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31 Cards in this Set
- Front
- Back
Polytrichia
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tufted or doll hair
- Loss of follicular openings; follicular pluggings Scalp surface changes may or may not relate to alopecia: Psoriasis: + scalp surface change; - hair loss Male pattern baldness: - scalp surface change; + hair loss |
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Lichenification criteria
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(must have all 3)
1) Palpable thickening 2) Accentuated skin markings 3) Lichen-type scale |
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AGA (Androgenetic Alopecia) occurance men/women
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80% of men; 40% of women by age 70
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AGA (Androgenetic Alopecia) cause & see
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- Increased 5α reduction of T -> DHT: Lose normal ratio of Terminal:Vellus (normal 2:1) -> vellus/indeterminate will outnumber
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Alopecia Areata/Totalis/Universalis
Cause |
Smooth patches; non-scarring T-cell disorder (HLA-DQ3; HLADRB1)
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Alopecia Areata/Totalis/Universalis Bad signs
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2) BAD SIGNS:
i. Onset before puberty ii. > 5 yr duration iii. FHx of AA or PMHx of Atopic Derm iv. Extensive dz like Ophiasis v. Worsening, Persistent, Recurrent vi. Onychodystrophy Always potentially reversible |
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2 Tests to order for DLE:
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1) ANA (lower titer; 10-20% positive
i. MAJORITY ANA Negative 2) Ro |
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Approach to pt w/ Suspected Cutaneous Lupus:
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1) ANA assay on HEP-2 cells ->
i. Negative (DLE)-> 1) No systemic symptoms & ongoing suspicion of anti-Ro assoc cutaneus dz? -> Ro-Ab ii. Titer < 1:160 (DLE) 1) No systemic symptoms & ongoing suspicion of anti-Ro assoc cutaneus dz? -> Ro-Ab 2) Systemic Symptoms -> Rheumatology consult iii. Titer 1:160 (SLE) 1) Autoab (anti-dsDNA; -Sm) if indicated by clinical findings -> anti-Ro; Cardiolipin a) Abnormal values -> Rheumatology 2) Other tests: a) CBC b) Chem screen for creatinin; albumin; protein c) ESR d) C3/C4 Abnormal -> Rheumatology |
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SCLE skin lesions have 2 types:
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1. Annular or polycyclic – no scales
DDx: Tinea infection, Erythema annulare centrifugum. 2. Papulosquamous or psoriasiform – scales are present |
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- 11 criteria (4 are derm findings) - 4 or more concurrent or serial = SLE
what are the 4 |
1) Malar erythema
2) Discoid rash 3) Photosensitivity 4) Oral or Nasopharyngeal uclers (often painless) "Photos of Malar Discoid Mouths/Noses" |
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NLE cause
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Crossing of Anti-Ro ab (SSA; Sjogrens Syndrome A) across placenta
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NLE Risk
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- Congenital heart block (dmg may be permanent) (ab settle 2% of time; if do -> 54% get heart block)
- Hepatic; hematologic; neurologic dmg - Dermatologic (50%) - analagous to SCLE (raccoon eyes; discoid) 7% (1/14) infants to anti-Ro moms |
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DILE drugs (6)
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Hydralazine,
Procainamide, Minocycline, TNF inhibitors, Methyldopa, Penicinlamine. |
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Dermatomyositis (DM): labs & features
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ALDOLASE is elevated (also ALT/AST; CPK; LDH)
Derm features: § HELIOTROPIC RASH (upper eyelids w/ violaceous edema) - pathognomonic GOTTRONS PAPULES (red scaly papules over knuckles, ip, mp, elbow, knee) - |
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Sclerodactyly
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- Sclerodactyly: no wrinkles despite old age; skin pulled tight (like collagen injection)
- Gross: salt and pepper in blacks, MAT type telangiectasia |
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Acne pathophys
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- Hormonally induced disruption of infundibular keratinocyte dynamics
o Superimposed epiphenomena of immune-mediated inflammation |
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Preadolescent Acne cause
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Preadolescent Acne: Androgen metabolism => acne via DHT formation
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Acne tx
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IMPORTANT TO KNOW
- Retinoid is 1st line - Individualized - COMBO - BPO is cheap and highest antimicrobial activity of topicals |
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Normal sebaceous follicle flora
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Normal Sebaceous follicle flora
1. Propionibacterium acnes 2. P. granulosum, P. parvum 3. Staphylococcus epidermis 4. Demodex folliculorum (mite) 5. Liphophilic yeast 6. Malassezia furfur, M.sympodalis |
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Melanoma risk factors
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Risk Factors: trauma, burn scars, albinism, X-ray radiation, pre-existing pigmented lesions
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ABCDE of nevi
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Asymmetry, Border, Color, Diameter, Evolution
Diameter > 6mm |
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Ugly Duckling Sign
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unusual very darkly pigmented/ugly mole or freckle that stands out from rest
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Little Red Riding Hood Sign
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persistent scaling pink/red patch that doesn’t respond to tx
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Biopsy melanoma effect?
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3/4 of all melanomas arise de novo,
§ removal of nevi inefficient to decrease melanoma risk, manage risk instead § Atypical nevi = risk MARKER (not pre-cancer c/o 3/4 arise de novo) |
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CUTANEOUS DRUG ERUPTIONS epidemiology
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95% of these immunological pathways are lymphocyte (T cell) mediated
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Mechanisms of Cutaneous Drug Eruption
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o Specific HLA molecules play an important role – presenting antigen to T-cells and confer a greater susceptibility to various drug eruptions
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Window of opportunity for cutaneous drug reaction
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closes after: ten weeks. >10 wks then most probably without problem
opens after: - a week for a new drug but - immediately for a drug the patient has previously taken. |
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Drug Reaction Patterns High risk
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- Urticaria and Angioedema
- EM, Stevens-Johnson Syndrome and TEN - Vasculitis - The Drug Hypersensitivity Syndrome/DRESS (Drug Rxn w/ Eosinophilia & Systemic Sx) - AGEP (Acute Generalized Exanthematous Pustulosis) - Erythroderma |
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Vascular Reactions morpho
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Lesions are typically red, without scaling lesions are typically flat-topped; often confluent
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"Fixed" erythemas morpho
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* Persistent flat erythema exanthem-like")
* Erythema multiforme (bullous and non-bullous) |
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BULLOUS FIXED DRUG ERUPTIONS
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Usually a single large blister (bulla) on an erythematous base
Lesions occur within 48 hours after exposure and last 7 to 10 days; no scaring, but with HYPERpigmentation |