Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

40 Cards in this Set

  • Front
  • Back
what is eczematous dermatitis?
- heterogenous group of PRURITIC inflmamatory disorders
what can cause eczematous dermatitis?
1. infection
2. chemicals (contact dermatitis)
3. Atopy (allergy)
how do chemicals cause contact dermatitis?
- can directly injure skin
- may acta s antigens of type IV cell-mediated hypersensitivity reactions from cooperation of skin macrophages (Langerhans cells) and helper T lymphocytes
- eczematous derm is often found in people with type I anaphylactic-type hypersensitivities (e.g. hay fever, broncial asthma)
- the skin manifestations themselves are most often caused by type IV rather than type I hypersensitivity
Type 1 hypersensitivity
Type 1 hypersensitivity is an allergic reaction provoked by reexposure to a specific antigen. Exposure may be by ingestion, inhalation, injection, or direct contact. The reaction is mediated by IgE antibodies and produced by the immediate release of histamine, tryptase, arachidonate and derivatives by basophils and mast cells. This causes an inflammatory response leading to an immediate (within seconds to minutes) reaction.
Type 2 hypersensitivity
In type 2 hypersensitivity, the antibodies produced by the immune response bind to antigens on the patient's own cell surfaces. The antigens recognized in this way may either be intrinsic ("self" antigen, innately part of the patient's cells) or extrinsic (absorbed onto the cells during exposure to some foreign antigen, possibly as part of infection with a pathogen). IgG and IgM antibodies bind to these antigens to form complexes that activate the classical pathway of complement activation for eliminating cells presenting foreign antigens (which are usually, but not in this case, pathogens). That is, mediators of acute inflammation are generated at the site and membrane attack complexes cause cell lysis and death. The reaction takes hours to a day.
Type 3 hypersensitivity
In type 3 hypersensitivity, soluble immune complexes (aggregations of antigens and IgG and IgM antibodies) form in the blood and are deposited in various tissues (typically the skin, kidney and joints) where they may trigger an immune response according to the classical pathway of complement activation (see above). The reaction takes hours to days to develop.
Type 4 hypersensitivity
Type 4 hypersensitivity is often called delayed type as the reaction takes two to three days to develop. Unlike the other types, it is not antibody mediated but rather is a type of cell-mediated response.
what do you see in the acue stage of eczematous dermatitis?
- spongiosis with vesicle formation
what do you see in the chronic stage of eczematous dermatitis?
- acanthosis
- hyperkeratosis
- lichenification
- focal lymphocytic dermal infiltrates
what do you see in the subacute stage of eczematous dermatitis?
- less songiosis and vesiculation
- less acanthiosis and hyperkeratosis
A benign abnormal thickening of the prickle cell layer of the epidermis (as in psoriasis)
A condition marked by thickening of the outer layer of the skin, which is made of keratin (a tough, protective protein). It can result from normal use (corns, calluses), chronic inflammation (eczema), or genetic disorders (X-linked ichthyosis, ichthyosis vulgaris).
aka lichen simplex chornicus
- clinically indistinguishable from chornic eczematous dermatitis
- produces changes entierly secondary to scratching
- cause of pruritus may be psychogenic
lichen simplex chronicus
aka neurodermatitis
- - Lichen simplex chornicus may result from an irritation of the skin, causing the person to rub or scratch the area. This causes thickening of the skin. The thickening skin itches, causing more scratching and more thickening.
- erythematous papules and plaques with silvery scaling
- lesions sharply demarcated
where are lesions most commonly found?
- extensor surfaces of the elbows and knees
- also scalp and sacral area
what is the histology of psoriasis?
- nonpuritic
- epidermal proliferation with acanthosis and PARAKERATOSIS
- neutrophilic abscesses (Munro abscesses) can be found within the parakerototic stratum corneum
Any abnormality of the horny layer of the outer skin which prevents the formation of keratin.
Munro abscesses
A microscopic collection of PMNs found in the stratum corneum in psoriasis. Also called Munro's abscess.
what is psoriasis associated with?
- psoriatic arthritis: severe destructive rheumatoid arthritis-like lesions
- affect fingers
flat, nonpalpable lesion of a different color than the surrounding skin
- less than 1cm in diameter
like a macule
- larger than 1cm in diameter
- small
- palpable
- less than 1cm in diameter
- palpable
- like a papule
- more than 1cm in diameter
- small fluid- containing blister
- large fluid containing blister
- more than 0.5cm in diameter
- blister with pus
dried exudate from a vesicle, bulla, or pustule
- increased thickness of the stratus corneum
hyperkeratosis with retention of nuclei of keratinocytes
thickening of the epidermis
epidermal intercellular edema with widening of intercellular spaces
- separation of epidermal cells one from the other
- cells appear to float within the extracellular fluid
accentuation of skin markings caused by scratching
- chickenpox
- viral infection in childhood
- fever and generalized vesicular eruption
- varicella zoster virus may remain latent in the DRG
- shingles -> dermatomes affected correspond to the affected DRG
pemphigus vulgaris
- acantholytic disorder in people 30-60 years old
- formation of severe intraepidermal bullae
- intraepideramlacantholysis but sparing of the basal layer
where is the first lesion found in pemphigus vulgaris?
- oral mucosa
- skin involvement then follows
- lesions rupture -> large denuded surfaces are at risk for secondary infection
what type of immune response do you see in pemphigus vulgaris?
- autoimmune disorder characterized by IgG autoantibodies against the epideraml intercellular cement substance
- you can see the autibodies in serum or by immunofluorescence surroudning the epidermal cells
can pemphigus vulgaris be fatal?