) Flashcards
Acute mastitis vs periduxtal mastitis
Acute- bacterial (S.aureus) infection from breast feeding; erythematous breast with purulent nipple discharge
Periductal- inflammation of the aubareolar duct due to cigarettes. Leads to columnar becoming squamous due to vitamin a deficiency and the duct gets blocked with keratin causing inflammation. Heals with fibrosis so myofibroblast pulls nipple inwards to ducts
Mammary duct extasía
Inflammation of the subsreolar duxts leads to dilation of the ducts causing inflammatory debris to create a mass and debris leaks out of breast as green brown nipple discharge; plasma cells
Fat necrosis
- presentation
Mass because of inflammatory and giant cells or as calcifications because fat binds calcium
Fibrocystic change
- pathophysiology
- subtypes
- complication
Development of fibrosis and cysts (dilation of lobules and ducts) in premenopausal women due to estrogen
- lumpy breast
Subtypes - fibrosis cysts apocrine metaplasia - no increase risk of invasive cancer
Ducts hyperplasia (>2 layers of cells in the duct and sclerosing adenosis (calcification and fibrosis - increased risk
Atypical hyperplasia - increased atypical cells in lobular or duct/ greatness increased risk of invasive carcinoma
Intraductal papilloma vs papillary carcinoma
Papillary duct growth into large duct
- intraductal- premenopausal; finger like projection is lined by luminal and myoepitheal : blood nipple discharge
- papillary carcinoma- post meno ; finger like projection is lined by luminal only
Fibroadenoma vs phyllodes tumor
Most common benign breasts mass is Fibroadenoma.
- tumor of fibrous tissue and glands in premenopausal ; responds heavily to estrogen so shrinks during menopause ; no increase risk of cancer
Phyllodes- fibroadenoma like tumor with overgrowth of fibrous tissue in postmenopausal ; May be malignant
Ducts carcinoma in situ (+subset)vs lobular carcinoma in situ
Dcis- malig proliferation of cells in ducts which doesn’t cross the basement membrane; present as calcification (no mass usually
- since there’s calcification need to biopsy calcification to distinguish between benign shit like fibrocystic sclerosing adenosis and fat necrosis
- subset is PAGET
Lobular carcinoma in situ - malignant proliferation of cells in lobular ; found incidentally bc no calcifications or mass primoduxed; cells lack ecadherin; treatment- TAMOXIFEN
Invasive Ducati carcinoma (+subtypes) vs invasive lobular
Ductal - most common invasive forms duct like structures ; presents as a mass
- tubular , mucinous , medullary (seen in brca; malignant cells with inflammation cells such as lymphocytes and plasma), inflammatory - grows in dermal lymphatics (so swelling)and presents like a mastitis that doesn’t resolve with antibiotics and
Lobular - lack ecadherin so can’t form duxts ; grows in single file
Male breast cancer
- location
- most common subtype
- possible symptoms
- risk factors
Subseeolar so can produce milk
Males only have ducts and no lobulares therefore more commonly would have invasive distal carcinoma
RF: Klein filter and BRCA2
Acne management
Comedones (whit and black heads ) topical retiñoids
Pustules - benzoyl peroxide
Clindamycin/ doxy/erythomycin antibiotics
Last resort -isoretinoin
Lichen planus association with what GI condition
Chronic hep c infection.
Pemphigus vulagaris vs pemphigoid
Vulgaris- IgG against desmoglein in desmorones; positive Nikolsky; blistering of skin and oral mucosa; iF - fish net
Pemphigoid - IgG against hemidesmisomes - negative nikolsky; blistering of skin only ; IF: liner
Erythema multiforme
- subtypes
- pathophysiology
- causes
Subtypes : SJs and TEN
- SJS (EM with oral mucosa and lip involvement plus fever)
- TEN : severe form of SJs with sloughing of skin at epidermal dermal junction due to adverse drug reaction
Hypersensitivity rxn associated with HSV, mycoplasma infection , AI diseases, malignancy and penicillin and sulfonamide ——-targetoid rash (with white center due to necrosis ) and bullae
Basal cell carcinoma vs squamous
- location; causes, appearance
BCC- top lip , UVB sun exposure , ulcerated ulcer with surrounding telangiectasia
SCC- lower lip; UVB sun exposure , but also immunosuppressive therapy, arsenic , chronic inflammation from burns or draining sinus tract
- dysplasia : actinic keratosis
- subtype : keratoacanthoma——occurs suddenly and resolves spontaneously
Vitiligo vs albinism
V- autoimmune destruction of melanocytes
A - enzyme deficieny (tyrosinase) so can’t make melanin; increased risk of SCC especially and other skin cancers
Freckles pathophysiology
Increases melanosomes( melanocytes are not increased