Often involutes and clears spontaneously within 3 to 4 months
- Histologically is SCC; now termed “Squamous cell carcinoma, Keratoacanthoma type” – like “grade 1 SCC of the skin”
- just need to resect these clinically
BCC
• Definition: Basal cell carcinoma (BCC) consists of several types of skin neoplasm originating from the basal regenerative epithelium of the epidermis that seldom - virtually never – metastasize.
most common!
always assoc. w/ sun exposure
- can become a “rodent ulcer”
Gorlin syndrome
Nevoid BCC syndrome
- autosomal dominant disorder
- multiple basal cell carcinomas before age 20
- pits of the palms and soles
- odontogenic keratocysts
- medulloblastomas: brain tumors
- ovarian fibromas
Genetics of BCC :
- sonic hedgehog binds patch gene and allows for patch to release smoothen à increased GLI1 à increased replication
if there is defect in Patch or smoothen – then its dissociated and smoothen is always turning on GLI1
nodular BCC
- Traditional or “classic” appearance of BCC
- Dome-shaped, pearly papule or nodule
- Prominent surface dilated dermal vessels (telangiectasia)
- Easily treated by excision if not large; may become quite large if neglected
sclerosing BCC
- Important clinical and pathologic type
- Occurs predominately on face
- “Rodent Ulcer”: Typically yellowish-white or pearly white, indurated plaque that may retract below plane of skin surface (leading to the designation rodent ulcer)
- Poorly defined margins (edge of lesion)
- Difficult to excise, high recurrence rate and may disfigure
- Reason MOHS surgery was invented (take tumor out without removing a lot of skin)
superficial BCC
- Multifocal erythematous, scaly plaque; elevated rolled edges.
- Occurs non-sun exposed skin sites on proximal limbs or trunk
- Multifocal growth pattern localized to dermal-epidermal junction
- Easily excised; do not become locally invasive or metastasize, but part of a “field defect” and therefore recur.
- May be confused clinically with melanoma, if pigmented
bednar tumor
pigmented variant of Dermatofibrosarcoma Protuberans
– Malignant superficial fibroblastic neoplasm (fibrosarcoma of skin)
– Locally aggressive but rarely metastasizes
The tumor usually presents as a flesh-colored fibrotic nodule on sectioning. B, The lesion often infiltrates the subcutis in a manner reminiscent of “Swiss cheese” to aficionados. C, A characteristic storiform (swirling) alignment of spindled cells is apparent.
Mycosis fungoides
cutaneous T cell lymphoma
- see inflammation of atypical lymphocytes underneath the epidermis: erythemaouts patches, pruritis, lymphadenopathy
may see “sezary cells” detected in the blood
- CD4+ T-cell lymphoma of the skin (CLA, CCR4 & CCR10)
- Aggressive neoplasm with median survival 8-9 years (M>F)
- erythematous patches/plaques present on trunk, usually over 5cm in diameter
- pruritis is common complaint
progression: premycotic, patch, plaque, tumor
PAS+ stain with CD4+ T cells in epidermis
sezary syndrome
cutaneous T cell lymphoma where skin shows generalized exfoliative erythroderma/dermatitis
scaling/erythema over most of body
itching, malaise, fever, chills, w/l
redness and scaling of skin >30%
icthyosis
scaling - looks like fish skin
- genetic abnormality leading to hyperkaratosis
- look for malignancy in LNs!
- worrisome when comes up suddenly
acute urticaria
hives often Mast cell-dependent and IgE-dependent
• All types can cause fatalities
– Systemic anaphylaxis
– Laryngeal edema
– Treat with antihistamines, subcutaneous epinephrine and IM injection corticosteroids (or with known C1 inhibitor deficiency use C1 inhibitor (C1-INH) concentrates, kallikrein inhibitor or fresh-frozen plasma)
• Classic skin lesion: Abrupt appearance of a wheal (always multiple) and area of wheal is intensely pruritic.
– Wheal: Transient edematous erythematous plaque secondary to an acute allergic reaction seen in hives (Urticaria)
– Bulla: Larger fluid-filled lesion (e.g., friction blister)
Eczema
Spongiotic Dermatitis – looks red and oozy
• Generalized term: numerous pathologic and clinical conditions: previous referred to “Chronic Dermatitis” or included collectively as “Spongiotic Dermatitis” because of common denominator of epidermal edema with prominent lymphocytes in dermis and epidermis
• spongiosis = intracellular edema
• Most commonly encountered in pediatric age groups
• Common denominator is acute onset of red, papulovesicular lesions (“boiling over” appearance) which may ooze or crust
• Usually driven by T cell mediated type IV hypersensitivity inflammation
• Acute lesions may evolve into raised, scaling plaques
type I HST?
IgE mediated = allergy
= anaphylaxis, wheels,
type II HST?
IgM or IgG mediated (i.e. autoimmune)
- antibody binds to antigen on target cell
- RHD
- Goodpasture’s
- Grave’s
- Myasthenia Gravis
type III HST?
IgG binds to soluble antigen –> circulating immune complex
- serum sickness
- RA
- post-strep pneumococcus
- SLE
type IV HST?
- T cell mediated “delayed type” cell mediated immune response
- contact dermatitis
- chronic transplant rejection
erythema multiforme
“target lesions”
• Hypersensitivity (CD8+ cytotoxic T cells) reaction to drugs, infections, malignancy, collagen vascular disorders
– Infections: Herpes simplex, deep fungal (Histoplasmosis), Salmonella typii, Leprosy
– Drugs: Antibiotics, Salicylates, Anti-malarials
– “Multiforme” because of wide variety of clinical appearances in addition to characteristic “target” lesions (red-pale-red)
– Other skin disorders have targetoid lesions but not the classic red-pale-red pattern
• Severe, systemic febrile form with mucosal involvement: Stevens-Johnson syndrome
• Toxic epidermal necrolysis is form with diffuse necrosis and sloughing of skin and mucosae (emergency situation – skin is like burn patient)
erythema minor - most often d/t herpes simplex
erythema major - most often d/t drugs
seborrheic dermatitis
“dandruff” = dry scales and underlying erythema - seen on scalp, face, back, glabella (upper eyebrow)
- Chronic “dermatitis” more common than Psoriasis (5% of population)
- Involves skin regions with high density of sebaceous glands (oil or sebum production)
• Infection with superficial yeast (Malassezia furfur) may play important role since condition is improved by use of topical antifungal agents
- often seen in hostpitalized patients with acute illness
** can be associated with parkinson’s disease!!! slow soft speech, swallowing, seborrheic dermatotis!
acute vs. chronic inflammatory conditions?
acute:
urticaria, eczema, erythema multiforme
chronic: seborrheic dermatitis psoriasis LSC lichen planus discoid lupus erythematosus rosacea
psoriasis
“AI disease” → results in plaques: silvery scales on bright red well demarcated plaques (knees, elbow, scalp)
• Chronic skin condition affects 1-2% of the US population
• Clinical association with arthritis
• Affects skin of elbows, knees, scalp, = EXTENSOR AREAS!!!!
Koebner phenomenon – trauma can induce psoriatic lesions – irritated skin sets of psoratic lesion
- Typical lesion: well-demarcated, pink- to salmon plaque
- Many different clinical presentations
- HLA-Cw*0602 association – increased CD4+TH1 sensitized cells set off other T-cells causing increased cytokines leading to epidermal proliferation.
tx: phototherapy - UV rays help it
- topical corticosteroids
associated with: MI, metabolic syndrome, IBD, depression, nail pits, koebner reaction, arthritis, +ASOT
LSC
Lichen Simplex Chronicus: chronic scratching!
• From chronic rubbing or scratching
• If nodular = Prurigo nodularis
• seen in nervous people
• see neoplasia of the epidermis
- see skin lines, well circumscribed and scaly plaque
civatte bodies
lichen planus
wickhan striae
lichen planus
lichen planus
: inflammation – see bandlike infiltrate of lymphocytes
pruritic, purple planar, papular - more often seen in oriental populations
- see wickam striae in mouth!
- Self-limiting chronic inflammatory condition of skin and mucous membranes (oral cavity)
- Usually resolves spontaneously 1-2 years after onset, but may persist for years in oral cavity
- Multiple plaques that are symmetrically distributed, particularly on extremities, often on wrists and elbows and on the glans penis, + Koebner phenomenon
** note: commonly assoc. w/ hep c, UC, vitiligo and MG — cell mediated immune response of u/k origin
Discoid Lupus Erythematosus:
• Localized cutaneous manifestation of Systemic Lupus Erythematosus (SLE) with no associated systemic manifestations
Excessive sun exposure may trigger cutaneous lesions or exacerbate them
– “butterfly rash”
REMEMBER:
- SLE type III HST, d/t ANA Abs directed against nuclear antigens, that result in immune complex formation
- linked with HLA-DQ
- see Antigen-Ab complexes stuck at the basement membrane: IgG and antigen along with complement C3 get stuck at the basal layer
- see : malar rash, discoid rash, photosensitivity, oral ulcers, arthritis, serositis (pleuritis, pericarditis), renal dysfunction, nseizures, hemolytic anemia
rosacea
see erythema and telangiectasias
flush easily
dfft. from acne b/c of neurovascular componenet and no comedones
bullous diseases
• Common Friction Blister – Intraepidermal blister usually just beneath the stratum granulosum with scant or no inflammation in papillary dermis. • Immune-Mediated – Pemphigus Group of Diseases – Bullous Pemphigoid – Dermatitis Herpetiformis • Genetic-Congenital – Epidermolysis Bullosa- inherited defects in collagen, laminin, etc leading to several disorders with weak skin and blistering – Porphyrias
subcorneal blister?
pemphigus follaceous
more benign course; involves face, scalp, chest and back and spares mucous membranes
– Epidemic form occurs in South America (fogo salvagem)
autoAbs against Dsg1 only (most superficial) - leads to subcorneal blisters
suprabasilar/intraepidermal blister
under epidermis, but above the BM
= pemphigus vulgaris
autoAbs against DSg1 and Dsg3 - cause blisters in the deep suprabasal epidermis
produce reticular “fishnet” like pattern
subepidermal blister
entire epidermis seperates from dermis
= bullous pemphigoid
autoAbs bind BPAG2 (component of hemidesmosomes, leading to blister formation) at level of basement membrane
- more resistant to rpture, look more like friction blister
- see linear deposition of C’ along dermo-epidermal junction
Dermatitis Herpetiformis:
– IgA to gliadin attacks reticulin in dermal papillae fibrils
– Rare skin bullous disorder
o Major association with Celiac Disease (Sprue, gluten- sensitive enteropathy)
o anti-gliadin antibodies cross-react with reticulin in the anchoring fibrils in dermal papillae
o Intensely pruritic plaques and vesicles
o located on extensor surfaces, elbows, knees, upper back and buttocks
• Note: Selective deposition of IgA autoantibody at the tips of dermal papillae is characteristic
erythema nodosum
panniculitis - painful red nodules w/out ulceration on anterior aspects of legs
- seen with drug exposure or inflammatory bowel disease
** strep infection is the most common cause *** 2nd most common is BCP’s
– Acute septal inflammation associated with infection by many agents [(e.g. Beta-strep, TB, sarcoidosis, inflammatory bowel disease, malignancies and drugs (e.g. sulfonamides , oral contraceptives)]
Erythema nodosum is a form of panniculitis characterised by tender red nodules, 1–10 cm, associated with systemic symptoms including fever, malaise, and joint pain. Nodules may become bluish-purple, yellowing, and green, and subside over a period of 2–6 weeks without ulcerating or scarring.
erythema induratum seen from TB: posterior surfaces of legs, may ulcerate
verruca vulgaris
warts
etiology - often d/t HPV virus
molluscum contagiosum
poxvirus
long incubation time, younger age group, umbilicated lesion, transmitted through contact
impetigo
= superficial blisters w/ purulent material that rupture easily w/ “honey colored crust”
** very contagious
** often gram + : most commonly caused by staph aureus, though historically seen with beta strep infections
different tinea infections
– Tinea capitis: scalp in children
– Tinea corporis (“ringworm”): trunk and extremities in all ages but more in children
– Tinea cruris: inguinal skin adjacent to genitalia, obese men in hot weather
– Tinea pedis (athlete’s foot): feet (between toes)
– Tinea barbae: beard area in men
– Onychomycosis: fungal infection of nail beds
– Tinea versicolor: this one is not named by a location and is a yeast (Malassezia furfur) infection (not a dermatophyte with hyphae, unlike the others)
tinea versicolor
a yeast skin (Malassezia furfur) infection (not a dermatophyte with hyphae, unlike the others)
would see pseudohyphae
epidermolysis bullosa
- genetic abnormalites in structural proteins keratin 14 or 5 –> lead to bulla forming that are massive!!! suprabasalar lesion
porphyrias
AD inheritence = non inflammatory blisters d/t sun
- hypertrichosis and skin fragility
- assoc. w/ liver disease and elevated urinary porphyrins
defects in heme synth, leads to increased intermediates causing urticaria and supepidermal vesicles (esp. in sun exposure)
atopic dermatitis
insect, light, drug, allergen, food allergy
- eos are prominent in inflamm.along with IgE
- humoral mediation - responds well to steroids
- pruritic, exudative, or lichenified eruption on face, neck trunk, wrists, hands
- onset often in children, rare after age 30
- flexural areas are common
note: often linked with staph - staph makes biofilm –> causing a rash that itches
allergic contact dermatitis
topically applied antigens
- t-cell mediated
- won’t respond well to steroids
- no inflamm. until second exposure
ex: poison ivy, nickel, jewelry
primary irritant dermatitis
- d/t chemicals
- no prior exposure necessary
- necrosis and ulceration w/ neutrophil response
NF1
NF1/neurofibromin gene
see neurofibromas, optic nerve gliomas, cafe au lait spots
NF2
NF2/merlin gene mutation
see neurofibromas, bilateral acoustic neuromas, CNS gliomas, cataracts
pityriasis rosea
oval, fawn-colored scaly eruption following cleavage lines of trunk - “christmas tree pattern”
common, mild inflamm. disease more common in females
d/t HHV 6 and 7
itching is mild and common
center of lesions have “cigarette paper” appearance - thin red scale around the outside, with clearing in the middle
“herald patch” - larger lesion that is usually seen before other lesions
NOTE: must rule out syphilis, with RPR - esp. if pregnant!
tinea corporis
“body ringworm”
- ring-shaped lesions with advancing scaly border, central clearing or scaly patches
often on trunk
ddx via culture/scrapings
trichophyton rubrum is most common pathogen
scaling of palms, soles, in between toes and fingers
think tinea pedis/manuum
bowen disease
intraepidermal SCC
folliculitis
itching and burning in hairy areas - pustules in hair follcicles
frequently caused by staph infections
“hot tub follcilitis” = pseudomonas aeruginosa
milaria
“heat rash”
burning, itching, small vesicles, usually on trunk in hot moist climates
steven johnson syndrome
erythema multiforme major where <10% BSA skin loss
caused by toxicity - often d/t sulfonamides, NSAIDs, allopurinol, antivonculscants
toxic epidermal necrolysis
see erythema multiforme major, TEN where there is >30% BSA skin loss
caused by toxicity - often d/t sulfonamides, NSAIDs, allopurinol, antivonculscants
must be tx like a burn patient
erythema migrans
think lyme disease - gradual expansion of red target
erysipelas
= an infectious erythema
edematous, spreading, hot erythematous region, pain chills, fever,
cellulitis d/t Beta-hemolytic strep
cellulitis
edematous, expanding, erythematous warm laque often involving lower leg
pain, chills, fever, may cause sepsis
Beta-hemolytic strep or staph aureus
leukocytosis is present throughout
kaposi sarcoma
Herpes Type 8
endemic in young black men in Africa
red/purple plaques or nodules on cutaneous or mucosa surfaces
seen in pts. with HIV/AIDS
scabies
generalized severe itching, burrows, especially on finger webs/wrist creases
red papules or nodules on scrotum and penil glands is pathognomonic
= “seven year itch”
pediculosis
pruritis with excoriation, nits on hair shafts, lice in skin/clothes
“crabs” or body lice — due to the pubic louse
do darrow’s slide show
do it NOW.
where does melanoma most often mets to?
liver. (shows elevated alk phos)
other places: LNs, lungs, brain
“the itch that rashes”
rash starts with pruritis –> rash = a type of atopic dermatitis, IgE mediated (seen at flexion of fossa, face, dorsal feet)
most often d/t staph - forms biofilm over the skin
Staphylococcal biofilm which block sweat glands. Toll-like receptor 2 is the protein that is involved in the innate immune system, which is activated in areas where there are blocked sweat ducts in cases of eczema.
treatment:
Current management for eczema includes the use of steroids to reduce inflammation and enhance the body’s ability to fight the bacteria. Patients should be instructed to be wary of soap, hot water, scrubbing, and clothing that can aggravate itching, scratching, and peeling. Oil rather than water-based moisturizers are recommended. Products containing dyes, perfumes, or peanuts should be avoided.
Job’s disease/ Hyper IgE syndrome
problem with phagocytic function- see recurrent staph absessess
- eczema + neutrophil problem
Job’s disease: white cells can’t get where they need to d/t no integrin CD11/CD18 - thus there are high WBC’s but recurrent bacterial infections = hyper IgE syndrome
- they present with atopic dermatitis and recurrent infections
- increased IL-4 –> results in increased TH2 response –> stimulates IL4, ** IL-5, –> production of B cells –> plasma cells (IgE)
- see decreased TH1 and CD8+ cells
case: An 8 year old child has a history of staphylococcal abscesses, a prior episode of pneumonia with pneumatoceles, high IgE levels,
eosinophilia, and rash as shown. He has lost none of his teeth. The primary problem in this patient is:
wiskott-aldrich
see eczema with combined immunodeficiency: this is a combined B and T cell immunodeficiency disorder
This 60 y/o male complains of dry itching skin with circular coin shaped lesions found in the winter. He bathes nightly. This is which eczema.
nummular eczema
drugs that can produce psoriasis?
stopping corticosteroids
Certain drugs can also produce psoriasis,
ie beta blockers, lithium, interferon, etc.
Flare up may be an HIV marker
koebner phenomenon
scratch skin and rash will break out where you scratch
- its more common for this to be associated with poison ivy
- almost like the itch that rashes
nail pitting, fungal looking nails, oil spots
think psoriasis
fungal infection that extends to the nail junction?
marker for immunodeficiency - think AIDS
trichophyton rubrum should be superficial and distal
dull yellow fluoresence under wood’s light
malassezia furfur = a genus of fungi that can cause hypopigmentation
“scraping show” - spaghetti/meatballs
can cause tinea versicolor - “sun fungus” that causes hypo or hyperpigmentation that is increased with sunlight - looks like small spots
Tinea versicolor = worsens with Cushings, malnutrition or immunosuppression
spaghetti and meatball
malassezia furfur, tinea versicolor
steroid acne
steroid dermatitis = small, firm follicular papules on the forehead, cheeks, and chest. They appear as pinkish maculopapular rash without any comedones or cyst
steroid acne is the same condition as malassezia folliculitis and is due to proliferation of malassezia yeasts (also known as pityrosporum).
pink florescence under wood’s lamp
cornebacterium
Bacterial infection in skin flexures due to erythrasma (Corynebacterium minutissimum)
green fluorescence under wood’s lamp
Cat ringworm Microsporum canis
porphyria cutanea tarda
hepatic uroporphyrinogen decarboxylase deficiency: disorder results from low levels of the enzyme responsible for the fifth step in heme production.
- see blistering of the skin, is a chronic condition and can result in chronic liver prolbmes, cirrhosis and inflammation and hepatic fibrosis
- void wine colored urine d/t increased uroporphyrin I enzyme
- see elevated ALT, hep C infection, photosensitivity
yields a pink fluorescence under Wood lamp (black light) radiation
b/l pneumonia w/ bullous myringitis (inflammation of TM) and dry cough,along with erythema multiforme
mycoplasma pneumonia
drugs causing SJS/TEN
West:
- oxicam NSAIDs***, ie perioxicam (Feldene)
- sulfas
East:
- carbamazepine (Tegretol) – HLA - B*1502
- allopurinol – HLA - B*5801
if from west think NSAIDs, if from east don’t give tegretol or allopurinol!!! (antiseizure drugs)
SJS works through FasR death receptor - drugs activate this pathway –> self breakdown
sharp demarcation of inflammation/rash
think strep = ‘st. anthony’s fire”
organism responsible for necrotizing cellulitis/ fascitis - associated with colon, gyn, or lymphoreticular malignancies.
Clostridium septicum - see “gas gangrene”
for some reason malignincies result in growth of C. septicum
Infections are typically seen in settings of trauma, surgery, malignancy, skin infections/burns, and septic abortions.
pt with rash after spending day in spa
pseudomonas aeruginosa
skin infection that feathers out around a central lesion - not sharp borders
think staph aureus or MRSA
what to worry about what with child w/ impetigo?
group A strep infection - can cause glomerulonephritis - child has puffy face d/t fluid retention and hematuria
what causes rosacea?
demodex mite or may be d/t intestinal bacterial overgrowth
see rinofina - large scarred nose
worry about Keratopathy. Corneal melting!
Corneal vascularization and thinning.
Associated with PD.
many have SIBO(small intestinal bacterial overgrowth) ad respond to rifamixin
see telangiectasias but no comedones
parkinson’s
think seborrheic dermatitis and malssezia furfur
complications of ioxides scapularis lyme disease?
Stage I: Flu syndrome with rash (ECM)
Stage II: Dissemination: heart, joints, nerves and skin (heart block, Bell’s palsy, migratory arthralgias, ECM)
Stage III: Late: joints and CNS and PNS (oligoarthritis, encephalitis/memory loss
- sleep disturbances, neuropathies/paresthesias)
“fifth’s disease”
slap cheek, reticulated rash that looks like giraffee
caused by parvovirus B19
Fifth disease starts with a low-grade fever, headache, rash, and cold-like symptoms, such as a runny or stuffy nose. These symptoms pass, then a few days later the rash appears. The bright red rash most commonly appears in the face, particularly the cheeks. This is a defining symptom of the infection in children (hence the name “slapped cheek disease”).
This ssDNA virus can also produce the glove and stocking purpuric syndrome. The mother may also develop a small joint arthritis resembling RA.
** worry about mom b/c can cause aplastic anemia
blueberry muffin baby, deafness, hematopoiesis, malaise, polyarthritis - see dark blue spots
congenital rubella syndrome = “german measles”
blueberry spots d/t extramedullary hematopoisis
The syndrome (CRS) follows intrauterine infection by the rubella virus and comprises cardiac, cerebral, ophthalmic and auditory defects- It may also cause prematurity, low birth weight, and neonatal thrombocytopenia, anemia and hepatitis.
This patient developed this rash on her forehead that is spreading
centifugally. She also has the
bluish white spots in the mouth
with fever, conjunctivitis, coryza, and cough.
rubeola virus = regular measels
problem if develops panencephalitis when older!
koplik spots = small red based lesions with blue white centers in mouth
levamisole
used to cut cocaine - causes arteritis and plugs up vesicles
see bubble fingers d/t?
caused by PDF/VEGF –> neoangiogenesis –> subperiosteal new bone formation
seen in lung cancer, lung infections, CF, cirrhosis, graves disease
DRESS syndrome
Drug Rash with Eosinophilia and Systemic Syndrome = DRESS
- 2-6 weeks after start of a new medicine
- Progression from acral edema to generalized rash to pinpoint pustules and desquamation
- Lymphadenopathy, hepatomegaly and abnormal LFTs
- An IL5 disease.
see progression from desquamation –> lymphadenopathy –> hepatomegaly and liver problems
type IV reaction d/t HHV6 induced CD8 T cell response
poison ivy is what response
T cell response with macrophage activation
Type IVa Gell-Combs
acquired C1 esterase deficiency
anyone with B cell lymphoma/leukemia forms antibodies, if you form Abs you tend to form them for C1 esterase, if C’ is activated you can’t shut it off and get angioedema, because you have formed Abs aainst C1 esterase
Angioedema: - Cause: Bradykinin - Screen with C4 for angioedema - Decreased CI level points to acquired C1 esterase deficiency rather than the hereditary type (It’s new and the body can’t keep up!)
hopefully won’t be on test…
urticaria >24 hours
means that its chronic = urticarial vasculitis
photosensitive pt. with RO/SSA antibody?
= subacute cutaneous lupus
- skin lesions that are scaly and evolve as polycyclic annular lesions or psoriasiform plaques
- lesions look annular and serpentine
- can be deficiency of the 2nd component of complement
- child could be born with heart block!!!
