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Diseases Flashcards

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Dermatology Board Prep flashcards
1
Q

Define hypersensitivity

A
  • immune response that causes collateral damage to self

- exaggeration of normal immune mechanisms

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2
Q

Describe allergy

A
  • hypersensitivity disorder of the immune system
  • allergic reactions occur when a persons immune system reacts to normally harmless substances in the environment
  • a substance that causes a reaction is called an allergen
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3
Q

Describe a type 1 allergy

A
  • immediate reaction; occurs within minutes and up to 2 hours after exposure to allergen
  • routes of exposure; skin contact, inhalation, ingestion and injection
  • history consistent with every exposure
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4
Q

Describe the clinical presentation of a type 1 allergy

A
  • utricaria; very itchy, lesions appear within 1 hour, lasts 2-6 hours sometimes 24 hours, hives, wheals, nettle rash
  • angioedema; localised swelling of subcutaneous tissue or mucous membranes, non pitting, not itchy
  • wheezing / asthma
  • anaphylaxis
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5
Q

Describe investigations for allergy

A
  • history (most important)
  • specific IgE (RAST)
  • skin prick or prick-prick testing
  • challenge test
  • serum mast cell tryptase level (during anaphylaxis)
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6
Q

Describe skin prick / prick-prick testing

A
  • cheap and quick
  • results in 15-20 minutes
  • specificity and sensitivity 90%+
  • anaphylaxis risk (1:3000)
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7
Q

When would you do a challenge test?

A

Only is skin prick test was negative but history is indicative of allergy

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8
Q

Describe the management of allergies

A
  • allergen avoidance
  • prevent effects of mast cell activation (anti-histamines)
  • anti inflammatory agent (corticosteroids)
  • adrenaline autoinjector (for anaphylaxis)
  • block mast cell activation (mast cell stabilisers - sodium cromogylcate)
  • immunotherapy
  • medic alert bracelet
  • information and education
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9
Q

Describe adrenaline auto-injectors

A
  • for anaphylaxis
  • pre-loaded adrenaline syringe
  • 300 nanograms in adults
  • 150 nanograms in children
  • all patients should be prescribed 2 pens
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10
Q

Describe non allergic reactions

A
  • not mediated by IgE (coeliac, eosinophilic gastroenteritis)
  • direct mast cell degranulation (morphine, aspirin, NSAIDs)
  • metabolic (lactose intolerance)
  • toxic (scombroid fish toxin)
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11
Q

Describe type 4 allergy

A
  • delayed hypersensitivity
  • antigen specific
  • t cell mediated
  • allergic contact dermatitis
  • onset of reaction typically after 24-48 hours
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12
Q

Describe irritant contact dermatitis

A
  • non immunological process
  • contact with agents that abrade, irritate and traumatize skin directly
  • does not require prior sensitisation
  • pattern depends on exposure
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13
Q

Describe the management of irritant contact dermatitis

A
  • allergen / irritant avoidance
  • allergen / irritant minimisation
  • emollients
  • topical steroids
  • UV phototherapy
  • immunosuppressants
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14
Q

Dermatitis is another name for which condition?

A

Eczema

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15
Q

Describe the appearance of the acute phase of dermatitis

A
  • papulovesicular
  • erthematous (red) lesions
  • oedema (spongiosis)
  • ooze or scaling and crusting
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16
Q

Describe the appearance of the chronic phase of dermatitis

A
  • thickening (lichenification)
  • elevated plaques
  • increased scaling
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17
Q

Names classifications of dermatitis

A
  • contact allergic
  • contact irritant
  • atopic
  • drug related
  • photo induced or photosensitive
  • lichen simplex
  • stasis dermatitis
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18
Q

What classification of dermatitis is a delayed type / type 4 hypersensitivity reaction?

A

Contact allergic or drug related

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19
Q

Describe the immunopathology of contact allergic dermatitis

A
  • langerhans cells in epidermis processes antigen (increased immunodeficiency)
  • 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
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20
Q

Describe irritant (contact) dermatitis

A
  • very common
  • non specific physical irritation rather than a specific allergic reaction eg soap etc
  • may be difficult to distinguish from allergic contact dermatitis
  • also may overlap with atopic dermatitis
  • NB types may co exist
  • implications for occupation
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21
Q

Describe atopic eczema

A
  • pruritus
  • ill defined erythema and scaling
  • generalised dry skin
  • flexural distribution (varies with age)
  • associated with other atopic diseases; asthma, allergic rhinitis, food allergy
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22
Q

Describe the chronic changes of atopic eczema

A
  • lichenification
  • excoriation
  • secondary infection
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23
Q

What is the most common secondary infection of atopic eczema?

A

Staph aureus

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24
Q

Describe eczema herpeticum

A
  • an infection to recognise early
  • herpes simplex virus
  • monomorphic punched out lesions
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25
Q

Describe the UK diagnostic criteria for atopic eczema

A
  • itching plus 3 or more of;
  • visible flexural rash (cheeks and extensor surfaces in infants)
  • history of flexural rash
  • personal history of atopy (or Fhx)
  • generally dry skin
  • onset before age 2 years
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26
Q

Describe the treatment of eczema

A
  • plenty of emollients
  • avoid irritants including shower gels and soaps
  • topical steroids
  • treat infection
  • phototherapy; mainly UVB
  • systemic immunosuppressants
  • biological agents
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27
Q

What is the most important gene in eczema?

A

Filaggrin

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28
Q

Stasis eczema can be secondary to what?

A
  • hydrostatic pressure
  • oedema
  • red cell extravasation
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29
Q

Define pruritus

A

A usually unpleasant, poorly localised, non adapting sensation that provokes the desire to scratch

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30
Q

What is the purpose of itch?

A
  • lots of animal itch (possibly all mammals)
  • itch always, or nearly always causes scratching
  • itch is predominately a skin symptoms
  • itch may be of different importance in different mammals
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31
Q

Describe the mediation of itch

A
  • chemical mediators in skin; histamine, PGE2, acetylcholine, serotonin, kallikrein, interleukin 2, substance P tryptase etc
  • nerve transmission; unmyelinated c fibres (different ones transmit itch and temperature from those that transmit pain)
  • central nervous system mediators; opiates (endogenous and exogenous)
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32
Q

Name some mast cell degranulating stimuli

A
  • allergen
  • anti-fcri
  • IgE
  • anti-IgE
  • substance P
  • stem cell factor
  • C5a
  • codeine
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33
Q

Name some pre formed mediators released from mast cell degranulation

A
  • proteases eg tryptase
  • heparin
  • histamine
  • cytokines
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34
Q

Name some newly formed mediators that are synthesised for mast cell degranulation

A
  • prostaglandin D2
  • leukotrienes C4, D4, E4
  • platelet activating factor
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35
Q

Name some causes of itch

A
  • pruritoceptive; something (usually associated with inflammation or dryness) in skin that triggers itch
  • neuropathic; damage of any sort to central or peripheral nerves causing itch
  • neurogenic; no evident damage in CNS, but itch caused by eg opiate effects on CNS effectors
  • psychogenic; psychological causes with no (currently detectable) CNS damage, eg itch in delusions of infestation
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36
Q

Name some systemic diseases associated with itch

A
  • (mostly, not all, neurogenic itch)
  • haematological
  • paraneoplastic
  • liver and bile duct
  • psychogenic
  • kidney disease
  • thyroid disease
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37
Q

Describe the management of itch

A
  • determine cause if possible
  • treat the cause
  • anti-itch treatments; sedative antihistamines, emollients, antidepressants, phototherapy, opiate antagonists
38
Q

Describe the morphologies / presentation of drug eruptions

A
  • exanthematous / morbilliform / maculopapular
  • urticarial
  • papulosquamous / pustular / bullous
  • pigmentation
  • itch pain
  • photosensitivity
39
Q

Describe the risk factors for drug eruptions

A
  • age (elderly over infants)
  • gender (females over males)
  • genetics
  • concomitant disease
  • immune status
40
Q

What is the most common type of drug eruption?

A

Exanthematous drug eruptions

41
Q

Describe exanthematous drug eruptions

A
  • most common type
  • idiosyncratic, t cell mediated delayed type hypersensitivity reaction
  • usually mild and self limiting
  • widespread symmetrically distributed rash
  • mucous membranes usually spared
  • pruritus is common
  • mild fever is common
  • onset is 4-21 days after first taking drug
42
Q

Describe indicators of a potentially severe drug eruption reaction

A
  • involvement of mucous membrane and face
  • facial erythema and oedema
  • widespread confluent erythema
  • fever
  • skin pain
  • blisters, purpura, necrosis
  • lymphadenopathy, arthralgia
  • shortness of breath, wheezing
43
Q

Name some drugs associated with exanthematous eruptions

A
  • penicillins
  • sulphonamides
  • erythromycin
  • streptomycin
  • allopurinol
  • anti-epileptics; carbamazepine, phenytoin
  • NSAIDs
  • chloramphenicol
44
Q

Describe urticarial drug reactions

A
  • usually an immediate IgE mediated hypersensitivity reaction
  • after rechallenge with drug
    OR
  • direct release of inflammatory mediators from mast cells on first exposure
45
Q

Describe pustular or bullous drug eruptions

A
  • acneiform (glucocorticoids, androgens, lithium, isoniazid, phenytoin)
  • acute generalised exanthematous pustulosis (rare, antibiotics, CCBs, antimalarials)
  • vesicular / bullous reactions can range from mild to severe
  • drug induced bullous pemphigoid
  • linear IgA disease can be triggered by drugs
46
Q

Describe fixed drug eruptions

A
  • well demarcated round / oviod plaques
  • red, painful
  • hands, genitalia, lips, occasionally oral mucosa
  • resolves with persistent pigmentation when drug stopped
  • can re-occur at same site on re-exposure to drug
  • usually mild when restricted to a single lesion
  • can present as eczematous lesions, papules, vesicles or urticaria
47
Q

Name drugs associated with fixed drug eruptions

A
  • tetracycline, doxycycline
  • paracetamol
  • NSAIDs
  • carbamazepine
48
Q

Name some conditions associated with severe cutaneous adverse drug eruptions

A
  • stevens johnson syndrokme (SJS)
  • toxic epidermal necrolysis (TEN)
  • drug reaction with eosinophilia and systemic symptoms (DRESS)
  • acute generalised exanthematous pustuloss
49
Q

Name some acute phototoxic drug reactions

A
  • skin toxicity (phototoxicity)
  • systemic toxicity
  • photodegeneration
50
Q

Name some chronic phototoxic drug reactions

A
  • pigmentation
  • photoageing
  • photocarcinogenesis
51
Q

Describe phototoxic cutaneous drug reactions

A
  • non immunological skin reaction arising in an individual exposed to enough photo reactive drug and light of the appropriate wavelengths
  • usually UVA / visible light
  • idiosyncratic reactions can occur
  • increased sensitivity to sunlight, caused by drugs, can also occur via other mechanisms eg immunosuppression or lupus
52
Q

Describe patterns of skin phototoxicity

A
  • immediate prickling with delayed erythema and pigmentation
  • exaggerated sunburn
  • exposed telangiectasia
  • delayed 3-5 days erythema and pigmentation
  • increased skin fragility
53
Q

Name some drugs associated with phototoxicity

A
  • antibiotics
  • thiazides
  • chlorpromazine
  • NSAIDs
  • quinine
  • psoralens
  • amiodarone
  • porphyrins
  • BRAF inhibitors
  • antifungals
  • immunosuppressants
54
Q

Name common culprits of drug eruptions

A
  • doxycycline
  • chlorpromazine
  • quinine
  • amiodarone
55
Q

Describe investigations for drug eruptions

A
  • history and physical examination are usually sufficient to spot likely drug
  • phototesting for suspected phototoxic drug eruptions
  • biopsies may be useful
  • patch and photopatch tests
  • skin prick / intradermao tests for specific drugs
  • skin testing is not indicated for serum sickness reactions or for t cell mediated reactions
56
Q

Describe the management for drug eruptions

A
  • discontinue the drug if possible
  • use an alternative
  • topical corticosteroids may be useful
  • antihistamines may help if type 1 or with symptoms of itch
  • allergy bracelets
  • reported via the yellow card scheme
57
Q

Define a chronic leg ulcer

A

An open lesion between the knee and ankle joint that remains unhealed for at least 4 weeks

58
Q

Most leg ulcers are what in nature?

A

Venous (although often multifactorial)

59
Q

Describe the assessment process of chronic leg ulcers

A

The main aims of assessment are to identify;

  • clues to the underlying aetiology
  • factors contributing to delayed healing
  • SIGN assessment tool
  • order of assessment is patient, leg, ulcer
60
Q

When assessing an ulcer, what would be recorded?

A
  • position of ulcer

- measure surface area

61
Q

Describe vasculitis

A
  • painful
  • sudden onset
  • purpuric rash / pustules
  • necrotic
62
Q

Describe investigations for leg ulcers

A
  • ABPI; establish if there is arterial disease
  • wound swab; only in ulcer increasingly painful, exudate, malodour or enlarging
  • bloods; FBC, LFTs, U and Es, CRP
  • patch testing; to previous ulcer treatments eg bandages, dressingsm creams
  • duplex scan if indicated
63
Q

Describe the treatment of venous ulcers

A
  • control pain
  • ABPI
  • non adherent dressing
  • de-sloughing agent if necessary eg hydrogel / honey
  • 4 layer compression bandaging
  • leg elevation
64
Q

Describe the 4 layer bandaging system

A
  • graduated compression
  • 40mmHg at ankle, 25mmHg below knee
  • latex / rubber free if possible
  • applied by a trained nurse
  • non-adherent dressing
  • leg padded to a cone shape
  • changed weekly, or as required
65
Q

Describe wound bed preparation

A
  • removal of devitalised tissue by debridement;
  • autolytic; the use of dressings to create moist wound environment and hydrate necrotic tissue or eschar - hydrogel, honey
  • sharp debridement; with scalpel or scissors
  • biological; larvae therapy
  • surgical; under general anaesthetic
66
Q

When do we aim to heal ulcers by?

A

12 weeks

67
Q

What is the result of vitamin D deficiency in children?

A

Ricketts

68
Q

What is the result of vitamin deficiency in adults?

A

Osteomalacia

69
Q

Name some indications for skin biopsy

A
  • skin rashes; assist in diagnosis

- skin tumours; assist in diagnosis, remove malignancy, remove unwanted skin growth

70
Q

Describe common melanocytic naevi

A
  • acquired during childhood and early adulthood
  • gradually lose pigment over years
  • usually regular, but not always
71
Q

Describe dermoscopy

A
  • diagnostic aid, mainly used for skin lesions but use extending into hair problems / inflammatory skin disease
  • recognition of morphologic structures not visible by the naked eye, thus opening up possibilities for clinical diagnosis based on dermoscopic features
72
Q

Name types of skin disease due to adverse reaction to amoxicillin

A
  • morbilliform (measles like) eruption
  • urticaria
  • angioedema
  • fixed drug eruption
  • generalised pustulosis
73
Q

Describe the treatment of common precancers

A
  • cryotherapy
  • solaraze
  • 5 FU
  • PDT
  • imiquimod
74
Q

Name the five layers of the scalp

A
  • skin
  • connective tissue
  • aponeurosis
  • loose connective tissue
  • periosteum
75
Q

What is the sensory nerve supply to the face?

A

The trigeminal nerve

76
Q

What is CN V1?

A

Ophthalmic division of trigeminal nerve

77
Q

What is CN V2?

A

Maxillary division of trigeminal nerve

78
Q

What is CN V3?

A

Mandibular division of trigeminal nerve

79
Q

Describe the clinical testing of the sensory component of the trigeminal nerve

A

Ask the patient to close their eyes. Gently brush the skin in each dermatome with a fine tip of cotton wool. Ask the patient to tell you when they feel their skin being touched. compare the two sides

80
Q

How do you test the CN VII (motor)?

A

Ask the patient to

  • frown
  • close eyes tightly
  • smile
  • puff out cheeks (if sphincter intact no air leaks from mouth)
81
Q

Describe methods of local anaesthesia

A
  • topical
  • local infiltration
  • nerve block
  • field block
82
Q

How can you reduce the pain during local anaesthesia?

A
  • relax patient
  • topical local
  • fine needle
  • warm local
  • omit adrenaline
  • neutralise acidity
  • massage skin
  • slow injection
  • subcutaneous injection
  • follicle opening
  • nerve blocks
83
Q

Describe complications of skin biopsy

A
  • bleeding
  • wound dehiscence
  • infection
  • scarring
  • motor or sensory nerve damage
  • loss of function
84
Q

Describe basic skin surgery methods

A
  • electrosurgery
  • snip excision
  • curettage
  • shave excision
  • punch biopsy
  • elliptical excision
85
Q

Describe electrosurgery

A
  • variety of electrosurgery units used for
  • haemostasis
  • treatment of minor skin lesions eg skin tags
86
Q

Describe snip excision

A
  • grasp lesion with skin hook

- cut across base of lesion

87
Q

Describe curettage and cautery

A
  • minimally invasive procedure

- pathology specimen does not accurately record the margins of the tumour

88
Q

Describe punch biopsy

A
  • quick
  • produces good wound edges but difficult to judge depth
  • round holes do not always heal well
  • pathology sample maybe too small
89
Q

Name the five main areas of potential impact of skin disease on quality of life

A
  • physical comfort and functioning
  • acceptability to self and others
  • emotional well being / self esteem
  • social functioning / behavioural
  • confidence in the nature and management of the condition
90
Q

Describe the three types of psychosomatic skin disease

A
  • primary skin disease precipitated or exacerbated by emotional factors
  • secondary psychiatric illness arising from or exacerbated by primary skin disease
  • primary psychiatric disorder which is manifest via skin lesions
91
Q

Describe psychosocial variables affecting vulnerability to illness

A
  • presence of abuse at some point in life
  • life events
  • grief reactions
  • perception of an environment as exceeding personal resources
  • interpersonal relationships providing a buffering role for stress
  • psychological assets and well being

Dermatology (10 decks)

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