Pathology 1 - Final - Part 2

davidwurbel7's version from 2016-04-11 19:41

Skin Disorders I

Question Answer
5.0 mm or lessVesicle
More than 5.0 mm or moreBullae
Autoimmune blistering disorder of skin & mucus membrane. Results in dissolution of intracellular attachments. Incidence during the 4th to 6th decadePemphigus
Caused by IgG autoantibodies against ‘desmogleins’. Desmosomal damage and consequent acantholysis may follow activation of chemical mediators. acantholysis, these cells are detached and appear rounded. the level of blistering: suprabasal. the row of suprabasal cells are referred to as ‘tombstones’. blister cavity contains few cells. Immunofluorescence: net-like pattern of intercellular IgGPemphigus vulgaris
Clinical features include oral lesions are seen. positive Nikolsky sign (with slight rubbing of skin, the superficial skin splits from basal layer). corticosteroid therapyPemphigus vulgaris
Chronic sub-epidermal blistering disease. mostly in elderly (60 to 70 years). multiple tense bullae of varying sizes. auto-antibodies against hemidesmosomesBullous Pemphigoid
Presence of circulating and tissue-bound autoantibodies against hemidesmosomes. blistering is due to antibodies raised against one of the hemidesmosome antigen (BPAG2). leading to neutrophil & eosinophil chemotaxis. proteolytic enzymes released by these cells produce blisters. subepidermal blister. scattered eosinophils, and other inflammatory are seen within the blisters. Immunoflourescence: linear deposition of IgG/C3. ‘ribbon candy’Bullous Pemphigoid
Clinical features include older people. eosinophilia in peripheral blood. inner aspect of thigh, flexors of forearm, groin, lower abdomen, and axillae. negative Nikolsky signBullous Pemphigoid
Rare, chronic, sub epidermal blistering disease. intensely pruritic, herpetiform grouping. predilection for extensor surfaces, symmetric. mostly early adults. 90% have gluten sensitive enteropathy (Celiac disease). gluten-free diet usually leads to reversalDermatitis Herpetiformis
Pathogenesis - IgA antibodies (against gluten) formed in the gut fixes on skin. IgA deposits in skin leads to complement activation. this brings neutrophils to papillary dermis. enzymes released by neutrophils destroy basement membrane components: laminin & Type IV collagenDermatitis Herpetiformis
Clinical features include intensely pruritic lesions (papule / vesicle) symmetric distribution of lesions on elbows, knees, buttocks, shoulders, and sacral areasDermatitis Herpetiformis
Acute self-limited, usually mild, and often relapsing mucocutaneous syndrome. may present with vesicles and bullae. Etiology includes infections - herpes simplex, mycoplasma, histoplasmosis, coccidiomycosis, typhoid, leprosy, drugs - sulfonamides, penicillin, barbiturates, salicylates, hydantoins, anti-malarial. Malignancies - carcinomas, lymphomas, Collagen vascular disease - SLE. Morphology - multiform lesions, typical targetoid symmetric involvements of limbs. Micro - superficial perivascular lymphocytic infiltrate. dermal edema, lymphocytes along dermal-epidermal junction. necrotic keratinocytesErythema Multiforme

Skin Disorder II

(Insert 1-4)
Question Answer
T cell mediated inflammatory reactions (type IV). triggered by contact antigens (example: uroshiol from poison ivy). Morphology - red, papulovesicular, oozing, and crusted lesions. Micro - spongiosis, superficial perivascular lymphocytic infiltrate, papillary edema, and mast cell degranulationAcute Eczematous Dermatitis
Self-limited disorder of the pilosebaceous unit. Seen primarily in adolescents, presents as comedones, papules, pustules, and nodules. The sequelae can be lifelong, with pitted or hypertrophic scar formationAcne vulgaris
Basic steps have been identified - follicular epidermal hyperproliferation (keratin), excess sebum production, inflammation, and the presence and activity of Propionibacterium acnesAcne vulgaris
Clinical features include the age of onset varies considerably. It may start as early as 6 to 8 years of age or it may not appear until the age of 20 or later. Course is one of several years duration followed by spontaneous remission in the majority of casesAcne Vulgaris
Characterized by epidermal hyperplasia with elongation of rete ridges in a regular mannerPsoriasiform
Chronic inflammatory dermatoses. autoimmune basis (HLA-C). common disorder. Genetic - HLA-C. Immune sensitized populations of CD4+ TH1 & TH17 cells, & activated CD8+ effector T cells enter skin, and accumulate in the epidermis leading to secretion of cytokines and growth factors keratinocyte proliferation. epidermal hyperplasia (acanthosis) elongation of rete ridges. parakeratosis. thinning of stratum granulosum. Monroe’s microabscesses in superficial epidermisPsoriasis
Clinical Features include lesions are present over the elbows, knees, scalp, lumbosacral areas, intragluteal cleft, glans penis. ‘salmon colored plaque covered loosely by silver-white scales’. involvement of nails in some patients. bleeding points. Treatment: PUVA (Psoralen, UV-A)Psoriasis
Clinical features include Pruritic, purple, polygonal, planar, papules, and plaques. a network of fine white lines: Wickham striae. Seen best in lesions present in oral cavity. Self limited disease, however oral lesions may persist association with chronic hepatitis CLichen Planus
Pathogenesis - expression of altered antigens at basal layer and epidermo-dermal junction. cell mediated immune response precipitated by altered epidermal antigens. draws in lymphocytic infiltrate. cytokines released damages epidermal basal cells/basement membrane. Morphology - interface dermatitis. apoptotic epidermal cells: Civatte bodies. band-like lymphocytic infiltrate. rete ridges show “saw tooth” appearanceLichen Planus
Also called as senile warts, very common. Seen in elderly, any part of the body except palms and soles. Morphology - sharply demarcated, gray-brown to black lesions. Basaloid cells, valleys filled with keratin, keratin cysts (horn cysts)Seborrheic Keratosis
Common skin tumor arising from skin. Predisposing factors include exposure to sunlight, fair skin, who tan poorly, industrial carcinogens, chronic ulcers (Marjolin’s ulcer), ionizing radiation and Xeroderma pigmentosum. Morphology - invasion into deeper stroma. Well differentiated will show formation of keratin pearlsSquamous Cell Carcinoma
Clinical features include early lesions appear as sharply defined, red scaly plaques. advanced lesions are nodular, ulcerated. lymph node metastasesSquamous Cell Carcinoma
These are common slow growing tumors that rarely metastasize. Predisposing factors include fair skin, sun exposure, Xeroderma pigmentosum, Nevoid Basal Cell Carcinoma Syndrome (associated with PTCH gene mutation affecting signaling pathway). Morphology - pearly plaques, telangietatic. tumor cell resemble normal basal cells of the epidermis. arranged in nests, with cells in the periphery forming ‘picket fence’ (pallisading)Basal Cell Carcinoma
Clinical features include later, ulceration seen, with can be extensive (rodent ulcer). “invades rather than metastasize”. Patient morbidity due to local tissue destruction and disfigurementBasal Cell Carcinoma
More common in darker pigmented individuals. Pathogenesis - autoimmune destruction of melanocytes. localized loss of pigmentationVitiligo
Clinical features include in light skinned people, localized depigmented areas appear following tanning. May be associated with other autoimmune diseasesVitiligo
Benign localized hyperplasia of melanocytes. Morphology - linear, distribution of melanocytic hyperplasia. hyperpigmented basal cell layerLentigo
Clinical features includes differs from freckle. freckles show increase in melanosomes, but no increase in melanocytesLentigo
Aggregates or nests of cells along dermo-epidermal junctionJunctional Nevi
Junctional nevi growing into dermisCompound Nevi
Only dermal present, the epidermal nests disappearIntradermal Nevi
Precursors to melanoma. dysplastic nevus syndrome in families. Pathogenesis - autosomal dominant in dysplastic nevi there is inherited loss of function mutations in CDKN2ADysplastic Nevi
Morphology - larger than usual type of nevi. may be numerous as in familial type. flat macules/raised plaques/pebbly surface. variability in pigmentation. irregular borders. seen in both sun exposed and not sun exposed areas. Micro - replace basal cells. lentiginous hyperplasia. cytologic atypiaDysplastic Nevi


Question Answer
Most common type of spreading melanomasuperficial spreading
in situ with a prolonged radial growth phase that may progress to invasivelentigo maligna
more often in an older population, most common site is the sole, with the palm and subungual locationsacral lentiginous
rapid evolution, lacks an radial growth phasenodular melanoma
Characteristic of superficial spreading, lentigo maligna and acral lentiginous typesradial growth
Depth of invasion can be measured. the nature and extent of vertical growth phase determine the biologic behavior of malignant melanomaVertical Growth

Renal Rejection

Question Answer
Complete graph destruction occurs in 24-48 hoursHyperacute Rejection
Kidney rapidly becomes cyanotic, mottled and flaccid with a dew drops of bloody urineHyperacute Rejection
Reversible reaction which occurs within days or weeksAcute Rejection
Interstitial inflammation composed of mononculear cells. Focal tubular inflammation and necrosis referred to as "tubulitis"Tubulointerstitial Pattern
Inflammation of vessels referred to as "endothelitis"Vascular Pattern
Irreversible reaction, usually happens in months to years in patients. Characterized by progressive renal failure indicated by elevated serum creatinine levelChronic Rejection
Characterized by obliterative intimal fibrosis resulting in renal ischemiaChronic Rejection