28. endocrine Flashcards
Inflammatory dermatosis include
Acute and Chronic
Acute inflammatory dermatosis include
Atopic dermatitis
Contact dermatitis
Chronic inflammatory dermatitis include
Psoriasis
Lichen planus
Atopic eczematous dermatitis
Define
Where
Type of hypersensitivity
Mutation
Type I hypersensitivity reaction
•Pruritic, erythematous, oozing rash with vesicles and edema
•On the cheeks, trunk and extensor surfaces in neonates, and moves to the flexor creases as the child aged
•Often associated with a personal or family history of AD, allergic rhinitis, and asthma; 35% of infants with AD develop asthma later in life
•Affect 15 to 20% of children
Defects in the keratinocyte barrier due to mutations in the filaggrin (filament aggregating protein) gene (FLG) is seen in
Contact dermatitis divided into
Allergic CD
Irritant CD
Allergic contact dermatitis (ACD)
Define
Subtype
Type IV hypersensitivity reaction against poison ivy, oak, nickel and chemicals found in the household cleaners, cosmetics, fabrics, dyes, medications (penicillin) and rubber products
•Photoeczematous dermatitis is a type of ACD that is caused by ultraviolet (UV) light reacting with drugs (e.g:- tetracycline, sulphonamides and thiazides).
Irritant Contact Dermatitis (ICD)
The most common type of eczematous dermatitis
•Non immunologic reaction due to the local toxic effect of a chemical on the skin (e.g, detergents in soaps and diaper dermatitis )
•The hands are the most important sites of ICD
CHRONIC INFLAMMATORY DERMATOSES
Psoriasis
Lichen planus
Psoriasis
Define
Cause
Also involves
Histologically
What sign is shown
Well-circumscribed, salmon-colored plaques with silvery scale, usually on extensor surfaces and the scalp.
Associated with HLA haplotypes Cw6, B13 and B17
Nail and psoriasis arthritis
Acanthosis
Parakeratosis
Munro abscess
Kojog pustules
Auspitz sign
Cause of silver color in psoriasis
Parakeratosis
Keratinocyte nuclei retention
What are Munro abscess
Neutrophil collection in corneum
What are kojog pustules
Neutrophil collection in sub corneum
Why auspitz sign seen
Because there is acanthosis
Capillaries dilates
And when scale is picked is bleeds
Lichen planus (LP)
Where
Male or female
Linked to
Patho genesis
6 ps
Histology
Clinically it shows
Skin and mucous membrane
Female more
Linked to hepatitis C
Cytotoxic T cell and memory cells response to change in antigen of basal cells
Plaque polygonal planar Pruritic papules
Hyperkeratosis no parakeratosis
Acanthosis saw tooth appearance
Wickham strae and kobener phenomenon linear
Vesicular and Bullous Disease
Include
Pemphigus
Bulluois pemphihoid
Dermatitic herpesform
Erythema multi forms
Pemphigus
Anti what?
Type what
Histology
What sign
Immunoflourence
Superficial soft blisters which ruptured easily
IgG antibody against desmosomes Type 2
Intraepidermal lesion
Basal cell attached to BM look like Tomb stones
Nikolsky sign - easily upper lid removed
Fish net appearance
Bullous pemphigoid
Anti what
Age and place
IgG
Histology
Older individuals oral mucosa spared
•Anti bullous pemphigoid-antigens 1 and 2 (a part of the keratinocyte hemidesmosome) IgG
•Deep tense bullae
IgG antibody against BM collagen
Subepidermal fluid
Eousinophil dominant in vesicle
No nikolsky sign
Dermatitis herpetiformis
Associated with
Place
Anti what antibody / what
Vesicle form when
Histology
Autoimmune deposition of IgA at dermal papillae
Associated with celiac sprue
•Itchy grouped vesicles and occasional bullae on the extensor surfaces
•IgA antibodies directed against gliadin and other antigens deposit in the tips of the dermal papillae and result in subepidermal blister formation
Papillary micro abscess
Erythema Multiforme (EM)
Patho genesis type ?
Bullous character and where
EM with fever and infection
An acute, self-limiting and commonly recurrent type IV hypersensitivity reaction to infections (Mycoplasma pneumoniae, herpes simplex) or drugs (sulfonamides, penicillin, barbiturates, phenytoin)
•Vesicles, bullae, and Symmetrically distributed of targetoid lesions often involving palms and soles
•EM with oral mucosa/lip involvement and fever is termed Stevens-Johnson syndrome (SJS)
Why targetoid appearance
Due to central necrosis
Toxic epidermal necrolysis
And how we say TEN
Severe form of SJS with sloughing off of skin
If greater than 30% of skin is affected
Pigment disorders include
Hypo
Vitiligo
Albinism
Post inflammatory depigmentation
Hyper
Freckle Ephelis
Melasma
Lentigo
Nevus
Vitiligo
Idiopathic possibly autoimmune destruction of melanocytes
Affected areas are devoid melanocytes
Albinism
Normal № of melanocytes, deficiency of tyrosinase
Freckle (ephelis);
melanocytes hyperreactivity to UV light. Change with seasons.
Increased melanosome not melanocytes
Lentigo
;↑ № of melanocytes. Do not change with sunlight.
Melasma;
associated with sun exposure, oral contraceptive use, and pregnancy (“mask of pregnancy”) and may
Melanocytic nevi (mole)
Types
And other
Two groups:
•Congenital nevi (birthmarks) present at the time of birth
•Acquired nevi appear at puberty, become more prominent during adult life, and then involute
Can be precursor to melanoma
Acquired nevi types
First as junctional nevi
Then to compound nevus by extension to dermis
Then Intradermal nevus
Tumors of skin
Fibro epithelial polyp
Acanthosis nigricans
Seborrheic keratosis
Cysts
