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musculoskeletal and skin > Non-neoplastic Skin Disorders > Flashcards

Non-neoplastic Skin Disorders Flashcards

1
Q

Layers of the skin

A

Know the layers of the
Granulosum
Spinosum- desmosomes –blister forming skin disorders.
Basale- mitosis in this area is normal

Confined to the epidermis- carcinoma in situ

Dermis
Papillary
Reticular

Subcutaneous fat

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2
Q

mechanism/function of the skin

A

Defense against potentially harmful infectious and physical agents
Synthesis of active vitamin D3

Epidermis cellular components

Keratinocytes majority of cells origin from surface ectoderm
Fluid balance and thermoregulation
Proliferating layer at base, stratum basale

Dendritic (Langerhans) cells in basal layer of monocytic origin
Antigen presenting immune cells in skin

Melanocytes in basal layer of neural crest origin
Melanin producing cells protective against UV radiation

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3
Q

What is the dermis composed of

A

Dermis:
Papillary: loose connective tissue beneath the epidermis
Reticular: Dense dermal collagen

Cells:
Lymphocytes (T>B)
Afferent nerve fibers and vessels
Adnexal components (sweat glands, hair follicles)
Fibroblasts
Elastic fibers

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4
Q

What is epidermis composed of

A

Stratum basalis:
Actively dividing stem cells
Mitosis limited to this area

Stratum spinosum: Contains prominent desmosome attachments

Stratum granulosum: granular layer with keratohyaline granules

Stratum corneum:
anucleate cells with keratin
Site for superficial dermophyte infection

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5
Q

Macule

A

circumscribed flat lesion ≤ 5 mm
Patch > 5 mm

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6
Q

Papule

A

elevated lesion ≤ 5 mm
Nodule > 5 mm

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7
Q

Plaque

A

– elevated flat topped lesion, usually > 5 mm

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8
Q

Scale

A

dry, horny, plate-like excrescence

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9
Q

excoriation

A

traumatic break in epidermis, raw linear area

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10
Q

Lichenification

A

thickened rough skin

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11
Q

Pustule

A

pus-filled raised lesion

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12
Q

vesicle

A

fluid filled raised lesion, ≤ 5 mm
Bulla > 5 mm

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13
Q

wheal

A

itchy transient elevated lesion
Variable blanching & erythema

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14
Q

onycholysis

A

separation of nail plate from nail bed

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15
Q

Macroscopic

A

Vesicle: fluid-filled lesion measuring = or < 5 mm in diameter, e.g. HSV vesicle (UL)
Bulla: fluid-filled lesion measuring > 5 mm in diameter, e.g. bullous pemphigoid (UR)
Blister: common term for vesicle or bulla
Pustule: circumscribed elevated pus-filled lesion (LL)
Wheal: pruritic elevated lesion with variable blanching and erythema due to acute dermal edema (LR)

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16
Q

Parakeratosis

A

the presence of nucleated keratinocytes in the stratum corneum

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17
Q

Hyperkeratosis:

A

: a condition marked by thickening of the stratus corneum

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18
Q

Acanthosis:

A

epidermal hyperplasia with thickening of epidermal layer

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19
Q

Orthokeratosis:

A

basket weave appearance to keratinized layers, classic finding in lichen planus

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20
Q

Dyskeratosis –

A

abnormal premature keratinization

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21
Q

Papillomatosis:

A

hyperplastic papillary dermis with elongation & widening of dermal papillae

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22
Q

Erosion –

A

incomplete loss of the epidermis

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23
Q

Ulceration –

A

complete loss of the epidermis

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24
Q

Exocytosis –

A

infiltration by inflammatory cells

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25
Q

Hydropic change –

A

INTRAcelluar edema

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26
Q

Spongiosis –

A

INTERcellular edema

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27
Q

Urticaria definition

A

Definition: Localized mast cell degranulation and release of histamine which leads to dermal microvascular hyperpermeability
Pathogenesis: Most cases stem from type I hypersensitivity reaction: IgE antibodies displayed on bodies of mast cells
Responsible antigens: pollens, food, drugs, insect venom
Hereditary angioedema: is caused by deficiency of C1 esterase inhibitor which results in uncontrolled activation of complement

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28
Q

Urticaria clinical features

A

Affects age 20-40 years but no age is immune
Individual lesions form and fade within hours
Episodes may persist for days and may be months
Lesions vary from small pruritic papules to large edematous plaques
Increased vascular permeability may lead to dermal edema
Lesions may be local or generalized

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29
Q

Eczema definition

A
30
Q

Eczema clinical features

A

Erythematous, papulovesicular, oozing, crusted lesions
Reactive acanthosis & hyperkeratosis
Raised scaling plaques
Pruritic
Classic ex: poison ivy/oak
Prone to bacterial superinfection
Yellow crust

31
Q

Eczema histology

A

Spongiosis: epidermal edema
Characterize all forms of acute eczematous dermatitis
Superficial perivascular lymphocytic infiltrate
Papillary dermal edema
Mast cell degranulation

32
Q

Eczema clinical

A

Lesions are pruritic, edematous
With persistent exposure, lesions may become scaly (hyperkeratotic), as the epidermis thickens: acanthosis
Susceptibility to atopic dermatitis is often inherited
Appears in early childhood and young adults
Children with atopic dermatitis often have asthma and allergic rhinitis: atopic triad

33
Q

Erythemal multiforme

A

Uncommon self limited disorder
Hypersensitivity response to certain infections and drugs
Drugs include: sulfonamides, penicillin, salicylates, hydantoins, antimalarial
Patients presents with variety of lesions hence called multiforme
Present with: macules, papules, vesicles, bullae
Epithelial damage is believed to result from the action of skin homing cytotoxic T cells
These cells attack the basal cells of the skin and the mucosae
Lesions have the characteristic targetoid appearance

34
Q
A

Early lesions show perivascular lymphocytic infiltrate along the dermoepidermal junction associated with dermal edema and degenerating keratinocytes
Chronic lesions will result in blister formation
Occasionally toxic epidermal necrolysis extending through the full thickness of the epidermis may occur
Erythema multiforme caused by medications may progress to life threatening eruptions such as Stevens-Johnson syndrome

35
Q

psoriasis definition

A

Common inflammatory dermatosis affecting 1-2% of people in US
Strong HLA association
No gender difference
Associated with increased risk of MI and strokes due to chronic inflammation
Aggravating factors:
streptococcal pharyngitis
HIV: sudden onset of psoriasis is highly suspicious for HIV
Drugs: NSAIDS, beta blockers, lithium
Scratching the skin: Koebner’s phenomenon

36
Q

psoriasis: pathogenesis

A

Uncontrolled proliferation of keratinocytes
Results from interaction of genetic and environmental factors
As in the case of many autoimmune diseases, it’s linked to genes within the HLA locus particularly with HLA-Cw*0602 allele
Sensitized CD4+ and activated CD8+ cytotoxic effector T cells stimulate the secretion of cytokines and growth factors causing keratinocytes proliferation
Koebner phenomenon – psoriatic lesions induced by local trauma

37
Q

presentation and histology

A

Elbows, knees, scalp, lumbosacral region, intergluteal cleft, glans penis
Pink-tan plaque
Silver-white scale

Histology:
Hyperkeratosis
Elongated rete ridges
Superficial dermis contains perivascular infiltrate
Stratum granulosum is almost absent

38
Q
A

Psoriasis

Nail changes in 30%
Yellow-brown discoloration
Pitting
Dimpling
Onycholysis
Thickening
Crumbling

39
Q
A

Psoriasis histology

•Marked acanthosis•Downward elongation of rete ridges•Thinned to absent granular layer•Extensive overlying parakeratotic scale

40
Q
A

•Spongiosis in epidermis•Spongiform pustules – aggregates of PMNs in epidermis•Munro mciroabscess – aggregates of PMNs in stratum corneum•Thinned epidermis overlying dermal papillae•Dilated tortuous blood vessels within dermal papillae•Auspitz sign – multiple, pinpoint spots of blood when scale is lifted

41
Q

Lichen Planus

A
  • Lichen Planus: Uncommon disorder seen in middle aged people
  • 6 ‘Ps” Pruritic purple, polygonal planar papules plaques
  • Flat-topped papules with coalescence
  • Seen on flexural surfaces wrists, forearms, and legs
  • Papules are often highlighted by white dots called Wickham’s striae
  • Nails are commonly dystrophic
  • Lesions develop in areas of scratching, Koebner’s phenomenon
  • Cell mediated immunity with CD4+ (T-helper) lymphocyte
42
Q

Pathophysiology lichen Planus

A

•The lymphocytes attack the basal layer keratinocytes at the dermoepidermal junction•Acanthosis with effaced ‘saw-tooth’ rete ridges•Colloid bodies or Civatte bodies are eosinophilic shrunken keratinocytes•Destroyed keratinocytes spill out melanin taken by macrophages causing pigmentation•Direct immunofluorescence (DIF): IgM colloid or Civatte bodies•Linear lesion with previous trauma or surgery called Koebner phenomenon•Associated with HEPATITIS C, Primary Biliary Cholangitis, diabetes mellitus

43
Q
A

Lichen Planus

•Dense lymphocytic infiltrate along DEJ•Intimately associated with basal keratinocytes•Civatte bodies – anucleate necrotic basal cells•Incorporated into inflamed papillary dermis•In active lesions destruction of the basal layer of the epidermis leak melanin•Melanin is taken by macrophages which give the clinical appearance of hyperpigmentation•Lesions are symmetrically distributed on the extremities•In 70% of cases oral mucosa is involved, lesions in buccal cavity are white papules with reticulate and netlike appearance•Cutaneous lesions resolve within 1 to 2 years

44
Q

LP pathogenesis and associations

A
  • LP pathogenesis is not known but it’s plausible that expression of altered antigen in basal epidermis or the dermoepidermal junctional elicit a cell mediated cytotoxic CD8 T cell response
  • LP is associated with:•Ulcerative colitis•Alopecia areata•Vitiligo•Dermatomyositis•Myasthenia gravis
45
Q

Erythema Nodosum

A

•Inflammatory lesion of subcutaneous fat (panniculitis)•More common in women•Erythema nodosum is characterized by tender, red bumps, usually found symmetrically on the shins.•Up to 55 percent of cases have no clear identifiable cause..•Rather, it is a sign of some other infection, disease, or of a sensitivity to a drug

46
Q

clinical presentation of ?

A

•The nodules are found on the anterior lower legs, knees and arms and rarely on the face and neck.•Nodules 3–20 cm in diameter erupting over one to several weeks•They are ill-defined, warm, oval, round, and without ulceration•The nodules are initially bright to deep red. •They spontaneously resolve within eight weeks, through a violaceous, brownish, or yellowish/green bruise-like appearance

47
Q

histology of ?

A
  • The classic histopathologic presentation of erythema nodosum is that of a septal panniculitis•With mixed cellular infiltrate of lymphocytes, histiocytes, giant cells and occasional eosinophils•Vasculitis is absent
  • Caused by:•Infections•Drugs•Sarcoidosis•Inflammatory bowel disease•Malignancy•Fever & malaise•Delayed hypersensitivity reaction
48
Q
A

Granuloma annulare

•Chronic inflammatory dermal disorder•Unknown etiology•Occurs in children and adults, more in females•Begins as erythematous papules progressing to annular plaques•Occurs on the dorsum of hands and feet•Disseminated type may be seen in diabetic patients•Spontaneously resolves in two years•Recurs in 40% of cases•The inflammatory infiltrate is predominantly within the deep dermis and extends into the subcutaneous tissue •Treatment with steroids locally or injections in the lesion itself

49
Q

Blistering: Pemphigus vulgaris

A

•It’s a rare autoimmune blistering disorder•Affects people 40-60 yrs•Men and women are affected equally•Blistering diseases can be complicated by secondary infections and extreme loss of fluid•Result of loss of intercellular attachments within the epidermis•Blistering diseases may be complicated by infections•Corticosteroid use reduced mortality in PV from 99% to 5-15%

50
Q

oral lesions are:

A

•Oral lesion in PV are:•Seen in 50-70% of patients•Blisters appear as erosions•Widespread in the mouth, may go into larynx•Painful and slow to heal•Difficult to eat and drink

51
Q

3 types of pemphigus vulgarisms

A

•Pemphigus vulgaris, the most common type occur in 80% of cases•Involves the scalp, face, axilla, groin, trunk and points of pressure•Caused by IgG antibodies against the intercellular desmosomal protein desmoglein type 3 and 1 in lower part of the epidermis•Floor is one layer of basal cell which look like a row of “tombstones•Pemphigus foliaceous, autoantibodies against desmoglein type I in upper epidermis•Mucous membranes are rarely affected•More benign than PV•Paraneoplastic pemphigus associated with various malignancies, most commonly non-Hodgkin lymphoma

52
Q

histology of?

A

•The histology of pemphigus vulgaris shows an intraepidermal blister.•The base of the blister consists of dermal collagen, covered by one layer of basal keratinocytes.•The basal keratinocytes not only lost contact with the upper layer of the epidermis, but also with each other.•The separation is caused by acantholysis.•A few acantholytic keratinocytes can be found in the blister.•Direct immunofluorescence of pemphigus vulgaris shows deposition of immunoglobulin between the epidermal keratinocytes in a fishnet-like pattern

53
Q

Bullous Pemphigouid

A

•Elderly patients, 50-70•Wide range of presentations•Oral lesions in 10-15%•IgG Autoantibodies that bind to hemidesmosomes at the dermoepidermal junction•Tense bullae, Do not rupture easily, usually < 2 cm•The histology of bullous pemphigoid shows a subepidermal blister with acantholysis•In bullous pemphigoid, direct immunofluorescence shows linear deposition of complement C3 and IgG along the dermoepidermal junction

54
Q

Dermatitis herpetiformis

A

•An autoimmune disease associated with celiac disease•Consumption of gluten-containing foods is a main risk factor for Dermatitis Herpetiformis•IgA antibodies are directed against epidermal transglutaminase.•Blisters appear on both sides of the body, most often on the forearms near the elbows, as well as on knees and buttocks, and along the hairline•Men, 3rd – 4th decades

55
Q
A

Dermatitis Herpetiformis

•Fibrin & PMNs at tips of dermal papillae•à microabscesses•Overlying basal – vacuolization & dermoepidermal separation•à subepidermal blister•DIF: Granular IgA in dermal papillae

56
Q

Ancanthosis Nigricans

A

•Thickened hyperpigmented skin•“velvet-like” texture•Flexural areas•Most commonly associated with diabetes & obesity•Can be associated with malignancy

57
Q
A

•Increased growth factor receptor signaling•Diabetes associated – increased IGFR1•Malignancy associated – increased TGF-α•Undulating epidermis & enlarged dermal papillae•Variable hyperplasia•Hyperkeratosis

58
Q
A

Epidermal Inclusion Cyst

•AKA infundibular cyst•Damage to pilosebaceous units•Dome-shaped swellings•Punctum present•May result from trauma causing dermal invagination•The cyst is filled with strands of keratin and lined by epithelium that resembles normal epidermis.•Adnexal structures are absent, which differentiate it from dermoid cyst

59
Q

Verrucae

A

•AKA warts•Children & adolescents• verruca plantaris is a symmetrical lesion composed of a thickened epidermis with hyperkeratosis and an undulating surface (papillomatosis)•They are numerous in patients with solid organ or stem cell transplant•Caused by HPV•Direct contact or autoinoculation•Self-limited, spontaneous regression within 6 months – 2 years

60
Q
A

•Verruca vulgaris – most common type•Hands most frequent: V palmaris•Grey-white to tan•Flat to rounded papules•Rough surface•Common lesion of children•Transmission by direct contact or autoinoculation•Generally self limited, regressing spontaneously in 6 month to 2 years

61
Q

Verrucae of gentialia

A

•HPV infection of the cervix or genitalia is caused by Condyloma acuminatum•Male & female genitalia, perineum, urethra, rectum•Soft, tan, cauliflower-like masses•HPV 6 & 11•HPV 16 and 18 are associated with dysplastic changes

62
Q
A

Verrucae

•Verrucous epidermal hyperplasia•Koilocytosis – cytoplasmic vacuolization•Cells infected with HPV•Histology:•The nuclei of the infected keratinocytes are surrounded by a pale halo•This phenomenon is called koilocytosis•The stratum granulosum is thickened and parakeratosis is present.•These histopathological changes are characteristic of human papillomavirus (HPV) infections

63
Q
A

muscollum contagiousum

•Self-limited•Poxvirus•Direct contact•Trunk & anogenital areas•Firm, pruritic, pink to flesh-colored umbilicated papules

64
Q
A

mulluscsm contagiousum

•Cuplike verrucous epidermal hyperplasia•Molluscum body – cytoplasmic inclusion•Contains numerous virions

65
Q

Impetigo

A

•Superficial bacterial infection of skin•Highly contagious and seen in healthy children•Skin of face & hands•Blister formation is related to bacterial production of toxins that cleaves desmoglein 1•Staphylococcus aureus•Evoke innate immune response à epidermal injury à local serous exudate & scab formation•Impetigo occurs in two forms, bullous and nonbullous•Nonbullous is the more common form 70%, affects skin on the face and extremities•Nonbullous impetigo is cause by staph aureus, and group A beta hemolytic streptococcus•Heals without scarring

66
Q
A

Impetigo

•Erythematous macule•Small pustules•Shallow erosions•Honey colored crust

67
Q
A

Impetigo

•Accumulation of PMNs beneath stratum corneum•Subcorneal pustule•Rupture à crust formation

68
Q

Skin Staphylococcal Scalded Skin Syndrome

A

•Staphylococcal scalded skin syndrome (SSSS) is a disorder that develops because of a toxin produced by a staphylococcal infection•It’s also called Ritters disease•Common in infants and young children < 6 years of age•This skin specimen shows a superficial blistering.•But it does not show inflammation, so the toxins must have been produced at a distance from this skin lesion (staphylococcal scalded skin syndrome)

69
Q
A

•The production of bacterial toxin cleaves the desmoglein 1 molecule and causes the blistering•The roof of the blister is the stratum corneum, and the remaining epidermis is present in the blister base.•This is very similar to impetigo bullosa•But in impetigo bullosa, a local infection with Staphylococcus aureus is present

70
Q

Typical SSS cutaneous features

A
  • A red rash with wrinkled tissue or paper-like consistency•Typically starts on the face and flexural regions (groin, axillae, and neck), then spreads rapidly to other parts of the body including the arms, legs, and trunk.•In newborns, lesions can be found around the umbilical cord.
  • Following the rash, the formation of large fluid-filled blisters•Frequently occur in areas of friction (such as axillae, groin, and buttocks), the center of the face and body orifices (such as the nose and ears).•Fluid contents range from a sterile cloudy fluid to frank yellow pus.
  • Blisters easily rupture leading to the top layer of the skin (epidermis) peeling off easily, often in large sheets.•Exposure of the underlying, moist, reddish tissue leaves the skin with a burned-like appearance

.•Gentle rubbing of the skin causes exfoliation (Nikolsky sign is positive)

71
Q

Mortality of SSS

A

•The mortality rate from SSSS in children is extremely low (1–5%),•The mortality rate in adults is higher (50–60%), likely due to an underlying condition which increases their predisposition to complications in itself

musculoskeletal and skin (17 decks)

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