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Immunology year 2 > Inflammatory dermatoses > Flashcards

Inflammatory dermatoses Flashcards

(52 cards)

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1
Q

Why should we learn about the skin

A

20% consultations in GP

Under represented in curriculum

Overlaps with many specialties

Largest organ (16% body mass, 1.8m2 surface area)

Clinical skills paramount in diagnosis

Over 2000 diseases affect the skin

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2
Q

What structures are found in the dermis

A

Dermis- collagen, GAGs, elastin, blood vessels, nerves and appendageal structures (hair folicles sebaceous glands and sweat glands)

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3
Q

Describe the basic micro anatomy of the skin

A

Epidermis
Dermis
Subcuteneous tissue

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4
Q

What are the black cells in the histology of the dermis

A

Black cells- fibroblasts- makle collagen, elastin and GAGs

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5
Q

Describe the histology of the skin

A 
Stratum cornea
Epidermis
Papillary dermis
reticular dermis
hypodermis
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6
Q

Describe the different glands found in the skin

A

Sebaceous glands- luybricate hair folliceles
Apcorine- axilla and groin- viscous sweat- degraded by bacteria

Eccrine- watery, most over places

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7
Q

What are the four different cell types found in the epidermis

A

Keratinocytes
Langerhan cells- APC
Merkel cells- nerve sensation

melanocytes

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8
Q

Describe the structure of the epidermis

A

Statum basale- melanocytes, dividing keratinocytes (stem cell), Merkel cells (tactile cells)

Stratum spinosum -spines between keratinocytes, dendritic cells

Startum granulosum- keratin granules in keratinocytes

Stratum lucidum -

Stratum corneum - dead keratinocytes- those on the surface flake off

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9
Q

Describe the keratinocyte differentiation pathway

A

 Keratinocyte differentiation pathway – basal cell  prickle cell  granular cell  keratin.

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10
Q

How will mealonocytes look in histology

A

Melanocytes are vacuolated

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11
Q

Describe the importance of the structure of the stratum corner

A

Very important for barrier function of the skin

Defects lead to eczema

Filagrin gene mutation common in eczema patients

Keratinocytes and lipid/protein glue – barrier function

Filagrin mutation- eczeman and other allergic diseases

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12
Q

Describe the stratum corner

A

 Stratum corneum:
o Very important barrier function of the skin.
o Defects lead to eczema.
o Composed of corneocytes (differentiated keratinocytes) with lipids in between each of them.

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13
Q

Describe atopic eczema

A

Atopy – tendency to develop hypersensitivity

Atopic diseases - eczema, asthma, hayfever

Atopic eczema – common, relapsing and remitting

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14
Q

Describe the atopic march

A

Food allergies and eczema may present early- food allergies- may have eczema on face- put food on face- sensitisation to food

Allergic rhinitis and eczema develop a little later on in childhood

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15
Q

Describe the pathophysiology of atopic eczema

A

Intrinsic factors – leading to defects in the epidermal skin barrier- filaggrin gene mutations

Extrinsic factors – penetration of exogenous agents:
allergens e.g house-dust mites
irritants e.g detergents in soaps
pathogens e.g staphylococcus

mast cell degranulation - releasing histamine

acute AD – activation of CD4 lymphocytes and Th2 immune response

Chronic AD- activation of CD4 and CD8, and the Th1 immune response

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16
Q

What is a clinical sign of the filaggrin gene mutation

A

Palmar hyper linearity

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17
Q

Where may atopic dermatitis present

A

Arreas where they riub themselves and on flexures

Face, elbows and knees

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18
Q

Describe the chronic changes in eczema

A

Eczema with lichenification
Looks like it’s thickened- with accentuated skin markings- area of involvement poorly defines

Red all over- erytheoderma

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19
Q

What infections are patients with eczema susceptible to

A

Suceptible to infections as a result of defective barrier function in skin

Staph aureus- superantigen- makes eczema worse
HSV
TREAT WITH AMOILIANTS, STEROIDS AND ACYCLOVIR

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20
Q

State some other types of eczema

A

Seborrhoeic

Allergic contact dermatitis

Discoid

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21
Q

Describe Seborrhoeic Eczema

Study These Flashcards
A

Same as dandruff, overgrowth of yeast
Nasal-labial folds, eyebrows, chest and back
Greasy scale, like dandrugg

Anti-fungal shampoo, cream and steroids, come back int imes of strefdf

22
Q

Describe allergic contact dermatitis

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A

Sesntiised to allergens- cosemtics, eyedrops, PPD in hair dye, henna in tattoos

23
Q

Describe discoid eczema

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A

Legs and skin
Dryness- people who was too much- don’t produce as much lipid in skin as you get older
Can be linked to atopic eczema
Avoid soap, steroid

24
Q

Summarise eczema

Study These Flashcards
A

Synonym: dermatitis

Types include:

Atopic
Seborrhoeic
Discoid
Allergic contact
Atopy: tendency to develop hypersensitivity

Atopic diseases include eczema, asthma and hayfever

25
What is meant by atopic eczema
Atopic eczema Very common itchy skin condition. Onset often within first 6 months of life. Many children will grow out of it, but a proportion does not. Biology Defective barrier function of the skin, leading to dry skin. Filagrin gene mutations in 10% of cases. Filagrin is an epidermal protein important in maintaining barrier function of the skin. Defective barrier function allows penetration of irritants, allergens (eg house dust mite particles) and pathogens eg staph aureus. Inflammation of the skin then occurs.
26
Describe the key features of seborrheic eczema
Seborrheic eczema A very common type of eczema affecting babies and adults. Often not itchy. There is overgrowth of malassezia species of yeast on the skin with associated skin inflammation. The rash has a distinctive distribution including nasolabial folds, eyebrows, scalp, central chest and sometimes axillae and groins.
27
Summarise psoriasis
Erythematous plaques- salmon pink colour, well defined Underlying genetic syceptibility- polygenic And environemtal triggers, beta blockers, lithium ,anti-malarials, strep infections, alcohol and stress Tonsils removed- improves psoriasis- less strep infections
28
Essentially, what happens in psoriasis
Overproliferation of keratinocytes- nuclei in corneal layer- shed when alive- scales
29
Describe the histological features of psoriasis
Hyperkeratosis- in stratum cornum Parakeratosis - stratum corner contains keratinocytes with nuclei Acanthosis - thickening of the epidermis Inflammation- lymphocytes in dermis, neutrophils in epidermis Dilated blood vessels
30
State the common locations of psoriasis
Extensor surfaces, scalp gential area, umbilicus and nails trunk, knees, elbows, buttock armpit face
31
What is a key feature of psoriasis
Psoriasis vulgaris: soles Well-demarcated, erythematous plaques with thick, yellowish scale and desquamation on sites of pressure arising on the plantar feet; similar lesions were present on the palms. Symmetrical- likely to be inflammatory
32
Describe how the nails may appear in a patient with psoriasis
Dystophic- roughening Cutiicle- seal proximal nail fold onto plate- allowing secondary infections Subungual hyperkeratosis Dystophic nail and loss of cuticle Nail plate- lifted off bed onycholysis Onycholysis and pitting
33
Summarise guttate psoriasis
Teens and young adults Little papules Salmon pink, scaly Strep infections associated Means raindrop
34
Summarise palmoplantar pustolosis
Pustules on hands and feet Different genes Exacerbates by smoking, stress and obesity
35
Describe generalised pustular psoriasis
Extensive pustules Infection Drug reactions Or psoriasis Pustules- neutrophils coagulating together in the epidermis- sterile- no infection in them Patinet will be febrile
36
Essentially, what is acne
Disorder of pilo-sebaceous unit
37
What are the factors that lead to acne formation
Other factors Comedone formation Genetic predisposition Propionibacteria acnes Androgenic stimulation
38
Describe the pathogenesis of acne
 Pathogenesis – multifactorial: o Hyperkeratinisation of the epidermis in the infundibulum of hair follicles.  Accumulation of dead keratinocytes in the lumen of the hair follicle. o Increase sebum production stimulated by androgens. o Proliferation of Propionibacterium acnes within pilosebaceous unit. o Rupture of inflamed pilosebaceous unit  further inflammation of surrounding skin (rupture of follicular canal).
39
What are the clinical features of acne
Whithead- comedone covered in skin Blackhead- open comedone Papule- small inflammatoty lesions Pustule- full of pus nodule- inflammation and pus
40
Summarise the treatment of acne
Benzoyl peroxide Topcial, lipophilic antibiotics Contraception to reduce free testosterone Atrithromycin and tetracylicn- antibiotic and anti-inflammatory
41
What is bullous pemphigoid
Deeper bilsteris | Pemphigoid- = deeper
42
Why do we need the basement membrane zone linking the dermis to the epidermis
Dermis- mesoderm Epidermis- ectoderm Need specialize proteins to link them
43
Describe the key features of bullous pemphigoid
An autoimmune bullous inflammatory condition most common in the elderly. Clinical features consist of intense pruritus followed by the development of tense blisters on an erythematous background of skin or mucous membranes. Biology IgG autoantibodies to basement membrane antigens BP180 (type XVII collagen) or BP230 result in cleavage of the skin at the dermo epidermal junction leading to sub epidermal blisters. Tonofillaments and anchoring fibrils
44
Summarise epidermolysis bullosa
Genetic Defective proteins Splititng of skin with minor trauma
45
What are the key complications and treatment of bullous pemphigoid
Infectious, septic and die Steroids and immunsuppressants Tense blisters (bullae)
46
Summarise pemphigus vulgaris
Vulgaris and foliaceous Superficial bilsters
47
Describe tha pathogenesis of pemphigus vulgaris
Autoantibodies against spines in spinosum Desmogleins autoantigen in PV (against plakophilin, plakoglobin and desmoplakin) essentially, destroys the connections between keratinocytes in the stratum spinosum
48
Describe the complications and treatment of pemphigus vulgarisms
Flaccid, fragile bilsrters Can be all over the bdoy Rarer= ,more likely to occur in Asians and in young age Oral steroids to suppress froamtion of antibodies And imunosuppresants.
49
Describe the key features of pemphigus vulgarisms
An uncommon autoimmune bullous inflammatory disease, which usually affects middle aged individuals. Clinical features include flaccid blisters which easily break leaving erosions and crusted lesions. Biology IgG autoantibodies to epidermal cell surface proteins desmogleins 1 and 3 lead to loss of cell-cell adhesion (acantholysis) within the epidermis causing flaccid blisters in the skin or mucous membranes.
50
Summarise the key features of acne
A very common condition which mainly affects teenagers and young adults. Biology Disease of the pilosebaceous unit of the skin. Pathogenesis is multifactorial and includes: Hyperkeratinisation of the epidermis in the infundibulum of the hair follicles Accumulation of dead keratinocytes in the lumen of the hair follicle Increase sebum production stimulated by androgens Proliferation of propionibacterium acnes within the pilosebaceous unit Rupture of the inflamed pilosebaceous unit, with further inflammation of the surrounding skin Key clinical features are: open and closed comedones, papules, pustules, nodules and scars on the face, chest and back.
51
Summarise the key features of psoriasis
Another common inflammatory dermatosis. Starts usually in teens or 40s / 50s. Types: ``` Chronic plaque Guttate Palmoplantar pustulosis Generalised pustular psoriasis Psoriatic arthritis affects approximately 30% of patients with cutaneous disease. ```
52
Summarise the pathogenesis of psoriasis
Genetic susceptibility and environmental triggers are the underlying cause. Many genes are implicated including PSOR1. Immune process occurs where T lymphocytes move out of blood vessels into the dermis and initiate the release of cytokines, eg Tumour Necrosis Factor Alpha. The Epidermis becomes thickened and produces more keratinocytes than normal, neutrophils infiltrate the epidermis and lymphocytes infiltrate the dermis. Triggers include infections, drugs and stress.

Immunology year 2 (5 decks)

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