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2nd Year Medicine > Dermatology > Flashcards

Dermatology Flashcards

1
Q

Type 1 hypersensitivity?

A

Immediate reaction

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2
Q

Pathophysiology type 1 hypersensitivity?

A
  • Activated TH2 cells release IL-4, IL-5, IL-13
  • Cause B cells to release IgE
  • IgE activates mast cells
  • Mast cells release histamine, leukotrienes and cytokines
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3
Q

Urticaria timeline?

A

Lesions appear within 1 hour + can last up to 24 hrs

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4
Q

Angioedema?

A

Localised swelling of subcutaneous tissue (non-pitting, not itchy)

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5
Q

Ix allergy? (4)

A
  • RAST (IgE test)
  • Skin prick
  • Challenge test
  • Serum mast cell tryptase level
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6
Q

Tx allergy? (6)

A

Allergen avoidance, anti-histamine, corticosteroids, adrenaline, sodium cromoglycate, immunotherapy

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7
Q

Adrenaline autoinjector?

A

For anaphylaxis

  • 300 ug adults
  • 150 ug children
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8
Q

Type IV hypersensitivity?

A

Delayed (24-48 hrs), T cell mediated

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9
Q

Ix type IV allergy?

A

Patch test

  • Allergens prepared on Finn chambers
  • Finn chambers placed on back and removed after 48 hrs
  • Readings at 48 and 96 hrs
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10
Q

Irritant contact dermatits?

A

Non-immunological process (irritants traumatise skin) e.g. nappy rash, lip-lick dermaitis

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11
Q

Dermatitis tx? (6)

A

Allergen avoidance, emollients, topical steroids, UV phototherapy, immunosuppressants

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12
Q

Epidermis composed of?

A

Stratified squamous epithlium

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13
Q

Embryological origin of epidermis? Dermis?

A 
Epidermis = ectoderm
Dermis = mesoderm
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14
Q

Melanocytes?

A

Pigment-producing cells from neural crest

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15
Q

Layers of epidermis? (4)

A

Keratin layer, glandular layer, prickle cell layer, basal layer

(+ appendages = nail, hair, glands, mucosae)

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16
Q

Blaschko’s lines?

A

Growth pattern of skin (does not follow nerves/lymphatics)

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17
Q

How long does it take keratinocytes to migrate from basement membrane?

A

28 days

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18
Q

Basal layer?

A

Small cuboidal, 1 cell thick

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19
Q

Prickle cell layer?

A

Large polyhedral cells (lots of desmosomes)

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20
Q

Granular layer?

A

ORIGIN OF CORNIFIED ENVELOPE (keratin layer)

2-3 layers of flatter cells

Contains: Lamellar (Odland) bodies, keratohyalin granules (contain filaggrin + involucrin)

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21
Q

A 3 year old boy presents on a sunny day in June. His mother reports he keeps crying and rubs at his skin when playing outside and this has been going on for a few weeks. His skin is sometimes a bit red, but there is never a rash and his skin is clear on examination now. He is skin type 1 with a few freckles evident, generally well, on no medication and there is no family history of skin problems.
What is the most likely diagnosis?

A

Erythropoietic protoporphyria

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22
Q

A 3 year old boy presents on a sunny day in June. His mother reports he keeps crying and rubs at his skin when playing outside and this has been going on for a few weeks. His skin is sometimes a bit red, but there is never a rash and his skin is clear on examination now. He is skin type 1 with a few freckles evident, generally well, on no medication and there is no family history of skin problems.
What is the most likely diagnosis?

A

Erythropoietic protoporphyria

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23
Q

Skin problems make up what percentage of all general practice consultations?

A

~19%

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24
Q

A 58 year old man presents in July with blisters on the dorsal aspect of his hands which have been appearing over the last few months, crust over and heal leaving scarring. He works as a joiner and is aware that his skin has also been more fragile than usual. You notice that he has a lot of hair growing on his cheeks. He is generally well and on no medication
What is the most likely diagnosis?

A

Porphyria cutanea tarda

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25
Q

Keratin layer?

A

Overlapping cell remnants (no nucleus)

also contain lamellar bodies

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26
Q

What does HPV do?

A

Infects keratinocytes and causes warts

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27
Q

Where are melanocytes found?

A

Basal layer

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28
Q

Function of melancoytes

A
  • Convert tyrosine to melanin pigment (Eumelanin = brown/black, Phaeomelanin = red/yellow)
  • Pigment stored in melanosomes
  • Melanosomes transferred to keratinocytes via DENDRITES
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29
Q

Vitiligo?

A

Autoimmune disease with loss of melanocytes

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30
Q

Albinism?

A

Genetic loss of pigment production

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31
Q

Nelson’s syndrome?

A

Melanin-stimulating hormone produced in excess by pituitary

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32
Q

Langerhans cells?

A

Produced in bone marrow, found in prickle cell, dermis + lymph nodes
* ANTIGEN PRESENTING CELLS

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33
Q

Merkel cells?

A

MECHANORECEPTORS (sensation)

* Present in BASAL cell layer

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34
Q

Merkel cell cancer?

A

Causes by virus, HIGH MORTALITY

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35
Q

Pilosebaceous unit?

A

Hair follicle + sebaceous gland

hair receives pigment from melanocytes above dermal papilla

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36
Q

Phases of hair growth?

A

Anagen (growing), catagen (involuting), telogen (resting)

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37
Q

Excess androgen from tumour results in?

A

Virilisation

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38
Q

Alopecia areata?

A

Autoimmune hair loss

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39
Q

Nails grow how much?

A

0.1 mm per day

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40
Q

Where are stem cells for nail growth located?

A

Nail matrix (trauma can irreversibly affect nail growth)

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41
Q

Bullous pemphigoid?

A

Antibody attacks DEJ (dx = immunofluorescence)

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42
Q

Dermis composed of?

A

Ground substance, fibroblasts, macrophages, mast cells, lymphocytes, langerhans, collagen, muscles, blood vessels, lymphatics, nerves

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43
Q

Deep vascular plexus supplies?

Superficial vascular plexus?

A 
Deep = hair follicle
Superficial = LSA allowing diffusion of nutrients to epidermis
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44
Q

Pacinian corpuscles?

A

Deep pressure, found in dermis (onion rings)

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45
Q

Meissners corpuscles?

A

Vibration

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46
Q

Function of sebaceous glands?

A

Produce sebum

* Controls moisture loss + protects against fungal infection

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47
Q

Apocrine glands?

A

Sweat glands in axilla and perineum (scent?)

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48
Q

Eccrine glands?

A

Sweat glands covering whole skin surface (esp. palms, feet, axilla)

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49
Q

Skin functions? (6)

A

Barrier, metabolism, thermoreg, immune defence, communication, sensory

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50
Q

Acute skin failure e.g.? Comps?

A
  • Toxic epidermal necrolysis, erythroderma

* Comps: dehydration, hypoalbuminaemia (protein loss), hypothermia, infection, disordered thyroxine metabolism, pain

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51
Q

Melanocyte:keratinocyte ratio?

A

1 melanocyte: 10 keratinocytes

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52
Q

Skin metabolism?

A

Vit D and thyroxine

  • Vit D stored as hydroxycholecalciferol in liver, converted to 1,25 - dihydroxycholecalciferol in kidney
  • Thyroxine -> thriiodothyronine (80% skin, 20% thyroid gland)
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53
Q

Eczema herpeticum?

A

Blindspot in immune system against herpes simplex virus

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54
Q

T lymphocytes found?

A

Both dermis and epidermis

  • Epidermis = CD8
  • Dermis = CD4 + CD8
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55
Q

T cells involved in systemic disease? (3)

A
  • TH1 = psoriasis
  • TH2 = atopic dermatitis
  • TH17 = psoriasis + atopic dermatitis
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56
Q

Function of TH1 cells? TH2?

A
  • TH1 = activate macrophages via IL2:IFNy

* TH2 = help B cells make antibodies via IL4, IL5 and IL6

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57
Q

Dendritic cells found?

A

In dermis

  • Dermal DC = Ag present
  • Plasmacytoid DC = produce IFNa (found in diseased skin)
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58
Q

MHC?

A

Chromosome 6

  • MHC class I = found on all cells, present endogenous Ag to CD8 cells
  • MHC II = found on APC, present exogenous Ag to CD4 cells
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59
Q

Psoriasis Ax?

A

Triggered by environmental factors in genetically susceptible individuals

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60
Q

Pathology psoriasis?

A
  • KC stimulate pDC to produce IFNa
  • Release IL-1B/Il-6 and TNF
  • Activate DC which activate TH1 and TH17
  • T cells release IL-17/22
  • Stimulates KC proliferation, AMP release, neutrophil-attracting chemokines
  • Dermal fibroblasts release epidermal growth factors
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61
Q

Atopic eczema Ax?

A

Genetic + environment

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62
Q

Pathology atopic eczema?

A

Impairment in skin barrier + abnormal immune response

impairment = mutations in fillagrin gene, decreased AMP in skin

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63
Q

Eczema lesions contain?

A

TH2, DC, KC, macrophages + mast cells

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64
Q

Primary immunodeficiency? Secondary?

A
  • Primary = genetic

* Secondary = acquired e.g. AIDS

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65
Q

Type I hypersensitvity? Type II? III? IV?

A
  • I = IgE mediated
  • II and III = IgG and IgM
  • IV = TH1 cell
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66
Q

Effects of ageing on skin? (3)

A

Decreased ability to detect malignant cells, decreased ability to detect Ag (infection), decreased ability to distinguish self from non-self (autoimmunity)

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67
Q

Photodermatoses?

A

Skin disease caused by exposure to sunlight

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68
Q

Porphyria?

A

Group of diseases due to deficiency of enzymes needed to make haem

(haem needed to make haemoglobin, myoglobin, cytochromes, peroxidases, catalases)

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69
Q

Types of porphyrias? (3)

A

Porphyria cutanea tarda, erythropoetic protoporphyria, acue intermittent porphyria

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70
Q

Porphyria cutanea tarda?

A

Uroporphyrinogen decarboxylase deficiency

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71
Q

s/s porphyria cutanea tarda? (6)

A

Blisters, milia, hyperpigmentation, hypertrichosis, solar uricaria, morphoea

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72
Q

Ix porphyria cutanea tarda? (2)

A

Woods lamp, spectrophometer

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73
Q

Ax + Tx porphyria cutanea tarda?

A
  • Ax: alcohol, viral hepatitis, oestrogens, haemochromatosis

* Tx = underlying cause + symptoms

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74
Q

Erythropoietic protoporphyria?

A

Deficiency in ferrochelatase

autosomal co-dominant inheritance

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75
Q

Ix erythropoietic protoporphyria?

A

RBC porphyrins, fluorocytes, transaminases, [Hb], biliary tract USS

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76
Q

S/s erythropoietic protoporphyria? (4)

A

redness, swelling, pain, itching

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77
Q

Mx and Tx erythropoietic protoporphyria?

A

Mx: 6 monthly LFTs and RBC prophyrins
Tx: visible light protection, prophylactic phototherapy, anti-oxidants (avoid iron)

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78
Q

Acute intermittent porphyria?

A

Deficiency of porphobilinogen deaminase

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79
Q

Types of allergic cutaneous drug eruptions? (4)

A
  • Type 1 anaphylactic = urticaria
  • Type II - pemphigus and pemphigoid
  • Type III - purpura/rash
  • Type IV - erythema/rash
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80
Q

Types of non-allergic cutaneous drug eruptions? (5)

A
  • Eczema
  • Psoriasis
  • Phototoxicity
  • Drug-induced alopecia
  • Cheilitis, xerosis
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81
Q

Morphologies of cutaneous drug eruptions? (3)

Presentation? (3)

A
  • Exanthematous/morbiliform/mculopapular (75%)
  • Urticarial (10%)
  • Pustular/bullous

2
* Pigmentation, itch/pain, photosensitivity

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82
Q

When to suspect cutaneous drug eruptions?

A

Any patient taking medication who suddenly develops a symmetrical skin eruption (usually resolves when drug is withdrawn)

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83
Q

Risk factors for drug eruptions? (5)

A
  • Young adults
  • Female
  • Genetics
  • Virus/lupus
  • Immunosuppression
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84
Q

Risk factors for drugs involved in eruptions? (4)

A
  • Chemistry (B lactams, NSAIDs, HMW, hapten-forming)
  • Route (systemic)
  • Dose
  • Half-life
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85
Q

Exanthematous drug eruption?

A
  • Most common (90%)

* Type IV hypersensitvity (4-21 days after taking drug)

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86
Q

s/s exanthematous drug eruption? (3)

A
  • Widespread symmetrical rash (mucous membranes spared)
  • Prutitus (itch)
  • Fever
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87
Q

Indicators of potentially severe exanthematous drug reaction? (7)

A
  • Involvement of mucous membrane + face
  • Facial erythema + oedema
  • Fever >38.5
  • Skin pain
  • Blisters, purpura, necrosis
  • Lymphadenopathy, arthlargia
  • SOB/wheezing
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88
Q

Drugs associated with exanthematous eruptions? (6)

A
  • Antibiotics, allopurinol, anti-epilecptics (carbamazepine), NSAIDs
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89
Q

Urticarial drug reactions?

A
  • Type I immediate

will blanche unlike purpura in exanthematous

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90
Q

Acute generalised exanthematous pustolsis (AGEP)? (3)

A
  • Anibiotics, CALCIUM CHANNEL BLOCKERS, antimalarials
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91
Q

Drug-induced bullous pemphigoid? (3)

A
  • ACE-I, penicillin, furosemide
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92
Q

Liner IgA disease?

A

Vancomycin = blistering rash in ring forms

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93
Q

Fixed drug eruptions?

A

Red, painful, well-demarcated round plaques

ALWAYS OCCURS in exactly the same spot!!!

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94
Q

Drugs associated with fixed drug eruptions?

A
  • Cyclines, paracetamol, NSAIDs, carbamazepine
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95
Q

Severe cutaneous adverse drug reactions? (4)

A
  • Stevens-Johnson syndrome
  • Toxic epidermal necrolysis
  • DRESS
  • AGEP
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96
Q

Phototoxic cutaneous drug reactions?

A

Non-immunological skin reaction - usually UVA

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97
Q

Drugs associated with phototoxicity? (6)

A

THIAZIDES, antibiotics, NSAIDs, amiodarone, chloropromazine, quinine

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98
Q

Skin prick test contraindicated in?

A

Type III and IV hypersensitivity as can cause SJS, TEN and DRESS

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99
Q

What infections/diseases can increase risk of drug eruptions? (4)

A
  • Immunosuppression, virus, CF, lupus
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100
Q

Tx cutaneous drug eruptions? (3)

A
  • Withdraw drug, topical corticosteroids, antihistamines (type I urticaria)
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101
Q

Creams?

Features of creams? (4)

A

Semisolid emulsion of oil in water

  • Contain emulsifier and preservative (antibac)
  • High water content (cools + moisturises)
  • Non-greasy
  • Cosmetically acceptable
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102
Q

Ointments?

Features of ointments? (3)

A

Semisolid grease/oil (soft paraffin)

  • No preservative
  • Occlusive + emolient
  • Greasy (less cosmetically attractive)
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103
Q

Lotions?

Tx?

A

Liquid forulation

Treat scalp, hair-bearing areas

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104
Q

Gels?

Tx?

A

Thickened aqueous solutions

* Treat scalp, hair-bearing areas, face

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105
Q

Pastes?

Tx?

A

Semisolids containing finely powdered ZNO

Tx: used in soothing bandages

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106
Q

Foams?

Advantage? (2)

A

Colloid with 2-3 phases

Advantage = increased penetration of active agents + can spread easily over large areas of skin without being greasy/oily

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107
Q

Emollients tx?

A

For dry/scaly conditions e.g/ eczema

prescribe 300-500g weekly

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108
Q

Sodium laurel sulphate?

A

Strong irritant found in some shampoos/creams

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109
Q

Topical steroid effects? (3)

Tx? (4)

A
  • Vasoconstrictive, anti-inflam, anti-prolif

Tx

  • Eczema
  • Psoriasis
  • Lichen planus
  • Keloid scars
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110
Q

Calicneurin inhibitors?

A

NSAID e.g. tacrolimus, pimecrolimus

avoids side effects of steroids

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111
Q

Antiviral agents used to treat? (3)

A

Herpes simplex - topical
Eczema herpeticum - oral antiviral
Herpes zoster - oral antiviral

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112
Q

Antipruritics? (4)

A
  • Menthol, caspaicin, camphor/phenol, crotamiton (e.g. eurax)
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113
Q

Keratolytics?

A

Used to soften keratin e.g. warts, eczema, psoriasis, corns

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114
Q

Commensal skin bacteria? (3)

A
  • Staph epidermidis
  • Corynebacterium (diptheroids)
  • Propionibacterium
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115
Q

Staph aureus culture? Coagulase neg staph?

A
  • Staph aureus = golden
  • Coagulase neg = white

(ONLY staph aureus is coagulase positive)

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116
Q

a-haemolytic strep? B-haemolytic? Non-haemolytic?

A
  • a-haemolytic = strep pneumoniae, veridans
  • B-haemolytic = GAS, group B, Group C
  • Non-haemolytic = enterococcus (common cause of UTI)
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117
Q

Coagulase test for staph?

A

Latex agglutination

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118
Q

Tx staph aureus?

A

Fluclox

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119
Q

Tx MRSA? (5)

A
  • Doxycycline
  • Co-trimoxazole
  • Clindamycin
  • Vancomycin
  • Linezolid
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120
Q

UTI infection in women of child-bearing age?

A

Staph. saprophyticus

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121
Q

Types of B-haemolytic strep? (2)

A
  • Group A (throat, severe skin infections)

* Group B (neonatal meningitis)

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122
Q

Diseases associated with strep pyogenes (GAS)? (5)

A
  • Infected eczema, impetigo, cellulitis, erysipelas, necrotising fasciitis
123
Q

Strep pyogenes (GAS) tx?

A

Penicillin

124
Q

Necrotising fasciitis tx?

A

SURGERY + antibiotics

125
Q

Types of necrotising fasciitis? (2)

A
  • Type I - mixed anaerobes + coliforms (usually post-abdominal surgery)
  • Type II - GAS
126
Q

Dermatophyte (fungal) infection (ringworm)? (7)

A
  • Tinea capitis - scalp
  • Tinea barbae - beard
  • Tinea corporis - body
  • Tinea manuum - hand
  • Tinea unguium - nails
  • Tinea cruris - groin
  • Tinea pedis - foot (athlete’s foot)
127
Q

Dermatophyte pathogenesis? (5)

A
  • Hyphae spread in stratum corneum (infects keratinised tissue only)
  • Increased epidermal turnover causes scaling
  • Inflammatory response
  • Hair follicles invaded
  • Lesion grows outward and heals in centre giving ring appearance
128
Q

Epidemiology dermatophyte infections? (3)

A
  • Males > females
  • Scalp ringworm mainly affects children
  • Foot + groin ringworm mainly affects men
129
Q

Dermatophyte organisms and transmission?

A

Trichophyton rubrum (most common!!) - human to human transmission

130
Q

Dx dermatophyte infection? (2)

A
  • Woods light

* Skin scrapings/nail clippings

131
Q

Dermatophyte infection tx? (3)

A
  • Small areas of infected skin/nails = clotrimazole cream or amorolfine nail paint
  • Severe skin/nail infection + scalp infections = oral terbinafine/itraconazole
  • Candida = clotrimazole cream + oral fluconazole
132
Q

Ax scabies?

A
  • Sarcoptes scabiei (chronic crusted form is called “Norweigan scabies” - HIGHLY CONTAGIOUS
133
Q

Tx scabies? (2)

A
  • Malathion lotion

* Benzyl benzoate (avoid in children)

134
Q

Type of lice infestations?

A
  • Pediculus capitis (head louse)
  • Pediculus corporis (body louse)
  • Phthirus pubis (pubic louse)

Tx = malathion

135
Q

Patients who need single room isolation and contact precautions? (3)

A
  • GAS infection
  • MRSA
  • Scabies
136
Q

Features of psoriasis? (4)

A
  • Commonest form is plaque psoriasis
  • Symmetrical
  • Common sites = extensors, scalp, sacrum, nails
  • Sharply demarcated, scaly, erythematous plaques
137
Q

Specific signs of psoriasis? (2)

A
  • Koebner phenomenon - areas of skin trauma e.g. scar

* Auspitz sign - removal of surface scale reveals tiny bleeding points

138
Q

Other types of psoriasis (other than plaque)? (3)

A
  • Guttate
  • Palmoplantar pustular
  • Erythrodermic or widespread pustular (rare)
139
Q

Psoriatic nail disease? (4)

A
  • Onycholysis
  • Nail pitting
  • Dystrophy
  • Subungal hyperkeratosis
140
Q

Psoriasis co-morbidities? (6)

A
  • Arthritis
  • Metabolic syndrome (hypertension/obesity)
  • Crohn’s
  • Uveitis
  • Cancer
  • SEVERE psoriasis = 3 x increased risk of MI!!!
141
Q

Psoriasis tx? (7)

A
  • Vitamin D analogues (calcipotriol, calcitriol), coal tar, dithranol, steroid ointments, EMOLLIENTS, phototherapy, immunosuppression (methotrexate)
142
Q

Acne vulgaris?

A

Chronic inflammatory disease of the pilosebaceous unit

143
Q

Acne pathogenesis?

A
  • Pore occluded
  • Bacterial colonisation
  • Dermal inflammation
  • Increased sebum production
144
Q

Acne vulgaris distribution? Morphology?

A
  • Distribution: face, upper back, chest

* Morphology: comedones (open = blackhead, closed = whitehead), cysts, pustules

145
Q

Acne treatment?

A
  • Topical: benzyl peroxide, retinoid, antibiotics

* Systemic: antibiotics, isotretinoin

146
Q

Rosacea distribution + epidemiology?

A
  • ose, chin, cheeks, forehead

* 30 – 60 years, male and female

147
Q

Features of rosacea? (4)

A
  • Papules, pustules and erythema with no comedones
    (NOT a disease of the pilosebaceous unit)
  • Prominent facial flushing exacerbated by sudden change in temperature, alcohol & spicy food
  • Enlarged / unshapely nose – rhinophyma
  • Conjunctivitis / gritty eyes
148
Q

Rosacea tx?

A
  • AVOID topical steroids
  • Topical therapy: metronidazole, ivermectin (to reduce demodex mite?)
  • Oral therapy: oral tetracycline, isotretinoin
  • Laser for telangiectasia
149
Q

Lichenoid eruptions? Types? (2)

A

Damage to basal epidermis

* Types = lichen planus + lichenoid drug eruption

150
Q

Lichen planus feautures? (5)

Tx?

A
  • pink/purple flat shiny papules
  • volar wrists/ forearms, shins and ankles
  • Wickham’s striae – whitish lines in papules
  • Intensely itchy
    (lasts 12- 18 months before burning out)

Treat symptoms - topical steroids (oral steroids if severe)

151
Q

Difference between pephigus and bullous pemphigoid? (2)

A
  • Bullous pemphigoiD –
    split is Deeper, through DEJ.
  • PemphiguS –
    split more Superficial, intra-epidermal

Nikolsky’s sign (top layers of skin slip away when rubbed)

  • Bullous pemphigoid = negative
  • Pemphigus = positive
152
Q

Epidemiology + distribution bullous pemphigoid?

A
  • Elderly patients

* Localised to one area OR widepsread on trunk + proximal limbs

153
Q

Feautures bullous pemphigoid? (6)

A
  • large tense bullae
  • blisters burst to leave erosions
  • non scarring
  • itchy erythematous plaques in early disease (blisters present later)
  • Nikolsky sign negative
  • No mucosal involvement
154
Q

Pemphigus vulgaris distribution?

A

Scalp, face, axilla, groin

155
Q

Features pemphigus vulgaris? (4)

A
  • Thin roofed bullae
  • Lesions rupture to leave raw areas (increased infection risk)
  • Nikolsky sign positive
  • Mucosal involvement (eyes, genitals)
156
Q

Prognosis bullous pemphigoid + pemphigus?

A
  • Pemphigus = high mortality if untreated

* Bullous pemphigoid = much lower risk

157
Q

Tx of bullous disease? (3)

A
  • Topical: emollients, steroids
  • Oral: steroids

If pemphigoid = tetracycline antibiotics

158
Q

Melanocytes found?

A

At DEJ

159
Q

Dermis composed of? (3)

A
  • Type I and type III collagen
  • Elastic fibres
  • Ground substance (hyaluronic acid + chondroitin sulphate)
160
Q

Layers of dermis? (2)

Epidermal basement membrane?

A
  • Papillary dermis = thin and lies just beneath epidermis
  • Reticular dermis = thick (contains appendages)
  • Epidermal basement membrane = composed of lamin + collagen IV
161
Q

Hyperkeratosis? Parakeratosis? Acanthosis? Papillomatosis? Spongiosis?

A
  • Hyperkeratosis = increased thickness of keratin layer
  • Parakeratosis = nuclei in keratin layer (normally un-nucleated)
  • Acanthosis - increased thickness of epithelium
  • Papillomatosis = irregular epithelial thickening e.g. wart
  • Spongiosis = oedema between prickle cells e.g. eczema
162
Q

4 main classifications of inflammatory skin diseases?

A
  • Spongiotic-intraepidermal oedema e.g. eczema
  • Psoriasiform-elongation of the rete ridges e.g. psoriasis
  • Lichenoid-basal layer damage e.g. lichen planus and lupus
  • Vesiculobullous-blistering e.g. pemphigoid, pemphigus + dermatitis herpetiformis
163
Q

Lichen planus histology? (4)

A
  • Irregular sawtooth acanthosis
  • Hypergranulosis and hyperkeratosis
  • Dermal infiltrate of lymphocytes
  • Basal damage with formation of cytoid bodies
164
Q

Immunobullous disorders? Examples? (3)

A

Blisters are MAIN feature

e.g. pemphigus, bullous pemphigoid, dermatitis herpetiformis

165
Q

Pathology pemphigus vulgaris?

A

AUTOIMMUNE

  • IgG antibodies made against desmoglein 3
  • Destruction of desmosomes
  • end result is ACANTHOLYSIS
166
Q

Bullous pemphigoid pathophysiology?

A
  • IgG attack hemidesmosomes (attach basal cells to basement membrane)
  • NO ACANTHOLYSIS
167
Q

Dx bullous pemphigoid?

A
  • Immunflourescence shows liner IgG around BM

always send EARLY lesions for histology - old lesions show re-epitelialisation mimicking pemphigus vulgaris

168
Q

Dermatitis herpetiformis? Features? (4)

A

Autoimmune bullous disease

  • Associated with coeliac
  • Itchy symmetrical lesions
  • Elbows, knees, buttocks
  • HALLMARK is papillary dermal microabscesses (neutrophils in papillary dermis)
169
Q

Neurophysiology of itch?

A
  • Unmyelinated C fibres in skin sense itch

* Sensation processed in forebrain then hypothalamus

170
Q

Mediation of itch? (3)

A
  • Chemical mediators: histaine, PGE2, IL-2
  • Nerve transmkssion: unmyelinated C fibres
  • CNS: opiates
171
Q

Causes of itch? (4)

A
  • Pruritoceptive: something in skin triggers itch
  • Neuropathic: damage to nerves that causes itch
  • Neurogenic: opiates etc
  • Psychogenic: psychological causes
172
Q

Example of neuropathic itch? Neurogenic?

A
  • Neuropathic = MS

* Neurogenic = opiates

173
Q

Pruritus tx? (5)

A
  • Sedative anti-histamines (non-sedative useless)
  • Emollients
  • Antidepressants
  • Phototherapy
  • Opiate antagonists/ondansetron (serotonin antagonist)
174
Q

Acute vs chronic eczema?

A
  • Acute: papulovesicular, erythema, oedema, ooze

* Chronic: lichenification, increased scaling

175
Q

Features of eczema? (4)

A
  • Itchy, ill-defined, erythematous + scaly
176
Q

Most common cause of contact allergic dermatitis?

A

Nickel

177
Q

Why does acute eczema “weep”?

A

Spongiosis occurs so rapidly that fluid accumulates as blisters rather than oozes

178
Q

Pathology contact allergic dermatitis?

A
  • Langerhans cell in skin presents antigen to CD4 cell
  • Type IV hypersensitivity (T cells sensitised)
  • On subsequent antigen challenge, sensitised T cells infiltrate skin (DERMATITIS)
179
Q

How to distinguish between nappy rash and fungal infection?

A
  • Fungi preferentially chose flexures

* In nappy rash, flexures are generally spared

180
Q

Atopic eczema associated with? (3)

A

Other atopic diseases: asthma, allergic rhinitis, food allergy

181
Q

Eczema distribution?

A

Flexures (+ neck & orbits)

182
Q

Fissure beneath ear lobe?

A

Pathopneumonic to eczema!!!

183
Q

Chronic changes atopic eczema? (3)

A
  • Lichenification
  • Exoriation
  • Secondary infection
184
Q

Crusting in eczema indicates?

A

Staph aureus

185
Q

Eczema herpeticum?

A
  • Herpes simplex virus

* Monomorphic (same shape + size) punched-out lesions

186
Q

UK diagnostic criteria for atopic eczema?

A

Itching + 3 or more of:

  • Visible flexural rash (cheeks + extnsor surfaces in infants)
  • History of flexural rash (cheeks + extensor surfaces in infants)
  • Personal history of atopy (or first degree relative if under 4 y/o)
  • Dry skin
  • Onset before age 2
187
Q

Tx eczema? (6)

A
  • Emollients, avoid irritants, topical steroids, infection tx, phototherapy, immunusuppressants
188
Q

Most important gene in eczema?

A

Filaggrin (controls skin barrier function)

189
Q

Other types of dermatitis/eczema? (6)

A
  • Discoid eczema
  • Photosensitive eczema
  • Stasis eczema
  • Seborrhoeic dermatitis (cradle cap)
  • Pompholyx eczema
  • Lichen simplex
190
Q

Features of stasis eczema? (3)

Where does it occur?

A
  • Hydrostatic pressure
  • Oedema
  • RBC extravasation

Often occurs along lateral malleolus (extending to calf)

191
Q

Pompholyx eczema?

A

Spongiotic vesicles occur due to acute eruption of eczema

192
Q

Lichen simplex?

A

Caused by scratching, will go away on its own (can be treated with potent topical steroids)

193
Q

s/s tuberous sclerosis? (9)

A
  • Infantile seizures
  • Ash-leaf macule
  • Periungal fibromata + longitudinal ridging
  • Facial angiofibromas
  • Hamartomas
  • Bone cysts
  • Shagreen patches
  • Enamel pitting
  • Cortical tubers
194
Q

Tuberous sclerosis?

A

Genodermatoses (autosomal dominant)

195
Q

What can cortical tubers in tuberous sclerosis lead to?

A

Epilepsy and mental impairment

196
Q

Genetic pathology tuberous sclerosis?

A
  • Autosomal dominant
  • Chromosomes 9 (TSC1) OR 16 (TSC2)
  • Code for tuberin and hamartin
197
Q

Tx tuberous sclerosis?

A
  • Topical rapamycin for angiofibromas
198
Q

Types of epidermolysis bullosa? (3)

A
  • Simplex - within epidermis
  • Junctional - DEJ
  • Dystrophic - within dermis (scarring)
199
Q

Epidermolysis bullosa?

A

10 genes involved

200
Q

Haploinsufficiency? Dominant negative? Gain of function? Complete loss of protein?

A
  • Hapoinsufficiency = only 1 copy of gene working (reduced protein production)
  • Dominant negative = expression of abnormal protein interferes with normal protein
  • Gain of function - mutant protein gains new function
  • Complete loss of protein - autosomal recessive, 2 faulty genes produce no protein
201
Q

Features of neurofibromatosis type 1? (7)

A
  • Cafe au lait macules
  • Neurofibromas
  • Plexiform neuroma
  • Axillary/inguinal freckling
  • Optic glioma
  • > 2 Lisch nodules
  • Bony lesion
202
Q

Filaggrin mutation associated with? (4)

A
  • Ichthyosis vulgaris
  • Eczema
  • Hay fever
  • Asthma
203
Q

2 main types of skin cancer?

A
  • Non-melanoma = BCC + SCC

* Melanoma

204
Q

Skin cancer prevalence?

A

1/3 of all cancers

205
Q

SSC incidence in Scotland?

A

334% increase from 1990 to 2011

206
Q

Melanoma mortality?

A

Only 6% of all skin cancers but 75% of skin cancer deaths!!

207
Q

Epidemiology melanoma?

A

Most common cancer in 15-24 year olds

208
Q

Why is early diagnosis essential for melanoma?

A

Much more likely to metastasise than keratinocyte skin cancers

209
Q

ABCDE rule for melanoma?

A 
A - asymmetry
B - border
C - colour
D - diameter
E - evolution
210
Q

Non-melanoma skin cancers prevalence?

A
  • 90-95% skin cancers
  • BCC = 75%
  • SCC = 20%
211
Q

BCC vs SCC? (4)

A

BCC

  • Slow growing lump or non-healing ulcer (“rodent ulcer”)
  • painless
  • locally invasive (doesn’t spread)

SCC

  • warty lump/ulcer
  • sun-damaged skin
  • grow faster, may be painful &/or bleed
  • more likely to spread
212
Q

Different types of BCC? (4)

A
  • Plaque
  • Nodular
  • Morphoeic
  • Pigmented
213
Q

Causes majority of non-melanoma deaths?

A

SCC

214
Q

Precursor lesions for SCC? (2)

A
  • Actinic keratoses

* Bowen’s disease (carcinoma in situ)

215
Q

Keratoacanthoma?

A

Self-resolving form of SCC

216
Q

Cutaneous horn?

A

SCC can present as cutaneous horn

217
Q

Sites of metastasis for SCC? (5)

A
  • Ear
  • Lips
  • Scalp
  • Lymph nodes
  • Bone
218
Q

Survival rate metastatic SCC?

A

5 ys SR = 25%

219
Q

What are chronic ulcers/wounds at risk of?

A

Developing SCC

220
Q

Xeroderma pigmentosum?

A

Defect in nucleotide excision repair gene

221
Q

Gorlin’s syndrome?

A

Naevoid basal cell carcinoma - autosomal dominant

*GENETIC PREDISPOSITION TO BCC!!!

222
Q

EB with regards to skin cancer?

A

Dystrophic form likely to develop SCC

223
Q

Risk factors for skin cancer? (3)

A
  • Genetic
  • Immunosuppression e.g. orga transplant recipients
  • Environmental carcinogens
224
Q

Hallmarks of cancer? (6)

A
  • Sustaining proliferative signalling
  • Evading growth suppressors
  • Activating invasion and metastasis
  • Enabling replicative immortality
  • Inducing angiogenesis
  • Resisting cell death
225
Q

Oncogene? Proto-oncogene?

A
  • Oncogene: positively regulates cell division (over-active) e.g. Ras
  • Proto-oncogene: normal (not mutated) form of oncogene
226
Q

Tumour suppressor?

A

Gene that negatively regulates cell division e.g. p53

227
Q

What pigment is seen in people who burn easily?

A

Pheomelanin

228
Q

Relevance of sun exposure to SCC? BCC? Melanoma?

A
  • SCC = life-long cumulative exposure e.g. outdoor workers

* Melanoma and BCC = intermittent burning episodes e.g. sunbed use

229
Q

Childhood suburn + melanoma risk?

A

Childhood sunburn increases melanoma risk 4-fold (rather than just 2-fold)

230
Q

Chemicals associated with NMSC? (4)

A
  • Coal tar, soot, creosate, arsenic
231
Q

Autoimmune conditions that increase skin cancer risk? (2)

A
  • UC incresases MM by 20%

* Crohns increases MM by 80%

232
Q

How UVB causes skin cancer? UVA?

A
  • UVB = causes direct DNA damage (1000 x more damaging than UVA when sun directly overhead)
  • UVA = causes indirect oxidative damage

(UV-induced immunosuppression also plays a role in skin cancer)

233
Q

DNA damage caused by UVB?

A

Pyrimidine dimer

  • cyclobutane pyrimidine dimer (more common)
  • pyrimidine-pyrimidone (more mutagenic)

Both are formed by covalent bonding between adjacent pyrimidines

234
Q

Nucelotide excision repair? (4)

A

For damage caused by UVB

  1. Recognition of damaged DNA
  2. Cleavage of damaged DNA
  3. DNA polymerase fills in gap using undamaged strand as a template
  4. DNA ligase seals the ends
235
Q

Indirect DNA damage by UVA?

A
  • Oxidation of DNA bases, especially deoxyguanosine to form 8-oxo-deoxyguanosine
  • 8-oxo-dG mispairs with deoxyadenosine rather than deoxycytosine
  • C -> A POINT MUTATION
236
Q

Base excision repair? (5)

A

For damage caused by UVA

  1. Recognition
  2. cleavage of the altered base by DNA glycosylase
  3. Base-free DNA cleaved away by endonuclease
  4. Single nucleotide gap filled by DNA polymerase β
  5. DNA ligase seals the ends
237
Q

UV-induced immunosuppression? (3)

A
  • decreased Langerhans cells in the skin so reduced ability to present antigens
  • T-reg cells with immune suppressive activity
  • anti-inflammatory cytokines e.g. IL-10 by macrophages and keratinocytes
238
Q

Mutation associated with BCC? Treatment developed as result?

A 
PTCH1 mutation (activates hedgehog signalling)
* Tx: vismodegib (hedgehod inhibitor)
239
Q

Mutation associated with melanoma? Treatment as result?

A
  • Ras/raf/MAPK pathway (mostly B-Raf mutation)

* Tx: tramatenib (target is MEK)

240
Q

Problem with vemurafenib in treating melanoma?

A
  • It is a B-Raf inhibitor

Only works for a few months until patient develops resistance to it (so used in combination with trametinib)

241
Q

Mutation associated with familial melanoma? (2)

A
  • CDKN2A mutation - inhibits CDKN2A which normally prevents cells from replicating when they contain damaged DNA
  • CDK4 (cyclin dependent kinase 4) = mutation accelerates cell cycle
242
Q

Ipilimumab?

A

PDL1 inhibitor

243
Q

Melanocytes formed from?

A

Melanoblasts which migrate from neural crest to skin

244
Q

Melanocortin 1 receptor (MC1R)?

A
  • Turns phaeomelanin (red hair) into eumelanin
  • One defective copy of MC1R causes freckling
  • 2 copies = red hair + freckles
245
Q

Ephilides?

A

Freckles (patchy increase in melanin pigmentation after UV exposure)

246
Q

Actinic lentigines?

A

Age/liver spots following UV exposure (found on face, arms, back of hands)

247
Q

Types of melanocytic naevi (moles)? (6)

A
  • Normal
  • Congenital
  • Dysplastic
  • Blue
  • Halo
  • Spitz
248
Q

Small congenital naevi? Medium? Risk with large lesions?

A
  • small = <2cm
  • medium = >2 but <20cm
  • large = 10% increased risk melanoma
249
Q

Why do children with leukaemia tend to have more moles?

A

Chemotherapy leadsto immunosuppression which has been linked to increased naevi

250
Q

Naevus development? (3)

A
  • Childhood = junctional naevus: clusters of melanocytes at DEJ
  • Adolescence = compound naevus: groups of melanocytes in dermis + junction
  • Adulthood = intradermal naevus: entirely dermal (no junction involvement)
251
Q

Features of dysplastic naevi? (3)

A
  • > 6mm diameter
  • Varied pigment
  • Border asymmetry
252
Q

2 types of dysplastic naevi?

A
  • Sporadic - not inherited, 1-2 atypical naevi, risk of MM slightly increased
  • Familial - inherited, high penetrance (CDKN2A mutation), lifetime risk of melanoma 100%
253
Q

What distinguishes dysplastic naevi from melanoma?

A

Unlike melanoma, epidermis is not affected (can be mistaken for melanoma-in-situ)

254
Q

Halo naevi?

A

Peripheral halo of depigmentation (lots of inflammatory lymphocytes)

255
Q

Blue naevi?

A

Entirely dermal and consist of dendritic spindle cells (may mimic melanoma)

256
Q

Spitz naevus?

A

Consist of large spindle/epitheloid cells (most are benign)

257
Q

Features of Spitz naevus?

A
  • Pink/red colour due to prominent vasculature

* Epidermal hyperplasia

258
Q

Epidemiology MM? (3)

A
  • Female > male
  • Middle-age
  • Can arise de novo (majority) or from dysplastic naevi
259
Q

Ax MM? (3)

A
  • Sunburn early childhood
  • UV exposure
  • Genetic i.e. skin colour + dysplastic naevi
260
Q

When to suspect melanoma? (6)

A
  • Change in shape
  • Bleeding
  • Different colours
  • Development of satellite nodules
  • Ulceration
  • New naevus in adulthood (naevi usually develop in childhood)
261
Q

4 types of melanoma?

A
  • Superficial spreading (commonest) - trunk and limbs
  • Acral/mucosal lentiginous -acral and mucosal
  • Lentigo maligna - sun damaged face/neck/scalp
  • Nodular - often trunk
262
Q

Why is nodular melanoma very dangerous?

A

It only has a vertical growth phase (no flat spreading growth phase) so suddenly appears as lump on skin

263
Q

Melanoma prognosis?

A

Related to Breslow’s thickness

  • PpTis (in-situ) - 100% survival
  • pT1 < 1mm - 90% survival
  • pT2- 1-2mm - 80% survival
  • pT3- 2-4mm - 55% survival
  • pT4 > 4mm - 20% survival
264
Q

Other adverse prognostic indicators (other than Breslow’s thickness) for melanoma? (4)

A
  • Ulceration (suffix is b e.g. pT3b)
  • High mitotic rate
  • Lymphovascular invasion
  • Satellites
265
Q

Melanoma tx? (4)

A
  • Excision (if sentinel node involvement, lymphadenectomy)
  • Chemo
  • Acral melanomas have c-kit mutation so can be treated with imatinib
  • BRAF inhibitor (vemurafenib) - only works for few months so paired with MEK inhibitor e.g. trametinib
266
Q

Epidermal tumours other than melanoma? (4)

A
  • Benign-seborrhoeic keratosis
  • Precancerous = Bowen’s, actinic keratosis, viral lesions
  • BCC
  • SCC
267
Q

Seborrhoeic keratosis? Features? (3)

A

Benign proliferation of keratinocytes

  • Common in ageing skin
  • Found on face + trunk
  • Stuck-on appearance
268
Q

Leser trelat sign?

A

Eruption of many seborrhoeic keratoses - can be sign of cancer

269
Q

3 types of BCC? (3)

A
  • Nodular
  • Superficial
  • Infiltrative (morphoeic)
270
Q

What is a chronic leg ulcer?

A

An open lesion between knee and ankle that remains unhealed for >4 weeks

271
Q

What are most chronic leg ulcers?

A

Venous

272
Q

Lipodermatosclerosis?

A

Sclerosis in response to venous hypertension

273
Q

Features of venous ulcer vs arterial ulcer? (2)

A
  • Venous = shallow

* Arterial = very sharp edges, punched-out deep ulcer (clues = hairless, cold leg)

274
Q

Features of Vasculitis? (4)

A
  • Painful
  • Sudden onset
  • Purpuric rash
  • Necrotic
275
Q

Non-healing shallow, well-defined leg ulcer?

A

BCC

276
Q

Ix chronic leg ulcer? (3)

A
  • ABPI (establish if arterial disease)
  • Wound swab (only if sign of infection)
  • Bloods - FBC, LFTs, U + E, CRP
277
Q

ABPI values?

A
  • 1.0 = normal
  • 0.8 - 1.3 = compress
  • <0.8 = vascular disease
  • > 1.5 = calcification
278
Q

Venous ulcer tx? (2)

A
  • Non-adherent dressing + COMPRESSION (4 layer compression bandaging)
  • Leg elevation
279
Q

Slough? How can slough be removed? (3)

A

Bacteria, exudate

  • Compression bandaging
  • Hydrogels
  • Manual debridement
280
Q

Commonest site for venous leg ulcers?

A

medial and lateral malleoli

281
Q

What shape are you aiming for when padding and shaping a leg prior to bandaging?

A

Cone

282
Q

Tinea pedis tx?

A

ORAL terbinafine (as topical clotrimazole cannot properly penetrate nail)

283
Q

Complication of facial shingles?

A

Ramsay Hunt syndrome (post-herpetic neuralgia)

284
Q

When may BCC kill?

A

Very unlikely to metastasise + very slow growing so can only kill when invading something like eye —> brain

285
Q

Precursors SCC? (3)

A
  • Bowen’s (especially on legs)
  • Actinic keratosis
  • Viral lesions
286
Q

Bowens disease? Epidemiology?

A
  • SCC in-situ (no dermal invasion)

* Usually older ladies’ legs

287
Q

Actinic keratosis?

A

Sun-exposed skin esp. scalp, face, hands

288
Q

Viral precursors SCC?

A
  • Viral genital lesions
  • Eythroplasia of Queryat (penile bowen’s)

Both associated with HPV

289
Q

Virulence factor examples? (5)

A
  • Adhesin – enables binding of the organism to host tissue
  • Invasin – enables organism to invade host
  • Impedin – enables organism to avoid immune system
  • Aggressin – causes damage to host directly
  • Modulin – induces damage to host indirectly
290
Q

Dangerous conditions associated with staph aureus? (2)

A

Toxic shock and SSS

291
Q

Staph aureus virulence factors? (5)

A
  • Capsule
  • Fibrinogen binding protein (adhesin)
  • Coagulase (clots plasma)
  • PVL (leukocidin)
  • TSST-1 (shock)
292
Q

Effects of TSST-1? (5)

A

Rapid (48 hrs)

  • high fever
  • vomiting
  • diarrhoea
  • sore throat
  • myalgia
293
Q

Staphylococcal food poisoning caused by? (3)

A
  • SeA, SeB, SeC
294
Q

Scalded skin syndrome caused by which staph aureus toxins? (2)

A

Exfoliatin toxins - often neonatal

* ETA and ETB target desmoglein-1

295
Q

what is significant about TSST-1 ?

A

it is a superantigen!!! Activates 1 in 5 Tcells (normal Ag 1:10,000)
* Cytokine storm

296
Q

Toxic shock syndrome diagnostic criteria? (4)

A
  • Fever
  • Macular rash + desquamation
  • Hypotension
  • > 3 organ systems involved
297
Q

Severe skin infections associated with PVL? (3)

A
  • Recurrent furunculosis
  • Sepsis
  • Necrotising fasciitis
298
Q

CA-MRSA? Associated diseases? (2)

A

PVL + a toxin

  • Necrotising pneumonia
  • Severe contagious skin infections
299
Q

Necrotising pneumonia?

A

Caused by CA-MRSA

  • Flu like symptoms that progresses to ARDS DESPITE ANTIBIOTICS!!!!!!
300
Q

GAS skin diseases? (3)

A
  • Impetigo
  • Cellulitis
  • Necrotising fasciitis
301
Q

Cellulitis?

A

Infection in dermis

302
Q

SLS?

A

Streptolysin - a haemolysin

303
Q

Toxic shock caused by? (2)

A

s.aureus (no bacteremia) OR s.pyogenes (invasive)

2nd Year Medicine (24 decks)

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