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Dermatology Flashcards

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USMLE® Step 1 flashcards
1
Q

Epidermis cell type

A

Stratified cellular epithelium

comes from ectoderm

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2
Q

Epidermis Layers

A

Basal layer
Prickle layer
Granular layer
Keratin layer

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3
Q

epidermal cell are …

A

95% keratinocytes

5%: Melonocytes, langerhands and merkel

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4
Q

Basal layer

A

Made of laminin and collagen IV

- one cell thick

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5
Q

Prickle cell layer

A
  • Larger polyhedral cells
  • Lots of desmosomes (connections)
  • Concur cohesive strength to the surrounding cells but also promoting movement
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6
Q

Granular layer

A

2-3 layers of flatter cells
• Large keratohyalin granules – contain structural filaggrin & involucrin proteins
- Bind intermediate keratin filaments together

• Odland bodies (lamellar bodies)
- Cells secrete these into extracellular space resulting in formation of hydrophobic lipid envelope (cornified envelope) – skin barrier
• Cell nuclei lost – non-viable corneocytes

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7
Q

Keratin layer

A
  • Corneocytes: overlapping non-nucleated cell remnants
  • Insoluble cornified envelope
  • 80% keratin & filaggrin
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8
Q

Melanocytes

A

Migrate from the neural crest to the epidermis in first 3 months of foetal development

Pigment producing dendrite cells - organelles called melanosome

Convert tyrosine to melanin pigament

  • eumelanin (Brown/black)
  • phaeomelanin (red/yellow)
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9
Q

Melanin

A

Melanin caps protect the nuclear DNA in basal cells (protective cap over nucleus) and absorb light

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10
Q

Langerhans cells

A

Mesenchymal origin – bone marrow

Prickle cell level in epidermis but also found in dermis and lymph nodes

Antigen presenting cells

Racket organelle (Birbeck granule): A rod or tennis racket-shaped cytoplasmic organelle solely found in Langerhans cells and hence a marker for Langerhans cell histiocytosis

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11
Q

Merkel cells

A
  • basal and found between keratinocytes & nerve fibres

* mechanoreceptors

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12
Q

Hair follicles “Pilosebaceous unit”

A
  • Epidermal component plus dermal papilla
  • Specialised keratins
  • Adjacent sebaceous gland – natural moistures
  • Hair pigmentation via melanocytes above dermal papilla
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13
Q

Phases of hair growth

A

Anagen = growing (2-6 years)

Catagen = involuting (4 week period)

Telogen = resting (5-10%)

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14
Q

Types of hair growth

A

lanugo, vellus and terminal

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15
Q

Nails

A 
• Specialised keratins
• Nail matrix / root similar to hair bulb
• Growth rate  0.1mm  per day
o Fingers > toes
o Summer > winter
• Some drugs increase nail / hair growth
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16
Q

Dermis layers

A

Papillary dermis is thin and lies just beneath epidermis

Reticular dermis thicker bundles type 1 collagen
• Reticular dermis contains appendage structures-sweat glands, pilosebaceous units

Ground substance – hyaluronic acid + chondroitin sulphate

Muscles, blood, lymph and nerves

Mesoderm

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17
Q

Lymphatics

A

Smaller non-contractile vessels ==> larger contractile lymphatic trunks

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18
Q

Sensory nerves

A

Free nerve endings

Pacinian (pressure and deep cutis) and Meissner (vibration and basal)

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19
Q

Sebaceous glands

A

holocrine secretion opening into pilary canal. Largest glands face and chest – clinical implications
• hormone sensitive – quiescent pre-puberty
• Produce sebum: squalene, wax esters, TG and FFA
• Functions: control moisture loss, helps protect against fungal infection

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20
Q

Apocrine sweat glands

A
  • Develop as part of pilosebaceous unit
  • Axillae and perineum
  • Androgen dependent
  • Produce oily fluid  odour after bacterial decomposition
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21
Q

Eccrine sweat glands

A 
• Whole skin surface
o palms, soles and axillae in particular
• Sympathetic cholinergic nerve supply – mental, thermal and gustatory stimulation
• Functions: cooling by evaporation
o moisten palms/soles to aid grip
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22
Q

Skin function

A

Barrier (physical, chemical and pathogens)

Vit D and thyroid hormone metabolism

thermoregulation

immune defence

communication

sensory function

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23
Q

Blaschko’s lines

A

developmental growth pattern of skin – not following vessels, nerves or lymphatics. The disease follows the lines

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24
Q

Cephalic Vein

A 
• arises from dorsal venous network
o lateral aspect of limb
o in deltopectoral groove
o drains into axillary vein
o becomes subclavian at lateral border of rib 1
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25
Q

Basilic Vein

A

• arises from dorsal venous network
o medial aspect of limb
o drains into brachial vein
o level of mid-arm

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26
Q

great saphenous vein:

A

• arises from dorsal venous arch
o medial aspect of limb
o drains into femoral vein
o femoral triangle

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27
Q

small saphenous vein:

A

• arises from dorsal venous arch
o posterior midline of leg
o drains into popliteal vein
o posterior to knee

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28
Q

Superficial lymphatics in arms

A

from plexuses in fingers and hand

  • Basilic => cubital lymph nodes => lateral axillary lymph nodes
  • Cephalic => mainly to apical axillary lymph nodes
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29
Q

Deep lymphatics of arm

A

o Follow deep veins of upper limb

o Drain into lateral axillary lymph nodes

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30
Q

Superficial lymphatics in legs

A

Great saphenous vein => superficial inguinal lymph nodes => external iliac nodes or deep inguinal nodes

Small saphenous vein => popliteal nodes => deep inguinal nodes => external iliac nodes

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31
Q

Deep lymphatics of legs

A

Drain into popliteal lymph nodes =>deep inguinal nodes => external iliac nodes

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32
Q

TH1?
TH2?
TH17?
Associated diseases

A

TH1 (psoriasis), TH2 (atopic dermatitis) & TH17 (psoriasis and atopic dermatitis).

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33
Q

Plasmacytoid DC (pDC):

A

produce IFNα. Found in diseased skin

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34
Q

Atopic eczema

A

• Impairment of skin barrier function is a key factor:
o Mutations in fillagrin gene associated with severe/early onset disease.
o ↓AMP in skin (antimicrobial proteins)
• T cells (TH2), DC, KC, macrophages and mast cells are involved/found in the lesions (probably attracted by stressed KC)
• The defective skin barrier allows access/sensitisation to allergen and promotes colonisation by micro-organisms.

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35
Q

Type 1 allergy

A
  • Immediate reaction - occurs within minutes & up to 2 hours after exposure to allergen
  • Routes of exposure – skin contact, inhalation, ingestion and injection
  • History – consistent reaction with every exposure
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36
Q

Type 1 allergy signs/symptoms

A

Urticaria: Lesions appear within 1 hour and last 2-6 hours, sometimes 24 hours

Angioedema: Localised swelling of subcutaneous tissue or mucous membranes

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37
Q

Type 1 allergy Ix

A

• History – most important!
• Specific IgE (RAST)
- Skin prick or prick-prick testing
• Challenge test: only do if skin prick test is negative
• Serum mast cell tryptase level (during anaphylaxis

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38
Q

Type 1 allergy Mx

A

Allergen avoidance
• Prevent effects of mast cell activation (anti-histamines)
• Anti-inflammatory agent (corticosteroids)
• Adrenaline autoinjector (for anaphylaxis): 300ug adults and 150ug children. Prescribed 2 pens
• Block mast cell activation (mast cell stabilisers – sodium cromoglycate)
• Immunotherapy – pollens but most allergies have no immunotherapy

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39
Q

Type IV Allergy

A
  • Delayed hypersensitivity
  • Antigen specific and T Cell mediated
  • Allergic contact dermatitis/eczema
  • Onset of reaction typically after 24-48 hours
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40
Q

Type IV allergy Ix

A

Patch testing. On finn chambers and Removed after 48 hours and read at 48 and 96 hours due to delayed hypersensitivity

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41
Q

Virulence Factors

A
  • Adhesin: Enables binding of the organism to host tissue
  • Invasin: Enables the organism to invade a host cell/tissue
  • Impedin: Enables the organism to avoid host defence mechanisms
  • Aggressin: Causes damage to the host directly
  • Modulin: Induces damage to the host indirectly
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42
Q

TSST

A

Toxic shock syndrome toxin - super antigen from staph aureus

Massive release of cytokines and inappropriate immune response

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43
Q

Toxins

A

TSST
SSS
Staphylococcal Food poisoning (enterotoxin SeA SeB & SeC)

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44
Q

Toxic shock syndrome diagnosis

A

Fever: 39˚C
Diffuse Macular rash & desquamation. diffuse macular erythroderma (“sunburn”)
• Hypotension (≤ 90 mm Hg (adults))
• ≥ 3 Organ systems involved e.g. liver, blood, renal, mucous membranes, GI, muscular, CNS.
o Whole body shock

Menstructual shock – staph colonies the tampon from perineum which passes to the vagina and then into the blood

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45
Q

PVL

A

Panton-Valentine Leukocidin. specific toxicity for Leukocytes

with CA-MRSA (community associated) responsible for necrotizing pnuemonia & contagious severe skin infections.

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46
Q

Staph Aureus infections

A 
Boils and Carbuncles
Other minor skin sepsis (infected cuts etc.)
Cellulitis
Infected eczema	Impetigo
Wound infection
Staphylococcal scalded skin syndrome
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47
Q

Coagulase negative Staphs (e.g. Staphylococcus epidermidis)

A

Skin commensals - not usually pathogenic

May cause infection in association with implanted artificial material, such as artificial joints, artificial heart valves, intravenous catheters (produces “slime” that allows it to stick to prosthetic material)

Staph. saprophyticus causes urinary tract infection in women of child-bearing age

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48
Q

Strep categories

A

alpha (viridans and pneuomaniae), beta (A: strep pyogenes, B: agalactiae, C), gamma

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49
Q

Throat, severe skin infections and scarlett fever

A

strep pyogenes

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50
Q

strep pyogenes infections

A 
•	Infected eczema
•	Impetigo
•	Cellulitis
Erysipelas
Necrotising fasciitis
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51
Q

strep and staph treatment

A

Flucloxacillin (staph and strep)
penicillin (strep)
Vancomycin (MRSA)

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52
Q

Tinea …

A 
o Tinea capitis - scalp
o Tinea barbae - beard
o Tinea corporis - body
o Tinea manuum – hand
o Tinea unguium - nails
o Tinea cruris - groin
o Tinea pedis – foot (athlete’s foot)
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53
Q

Dermatophyte pathogenesis

A
  • Fungus enters abraded or soggy skin
  • Hyphae spread in stratum corneum
  • Infects keratinised tissues only (skin, hair, nails)
  • Increased epidermal turnover causes scaling
  • Inflammatory response provoked (dermis)
  • Hair follicles and shafts invaded
  • Lesion grows outward and heals in centre, giving a “ring” appearance
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54
Q

Fungal infection organisms

A
  • Trichophyton rubrum** (accounts for >70% of lab isolates): Human- human transmission
  • Trichophyton mentagraphytes (next most common isolate (>20%): Human-human transmission
  • Microsporum canis (occasional isolate): cats, dogs-humans
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55
Q

Exanthematous drug eruptions

A

measles like, macuale, popular like
• Most common type of drug eruption (90%)
• Idiosyncratic, T-cell mediated delayed type hypersensitivity (Type IV) reaction
• Usually mild & self-limiting – most go away when the drug is stopped
• Widespread symmetrically distributed rash
• Mild fever is common – can make it confusing to differentiate between viral and drug eruption
Onset is 4-21 days after first taking drug

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56
Q

Drugs associated with exanthematous eruptions

A
  • Penicillins esp if glandular fever
  • Sulphonamides
  • Erythromycin
  • Streptomycin
  • Allopurinol
  • Anti-epileptics: carbamazepine, phenytoin
  • NSAIDs
  • Chloramphenicol
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57
Q

Urticarial drug reactions

A

itchy erythematous wheals that move around appear rapidly after drug exposure+/- angioedema/analphyxis
• Usually an immediate IgE-mediated hypersensitivity reaction (Type I) after rechallenge with drug (β-lactam antibiotics, carbamazepine, many other drugs)
• Some drugs can directly release of inflammatory mediators (histamine) from mast cells on first exposure (aspirin, opiates, NSAIDs, muscle relaxants, vancomycin, quinolones)

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58
Q

Pustular or bullous drug eruptions

A

• Acneiform
o Glucocorticoids (steroid acne)
o Androgens, lithium, isoniazid, phenytoin

• Acute generalised exanthematous pustulosis (AGEP)
o Antibiotics, calcium channel blockers, antimalarials

• Vesicular/bullous reactions can range from mild to severe

• Drug-induced bullous pemphigoid
o ACE inhibitors, penicillin, furosemide

• Linear IgA disease can be triggered by drugs
o Vancomycin

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59
Q

Fixed drug eruptions

A
  • Well demarcated round/ovoid plaques (Red, painful)
  • Hands, genitalia, lips, occasionally oral mucosa
  • Resolves with persistent pigmentation when drug stopped
  • Tetracycline, doxycycline, paracemtol, NSAIDS, carbamazepine, sulfaminades and aspirin
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60
Q

Stevens-Johnson syndrome (SJS)

A

rare, serious disorder of your skin and mucous membranes. It’s usually a reaction to a medication or an infection. Often, it begins with flu-like symptoms (vague upper respiratory symptoms), followed by a painful red or purplish rash that spreads and blisters

Painful erythematous macules - target lesions. Severe mucosal ulceration of more than 2 surfaces

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61
Q

Toxic epidermal necrolysis (TEN)

A

o Systemic and multi-organ failure. Flu like symptoms precede skin involvement
o Widespread dusky painful erythema then necrosis of epidermis. Musose affected
o Sulfonamides, cephalosporins, carbamazepine, phenytoin, NSAIDs, nevirapine, lamotrigine, sertraline, pantoprazole, tramadol
o ICU, relieve pain, protect skin and avoid steroids due to risk of infection

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62
Q

Drug reaction with eosinophilia & systemic symptoms (DRESS)

A

Sulfonamides, anticonvulsants, allopurinol, minocycline, dapsone, NSAIDs, abacavir, nevirapine, vancomycin

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63
Q

Causes of itch:

A

Pruritoceptive
Neuropathic
Neurogenic
Psychogenic

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64
Q

Itch Mx

A
  • Sedative: anti-histamines (non-sedative antihistamines useless for most itch except where excess histamine in the skin is part of the mechanism)
  • Emollients (with menthol, or cooled in fridge – counter-irritant effects)
  • Antidepressants, e.g. doxepin and some of the newer ones including SSRIs
  • (For some types of neuropathic itch, anti-epileptics)
  • Phototherapy
  • Opiate antagonists, ondansetron (a serotonin antagonist), etc
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65
Q

Creams

A

Semisolid emulsion of oil in water

Contain emulsifier & preservative

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66
Q

Ointments

A

o Semisolid grease/oil (soft paraffin)
o No preservative – be careful because you don’t want bacterial spread
o Occlusive and emollient

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67
Q

Lotions

A

Liquid formulation

Suspension or solution of medication in water, alcohol or other liquids

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68
Q

Gels

A

o Thickened aqueous lotions

o Semi-solids, containing high molecular weight polymers eg methylcellulose

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69
Q

Pastes

A

Semisolids
o Often used in cooling, drying, soothing bandages
o Could at preventing macerating of the skin surrounding the ulcer

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70
Q

• Foams

A

o Colloid with two – three phases

o Usually hydrophilic liquid in continuous phase with foaming agent dispersed in gaseous phase

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71
Q

Emollients

A
  • Enhance rehydration of epidermis
  • For all dry/scaly conditions esp. eczema
  • Need to be effective and cosmetically acceptable
  • Prescribe 300-500g weekly -see BNF
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72
Q

Topical corticosteroids mechanism

A
  • Vasoconstrictive
  • Anti-inflammatory
  • Antiproliferative
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73
Q

Examples of corticosteroids and potency

A

Hydrocortisone mild

Modrasone clobetsone butyrate - moderate

betamethasone valerate potent

clobetasol proprionate - very potent

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74
Q 
HYPERKERATOSIS
PARAKERATOSIS
ACANTHOSIS
PAPILLOMATOSIS
SPONGIOSIS
A

• Increased thickness of keratin layer
Persistence of nuclei in the keratin layer
Increased thickness of epithelium
Irregular epithelial thickening
Oedema fluid between squames appears to increase prominence of intercellular prickles. If severe vesicles filled by oedema fluid develop.

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75
Q

UVB leads to direct DNA damage: what are the photo products?

A

cyclobutane pyrimidine dimers (CPDs) – more common

pyrimidine–pyrimidone (6–4) photo-products – more mutagenic

o Repaired by nucleotide excision repair
o CC → TT UV signature mutation

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76
Q

UVA causes indirect DNA damage: what are the photo products?

A

o Oxidation of deoxyguanosine forming 8-oxo-deoxyguanosine
o Repaired by base excision repair
o C → A point mutation

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77
Q

MCR1

A
  • One defective copy of MC1R causes freckling

* Two defective copies-red hair and freckles

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78
Q

Freckles (ephilides)

A
  • Patchy increase in melanin pigmentation
  • Occurs after UV exposure
  • Reflects clumpy distribution of melanocytes
79
Q

Actinic lentigines

A
  • Related to UV exposure – chronic exposure
  • Epidermis elongated rete ridges
  • Increase melanin and basal melanocytes
80
Q

Congenital melanocytic naevi

A
  • Small <2cm diameter
  • Medium >2cm but <20cm diameter
  • Giant-garment type lesions
  • Large lesions 10-15% risk of melanoma so may need surgical excision
81
Q

Usual type acquired naevi

A

Junctional naevus (DEJ) - CHILDHOOD

compound naevus - junctional clusters and groups of cells in dermis - early adulthood

intradermal naevus - all junctional activity had ceased - adult

82
Q

Dysplastic Naevi (DN)

A
  • Generally >6mm diameter, variegated pigment and border asymmetry
  • Architectural atypia AND cellular atypia
  • Unlike melanoma epidermis not effaced
  • Severe dysplasia may be difficult to distinguish from melanoma in-situ
83
Q

Halo naevi

A

Peripheral halo of depigmentation. They show inflammatory regression and are overrun by lymphocytes. Young adults – full of lymphocytes attack it and the melanocytes

84
Q

Blue naevi

A

entirely dermal and consist of pigment rich dendritic spindle cells

85
Q

The Spitz naevus

A

• Consist of large spindle and/or epithelioid cells – melanocytes becomes spindle
• May closely mimic melanoma
• Most are entirely benign
• Spitz naevus-note pink coloration due to prominent vasculature
o Small and well defined
o Epidermal hyperplasia

86
Q

Alopecia areata

A

condition that causes hair to fall out in small patches, which can be unnoticeable. These patches may connect, however, and then become noticeable. The condition develops when the immune system attacks the hair follicles, resulting in hair loss.

87
Q

Hirsutism

A

Excess hair growth

88
Q

Vitiligo

A

autoimmune disease with loss of melanocytes

89
Q

X-linked ichthyosis

A

genetic skin disorder that affects males. It is an inborn error of metabolism characterized by a deficiency of the enzyme steroid sulfatase. … The normal shedding of dead skin cells is inhibited and the skin cells build up and clump into scales.

90
Q

ALBINISM

A

genetic partial loss of pigment production
• Does have melanocytes but doesn’t produce melanin

congenital disorder characterized in humans by the complete or partial absence of pigment in the skin, hair and eyes.

Albinism is associated with a number of vision defects, such as photophobia, nystagmus, and amblyopia.

91
Q

NELSON’S SYNDROME

A

melanin stimulating hormone is produced in excess by the pituitary

  • hyperpigmentation is caused by high levels of circulating ACTH that bind to the melanocortin 1 receptor on the surface of dermal melanocytes
  • increase in skin pigmentation, so patients may look as if they have a suntan
92
Q

Merkel cell cancer

A

Rare and high mortality

caused by viral infection

93
Q

Contact allergic dermatitis (type IV reaction)

A

Response to chemicals, topical therapies, nickel, plants etc. Has to be something in contact with the skin e.g. nickel or latex

94
Q

Pathology of contact dermatitis (IV)

A

• Langerhans cell in epidermis processes antigen (immunogenicity).
• Processed antigen is then presented to Th cells in dermis
• Sensitised Th cells migrate into lymphatics and then to regional nodes where antigen presentation is amplified
• On subsequent antigen challenge specifically sensitised T-cells proliferate and migrate to and infiltrate skin
o dermatitis

95
Q

contact allergic dermatitis signs/symptoms

A

Erythema, scaling, fissuring, lichenification (thick and leathery), nail dystrophy, crusting

96
Q

contact allergic dermatitis Ix and Mx

A

Ix: Patch testing

Mx: 
• Avoid allergens 
• Cover exposed areas 
• Treat eczema with emollients 
• Topical steroid depending on severity  
• Treat infection
97
Q

Irritant (contact) dermatitis

A

• Non-specific physical irritation rather than a specific allergic reaction
E.g.Soap/detergent/cleaning products, water, oil

98
Q

Irritant (contact) dermatitis signs/symptoms

A

fissuring, erythema, scaling, crusting, lichenifcation and nail dystrophy

sparing of flexures

99
Q

Irritant (contact) dermatitis Mx

A
  • Avoid all irritants, hand care (soap subisitiues, regular emollients, careful drying, cotton or cotton lined gloves for wet and dry work
  • Topical steroids for acute flare up
100
Q

Atopic eczema gene

A

filaggrin

101
Q

Atopic eczema signs/symptoms

A 
• Pruritus
• Ill-defined erythema & scaling
• Generalised dry skin
• Flexural distribution (varies with age) – folds in the wrist 
• Associated with other atopic diseases:
• ichthyosis vulgaris from filaggrin mutations (dry, thick and itchy skin)
- Lichenification 
- Excoriation
102
Q

Atopic eczema Ix

A 
Itching plus 3 or more:
•	Visible flexural rash*
•	History of flexural rash*
•	Personal history of atopy (or first degree relative if under 4 yo)
•	Generally dry skin 
•	Onset before age 2 years
103
Q

Atopic eczema Mx

A
  1. Education
  2. Plenty of emollients
  3. Avoid irritants/allergens including shower gels and soaps – washing hear in the sink so the shampoo does not go on the skin
  4. Topical steroids – exacerbations
  5. Treat infection
  6. Phototherapy – mainly UVB
  7. Systemic immunosuppressants
  8. (Biologic agents)
104
Q

complications of atopic eczema

A

• Crusting indicates Staph aureus infection
• Eczema herpeticum
o Herpes simplex virus
o Monomorphic punched-out lesions

105
Q

Discoid Eczema

A

long-term skin condition that causes skin to become itchy, reddened, swollen and cracked in circular or oval patches.

106
Q

Photosensitive eczema

A
  • Chronic Actinic Dermatitis
  • Look for cut offs e.g. cut-off at collar
  • These patients are often atopic too
  • Drug induced: clinical history showing that drug use is causing it: Secondary to photosensitising drugs
107
Q

Stasis eczema

A

need to treat underlying condition issues e.g. varicose vein

  • hydrostatic pressure
  • oedema
  • red cell extravasation
108
Q

Pompholyx eczema

A

usually restricted to the hands and feet.

In most cases, pompholyx eczema involves the development of intensely itchy watery blisters, mostly affecting the sides of the fingers, the palms of the hands and the soles of feet.

rapid onset

109
Q

Psoriasis

A

Chronic inflammatory skin condition characterised by scaly erythematous plaques which typically follows relapsing remitting course

110
Q

Psoriasis pathology

A

Proliferation and dilation of blood vessels in epidermis – infiltration of inflammatory cells such as T cells and neutrophils
o ?Complement mediated attack on keratin layer
o Complement attracts neutrophils to keratin layer
o Munro micro abscesses – a useful diagnostic clue

111
Q

Psoriasis triggers

A

Stress, infections (strep pneumonia), koebner phenomenon (trauma), drugs (lithium, NSAIDS and beta-blockers), alcohol, obesity and smoking

112
Q

Psoriasis types

A

Chronic plaque psoriasis: symmetrical well-defined red plaques with silvery scale on extensor aspects of the elbows, knees, scalp, sacrum and feet.

Flexural psoriasis: plaques in moist flexural areas (axillary, groins, sub mammary)

Guttate psoriasis: Large numbers of small plaques over the trunk and limbs (young).

Pustular psoriasis (palmoplantar): yellow-brown pustules with plaques affecting palms and soles

Erythrodermic psoriasis (widespread pustular): systemic upset (fever, increase in WBC, dehydration). Medical emergency 
Nail changes
113
Q

Psoriasis Ix

A

Koebner phenomenon: psoriasis develops in area of skin trauma e.g. scratch mark or scar

Auspitz sign: removal of surface scale reveals tiny bleeding points (dilated capillaries in elongated dermal papillae

114
Q

Psoriasis Mx (mild)

A

1) EMOLLIENTS
2) Vitamin D analogues
o Calcipotriol (Dovonex)
o Calcitriol (Silkis)
3) Steroid ointments – usually in combination with Vitamin D/ risk of rebound e.g. Betamethasone valerate 0.1% + calcipotriol
o Don’t use for more than 8 weeks and 4 week break before restarting
4) Coal tar – if Vitamin D has failed or widespread: anywhere no limit
5) Dithranol

115
Q

Psoriasis Mx (moderate to severe)

A

Phototherapy e.g. Narrowband UVB and PUVA (guttate or plaque)

Systemic treatments e.g. immunosuppresion such as methotrexate
or Immune modulation such as targeted biological agents
e.g. infliximab & etanercept (TNF antagonist), Apremilast (PDE-4 inhibitor)

116
Q

Guttate Psoriasis Mx

A

o 1st line = narrow band UVB therapy

o 2nd line = Methotrexate and/or oral retinoid

117
Q

Scalp Psoriasis Mx

A

o Potent topical steroid lotion or Vit D analogue scalp prep. Coal tar shampoos may help

118
Q

Lichenoid disorders

A

damage to basal epidermis and infiltration between the epidermis and dermis

119
Q

Lichenoid disorders signs/symptoms

A

Itchy flat-topped violaceous papules (raised area less than 1cm)

120
Q

Lichen planus

A

lesions (flexor aspects of wrists, forearms, ankles and legs) are purple, pruritic, poly-angular, plantar (flat topped), papules seem at any age and have white lacy markings on surface of papules and buccal mucosa (Wickhams straie)

  • T cell-mediated inflammation targeting an unknown protein within the skin and mucosal keratinocytes.
  • Other lesions: scalp, nails, tongue, mouth (lacy white areas on inner cheek) and gentials
121
Q

Lichen planus biopsy

A

o Irregular sawtooth acanthosis (diffuse epidermal hyperplasia)
o Hypergranulosis and orthohyperkeratosis
o Band-like upper dermal infiltrate of lymphocytes
o Basal damage with formation of cytoid bodies

122
Q

Lichen planus Mx

A 
• Check for possible drug percipient 
• Emollients
• Treat symptomatically 
o topical steroids (potent or very potent)
o oral steroids if extensive

UVB Phototherapy or PUVA

Oral disease: fluticasone spray

123
Q

Pemphigus Vulgaris

A

• Loss of integrity of epidermal cell adhesion
o IgG autoantibodies made against desmoglein 1 and 3
• Desmoglein 3 maintains desmosomal attachments
• Immune complexes form on cell surface
• Complement activation and protease release
• Disruption of desmosomes
• End result is ACANTHOLYSIS

124
Q

Pemphigus Vulgaris signs/symptoms

A

Flaccid superficial blisters which rupture easily to leave widespread shallow erosions
• Involves skin esp. scalp, face, axillae, groin, trunk
• May affect mucosa e.g. mouth, resp.tract. Extensive mucosal involvement may be fatal

125
Q

Pemphigus Vulgaris Ix

A
  • Skin biopsy: +ve immunofluorescence (intercellular IgG giving a crazy paving affect)
  • Nikolsky’s sign = positive
  • Circulating anti-epidermal antibodies can be detected by a blood test (indirect immunofluorescence test).
126
Q

Pemphigus Vulgaris Mx

A
  • Prednisolone (40-60mg/day PO) with gradual tapering
  • Steroid sparing: azathioprine, methotrexate or cyclophosphamide
  • Rituximab (anti-CD-20) and IV immunoglobulin in resistant cases
127
Q

Bullous Pemphigoid

A

Fragility at the dermo epidermal junction
elderly >80 years old
• Autoimmune disease
• Circulating antibodies (IgG) react with a major and/or minor antigen of the hemidesmosomes anchoring basal cells to basement membrane. The result is local complement activation and tissue damage

128
Q

Bullous Pemphigoid signs/symptoms and Ix

A

• Non-specific rash for several weeks before blisters appear
o Urticated itchy plaques rather bullae in early disease
• Subepidermal blister – tense (1-3 cm in size) on inflamed or normal skin
• They develop on areas of skin that often flex — such as the lower abdomen, upper thighs or armpits.
• localized to one area, or widespread on the trunk and proximal limbs
- Skin biopsy +ve IgG and C3 on BM
- Nikolsy sign negative

129
Q

Bullous Pemphigoid Mx

A
  • Emollients
  • Topical antisepsis/hygiene measures
  • Very potent topical steroids e.g. clobetasol
  • Prednisolone (0.3-1.0mg/kg/day PO)
  • Blisters heal however relapsing course 5-10 years
  • Tetracycline antibiotics
130
Q

Dermatitis Herpetiformis

A
  • Strong association with coeliac disease
  • IgA antibodies target gliadin component of gluten but cross react with connective tissue matrix proteins
  • Immune complexes form in dermal papillae and activate complement and generate neutrophil chemotaxins.
131
Q

Dermatitis Herpetiformis Ix

A
  • Hallmark is papillary dermal micro abscesses

* DIF shows deposits of IgA in dermal papillae

132
Q

Epidermolysis Bullosa types

A
  • EB simplex – cells stop sticking together in the epidermis
  • Junctional – cells stop sticking together at epidermal-dermis junction
  • Dystrophic – at the dermis – scarring – recurring over lifetime. Gradually the digits become shorter and become a stump (very disabling)
133
Q

Epidermolysis Bullosa signs/symptoms

A

• Blisters occur with minor trauma or friction and are painful. Its severity can range from mild to fatal.

134
Q

Acne

A

Chronic inflammatory disease of the pilosebaceous unit

135
Q

Acne pathology

A
  1. Basal keratinocyte proliferation in pilosebaceous follicles (androgen drive) – poral occlusion
  2. Increase in sebum production: increase in androgens and androgen sensitivity
  3. Propionibacterium acnes colinsation
  4. Inflammation (dermal) and foreign body granulomas
  5. Comedones (white and black) blocking secretions, hence papules, nodules, cysts and scars
136
Q

Acne diagnosis

A
  • Mild- scattered papules and pustules, comedones
  • Moderate - numerous papules, pustules & mild atrophic scarring
  • Severe - cysts, nodules and significant scarring
137
Q

Mild acne Mx

A

Topical treatment (mild/moderate acne)
o Benzoyl peroxide – keratolytic, antibacterial
o Topical vitamin A derivatives (retinoid) - drying effect
o Topical antibiotics – antibacterial and anti-inflammatory – clindamycin 1%

138
Q

Moderate acne Mx

A

o 1st line: Tetracycline, doxycycline or erythromycin if preg or under 12
o Topical retinoid

139
Q

Severe acne Mx

A

Isotretinoin (oral retinoid) –
• +/- oral prednisolone (not long term)
• Laser therapy and dermabrasion for scarring.

140
Q

Rosacea

A

Chronic and relapsing disorder of blood vessels and pilosebaceous units in central facial areas typically in fair skinned people
o Patchy inflammation with plasma cells
o Pustules
o Perifollicular granulomas
o Follicular Demodex mites often noted (Allergic reaction to mites)

• Triggered by stress/blushing, alcohol, sunlight and spices

141
Q

Rosacea signs/symptoms

A
  • Recurrent facial flushing – central with erythema, telangestia
  • Visible blood vessels
  • Pustules and papules (without comedones)
  • Inflammatory nodules
  • Thickening of skin - rhinophyma
142
Q

Rosacea Mx

A

Reduce aggravating factors:

Metronidazole gel, Ivermectin (to reduce demodex mite)

Oral tetracycline long term or erythromycin if contradicted

Isotretinoin low dose if severe

Telangiectasia : vascular laser

Rhinophyma: surgery/ laser shaving

143
Q

Porphyria cutanea tarda (PCT)

A

reduced enzyme activity of uroporphyrinogen decarboxylase resulting in overproduction of photoactive porphyrins

  • Triggers e.g. HIV, Hep C, alcohol, increase iron levels (Fe supplements/hemochromatosis)
  • Caused chronic liver disease and excess iron build up
144
Q

Porphyria cutanea tarda (PCT) signs/symptoms

A

• Vesicles/bullae in sun exposed sites – visible light not UV light
• Hypertrichosis: abnormal amount of hair growth over the body
• Solar urticaria
Hyperpigmentation
• Morphoea: patch or patches of discoloured or hardened skin on the face neck, hands, torso or feet
• Skin fragility
• Scarring (milia)

145
Q

Porphyria cutanea tarda (PCT) dx

A
  • Faecal & urinary porphyrins (woods lamp – goes red)
  • Spectrophotomterer
  • Skin biopsy
146
Q

Porphyria cutanea tarda (PCT) Mx

A 
• Remove and treat percipients (underlying cause)
o	Alcohol
o	Viral hepatitis
o	Oestrogens
o	Haemochromatosis
• Sun avoidance/protection 
• Regular venesection
• Low dose chloroquine
147
Q

Erythropoietic protoporphyria

A

deficiency in the enzyme ferrochelatase, leading to abnormally high levels of protoporphyrin in the red blood cells (erythrocytes), plasma, skin, and liver.

148
Q

Erythropoietic protoporphyria signs/symptoms

A
  • Mild anaemia
  • Gallstones by 40 – multiple pigment gallstones
  • Pain/unpleasant sensation with physical light exposure but no blistering or erythema
149
Q

Erythropoietic protoporphyria Mx

A

6 monthly LFTs and RBC porphyrins
• Visible light photoprotection measures
o Behavioural (e.g. avoid middle of day sunlight)
o Clothing (importance of weave, colour, etc)
o Environmental (e.g. shade trees, window films)
o Topical sunscreen
• May need liver and bone marrow transplant

150
Q

Acute intermittent porphyria

A

partial deficiency of the enzyme hydroxymethylbilane synthase (also known as porphobilinogen deaminase). This enzyme deficiency can result in the accumulation of porphyrin precursors in the body.

151
Q

Acute intermittent porphyria signs/symptoms

A
  • Severe abdominal pain.
  • Pain in your chest, legs or back.
  • Constipation or diarrhoea.
  • Nausea and vomiting.
  • Muscle pain, tingling, numbness, weakness or paralysis.
  • Red or brown urine.
  • Mental changes, such as anxiety, confusion, hallucinations, disorientation or paranoia.
152
Q

Acute intermittent porphyria Ix and Mx

A

increased urinary porphobilinogen secretion

  • Mild attacks can be managed with increased caloric intake and fluid replacement. Recurrent acute attacks should be managed by a porphyria specialist. Hospitalization is often necessary.
  • Panhematin, an intravenous medication used to correct heme deficiency, may also be prescribed.
153
Q

Necrotising faciitis

A

Bacterial infection spreading along fascial planes below skin surface → rapid tissue destruction

• 2 types:
o Type I – mixed anaerobes & coliforms, usually post-abdominal surgery
o Type II – Group A Strep infection

154
Q

Necrotising faciitis Mx

A

surgical debridement

antibiotics

155
Q

Fungal infections Diagnosis

A

• Clinical appearance
• Woods light (fluorescence)
• Skin scrapings, nail clippings, hair – taken from the scaly edge of the lesion
o Send to laboratory in a “Dermapak” for microscopy and culture
o N.B. Culture takes 2 weeks +

156
Q

Fungal infections Mx

A 
Small areas of infected skin, nails
o Clotrimazole (Canestan) cream or similar
o Topical nail paint (amorolfine)

• Extensive skin infections, nail infections and scalp infections
o Terbinafine orally
o Itraconazole orally

157
Q

Candida Mx

A

oral fluconazole

158
Q

Scabies signs/symptoms

A

Intensely itchy rash affecting finger webs, wrists, genital area

159
Q

Scabies Mx

A
  • Permethrin 5% cream (first choice) should be applied all over and left on for 8 hours
  • malathion lotion, applied overnight to whole body and washed off next day (second choice)
  • Treat again after 7 days
  • benzyl benzoate (avoid in children)
160
Q

Pubic lice Mx

A

Malathion

161
Q

Chicken pox and signs/symptoms

A

Varicella virus

Macules to papules to vesicles to scabs to recovery

fever and itch

162
Q

Chicken pox Mx

A
  • Live attenuated vaccine is available for chickenpox
  • Calamine lotion to keep lesions cool
  • Trim nails – lessen damage from scratching
  • Flucloxacillin if bacterial superinfection
  • Varicella Zoster Immune Globulin
  • Acyclovir if immunocompromised or on steroids
163
Q

shingles

A

Zoster or Herpes Zoster (reactivation in later age)

Tingling/pain to erythema (see photo) to vesicles to crusts

164
Q

Post Herpetic Neuralgia

A

Zoster associated pain (beyond week 4)

165
Q

Ramsay-Hunt syndrome

A

Vesicles and pain in auditory canal and throat

Facial palsy (7th nerve palsy): Poorer prognosis than Bell’s palsy (idiopathic 7th nerve palsy)

Irritation of the 8th cranial nerve
– Deafness
– Vertigo
– Tinnitus

166
Q

Herpes simplex types

A 
HSV Type 1
o	main cause of oral lesions
HSV Type 2
o	rare cause of oral lesions
o	causes half of genital cases
o	encephalitis / disseminated infection (particularly in neonates)
167
Q

Erythema multiforme

A

Erythema multiforme (EM) is a skin condition of unknown cause; it is a type of erythema possibly mediated by deposition of immune complexes (mostly IgM-bound complexes) in the superficial microvasculature of the skin and oral mucous membrane that usually follows an infection or drug exposure.

Many triggers including drug reactions and some infections
o Herpes simplex virus
o Mycoplasma pneumoniae bacterium

168
Q

Molluscum contagiosum (pox virus) and Mx

A

Fleshy, firm, umbilicated, pearlescent nodules

Mx: self limiting but can use local application of liquid nitrogen

169
Q

Warts (Human papilloma virus) or Verracus (feet) Mx

A

1st line: Keratolytics – topical salicylic acid
2nd line: Cryotherapy
3rd line: Imiquimod

170
Q

Erythema infectiosum (slapped cheek syndrome)

A

Erythrovirus (formerly parvovirus) B19.

Note slapped cheek appearance.. As the rash on the face fades a lacy macular rash on the body appears.

In adults rash may be absent and an acute polyarthritis of the small joints eg of the hands may be more prominent.

171
Q

Complications of parvovirus 19

A

spontaneous abortion

Aplastic crises:
• sudden drop in haemoglobin
• seen in patients with short red cell life span: Thalassaemia, Hereditary spherocytosis and Sickle cell anaemia

Chronic anaemia
• in immunosuppressed patients

172
Q

Orf

A
  • Firm, fleshy nodule on hands of farmers
  • Constitutional symptoms rare

virus of sheep

173
Q

Tuberous sclerosis signs/symptoms

A 
•	Periungual fibromas – around nails 
•	Facial angiofibromas 
Cortical tubers and/or calcification of falx cerebri 
Hamartomas 
Bone cysts 
•	Shagreen patches
•	Enamel pitting
174
Q

Xeroderma Pigmentosum (DNA repair syndrome) and complications

A

Defect in one of seven Nucleotide Excision Repair (NER) genes (XPA - G)

Photosenstivity
Photodamage

175
Q

Oculocutaneous albinism

A 
• congenital absence of melanin
• autosomal recessive
• visual defects including: 
o photophobia
o nystagmus
o amblyobia
176
Q

Seborrhoeic keratosis

A

Benign proliferation of epidermal keratinocytes

Epidermal acanthosis, hyperkeratosis, horn cysts

177
Q

Malignant Melanoma risk factors

A

UV exposure (intermittent), sunburn, fair complexion, many (>50) melanocytic or dysplastic naevi, positive family history, childhood sunburn, previous melanoma, old age (>80 years)

178
Q

Malignant Melanoma signs/symptoms

A

Melanoma most common on sun-exposed sites scalp, face, neck, arm, trunk, leg
• A – Asymmetry in the outline of the lesion
• B – Border – irregular
• C – Colour variation (more than 2) with shades of black, brown, blue or pink
• D – Diameter >6mm
• E – Evolution – all changing moles e.g. size, elvation and colour

179
Q

Malignant Melanoma types

A

Superficial spreading
Acral/mucosal lentiginous

acral and mucosal: palms, soles and subungual

Lentigo maligna: sun-damaged face/neck/scalp: arises from lentigo melanoma

Nodular

180
Q

Malignant Melanoma Mx

A

Depends on the tumour depth (Breslow thickness) and ulceration
- Primary excision to give clear margins (1-2cm)
- Some also receive a sentinel node biopsy
o If SN positive - regional lymphadenectomy

Treatment of advanced disease difficult
o Chemo, immunotherapy, genetic therapies

Some acral melanomas have c-kit mutations and may be treated with imatinib (tyrosine kinase inhibitor)

Melanomas on intermittently sun-exposed skin may have a BRAF mutation
- Vemurafenib and Dabrafenib: target the mutated form of B-RAF

Trametinib targets MEK: Inhibiting the downstream signals, blocks proliferation, survival, cell cycle

However, B-RAF resistance increases, better if you use the two in combination

181
Q

Basal cell carcinoma

A

pluripotent stem cells in basal epidermis

Most common of malignant skin tumours

182
Q

Basal cell carcinoma signs/symptoms

A
  • sun exposed sites (head and neck area)
  • slow growing lump or non-healing ulcer
  • painless and often ignored
  • ‘pearly’ or translucent with visible, arborising blood vessels
  • Overlying telangiectasia
  • central ulceration - “rodent ulcer”
183
Q

BCC types

A

‘superficial’: red scaly plaques with raised smooth edge, often on trunk or shoulder.

nodular or nodulocystic (most common): a pearly nodule with rolled telangiectatic edge on the face or on a sun exposed site with or without central ulceration

infiltrative - ‘morphoeic’. Poorly defined, mid facial sites, infiltrate cutaneous nerves (perineural spread). Waxy, scar-like plaque with indistinct borders. Wide and deep subclinical extension

pigmented

184
Q

BCC Mx

A
  • most can be treated by skin surgery esp nodular (excision of 4mm margin with histology)
  • Mohs micrographic surgery for morphoeic variant
  • sBCC – topical imiquimod, Photodynamic treatment, cryotherapy
  • Vismodegib binds to Smoothened to block hedgehog signalling and prevent cell cycle activation and angiogenesis
185
Q

squamous cell carcinoma precursor

A

actinic keratoses: partial thickness dysplasia: scalp, face and hands: precursor to invasive squamous cell carcinoma

Bowen’s disease (carcinoma-in-situ): full thickness dysplasia: lower leg. Scaly patch/plaque, Irregular border, No dermal invasion

186
Q

squamous cell carcinoma signs/symptoms

A
  • Sun exposed sites: face, scalp, ears, hands
  • hyperkeratotic (crusted) lump or ulcer: warty or crusted lump or ulcer
  • grow relatively fast, may be painful &/or bleed
  • ear, nose, lip and scalp are high risk sites
187
Q

SSC Mx

A

• SCC precursors: cryotherapy, 5-Fluorouracil cream, imiquimod, photodynamic therapy

local complete excision: 6mm margin with histology

Radiotherapy

188
Q

Venous leg ulcer

A
  • Open lesion between knee and ankle unhealed for at least 4 weeks caused by venous hypertension in superficial veins (incompetent valves, DVT).
  • Increased pressure leads to poor oxygenation of surrounding skin
189
Q

Venous leg ulcer signs/symptoms

A
  • Chronic and recurrent lower leg ulceration
  • Shallow, sloping-edge ulcer varying size
  • Commonly in gaiter area
  • Surface slough (dead skin and bacteria)
190
Q

Venous leg ulcer Ix

A 
• ABPI (Ankle-Brachial Pressure Index) 
 - 0.8-1.3: compression
<0.8 arterial 
>1.3 calcification 
• Duplex USS
• Swab ONLY if clinical signs of infection
191
Q

Venous leg ulcer Mx

A
  • Analgesia
  • Debridement of dead tissue
  • Non-adherent dressings +/- desloughing agent
  • High compression (four-layer bandaging)
  • Leg elevation
  • Supporting stocking worn for life after healing to prevent recurrence.
192
Q

Arterial Leg Ulcer

A

• Open lesion between knee and ankle unhealed for at least 4 weeks caused by arterial insufficiency

193
Q

Arterial Leg Ulcer signs/symptoms

A
  • Punched out deep painful ulcers
  • Higher (lower?) on the leg, common on the feet
  • Cold
  • Pale
  • Pulseless
  • Hairless
  • Absent peripheral pulses
194
Q

Arterial Leg Ulcer Mx

A
  • DO NOT USE COMPRESSION
  • Keep clean and covered
  • Adequate analgesia
  • Referral to vascular surgery

Medical Diseases (18 decks)

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