Week 2 Flashcards
What are the chemical mediators that causes pruritus
PGE2
IL2
Histamine
Substance P
Acetylcholine
What type of nerve transmits the sense of pruritus to the brain
Unmyelinated C fibres
Describe the synergism between PGE2 and histamine
PGE2 reduces the threshold of human skin to histamine evoked itching
Different causes of pruritus
Pruriceptive
Neuropathic
Neurogeic
Psychogenic
What mediates neurogenic cause of itch
Opiates (exogenous or endogenous)
What is pruritoceptive cause of pruritus
When something in the skin that triggers the itch e.g. inflammation / dryness
What is neuropathic cause of pruritus
Damage to central or peripheral nerves causing itch
What is psychogenic cause of pruritus
Psychological causes with no CNS damage
Presentation of acne vulgaris
Non-inflammatory lesions: comedones (open or closed)
Inflammatory lesions: papules, nodules, pustules
Cysts
Scarring
Erythema
Difference between papules and pustules
Papules are solid raised bumps that are not pus filled whereas pustules are
Difference between pustules and cysts
Cysts = multiple pustules joined together to form a larger pus filled cyst
What are open comedones
Blackheads
What are closed comedones
White heads
Cause of acne vulgaris
Increase in sebum production / hyperplasia of sebaceous glands causing occlusion of pores allowing bacterial colonisation hence causing inflammation
What causes hyperplasia of sebaceous glands
Increase in androgens
What is considered as mild acne
Scattered papules, pustules and comedones
What is considered as moderate acne
Numerous papules, pustules
mild atrophic scarring
What is considered as severe acne
extensive inflammatory lesions including nodules, cysts
Significant atrophic scarring
Example of atrophic scarring
Ice pick scarring - small indentations on the skin due to acne
Why does acne mostly appear during puberty
Because during puberty, there is an increase in androgen. Increase in androgens then cause increase in sebum and hyperplasia of sebaceous glands
Describe the distribution of acne vulgaris
Reflects sebaceous glands sites
- face
- back
- chest
Management for mild acne
Topical benzoyl peroxide + topical clindamycin
Or
topical benzoyl peroxide + topical adapalene
Or
Clindamycin + tetrinoin
Management for moderate acne vulgaris
Topical benzoyl peroxide + topical adapalene / Clindamycin + topical tetrinoin / topical benzoyl peroxide + topical clindamycin
Or
Azelaic acid + oral tetracycline
Or
Oral anti-androgen
Examples of topical retinoids
adapalene
isotretinoin
tretinoin
What effect does topical retinoid have on the skin
Drying effect which removes excess sebum
What effect does topical benzoyl peroxide have on the skin
Keratolytic (keratin builds up in acne)
Antibacterial
What are the oral antibiotics used for acne vulgaris
Tetracyclines: doxycycline, Lymecycline
Contraindications for tetracyclines
Pregnancy
Breastfeeding
What are the oral anti-androgens that females can take to treat moderate acne
Oral contraceptive pill
Spironolactone
Why are oral anti-androgens not used in males
Due to feminising effects
Management for severe acne
Oral isotretinoin
What should patients be aware of when taking oral isotretinoin
There will be an initial aggravation of acne before it gets better
Contraindications for oral retinoids
Pregnancy
Liver impairment
Side effects of oral retinoids
Dry mucous membranes
Hair thinning
Hair loss
Headaches
What 2 things should be monitored when taking oral retinoids and why
LFT due to risk of hepatitis
Any changes in mood due to risk of depression
What is rosacea
chronic skin condition causing flushing of the forehead, nose, cheeks and chin
Rosacea is more common in females / males
Females
Rosacea most commonly affects which age group
30-60 years old
Presentation of Rosacea
Facial flushing
Rash
- Erythema
- Papules and pustules
- telangiectasia
- Rhinophyma
What is rhinophyma
Enlarged red nose, a bulb shape
Facial flushing in rosacea can be exacerbated by
Increase in temperature
Alcohol
Spicy foods
Sun exposure
Warm baths
Difference between rosacea and acne
Rosacea is not due to inflammation in pilosebaceous unit
Rosacea does not have comedones
Management for rosacea
Avoid triggers
Use sun protection creams
1. Topical treatment (brimonidine / metronidazole)
2. Oral therapies (tetracycline / isotretinoin if severe)
Laser therapy (for persistent telangiectasia)
Surgery (for rhinophyma)
Describe the topical therapies for rosacea
Topical brimonidine or Ivermectin
Topical metronidazole (antibiotic)
Describe the oral therapies for rosacea
Oral tetracycline
Low dose oral isotretinoin for severe rosacea
Rosacea increases risk for infestation of which organism
Demodex mites infestation at eyelashes
Laser therapy for rosacea is indicated when
Patient has persistent telangiectasia
Complications of rosacea
Rhinophyma
Ocular involvement - conjunctivitis, blepharitis (Gritty eyes)
What are lichen disorders
Conditions characterised by damage to basal epidermis
Differences between lichen planus and psoriasis
Psoriasis is scaly whereas lichen planus isn’t
Psoriasis doesn’t involve the oral cavity whereas lichen planus does
What are the 6 Ps that characterise lesions of lichen planus
very Pruritic
Polygonal
Purple
Planar (flat topped)
Papules or Plaques
Symptoms of lichen planus
6Ps
Very itchy
Oral involvement
Wickham’s striae
Longitudinal ridging of the nails
How does lichen planus affect the mouth
Mucosal ulceration
Wickham’s striae inside of the mouth
What is Wickham’s striae
Lacy white lesions
Oral candida also causes white lesions. How can you differentiate it from Wickham’s lesions in Lichen Planus
The white lesion in Lichen Planus cannot be wiped off
Describe the distribution of lesions in Lichen planus
Flexural distribution - wrists, ankles
Legs
Histological features of lichen planus
Irregular sawtooth acanthosis
Cytoid bodies
Inflammatory cells infiltrate at upper dermis
Orthohyperkeratosis
What is orthohyperkeratosis
Thickening of stratum corneum (outermost layer) with non-nucleated keratinocytes
so this is not parakeratosis because parakeratosis involves retaining the nuclei
Management for Lichen planus
Emollients
Topical steroid
PUVA / UVB phototherapy
Oral steroids if lesions do not resolve after 12 months
What is lichenoid eruption
Lichenoid disorder due to medication
Difference between lichen planus and lichenoid eruption
Lichenoid eruption affects the trunk, it does not have a flexural distribution
Lichenoid eruption does not usually cause Wickham’s striae
Lichenoid eruption is due to a specific trigger - medications
When do symptoms of lichenoid eruption usually occur
2 months after starting a medication
Drugs that commonly causes lichenoid eruption (BA GPT)
Beta blockers
ACEi
Gold
Thiazides
Penicillamine
Management for lichenoid eruption
Discontinue the drug and use alternative
Topical steroids
Emollients
What can cause bullae to form
Burn
Eczema
Herpes infection
Immunobullous disorders
List the 3 immunobullous disorders
Dermatitis herpetiformis
Bullous pemphigoid
Pemphigus Vulgaris
What is the general cause of the immunobullous disorders
Autoimmune disorders causing damage to adhesion mechanisms in the skin
What causes bullous pemphigoid
IgG antibodies attacking the hemidesmosomes that anchor the basal cells to basement membrane
Causes interruption of the dermo-epidermal junction
= the pathology is at the DEJ
Bullous pemphigoid most commonly occur in
Elderly patients
Presentation of bullous pemphigoid
1) Only pruritus before plaques
2) Itchy erythematous plaques and papules
3) Large deep bullae on erythematous base
4) Erosions when blisters burst
Distribution of bullous pemphigoid
Proximal limbs
Trunk
Can be localised
Investigations for bullous pemphigoid
Nikolsky sign - negative
Immunofluorescence
Skin Biopsy
What would immunofluorescence show in bullous pemphigoid
IgG deposition at basal membrane
Dermal papillae (thin top layer of dermis) projecting into bulla
What would immunofluorescence show in bullous pemphigoid
IgG deposition at basal membrane
Dermal papillae (thin top layer of dermis) projecting into bulla
Management of bullous pemphigoid
High potency topical steroids
Oral tetracycline antibiotic
Oral steroids
Immunosuppressive drugs
Which high potency topical steroid is used for bullous pemphigoid
Dermovate
Which oral tetracycline antibiotic is used in bullous pemphigoid
Doxycycline
Lymecycline
Which oral steroid is used for bullous pemphigoid
Oral prednisolone
What should you monitor when giving oral steroids
Glucose level
Blood pressure
Why should you monitor glucose level when giving oral steroids
Because steroids act like glucagon where they increase blood sugar
How should you adjust the dose of oral steroid for bullous pemphigoid
Reduce quickly at first to 15-20mg per day then more slowly afterwards.
Increase the dose if blisters start again then reduce again when blisters resolve
Cause of pemphigus vulgaris
IgG antibodies depositing in epidermis and attacking the desmosomes between keratinocytes in the epidermis causing the cells to separate
= pathology is at epidermis
What is the protein that maintains desmosomal attachments between keratinocytes
Desmoglein 3
Difference between pemphigus vulgaris and bullous pemphigoid (bullous pemphigoiD and pemphiguS)
Bullous pemphigoid pathology is at Dermo-epidermal junction whereas pemphigus vulgaris is within epidermis
Bullous pemphigoid- deep blisters
pemphigus vulgaris- superficial blisters
Bullous pemphigoid Nikolsky’s sign - negative
Pemphigus vulgaris Nikolsky’s sign - positive
Bullous pemphigoid does not affect mucosal membranes whereas pemphigus vulgaris does
Presentation of pemphigus vulgaris
Thin roofed, fragile lesions
Superficial lesions
Raw areas left after blisters burst
Distribution of pemphigus vulgaris
Face
Scalp
Axillae
Groin
Mucosa
Which mucosal membranes are commonly affected by pemphigus vulgaris
Oral mucosa
Eyes
Genitals
What is at an increased risk due to rupture of blisters in pemphigus vulgaris
Infection because the rupture of blisters leave raw areas = ineffective skin barrier
Investigations for pemphigus vulgaris
Nikolsky’s sign
Immunofluorescence
Skin biopsy
Nikolsky’s sign in pemphigus vulgaris is
Positive
Immunofluorescence of pemphigus vulgaris will show
IgG antibodies deposited within the epidermis
Chicken wire appearance
Histology of pemphigus vulgaris
Intra-epidermal blister
Acantholysis
Management of pemphigus vulgaris
Topical steroids
Oral steroids
Immunosuppressive agents
Bullous pemphigoid and pemphigus vulgaris are both part of which type of hypersensitivity
Type 2 - IgG or IgM mediated
What is dermatitis herpetiformis
Autoimmune bullous disorder associated with coeliac disease
Cause of dermatitis herpetiformis
IgA antibodies targeting gluten and causing immune complexes to form in dermal papillae -> triggers inflammation -> sub epidermal blisters
Presentation of dermatitis herpetiformis
VERY itchy lesions
Symmetrical lesions on erythematous base
Distribution of dermatitis herpetiformis
Buttocks
Extensor surfaces - inner elbow, front of knee
Investigations for dermatitis herpetiformis
Serum anti TTG IgA antibodies
Immunofluorescence
Skin biopsy
2% of Coeliac patients have IgA deficiency. How should you test for Coeliac if the patient has IgA deficiency
Do Serum Anti-TTG IgG instead
What would immunofluorescence show in dermatitis herpetiformis
IgA deposits in dermal papillae
What would histology show in dermatitis herpetiformis
Sub-epidermal blisters
Management of dermatitis herpetiformis
Treat Coeliac - gluten free diet
What is photosensitivity
Group of disorders that result from exposure to normal levels of UV light
Cause of photosensitivity
Multifactorial - genetics, environment, skin type
What environmental factors may cause photosensitivity
Use of photosensitive drug
Intensity of UV light
How many skin types are there in Fitzpatrick skin type
6
Which skin type has higher tendency to be photosensitive
Skin type 1
Describe skin type 1
Very fair skin colour
Always burns
Never tans
People with what colour of hair tends to be skin type 1 and why
Red hair
Because those people have less eumelanin and more pheomelanin
2 types of melanin
Eumelanin
Pheomelanin
Which gene controls which melanin is produced
MC1R (Melanocortin 1 receptor gene)
What happens when MC1R is switched on
Switches from producing pheomelanin to eumelanin
Function of pheomelanin
Causes yellowish to reddish colour
Gives pinkish fairer skin type
Does not absorb UV light hence does not protect skin from UV light damage
What is eumelanin
Type of melanin that gives dark pigmentation to skin and hair
Where is pheomelanin most abundant in
Nipples
Lips
Vagina
Glans of penis
Skin and hair (causes red hair and fair skin)
People with type 1 skin colour are at risk of
Skin cancer
Photosensitivity
Describe skin type 6
Black
Never burns
Always tans
What is xeroderma pigmentosum
Genetic condition characterised by extreme photosensitivity
Inheritance pattern of xeroderma pigmentosum
Autosomal recessive
What causes xeroderma pigmentosum
Deficiency in DNA repair mechanism in skin hence unable to repair the DNA damage caused by UV light
Xeroderma pigmentosum increases the risk for
Skin cancer
Severe sunburn
Accelerated photoaging
Ocular damage
Management for xeroderma pigmentosum
Sun avoidance and protection
Vitamin D supplements
Life expectancy for patients with xeroderma pigmentosum
Teenage - young adults
Most die young due to skin cancer
What is porphyria
Group of photosensitivity disorders resulting from defects in enzymes required to produce adequate amount of haem or unable to break down porphyrin resulting in accumulation of porphyrins
Porphyrin is required in
Haemoglobin
Conditions in porphyria
Porphyria Cutanea Tarda
Erythropeotic protoprophyria
Porphyria Cutanea tarda is caused by deficiency in ___ causing ____
Uroporphyrinogen decarboxylase enzyme causing accumulation of uroporphyrinogen
What factors can cause deficiency in uroporphyrinogen decarboxylase hence PCT
Genetics
Alcohol (50% case)
Oestrogen replacement
Symptoms of PCT
Painful blisters on sun exposed sites
Scarring and Hyperpigmentation after blisters heal
Hypertrichosis
What is hypertrichosis
Excessive hair growth
Where is hypertrichosis mainly seen in PCT
Top of cheeks
Where are symptoms of PCT commonly seen
Dorsum of hands
PCT is associated with which conditions
Hepatitis
Alcohol abuse
Haemochromatosis
Investigations for PCT
Urinary porphyrin
Skin biopsy
Management for PCT
Sun avoidance
Treat hepatitis / alcohol misuse/ haemochromatosis
Stop oestrogen replacement therapy / find alternative
What causes erythropeotic protoporphyria
Ferrochelatase deficiency causing accumulatino of protoporphyrin IX
Inheritance pattern of erythropeotic protoporphyria
Autosomal dominant
Erythropeotic protoporphyria most commonly seen in
Children
Symptoms of erythropeotic protoporphyria
Burning and itching with sun exposure
Child screaming when out in the sun
What is seborrheic dermatitis
dermatitis affecting areas of skin rich in sebaceous glands
Cause of seborrheic dermatitis
inflammatory reaction to the proliferation of Malassezia furfur (a yeast normally found on the skin.)
Risk factors for seborrheic dermatitis
Family history
Oily skin
Immunosuppression (such as HIV)
Neurological and psychiatric diseases (such as Parkinson’s Disease or Depression)
Stress
Presentation of seborrheic dermatitis
Greasy, flaky scales
Ill defined margins
Erythematous base
Where does seborrheic dermatitis usually present on
nasolabial folds
posterior auricular skin
scalp
The distribution of seborrheic dermatitis reflects
sebum rich areas
What is a term used to describe mild seborrheic dermatitis
Dandruff
Management of seborrheic dermatitis
Zinc Pyrithione shampoo
Ketoconazole shampoo or cream
Short course of topical corticosteroid
What is the other term for infantile seborrheic dermatitis
Cradle cap
Presentation of infantile seborrheic dermatitis
diffuse, yellow, greasy scales
No underlying erythema
Where is infantile seborrheic dermatitis most commonly found on
Scalp
management of infantile seborrheic dermatitis
topical emollient, commonly olive oil
scales are brushed off gently
use normal baby shampoo
