Dermatology 538/17 Flashcards

1
Q
  1. Rosacea- History and examination
A
  • Are there any triggers that exacerbate the flushing or redness? - any treatment for the redness or the bumpiness, in particular, has she been using topical corticosteroids? - Does she have any ocular symptoms? Examine face closely, looking for - background erythema, - telangiectasia and - superimposed papules and pustules. These changes are usually more apparent on the nose, cheeks and chin.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
  1. Rosacea- types
A

The clinical presentation for rosacea is varied. There are four primary subtypes: Inflammatory papulopustular rosacea - inflammatory papules and pustules consistent with - erythrotelangiectatic rosacea and papulopustular rosacea often co-exist. Erythrotelangiectatic rosacea - characterised by chronic background erythema, facial flushing and telangiectasia, particularly of the central face. Ocular rosacea - dry, gritty and inflamed eyes - Patients with ocular rosacea often report a sense of dryness or pain, and - ocular manifestations may precede cutaneous signs. - Blepharitis and conjunctivitis are the most common findings. Phymatous rosacea - characterised by tissue hyperplasia after chronic inflammation (eg rhinophyma) - This subtype occurs mainly in older men. Persistent erythema of the central portion of the face lasting for at least three months is an important primary feature of rosacea. Other characteristic findings of rosacea that are often present but not needed for diagnosis, include - oedema, - rhinophyma or - hyperplasia of the connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  1. Rosacea- Ddx
A

Other skin conditions to consider, which have features similar: Seborrhoeic dermatitis – This chronic inflammatory condition is characterised by erythema and scaling of the eyebrows, nasolabial folds, scalp and chest. Rosacea is usually not scaly. The erythrotelangiectatic subtype of rosacea can at times coexist with rosacea (sebo-rosacea). Periorofacial dermatitis – This condition most commonly presents with inflammatory papules around the mouth, eyes and nasal area, and is sometimes caused by the prolonged use of potent topical steroids on facial skin. Acne vulgaris – This is typically seen in a younger age group and is characterised by comedonal lesions, inflammatory papules, pustules, nodules, cysts and scarring. Rosacea does not present with comedones and seldom scars. Keratosis pilaris – This facial disease can be difficult to differentiate from rosacea and may occur simultaneously with rosacea in patients. It is characterised by a fixed blush appearance, especially on the lateral cheeks, and fine follicular keratotic plugs. Keratosis pilaris most commonly affects the extensor surface of the upper arms. Systemic lupus erythematous (SLE) – Patients with SLE may have a malar erythema, which is difficult to differentiate from rosacea, and are often extremely photosensitive. Patients with SLE may also have other systemic symptoms, such as arthritis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
  1. Rosacea- population
A

Rosacea is most commonly seen in individuals with - fair skin, - blue eyes and - of European and Celtic origin. However, patients of any ethnic group may experience rosacea. Typically, symptoms of rosacea peak in those aged 30–50 years. Most studies report it to be more common in women; however, phymatous rosacea develops most frequently in males.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
  1. Rosacea - aetiology
A

The aetiology of rosacea is multifactorial. - the number of facial sebaceous glands, - the innervation and vasculature of the skin all contribute to the pathophysiology of rosacea. - demodex mites may also be implicated in the pathogenesis of rosacea.

Triggers of rosacea that may initiate or aggravate the clinical manifestations…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  1. Rosacea- management
A

Rosacea is managed mainly with general measures and pharmacological treatments targeted at the specific presenting symptoms.

The pharmacotherapy goals for rosacea are to reduce morbidity and symptoms. However, rosacea is not curable and symptoms often recur on cessation of treatment.

First-line pharmacological treatment is with topical agents, including:

  • metronidazole 0.75% gel or cream daily
  • ivermectin 1% gel
  • azelaic acid 15%12

Treatment should be reviewed after four to six weeks and, if there is no improvement, oral antibiotics can be prescribed for six to eight weeks to reduce the inflammatory lesions (papules and pustules) and ocular symptoms of rosacea. Antibiotics that can be used include the following, given orally:

  • doxycycline 50–100 mg daily
  • erythromycin (ethyl succinate formulation) 400–800 mg twice daily
  • minocycline 50 mg twice daily
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  1. Rosacea- recurrent management
A

Recurrent papulopustular rosacea, the following line of treatment should be considered:

  • Topical ivermectin 1% gel daily, initially for three months, as an anti-inflammatory agent to control demodex mites
  • Repeat course of oral antibiotics: doxycycline 100 mg daily for two to three months at a time
  • Trial a different oral antibiotic (eg minocycline 100 mg daily for two to three months at a time).
  • Referral to specialist dermatologist for consideration of oral isotretinoin at a low dose of 10–20 mg daily, which is particularly useful for inflammatory lesions and refractory nodules. It is also useful for preventing the progression of rhinophyma. Isotretinoin is not Pharmaceutical Benefits Scheme (PBS)-subsidised for rosacea.

For erythrotelangiectatic rosacea, vascular laser therapy could be considered. It is an effective treatment for background erythema and telangiectasia; however, these tend to recur with time.

Episodes of papulopustular rosacea would require episodic therapy described above.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  1. Scabies- History
A
  • location of the rash
  • onset of symptoms
  • subsequent spread
  • aggravating/associated factors
  • any identified relievers.
  • treatment tried to date, including any local medicine.

Past history should consider

  • previous similar episodes,
  • how they were treated and responded.

Social history would include whether anyone else in the household currently has, or previously had, symptoms.

Ideally, management of this patient should be done with knowledge of the local context, including:

current outbreaks of skin infections and infestations

local disease patterns, including common skin conditions, incidence/prevalence of possible infectious sequelae, such as post- streptococcal glomerulonephritis (PSGN) and acute rheumatic fever (ARF)/rheumatic heart disease (RHD)

commonly occurring bacteria and known antibiotic susceptibility

local health literacy levels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  1. Scabies examination
A

Examination should incorporate a full set of observations and a complete head-to-toe skin examination.

Look for scratches and sores around the fingers, wrists, elbows, knees and ankles. In particular, include external genitalia, head and face, and inguinal region and axillae for nodules if permitted.

Where appropriate, a complete health check may also be considered, including checking growth, vision, oral health, nutrition and physical activity. In some settings, it may be appropriate to give six-monthly albendazole stat dose and investigate for anaemia.

Examination specific to Scabies

  • excoriated skin on both of her hands and wrists.
  • track marks and burrows.
  • crusted pustules present on the anterior surface of both wrists.
  • webbing between fingers, you may also see significant excoriation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  1. Scabies DDx
A
  • insect bites,
  • papular dermatitis,
  • skin infections,
  • dermatitis,
  • urticarial and bullous pemphigoid.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  1. Scabies Inx
A

Scabies is a parasitic infection of the skin caused by a mite, Sarcoptes scabiei.

The impetigo occurs as a result of bacterial infection secondary to scratching from the pruritis.

Scabies is typically a clinical diagnosis; however, it is possible to confirm the diagnosis.

  • using dermatoscopy, it may be possible to see the typical ‘hang-glider’ appearance
  • Alternatively, a skin scraping from the end of a burrow may reveal mites on microscopy. Ideally, this skin scraping should be performed using dermatoscopy to improve accuracy.
  • Response to treatment may also be used as a confirmation of diagnosis.

In severe cases of scabies, patients may also develop eosinophilia.

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

Treatment of scabies infection

  • permethrin 5% applied late in the evening. It should be left on overnight (minimum eight hours) and washed off in the morning.
  • Application should be from head to toe, from the hairline down, avoiding the face.
  • It is important to include the webbings, soles of the feet, beneath the nails, behind the ears and around the groin and genitalia. Note that in infants and elderly, it may also be appropriate to apply to the face and hair, avoiding contact with mucous membranes.

Treatment of concurrent impetigo:

oral treatment using trimethoprim plus sulphamethoxazole 8/40 mg/kg oral daily for five days; OR

benzathine penicillin (by weight) stat dose intramuscular

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

To prevent re-infection:

Household contacts should be treated concurrently. As scabies has a long incubation period, contacts may be infected but asymptomatic. Treatment for contacts is the same as those confirmed:

permethrin 5% (or crotamiton 10% daily for two to three days if any contacts are <2 months of age) applied as described above.

Fomites need to be managed concurrently with application of the scabicide. Ensure that towels, clothes and bedding are either exposed to heat (eg washing at 50–60°C) or separated from contacts for a minimum of three days to let any mites on them die.

Eggs may hatch up to one week later, hence any scabies treatment given to the patient and their contacts should be repeated seven days later to ensure any eggs that have subsequently hatched have also been dealt with.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  1. Scabies; community Mx
A

Scabies has been hypothesised to contribute to streptococcal infections and their sequelae of PSGN and ARF. Community control of scabies has been shown to reduce the prevalence of impetigo.

Current recommendations for impetigo are to exclude from school until 24 hours after treatment has commenced.

Any weeping sores that are present should be covered before she goes to school. Current National Health and Medical Research Council (NHMRC) guidelines recommend excluding school until after initiation of appropriate treatment for scabies.

In some locations, there are trials or localised protocols using oral ivermectin 200 µg/kg as a stat dose and repeated seven to 14 days later to reduce community outbreaks.

In the event of a high community-wide prevalence, a public health intervention could be considered in this way.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  1. Scabies- persistent Sx
A

Persistent itch is common after treatment for scabies and may occur for some weeks afterwards. It is thought to be linked to the immune- mediated response to the dead mites. This can be treated in a number of ways including use of an emollient, topical steroids or oral antihistamines.

In the event of itch and recurrent signs of infection, consider the following possibilities:

Inadequate treatment:

Is there resistance to the treatment given?

Was it applied incorrectly or removed prematurely?

Did it not penetrate (eg because of crusting)?

Supervised treatment may be required, or changing to an alternative such as benzyl benzoate or ivermectin.

Incorrect diagnosis:

Use dermatoscopy and scrapings to confirm the diagnosis.

Re-infestation:

In some locations, once topical treatment has failed twice, a home visit may be done to perform a ‘mini-skin’ day. This includes treatment as mentioned above to patient, identification and treatment of all contacts, and clearance of household items.

On occasion, an insecticide bomb may be used in each bedroom.

Directly observed treatment to the entire household, which is repeated seven to 14 days later, improves coverage.

A home visit may also include promotion of home hygiene practices, and reviewing the household’s access to adequate washing facilities and bathrooms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  1. Penile Lumps- Pearly papules
A

Pearly penile papules are normal anatomical variants. They classically present as papillae arranged in rows around the coronal sulcus and may be mistaken for warts. Laser ablation or shave excision is a possible approach to treatment, but the main management is reassurance of their normality and advice to leave them alone.

17
Q
  1. Balinitis
A
  • is an inflammation of the glans penis
  • may be associated with other dermatological conditions, such as dermatitis or psoriasis

Non-specific balanitis refers to an irritant reaction to bacteria (eg Pseudomonas, anaerobes) and yeasts (eg Candida albicans)

management would be

  • encourage to keep his skin clean and dry, and not to use soaps to wash his genitalia (try lukewarm water or sorbolene cream instead).
  • salt water baths may help soothe the itch and discomfort.
  • Treat any obvious underlying cause (eg candidal balanitis can be treated with clotrimazole 1% cream).
18
Q
  1. Genital warts
A

Growths or bumps that may be raised or flat, single or multiple, small or large.

Some are clustered together, forming a cauliflower-like shape.

Warts are caused by human papillomavirus (HPV); approximately 90% are caused by HPV types 6 and 11. These HPV types are different from the oncogenic types (HPV 16 and 18) that are associated with HPV-related (ie cervical, anal, oropharyngeal) cancers.

19
Q
  1. Genital warts Rx
A

The HPV infection will usually resolve within 12–24 months. It is important to note that treatment will not get rid of the HPV virus but only treats the visible warts.

Treatment options include patient-applied methods:

  • podophyllotoxin cream 0.15% or 0.5% paint applied topically twice daily for three days in a row, then no application for four days, repeated every week for up to four weeks and review; OR
  • imiquimod 5% cream once a day, three times a week for 4–16 weeks.

In general, warts that are soft, mucosal, vulval or perianal, or are on or under the prepuce respond well to these topical agents.

Keratinised or longstanding warts usually need ablative therapies. These include clinician-applied cryotherapy, laser, diathermy, electrocautery or excision (only for very large warts). Long-term complications of treatment are very rare and may include hypopigmentation or hyperpigmentation.

20
Q
  1. Genital Herpes
A

Suggestive sexual history and combination of symptoms (including his flu-like symptoms), the likely diagnosis now is primary genital herpes.

Genital herpes is caused by Herpes simplex virus (HSV) 1 or 2. This may be acquired from symptomatic or asymptomatic partners.

Sexually acquired manifestations include genital ulceration, gingivostomatitis, urethritis, cervicitis and proctitis.

21
Q
  1. Genital Herpes- Inx
A

The most sensitive and specific investigation would be to do a swab for viral HSV polymerase chain reaction (PCR).

It is advisable to also request testing for syphilis PCR from the same swab, particularly for men who have sex with men, as syphilis rates in Australia are rising rapidly.

Further, the majority of sexually acquired genital ulcers in Australia are caused by HSV or syphilis, which may present with overlapping symptoms and signs.

Note that serology should not be used to screen for HSV as it lacks positive predictive value in low prevalence populations and antibody results are not specific to anatomical sites of infection.

22
Q
  1. Genital Herpes Rx
A

Education, patient information leaflets and referral for counselling where necessary.

Antiretroviral treatment:
valaciclovir 500 mg, twice daily for 7–10 days; OR

• acyclovir 400 mg, three times a day for 7–10 days.

Oral valaciclovir and acyclovir are equally effective treatments. Topical antivirals are ineffective.

Lignocaine 2% jelly topically may be useful if the lesions are particularly painful.

Simple analgesics (paracetamol, codeine) may also be considered for pain relief.

23
Q
  1. Atopic dermatitis (eczema) Hx
A
  • onset of symptoms
  • symptoms and severity in childhood.
  • clinical course of the disease, which tends to follow a chronic, relapsing pattern over months to years.
  • periods of flares and remission, and whether remission is ever achieved without treatment.

Patients with mild disease may experience intermittent flares and spontaneous remission, but those with moderate-to- severe disease rarely experience remission without direct treatment.

Documenting fully failed therapies is important for directing treatment.

Establish whether general measures, topical therapy and systemic therapy have been trialed, and whether remission was achieved.

Lack of adherence to treatment is the most common reason for poor response to treatment.

More than 50% of patients (and parents) with atopic dermatitis do not administer therapy as directed. The most common reasons for poor compliance include concerns about side effects, dislike of topical preparations and insufficient education by practitioners about skin care.

24
Q
  1. Atopic dermatitis- Examination
A

A full-body examination is required. Acute atopic dermatitis is characterised by intensely pruritic, erythematous papules and vesicles, with exudation and crusting. Chronic atopic dertmatitis is characterised by dry, scaly or excoriated erythematous papules.

Other signs of chronic atopic dertmatitis are skin thickening from itching (lichenification) and fissuring. Infants and young children typically present with lesions on the extensor surfaces, cheeks and scalp. The diaper region is usually spared.

Older children and adolescents typically present with lesions in the antecubital and popliteal fossae, volar aspect of the wrists, ankles and neck.

Adults typically present with lesions in skin flexures and, less commonly, on the face, neck and hands.

25
Q
  1. Atopic Dermatitis DDx
A

Differential diagnoses for atopic dermatitis include:

Allergic or irritant contact dermatitis – Features of the history include lesion distribution (particularly the hands, face and eyelids), exposure to irritants and sensitisers and positive patch testing.

Seborrhoeic dermatitis – This is a common differential diagnosis in infants and may coexist with atopic dermatitis. Lesions are salmon-red, erythematous and have a greasy scale. Lesions are typically distributed on the scalp and are not pruritic.

Psoriasis – In infants and young children, psoriasis presents with lesions in the diaper area with well-demarcated patches with minimal scale.

Scabies presents with diffuse pruritic lesions that mimic dermatitis – Consider scabies when the skin folds are involved and vesicopustules are present on the palms and soles.

Other less common differential diagnoses include cutaneous T-cell lymphoma, autoimmune disorders, and nutritional and immune deficiencies.

26
Q
  1. Atopic Dermatitis Dx
A

Skin biopsy and laboratory tests are not routinely performed or recommended. Consider investigations only if there is high suspicion of an alternative diagnosis.

The diagnosis is dependent on the history, morphology and distribution of lesions, and clinical signs. The UK working group for atopic dermatitis proposes the following diagnostic criteria:

One mandatory criterion:

• Evidence of pruritic skin, including the report by a parent of a child rubbing or scratching.

Three or more of the following criteria:

History of skin creases being involved. These include antecubital fossae, popliteal fossae, neck, areas around eyes, fronts of ankles.

History of asthma or hay fever (or history of atopic disease in a first-degree relative for children under four years of age).

The presence of generally dry skin within the past year.

Symptoms beginning in a child before the age of two years (this criterion is not used to make the diagnosis in a child who is under four years old).

Visible dermatitis involving flexural surfaces.

For children under four years of age, this criterion is met by dermatitis affecting the cheeks or forehead and outer aspects of the extremities.

27
Q
  1. Atopic dermatitis severity assessment
A

Most patients with atopic dermatitis have mild-to-moderate disease that is amenable to topical therapy.

A number of disease severity scores (eg SCORAD index, Eczema Area and Severity Index, patient- oriented eczema measure) have been devised and validated in clinical trials, but their use is limited in clinical practice.

A severity classification accounting for skin involvement, and impact on quality of life and psychological wellbeing has been proposed by the National Institute for Health and Care Excellence (NICE):

Mild: Areas of dry skin, infrequent itching (with or without small areas of redness). Little impact on everyday activities, sleep and psychosocial wellbeing.

Moderate: Areas of dry skin, frequent itching, redness (with or without excoriation and localised skin thickening). Moderate impact on everyday activities and psychosocial wellbeing, frequently disturbed sleep.

Severe: Widespread areas of dry skin, incessant itching, redness (with or without excoriation, extensive skin thickening, bleeding, oozing, cracking and alteration of pigmentation). Severe limitation of everyday activities and psychosocial functioning, and nightly loss of sleep.

Atopic dermatitis that does not respond to conventional therapy is classified as severe, refractory dermatitis.

Always consider alternative diagnoses if the patient is not responding to conventional treatment.

28
Q
  1. Atopic dermatitis Rx
A

Current guidelines recommend

  • managing aggravating factors, (identifying and minising contact)
  • improving skin condition, (washing and emollient use)
  • treating infections, and
  • applying topical anti- inflammatory therapy.

–> initiating an appropriate topical corticosteroid.

29
Q
  1. Atopic dermatitis and topical steroids
A

One of the most common reasons for unsatisfactory treatment of childhood atopic dermatitis is inadequate compliance with topical corticosteroids.

Advice for parents should note that:

  • Topical corticosteroids are safe and effective when used appropriately in the treatment of inflammatory skin diseases. Corticosteroids are an important part of a treatment plan.
  • Scarring and permanent disability results from the under-treatment of eczema and the trauma caused by itching.
  • Understand the type of corticosteroid used, expected length of treatment and body areas where its use is safe.
  • Topical corticosteroids should be applied liberally until the rash disappears and the skin appears normal.

A written treatment plan should be supplied that includes patient education, topical therapy, identification of triggers and use of emollients.

30
Q
  1. Atopic dermatitis- referral to specialist
A

Patients with severe refractory atopic dermatitis should be referred to a dermatologist for consideration of phototherapy and immunosuppressive therapy.

Any treatment involves the standard care of atopic dermatitis, namely skin hydration, management of pruritus and inflammation, management of infection, and avoidance of exacerbating factors.

Systemic corticosteroids are only recommended for a short, tapering course to manage an acute exacerbation. Systemic corticosteroid is not recommended unless guided by a dermatologist or immunologist. A dose of 1 mg/kg/day tapered over two weeks is generally sufficient to settle a flare.

Ultraviolet (UV) light therapy is a second-line treatment for severe refractory atopic dermatitis in adolescents and adults. Although there are numerous options for UV therapy, narrowband UVB therapy is almost exclusively used. Side effects of treatment may be short-term (eg itch, acute burns, skin dryness) or long-term (eg premature skin ageing, increased risk of skin cancer). The increased risk of skin cancer is related to the total dose (wavelength and number of treatments). UV therapy cannot be used on the scalp or hairy skin areas. Although moderately effective, there is little evidence regarding the long-term effects of UV therapy in children. UV therapy should therefore be reserved for particularly severe cases in children.

Several immunosuppressive agents are effective in treating severe refractory eczema. These drugs include cyclosporine, mycophenolate mofetil, azathioprine and methotrexate. The use of these medications is limited by respective side effects, including increased risk of infection, hepatotoxicity and renal toxicity, malignancy and bone marrow suppression. Therefore, the aim of treatment is to establish remission on the lowest maintenance dose possible, then taper the dose over three to six months.

There is limited evidence that biological agents, including dupilumab, omalizumab, rituximab, infliximab, alefacept, interferon-gamma and mepolizumab are effective in a small number of patients. Further studies are required before any of these agents are routinely used in severe atopic dermatitis.

31
Q
  1. Atopic dermatitis; preventing relapse
A

For successful treatment of atopic dermatitis, it is imperative to eliminate exacerbating factors that disrupt the epithelia barrier. It is also important to maintain skin hydration and barrier functions, and provide patient education.

Exacerbating factors that worsen chronic atopic dermatitis include excessive bathing without moisturising, low humidity environments, emotional stress, overheating skin, and exposure to detergents and irritants.

Advise patients to avoid trigger factors such as heat and humidity, seek treatment for skin infections promptly, and manage stress and anxiety.

Establish the frequency of exposure to pruritic stimuli on the skin.

  • Exposure to dust mites, animals, moulds and pollen is associated with flares of atopic dermatitis. Many children with atopic dermatitis

may have positive skin-prick tests to food allergens (most often cow’s milk, egg, wheat, peanut), but the role of food in reducing flares is not established.

Managing itch and breaking the itch–scratch cycle is crucial for allowing skin to heal and regain its barrier function. Antihistamines are widely used to control itch, although their use is not supported with clinical evidence. The use of sedating antihistamines is effective for promoting sleep. Tepid baths and wet dressings (wet wraps) help soothe skin and reduce itch.

32
Q
  1. Psoriasis- nail changes
A

Onycholysis refers to detachment of the nail plate from the nail bed (Figure 3). It usually starts at the distal free edge of the nail and progresses proximally. Air trapped in the subungual space gives the detached nail a smooth and white-to-yellow appearance. Onycholysis may be idiopathic, related to trauma, or due to nail bed disorders (Table 1). If all nails are involved, a drug or systemic disease is likely. Fingernail involvement is more suggestive of a local cause or cutaneous pathology such as psoriasis. The two main causes of onycholysis of the toenail, usually the great toe, are infection and trauma. Infection with fungi can lead to onychomycosis, and secondary infection with Pseudomonas species can cause green–brown discolouration of the nail.

Subungual hyperkeratosis is thickening beneath the nail plate involving either the nail bed or the free edge of the nail. Normal nail thickness is 0.5 mm. The most common causes of subungual hyperkeratosis include onychomycosis (fungal nail infection; psoriasis, contact eczema and trauma. Less common causes include lichen planus, and crusted scabies.

Three conditions that can present with onycholysis and subungual hyperkeratosis of multiple nails include
- psoriasis,

- onychomycosis or

- lichen planus.

33
Q
A