DERM Revision 3 Flashcards

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1
Q
A
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2
Q

Describe what is meant by bullous pemphigoid [1]

It is caused by antibodies agaisnt which basement membrane proteins? [2]

Which patients is it commonly found in?

A

In frail patients
Autoimmune blistering condition
Antibodies against basement membrane proteins which are key components of hemidesmosomes
* BP 180
* BP 230

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3
Q

Which neurological conditions is Bullous Pemphigoid associated with? [3]

Which medications are Bullous Pemphigoid associated with? [2]

A

Neurological disease (that cause frailty)
* Stroke
* Dementia
* Parkinson’s Disease

Drugs:
* PD-1 Inhibitors (used in the treatment of metastatic melanoma)
* Gliptins (diabetic medication)

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4
Q

Describe the clinical manifestations of Bullous Pemphigoid [5]

A
  • Severe itch
  • Pre-bullous rash
  • Large tense bullae and erosions on rupture
  • Milia in healed areas
  • Multple, large tense blisters - that leave eriosions after they burst
  • Mucosal lesions uncommon

NB: top right shows the erosion after a blister has gone

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5
Q

Describe the topical treatments [4] and systemic therapy [5] used to treat Bullous Pemphigoid

A

Topical Treatments
* Super potent topical steroid
* Non adhesive dressings
* Potassium per manganate soaks
* Pop large blisters

Systemic therapy
* Antihistamines
* Tetracycline antibiotic vs oral steroid (BLISTER trial)
* Methotrexate
* Mycophenolate Mofetil
* Biologic therapy - Rituxumab

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6
Q

Describe the pathophysiology of Pemphigus Vulgaris [1]

A

Autoimmune blistering condition
- Autoantibodies to Desmoglein-3 (and sometimes also Desmoglein-1) which are found in desmosomes
- The autoantibodies belong to the IgG class, specifically IgG4

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7
Q

Describe the clinical features of pemphigus vulgaris [+]

A
  • Mucosal involvement usually precedes skin involvement – mouth + genitals: oral lesions are common and often present as the initial clinical feature.
  • Thin-walled flaccid blisters filled with clear fluid
  • Rupture easily
  • Itchy, painful erosions
  • Painful ! :( - epidermis has gone and exposing the dermis
  • Often lose weight (due to mouth ulcers stopping eating)
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8
Q

Which drugs can induce PV? [2]

A

Penicillamine
ACE-inhibitors

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9
Q

Dx of Pemphigus Vulgaris ?

A

Punch/incisional biopsy of:
* Lesional skin for H&E
* Peri-lesional skin direct immunofluorescence
- Fishnet pattern of intercellular IgG and C3 deposits within the epidermis

Serum Autoantibody Testing:
- test measures circulating autoantibodies against desmoglein 1 and 3

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10
Q

Tx of Pemphigus Vulgaris? [4]

A

First-Line Treatment
- oral corticosteroid ± azathioprine or mycophenolate

Second line:
- Rituximab

Intravenous immunoglobulin (IVIG) and plasmapheresis are adjunctive therapies for severe or refractory cases.

Patients on high-dose steroids or other immunosuppressants should receive prophylaxis against Pneumocystis jirovecii pneumonia with co-trimoxazole.

Notes: BMJ BP

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11
Q

Tx for Dermatitis Herpetiformis? [2]

A

Gluten free diet for life
Dapsone

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12
Q

Define erythroderma [1]

Name 5 causes

A

Widespread erythema of skin (over 90% of body surface area)

Causes
* Idiopathic (30%)
* Adverse drug reaction (gold)
* Known inflammatory skin disease (eczema, psoriasis)
* Cutaneous lymphoma

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13
Q

Tx for Eczema Herpeticum? [2]

A

Acyclovir
Flucoxacillin

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14
Q

What commonly causes erytherma multiforme? [3]

Describe the two types (EM minor/major) [2]

A

Causes:
Drugs or Infections (HSV, Mycoplasma)

EM Minor
– target lesions + mild/ no mucosal involvement

EM Major
– target lesions + 1 or more mucosal surfaces involved

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15
Q

Describe in detail the skin lesions seen in SJS / TENs [4]

A
  • Erythematous or purpuric macules
  • Diffuse erythema
  • Targetoid/ atypical target lesions
  • Flaccid blisters
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16
Q

What is a classic differentiating feature between pemphigoid and pemphigus? [2]

A

Bullous pemphigoid:
- mouth is usually spared
- blisters are more tense

Pemphigus vulgaris:
- Mouth commonly involved
- blisters commonly burst

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17
Q

Complications associated with BP? [4]

A

Secondary infections:
* Staphylococcus aureus and Pseudomonas aeruginosa are the most common organisms
* risk of sepsis is significant due to disrupted skin integrity

Side effects from treatment:
- significant corticosteroid use: osteoporosis, diabetes mellitus, hypertension, glaucoma or cataracts

Elderly-related complications::
- Cognitive impairment has been linked with bullous pemphigoid

Increased risk of cardiovascular disease and stroke

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18
Q

PV can be a pareneoplastic disease of which cancers? [2]

A

Lymphomas
Castleman disease

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19
Q

Dapsone can be used to treat dermatitis herpetiformis.

Name some side effects of using as treatment [2]

A

hemolytic anaemia and methemoglobinemia

  • regular monitoring of complete blood counts and methemoglobin levels.
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20
Q

Patients with dermatitis herpetiformis have an increased risk of developing [], a rare but aggressive form of non-Hodgkin lymphoma.

A

Patients with dermatitis herpetiformis have an increased risk of developing Enteropathy-associated T-cell lymphoma (EATL), a rare but aggressive form of non-Hodgkin lymphoma.

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21
Q

Explain some complications of erythroderma

A

Secondary infection
Acute renal failure
- water loss from skin; immune deposits in kidney

High output cardiac failure

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22
Q

Describe the clinical presentation of eczema herpticum [6]

A

The skin lesions of eczema herpeticum typically present as painful clusters of blisters, fluid-filled elevations of the skin

Areas of rapidly worsening, painful eczema

The blisters appear widely over the body but are most common on the face, neck, and trunk.

Older blisters that have burst and dried commonly form “punched out” erosions, which are circular breaks in the continuity of the skin that may bleed or produce pus.

Possible fever, lethargy, lymphadenopathy or distress

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23
Q

What is meant by ‘eczema herpeticum incognito’? [1]

A

presentation of EH that is easily mistaken for impetigo and most often seen in patients with severe AD and recurrent EH

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24
Q

What is the name for when HSV can spread to the eye? [1]

What is the management? [1]

A

Rarely, HSV may spread to the eye resulting in herpes keratitis

Ganciclovir ointment five times daily (3 hourly) for 7-10 days

25
Q

A patient takes penicillin for an infection.

They come out in targetoid lesions.

What type of hypersensitivty reaction is this?

Type 1
Type 2
Type 3
Type 4

A

Type 1
Type 2
Type 3
Type 4

EM is considered a cell-mediated (type IV) hypersensitivity reaction, which is an abnormal cell-mediated reaction initiated by T cells.

The exact mechanism leading to EM is incompletely understood, but it appears to be an abnormal immune reaction to a drug metabolite or viral antigen that becomes expressed by keratinocytes within the skin

26
Q

What is the management for EM? [3]

A

Management

  • EM typically develops over 3-5 days and improves over 2 weeks. Some patients may get persistent or recurrent episodes.
  • Stop the drug
  • Treat the underlying infection
  • Treat with a week of oral prednisolone if severe mucosal pain/ difficulty eating
27
Q

Describe what is meant by SJS [1]

Describe the presentation of SJS [3]

A

Stevens-Johnson syndrome is a severe systemic reaction affecting the skin and mucosa that is almost always caused by a drug reaction.

Presentation:
* 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.
* Nikolsky sign is positive in erythematous areas - blisters and erosions appear when the skin is rubbed gently

NB: Nikolsky sign = where very gentle rubbing of the skin causes it to peel away

28
Q

Which drugs cause SJS? [7]
Which infection can also can? [1]

A

SPANLOC
* Sulphonamide
* Penicillin
* Phenytoin
* Allopurinol
* NSAIDS
* Lamotrigine
* OCP
* Carbamazepine

Most commonly caused by drugs. Less commonly infection eg Mycoplasma

29
Q

How do you dx SJS / TEN? [1]
What score is used for to classifiy the severity of SJS / TEN? [1]

A

Dx:
- skin biopsy

Severity:
- SCORTEN

sum of five points or more indicates a mortality risk of over 90%

30
Q

Pathophysiology of staphylococcal scalded skin syndrome (SSSS)? [1]

A

staphylococcus aureus bacteria that produces epidermolytic toxins. These toxins are protease enzymes that break down the proteins that hold skin cells together

When a skin infection occurs and these toxins are produced, the skin is damaged and breaks down.

This condition usually affects children under 5 years. Older children and adults have usually developed immunity to the epidermolytic toxins.

31
Q

Clinical presentation of SSSS? [5]

A

Fever:
- High fever (>38.9°C)

Rash:
- A diffuse, blanching erythroderma resembling sunburn usually appears early in the disease course.
- Desquamation, particularly on the palms and soles, typically occurs one to two weeks after the onset of illness

Myalgias and arthralgias are frequently reported;

Hypotension:
- Hypotension or shock may be present, often manifesting as systolic blood pressure less than 90 mmHg.

32
Q

Management for SSSS? [1]

A
  • Admit
  • Fluids
  • IV flucloxacillin and clindamycin Clindamycin suppresses toxin production, while flucloxacillin targets the bacterial cell wall.
  • If methicillin-resistant Staphylococcus aureus (MRSA) is suspected, vancomycin or daptomycin can replace flucloxacillin.
33
Q

What are the four types / causes of necrotising fasciitis? [4]

A

Type 1 – Polymicrobial (anaerobes + aerobes)
Type 2 – Group A beta-haemolytic streptococci
Type 3 – Clostridium perfringens; also associated with Vibrio species infection from seafood ingestion or water contamination of wounds.
Type 4 - Fungal infection

34
Q
A

Co-amoxiclav

35
Q
A
36
Q

Tx for athletes foot? [3]

A

Clinical knowledge summaries recommend a topical imidazole, undecenoate, or terbinafine first-line

37
Q

Dx? [1]
Risk factor for..? [1]

A

Erythema ab igne

If the cause is not treated then patients may go on to develop squamous cell skin cancer.

38
Q

What are the features of erythema multiforme? [3]

A

Features
* target lesions
* initially seen on the back of the hands / feet before spreading to the torso
* upper limbs are more commonly affected than the lower limbs
* pruritus is occasionally seen and is usually mild

39
Q

How do you dx erythrasma? [1]

What is the treatment? [1]

A

Examination with Wood’s light reveals a coral-red fluorescence.

Topical miconazole or antibacterial are usually effective. Oral erythromycin may be used for more extensive infection

40
Q

What is meant by erythrasma? [1]

A

Erythrasma is a generally asymptomatic, flat, slightly scaly, pink or brown rash usually found in the groin or axillae.

It is caused by an overgrowth of the diphtheroid Corynebacterium minutissimum

Looks the same as acanthosis nigricans WITHOUT thickening/velvet like texture of the skin

41
Q

Fungal nail infections:

Causative organisms:
- dermatophytes account for around 90% of cases mainly []
- yeasts account for around 5-10% of cases
e.g. []

A

Causative organisms
dermatophytes account for around 90% of cases mainly Trichophyton rubrum

yeasts account for around 5-10% of cases e.g. Candida

42
Q

Investigation and mangement for fungal nail infections?

A

Investigation:
- nail clippings +/- scrapings of the affected nail for microscopy and culture
- should be done for all patients if antifungal treatment is being considered

Mangement:
- None if asymptomatic and unbothered
- if limited involvement (≤50% nail affected, ≤ 2 nails affected, more superficial white onychomycosis): topical treatment with amorolfine 5% nail lacquer; 6 months for fingernails and 9 - 12 months for toenails
- extensive: oral terbinafine is currently recommended first-line; 6 weeks - 3 months therapy is needed for fingernail infections whilst toenails should be treated for 3 - 6 months

43
Q

Which drugs are used for fungal nail infection, for both fingernails and nails, if:

  • Limited involvement
  • Extensive involvement
  • Extensive involvement due to Candida infection
A

Limited involvement: - Topical treatment with amorolfine 5% nail lacquer
- Fingernails: 6 months
- Toe nails: 9-12 months

Extensive involvement - : oral terbinafin
- Fingernails: 6 weeks-3 months
- Toe nails: 3-6 months

Candida:
- oral itraconazole is recommended first-line;
- ‘pulsed’ weekly therapy is recommended

44
Q

Which four factors are in the criteria for hereditary haemorrhagic telangiectasia? [4]

A

epistaxis :
- spontaneous, recurrent nosebleeds

telangiectases:
- multiple at characteristic sites (lips, oral cavity, fingers, nose)

visceral lesions:
- for example gastrointestinal telangiectasia (with or without bleeding), pulmonary arteriovenous malformations (AVM), hepatic AVM, cerebral AVM, spinal AVM

family history:
- a first-degree relative with HHT

NB only 3 are needed for a definite diagnosis; 2 is a possible diagnosis

45
Q

Describe what is meant by Hidradenitis suppurativa

A

Hidradenitis suppurativa
* Chronic, painful, inflammatory skin disorder.
* It is characterized by the development of inflammatory nodules, pustules, sinus tracts, and scars in intertriginous areas
* The axilla is the most common site
* Coalescence of nodules can result in plaques, sinus tracts and ‘rope-like’ scarring.

46
Q

Treatment of acute and chronic Hidradenitis suppurativa?

A

Acute flares:
- can be treated with steroids (intra-lesional or oral) or flucloxacillin.
- Surgical incision and drainage may be needed in some cases.

Long-term disease:
- can be treated with topical (clindamycin) or oral (lymecycline or clindamycin and rifampicin) antibiotics.

47
Q

Hyperhidrosis describes the excessive production of sweat.

What are 4 managment options? [4]

A
  1. topical aluminium chloride preparations are first-line. Main side effect is skin irritation
  2. iontophoresis: particularly useful for patients with palmar, plantar and axillary hyperhidrosis
  3. botulinum toxin: currently licensed for axillary symptoms
  4. surgery: e.g. Endoscopic transthoracic sympathectomy. Patients should be made aware of the risk of compensatory sweating
48
Q

What is the treatment algorithm for impetigo? [3]

A

Tx:
- Hydrogen peroxide 1% cream for ‘people who are not systemically unwell or at a high risk of complications’
- topical antibiotic creams: topical fusidic acid; topical mupirocin should be used if fusidic acid resistance is suspected
- Extensive disease: oral flucloxacillin; oral erythromycin if penicillin-allergic

49
Q

How do you treat keloid scars? [2]

A

Early keloids:
- triamcinolone

Excision is sometimes used (but can risk further keloid scarring)

50
Q

Describe what is meant by a leukoplakia [1]

How can you distinguish it from candidiasis and lichen planus? [1]

What is there a risk of transformation to? [1]

A

Leukoplakia
- is a premalignant condition which presents as white, hard spots on the mucous membranes of the mouth.
- Differentiae from candiasis and lichen planus if they can be ‘rubbed off
- Need a biopsy to exclude squamous cell carcinoma as this can transform in about 1% patients

51
Q

Dx? [1]

A

Lichen planus - pruritic eruption on the shins

Skin disorder of unknown aetiology, most probably being immune-mediated.

52
Q

What are the 6Ps of LP? [6]

A

Pruritic
Purple
Polygonal
Planar
Papules
Plaques

53
Q

Management of LP? [2]

A

potent topical steroids are the mainstay of treatment
benzydamine mouthwash or spray is recommended for oral lichen planus

54
Q

Describe what is meany by lichen sclerosus [1]

What are the characteristic features? [3]

A

It is an inflammatory condition that usually affects the genitalia and is more common in elderly females.

Lichen sclerosus leads to atrophy of the epidermis with white plaques forming.

Features:
* white patches that may scar
* itch is prominent
* may result in pain during intercourse or urination

55
Q

How do you treat lichen sclerosus? [2]

Why do you follow up patients? [1]

A

Treatment:
* topical steroids and emollients

Follow up due to risk of vulval cancer

56
Q

What is mycosis fungoides? [1]

A

Mycosis fungoides is a rare form of T-cell lymphoma that affects the skin.

57
Q

How do you differentiate mycosis fungoides from eczema and psoriasis?

A

lesions tend to be of different colours in contrast to eczema/psoriasis where there is greater homogenicity

58
Q

This patient is suffering from dermatitis due a deficiency in a vitamin - which one? [1]

A

Pellegra - B3 deficiency
The classical features are the 3 D’s - dermatitis, diarrhoea and dementia.

Dermatitis (brown scaly rash on sun-exposed sites - termed Casal’s necklace if around neck)

59
Q

What is meant by Periorificial dermatitis? [1]

Management? [2]

A

A condition typically seen in women aged 20-45 years old. Topical corticosteroids, and to a lesser extent, inhaled corticosteroids are often implicated in the development of the condition.

Management:
* steroids may worsen symptoms
* should be treated with topical or oral antibiotics