Case 9 Psoriasis, Dermatitis Flashcards

1
Q

General histories for dermatology

A

Presenting complaint
- Site and duration
- Initial appearance and evolution of rash
- Onset of rash: specific triggers, aggregating or relieving factors
- Site of rash: unilateral/bilateral
- Character of lesion: itch, pain
- Crouse of rash: constant, come and go
PMHx
- History of atopy: atopic triad
- Medication, especially any recent changes
- Family history of skin disease
Social history
- Occupation/any improvement of lesion when away from work
- new changes to shampoo/detergents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

General physical exams for dermatology

A
-	General observations (SCAM)
Size, shape
Colour
Associated secondary change
Margin, morphology
-	If the lesion is pigmented (ABCDE), melanoma
Asymmetry
Border irregular
Colours 2 or more
Diameter > 6 mm
Elevation 
-	Palpate
Surface, consistency, mobility, tenderness, temperature
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are some characteristics of psoriasis?

A

Pink papules/plaques covered by loosely adherent silver-white scales
less itchy comparing to eczema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are some risk factors of psoriasis?

A
  • Genetic: ask about family history of psoriasis/psoriatic arthritis
  • Trauma, previous infection
  • Drug eruption, smoking
  • HIV, stress
  • Medication: lithium, beta blockers
  • Might worse in winter due to lack of sun and humidity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the mechanism of psoriasis?

A

AUTO-IMMUNE
When skin breaks and pathogen invades, dendritic cells present the antigen to T cells, who release cytokines –> excessive inflammation –> inc keratinocytes proliferation in the skin (parakeratosis, scaly appearance) + recruitment of immune cells (collection of neutrophils in the stratum corneum layer)

Excessive inflammation –> vasodilation of blood vessels between dermis and epidermis –> inc recruitment of immune cells such as neutrophils –> neutrophils collect in the stratum corneum layer

Excessive inflammation –> excessive keratinocytes proliferation and abnormal maturation –> thinning of stratum Basale and thickens the other layers especially stratum corneum and stratum spinosum –> keratinocytes retain nuclei (parakeratosis) and do not adhere to each other properly (breaks in epidermis leading to the scaly appearance ) –> When scales are picked off, blood vessels in dermis can get injured and cause localised spots of bleeding called auspitz sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are some symptoms and signs of psoriasis?

A
  • Erythema  superficial elongated and dilated capillaries
  • Thickening  thicker epidermis/acanthosis
  • Scale – abnormal keratinisation
  • Auspitz sign – removing scale reveals wet surface with pinpoint bleeding
  • Less itchy than eczema, well-demarcated than eczema
  • Symmetrical – scalps, elbows, knees, lumbosacral
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are some comorbidities of psoriasis?

A
  • 10-15% people develop psoriatic arthritis: ask about joint pain/swelling or finger pain
  • Inc risk of CVS ,renal disease
  • Metabolic syndrome  central obesity, impaired glucose tolerance, dyslipidaemia, hypertension
  • Crohn’s disease/IBD
  • Depression/psychosocial issues, low self-esteem, social isolation, sexual dysfunction, suicidal ideation in 10%
  • Dec vocational opportunities and economic impact
  • Depression and stress triggers flares and reduce motivation to improve health
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How to diagnose psoriasis?

A
  • Usually clinical
  • Tissue biopsy to look for the classic change in epidermal layers
    Acanthosis (epidermal thickening), parakeratosis (retention of nuclei in stratum corneum), accumulation of neutrophils in superficial epidermis, dilated capillaries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some treatment of psoriasis

A
  • Avoid triggers: stress, medication (NSAIDs, beta blockers, lithium, ACE inhibitors)
  • Moisturisers: clear plaques and minimise itchiness
  • Topical corticosteroids
  • Topical calcipotriol
  • Keratolytic agents: urea, salicylic acid, fruit acid
  • Vit D (Calcipotiol)
    Inhibits hyperproliferation and abnormal differentiation
  • UV therapy (dermatology day unit)  induce DNA damage in keratinocytes
  • Coal tar preparations
    Suppress DNA synthesis, reduce epidermal thickness
  • Depression and anxiety  psychological counselling/psycho-dermatology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why is oral preferred over topical?

A

When rash is wide-spread, oral antibiotics are usually preferred over topical –> several tubes are needs to cover all infected areas + costs –> lead to incorrect application techniques and non-adherence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Rash due to hypersensitivity to penicillin?

A

Urticaria
Acute onset, after antibiotics
angioedema/swollen face, anaphylaxis (SOB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are some characteristics of eczema/atopic dermatitis?

A

Dry, itchy and erythematous patches, vesicular and weepy, poorly defined

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the mechanism of atopic dermatitis?

A

inflammatory condition: Type 1 hypersensitivity (IgE-mediated, prior sensitisation leading to degranulation of mast cells + HISTAMINE RELEASE)

  • Epidermal barrier dysfunction due to genetics
    Dec filaggrin, which is a protein that holds skin together (25-50%)
    In proteases, inc breakdown due to pathogens invasions
    Abnormal stratum corneum lipids
  • Immune dysfunction
    Predominant Th2 cell response –> IL 4, 5 and 13 cytokine release –> stimulate isotope switching to IgE –> eosinophils and mast cell degranulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some risk factors of eczema?

A
  • Atopic triad or family history of atopy/eczema
  • Allergic rhino-conjunctivitis, eosinophilic oesophagitis
  • Food allergies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are some triggers of eczema?

A

Airborne allergens: house dust mites, animal feathers, moulds, pollens, fragrances
Food allergens: egg, milk, soy, peanuts, fish
Irritants: prolonged water immersion, soap, shampoo, chlorinated pools, clothing (laundry, detergent, wool, synthetic fibres)
Climate: temp extremes, low humidity, +/- sunlight
Microbes (bacteria, fungi, viruses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are some examination findings of eczema?

A
  • Dry, itchy and erythematous patches, vesicular and weepy, poorly defined
  • More often in extensors in infants, flexors in children and adult
  • Distribution of disease – consider irritant/contact patterns of disease
  • Morphology – erythema poorly defined patches and indurated plaques
  • Excoriation – loss of surface of skin from scratching
  • Lichenification – skin thickening from hypertrophy
  • Secondary signs of infection: crusting, weeping, vesicles
17
Q

What are some investigations for eczema?

A
  • Usually clinical
  • Skin biopsy
  • Immunoglobulin
  • Scrape to exclude tinea infection
  • CBE: eosinophilia, total IgE
  • Patch testing (NOT to diagnose eczema, FOR ALLERGIC DERMATITIS)
  • Repeat open application test (ROAT)
  • RAST testing (radio-allergo Sorbent test) – allergen specific IgE in serum
  • Complications: Swab MCS, Swabs for MRSA (nasal if recurrent infection), viral PCR
18
Q

What are some treatment for eczema?

A
  • identify and eliminate exacerbating factors
  • skin hydration: emollients
  • antihistamine - pruritis
  • topical steroids
  • UV therapy
19
Q

What are some adverse effects of topical steroids?

A
  • Short term: inc blood glucose level, inc BP, fluids retention, hypokalaemia, poor memory with poor retention of new info, inc infection risk and reactivation of previous infection, poor sleep, altered mood
  • Long term (short term + protein changes): proximal myopathy, osteoporosis, cataracts, poor wound healing/easy bruising, weight gain, phycological changes due to poor sleep
20
Q

What conditions do antihistamine work on?

A

o Do not work on irritant or allergic dermatitis as there’s no histamine involvement
work on eczema as Type 1
o Prescribe sedating antihistamine  minimise itching to prevent any secondary changes
- Sedative
Reduce the effect of histamine by binding to H1 receptor and stablising it in an inactive form.
Side effect: sedation/psychomotor impairment (excessive sleepiness so no driving and no alcohol) + anticholinergic effects: dry mouth, blurred vision, constipation

  • Newer, less sedating
    Side effect: drowsiness, fatigue, headache
    Cetirizine
21
Q

What is the difference between irritant and allergic dermatitis?

A

Mechanism

  • ID: acute exposure/accumulation of toxic exposures causes direct injury to skin
  • AD: delayed Type 4 sensitivity (cell-mediated: sensitised Helper T cells –> release cytokines to activate macrophages)

Concentration dependent

  • ID: yes
  • AD: No

Causes

  • ID: common washing items (soap, shampoo, body wash, detergents, chlorine in pool)
  • AD: jewellery (nickel), perfume, hair dye, leather and latex

Onset

  • ID: min to hours
  • AD: hours to days

Distribution

  • ID: confined to area of exposure, well-defined
  • AD: begins in area of exposure but can spread, ill-defined

Patch test

  • ID: negative
  • AD: positive
22
Q

Other common differentials mimic dermatitis?

A

tinea corporis
- fungal, annular lesions
pityriasis rosea
- start with herald patch

23
Q

Define bulla

A

circumscribed superficial collection of fluid > 5mm

if < 5mm it’s vesicle

24
Q

Define Lichenfication

A

leathery and thickened skin with hyperkeratosis due to chronic scratching

25
Q

Define macule

A

flat, non-palpable lesion with colour change, less than 1 cm

26
Q

Define Nodule

A

a sold and rounded lesion with an appreciable deep component > 1cm

27
Q

Define papule

A

raised lesion < 1cm

larger than 10 mm –> nodule/plaque

28
Q

Define plaque

A

a well-circumscribed elevated area of the skin larger than 5-10mm

29
Q

Define vesicle

A

well-circumscribed fluid-filled lesion up to 5-10mm

30
Q

How does size change and definitions change?

A

macules –> patches
papules –> plaques/nodules
vesicles –> bullae

31
Q

Define patches

A

flat, non-palpable lesion with colour change, more than 1 cm

32
Q

What are some functions of skin?

A
maintains fluid homeostasis (prevent dehydration)
mechanical barrier to pathogens
thermoregulatory function
UV radiation protection
excretory function
Vit D production
33
Q

What is the layer of skin?

A

Up to down
- Epidermis
multiple layers of developing keratinocytes filled with keratin proteins
langerhan cells, merkel cells (sensory)
- dermis (nerves, sweat glands, lymph, blood vessels)
- hypodermis (fat and connective tissue, anchor skin to muscles)
- muscles

34
Q

What are different layers of epidermis?

A

From bottom to top
- stratum basale
mitosis of keratinocytes, when they lose the ability to divide –> move up to stratum spinosum
- stratum spinosum
- stratum granulosum (3-5 layer thick)
keratinisation (keratinocytes flatten out by removing intracellular structures and die to form epidermal skin barriers
secretion of lipids and other waterproofing molecules
- stratum lucidum
(2-3 cell thick): translucent, dead keratinocytes, only find in thick skin such as palm and soles of the feet
- stratum corneum
(20-30 cell thick, uppermost layer) complete loss of all organelles and production keratin
as new keratinocytes push up, old/dead cells shed off so that the thickness of the epidermis layer is constant

35
Q

What is the blood supply of skin?

A

subpapillary plexus

cutaneous plexus