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MCD: Immunology > Inflammatory dermatoses > Flashcards

Inflammatory dermatoses Flashcards

1
Q

What are the 2 types of sweat glands?

A

Eccrine and apocrine.
Eccrine sweat glands produce watery sweat and are distributed all over the body.
Apocrine sweat glands produce more viscous sweat and are distributed mainly in the axillae and groin.

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2
Q

What makes up the matrix of the dermis?

A

Collagen, elastin, glycosaminoglycans, blood vessels and nerves.

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3
Q

Describe the basic micro anatomy of the skin.

A

Epidermis sits on top of the dermis (epidermis is top layer), with basement membrane in between.

Within dermis, there are hair follicles (pilosebaceous unit- consists of hair follicle, sebaceous gland and arrector pili muscle) and sweat glands (eccrine and apocrine).

Matrix of dermis sits on subcutaneous tissue- consists of adipose tissue and connective tissue.

Below that is fascia.

Below that is e.g. muscle.

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4
Q

Describe the histology of hairless skin.

A

Epidermis at the top, below which is the dermis.
Collagen stains well in H&E staining- pink.
Most cells within the dermis are fibroblasts.

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5
Q

What do fibroblasts make?

A

Collagen, elastin and glycosaminoglycans.

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6
Q

Describe the histology of hairy skin.

A

Hair follicles
Shaft, bulb, sebaceous glands etc.
Apocrine glands
Papillary dermis- just below epidermis, and deep to it is the reticular dermis

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7
Q

What are the layers of the epidermis from deep to superficial?

A 
Stratum basale
Stratum spinosum
Stratum granulosum
Stratum lucidum
Stratum corneum
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8
Q

What cells make up to epidermis?

A

Dendritic cells
Melanocytes sit on the basement membrane and make melanin, protecting nuclei of keratinocytes from UV damage
Langerhans cells- antigen presenting cells within epidermis
Merkel cells- involved in sensation, sit on basement membrane

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9
Q

How do keratinocytes differentiate, and what is their function?

A

Keratinocytes start off at the bottom in the stratum basale, proliferate, and as they move on up through the epidermis they differentiate.

Keratohyalin granules in the stratum granulosum, go on to form keratin which makes up the bulk of stratum corneum.

By the time cells have reached the stratum corneum, they have lost their nuclei and are essentially dead.

Important function: form the barrier function of the skin, don’t just flake off.

Basal cell → prickle cell → granular cell → keratin.

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10
Q

What is the structure and function of the stratum corneum?

A

Keratinocytes sealed together with lipids and proteins- tight seal protective against irritants and allergens, bacteria etc.

Very important barrier function of the skin.

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11
Q

What do defects in the stratum corneum lead to?

A

Eczema and dry skin.

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12
Q

What gene mutation is common in eczema patients?

A

Filaggrin gene mutation.

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13
Q

Define atopy.

A

Tendency to develop hypersensitivity.

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14
Q

What is atopic eczema?

A

Atopic eczema is a skin disease caused by dryness of the skin that leads on to inflammation.
Common, relapsing and remitting.

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15
Q

List atopic diseases.

A

Eczema
Asthma
Hayfever

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16
Q

What is the atopic march?

A

Diseases come on at different time points in an individual’s life.
Eczema, food allergies, asthma, rhinitis.
Might not get all of them, but happens in that order.
Underlying problem is defective barrier function of skin.
Leads to sensitisation.

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17
Q

What factors can influence development of atopic eczema?

A

Intrinsic factors leading to defects in the epidermal skin barrier, e.g. filaggrin gene mutations.

Extrinsic factors:

  • penetration of exogenous agents
  • allergens, e.g. house dust mite, pollen, food
  • irritants, e.g. detergents in soaps
  • pathogens, e.g. staphylococcus

Mast cell degranulation releasing histamine.

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18
Q

What is the difference between chronic and acute atopic dermatitis?

A

Chronic AD: activation of CD4+ and CD8+ lymphocytes and the Th1 immune response.

Acute AD: activation of CD4+ lymphocytes and the Th2 immune response.

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19
Q

What is palmar hyperlinearity, and in what patients can it be seen?

A

Sign of filaggrin gene mutation.
Very visible lines on the palms of the hands (more so than is normal).
5-10% of the population have this.
Genetically dry skin, more likely to get eczema.

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20
Q

What is infantile atopic eczema?

A

Red, raw, weepy, itchy.

Baby won’t be sleeping or feeding properly.

Happens around the mouth.

Worst areas are those the baby can reach easily or rub on other things- infants affected on face, elbows and knees.

As the child grows up, pattern of eczema changes.

Progresses to be more on areas with a build-up of sweat- antecubital hypoxial fossae, face and neck.

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21
Q

What is lichenification of eczema?

A

Chronic changes.

Less red, appears scratched and lichenified.

Skin looks thickened, accentuation of skin lines.

22
Q

What is severe eczema, what causes it and how is it treated?

A

Very widespread, affects more than 90% = erythrodermic eczema (red all over).

Colonisation with Staphylococcus aureus- activates eczema so it gets worse.

Course of antibiotics (flucloxacillin) to treat the S. aureus, plenty of emollients, topical steroid, and a short course of oral steroids.

23
Q

What is eczema herpeticum?

A

Because the barrier function is defective, certain viruses can proliferate and spread on the skin.

Herpes simplex can proliferate on the surface of the skin- spreads from the lips to anywhere involved with eczema, dry skin.

Consists of punched out vesicles, can progress to encephalitis and cause brain damage and death.

24
Q

List other types of eczema.

A

Seborrheic.
Allergic contact dermatitis.
Discoid.

25
Q

What is seborrheic eczema?

A

Same as dandruff.

Can affect face- poorly defined areas of redness, greasy scale, mainly affecting nasolabial folds, eyebrows, forehead, beard, chest and back.

Generally not itchy, but annoying and sore.

26
Q

What is dandruff?

A

Dandruff is mild, seborrhoeic dermatitis affecting scalp only- greasy, scaly, flaking of scalp.

27
Q

How is seborrheic eczema treated?

A

Treat with anti-dandruff/anti-fungal shampoo, anti-fungal cream, mild topical steroid.

28
Q

What causes seborrheic eczema?

A

Caused by overgrowth of a naturally occurring yeast on the skin, along with a reaction to that.

29
Q

What are exacerbating factors of seborrheic eczema?

A

Gets worse in times of stress, lack of sun exposure, staying up late or drinking too much alcohol, and improves in absence of those factors.
Worse in some underlying medical conditions, e.g. HIV and other immunodeficiencies.

30
Q

What is allergic contact dermatitis?

A

Different to atopic eczema, but patients with atopic eczema can get and are more likely to get allergic contact dermatitis too.

Patients are sensitised to allergens in the environment- very allergic, e.g. makeup, preservatives in eye drops or contact lens fluid, henna tattoos.

Type 4 hypersensitivity reaction.

31
Q

What is discoid eczema?

A

Atopic eczema might predispose.
Eczema occurs in discoid areas, often on legs.
Caused by dry skin with secondary dermatitis.
Treatment is emollients, topical steroids, and avoiding soap and shower gel that dry out the skin.

32
Q

What is psoriasis?

A

Inflammatory dermatosis
Patients present with psoriatic plaques
Salmon pink plaques with silvery scale
Genetic condition, multigenetic (not single gene)
15-20% of patients have a family history of psoriasis
Monozygotic twins more likely to both have it than dizygotic twins
Environmental triggers, e.g. infection, stress, drugs
Very well defined plaques
Bilateral symmetrical eruption

33
Q

List histological features of psoriasis.

A 
Hyperkeratosis.
Parakeratosis.
Acanthosis.
Inflammation.
Dilated blood vessels.
34
Q

What is hyperkeratosis?

A

Stratum corneum becomes thicker.

35
Q

What is parakeratosis?

A

Individual cells in the stratum corneum do not lose their nuclei in the differentiation process.

36
Q

What is acanthosis?

A

Epidermis becomes thicker.

37
Q

What causes inflammation in psoriasis?

A

Influx of neutrophils within epidermis- can be so prevalent that they form pustules; lymphocytes within dermis.

38
Q

What drives the immune reaction in psoriasis?

A

Lymphocytes, excess cytokines, and TNF-alpha.

39
Q

What are the common locations of psoriasis?

A 
Scalp
Elbows
Knees
Genital area
Around the umbilicus
Natal cleft of the buttocks
Hands
40
Q

What is guttate psoriasis?

A

Raindrops pattern, usually on trunk
Usually affects young people- teenage/20s
Occurs after sore throat (streptococcal)
Rash can last weeks or months
Swab throat to demonstrate Streptococcus, give course of antibiotics e.g. penicillin B, topical steroids and a course of light therapy to clear psoriasis
Underlying genetic susceptibility

41
Q

List some distinctive patterns of psoriasis.

A

Psoriasis soles- pressure and trauma
Subungual hyperkeratosis
Dystophic nail and loss of cuticle
Onycholysis and pitting
Guttate psoriasis
Palmoplantar pustulosis- pustules on palms of the hands
Generalised pustular psoriasis- treated with emollients, topical steroids and immunosuppressants (e.g. methotrexate, cyclosporin), high mortality rate without treatment

42
Q

What is acne?

A 
Inflammatory dermatosis.
Disease of the pilosebaceous unit- follicle and sebaceous gland.
Comedone formation.
Genetic predisposition.
Propionibacteria acnes.
Androgenic stimulation.
43
Q

What are the clinical features of acne?

A

Open comedones (blackheads)- buildup of keratin in hair follicle pore.
Closed comedones (whiteheads)- blackhead covered with skin.
Inflammatory nodules- papules, pustules and nodules.
As the lesion heals, it can cause scarring.
Areas affected are areas of predominance of sebaceous glands: face, neck, upper back and upper chest.

44
Q

What is bullous pemphigoid?

A

Autoimmune condition.
Production of autoantibody that acts against protein in basement membrane.
BPAg1 and BPAg2- target of autoantibodies.
Tense blisters.
Elderly patients.
Starts off as rash that looks like eczema, then develop blisters, blisters progress, get infected and without treatment cause sepsis and death.

45
Q

How is bullous pemphigoid treated?

A

Treated with high dose oral steroids, immunosuppressants, e.g. methotrexate, stay on treatment for years.

46
Q

What is the basement membrane?

A

Very specialised area between epidermis and dermis.

Proteins adhere epidermis to basement membrane, and basement membrane to dermis.

Tonofilaments and anchoring fibrils.

47
Q

What is the embryological origin of the epidermis?

A

Ectoderm

48
Q

What is the embryological origin of the dermis?

A

Mesoderm

49
Q

Describe the pathology of bullous pemphigoid.

A

BPAg1 and BPAg2 proteins located on basement membrane.
Inflammation and splitting of epidermis off the dermis.
Deep blister split at basement membrane.

50
Q

What is epidermolysis bullosa?

A

If a patient has a genetic abnormality in BPAg1 and BPAg2 proteins, causes blistering.
Any genetic condition causing problem with basement membrane zone leads to epidermolysis bullosa, can be mild or severe.

51
Q

What is pemphigus vulgaris?

A

Superficial blisters- don’t last, cause erosions as they break down and flake off.
Autoantibody directed against component of a hemidesmosome within epidermis.
Split is usually somewhere in the middle of the epidermis, in hemidesomosomes between keratinocytes.

52
Q

What connections between keratinocytes are targeted by pemphigus vulgaris?

A

Desmogleins autoantigen in pemphigus vulgaris- target of autoantibody.
Different proteins targeted in different types of pemphigus.

MCD: Immunology (5 decks)

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