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Phase 3 > Week 10 - Dermatology > Flashcards

Week 10 - Dermatology Flashcards

1
Q

What are the 3 main functions of the skin? Include some examples of each.

A

Protection - i.e. barrier to microorganisms, detects temperature variations, detects and protects pressure.
Physiological regulation - body temperature via sweat, hair and changes in peripheral circulation, vitamin D synthesis.
Sensation - detects heat, cold, touch, pressure, pain.

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2
Q

What are the layers of the epidermis from superficial to deep?

A 
Stratum corneum
Stratum lucidum (palms and soles only)
Stratum granulosum 
Stratum spinosum 
Stratum basale

Come, Let’s Get Sun Burned

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3
Q

Which embryological layer is the skin derived from?

A

Ectoderm.

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4
Q

Describe the embryological development of the skin.

A
  • week 5, skin covered by simple cuboidal epithelium.
  • week 7, this splits into single squamous layer (periderm) and a basal layer.
  • 3rd month, hair develops as an epidermal proliferation into the dermis.
  • 4th month, an intermediate layer containing several cell layers forms between basal layer and periderm.
  • early fetal period, epidermis invaded by melanoblasts.
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5
Q

What immune cells reside in the skin? What layer of skin would they be found it?

A 
Langerhans cells (dendritic cell family). 
Reside in the basal layers.
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6
Q

How do langerhans cells work as the immune cells of the skin?

A

Specialize in antigen presentation. They acquire antigens in the peripheral tissues and transport them to regional lymph nodes, present to naive T cells and initiate adaptive immune response.

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7
Q

In what ways can ultraviolet light harm the skin?

A

Photoaging, DNA damage, carcinogenesis.

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8
Q

Which tumour suppressor gene can be mutated by UV light?

A

P53

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9
Q

Which cells work together to protect cells from UV DNA damage?

A

Keratinocytes and melanocytes.

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10
Q

Describe how UV light results in the production of vitamin D.

A

During sunlight exposure, UVB photons are absorbed by cholesterol in the skin and converted to pre-vitamin D3. Pre-vitamin D3 undergoes transformation in the plasma membrane to form active vitamin D3. It is then activated in the liver and kidney to finally form the active 1.25 DHCC.

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11
Q

Name 3 aetiological factors contributing towards acne.

A

Keratin and thick sebum blockage of sebaceous gland.
Androgenic increased sebum production and viscosity.
Proprioni bacterium inflammation.

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12
Q

What are the clinical features of acne?

A

Papules, pustules, erythema, comedones, nodules, cysts, scarring.

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13
Q

Where is acne commonly found?

A

Face, chest, back, shoulders, occasionally legs scalp.

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14
Q

What treatment options are available for acne?

A

Reduce plugging: topical retinoid, topical benzoyl peroxide.
Reduce bacteria: topical antibiotics (erythromycin, clindamycin), oral antibiotics (tetracyclines, erythromycin). Benzoyl peroxide.
Reduce sebum production: hormones - anti-androgens i.e. dianette/OCP.

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15
Q

Inflammation in eczema primarily due to inherited abnormalities in skin so called “barrier defect”. Abnormalities in what protein can result in disordered barrier function?

A

Filaggrins

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16
Q

What other atopic conditions is atopic eczema associated with? What antibodies have high levels in this condition?

A

Asthma, allergic rhinitis, conjunctivitis, hayfever.

High IgE.

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17
Q

What are the features of infant atopic eczema?

A

Itchy, occasionally vesicular, often facial component, secondary infection.

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18
Q

What are the complications of atopic eczema?

A 
Bacterial infection: staph. aureas.
Viral infection: molluscum, viral warts, eczema herpeticum. 
Tiredness
Growth reduction
Psychological impact
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19
Q

How is atopic eczema managed?

A

Emollients
Topical steroids
Bandages
Anti-histamines
Antibiotics/antivirals
Avoidance of exacerbating factors i.e. house dust mites.
Systemic drugs i.e. ciclosporin, methotrexate.
Biologic agent: IL4/13 blocker Dupilumab.

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20
Q

What is contact dermatitis caused by?

A

Precipitated by an exogenous agent i.e. an irritant which has a direct noxious effect on the skin barrier or by a type 4 hypersensitivity reaction.

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21
Q

What common allergens cause contact dermatitis?

A

Nickel, chromate, cobalt, colophony, fragrance.

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22
Q

What is Seborrhoeic Dermatitis? What causes it?

A

Chronic, scaly inflammatory condition, often thought to be dandruff, seen on the face, scalp, eyebrows, occasionally upper chest.
Overgrowth of Pityrosporum Ovale yeast.

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23
Q

What is the management of Seborrhoeic Dermatitis?

A

Scalp - medicated anti yeast shampoo (i.e. antifungal ketoconazole)
Face - anti-microbial, mild steroid (i.e. daktacort cream)

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24
Q

What is venous dermatitis? What is the management?

A

A conditions affecting the lower legs. Incompetence of deep perforating veins, leads to increased hydrostatic pressure.

Emollients
Mild / moderate topical steroid
Compression bandaging / stockings
Consider early venous surgical intervention

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25
Q

Define psoriasis.

A

A chronic relapsing and remitting scaling skin disease which may appear at any age and affect any part of the skin.

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26
Q

What is the pathophysiology of psoriasis?

A

T cell mediated autoimmune disease.
Abnormal infiltration of T cells leading to release of inflammatory cytokines including interferon, interleukins and TNF, leading to increased keratinocyte proliferation.

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27
Q

Psoriasis has a strong genetic component. What genes are associated with the condition?

A

PRORS1, HLA-Cw0602.

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28
Q

What scoring systems can be used to assess the severity of psoriasis?

A

DLQI PASI PEST

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29
Q

What treatments are available for psoriasis?

A 
Topical creams and ointments  
Phototherapy light treatment
Acitretin
Methotrexate
Ciclosporin

Biologic therapies i.e. adalumimab

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30
Q

There are two distinct pathways involving UV light which interact to cause skin cancer. Describe these pathways.

A

Direct action of UV light on keratinocytes for neoplastic transformation via DNA damage.

Effects of UV light on the immune system.

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31
Q

What gene mutation may predispose to basal cell carcinoma?

A

PTCH gene.

32
Q

List the 4 different types of basal cell carcinoma.

A

Nodular, superficial, pigmented, morphoeic/sclerotic.

33
Q

How is basal cell carcinoma treated?

A

Gold standard - surgical excision 3-4 mm margin.
Curettage and cautery (scraped off and heat applied).
Photodynamic therapy
Topical imiquimod/5-florouracil cream.
Mohs micrographic surgery.

34
Q

What pre malignant variants are there to squamous cell carcinoma? What cell type does it originate from?

A

Actinic keratoses, Bowens disease.

Keratinocytes

35
Q

What is the risk of metastasis from a high risk SCC?

A

10-30%

36
Q

What are the treatment options for squamous cell carcinoma?

A

Gold standard – Surgical excision 4mm margin
Curettage and cautery

Pre-malignant /squamous cell in-situ
Topical imiquimod / 5-fluorouracil cream
Cryotherapy
Photodynamic therapy

Sun protection

37
Q

What are 4 risk factors for developing melanoma?

A

Genetic markers (e.g. CDKN2A)
Family history
UV radiation exposure
Sunburns in childhoo

38
Q

How is melanoma treated?

A

Surgical excision
Immunotherapy - ipilimumab
Immune checkpoint/MEK inhibitors
Biologic antibodies e.g. BRAF genetic defects (debrafanib)

39
Q

What would be the treatment for necrotising faciitis?

A 
Flucluxocillin 
Benzylpenicillin 
Gentamicin 
Clindamycin 
Metronidazole 
Surgical intervention
40
Q

What drug can induce psoriasis?

A

Lithium

41
Q

Where are merkel cells located in the skin? What is their function?

A

Base of epidermis

Assess shape and edge

42
Q

Where are meissner corpuscles located in the skin? What is their function?

A

Immediately below the epidermis, especially on fingertips and lips.
Sensitive to light touch.

43
Q

Where are ruffini corpuscles located in the skin? What is their function?

A

In the dermis, sensing deep pressure and stretching.

44
Q

Where are pacinian corpsucles located in the skin? What is their function?

A

Mechanoreceptors of the deep dermis. Sensitive to deep touch and position/proprioception.

45
Q

Name 3 drugs which can cause acute rashes?

A

Penicillins, trimethoprim, NSAIDs

46
Q

Name 2 drugs which can cause a photo-toxic drug rash.

A

Quinine, bendroflumethiazide.

47
Q

What are the triggers for vasculitis?

A

Infection
Drugs
Connective tissue disease i.e. RA

48
Q

What is bullous pemphigoid?

A

Immunobullous disorder where there are autoantibodies to the basement membrane, causing the epidermis to lift off as a blister.

49
Q

Describe the treatment of immunobullous disorders.

A

Oral steroids
Steroid sparing agents i.e. azathioprine
Burst any blisters
Dressings and infection control
Check for oral/mucosal involvement
Consider screen for underlying malignancy.

50
Q

What is urticaria?

A

Immune mediated type 1 allergic IgE response.

51
Q

What are the different causes of acute urticaria?

A 
Viral infections
Medication i.e. NSAIDs, aspirin, ACE
Food 
Parasitic infections 
Physical stimulants - cold, pressure, cholinergic, aquagenic.
52
Q

What is the treatment of urticaria?

A

Anti-histamines, steroids, immunosuppression, omiluzimab.

53
Q

What is erythema multiforme? What are some of its causes?

A

A self limiting allergic reaction causing target lesions.

HSV, EBV, occasionally drug.

54
Q

What is the treatment of Dermatitis Herpetiformus (coeliac disease)?

A

Topical steroids
Gluten free diet
Oral dapsone

55
Q

What is erythroderma? What can cause it?

A

Diffuse erythema of 80-90% of the skin surface.

Psoriasis, eczema, drug reaction, cutaneous lymphoma.

56
Q

Describe how basal cell carcinoma forms. Where are they most commonly found?

A

DNA damage to basal skin cell causing rapid multiplication of abnormal cells forming a tumour.
Most found on the head and neck/UV exposed areas.

57
Q

Name 3 types of skin allergy testing and discuss the place for each.

A

RAST test - useful for testing single agents
Contact patch testing - chemical contact allergy i.e. nicker, rubber, fragrance
Skin prick testing - used more in children for food allergy.

58
Q

Name a few organisms found normally on the skin.

A

Coagulase negative staphylocci, corynebacterium sp, staphylococcus aureas, streptococcus pyogenes.

59
Q

Describe Impetigo, the causative organism and its treatment.

A

Golden encrusted skin lesions with inflammation localised to the dermis.
Caused by staph. aureas.
Usually self-limiting but can treat with topical fusidic acid or systemic antibiotics if required.

60
Q

Describe Tinea, a possible cause, diagnosis and treatment.

A

Superficial fungal infection of the skin or nails.
Most common causes: microsporum.
Diagnosis can be made on skin scraping.
Treatment: topical or systemic anti-fungals.

61
Q

What is a soft tissue abscess? How is it treated?

A

Infection within the dermis or fat layers with development of walled off infection and pooled pus. Limited antibiotic penetration into into abscess so surgical drainage is the best option.

62
Q

Which layer of skin is cellulitis normally involving? What organisms normally cause it?

A

The dermis.

β-haemolytic streptococci (Group A Strep most common) and S. aureus

63
Q

Describe the 4 classes of cellulitis according to the Enron Classification.

A

I. Patient not systemically unwell and no significant co-morbidities
II. Patient systemically unwell or has significant co-morbidities which may complicate or delay resolution of infection.
III. Patient has significant systemic upset or unstable co-morbidities that will interfere with response to treatment or limb threatening vascular compromise.
IV. Presence of sepsis or severe, life threatening complications.

64
Q

What would be appropriate therapy for someone with Class I cellulitis who had not yet received antibiotics?

A

Oral flucloxacillin or doxycycline for 7 days.

65
Q

What would be appropriate therapy for someone with Class I cellulitis who had not responded to 48 hours of oral antibiotics?

A

IV flucloxacillin or vancomycin. Can be switched to oral therapy after 48-72 hours.

66
Q

What would be the appropriate therapy for someone with class III or IV cellulitis?

A

Require admission to hospital for IV therapy and consideration of surgical management.

67
Q

What is Streptococcal Toxic Shock, the causative agent and the clinical presentation?

A

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

Causative agent - Group A Streptococcus.

Patients present with localised infection (not necessarily severe), fever, shock. Often have diffuse faint rash over body/limbs.

68
Q

How is Streptococcal Toxic Shock treated?

A

Surgery - aggressively seek out abscesses for drainage.
Antibiotics - penicillin + clindamycin
Consider pooled human immunoglobulin in severe cases.

69
Q

What is the treatment for necrotising fasciitis?

A

Extensive surgical debridement - consult surgeon if suspected necrotising fasciitis.

70
Q

What are the signs/symptoms of necrotising fasciitis?

A

Rapidly progressive
Pain out of proportion to clinical signs.
Severe systemic upset.
Presence of visible necrotic tissue.

71
Q

Name two conditions that can mimic cellulitis?

A 
Lyme disease (erythema migrans)
DVT
72
Q

What would be the treatment of bite injuries?

A

Antibiotic treatment:
1st line - co-amoxiclav
2nd line - doxycycline and metronidazole

Surgical treatment:
Need to consider early exploration and debridement.

Prophylactic treatment: need to consider prophylactic antibiotics, tetanus prophylaxis, rabies prophylaxis.

73
Q

Name some types of non-scarring hair loss.

A

Alopecia areata, telogen effluvium (hair cycle disorder), drug induced - chemotherapy, androgenic alopecia, anorexia/vitamin deficiency, syphilis.

74
Q

Name some types of scarring hair loss.

A

Discoid cutaneous lupus, folliculitis, fibrosing alopecia, lichen planus, fungal infection.

75
Q

What are the possible treatment options for alopecia areata?

A 
Super potent topical corticosteroids
Intralesional oral corticosteroids. 
High dose oral corticosteroids. 
Immunotherapy 
Biologics i.e. JAK2 inhibitors

Phase 3 (14 decks)

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