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J3 > Huid > Flashcards

Huid Flashcards

1
Q

Functions of the skin

A

1) Protection - barrier (physical and immunological)
2) Regulation - body temperature, fluid balance, vit D
3) Sensation - heat, cold, touch, and pain. Network of nerve cells detect and relay changes in the environment

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2
Q

What are the layers of the epidermis?

A
  • Stratum corneum
  • Stratum Lucidum
  • Stratum Granulosum
  • Stratum Spinosum
  • Stratum Basale

• Basement membrane

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3
Q

In which layer of the epidermis is filaggrin found?

A

stratum corneum

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4
Q

Embryology of the skin

A

Epidermis is derived from the ectoderm

5th week - skin of the embryo is covered by simple cuboidal epithelium

7th week - single squamous layer (periderm), and a basal layer

4th month - an intermediate layer, containing several cell layers, is interposed between the basal cells and the periderm

Early foetal period - the epidermis invaded by melanoblasts, cells of the neural crest origin

Hair- 3rd month as an epidermal proliferation into dermis.

Cells of the epithelial root sheath proliferate to form a sebaceous gland bud.

Sweat glands develop as down growths of epithelial cords into dermis.

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5
Q

Where in the skin are Langerhans cells found?

A

basal layer

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6
Q

How does skin allergy develop?

A

Skin irritation can be nonallergenic or allergenic

Irritation by nonallergenic and allergenic compounds induces Langerhans cell migration and maturation

Langerhans cells migrate from epidermis to draining lymph nodes

Initial sensitization takes 10-14 days from initial exposure to allergen (nickel, dye, rubber etc.)

This is why there may be no response on initial exposure to an allergen

Once an individual is sensitized to a chemical, allergic contact dermatitis can then develop within hours of repeat exposure

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7
Q

Damaging effects of ultraviolet light on skin:

A

1) direct cellular damage
• Photoaging
• DNA damage
• Carcinogenesis

2) alterations in immunologic function.
• P53 TSGs are mutated by DNA damage
• implicated in development of (non-) melanoma skin cancers

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8
Q

What are effects of Chronic UV exposure?

A
  • loss of skin elasticity
  • fragility
  • abnormal pigmentation
  • haemorrhage of blood vessels - bruising/fragility
  • Wrinkles and premature ageing
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9
Q

Merkel cells

A

Located at the base of the epidermis

respond to sustained gentle and localised pressure

remember: MerkeL respond to Localised pressure

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10
Q

Meissner corpuscles

A

situated immediately below epidermis

particularly well represented on the palmar surfaces of the fingers and lips

especially sensitive to light touch (cotton-wool type sensation)

remember: • MeiSSner respond to Soft (light) touch

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11
Q

Ruffini’s corpuscles

A
  • situated in the dermis
  • sensitive to deep pressure and stretching

remember: RUFFini corpuscles respond to “rough” (deep) pressure

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12
Q

Pacinian corpuscles

A

mechanoreceptors present deep in the dermis

sensitive only to deep touch, rapid deformation of skin surface and around joints for position/proprioception

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13
Q

Macule

A
  • Flat area of the skin that is abnormal

* area of skin discoloration

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14
Q

Papule

A

• A circumscribed, elevated, solid lesion

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15
Q

Pustule

A
  • Papule containing purulent material

* i.e. raised and full of puss

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16
Q

Plaque

A

elevated, superficial, solid lesion, greater than 1 cm in diameter

Raised, tends to be big

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17
Q

Vesicle

A
  • Papule containing serous fluid

* i.e. a tiny blister

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18
Q

Bulla

A

A raised, circumscribed lesion greater than 0.5 cm that contains serous fluid.

I.e. a giant blister

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19
Q

Erythema

A

superficial reddening of the skin, usually in patches

result of injury or irritation causing dilatation of the blood capillaries

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20
Q

Ulceration

A

loss of the epidermis

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21
Q

Aetiology of acne

A

Androgens increase sebum production and viscosity

Lining of the hair follicles and sebaceous (oil) glands gets blocked by keratin and sebum build up

This causes narrowing

P. acnes bacteria on the skin thrives on trapped sebum
It invades into the oil glands causing a characteristic spot

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22
Q

Diagnosis of acne

A

Diagnosis of acne requires a mixture of all three of:
• Papules
• Pustules
• Erythema

May also have:
• Comedones (black heads/white heads)

Markers of much more severe disease:
• Nodules
• Cysts
• Scarring

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23
Q

Distribution of acne

A
  • Face – most common area
  • Chest
  • Back / Shoulders – more common in males
  • Occasionally legs, scalp
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24
Q

Acne subtypes

A

Acne vulgaris
• Papulopustular
• Nodulocystic
• Comedonal

Steroid induced – more truncal distribution than face

Acne fulminans – dermatological emergency

Acne rosacea – tends to affect adults

Acne Inversus (Hidradenitis suppurativa) - Papules, pustules and cysts on the groin, buttocks and other areas

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25
Q

How do you grade the severity of acne?

A

Leeds grading system, grades 1 to 12

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26
Q

Treatment of acne

A

Reduce plugging
• Topical retinoid
• Topical benzoyl peroxide

Reduce bacteria
• Topical antibiotics (erythromycin, clindamycin)
• Oral antibiotics (tetracyclines, erythromycin)
• Benzoyl peroxide reduces bacterial resistance

Reduce sebum production
• Hormones – anti-androgen i.e. Dianette / OCP
• Changes the viscosity of the oil produced and also leads to less sebum production

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27
Q

Oral isotretinoin

A

Roaccutane

  • Oral retinoid for severe acne vulgaris
  • Concentrated vitamin A
  • Reduces sebum, plugging and bacteria
  • Remission of acne in around 80% teenagers
  • Standard course for 16 weeks
Multiple side effects – most are trivial
•	Dry lips
•	nose bleeds
•	dry skin
•	myalgia 
Serious side effects
•	Deranged LFTs
•	Raised lipids
•	Mood disturbance 
•	Teratogenicity - pregnancy prevention programme
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28
Q

Keloid scarring

A

• Overgrown scar tissue

Causes:
• Physical trauma
• Burns
• Hugely exaggerated scars as a result of acne

Cannot be reversed

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29
Q

Which two pathways lead to the development of skin cancer?

A

Direct action of UV on target cells (keratinocytes) for neoplastic transformation via DNA damage

Effects of UV on the host’s immune system

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30
Q

What is the most common type of skin cancer?

A

basal cell carcinoma

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31
Q

Which gene mutation may predispose to BCC?

A

PTCH gene mutation may predispose to BCC (pronounced ‘patch gene’)

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32
Q

Basal cell carcinoma subtypes

A
  • Nodular
  • Superficial
  • Pigmented
  • Morphoeic
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33
Q

Nodular Basal cell carcinoma

A
  • Nodule i.e. raised lesion ( > 0.5cm)
  • Rolled shiny margin
  • Shiny “pearly”
  • Telangectasia (broken blood vessels)
  • Often ulcerated centrally
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34
Q

Superficial Basal cell carcinoma

A
  • No raised nodular appearance
  • Rolled shiny margin
  • Broken blood vessels
  • Usually doesn’t ulcerate
  • Indolent superficial spread
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35
Q

Pigmented Basal cell carcinoma

A
  • Rolled shiny margin
  • Telangiectasia
  • Ulceration
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36
Q

Treatment – Basal cell carcinoma

A

Gold standard – Surgical excision with an adequate margin

3-4mm margin of normal looking skin

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37
Q

Squamous Cell Carcinoma

A
  • Originates from keratinocytes
  • 2nd commonest skin cancer

Appearance:
• keratin – crusty
• no rolled shiny margin
• inflamed, but no specific blood vessels
• no area of skin ulceration unless very aggressive

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38
Q

Pre-malignant variants of Squamous Cell Carcinoma

A
  • actinic keratoses

* Bowens disease = SSC in situ

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39
Q

Treatment – Squamous cell carcinoma

A
  • Gold standard - Surgical excision
  • 4-5mm margin due to risk of metastasis
  • Curettage and cautery in elderly patients
  • Symptomatically debulk the tumour
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40
Q

management of Pre-malignant skin lesions

A

• Topical imiquimod / 5-fluorouracil cream

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41
Q

Malignant melanoma

A
  • Malignant tumour of melanocytes
  • Most common in skin (but can be bowel/eye)
  • Accounts for 75% of deaths from skin cancer
  • Often affects young, fit people – hard to diagnose

Depth of tumour penetration into skin at presentation determines prognosis

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42
Q

Spread of malignant melanoma

A

Metastatic spread is via lymphatics, but rarely can spread haematogenously or along the skin

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43
Q

Risk factors for development of malignant melanoma

A 
family history
UV irradiation
sunburns during childhood
high SE status
intermittent burning in fair unacclimatised skin
skin type I/II
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44
Q

what determines melanoma prognosis?

A

Breslow depth score

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45
Q

Subungual melanoma

A

under the nail (nailbed is skin)

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46
Q

Acral melanoma

A
  • Affects hands and feet
  • Tend to present late
  • Poor prognosis
  • More common in darker skin types
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47
Q

Lentigo maligna

A

• melanoma in situ lesion on sun-damaged skin

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48
Q

Melanoma treatment

A

Surgical excision:
• (Breslow < 1mm) – 1cm margin
• (Breslow > 1mm) – 2cm margin

If metastatic:
• Chemotherapy
• isolated limb perfusion

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49
Q

Biologic therapies for melanoma

A
  • Immunotherapy (ipilimumab)
  • Immune checkpoint/MEK inhibitors
  • antibodies to BRAF genetic defects (vemurafenib)
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50
Q

Name 2 Cutaneous tumour syndromes

A

Gardner Syndrome – soft tissue tumours, polyps, bowel ca

Cowden’s Syndrome – multiple hamartomas thyroid, breast ca

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51
Q

Eczema

A

= Dermatitis - inflammation of the skin

Inflammation in eczema is primarily due to inherited abnormalities in skin “barrier defect”, causing increased permeability and reduces its antimicrobial function

An inherited abnormality in filaggrin expression is considered a primary cause of disordered barrier function.

The gene for filaggrin is on Chromosome 1

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52
Q

what is filaggrin?

A

Filaggrins are filament-associated proteins which bind to keratin fibres in the epidermal cells.

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53
Q

Types of eczema

A

Endogenous
• Atopic eczema – classical type
• Seborrhoeic eczema
• Varicose eczema

Exogenous (external irritants to the skin)
• Contact (allergic, irritant)
• Photoreaction (allergic, drug)

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54
Q

Atopic eczema

A
  • Itchy inflammatory skin condition
  • Yellow crusting suggests a secondary bacterial infection
Associated with atopic conditions:
•	Asthma
•	allergic rhinitis 
•	conjunctivitis 
•	hay fever
  • high IgE levels
  • Genetic and immune aetiology
  • 10% of infants affected
  • Remission occurs in majority by 15 years
  • 2/3 have a family history of atopy
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55
Q

Infant atopic eczema

A
  • Itchy
  • occasionally vesicular (small blisters)
  • often facial component
  • secondary infection (yellow crusting)
  • < 50% still have eczema by 18 months

occasionally aggravated by food (i.e. milk, eggs, wheat) unlike in adult eczema

Symmetrical distribution

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56
Q

complications of infant atopic eczema

A
  • Growth reduction
  • Psychological impact
  • Bacterial infection due to broken skin
  • Viral infection
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57
Q

Management of infant atopic eczema

A

Emollients – ‘reseal’ the skin with a protective film

Topical steroids – targets the inflammatory component

Bandages, antihistamines (sedative) – to prevent scratching

Antibiotics / antivirals (if prone to HSV/eczema herpeticum)

Education for parents and child – specialised eczema nurses

Avoidance of exacerbating factors

Systemic drugs – immune modifications. Very potent drugs
• Ciclosporin
• Methotrexate

Newer biological agents
• Dupilumab – IL-4/IL-13 blocker

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58
Q

Contact dermatitis

A

Precipitated by an exogenous agent

Two types:
• Irritant - direct noxious effect on skin barrier
• Allergic - Type IV hypersensitivity reaction. Immune system is sensitised and reaction occurs on repeated exposure

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59
Q

Common allergens causing contact dermatitis

A

Nickel - Jewellery, zips, scissors, coins, door handles

Fragrance - Cosmetics, creams, soaps

Chromate - Cement, tanned leather

Cobalt - Pigment

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60
Q

Seborrhoeic Dermatitis

A
  • Chronic, scaly inflammatory condition
  • Often thought to be “dandruff”
  • Face, scalp, and eyebrows
  • Overgrowth of Pityrosporum Ovale yeast. Natural commensal organism. Thrives on oily parts of the skin
  • Can be worse in teenagers
  • Identifying illness for HIV
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61
Q

Management of Seborrhoeic Dermatitis

A

Scalp - medicated anti yeast shampoo

Face - anti-microbial, mild steroid

Simple moisturizer

Often improves with UV/sunlight

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62
Q

Venous dermatitis

A

Underlying venous disease causing incompetence of deep perforating veins

This leads to increased hydrostatic pressure

Skin gradually starts to stretch out, and ultimately this causes inflammation and external dermatitis

Symmetrical

Usually in the area with the most gravitational pressure - affects lower legs

Brown discolouration due to haemosiderin deposition

Can cause areas of superficial ulceration

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63
Q

Management of Venous dermatitis

A

Emollient

Mild/moderate topical steroid to target inflammation

Compression bandaging / stockings – to target the valve issues/gravitational effects

Consider venous surgical intervention

64
Q

Psoriasis

A

a chronic relapsing and remitting scaling skin disease

may appear at any age and affect any part of the skin

common on the lower back

Age onset often two peaks:
• Early onset 20-30y
• Late onset 50-60y

65
Q

psoriasis pathophysiology

A

T cell mediated autoimmune disease

Abnormal infiltration of T Cells causes release of inflammatory cytokines

Inflammation causes increased keratinocyte proliferation
This is what causes the skin to become scaly and build up (turnover is too fast)
- Inflammation is what causes the redness

Environmental and genetic factors

66
Q

Koebner phenomenon

A

formation of psoriatic skin lesions on parts of the body that aren’t typically where a person with psoriasis experiences lesions

Can appear at the sites of trauma/scars

67
Q

Auspitz’s sign

A

the appearance of punctate bleeding spots when psoriasis scales are scraped off

68
Q

Plaque psoriasis

A

Most common type of psoriasis

Appearance:
	salmon pink
	well-demarcated
	scaly on top
	symmetrical

Changes seen in the nails:
 Onycholysis - nail end lifts off due to plaques underneath the nail
 Nail pitting
 Dystrophic nails

psoriatic arthritis

69
Q

Guttate psoriasis

A
  • Teardrop/raindrop shape
  • Comes on very quickly, often in unwell patients
  • Can be triggered by infection (e.g. streptococcal throat infection)
70
Q

pustular psoriasis

A
  • Very inflammatory
  • Acute presentation
  • Pustules are not infective, but markers of acute inflammation
71
Q

Treatments for psoriasis

A

In order of increasing effectiveness (and toxicity)
• Topical therapies - moisturisers, steroids
• Phototherapy light treatment
• Acitretin
• Methotrexate
• Ciclosporin

• Biologic therapies

72
Q

Ultraviolet Phototherapy

A

Non-specific immunosuppressant therapy to the skin
• Eczema
• Acne
• Seborrhoeic dermatitis

  • Can reduce T cell proliferations
  • Decreases release of inflammatory cytokines

• Encourages Vitamin D (reduces skin turnover)

UV-B light most commonly used – less damaging

73
Q

List some commensal organisms of the skin

A
  • Coagulase negative staphylococci
  • Corynebacterium sp.

In areas of skin with less acidic pH:
• Staphylococcus aureus
• Streptococcus pyogenes

Usually not Gram negative bacteria or anaerobic organisms

NB: Anaerobe P. acnes dwells in sweat and sebacious glands

74
Q

Most common organisms causing bacterial skin infection

A
  • Staphylococcus aureus

* Group A streptococcus

75
Q

Impetigo

A

Golden encrusted skin lesions with inflammation localised to the dermis.

Most common in children

Highly contagious and may occur in small outbreaks

Caused by S. aureus; usually mild and self limiting

Can treat with topical fusidic acid or topical mupiricin
Usually not severe enough to require oral or systemic antibiotics

NB: Staphylococcus aureus classically crusts

76
Q

how do bacterial and fungal infections of the skin differ?

A

bacterial infections cause much more inflammation than fungal infections
• Redder
• Hotter
• Erythematous

Fungal infections tend to be less red and not too painful to touch

77
Q

Tinea

A

Superficial fungal infection of the skin or nails

Very common, particularly on the feet

Demarcated appearance, but appears to be spreading

78
Q

Diagnosis and treatment of tinea

A

Diagnosis can be made on skin scrapings

Treatment with topical therapy in non-severe cases involving skin alone: terbinafine cream

Systemic therapy in severe cases and those involving hair/nails:
• Terbinafine or itraconazole

Fungal nail infections may require an extended period of oral antifungal therapy

79
Q

Soft tissue abscess

A

Infection within the dermis or fat layers with development of walled off infection and pooled pus

Best treatment for abscess is always surgical drainage
because antibiotics cannot penetrate abscesses very well

Antibiotics not usually required if abscess fully drained and no surrounding cellulitis

Same causative organisms as cellulitis
• Staph aureus
• Group A strep

80
Q

Panton valentine toxin

A

Virulence factor (cytotoxin) carried by some Staphylococcus aureus

Association with recurrent soft tissue boils and abscesses

Transmissible – outbreaks occur in families and others living closely together

81
Q

Cellulitis

A

Infection involving dermis

Usually caused by β-haemolytic streptococci (Gp A Strep most common) and S. aureus

Most commonly begins on the lower limbs

Often tracks through the lymphatic system and may involve localised lymph nodes

May be associated with systemic upset although bacteraemia is relatively uncommon

82
Q

Classification of cellulitis

A

Enron Classification:

I. Patient not systemically unwell and no significant co-morbidites (i.e. diabetes)

a) <48h antibiotic therapy
b) failure to respond to >48h antibiotic therapy

II. Patient systemically unwell or has significant co-morbidities which may delay resolution of infection

III. Patient has significant systemic upset or unstable co-morbitidies that will interfere with response to treatment

IV. sepsis or life threatening complications

83
Q

Streptococcal Toxic Shock

A

Caused by toxin producing Group A Streptococcus

Primary infection is typically within the throat or skin/soft tissue

Patients present with localised infection (not necessarily severe), fever and shock

Exotoxins cause massive immune stimulation and cytokine cascade causes blood vessel dilation –> patients often present with a diffuse, faint rash over body/limbs

84
Q

Necrotising fasciitis

A

Immediately life threatening soft tissue infection with deep tissue involvement

Rapidly progressive (within hours) with extensive tissue damage requiring extensive surgical debridement

85
Q

Signs/symptoms of necrotising fasciitis

A
  • Rapidly progressive
  • Pain out of proportion to clinical signs
  • Severe systemic upset
  • Presence of visible necrotic tissue
86
Q

Antimicrobial treatment of necrotising fasciitis

A
  • Flucloxacillin
  • Benzylpenicillin
  • Gentamicin
  • Metronidazole
  • Clindamycin

Remember: Fight Back GMC

NB: Antibiotics are no substitute for surgical intervention

87
Q

Cellulitis differential diagnosis

A
  • DVT
  • Thrombophlebitis
  • Lyme disease
88
Q

PWID soft tissue infections

A

Often present late with neglected soft tissue infection

Staphylococcus aureus predominates but infections often polymicrobial

High rates of bacteraemia and disseminated infection

Triad of:
• S. aureus bacteraemia
• DVT
• multiple pulmonary abscesses

Often have endocarditis
Must offer BBV testing

89
Q

Urticaria (hives)

A
  • Itchy, wheals (hives) - red, raised, itchy bumps
  • Lesions last <24 hours
  • Non-scarring

Immune-mediated
– type 1 allergic IgE response

Non-immune-mediated
– direct mast cell degranulation
– e.g. opiates, antibiotics, contrast media, NSAIDs

90
Q

Morbilliform rash

A

measles-like rash (red macular rash)

91
Q

Fixed drug rash

A

causes a rash in a specific place every time you take a drug

can be caused by paracetamol

92
Q

Which drugs commonly cause angioedema?

A

ACEi

93
Q

Which drugs commonly cause photo-toxic drug rash?

A

• Affects areas exposed to UV light

Systemic reaction between absorbed drug that has leaked into the skin and UV light

– Tetracyclines
– Isotretinoin (roaccutane)
– Quinine
– bendroflumethiazide

94
Q

What can cause a Pustular drug rash?

A

antibiotics

95
Q

Lichenoid rash

A
  • Purply itchy rash
  • Looks similar to the rash “Lichen planus”
  • Can be drug-induced
  • Tends to have a white network pattern on top
96
Q

COMMON EXAM QUESTION

what is a drug trigger for psoriasis?

A

Lithium, Beta blockers

rash that resembles the plaquelike erythematous lesions of psoriasis (Psoriasis–like)

Well demarcated pink erythema with scale

Sudden onset, no FHx

97
Q

Name two Drug induced Blistering disorders

A

– Steven Johnson Syndrome

– Toxic epidermal necrolysis

98
Q

Name two Immunobullous diseases

A

– Bullous pemphigoid
– Pemphigus

immunobullous conditions are characterised by pathogenic autoantibodies directed at target antigens whose function is either cell-to-cell adhesion within the epidermis or adhesion of stratified squamous epithelium to the dermis

target antigens are components of desmosomes or the functional unit of the basement membrane

screen for underlying malignancy – immunobullous diseases can be associated with malignancy

99
Q

Stevens Johnson Syndrome

A
  • Blistering condition
  • Often affects mucosal areas
  • Some blistering on skin possible
  • Can have haemorrhagic crusting on the lips

NB: If < 10% skin involvement, it is SJS not Toxic epidermal necrolysis

100
Q

Toxic epidermal necrolysis (TEN)

A

Much more extensive than SJS

Looks like a 3rd degree burn, skin becomes necrotic and essentially falls off

Dermatological emergency

Majority of cases are drug induced

If < 10% skin involvement, it is SJS not TEN
>10% of skin involvement = TEN

Common cause of mortality is secondary sepsis

101
Q

Staphylococcal scalded skin syndrome

A

Characterised by red blistering skin that looks like a burn or scald

caused by the release of exotoxins from S. aureus

Not very systemically unwell
No mucosal involvement
Generalized redness and some peeling

102
Q

Erythema multiforme

A

hypersensitivity reaction usually triggered by infections, most commonly HSV

presents with a skin eruption characterised by typical Target lesions

acute and self-limiting

103
Q

which skin condition is characterised by target lesions?

A

Erythema multiforme

104
Q

Bullous pemphigoid

A

Autoimmune pruritic skin disease

preferentially affects elderly people

formation of blisters (bullae) at the space between the epidermis and dermis skin layers.

classified as a type II hypersensitivity reaction, with the formation of anti-hemidesmosome antibodies

105
Q

Pemphigus

A

More severe than bullous pemphigoid

Pemphigus is unique from pemphigoid in that the blistering can involve the mucous membranes as well as skin.

causes blisters that slough off and turn into sores
– Sheared pattern
– Superficial split (pemphigus)

Autoantibodies to various skin components
– i.e. basement membrane proteins in BP

106
Q

Dermatitis herpetiformis

A

(coeliac disease)

Tiny blisters on elbows, knees and buttocks (extensor surfaces)

Topical steroids to treat autoimmune component

Gluten free diet

Oral dapsone

107
Q

Causes of Acute urticaria

A
  • Unknown
  • Viral infections
  • Medication
  • Foods
  • Physical stimulants
108
Q

Erythroderma

A
  • Descriptive term
  • erythema with >80-90% involvement
Causes: 
–	Psoriasis
–	Eczema
–	Drug reaction
–	Cutaneous lymphoma (unusual)
–	others

Treat underlying skin disorder

109
Q

Acute generalized exanthematous pustulosis (AGEP)

A

also known as pustular drug eruption / toxic pustuloderma

rare skin reaction

related to medication administration in 90% of cases

characterized by sudden skin eruptions (numerous sterile pustules)

appear on average five days after medication is started

110
Q

What kinds of systemic disease can manifest with skin changes?

A 
o	Endocrine disease
o	Internal malignancy
o	Nutritional deficiency
o	Systemic infection
o	Systemic inflammatory disease
111
Q

Thyroid dermopathy

A

= pretibial myxoedema

Seen in Grave’s disease

an infiltrative dermopathy

most commonly seen on the shins (pretibial areas)

characterised by swelling and lumpiness of lower legs.

112
Q

Thyroid acropachy

A

Seen in Grave’s disease

extreme manifestation of autoimmune thyroid disease.

presents with finger clubbing, swelling of digits and toes, and periosteal reaction of extremity bones.

almost always associated with ophthalmopathy and thyroid dermopathy

113
Q

Necrobiosis lipoidica

A

Seen in diabetes

waxy appearance

yellow discolouration

often localized to bilateral shins

occasionally ulcerates and scars (“shopping trolley distribution” – the area where a shopping trolley would hit) if chronic or with trauma

114
Q

Diabetic dermopathy

A

The lesions are asymptomatic

red crusted papules

occur on the shins of patients with diabetes.

115
Q

which skin condition is described as having a “Woody texture” and what disease is it associated with?

A

Scleredema (NB: not scleroderma)

associated with diabetes

116
Q

Which skin condition may be a marker as a precursor to diabetes?

A

Granuloma annulare

117
Q

Possible skin manifestations of Cushings syndrome/steroid excess

A

Acne – disproportionate aggressive acne, particularly on the trunk

Striae

Erythema – generalized redness

Gynaecomastia

Global skin atrophy –> easy bruising

118
Q

Possible skin manifestations of Addison’s disease /steroid insufficiency

A

Hyperpigmentation – distinctive bronze discoloration
o Seen in palmar creases and old scars
o Areas of increased skin markings e.g. over extensor surfaces of knees

Acanthosis nigricans

119
Q

Possible skin manifestations of testosterone excess and conditions/treatments that may cause this.

A
  • Acne
  • Hirsutism – male pattern

e.g.
Polycystic Ovarian Syndrome
Testicular tumours
Testosterone drug therapy – e.g. topical androgen gels

120
Q

Possible skin manifestations of progesterone excess and conditions/treatments that may cause this.

A
  • Acne
  • Dermatitis

E.g.
o Congenital adrenal hyperplasia
o Contraceptive treatment

121
Q

list 3 Cutaneous Signs of Internal Malignancy

A
  • Necrolytic migratory erythema
  • Erythema gyratum repens
  • Acanthosis nigricans
122
Q

Which skin condition is strongly associated with glucagonomas?

A

Necrolytic Migratory Erythema

Red, blistering rash that spreads across the skin. Haphazard, irregular plaques

particularly affects the skin around the mouth and distal extremities
o Erythematous
o scaly plaques on acral (peripheral body parts), intertriginous (where two skin areas may touch or rub together), and periorificial areas

123
Q

Which skin condition presents with a whorled woodgrain pattern? What kind of systemic disease is it associated with?

A

Erythema Gyratum Repens

Significant disproportionate itch and peripheral eosinophilia

Strong association with solid organ malignancy, especially lung cancer

124
Q

Which skin condition is strongly associated with uterine/ovarian tumours?

A

Sister Mary Joseph Nodule

originates from the umbilicus

125
Q

Describe the cutaneous features associated with Vitamin B Deficiencies

A

B6 - pyridoxine
• Dermatitis (disproportionate)

B12 - cobalamin
• Angular chelitis

B3 - niacin
• Pellagra (dementia, dermatitis, diarrhoea)

126
Q

Describe the cutaneous features associated with zinc Deficiency

A

Acrodermatitis Enteropathica

autosomal recessive

caused by mutations in the gene that encodes a membrane protein that binds zinc

In infants, deficiency can follow breast-feeding, when breast milk contains low levels of zinc

In adults, disease can occur with:
o	total parenteral nutrition without zinc supplements
o	alcoholism
o	malabsorption states 
o	inflammatory bowel disease 
o	bowel surgery
127
Q

Describe the cutaneous features associated with Vitamin C Deficiency

A 
Scurvy
•	Punctate purpura / bruising
•	“Corkscrew” spiral curly hairs 
•	Patchy hyperpimentation
•	Dry skin
•	Dry hair
•	Non-healing wounds
•	Inflamed gums
128
Q

Erythema nodosum

A

inflammatory condition

characterized by inflammation of the fat cells under the skin, resulting in tender red nodules or lumps

usually seen on both shins

causes severe pain

Underlying causes:
•	Streptococcal infection
•	Pregnancy 
•	Sarcoidosis
•	Drug induced
•	Bacterial / Viral infection
129
Q

Pyoderma gangrenosum

A

condition that causes tissue to become necrotic, causing deep ulcers that usually occur on the legs.

Ulcers usually initially look like small bug bites or papules, and they progress to larger ulcers.

Often affects the shins
• Central area of ulceration with purple rim
• “Overhanging” edge

Associated with:
• Inflammatory Bowel Disease
• Rheumatoid arthritis
• Myeloma

130
Q

Which conditions are associated with pyoderma gangrenosum?

A
  • Inflammatory Bowel Disease
  • Rheumatoid arthritis
  • Myeloma
131
Q

Which conditions are associated with Generalised hair thinning?

A

o B12 deficiency
o Iron deficiency
o lupus
o hypothyroidism

132
Q

What kind of conditions cause nail clubbing/nail fold telangectasia?

A 
Connective tissue diseases 
	RA
	SLE
	scleroderma
	dermatomyositis
133
Q

differential diagnosis of chronic, red scaly skin

A

eczema
psoriasis
Seborrheoic dermatitis

134
Q

Urticaria

A

Condition caused by the abnormal release of histamine within the skin

Not normally the result of allergy

135
Q

Urticaria presentation

A

characterized by blanching, raised, palpable wheals (hives)

can vary in shape

occur on any skin area; usually transient and migratory.

lesions are often separated by normal skin, but may coalesce rapidly to form large areas of erythematous,
raised lesions that blanch with pressure.

Dermographismmay occur (urticarial lesions resulting from light scratching)

136
Q

Urticaria precipitants

A 
 Heat/cold
 pressure
 exercise
 sunlight
 emotional stress
 chronic medical conditions (hyperthyroidism, RA, SLE)
137
Q

Urticaria treatment

A

Mainstay – antihistamines. Higher dose than hayfever

 Cetirizine
 Fexofenadine
 Loratidine
 Chlorpheniramine
 Hydroxyzine
138
Q

Urticaria - Differential Diagnoses

A
  • Allergic Contact Dermatitis
  • Atopic Dermatitis
  • Erythema Multiforme
139
Q

Risk factors for leg ulceration

A

o obesity
o smoking
o hypertension
o history of deep vein thrombosis

140
Q

venous ulcers

A

usually in gaiter area

caused by sustained venous HTN due to venous insufficiency (e.g. varicose veins, pregnancy, trauma)

RBC pushed out of capillaries due to HTN -> haemosiderin deposition from RBC breakdown

can develop venous eczema due to irritation of the skin by waste products leaking from the blood

Tends to be less painful than arterial, usual more superficial and diffuse with more surrounding skin
changes

141
Q

Arterial ulcers

A

result of reduced arterial blood flow/tissue perfusion.

Atherosclerosis or peripheral vascular disease is the most common cause

if left untreated, can cause death of tissue

Ulcer development is often rapid with deep destruction of tissue.

limb looks pale and there is a noticeable lack of hair.

Capillary refill is reduced; pedal pulses weak or absent.

classically look punched out and deep

142
Q

What would be the most important initial investigation in a patient with a leg ulcer?

A

Ankle Brachial Pressure Index ABPI (blood pressure comparison between upper and lower limbs)

should be roughly equal

0.8 ratio might suggest occlusion and need vascular arterial assessment

NB: Compression bandages are used for venous ulcers
If a patient has arterial disease with occlusion, compression bandages will worsen the supply to the
distal limbs, which will cause ischaemic disease

143
Q

What initial treatment would you suggest for a venous leg ulcer?

A

compression bandages

emollient, topical steroid, avoidance of irritant soaps

Topical steroid

144
Q

Name some other causes for leg ulceration

A 
 Arterial disease
 Connective Tissue Disease ie Lupus
 Diabetic
 Pressure sores
 Skin cancer – eg basal cell ca
 Infection, deep fungal
 Trauma
 Necrobiosis lipoidica
 Drug induced 
 Pyoderma gangrenosum
145
Q

How would you confirm a diagnosis of malignant melanoma?

A

full excision of the whole lesion for diagnostic biopsy and histology

146
Q

Breslow thickness

A

distance in mm of the furthest tumour cell from the basal layer of the epidermis

prognostic tool for malignant melanoma

147
Q

Prognostic factors in melanoma

A

 Size of presenting lesion
 depth of clinical pigmentation (Blue / grey colours)
 Anatomical location (e.g. poor prognosis for late presentation acral melanoma e.g. sole foot
 Evidence of clinical ulceration
 Evidence of resorption e.g. regression
 Obvious local metastases / satellites (eg in transit)

148
Q

Assessment of a pigmented lesion

A 
A - asymmetry
B - border
C - colour
D - diameter
E - evolution
149
Q

treatment options for melanoma

A

Surgical excision with wide local excision - margin based on Breslow thickness 1cm margin Breslow <1mm

Lymph node dissection if LN involved

Chemotherapeutic agents e.g. BRAF inhibitors
o Vemurafenib

Immunotherapy e.g. nivolumab, ipilimumab

150
Q

Non scarring hair loss - 4 examples

A

 alopecia areata
 telogen effluvium (hair cycle disorder)
 Drug induced, e.g. Chemotherapy
 anorexia / vitamin deficiency

151
Q

scarring hair loss - 4 examples

A

 discoid cutaneous lupus
 fibrosing alopecia
 lichen planus
 fungal infection

152
Q

Localised hair loss causes

A

 alopecia areata

 fungal infection

153
Q

Alopecia Areata

A

autoimmune disease that causes hair to fall out in round patches

Immune phenomenon against hair follicles and follicular melanocytes (regrowth will be white)

 Alopecia Totalis (whole scalp hair loss)
 Alopecia Universalis (whole body hair loss)

154
Q

treatment options for the management of alopecia areata

A

Super potent topical corticosteroid

Intralesional corticosteroid injections

High dose oral corticosteroids (in very rapid onset progressive AA)

Allergic contact immunotherapy
o Induces contact dermatitis
o This makes the immune system distracted from the hair follicle, and allows the hair to grow

biologic agents eg Jak2 Inhibitors

155
Q

Some causes of hair loss

A

Alopecia Areata

psoriasis
eczema
Fungal infection/ringworm
Syphilis

Secondary medical causes
 Thyroid disease
 systemic lupus
 vitamin deficiencies eg iron, B12, zinc
 Hormonal
156
Q

investigations in hair loss

A

Dermoscopy

Associated autoimmune bloods
o Thyroid
o Glucose - diabetic
o B12

Fungal mycology

check ANA antibodies

Syphilis serology (multi patch moth eaten hair loss)

Diagnostic skin biopsy including hair follicles

J3 (18 decks)

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