Pathology (skin, Inflammatory dermatosis)

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amirh899
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Pathology (skin, Inflammatory dermatosis)
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2013-09-25 14:58:02
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Pathology skin Inflammatory dermatosis
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Pathology (skin, Inflammatory dermatosis)
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  1. What are the diagnostic clue to TEN, SJS, EM, SSSS, and TSS?
    • 1. EM--> HSV, Mycoplasma--> MC, also drugs, malignancy, autoimmune. Target lesion (a dusky central area or blister, a dark red inflammatory zone surrounded by a pale ring of edema, and an erythematous halo on the extreme periphery of the lesion), also mucosal
    • 2. SJS, TEN--><10% >30%, drugs , mucosa, prodrome, macules and patches, skin pain in TEN, subepidermal blister, 2 mucosal surface
    • 3. SSSS, children, stratum granulosum, Adults can clear by kidney, exfoliative phase is heralded by perioral exudation and crusting with large radial fissures, no mucosal involvement
    • 4. TSS: diffuse, red, macular rash resembling sunburn that may involve the palms and soles, Hypotension, fever, hyperemia of mucosa, MOF, desquamation of palm and sole after 1-2 w
  2. What are the features of urticaria and angioedema?
    • localized mast cell degranulation and resultant dermal microvascular hyperpermeability
    • Angioedema is closely related to urticaria and is characterized by deeper edema of both the dermis and the subcutaneous fat.
  3. What is the mc location for urticaria?
    area exposed to pressure, such as the trunk, distal extremities, and ears
  4. What is the association of persistent urticaria?
    underlying disease (e.g., collagen vascular disorders, Hodgkin lymphoma)
  5. What is the histology of urticaria?
    • Sparse superficial perivenular infiltrate consisting of mononuclear cells. Eosinophils may also be present.
    • Collagen bundles are more widely spaced than in normal skin, a result of superficial dermal edema.
    • Superficial lymphatic channels are dilated due to increased absorption of edema fluid.
    • Epidermal changes are typically absent
  6. What is the pathogenesis of urticaria?
    • MC--> Antigen-induced release of vasoactive mediators from mast cell granules through sensitization with specific IgE antibodies. 
    • IgE-independent--> direct degranulation of mast cells, such as opiates, certain antibiotics, curare, and radiographic contrast media. Another cause of IgE-independent urticaria is exposure to chemicals, such as aspirin, that suppress prostaglandin synthesis from arachidonic acid. 
    • Complement-mediated urticaria is seen in hereditary angioneurotic edema , caused by an inherited deficiency of C1 inhibitor that results in uncontrolled activation of the early components of the complement system and production of vasoactive mediators.
  7. What is the clinical presentation of eczema?
    All forms of eczema are characterized by red, papulovesicular, oozing, and crusted lesions that, if persistent, develop into raised, scaling plaques due to reactive acanthosis and hyperkeratosis
  8. What are the earliest skin change in eczema?
    Initial dermal edema and perivascular infiltration by inflammatory cells is followed within 24 to 48 hours by epidermal spongiosis and microvesicle formation
  9. What is the histologic hallmark of acute eczema?
    Spongiosis
  10. What are the types of eczema?
    (1) allergic contact dermatitis, (2) atopic dermatitis, (3) drug-related eczematous dermatitis, (4) photoeczematous dermatitis, and (5) primary irritant dermatitis
  11. What is the hallmark of chronic eczema?
    Scale (hyperkeratotic) and epidermal thickening (acanthosis)
  12. What are the histological features of eczema?
    • Spongiosis characterizes acute eczematous dermatitis. Unlike urticaria, in which edema is restricted to the superficial dermis, edema seeps into the intercellular spaces of the epidermis, splaying apart keratinocytes, particularly in the stratum spinosum. Mechanical shearing of intercellular attachment sites (desmosomes) and cell membranes by progressive accumulation of intercellular fluid may result in the formation of intraepidermal vesicles
    • During the earliest stages of eczematous dermatitis, there is a superficial, perivascular, lymphocytic infiltrate associated with papillary dermal edema and mast cell degranulation.
  13. How is eczema resulting from certain ingested drugs different from contact antigens ?
    eczema resulting from certain ingested drugs is marked by a lymphocytic infiltrate, often containing eosinophils, around deep as well as superficial dermal vessels. By contrast, eczematous dermatitis resulting from contact antigens tends to produce an inflammatory reaction that preferentially affects the superficial dermal layer.
  14. What are the hallmark symptoms of AD?
    Pruritus and dry skin
  15. What is the first manifestation of atopy?
    AD
  16. What is the diagnostic features for atopy?
    • Infantile< 2y stage may present with pruritic, red, scaly, and crusted lesions on the extensor surfaces and cheeks or scalp. There is usually sparing of the diaper area
    • Childhood stage (2-12y) is characterized by less exudation and often demonstrates lichenified plaques in a flexural distribution, especially of the antecubital and popliteal fossae, volar aspect of the wrists, ankles, and neck 
    • Adult stage(>12y) of atopic dermatitis is considerably more localized and lichenified and has a similar distribution to the childhood stage, or may be primarily located on the hands and feet
  17. AD
  18. How can Chronic exposure to UV can prevent sensitization to contact antigens?
    Chronic exposure to UV light is injurious to epidermal Langerhans cells and can prevent sensitization to contact antigens
  19. Which cell play a central role in ACD?
    Langerhans
  20. What are the stages of ACD?
    Initially, antigens at the epidermal surface are taken up by dendritic Langerhans cells, which then migrate by way of dermal lymphatics to draining lymph nodes. Here, antigens, now processed by the Langerhans cell, are presented to naive CD4+ T cells, which are activated and develop into effector and memory cells. On antigen re-exposure, these memory T cells migrate to affected skin sites of antigen localization, where they adhere to post-capillary venules, extravasate into tissues, and release cytokines and chemokines that recruit the numerous inflammatory cells characteristic of eczema. This process occurs within 24 hours and accounts for the initial erythema and pruritus that characterize cutaneous delayed hypersensitivity in the acute, spongiotic phase
  21. What is the mcc of EM, SJS, and TEN?
    • EM--> HSV
    • SJS, TEN: drugs
  22. What are the causes of EM?
    (1) infections such as herpes simplex, mycoplasmal infections, histoplasmosis, coccidioidomycosis, typhoid, and leprosy, among others; (2) administration of certain drugs (sulfonamides, penicillin, barbiturates, salicylates, hydantoins, and antimalarials); (3) malignant disease (carcinomas and lymphomas); and (4) collagen vascular diseases (lupus erythematosus, dermatomyositis, and polyarteritis nodosa)
  23. What are the most important drugs associated with SJS and TEN?
    • Allopurinol
    • sulfunamide
    • Carbamazepine
    • Phenytoin
    • Phenobarbital
    • Lamotrigine
    • Piroxicam
    • Penicillin
    • Nevirapine
  24. What is a target lesion?
    • red macule or papule with a pale, vesicular, or eroded center (a dusky central area or blister, a dark red inflammatory zone surrounded by a pale ring of edema, and an erythematous halo on the extreme periphery of the lesion)
    • Symmetric involvement of extremities
  25. What are the major problems associated with TEN and SJS?
    secondary infection and fluid loss
  26. What are the histological hallmarks of EM?
    • Early lesions show a superficial perivascular, lymphocytic infiltrate associated with dermal edema and accumulation of lymphocytes along the dermoepidermal junction, where they are intimately associated with degenerating and necrotic keratinocytes, a pattern termed interface dermatitis.
    • With time there is upward migration of lymphocytes into the epidermis. Discrete and confluent zones of epidermal necrosis occur with concomitant blister formation. Epidermal sloughing leads to shallow erosions.
    • The clinical targetoid (target-like) lesion shows central necrosis surrounded by a rim of perivenular inflammation
  27. Pathophysiologically EM resembles .................
    acute graft-versus-host disease, skin allograft rejection, and fixed drug eruptions
  28. What is the mechanism of keratinocyte necrosis in EM, acute graft-versus-host disease, skin allograft rejection, and fixed drug eruptions?
    skin-homing (CLA+) CD8+ cytotoxic T lymphocytes (CTLs).
  29. In erythema multiforme ......... are more prominent in the central portion of the lesions while ...... and ........ cells are more common in the raised, erythematous periphery
    CTL/ CD4, Langerhans
  30. How is Granuloma annulare presented?
    • erythematous, non-scaly, annular plaque on distal extremity (hand and foot)
    • generalized type may be associated with DM
  31. What are the features of pityriasis rosea?
    • The eruption commonly begins with a "herald" or "mother" patch, a single round or oval, rather sharply delimited pink or salmon-colored lesion on the chest, neck, or back, 2 to 5 cm in diameter.
    •  The lesion soon becomes scaly and begins to clear centrally, leaving the free edge of the cigarette paper-like scale directed inwards toward the center. This clinical finding is often described as a “collarette” of scale.
    • A few days or a week or two later oval lesions similar in appearance to the herald patch, but smaller, appear in crops on the trunk and proximal areas of the extremities
    • The long axes of these oval lesions tend to be oriented along the lines of cleavage of the skin
    • Pruritus
  32. Psoriasis might be associated with.......
    AIDS
  33. What are the locations for psoriasis?
    skin of the elbows, knees, scalp, lumbosacral areas, intergluteal cleft, and glans penis
  34. What are the features of guttate psoriais?
    Drop or lancet shape papules following streptococcal infection in the upper torso and proximal extremity
  35. What are the hallmark of skin lesions in psoriasis?
    • Well-demarcated symmetric
    • pink to salmon-colored plaque covered by loosely adherent scale that is characteristically silver-white in color
    • No pruritus

  36. What are the characteristics of pustular psoriasis?
    Spreading bright red plaques with the sudden onset of 2-3 mm sterile pustules at the periphery --> palms and soles
  37. What is an important complication of skin psoriasis?
    Eythroderma
  38. What are the nail changes in psoriasis?
    yellow-brown discoloration (often likened to an oil slick), with pitting, dimpling, separation of the nail plate from the underlying bed (onycholysis), thickening, and crumbling
  39. What are the histological features of psoriasis?
    • 1) Increased epidermal cell turnover results in marked epidermal thickening (acanthosis), with regular downward elongation of the rete ridges sometimes described as appearing like test tubes in a rack.
    • 2) Mitotic figures are easily identified well above the basal cell layer, where mitotic activity is confined in normal skin. 
    • 3) The stratum granulosum is thinned or absent (unlike LP where there is hypergranulosis), and extensive overlying parakeratotic scale is seen.
    • 4) Typical of psoriatic plaques is thinning of the portion of the epidermal cell layer that overlies the tips of dermal papillae (suprapapillary plates) and dilated, tortuous blood vessels within these papillae. This constellation of changes results in abnormal proximity of vessels within the dermal papillae to the overlying parakeratotic scale, and accounts for the characteristic clinical phenomenon of multiple, minute, bleeding points when the scale is lifted from the plaque (Auspitz sign)
    • 5) Neutrophils form small aggregates within slightly spongiotic foci of the superficial epidermis (spongiform pustules) and within the parakeratotic stratum corneum (Munro microabscesses).
    • 6) In pustular psoriasis, larger abscess-like accumulations of neutrophils are present directly beneath the stratum corneum.
  40. What is the most important genetic association of psoriasis?
    HLA-Cw*0602
  41. What is the dominated inflammatory response in psoriasis?
    TH17 TH1
  42. What are the underlying mechanisms of psoriasis?
    • IFN-alpha produced by plasmacytoid dendritic cells stimulates the activation of myeloid dendritic cells, which contribute to the adaptive immune response through the activation of T cells
    • IL-23 and IL-12 produced by activated myeloid dendritic cells promote the development of Th17 and Th1 cells, respectively. Th17 cells appear to play a major role in the pathogenesis of psoriasis
  43. What is Koebner phenomenon?
    The trauma may induce a local inflammatory response that promotes lesion development
  44. What are the features of Lichen planus?
    • Pruritic, purple, polygonal, planar papules, and plaques
    • usually self-limited and most commonly resolves spontaneously 1 to 2 years after onset, often leaving zones of postinflammatory hyperpigmentation.
    • Oral lesions may persist
    • Papules are often highlighted by white dots or lines called Wickham striae
    • Symmetric wrists and elbows, and on the glans penis
    • Oral lesions are present as white, reticulated, or netlike areas involving the mucosa
    • Koebner phenomenon
  45. What is the pathophysiology of Wickham striae?
    Hypergranulosis
  46. What is the main difference in pathology of Lichen planus and psoriasis?
    • LP--> hypergranulosis
    • Psoriasis--> hypogranulosis
  47. What skin lesion is prototype of interface dermatitis?
    Lichen planus
  48. What are the histological features of LP?
    • Dense, continuous infiltrate of lymphocytes along the DEJ(interface dermatitis
    • Basal keratinocytes, which show degeneration, necrosis, and a resemblance in size and contour to more mature cells of the stratum spinosum (squamatization).
    • Angulated zigzag contour (sawtoothing) of DEJ.
    • Anucleate, necrotic basal cells may become incorporated into the inflamed papillary dermis, where they are referred to as colloid or Civatte bodies.
    • Epidermal hyperplasia and thickening of the granular cell layer and stratum corneum (hypergranulosis and hyperkeratosis).

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