Inflammatory Dermatoses Flashcards

(37 cards)

1
Q

what kind of cells are found in the stratum corneum?

A

dead keratinocytes which have lost their nuclei

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2
Q

what kind of cells are found in the stratum granulosum?

A

cells with keratin granules

much flatter

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3
Q

what kind of cells are found in the stratum spinosum?

A
  • living keratinocytes

- dendritic cells (Langerhan cells)

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4
Q

what kind of cells are found in the stratum basale?

A
  • melanocyte
  • dividing keratinocyte (stem cell)
  • tactile cell with sensory nerve ending (Merkel cells)
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5
Q

where are the youngest and oldest cells found in the epidermis?

A

the youngest cells are near the basement membrane where they freshly differentiate

the older cells are closest to the stratum corneum

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6
Q

what are the stages of differentiation of basal cells into keratinocytes?

A

basal cell

  • to prickle/spinous cell (in the spinosum layer)
  • to granular cell (in the granulosum layer)
  • to keratin producing cell
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7
Q

what are the two layers of the dermis layer?

A

papillary dermis

reticular dermis

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8
Q

what function does the stratum corneum have and how is this achieved?

A

barrier function:

corneocytes (differentiated keratinocytes) have a glue around them made of lipids (filaggrin)

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9
Q

what protein is required for the glue around the corneocytes?
what is the result of a defect in this protein (gene) ?

A

filaggrin

a defect in the protein’s gene predisposes you to eczema

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10
Q

what are the 4 main types of eczema/dermatitis?

A
  • atopic
  • seborrhoeic
  • discoid
  • allergic contact

ASDA

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11
Q

what is the associated tendency with atopic diseases?

A

the tendency to develop hypersensitivity – includes eczema, hay fever & asthma:

from early life. Many grow out of it

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12
Q

what is the cause of atopic dermatitis?

A

defective barrier of skin e.g. filagrin epidermal protein gene mutation

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13
Q

what is a sign of filagrin mutation?

A

palmar hyperlinearity

the lines of the palm are more prominent

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14
Q

what is the consequence of a defective skin barrier due to the mutation in filagrin?

A

Defective barrier then allows entry of irritants, allergens and pathogens which then cause inflammation.

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15
Q

what is the consequence of chronic scratching and rubbing of atopic dermatitis?

A

lichenification where the skin becomes thick and leathery

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16
Q

how is severe eczema described?

A

erythroderma

describe intense and usually widespread reddening of the skin due to inflammatory skin disease.

17
Q

what are some microbial infections that lead to severe eczema?

A

staphylococcus, streptococcus and herpes simplex

susceptible to these infection due to eczema

18
Q

what is seborrhoeic eczema?

A

Associated with an overgrowth of malassezia (species of yeast on the skin that causes inflammation) with eczema

19
Q

who does seborrhoeic eczema affect?

A

Common skin condition affecting babies and adults but is NOT itchy.

distinctive distribution involving
– nasolabial folds, eyebrows, scalp, central chest, axilla and groin.

20
Q

in what sort of skin is discoid eczema common?

A

small discrete discs common in overwashed skin due to lack of skin oils

21
Q

what are the types of psoriasis?

A

o Chronic plaque.
o Guttate.
o Palmoplantar pustulosis.
o Generalised pustular psoriasis

22
Q

what is the cause of psoriasis?

A

many genes are implicated including PSOR1 alongside Environmental causes i.e. triggers like
- alcohol, stress, smoking, drugs (antimalarials, beta blockers) infection (strep)

in infection, tonsillectomy can improve psoriasis

23
Q

what is the mechanism resulting in psoriasis?

A
  • T-lymphocytes move out of blood vessels into the dermis
  • initiate release of cytokines (e.g. TNFa)
  • the epidermis thickens in response (produces more keratinocytes)
  • Neutrophils infiltrate the epidermis and lymphocytes infiltrate the dermis.
24
Q

what are the histological features of psoriasis?

A

proliferation effects:

  • hyperkeratosis: thickening due to overproliferation
  • parakeratosis: top layer of keratinocytes have not lost their nuclei
  • acanthosis: thickening
  • inflammation
  • dilated blood vessels
25
info about Guttate psoriasis
smaller plaques (papule) pink and scaly exacerbated by strep infections
26
info about palmoplantar pustolosis
pustules on the hands or feet | exacerbated by smoking, stress and obesity
27
what is acne the disease of?
disease of the pilosebaceous unit of the skin involving the hair follicle at its opening
28
what is the process that leads to acne formation?
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 (bacteria) within pilosebaceous unit. o Rupture of inflamed pilosebaceous unit --> further inflammation of surrounding skin important drivers: propionibacteria and androgenic stimulation
29
what are the clinical features of acne?
- open (blackhead) comedones - closed (whitehead) comedones - papules - pustules - nodules - scars on face, chest and back.
30
what is Bullous Pemphigoid?
autoimmune bullous inflammatory condition most common in the elderly
31
what are the clinical features of bullous pemphigoid?
- pruritis (itch) - deep blistering (tense blisters/bullae) on an erythematous background of skin or mucous membrane e.g. epidermolysis bullosa
32
what is the autoimmune mechanism of bullous pemphigoid?
IgG auto-antibodies against basement membrane antigens - BP180 (T17 collagen) - BP230 leads to an inflammatory response: result in cleavage of skin at the dermo-epidermal (between dermis and epidermis) junction leading to sub-epidermal blisters. (?) antigens: BPAg1 and BPAg2
33
in embryology, where is the epidermis and dermis derived from?
epidermis from ectoderm | dermis from mesoderm
34
what is pemphigus vulgaris?
uncommon AI bullous inflammatory disease most common in middle-aged people more likely in Asians than whites (at a younger age group)
35
what are the clinical features of pemphigus vulgaris?
flaccid blisters which break easily leaving erosions and crusted lesions
36
what is the autoimmune mechanism in pemphigus vulgaris?
IgG auto-antibodies to epidermal cell surface proteins desmogleins 1 & 3 (cadherins) this results in the loss of cell-cell adhesion (acantholysis) between keratinocytes within the epidermis causing flaccid blisters in the skin or mucous membranes summary: AI reaction affects intercellular adhesions between keratinocytes at cell-cell junction NB pemphigoid is to do with basement membrane
37
what is the difference between bullous pemphigoid and pemphigus vulgaris?
BP: - Affects the junction between the epidermis and dermis. - Affects an older age group (elderly) PV: - Effect is within the epidermal layer (due to keratinocyte adhesions) - Affects a younger age group (at middle age)