Immuno 5: Inflammatory dermatoses Flashcards
Outline important structural features of skin microanatomy
Basement membrane between epidermis and dermis Underlying the fat is fascia then muscle Within the dermis there are ADNEXAL structures hair follicles and sebaceous glands, sweat glands. Also matrix
What is a pilosebaceous unit
Hair follice + sebaceous gland + pioerecti muscle
T/f sebaceous gland= sweat gland
F…. sebaceous associated with hair follice The sweat glands are eccrine and apocrine
Distributin of each sweat gland
Eccrine= all over the body Apocrine= axilla and groins (smelly sweat)
What is the rest of the dermis made of aside from the pilosebaceous unit
Collagen, elastin, connective tissue, fibroblasts and immune cells, GAGs, blood vessels
What is all the pink on H&E in the dermis
Collagen. The cells in the dermis are mostly fibroblasts
What is the difference in the substance produced by sweat glands and sebaceous glands
Sweat obs sweat Sebaceous produces sebum which is a oil that lubricates the hair and also kills bacteria and fungi
Where are langerhans cell, merkel cell mostly located
Langerhans= in the stratum spinosum Merkel=stratum basale
What happens to keratinocytes after production in the stratum basale from stem cell
They differentiate as they move up, eventually to become the keratines stratified epithelim in the stratus corneum to perform barrier function
Outline differentiation of keratinocytes
Basal cell Prickle cell Granular cell Keratin
What is contained within the granules of cells of the granular layer
Keratin
What is the difference between cells in the granular and the corneum layer
In the corneum has no nucleus (effectively dead cells)
Outline the structure of the straum corneum
BARRIER Corneocytes bound together in a glue which is rich in lipids and proteins Dead cells flaking off the top Filagrin part of this glue Defects in the barrier lead to eczema
What gene mutation is common in eczema patients
Filgarin gene mtutation
Define atopy
tendency to develop hypersensitivity
What are the 2 atopic diseases
Eczema, asthama, allergic rhinitis (hayfever)
What is the pattern in atopic eczema
Common Relapsing and remitting
What is the problem in atopic eczema
Related to the reduced barrier function of the skin
What is the atopic march
People tend to develop Eczema, then food allergy, then asthma and then rhinitis (the initial eczema allows sensitisation to allergens which then manigest in other atopic disease later in life)
Outline the basic pathology in eczema
Reduce barrier function of skin and dryness(i.e. due to filagrin or other polymoprhism) Infiltration of bacteria (S. Aureus) or other irritants (soap etc), further drying skin and reducing barrier function. Immune response activated. APC (langerhans) leads to activation of CD4+ lymphocytes in a Th2 response. IgE production, mast cells degranulate If it persists from acute to chronic, then it changes to Th1 response
Signs of a filagrin gene mutation
Palmar Hyperlinearity (more prominent lines) … so more likely eczema
What does acute eczema often look like
Red, raw, weepy, vesicles, food likely to get in contact with it and lead to food allergies later due to sensitisatin
What sites are most affected in infantile atopic eczema
The most affected areas are those that the baby can access easily (face, arms, elbows, knees).
Common site of eczema outbreak in infant vs child
From infant to child: Infant: arms, face, knee etc. wherever they can access child
now affects: antecubital fossa, the popliteal fossa, hands, face and neck, legs and feet (flexural areas, and areas where there is build up of sweat).
Differentiate acute and chronic eczema
Acute is when it is very red and raw and weepy Chronic is when it now looks more skil coloured: appear excoriated and lichenified Lichenification: the skin looks thickened and there is accentuation of the skin lines
What is erythrodermic eczema
The redness is all oer and the patient is systemically unwell
What can be consequence of inflammed skin in eczema
S. Aureus can colonise on the skin and activate immune response to perpetuate the eczema Can also cause infections
What other infection are eczema patient more likely to get
Herpes Simplex Virus Punched out blisters which break down to form ulcers =Eczema herpeticum Patient can become very unwell, and virus can spread into blood and this can cause herpes encepalitis. Patient would also need to be admitted for antiretroviral treatmet e.g. acyclovir
Other types of eczema than atopic
Seborrhoeic Allergic contact dermatitis Discoid
Outline seborrhoeic eczema
Greasy scaly skin with redness around nasal labial folds, forehead and eyebrows or scalp The overgrowth of yeast and the dermatitis occur at the same time(includes dandruff) Not as itchy • It can be treated with anti-dandruff/anti-fungal shampoo, antifungal cream and topical steroid • This gets worse in times of stress, staying up late or drinking too much alcohol
What is allergic contact dermatitis
Reaction to an individual product Common: makeup, perfume, fragrance, nickel, rubber, PPD in henna
Why is S Aureus called super antigen
• Often, there is colonisation of the skin with staphylococcus aureus • S. aureus acts as a super antigen activates the eczema worsening of eczema in a topic eczema
What is discoid eczema
• This is descriptive of the pattern • It occurs in discoid areas (often on the legs, but can be anywhere • Each individual disc looks like eczema • But the intervening skin may look normal Over washing can cause it
Cause of discoid eczema and treatmnet
• The cause of this is often just dry skin with secondary dermatitis • Treatment involves: o Emollient use o Topical steroid o Avoidance of soap/shower gel
What is psoriasis
Psoriasis is another inflammatory dermatoses, in which patients present with psoriatic plaques. There are a number of patterns that allows us to identify this. Patients have salmon pink coloured plaques, with a silvery scale.
T/f psoriasis is a monogenetic confition F
F Psoriasis is a genetic condition, but it is polygenetic – a number of different genes can cause it
Environmental triggers of psoriasis
Psoriasis has environmental triggers as well as genetic susceptibility. This may include an infection, stress or certain drugs or alcohol .
Histology of psoriasis
• The epidermis becomes thicker – this is called acanthosis • The stratum corneum also becomes thicker – this is hyperkeratosis • The individual cells are not losing their nuclei – this is parakeratosis • There’s dilatation of blood vessels in the dermis so red colour Scaling
What immune cells are involved in psoriasis
• There are lymphocytes within the dermis • This immune reaction is being driven by T cells and excess cytokines/TNF-alpha -neutrophils recruited to epidermis and over production of keratinocytes….. thickening of epidermis
Common sites of psoriasis
Psoriasis is commonly seen at the scalp, elbows, knees, and genital areas, around the umbilicus and at the natal cleft of the buttocks. It is also seen on the hands and feet Note the difference to eczema, which was on inside of elbow and knees and psoriasis is on the outside
Differentiate the skin lesions in atopic eczema and psoriasis
Atopic eczema not well defined skin lesions In psoriasis , the plaques are very well defined Generally, it is rare for someone to have BOTH atopic eczema and psoriasis.
Triggers for psoriasis How can it be distinguished from athletes foot on the feet
It can be triggered by pressure and trauma to areas of skin. I.e. in the feet on sites of pressure and symmetrical whereas fungal infection would not be
Pattern of psoriasis What are the nail signs for psoriasis. How do you differentiate them from fungal infection nail signs
In psoriasis; if not all, then most of the nails are affected with these patterns : Subungual hyperkeratosis, Dystophic nail and loss of cuticle Onycholysis and pitting
In fungal infection just one or two nails(nails willhave a yellow crumbly appearance),
What is guttate psoriasis
lots of little, raindrop like lesions on the skin
When is guttate psoriasis affecting patients
- This generally affects young people (teenagers), and can occur after a streptococcal sore throat
How long does rash last in gutate psoriasis How is pateint treated
- The rash can persist for weeks or - We can treat the patient with antibiotics and topical steroids to clear the psoriasismonths
T/f there is no relationship between guttate psoriasis and later development of chronc plaque psoriasis
F - These patients have a genetic susceptibility – they are more likely to develop chronic plaque psoriasis
What is palmoplantar pustolosis
This is where, instead of plaques forming on the body, pustules form on the palms of the hands and soles of the feet. The patients are otherwise well, however this can be itchy and sore.
What is palmoplantar pustolosis often linked to
This must be driven by a different genetic susceptibility. These patients are often smokers, but cessation of smoking doesn’t seem to make it better.
What is generalised pustular psoriasis
Pustules on a background of inflammation the condition makes patients very unwell. They are febrile and toxic. They have a high HR, and low BP. They are so unwell that they cannot function. High mortality without treatment
How is generalised poustular psoriasis treated
They are treated with immunosuppressants. Patients are also given emollients and topical steroid treatment
What does acne affect
Pilosebaceous unit
Acne development
Comedone caused by build up of keratin (hyperkeratinisation, thickening of infundibulum of hair follice), creating a plug Increased sebum production due to androgenic stimulation Growth of propionibacteria acnes causing inflammation Turns into cyst Inflammatory cells spilling into the dermis (out of the follice), causing even more inflammation
Why does acne happens
Genetic factors + hormones
Differentiate white head and black head
White head is the comidone covered with skin. Blackhead is where there is no skin(an open comedone) and you can see dead follicl cells within it. Papules are raised inflammatory lesions.Nodules are where these raised inflammatory lesions are thickened and pustules are where there is pus within these raised inflammatory lesions.
Outline hormonal basis of acne
It is driven by hormones (androgenic stimulation causes hypertrophy of sebaceous glands excess production of sebum).
What can be the result of lesion healing
Scarring
Where is acne most common
Where the sebaceous glands are present: Face neck upper chest
What is bullous pemphigoud
AI condition… antibody against component of basement membrane… often in elderly
blister forms
Why are special proteins required for the epitdermis and the dermis
BECAUSE the epitdermis is derived from the ecoderm and the dermis is derived from the mesoderm so you need proteins to hold them toegether via the basement membrane
Which proteins are found between the epidermis and the dermis
Tonofilaments from epidermis linking to the basement membrane anchoring fibrils in the dermis linking to basement membrane too
lots of proteins involved
Which anitgens are involved in bollous pemphigoid
BPAg 1 and BPAg 2 Involved in hemidesmosome B cells produce produce ABs against them
Pathology of bollous pemphigoid
- The BPAg proteins are located on the basement membrane - This AI disease has autoantibodies against these proteins. Causes inflammation at the BM zone, and splitting of the epidermis from the dermis - This is a deep blister, where the deep blister split is at the location of the basement membrane (subepidermal blister)
Treatment for bollous pemphigoid
high dose oral steroids, and other immunosuppressant drugs (methotrexate) Suppresses formation of autoantibodies and allows skin to recover Must be maintained for number of years
Who does bollous pemphigoid often occur in adn what is the effect
In bullous pemphigoid, you get tense blisters. It is usually an elderly patient in their 70s/80s/90s. The condition begins with a rash (looks like eczema), followed by the development of blisters. The blisters progress, and without treatment, they become infected. Patients can then die from sepsis.
What is epidermolysis bullosa
IN BULLOUS PEMPHIGOID AND PEMPHIGUS, THERE IS AN AUTO-ANTIBODY ATTACKING THE BP PROTEIN. IF SOMEONE HAS A MUTATION IN ONE OF THE GENES FOR THESE PROTIENS, THEY GET A GENETIC BLISTERING CONDITION, CALLED EPIDERMOLYSIS BULLOSA.
Differentiate the blisters in bollous pemphigoid and pemphigus
In bullous pemphigoid, the blisters are deep. In pemphigus, the blisters are superficial.
What is the protein affected in pehmphigus vulgaris and what is the consequence
There is an auto-antibody, but this time it is directed at a component of the desmosomes(connections between the keratinocytes) within the epidermis called DESMOGLEINS 1&3 (especially between stratum spinosum.. the spinous processes in the stratum spinosum are desmosomes) It causes blisters, but these are much more superficial. Because of this, they break down and flake off ….erosions of skin.
Differentite where the split occurs in pemphigoi and pemphigus
In pemphigus within the epidermis In pemphigoid it is between epidermis and dermis
What are the causes of pustules on the skin
Infection Psoriasis Drug reaction
How is acne treated
Start off with topicals(include benzyl peroxide,topical antibiotics[like erythromycin and cindamycin-which both work against bacterial acnes and are lipd soluble so that they penetrate into the sebum]), then use systemic agents(like oral antibiotics,which have an anti-inflammatory effect on top of their antibiotic effect, and for females we can use a contraceptive pill ,which are formulated to be good for acne,such as yasmin, and if all of this does not work you can use isotretonoin, whcih has an anti-inflammatory and antiproliferative effects on the acne.
Treatment of pempigus vulgaris , and what happens without treatment
Oral steriods , oral immunosupressants, to supress the fomration of the autoantibodies, for the skin to revcover, WIthout tretament patients can become septic and die
