5: Inflammatory dermatoses Flashcards

1
Q

Which layer of the skin is associated with its normal barrier function?

What is it made of?

A

It is mainly situaties in the stratum Corneum

It contains of

  • Kerationocytes (differentiated as Corneocytes)
  • and a “special glue”
    • made up of lipids and filagrin
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2
Q

What is the main risk factor for development of eczema?

A

Defect Skin Barrier Function

  • makes it easier for pathogens to enter the skin
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3
Q

Explain the pathophysiology of atopic eczema

A
  1. Defective barrier function of the skin allows
  2. extrinsic factors to enter the skin
    • e.g. allergens
    • irritangs (e.g. soaps)
    • pathogens
  3. Leading to
  4. Acute Eczema
    1. Activation of the immune system (CD4+ T cells and Th2 cells)
    2. Trigger B-cell to produce antibodies
      1. Mast cell degradation and inflammatory response (histamine release)
  5. Chronic Eczema
    1. Activation of CD4+, Th1 and CD8+ T-cells (mediated via eosinophils)
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4
Q

Explain the relationship betwen hyperlinearity and eczema

A

It is a sign of sign of filagrin gene mutation –> sign of defect barrier function of the skin

–> people are more prone to eczema

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5
Q

What is the clinical presentation of actute atopic dermatitis?

A

Generally: ichy, red, inflammes plaques (exzema)

Site changes with age

  • Children:
    • extensor sites of limbs (elbow/knee)
    • face
  • Adults
    • neck
    • flexor (cubital and polpiteal fossas)
    • bakc of hands
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6
Q

What is the clinical presentation of chronic atopic dermatitis?

A

lichenification (Thickening of the skin with accentuated skin markings) but associated with less redness

  • poorly defined borders
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7
Q

What is Erythidema?

A

Severe eczema over whole body

(patients are unwell and miht require hispilalisation)

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8
Q

Explain the relationship between eczema and infections

A

Because of defect skin barrier:

  • increased risk of infection
    • e.g. staph A
    • Herpes simplex wich might lead to eczema herpeticum
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9
Q

What is atopic eczema?

A

It is an actopic disease –> hypersensitivity in skin

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10
Q

What is Seborrhoeic Eczema?

A

Same as dandruffs on other parts of body (often in face)

  • increased yeast growth on skin
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11
Q

What is Allergic contact dermatitis?

A

sensitisation to specific allergens e.g. cosmetics, hair dye, henna tattoos (PPD), Nickel etc.

–> When contact: dermatitis and inflammation

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12
Q

What is Discoid eczema?

A
  • related to dryness of skin with
    • often in elderly that whash themselves a lot
  • round/coin shaped eczemas
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13
Q

What is psoriasisi?

What is its clinical presenation?

A

It is a disease that causes well defined, several larger patches which have cales and plaques on them

often symmetrical on

  • scalp
  • trunk
  • armpit
  • elbows
    *
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14
Q

What are the pathophysiological and histological changes in psoriasis

A

Hyperproliferation of keratinocytes leading to

  • hyperkeratosis –> too much formation of keratin
  • Parakreatosis –> no loss of cell nuclei at the top of epidermis
  • Acanthosis –> thickened epidermis

Also

Inflammation

Dilated blood vessels –> redness

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15
Q

What is Psoriasis Soles?

A

Psoriasis at the soles of the feet

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16
Q

What are the changes in nails that can often be seen in psoriasis?

A
  • Subungual hyperkeratosis
    • increased Keratine under nail
  • Dystophic nail and loss of cuticle
    • might make it more prone to infection
  • Onycholysis and pitting
    • seperation of nail from nailbed
    • pitting= pits on nail
17
Q

Which cells usually mediate inflammation of the skin?

A
  • In the epidermis= neutrophils
  • in the dermis= lymphocytes
18
Q

What is Guttate psoriasis

A

Type of psoriasis (“Raindrop like) with

  • many small plaqules
  • presenting in teenagers and young adults

exaggabated by streptococcal infections

19
Q

What is Palmoplantar pustulosis?

A

blister-like sores on the palms of your hands and the soles of your feet

20
Q

What is Generalised pustular psoriasis?

What is its prognosis?

A

Many pustulars form due to clustering of neutrophils in epidermis

21
Q

What are the possible causes of postules?

A
  1. Infection
  2. Drug reaciton
  3. Psoriasis
    1. sterile neutrophil accumulation
22
Q

What is the clinical presentation of Acne?

A

Present with

  • whitehead closed comedo
  • blackheads (open comedo)
  • pustules
  • nodules
  • papules
23
Q

Explain the pathophysiology of acne

A
  1. Overproduction of keratine by keratinocytes that line the sebaceous follicle blocks hair follicle/sebacous gland –> formation tof micro comodo
  2. Accumulation of sebum and dead cells around hair follicle
  3. Infection with bacteria Propionibacterium acnes and further production of sebum
  4. Rupture with excretion and pus going into adjacent areas/follicles
  5. Might be also influenced by
    • genetic predisposition
    • other comedone formation
    • androgen stimmulation —> leding to sebum production
    • propionibacterium acnes
24
Q

What is Bullus pemphigoid?

A

It is a condition that causes separation of the epidermis from the dermis leading to deep blister formation

25
Q

Explain the pathophysiology of bullous pemphigoid

A

Auto-immune disease: antibodys against BP1 and BP2 proteins

  • part of the hemidesmosome of the basal keratinocytes that anchor the epidermis to the basement membrane
26
Q

What is the clinical presentation and treatment of bullouw pemphigoid?

A
  1. Deep, tense blistering

–> treatment required otherwise infection –> sepsis –> death

  • steroid treatment (immunosuppression)
27
Q

What is Pempigus Vularis?

A

A skin connection where theintracellular connections between Keratinocytes are attacked and lead to a splin in the stratum spinosum

28
Q

Explain the pathophysiology of Pempigus Vulgaris

A

Antibody production against Desmogleins

  • needed to form the intracellular connection betwenn keratinocytes in the stratum spinosum
29
Q

What is the clinical presentation of pempigus vularis?

A
  • flaccis, thin blistering
  • that break early