The Itchy Skin Flashcards

1
Q

What is itch?

A
  • sensation (usually unpleasant) = desire to scratch
  • NB protective mechanism = animal detect harmful substances
  • scratching behavior, pleasant feeling = itch-scratch cycle
  • cycle= serious skin damage & propagates itch
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2
Q

Itch-scratch cycle

A
  1. Scratch (automatic usually)
  2. Epidermal barrier/skin (damage)
  3. Production of Neuropeptides, tryptase
  4. Stimulate C nerve fibers (more itching, scratching etc)
  5. Itch
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3
Q

Pruritus

A
  • most common complaint of patients with dermatologic disease
  • arises from primary skin disorder
  • manifestation of underlying systemic disease = 10% - 25% affected individuals
  • occurs in absence of visible skin signs (have to be careful)
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4
Q

Classification of an itch

A

— mechanical - physical stimulus (wind blowing over skin/ tickle)
— chemical itch
- histamine-dependent
- histamine-independent
— ‘contagious itch’ (yawn)
- watching others scratching themselves/ talking about itchiness = desire to scratch, despite no chemical/ mechanical pruritic input

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5
Q

Itch pathway

A

Complex
- itch signal transmitted mainly through small, itch-selective C-fibers, histamine & non-histamine triggered neurons
- connects secondary neurons in dorsal root ganglion
- cross opposite side of spinothalamic tract
- ascend to parts of brain involved in sensation, emotion, reward & memory

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6
Q

Primary mediators of pruritus

A
  • Histamine
  • Tryptase
  • Cathepsin S
  • IL-31
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7
Q

Secondary mediators of pruritus

A
  • Prostaglandins E1,2
  • Substance P
  • Opioid receptor agonists
  • Nerve growth factor
  • IL-2
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8
Q

Causes of itch = with skin rash (primary skin changes)

A

Skin disease with primary skin changes
- atopic eczema
- psoriasis
- fungal infection
- popular urticaria
- insect bites
- scabies

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9
Q

Causes of itch = no skin rash

A
  • systemic disease
  • underlying malignancy (paraneoplastic)
  • medication
  • advanced aging
  • neurogenic/ neuropathic itch (stroke/ trigeminal neuralgia)
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10
Q

Causes of itch = with skin rash (secondary skin changes)

A

Secondary skin changes = scratching (itch-scratch cycle = local small fiber neuropathy)
- lichen simplex chronicus
(Habitual scratching eg: sitting in front of tv)

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11
Q

Atopic eczema/dermatitis

A
  • chronically relapsing
  • inflammatory
  • non-contagious
  • extremely pruritic skin disease
  • families with atopic diseases (group of conditions inherited tog. = asthma, allergic rhinitis, conjunctivitis, food allergies)
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12
Q

Pathogenesis of AD

A
  • complex genetic disease = gene-gene & gene-environment interactions
  • genetic predisposition to very dry skin & overactive immune system
    Epigenetics + genetics
  • polygenetic incl: FLG-mutation (well known but others)
    Non-genetics
  • allergic incl: HDM (house dust mites) & food allergens
  • non-allergic incl: Staph superAg + irritants (soap)
  • dysbiosis
    = barrier dysfunction + Th2-immunological response
    (Type 2 inflammation contributes to skin barrier dysfunction in atopic dermatitis)
  • sub clinically, cytokine involvement = whole body affected
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13
Q

Skin barrier

A
  • brick & motor model = stratum corneum (outermost layer) - prevents from evaporating
  • brick = corneocyte
  • motor = lipid lamellae
  • steel rods = desmosomes keeping cells tog.
  • lipid gets washed out = skin desquamantes earlier, desmosomes break down, infections get access to immune system
  • increase in trans epidermal water loss
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14
Q

TH2 pathway of AD

A
  1. Dendricyte (APC)
  2. Stimulate IL-4 production
  3. Stimulate TH2 cell to produce IL4 & IL13 (NB cytokines)
  4. Triggers type 2 inflammation
    (Back to 1.)
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15
Q

Psoriasis

A
  • complex, chronic, multi factorial, immune-mediated, inflammatory disease = clearly defined, red & scaly plaques
  • hyperproliferation of keratinocytes in epidermis, increase in epidermal cell turnover rate
  • normal skin in between plaques, not like AD where there is whole body involvement
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16
Q

Psoriasis pathogenesis

A

Multi factorial
1. Genetic (certain HLA-alleles)
2. environmental:
— stress
— cold, trauma
— infections (Eg: strep, staph, HIV)
— alcohol & drugs (eg: iodides, steroid withdrawal, aspirin, lithium, beta-blockers, botulinum A, antimalarials)
3. Immunologic

17
Q

Inflammatory pathway involved in Psoriasis

A

Type 1 inflammation - Th1 disease
1. DC
2. IL 23
3. Th17
4. IL-17A
5. Keratinocytes proliferate
(Back to 1. = inflammation neutrophilic)

18
Q

Fungal skin infections

A

Dermatophytes
Non-Dermatophytes
- yeast-like fungus = Candida albicans
- molds = eg: malassezia furfur

19
Q

KOH

A

Postassiez hydroxide scrape (skin scrape)
Dermatophyte
- septate hyphae
Candida
- round / oval cells
- pseudohyphae
- septate hyphae
Malassezia
- yeasts & hyphae = “spaghetti & meatballs”

20
Q

Dermatophyte infection

A
  • ringworm
  • tinea
  • only grow in keratin
    (Stratum corneum, hair, nail)
    Organism is most common depends on area to area
  • Microsporum = canis
  • trichophyton = violaceum
  • Epidermophyton = floccosum
21
Q

Types of Dermatophytes based on mode of transmission

A

Anthrophilic = human to human = mild, inflammatory, chronic (mostly - urbanization)
Zoophilic = animal to human = intense inflammation (pustules & vesicles possible), acute
Geophilic = soil to human/ animal = moderate inflammation

22
Q

Papular urticaria

A
  • very common = children
  • hypersensitivity response to antigens in arthropods’ saliva
  • immunological tolerance develops = less common in adults
    — arthropods
  • fleas
    (Dogs, cats, birds = can be aggressive)
  • bed bugs
  • mosquitoes
  • mites
    Often recurs when exposed to new insects at new venues
23
Q

Insect bites

A
  • vectors for major infections eg: Black Death/ tick bite fever/ malaria
    Lice
  • pediculosis: head lice (pediculus capitis)
  • clothing lice (pediculus humanus)
  • crab lice (pthirus pubis)
    Fleas
    Bed bugs (cimex lectularius)
    Animal mites
    Ticks
24
Q

Paraneoplastic pruritus

A
  • precede, follow or occur concurrently
  • improves when malignancy cleared
  • often recurs during remission
  • skin appear normal, except for secondary changes (eg: excoriations)
  • mechanism not fully understood
    Any malig. But commonest
  • haemtological malignancies (leukemia & lymphoma)
  • cholangiocardinoma
25
Q

Advanced age

A

Dry skin
- inherited factors
- increasing age = decreased production of ceramides in stratum corneum
- mostly legs, widespread
- cool weather, windy/ low humidity
- air conditioning, central heating
- excessive bathing, showering/ swimming, strong chlorination
- soap, detergents & solvents