Dermatology Flashcards

1
Q
A
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2
Q

What is Eczema?

A

Skin inflammation which is dry patchy that results from allergy

common in children which can progress to adulthood

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3
Q

Is eczema contagious?

A

autoimmune

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4
Q

eczema is also known as?

A

atopic dermatitis

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5
Q

Common paces eczema can be found on the skin?

A

Flexor surfaces like: wrist creases, elbows (inside), back of knee

Exposed surfaces: Hands, face, scalp (most common in infants) , feet

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6
Q

is eczema worse in the morning or night

A

night

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7
Q

What is the atopy triad?

A

Atopic dermatitis

Asthma

Allergic Rhinitis

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8
Q

What type of hypersensitivity eczema?

A

1

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9
Q

Explain eczema sensitivity?

A

Type 1 hypersenistivity

  • Starts with environment allergey eg pollen
  • Pollen picked up by APC
  • presents to naive T helper cell- activates to Th2 cell
  • Th2 cell stimulates B cells which produces IgE antibodies
  • IgE bind to mast cells +basophils (sensitisation)
  • Degranulation: histamine, leukotriene
  • Inflammation causes skin to be leaky
  • allows more of the allergen
  • allows more water to escape=skin dry +scaly+itchy
  • scrathng further damages skin layers
  • skin can blister + peel
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10
Q

What are Emollients?

A

thick greasy soap substitues

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11
Q

Examples of thin creams for eczema?

A

E45

Diprobase cream

Oilatum cream

Aveeno cream

Cetraben cream

Epaderm cream

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12
Q

Examples of thick, greasy emollients for eczema?

A

50:50 ointment (50% liquid paraffin)

Hydromol ointment

Diprobase ointment

Cetraben ointment

Epaderm ointment

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13
Q

The purpose of steroids in ezema?

A

Steroids are very good for settling down the immune activity in the skin and reducing inflammation, but they do come with side effects.

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14
Q

Side effects of topical steroids

A

thinning of skin - prune to more flares, brusing, tearing,

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15
Q

enlarged blood vessels under the surface of the skin called _________

A

enlarged blood vessels under the surface of the skin called telangiectasia

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16
Q

The thicker the skin, the ______ the steroid required.

A

The thicker the skin, the stronger the steroid required.

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17
Q

State the steriod ladder from weakest to most potent?

State some examples?

A

Mild: Hydrocortisone 0.5%, 1% and 2.5%

Moderate: Eumovate (clobetasone butyrate 0.05%)

Potent: Betnovate (betamethasone 0.1%)

Very potent: Dermovate (clobetasol propionate 0.05%)

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18
Q

Opportunistic bacterial infection of the skin is common in eczema.The breakdown in the skin’s protective barrier allows an entry point for infective organisms. The most common organism is ___________ _____

A

staphylococcus aureus

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19
Q

WHat is the treatment for bacterial infection in eczema?

A

flucloxacillin.

More severe cases may require admission and intravenous antibiotics.

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20
Q

What is Eczema Herpeticum?

What organism causes this?

A

Eczema herpeticum is a viral skin infection in patients with eczema

caused by the herpes simplex virus (HSV) or varicella zoster virus (VZV).

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21
Q

Mx for Eczema?

A

Allergy mediated inflammation- avoid overheating, dressing in soft fabric, manage stress

Dry skin- frequen moisturisation after warm bath

Itching- short finger nails, anti histamines

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22
Q

What is HSP

A

Henoch-Schonlein Purpura (HSP)

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23
Q

Definition of HSP?

A

is an IgA vasculitis that presents with a purpuric rash affecting the lower limbs and buttocks in children. Inflammation occurs in the affected organs due to IgA deposits in the blood vessels.

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24
Q

HPS affectsskin, kidneys and gastro-intestinal tract

TRUE OR FALSE

A

TRUE

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25
Q

HPS is often triggered by?

A

upper airway infection or gastroenteritis.

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26
Q

Who is HSP common in?

A

most common in children under the age of 10 years.

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27
Q

HSP

The four classic features are:

A

Purpura (100%),

Joint pain (75%),

Abdominal pain (50%)

Renal involvement (50%) - IgA nephritis

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28
Q

What causes the HSP rash?

A

The rash is caused by inflammation and leaking of blood from small blood vessels under the skin, forming purpura. Purpura are red-purple lumps under the skin containing blood.

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29
Q

What is purpura?

What condition is purpura?

A

They are red-purple in colour and are palpable under the skin. Typically they start on the legs and spread to the buttocks. They can also affect the trunk and arms. In severe cases, skin ulceration and necrosis can develop.

Purpura are seen in practically 100% of patients with HSP

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30
Q

in 75% patients HSP develops into

A

arthralgia or arthritis

mostly affecting the knees and ankles.

The joints can become swollen and painful, with a reduced range of movement.

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31
Q

HSP- abdominal pain in severe cases can lead to?

A

gastrointestinal haemorrhage, intussusception and bowel infarction.

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32
Q

HSP affects the kidneys in around 50% of patients, causing an IgA nephritis. This is sometimes referred to as ____ _______. This can lead to microscopic or macroscopic _________ and ________

A

HSP affects the kidneys in around 50% of patients, causing an IgA nephritis. This is sometimes referred to as HSP nephritis. This can lead to microscopic or macroscopic haematuria and proteinuria

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33
Q

How do you diagnose HPS?

A

Full blood count and blood film for thrombocytopenia, sepsis and leukaemia

Renal profile for kidney involvement

Serum albumin for nephrotic syndrome

CRP for sepsis

Blood cultures for sepsis

Urine dipstick for proteinuria

Urine protein:creatinine ratio to quantify the proteinuria

Blood pressure for hypertension

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34
Q

What is EULAR/PRINTO/PRES criteria ?

A

There are many different sets of criteria for diagnosing HSP, the most recent being the EULAR/PRINTO/PRES criteria from 2010. This requires the patient to have palpable purpura (not petichiae) + at least one of:

  • Diffuse abdominal pain
  • Arthritis or arthralgia
  • IgA deposits on histology (biopsy)
  • Proteinuria or haematuria
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35
Q

Differentials for HSP

A

The most important initial step is to exclude other serious pathology, such as meningococcal septicaemia and leukaemia. Idiopathic thrombocytopenic purpura and haemolytic uraemic syndrome are also differentials for a non-blanching rash

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36
Q

Management for HSP

A

Management is supportive, with simple analgesia, rest and proper hydration.

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37
Q

Prognosis for HSP

A

Abdominal pain usually settles within a few days. Patients without kidney involvement can expect to fully recover within 4 to 6 weeks. A third of patients have a recurrence of the disease within 6 months. A very small proportion of patients will develop end stage renal failure.

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38
Q

WHat is ITP?

A

Idiopathic thrombocytopenic purpura (ITP) is a condition characterised by idiopathic (spontaneous) thrombocytopenia (low platelet count) causing a purpuric rash (non-blanching rash).

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39
Q

Cause of ITP?

A

ITP is caused by a type II hypersensitivity reaction. It is caused by the production of antibodies that target and destroy platelets. This can happen spontaneously, or it can be triggered by something, such as a viral infection.

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40
Q

Presentation of ITP

A

diopathic thrombocytopenic purpura usually present in children under 10 years old. Often there is a history of a recent viral illness. The onset of symptoms occurs over 24 – 48 hours:

  • Bleeding, for example from the gums, epistaxis or menorrhagia
  • Bruising
  • Petechial or purpuric rash, caused by bleeding under the skin
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41
Q

Diagnosis of ITP?

A

The condition can be confirmed by doing an urgent full blood count for the platelet count. Other values on the FBC should be normal. Other causes of a low platelet count should be excluded, for example heparin induced thrombocytopenia and leukaemia.

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42
Q

Tx for ITP?

A

Treatment may be required if the patient is actively bleeding or severe thrombocytopenia (platelets below 10):

  • Prednisolone
  • IV immunoglobulins
  • Blood transfusions if required
  • Platelet transfusions only work temporarily
  • Platelet transfusions only work temporarily because the antibodies against platelets will begin destroying the transfused platelets as soon as they are infused.
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43
Q

ITP

WHat are some key education and advice?

A
  • Avoid contact sports
  • Avoid intramuscular injections and procedures such as lumbar punctures
  • Avoid NSAIDs, aspirin and blood thinning medications
  • Advice on managing nosebleeds
  • Seek help after any injury that may cause internal bleeding, for example car accidents or head injuries
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44
Q

Complications of ITP

A
  • Chronic ITP
  • Anaemia
  • Intracranial and subarachnoid haemorrhage
  • Gastrointestinal bleeding
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45
Q

WHat is psorasis?

A

Psoriasis is a chronic autoimmune condition that causes recurrent symptoms of psoriatic skin lesions.

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46
Q

Causes of psoriasis?

A

There is a large variation in how severely patients are affected with psoriasis. There appears to be a genetic component but no clear genetic inheritance has been established. Around a third of patients have a first degree relative with psoriasis. The symptoms start in childhood in a third of patients.

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47
Q

Patches of psoriasis are ____ _____ ____, faintly _______ skin lesions that appear in ______ and ______ plaques, commonly over the _______ ______ of the ________ and ________and on the scalp

A

Patches of psoriasis are dry, flaky, scaly, faintly erythematous skin lesions that appear in raised and rough plaques, commonly over the extensor surfaces of the elbows and knees and on the scalp

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48
Q

What are the different types of psoriasis?

A

Plaque psoriasis

Guttate psoriasis

Pustular psoriasis

Erythrodermic psoriasis

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49
Q

NAme rare severe form of psoriasis?

A

Pustular psoriasis

Erythrodermic psoriasis

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50
Q

Most common form of psoriasis?

A

Plaque psoriasis

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51
Q

Which type of psoriasis is triggered by a streptococcal throat infection, stress or medications.

A

Guttate psoriasis

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52
Q

Presentation for psoriasis?

A

n children the distribution and presentation of psoriasis may differ from adults. Guttate psoriasis is more common in children, often triggered by a throat infection. Plaques of psoriasis are likely to be smaller, softer and less prominent.

There are a few specific signs suggestive of psoriasis:

  • Auspitz sign refers to small points of bleeding when plaques are scraped off
  • Koebner phenomenon refers to the development of psoriatic lesions to areas of skin affected by trauma
  • Residual pigmentation of the skin after the lesions resolve
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53
Q

Management for psorisis?

A

The treatment options include:

  • Topical steroids
  • Topical vitamin D analogues (calcipotriol)
  • Topical dithranol
  • Topical calcineurin inhibitors (tacrolimus) are usually only used in adults
  • Phototherapy with narrow band ultraviolet B light is particularly useful in extensive guttate psoriasis
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54
Q

There are two products that contain both a potent steroid and vitamin D analogue that are commonly prescribed for psorasis and worth being aware of. These not licensed in children and will be guided by a specialist.

What are they?

A
  • Dovobet
  • Enstilar
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55
Q

Associations of psoriasis?

A

Nail psoriasis

Psoriatic arthritis

depression and anxiety

obesity

hyperlipidaemia

hypertension

type 2 diabetes.

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56
Q

WHat is Erythema nodosum?

A

Erythema nodosum is a condition where red lumps appear across the patient’s shins. Erythema means red and nodosum directly translates from Latin as “knots”, referring to lumps.

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57
Q

Causes of erythema nodosum?

A

It is caused by inflammation of the subcutaneous fat on the shins. Inflammation of fat is called panniculitis. It is caused by a hypersensitivity reaction. In around half of patients there is no identifiable cause. It is associated with a number of triggers and underlying conditions.

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58
Q

Associations with erythema nodosum?

A

Erythema nodosum is caused by a hypersensitivity reaction, and there is often an identifiable cause:

  • Streptococcal throat infections
  • Gastroenteritis
  • Mycoplasma pneumoniae
  • Tuberculosis
  • Pregnancy
  • Medications, such as the oral contraceptive pill and NSAIDs

It is also associated with chronic diseases:

  • Inflammatory bowel disease
  • Sarcoidosis
  • Lymphoma
  • Leukaemia
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59
Q

Erythema nodosum often indicates ________ ______ ________ or _________ in exams.

A

Erythema nodosum often indicates inflammatory bowel disease or sarcoidosis in exams.

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60
Q

Presentation

Erythema nodosum

A

Erythema nodosum presents with red, inflamed, subcutaneous nodules across both shins. The nodules are raised and can be painful and tender. Over time the nodules settle and appears as bruises.

When you suspect someone has erythema nodosum it is important to look for signs and symptoms of potential triggers and underlying medical conditions.

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61
Q

Investigations Erythema nodosum

A

The diagnosis of erythema nodosum is based on the clinical presentation. Investigations can be helpful in assessing the underlying cause:

  • Inflammatory markers (CRP and ESR)
  • Throat swab for streptococcal infection
  • Chest xray can help identify mycoplasma, tuberculosis, sarcoidosis and lymphoma
  • Stool microscopy and culture for campylobacter and salmonella
  • Faecal calprotectin for inflammatory bowel disease
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62
Q

Mx for erythema nodosum?

A

Management mainly involves investigating for an underlying condition and treating the underlying cause.

Erythema nodosum is managed conservatively with rest and analgesia. Steroids may be used to help settle the inflammation.

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63
Q

Most cases of eythema nodosum will fully resolve within _ _____, however it can last longer.

A

Most cases of eythema nodosum will fully resolve within 6 weeks, however it can last longer.

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64
Q

WHat is acne vulgaris?

A

Acne vulgaris (acne) is an extremely common condition, often affecting people during puberty and adolescence. Most people are affected at some point during their lives, and symptoms can range from mild to severe.

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65
Q

patho of acne vulgaris

A

Acne is caused by chronic inflammation, with or without localised infection, in pockets within the skin known as the pilosebaceous unit. The pilosebaceous units are the tiny dimples in the skin that contain the hair follicles and sebaceous glands. The sebaceous glands produce the natural skin oils and a waxy substance known as sebum.

Acne results from increased production of sebum, trapping of keratin (dead skin cells) and blockage of the pilosebaceous unit. This leads to swelling and inflammation in the pilosebaceous unit. Androgenic hormones increase the production of sebum, which is why acne is exacerbated by puberty and improves with anti-androgenic hormonal contraception. Swollen and inflamed units are called comedones.

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66
Q

Which bacteria plays an important part in acne?

A

Propionibacterium acnes bacteria

colonises the skin.

It is thought that excessive growth of this bacteria can exacerbate acne. Many of the treatments of acne aim to reduce these bacteria.

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67
Q

Presentation of acne

A

There is significant variation in the severity of acne. It presents with red, inflamed and sore “spots” on the skin, typically distributed across the face, upper chest and upper back.

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68
Q

Management for acne

A

Treatment is initiated in a stepwise fashion based on the severity and response to treatment:

  • No treatment may be acceptable if mild
  • Topical benzoyl peroxide reduces inflammation, helps unblock the skin and is toxic to the P. acnes bacteria
  • Topical retinoids (chemicals related to vitamin A) slow the production of sebum (women of childbearing age need effective contraception)
  • Topical antibiotics such as clindamycin (prescribed with benzoyl peroxide to reduce bacterial resistance)
  • Oral antibiotics such as lymecycline
  • Oral contraceptive pill can help female patients stabilise their hormones and slow the production of sebum
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69
Q

What is a last line option for severe acne

A

Oral retinoids for severe acne (i.e. isotretinoin) is an effective last-line option, although it is only prescribed by a specialist after other methods fail. This needs careful follow-up and monitoring and reliable contraception in females. Retinoids are highly teratogenic.

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70
Q

What is the most effective combined contraceptive pill for acne?

S/E

A

Co-cyprindiol (Dianette) is the most effective combined contraceptive pill for acne due to it’s anti-androgen effects.

It has a higher risk of thromboembolism, so treatment is usually discontinued once acne is controlled and it is not prescribed long term.

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71
Q

Side effects of isotretinoin include:

A
  • Dry skin and lips
  • Photosensitivity of the skin to sunlight
  • Depression, anxiety, aggression and suicidal ideation. Patients should be screened for mental health issues prior to starting treatment.
  • Rarely Stevens-Johnson syndrome and toxic epidermal necrolysis
72
Q

Basal cell carcinoma is also known as?

A

rodent ulcers

73
Q

What is the most common skin malignancy?

A

basal cell carcinoma

74
Q

Basal cell carcinoma

Malignant tumour of _________ ________
Normally affects ______ ______ ____ individuals

A

Malignant tumour of epidermal keratinocytes
Normally affects middle aged-older individuals

75
Q

RF for BCC

A

Risk factors include pale skin type, UV sun exposure,
immunosuppression, previous skin cancer, inherited syndromes

76
Q

Common sites of BCC

A

Common sites include face, arms, legs (sun exposed areas)

77
Q

Name the different types of BCC

A

Nodular

Superficial

Sclerosing

Pigmented

78
Q

Which BCC is most common type on the face?

A

Nodular BCC

79
Q

Which BCC tends to occur in younger patients?

A

Superficial

80
Q

Which BCC is skincoloured waxy, scar-like ?

A

Sclerosing

81
Q

Which BCC is brown, blue or greyish lesion that may resemble melanoma?

A

Pigmented

82
Q

What is the managemenf of BCC

A

• Surgical excision is usual treatment of choice - allows histological examination of
the tumour and margins
• Radiotherapy when surgery is inappropriate
• Topical treatment (imiquimod cream) or photodynamic therapy for superficial
subtype
• Prognosis is excellent especially for smaller lesions - locally invasive if untreated
but metastatic spread is extremely rare
• High risk of developing further lesions (~50% ppl develop further lesion within 5
years) and affected individuals at ^ risk of developing other forms of skin cancer

83
Q

Which skin malignacy is most common in black people?

A

Squamous Cell Carinoma

84
Q

TRUE OR FALSE

BCC

Usually grow over weeks – months, can be painful, often ulcerated

A

FASLE

SCC

85
Q

RF for SCC

A

Risk factors include UV sun exposure, (HPV infection in Black
people), immunosuppression and smoking (particularly SCC of lips)

86
Q

Common sites SCC

A

Most SCCs are found on sun-exposed sites, particularly the face,
lips, ears, hands, forearms, lower legs & anogenital region in Black
people

87
Q

Management of SCC

A
  • Surgical excision - treatment of choice
  • Radiotherapy - for large, non-resectable tumours
  • Early stage tumours >90% 5 year survival
  • Approximately 10% rate of metastasis overall
88
Q

________ ____– excessive
keratin production results in a
hard horn; this can overlie SCC,
pre-cancerous lesions or warts

A

Cutaneous horn – excessive
keratin production results in a
hard horn; this can overlie SCC,
pre-cancerous lesions or warts

89
Q

______________ – a rapidly
growing keratinising skin nodule
which can look identical to SCC
but resolves without treatment.

A

Keratoacanthoma – a rapidly
growing keratinising skin nodule
which can look identical to SCC
but resolves without treatment.

90
Q

Actinic Keratoses is also known as

A

solar keartosis

91
Q

Where does Actinic Keratoses develop usually?

A

Develop in areas of sun damage (face,
backs of hands, bald scalps), usually
older individuals. Rarely seen in Black
people

92
Q

Actinic Keratoses is a maligannt tumour

TRUE OR FALSE

A

FALSE

Premalignant - small minority (<1%)
may eventually progress to SCC

93
Q

Actinic Keratoses treatment options?

A

• Treatment options include cryotherapy and curettage for individual lesions or topical 5-fluorouracil for field treatment

94
Q

WHat is bowne’s disease

A

SCC in situ

95
Q

Where is bowen’s disease found?

A

Commonly found on the lower leg or trunk, more
often in women.

96
Q

Bowen’s Disease can be mistaken for?

A

Bowen’s disease may resemble discoid eczema,
psoriasis or superficial basal cell carcinoma.

97
Q

Bowen’s disease treatment?

A

Treated by cryotherapy, curettage, topical 5- fluorouracil or imiquimod, or photodynamic therapy.

98
Q

What is the ABCDE rule for Malignant melanoma

A
99
Q

What is the weighted 7 point checklist?

Malignant melanoma

A
100
Q

Basal cell carcinoma is also known as?

A

rodent ulcers

102
Q

What is a Malignant melanoma

A

An invasive malignant tumour of the epidermal melanocytes, which has
the potential to metastasise

103
Q

RF for Malignant melanoma

A
  • Increasing age
  • UV exposure
  • Previous invasive melanoma or melanoma in situ
  • Previous non-melanoma skin cancer
  • Many melanocytic naevi (moles) especially if atypical naevi
  • Strong family history of melanoma with 2 or more first-degree relatives affected
  • Fair skin that burns easily
104
Q

Different types of malignant melanoma?

A

Superficial Spreading

Mucosal and Ocular Melanomas

Lentigo Maligna Melanoma

Nodular Melanoma

105
Q

Which melanoma is common on the face in elderly population; Related to long-term cumulative UV exposure

A

Lentigo Maligna Melanoma

106
Q

Which melanoma is

  • Common on the lower limbs
  • Young and middle-aged adults
  • Related to intermittent high intensity UV exposure
A

Superficial Spreading

107
Q

Which melanoma arise on lips, eyelids, vulva, penis, anus and on sclera

A

Mucosal and Ocular Melanomas

108
Q
A
109
Q

Which melanoma is

  • Common on the trunk
  • Young and middle aged adults
  • Related to intermittent high- intensity UV exposure
A

Nodular Melanoma

110
Q

Management for Malignant melanoma?

A

Surgical excision - definitive treatment
•Sentinel lymph node biopsy for higher risk lesions
•Surgery if nodal disease
•Radiotherapy – only for metastatic disease
•Targeted or immunotherapy if systemic metastases

111
Q

Recurrence of melanoma based on _______ thickness (thickness of tumour):

Explain this?

A

Recurrence of melanoma based on Breslow thickness (thickness of tumour):

  • <0.76mm thick – low risk,
  • 0.76mm-1.5mm thick – medium risk,
  • >1.5mm thick – high risk
112
Q

Prognosis of rmelanoma?

A
  • 5 year survival rates based on the TNM classification:
  • Stage 1 (T <2mm thick, N0, M0) – 90%,
  • Stage 2 (T>2mm thick, N0, M0) – 80%
  • Stage 3 (N≥1, M0) – 40-50%
  • Stage 4 (M ≥ 1) – 20-30%
113
Q

What is Erythema Multiforme

Most common cause?

A

Erythema multiforme is an erythematous rash caused by a hypersensitivity reaction.

The most common causes are viral infections and medications. It is also notably associated with the herpes simplex virus (causing coldsores) and mycoplasma pneumonia.

114
Q

Presentation

Erythema multiforme

A

Erythema multiforme produces a widespread, itchy, erythematous rash. It produces characteristic “target lesions”. Target lesions are red rings within larger red rings, with the darkest red at the centre, similar to a bulls-eye target. It does not usually affect the mucous membranes but can cause a sore mouth (stomatitis).

The symptoms come on abruptly over a few days. It may be associated with other symptoms of mild fever, stomatitis, muscle and joint aches, headaches and general flu-like symptoms

115
Q

Management of Erythema multiforme

A

The diagnosis is made clinically based on the appearance of the rash.

It is important to identify the underlying cause. Where there is a clear underlying cause, for example a recent coldsore or treatment with penicillin, it may be managed supportively. Where there is no clear underlying cause it may be worth investigating further, for example doing a chest xray to look for mycoplasma pneumonia.

Most of the time erythema multiforme is mild and resolves spontaneously within 1 to 4 weeks without any treatment or lasting effects. Cases may be recurrent, particularly associated with recurrent coldsores.

Severe cases may require admission to hospital, particularly where it affects the oral mucosa. Treatments used in severe cases include IV fluids, analgesia and steroids (systemic or topical). The use of systemic steroids is controversial. Antibiotics or antivirals may be used where infection is present.

116
Q

WHat is Urticaria

Associations?

A

Urticaria are also known as hives. They are small itchy lumps that appear on the skin. This can be localised to a specific area or widespread.

They may be associated with a patchy erythematous rash. They may be associated with angioedema and flushing of the skin. Urticaria can be classified as acute urticaria or chronic urticaria.

117
Q

Patho of Urticaria

A

Urticaria are caused the release of histamine and other pro-inflammatory chemicals by mast cells in the skin. This may be part of an allergic reaction in acute urticaria or an autoimmune reaction in chronic idiopathic urticaria.

118
Q

Causes of Acute Urticaria

A

Acute urticaria is typically triggered by something that stimulates the mast cells to release histamine. This may be:

  • Allergies to food, medications or animals
  • Contact with chemicals, latex or stinging nettles
  • Medications
  • Viral infections
  • Insect bites
  • Dermatographism (rubbing of the skin)
119
Q

Chronic urticaria is an autoimmune condition, where autoantibodies target mast cells and trigger them to release histamines and other chemicals. It can be sub-classified depending on the cause:

A

Chronic idiopathic urticaria

Chronic inducible urticaria

Autoimmune urticaria

120
Q

Explain what these mean?

Chronic idiopathic urticaria

Chronic inducible urticaria

Autoimmune urticaria

A

Chronic idiopathic urticaria describes recurrent episodes of chronic urticaria without a clear underlying cause or trigger.

Chronic inducible urticaria describes episodes of chronic urticaria that can be induced by certain triggers, such as:

  • Sunlight
  • Temperature change
  • Exercise
  • Strong emotions
  • Hot or cold weather
  • Pressure (dermatographism)

Autoimmune urticaria describes chronic urticaria associated with an underlying autoimmune condition, such as systemic lupus erythematosus.

121
Q

Management Urticaria

A

Antihistamines are the main treatment for urticaria. Fexofenadine is usually the antihistamine of choice for chronic urticaria. Oral steroids may be considered as a short course for severe flares.

In very problematic cases referral to a specialist may be required to consider treatment with:

  • Anti-leukotrienes such as montelukast
  • Omalizumab, which targets IgE
  • Cyclosporin
122
Q

What is chicken pox

A

Chickenpox is caused by the varicella zoster virus (VZV). It causes a highly contagious, generalised vesicular rash. It is common in children. Once a child has had an episode of chickenpox, they develop immunity to the VZV virus and will not be affected again.

123
Q

Varicella zoster Presentation

A

Chickenpox is characterised by widespread, erythematous, raised, vesicular (fluid filled), blistering lesions. The rash usually starts on the trunk or face and spreads outwards affecting the whole body over 2 – 5 days. Eventually the lesions scab over, at which point they stop being contagious.

  • Other symptoms:
  • Fever is often the first symptom
  • Itch
  • General fatigue and malaise
    *
124
Q

Chickenpox is highly contagious and spread through direct contact with the lesions or through infected droplets from a cough or sneeze. Patients become symptomatic __ days to __ weeks after exposure. The stop being contagious after all the lesions have crusted over.

A

Chickenpox is highly contagious and spread through direct contact with the lesions or through infected droplets from a cough or sneeze. Patients become symptomatic 10 days to 3 weeks after exposure. The stop being contagious after all the lesions have crusted over.

125
Q

Complications of chicken pox?

A
  • Bacterial superinfection
  • Dehydration
  • Conjunctival lesions
  • Pneumonia
  • Encephalitis (presenting as ataxia

.

126
Q

Chickenpox

After the infection the virus can lie dormant in the _______ ______ ____ ________ cells and chicken pox cranial nerves reactivate later in life as ______ or _____ ______ syndrome

A

After the infection the virus can lie dormant in the sensory dorsal root ganglion cells and cranial nerves reactivate later in life as shingles or Ramsay Hunt syndrome

127
Q

Antenatal and Neonatal Chickenpox

Preganancy

What happens if they are exposed to chicken pox

A

Pregnant women that are known to be immune to chickenpox are not at risk when in contact with chickenpox. When they are not immune, varicella zoster immunoglobulins can be given to protect them against the virus after exposure.

Chickenpox in pregnancy, before 28 weeks gestation, can cause developmental problems in the fetus in a small portion of patients. This is known as congenital varicella syndrome.

Chickenpox in the mother around the time of delivery can lead to life threatening neonatal infection and is treated with varicella zoster immunoglobulins and aciclovir.

128
Q

Management of chicken pox

A

Chickenpox is usually a mild self limiting condition that does not require treatment in otherwise healthy children.

Aciclovir may be considered in immunocompromised patients, adults and adolescents over 14 years presenting within 24 hours, neonates or those at risk of complications.

Complications such as encephalitis require admission for inpatient management.

Symptoms of itching can be treated with calamine lotion and chlorphenamine (antihistamine).

Patients should be kept off school and avoid pregnant women and immunocompromised patients until all the lesions are dry and crusted over. This is usually around 5 days after the rash appears.

129
Q

Hand, foot and mouth disease is caused by the _______ __virus. Incubation is usually __ __ days.

A

Hand, foot and mouth disease is caused by the coxsackie A virus. Incubation is usually 3 – 5 days.

130
Q

Hand, Foot and Mouth Disease

Presentation

A

The illness starts with typical viral upper respiratory tract symptoms such as tiredness, sore throat, dry cough and raised temperature. After 1 – 2 days small mouth ulcers appear, followed by blistering red spots across the body. As the name suggests, these spots are most notable on the hands, feet and around the mouth. Painful mouth ulcers, particularly on the tongue are also a key feature. The rash may be itchy.

131
Q

Hand, Foot and Mouth Disease

Management

A

Diagnosis is made based on the clinical appearance of the rash.

There is no treatment for hand, foot and mouth disease. Management is supportive, with adequate fluid intake and simple analgesia such as paracetamol if required. The rash and illness resolve spontaneously without treatment after a week to 10 days

It is highly contagious and advice should be give about measures to avoid transmission, such as avoiding sharing towels and bedding, washing hands and careful handling of dirty nappies.

132
Q

Complications of Hand foot mouth disease

A

Rarely it can cause complications:

  • Dehydration
  • Bacterial superinfection
  • Encephalitis
133
Q

Molluscum contagiosum is a viral skin infection caused by the _________ _______ virus, which is a type of _______

A

Molluscum contagiosum is a viral skin infection caused by the molluscum contagiosum virus, which is a type of poxvirus.

134
Q

Molluscum Contagiosum Features

A

Molluscum contagiosum is characterised by small, flesh coloured papules (raised individual bumps on the skin) that characteristically have a central dimple. They typically appear in “crops” of multiple lesions in a local area. It is spread through direct contact or by sharing items like towels or bedsheets.

The papules resolve by themselves without any treatment, however this can take up to 18 months. Once they resolve the skin returns to normal. Scratching or picking the lesions should be avoided as it can lead to spreading, scarring and infection.

135
Q

Molluscum Contagiosum Management

A

No treatment or change in lifestyle is required and children can continue all their normal activities. They should avoid sharing towels or other close contact with the lesions to minimise the risk of spreading the infection. Usually just simple reassurance and education is enough.

Rarely, if bacterial superinfection infection occurs in the lesions as a result of scratching, this may require treatment with antibiotics. Options include topical fuscidic acid or oral flucloxacillin.

Immunocompromised patients and those with very extensive lesions or lesions in problematic areas such as the eyelid or anogenital area may require referral to a specialist. Specialist treatment options include:

Topical potassium hydroxide, benzoyl peroxide, podophyllotoxin, imiquimod or tretinoin

Surgical removal and cryotherapy (freezing with liquid nitrogen) is an option but can lead to scarring

136
Q

Pityriasis Rosea

WHat is it

A

Pityriasis rosea a generalised, self limiting rash that has an unknown cause. It often occurs in adolescents and young adults. It may be caused by a virus such as human herpes virus (HHV-6 or HHV-7), but no definitive causative organism had been established.

137
Q

Presentation of Pityriasis Rosea

A

There may be prodromal symptoms prior to the rash developing. These include headache, tiredness, loss of appetite and flu-like symptoms.

The rash starts with a characteristic herald patch. This is a faint red or pink, scaly, oval shaped lesion that is 2cm or more in diameter, usually occurring somewhere on the torso. It appears 2 or more days prior to the rest of the rash. If you suspect pityriasis, ask and look for a herald patch. Most, but not all, patients have a herald patch.

The rash consists of widespread faint red or pink, slightly scaly, oval shaped lesions, usually less than 2 cm in diameter. On the torso they can be arranged in a characteristic “christmas tree” fashion, following the lines of the ribs.

In dark skinned patients the lesions can be grey coloured, lighter or darker than their skin colour.

Other symptoms may be present:

  • Generalised itch
  • Low grade pyrexia
  • Headache
  • Lethargy
138
Q

Pityriasis Rosea Disease Course

A

The rash resolves without treatment within 3 months. It can leave a discolouration of the skin where the lesions were, however these will also resolved within another few months.

139
Q

Pityriasis Rosea Management

A

There is no treatment for the rash. It will resolve spontaneously without any long term effects. Patient education and reassurance is all that is required. It is not contagious and they can continue all their normal activities.

They may require symptomatic treatment if bothered by itching. This may include emollients, topical steroids or sedating antihistamines at night to help with sleep (e.g. chlorphenamine).

140
Q

Seborrhoeic Dermatitis

What is it

A

Seborrhoeic dermatitis is an inflammatory skin condition that affects the sebaceous glands. The sebaceous glands are the oil producing glands in the skin. It affects areas that have a lot of these glands, such as the scalp, nasolabial folds and eyebrows. It causes erythema, dermatitis and crusted dry skin. In infants it causes a crusted dry flaky scalp, often called cradle cap. It is thought that Malassezia yeast colonisation has a role to play in the development of seborrhoeic dermatitis, and the condition improves with anti-fungal treatment

141
Q

WHat is Infantile Seborrhoeic Dermatitis

Tx?

A

Infantile seborrhoeic dermatitis (cradle cap) causes a crusted flaky scalp. It is a self limiting condition and usually resolves by 4 months of age, but can last until 12 months.

First line treatment is by applying baby oil, vegetable oil or olive oil, gently brushing the scalp then washing off. When this is not effective, white petroleum jelly can be used overnight to soften the crusted areas before washing off in the morning.

The next step is a topical anti-fungal cream such as clotrimazole or miconazole, used for up to 4 weeks. Severe or unresponsive cases may need referral to a dermatologist.

142
Q

Mx for Seborrhoeic Dermatitis of the Scalp

A

Mild seborrhoeic dermatitis of the scalp presents with flaky itchy skin on the scalp (dandruff). More severe cases cause more dense oily scaly brown crusting. This commonly occurs in adolescents and adults rather than children.

First line treatment is with ketoconazole shampoo, left on for 5 minutes before washing off. Topical steroids may be used if there is severe itching. It often reoccurs after successful treatment.

143
Q

Mx for Seborrhoeic Dermatitis of the Face and Body

A

Seborrhoeic dermatitis of the face and body presents with red, flaky, crusted, itchy skin. It commonly affects the eyelids, nasolabial folds, ears, upper chest and back.

First line treatment is with an anti fungal cream, such as clotrimazole or miconazole, used for up to 4 weeks. Localised inflamed areas may benefit from a topical steroids, such as hydrocortisone 1%.

Severe or unresponsive cases should be referred to a dermatologist or paediatrician.

144
Q

What is ringworm

A

Ringworm is a fungal infection of the skin. It is also known as tinea and dermatophytosis. Fungal infections have specific names depending on the area they affect:

145
Q

Tinea capitis refers

Tinea pedis

Tinea cruris

Tinea corporis

Onychomycosis

What do these mean?

A

Tinea capitis refers to ringworm affecting the scalp (caput meaning head)

Tinea pedis refers to ringworm affecting the feet, also known as athletes foot (pedis meaning foot)

Tinea cruris refers to ringworm of the groin (cruris meaning leg)

Tinea corporis refers to ringworm on the body (corporis meaning body)

Onychomycosis refers to a fungal nail infection

146
Q

The most common type of fungus that causes ringworm is called_______ It is spread through contact with infected individuals, animals or soil.

A

The most common type of fungus that causes ringworm is called trichophyton. It is spread through contact with infected individuals, animals or soil.

147
Q

Presentation

Ringworm

A

Ringworm presents as an itchy rash that is erythematous, scaly and well demarcated. There is often one or several rings or circular shaped areas that spread outwards, with a well demarcated edge. The edge is more prominent and red and the area in the centre is more faint in colour.

148
Q

Presentation of Tinea capitis

A

Tinea capitis can present with well demarcated hair loss. There will also be itching, dryness and erythema of the scalp. This is more common in children than adults.

149
Q

Presentation of Tinea pedis (athletes foot)

A

Tinea pedis (athletes foot) presents with white or red, flaky, cracked, itchy patches between the toes. The skin may split and bleed. This is often the result of sharing changing rooms with someone that has athletes foot and is more likely to occur when feet are sweaty and damp for prolonged periods.

150
Q

Presentation of Onychomycosis

A

(fungal nail infections) presents with thickened, discoloured and deformed nails.

151
Q

Management of Ringoworm

A

Treatment of ringworm is with anti-fungal medications:

  • Anti-fungal creams such as clotrimazole and miconazole
  • Anti-fungal shampoo such as ketoconazole for tinea capitis
  • Oral anti-fungal medications such as fluconazole, griseofulvin and itraconazole

Fungal nail infections can be treated with amorolfine nail lacquer for 6 – 12 months. Resistant cases may need oral terbinafine, however the patient will need their LFTs monitoring before and whilst taking this.

A mild topical steroid can help settle the inflammation and itching. A common combination is miconazole 2% and hydrocortisone 1% cream (Daktacort).

152
Q

Ringwom

Simple advice should be given to help recovery, prevent spread and avoid recurrence. Fungal infections grow best in warm, moist areas. Advise includes

A
  • Wear loose breathable clothing
  • Keep the affected area clean and dry
  • Avoid sharing towels, clothes and bedding
  • Use a separate towel for the feet with tinea pedis
  • Avoid scratching and spreading to other areas
  • Wear clean dry socks every day
153
Q

What is

Tinea Incognito

A

Tinea incognito refers to a more extensive and less well recognised fungal skin infection that results from the use of steroids to treat an initial fungal infection.

This often occurs when the initial presentation of ringworm was misdiagnosed as dermatitis and a topical steroid was prescribed. The steroid improves the itching and inflammation but accelerates the growth of the fungal infection by dampening the immune response in the local area. When the steroid is stopped the itchy rash caused by the fungus returns and is much worse than previously. It may be less recognisable as ringworm due to a less well-demarcated border and fewer scales, giving rise to the incognito name.

154
Q

What are scabies

A

Scabies are tiny mites called Sarcoptes scabiei that burrow under the skin causing infection and intense itching. They lay eggs in the skin, leading to further infection and symptoms. It can take up to 8 weeks for any symptoms or rash to appear after the initial infestation.

155
Q

Presentation

Scabies

A

Scabies presents with incredibly itchy small red spots, possibly with track marks where the mites have burrowed. The classic location of the rash is between the finger webs, but it can spread to the whole body.

TOM TIP: Scabies is more common than you may think. When someone presents with an itchy rash, ask whether anyone they live with has a similar rash and check between their finger webs for little red dots and track marks that may indicate scabies.

156
Q

Management of sacbies

A

Treatment is with permethrin cream. left on for 8 – 12 hours and then washed off. This should be repeated a week later to kill all the eggs that survived the first treatment and have now hatched.

Oral ivermectin as a single dose that can be repeated a week later is an option for difficult to treat or crusted scabies.

Scabies is contagious to all household and close contacts. When one person is diagnosed, all household and close contacts should also be treated in exactly the same way, even if asymptomatic. This is because they may be infected and not yet have symptoms.

All clothes, bedclothes, towels and other materials in contact with scabies need to be washed on a hot wash to destroy the mites. Thorough hoovering of carpets and furniture is also essential.

Itching can continue for up to 4 weeks after successful treatment. Crotamiton cream and chlorphenamine at night at night can help with the itching.

157
Q

What are Crusted Scabies

A

Crusted scabies is also known as Norwegian scabies. It is a serious infestation with scabies in patients that are immunocompromised. These patient may have over a million mites in their skin. They are extremely contagious. Rather than individual spots and burrows, they have patches of red skin that turn into scaly plaques. These can be misdiagnosed as psoriasis. Immunocompromised patients may not have an itch as they do not mount an immune response to the infestation. They may need admission for treatment as an inpatient with oral ivermectin and isolation.

158
Q

What is Impetigo

A

Impetigo is a superficial bacterial skin infection, usually caused by the staphylococcus aureus bacteria. A “golden crust” is characteristic of a staphylococcus skin infection. It is also less commonly caused by the streptococcus pyogenes bacteria. Impetigo is contagious and children should be kept off school during the infection.

Impetigo occurs when bacteria enter via a break in the skin. This may be in otherwise healthy skin or may be related to eczema or dermatitis.

159
Q

Impetigo can be classified as ___ _____ or _____

A

mpetigo can be classified as non-bullous or bullous.

160
Q

Non-Bullous Impetigo

Presentation

Tx?

A

Non-bullous impetigo typically occurs around the nose or mouth. The exudate from the lesions dries to form a “golden crust”. They are often unsightly but do not usually cause systemic symptoms or make the person unwell.

Topical fusidic acid can be used to treat localised non-bullous impetigo. Draft NICE guidelines from August 2019 suggest using antiseptic cream (hydrogen peroxide 1% cream) first line rather than antibiotics for localised non-bullous impetigo.

Oral flucloxacillin is used to treat more wide spread or severe impetigo. Flucloxacillin is the antibiotic of choice for staphylococcal infections.

Advise about measure to avoid spreading the impetigo. Patients should be given advice about not touching or scratching the lesions, hand hygiene and avoiding sharing face towels and cutlery. They need to be off school until all the lesions have healed or they have been treated with antibiotics for at least 48 hours.

161
Q

Bullous Impetigo what is caused by?

A

Bullous impetigo is always caused by the staphylococcus aureus bacteria. These bacteria can produce epidermolytic toxins that break down the proteins that hold skin cells together. This causes 1 – 2 cm fluid filled vesicles to form on the skin. These vesicles grow in size and then burst, forming a “golden crust”. Eventually they heal without scarring. These lesions can be painful and itchy.

162
Q

Which one is more common in neonates and children under 2 year

Bullous Impetigo or Non Bullous

A

bullous

163
Q

Mx for bullus impetigo

A

reatment of bullous impetigo is with antibiotics, usually flucloxacillin. This may be given orally or intravenously if they are very unwell or at risk of complications. The condition is very contagious and patients should be isolated where possible.

164
Q

Complications of Impetigo

A

Impetigo usually responds well to treatment without any long term adverse effects. Rarely there can be complications:

  • Cellulitis if the infection gets deeper in the skin
  • Sepsis
  • Scarring
  • Post streptococcal glomerulonephritis
  • Staphylococcus scalded skin syndrome
  • Scarlet fever
165
Q

What is Nappy Rash versus Candidal Infection

A

Candida in the nappy area (thrush) is a common finding. Signs that would point to a candidal infection rather than simple nappy rash are:

  • Rash extending into the skin folds
  • Larger red macules
  • Well demarcated scaly border
  • Circular pattern to the rash spreading outwards, similar to ringworm
  • Satellite lesions, which are small similar patches of rash or pustules near the main rash

Check for oral thrush with a white coating on the tongue, as this is likely to indicate a fungal infection in the nappy area.

166
Q

Management Nappy Rash

A

Simple measures can be taken to improve skin health and treat nappy rash within a few days:

  • Switching to highly absorbent nappies (disposable gel matrix nappies)
  • Change the nappy and clean the skin as soon as possible after wetting or soiling
  • Use water or gentle alcohol free products for cleaning the nappy area
  • Ensure the nappy area is dry before replacing the nappy
  • Maximise time not wearing a nappy

Infection with candida or bacteria warrants treatment with an anti-fungal cream (clotrimazole or miconazole) or antibiotic (fusidic acid cream or oral flucloxacillin).

167
Q

Nappy Rash

Complications

A

Candida infection

Cellulitis

Jacquet’s erosive diaper dermatitis

Perianal pseudoverrucous papules and nodules

168
Q

Patho of a non blanching rash

A

Non-blanching rashes are caused by bleeding under the skin. Petechiae are small (< 3mm), non blanching, red spots on the skin caused by burst capillaries. Purpura are larger (3 – 10mm) non-blanching, red-purple, macules or papules created by leaking of blood from vessels under the skin.

169
Q

Any child presenting with a non-blanching rash needs immediate investigation for the underlying cause. The most concerning differential is ___________ ______. Patients with features of sepsis need immediate management for life threatening ___________ ______

A

Any child presenting with a non-blanching rash needs immediate investigation for the underlying cause. The most concerning differential is meningococcal septicaemia. Patients with features of sepsis need immediate management for life threatening meningococcal sepsis.

170
Q

Non-Blanching Rashes in Children Differentials

A

Meningococcal septicaemia or other bacterial sepsis: This presents with a feverish unwell child. Any features of meningococcal septicaemia indicate emergency management with immediate antibiotics. This can lead to significant morbidity and mortality if treatment is delayed.

Henoch-Schonlein purpura (HSP): This typically presents as a purpuric rash on the legs and buttocks and may have associated abdominal or joint pain.

Idiopathic thrombocytopenic purpura (ITP): This develops over several days in an otherwise well child.

Acute leukaemias: This presents with a gradual development of petechiae, potentially with other signs such as anaemia, lymphadenopathy and hepatosplenomegaly.

Haemolytic uraemic syndrome (HUS): This is associated with oliguria (very low urine output) and signs of anaemia. This often presents in a child with recent diarrhoea.

Mechanical: Strong coughing, vomiting or breath holding can produce petechiae in a “superior vena cava distribution”, above the neck and most prominently around the eyes.

Traumatic: Tight pressure on the skin, for example in non-accidental injury, or occlusion of blood in an area of skin can lead to traumatic petechiae.

Viral illness: This is often the explanation when other causes and serious illness are excluded. Typical causes are influenza and enterovirus.

171
Q

Investigations for non blanching

A
  • Full blood count: Anaemia can suggest HUS or leukaemia. Low white cells can suggest neutropenic sepsis or leukaemia. Low platelets can suggest ITP or HUS.
  • Urea and electrolytes: High urea and creatinine can indicate HUS or HSP with renal involvement.
  • C-reactive protein (CRP): This is a non-specific indication of inflammation or infection and can be useful but not definitive in excluding sepsis.
  • Erythrocyte sedimentation rate (ESR): This is a non-specific indication of inflammatory illness such as a vasculitis (HSP) or infection.
  • Coagulation screen, including PT, APTT, INR and fibrinogen can diagnose clotting abnormalities.
  • Blood culture: This can be useful but not definitive in diagnosing or excluding sepsis.
  • Meningococcal PCR: This can confirm meningococcal disease, although this should not delay treatment.
  • Lumbar puncture: To diagnose meningitis or encephalitis.
  • Blood pressure: Hypertension can occur in HSP and HUS. Hypotension can occur in septic shock.
  • Urine dipstick: Proteinuria and haematuria can suggest HSP with renal involvement, or HUS.
172
Q

Causes of Stevens-Johnson syndrome (SJS)

A

Medications

  • Anti-epileptics
  • Antibiotics
  • Allopurinol
  • NSAIDs

Infections

  • Herpes simplex
  • Mycoplasma pneumonia
  • Cytomegalovirus
  • HIV
173
Q

Stevens-Johnson syndrome (SJS) Presentation

A

The condition has a spectrum of severity. Some cases are mild whilst others are very severe and can potentially be fatal.

Patients usually start with non-specific symptoms of fever, cough, sore throat, sore mouth, sore eyes and itchy skin. They then develop a purple or red rash that spreads across the skin and starts to blister.

A few days after the blistering starts, the skin starts to break away and shed leaving the raw tissue underneath. Pain, erythema, blistering and shedding can also happen to the lips and mucous membranes. Eyes can become inflamed and ulcerated. It can also affect the urinary tract, lungs and internal organs.

174
Q

Management Stevens-Johnson Syndrome

A

SJS and TEN are medical emergencies and patients should be admitted to a suitable dermatology or burns unit for treatment. Good supportive care is essential, including nutritional care, antiseptics, analgesia and ophthalmology input. Treatment options include steroids, immunoglobulins and immunosuppressant medications guided by a specialist.

175
Q

Stevens-Johnson Syndrome Management

A
  • Secondary infection: The breaks in the skin can lead to secondary bacterial infection, cellulitis and sepsis.
  • Permanent skin damage: Skin involvement can lead to scarring and damage to skin, hair, nails, lungs and genitals.
  • Visual complications: Depending on the severity, eye involvement can range from sore eyes to severe scarring and blindness.
176
Q
A