Dermatology: Other Skin Disorders Flashcards

1
Q

State and describe the two types of contact dermatitis

A

Contact dermatitis is an inflammatory skin condition which occurs as a result of exposure to an external irritant or allergen. Two types:

  • Irritant contact dermatitis: non-immunological localised skin reaction to due direct contact with irritant (usually due to weak acids or alkalis e.g. detergents)
  • Allergic contact dermatitis: type IV hypersensitivity reaction due to contact with re-exposure to allergens after sensitisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Compare and contrast typical presentation of irritant contact dermatitis and allergic contact dermatitis

A

Irritant contact dermatitis

  • Immediate or delayed gradual reaction (depending on whether strong or mild irritant)
  • Common symptoms= stinging, burning, erythema, dryness, chapping
  • Skin changes restricted to area in contact with irritant

Allergic contact dermatitis

  • Usually develop 24-72hrs after exposure
  • Itching is predominant symptom but may have blistering, weeping & oedema
  • May affect areas not in direct contact with irritant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Discuss the management of contact dermatitis

A
  • Avoiding contact with the irritant or allergen
  • Liberal application of an emollient
  • Consideration of topical corticosteroids (depending on the clinical situation).
  • Appropriate treatment of secondary skin infection, if present
  • Consider skin patch testing (for type IV hypersensitivity)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is urticaria?

What are causes?

How can urticaria be classified?

A
  • Superficial swelling of skin (superficial dermis)
  • Can occur spontaneously or due to trigger (e.g. allergy or viral infection)
  • Classified into:
    • Acute: < 6 weeks
    • Chronic: >6 weeks
      • Chronic spontaenous
      • Autoimmune
      • Chronic inducible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe typical presentation of urticaria

A
  • Areas of raised skin (pale & pink on fair skin)
  • Pruritic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Discuss the management of urticaria

A
  • First line= non-sedating antihistamine (daily up to 6 weeks)
  • Consider short course PO prednisolone if severe or persistent (up to 7 days)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

State some examples of:

  • Sedating antihistamines
  • Non-sedating antihistamines
A
  • Sedating: chlorpheniramine
  • Non-sedating: loratadine, cetirizine, fexofenadine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is angioedema?

State some potential causes of angioedema

A
  • Swelling of deep dermis & subcutaneous and/or submucosal tissue often affecting the face, genitalia, hands or feet (but can affect airway & bowel). Not usually itchy,
  • Some causes:
    • Allergic
    • Non-allergic drug reaction e.g. ACE inhibitor treatment
    • Hereditary angioedema
  • Management:
    • Mild allergic or idiopathic: antihistamines
    • Moderate/more severe: oral corticosteroids

*Remember angioedema can occur in anaphylaxis (hence usual anaphylaxis mangagment)

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

For bullous pemphigoid, discuss:

  • What it is/cause
  • Who it usually affects
  • Presentation
  • Management
A
  • Blistering skin disorder due to autoantibodies against antigens between epidermis & dermis causing sub-epidermal split in skin (antibodies against basement membrane)
  • Elderly
  • Presentation:
    • May have non-specific rash preceding….
    • ….Tense, fluid filled blisters on erythematous base
    • Itchy
    • Often affects trunk & limbs
  • Management:
    • Wound dressings
    • Localised disease: topical steroids
    • Widespread disease: oral steroids (PASSMED says oral steroids= main stay)
    • May also use oral antibiotics & immunosuppressants

**Pt in clinic was on oral steroids, oral abx and they were considering adding azathioprine as a steroid sparing agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

For pemphigus vulgaris, discuss:

  • What it is/cause
  • Who usually affects
  • Presentation
  • Management
A
  • Blistering disorder due to autoantibodies against antigens within the epidermis causing an intra-epidermal split (antibodies against desmosomes that connect cells)
  • Middle aged
  • Presentation:
    • Flaccid, easily ruptured blisters
    • Painful
    • Mucosal involvement common
  • Management:
    • General measures: wound care, oral care, monitor signs infection
    • First line= high dose oral steroids
    • Immunosuppressants

********The fragility of blisters depends on the level of split within the skin – an intra-epidermal split (a split within the epidermis) causes blisters to rupture easily; whereas a sub-epidermal split (a split between the epidermis and dermis) causes blisters to be less fragile. This can help you remember difference in blisters between bullous pemphigoid and pemphigus vulgaris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is erythema multiforme?

State some potential causes

Describe typical presentation

A
  • Hypersensitivity reaction most commonly triggered by infections
  • Causes:
    • Viruses: HSV (MOST COMMON)
    • Drugs e.g. penicillin, sulphonamides, allopurinol, carbamezapine
    • Sarcoidosis
    • Idiopathic
  • Presentation:
    • Target lesions
    • Start on back of hands/feet then spread to torso
    • Mild itching
    • May have mucosal involvement (limited to one surface)
    • Systemic symptoms: mild fever, headache, flu-like symptoms
  • Management:
    • Most of time it is mild and resolves on own without treatment
    • Severe cases may need admission to hospital
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is erythema nodosum?

State some potential causes

Describe presentation

A
  • Hypersensitivity reaction causing inflammation of subcutaneous fat
  • Causes:
    • Infection (e.g. TB, Streptococcus pyogenes)
    • Systemic disease (e.g. IBD, sarcoidosis, Behcet’s)
    • Malignancy
    • Pregnancy
    • Drugs (e.g. penicillin’s, sulphonamides)
  • Presentation:
    • Discrete, tender nodules (may become confluent)
    • Shins common site

*HINT: can also remember causes using mneumonic:

  • NO – idiopathic*
  • D – drugs (penicillin sulphonamides)*
  • O – oral contraceptive/pregnancy*
  • S – arcoidosis/TB*
  • U – ulcerative colitis/Crohn’s disease/Behçet’s disease*
  • M – microbiology (streptococcus, mycoplasma, EBV and more)*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is pyoderma gangrenosum?

State some causes

Describe presentation

Discuss management

A
  • One of a group of autoinflammatory disorders known as neutrophilic dermatoses (infiltration of neutrophils in tissue) which presents as rapidly enlarging, painful ulcer (commonly on lower legs)
  • Causes;
    • Idiopathic (50%)
    • IBD
    • Rheumatological: RA, SLE
    • Haematological: MPN, lymphoma
  • Presentation:
    • Often lower leg
    • Starts as pustule, red bump or blood blister
    • Acute development of painful ulcer
    • May have fever & myalgia
  • Management:
    • Oral steroids
    • Can add immunosuppressants in difficult cases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

For vitiligo, discuss:

  • What it is
  • Associated conditions
  • Presentation
  • Management
A
  • Autoimmune condition which results in loss of melanocytes and subsequent depigmentation of skin
  • Associated conditions:
    • T1DM
    • Addison’s disease
    • Autoimmune thyroid disorders
    • Pernicious anaemia
    • Alopecia areata
  • Presentation:
    • Well demarcated patches of depigmented skin
    • Koebner phenomenon
  • Management:
    • Camouflage makeup
    • Advise on sun protection on affected areas
    • Topical steroids may reverse changes if applied early
    • Other treatments: topical tacrolimus (calcineurin inhibitor), phototherapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is alopecia areta?

Discuss the prognosis

A
  • Autoimmune condition leading to well demarcated patches of hair loss
  • Hair will regrow in 50% pts by 1 year and in 80-90% eventually therefore pts often accept this explanation and no treatment needed. Treatment options include wigs, topical steroids, intra-lesional steroids, DCP therapy etc…
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is dermatitis herpetiformis?

Discuss the management

A
  • Autoimmune blistering disorder associated with coeliac disease due to deposition of IgA in dermis; causes itchy, vesicular lesions on extensor surfaces. Confirmed by biopsy (IgA deposits in dermis)
  • Management:
    • Gluten free diet
    • Dapsone to help symptoms
17
Q

What are dermatofibromas?

Describe appearance

A
  • Common benign, fibrous skin lesions (often follow injury)
  • Presentation:
    • Solitary firm papule or nodule
    • Overlying skin dimples on pinching the lesion
18
Q

What are seborrheic keratoses?

A
  • Benign epidermal skin lesions in older people
  • Presentation:
    • Vary in their colour (flesh → black)
    • Stuck on appearance
    • Keratotic plugs may be seen on surface
  • Management:
    • Reassurance
    • Can be removed if pt wants
19
Q

Describe typical presentation of both epidermoid and pilar cysts

What is the difference in their pathophysiology?

A

Presentation

  • Round bumps just under the skin surface
  • May be yellow or whitish
  • Small dark plug is often present, through which it may be possible to squeeze out some of the cyst’s contents

Pathophysiology

  • Cyst made of lining and contents
  • Difference is in the lining:
    • Epidermoid cyst lining looks like epidermis
    • Pilar cyst lining looks like cells that are found in hair follicles
  • Both contain substance made of keratin
20
Q

For keloid scars, discuss:

  • What they are
  • Who more common in
  • Management
A
  • Tumour-like lesions that arise from connective tissue of a scar and extend beyond the dimensions of the original wound
  • More common in those with darker skin
  • Management:
    • Intra-lesional steroids (early)
    • Excision
21
Q

For polymorphic eruption of pregnancy, discuss:

  • What it is
  • Presentation
  • Management
A
  • Pruritic rash associated with the last trimester
  • Presentation:
    • Starts as small pink papules
    • Enlarge and coalesce to form plaques
    • Sometimes vesicles present
    • Lesions start in abdominal striae then extend to buttocks & thighs (lesions above breast rare)
    • Itchy
  • Management (depends on severity):
    • Emollients
    • Mild topical steroids
    • Oral steroids
22
Q

For cherry haemangiomas, discuss:

  • What they are
  • Who more common in
  • Presentation/features
  • Management
A
  • Benign skin lesions containing abnormal proliferation of capillaries
  • More common with advancing age
  • Presentation:
    • Erythematous, papular lesion
    • 1-3mm in size
    • Non-blanching
    • Not found on mucous membranes
  • No treatment required
23
Q

State some conditions associated with acanthosis nigricans

A
  • T2DM
  • Obesity
  • PCOS
  • Cushing’s disease
  • Acromegaly
  • Prader-Willi
  • Drugs (e.g. COCP)

(due to insulin resistance → hyperinsulinemia → stimulation of keratinocytes and dermal fibroblast proliferation

24
Q

For erythema ab igne, discuss:

  • Cause
  • Presentation
  • Risks
A
  • Over exposure to infrared radiation
  • Presentation:
    • Erythematous patches with hyperpigmentation and telangiectasia often in lace-like pattern or like a fishing net
  • Risks: development of SCC
25
Q

What is erythrasma?

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
  • Topical miconazole or antibacterial are usually effective. Oral erythromycin may be used for more extensive infection
26
Q

Briefly discuss pathophysiology of burns/how burns can lead to a pt being unstable

A
27
Q

Discuss the immediate management of burns

A
  • Remove person from source
  • Immediate first aid:
    • ABC
    • Irrigate injury with cool (not iced) water for between 10-30 minutes
    • Cover burn using cling film (layered rather than wrapped)

Then assess if need referral to secondary care. Severe burns will require supportive care including careful fluid resuscitation, temperature regulation, recognition and treatment of infections etc…. Can use Wallace’s Rule of Nines or Lund & Browder chart to assess extent of burn. Know that formulas exist to guide fluid resuscitation in burn’s pts.

Parkland formula: volume of fluid= total body surface area of the burn % x weight (Kg) x4. Half of the fluid is administered in the first 8 hours.

28
Q

For pityriasis rosea, discuss:

  • What it is & who it affects
  • Aetiology
  • Whether it is contagious
  • Presentation
  • Management
A
  • Acute, self-limiting rash which tends to affect young adults
  • The aetiology is not fully understood but is thought that herpes hominis virus 7 (HHV-7) may play a role.
  • Not contagious
  • Presentation:
    • May have hx of viral infection (most don’t)
    • herald patch (usually on trunk)
    • followed by erythematous, oval, scaly patches which follow a characteristic distribution with the longitudinal diameters of the oval lesions running parallel to the line of Langer. This may produce a ‘fir-tree’ appearance
  • Management: self-limiting - usually disappears after 6-12 weeks