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Flashcards

Dermatology

Keith Allen English 159 cards

Cards in this deck (159)

  1. 1What are the layers of the epidermis from deep to superficial?Basal layer
    Spindle cell layer
    Granular layer
    Stratum corneum
  2. 2What are the three major proteins produced in the epidermis?Keratinise
    Filaggrins
    Involucrins
  3. 3If drugs are to be delivered transdermally, what 2 properties must they have?Lipid soluble and small
  4. 4Briefly describe the bricks and mortar model of the epidermisThe bricks are made up of the individual dead keratinocytes. Their outer surface is made from involucrins. The mortar in between these bricks is made from lipids produced by the keratinocytes.
    The result is a hydrophobic barrier which is relatively impermeable to water.
  5. 5What are the two main types of melanin and what colour are they?Eumelanin - brown/black
    Pheomelanin - red/yellow
  6. 6What is the key enzyme involved in melanin synthesis?Tyrosinase
  7. 7What determines skin and hair colour?Everyone in the world has the same number of melanocytes in their skin. The colour is determined my the ratio of different types of melanin
  8. 8Does melanin in melanocytes reflect skin colour?No. Once produced, melanin is passed along the dendrites of the melanocytes into keratinocytes. There are a lot more keratinocytes than melanocytes. Therefore amount of melanin in keratinocytes actually influences colour of skin
  9. 9What are langerhans cells and where are they found?Langerhans cells are antigen presenting cells found in the epidermis. They are thought to collect haptins/antigens and present them to T cells at regional lymph nodes
  10. 10What is the basement membrane? What attaches the dermis and epidermis to it?The basement membrane separates the dermis and epidermis. It is an acellular structure made from a complex mixture of proteins and gene products. Basal cell keratinocytes are attached to it via hemidesmosomes. The basement membrane is attached to the dermis by a number of molecules, most notably collagen vii
  11. 11Blisters often result from interference of structures which join both cells and layers within the skin. Name a blistering disease and the corresponding defect in adhesionEpidermolysis simplex - keratin mutations
    Dystrophic epidermolysis bullosa - collagen via mutation
    Bullous pemphigoid - interference of attachment of epidermis to basement membrane.
    Bullous pemphigus - autoantibodies target desmosomes adhesion between keratinocytes
  12. 12What is the bulk of the dermis made up of?Collagen
  13. 13What is the dominant cell type in the dermis?The fibroblast
  14. 14What are the two layers of the dermis?The superficial papillary dermis and the deeper reticular dermis
  15. 15What causes helpers danlos syndrome?Collagen mutation
  16. 16Name two things which can cause a decrease in the collagen content of the dermis.Corticosteroids (interfere with collagen synthesis). Chronic uv exposure (increased collagen cross linking)
  17. 17What vitamin is essential for collagen synthesis?Vitamin c. In scurvy, dermatological features such as corkscrew hairs, peri follicular haemorrhages and gingivitis are present.
  18. 18A mutation in the fibrillation gene causes which diseasemarfans
  19. 19In the dermis, what surrounds the fibroblasts and various protein structures?Proteoglycans - consisting of core proteins and gags. Common gags found in skin include - hyaluronic acid, chondroitin sulphate, heparin sulphate and keratin sulphate
  20. 20What is the clinical lesion seen as a result of mast cell degranulation?Weal. Widespread weals is called urticaria
  21. 21How good is the blood supply to the skin?Larger than the blood supply to the brain
  22. 22What is the nervous supply of eccrine sweat glandsCholinergic post ganglionic fibres of the sympathetic nervous system
  23. 23What two functions does sweat serve in man?Cooling
    Functional grip on palms and soles in fight or flight response
  24. 24What is normal sweating1litre per day. Can increase to 4 litres per hour. Sweat gland training can occur where although the same volume ofmsweat is produced, the electrolytes lost in it can be reduced
  25. 25What type of cell are eccrine, apocrine and sebaceous glads derived from?Keratinocyte
  26. 26What are the two main types of post natal hair?Vellus (short, white and thin) or terminal (thick, black, long)
  27. 27How are sexual hairs formed?These are formed by the action of androgens on vellum hairs
  28. 28What are the three phases in the hair growth cycle?Anagen - growth phase, typically lasting 3 years
    Catogen - a transition period lasting about 3 weeks where the bulbs undergo apoptosis and the lower hair moves closer to the surface.
    Telegen- a 3 month perios where the new hair is formed below the old, eventually pushing the old out
  29. 29How is the sensation of itch transmitted?It is transmitted through unmyelinated c fibres which cover a great area. Distinct from the fibres which Cary the neural response to pain
  30. 30How do anti histamine s work to relieve itch?They cause a central sedative effect which is thought to relieve the itch because patients are too sedated to scratch
  31. 31What are type 2 hypersensitivity reactions?They are gig mediated cytotoxic reactions. Examples include pemphigus, pemphigoid and systemic vascularises involving ANCA
  32. 32What's a type 3 hypersensitivity reaction?Immune complexes develop and are deposited in the blood vessels. Cause complement and polymorph activation. Can be caused by infection, drugs or may be the cutaneous manefestation of a systemic disease e.g. Ra
  33. 33What's a type Iv hypersensitivity reaction?This a delayed, T cell mediated reaction. A common example in nickel allergy. The presentation of haptens to T cells creates an immunological memory, meaning that future exposure causes an eczematous response. Investigated by patch testing.
  34. 34Name three types on common type 1 hypersensitivity reactionPeanut, latex, penicillin
  35. 35What is acanthosis?Thickening in the epidermis due to an increase in the number of keratinocytes. Also called hyperplasia, may be caused by
    Scratching
  36. 36What is acantholysis?It is a defect in the adhesion between keratinocytes. Seen in pemphigus, where cells float free from one another
  37. 37What is a crust?Crust is dried exudate. It is seen in conditions such as eczema and impetigo
  38. 38What is erythema?Increased redness of the skin due to an increase in intravascular blood
  39. 39What is hyper keratosis?Increased thickness of the striatum corneum where there are more layers of corner yes than there should be.
  40. 40What is parakeratosis?Cells in the striatum corneum are normally anucleate. In diseases such as psoriasis, they have nuclei, this is called parakeratosis
  41. 41What is necrobiosis?A degeneration of collagen normally found within palisading granulomas
  42. 42What is nikolskys sign?Ability to induce a blister on the skin by simple frictional pressure. It is a feature of diseases such as pemphigus and toxic epidermal necrolysis
  43. 43Name 2 common conditions where onycholysis is seenpsoriasis
    Dermatophyte nail infections
  44. 44What is panniculitis?Inflammation of the subcutaneous fat e.g. Erythema nodosum
  45. 45When would you see sterile and non sterile pustules?Sterile - psoriasis
    Non sterile - impetigo
  46. 46What is purpura?blood outside the blood vessel. If it is small, it is called petechiae, if it is larger it is termed a bruise. Palpable purpuri is a sign of vasculitis
  47. 47What is sclerosis?cChanges within the dermis which lead to it feeling harder and stiffer than it sHould. Due to an increased production of collagen. Best example is systemic sclerosis
  48. 48What is spongiosis?Intracellular oedema within the epidermis
  49. 49What is an ulcer.A full thickness break in the dermis and epidermis
  50. 50What is a weal?An area of focal dermal oedema. Fluid is deeper than in a blister
  51. 51What are the two peaks in psoriasis incidence?- type 1: late teenage, early adulthood. Associated with Hla
    - type 2: 5th and 6th decade
  52. 52What drugs are thought to worsen psoriasis?Beta-blockers, lithium, interferon alpha, choloquine
  53. 53What Hla type is associated with psoriasis?Hla cw6
  54. 54What are the 2 cardinal histology cal features of psoriasisEpidermal hyperproliferation
    Pronounced inflammatory infiltrate
  55. 55What are Munro micro abscesses? What disease are they found in?They are found in psoriasis. They are secondary to the inflammatory infiltrate and consist of polymorphs within the epidermis
  56. 56Koebner phenomenonWhen psoriasis is active, trauma to the skin results in psoriasis developing at that area
  57. 57Name the 7 descriptive terms for types of psoriasisStable plaque psoriasis, guttate psoriasis, flexural psoriasis, erythrodermic, pustular, palmoplantar, nail
  58. 58What does guttate psoriasis usually proceed?A streptococcal sore throat by 2-3 weeks
  59. 59What are the two main forms of pustular psoriasis?Palmoplantar and generalised
  60. 60Can topical treatments make pustular psoriasis worse?Yes, inappropriate steroid use can cause pustules to become more widespread. When withdrawn, the pustules can become even worse.
  61. 61What three classic nail changes are seen in psoriasis?Pitting, onycholysis and oily spots
  62. 62What are the differential diagnoses for erythroderma?Eczema, drug reaction, lymphoma, idiopathic
  63. 63What precipitating factors can be removed in the management of psoriasis?Few environmental factors can be managed. HIV, drugs, heavy drinking
  64. 64What are the three steps in psoriasis treatment?1. Topical agents ( creams and ointments)
    2. UVR (UVB and puva)
    3. systemic agents (methotrexate and cyclosporine)
  65. 65Why use emollients in psoriasis?Renders plaques less visible. If scalicylic acid is added, it helps to break up plaques
  66. 66Hat are the 4 main topical options for psoriasis treament?Emollients, corticosteroids, vitamin d analogues, tar
  67. 67What effect does activated psoralen have on DNA?When activated, psoralen intercalated between two strands of DNA and cross links them. This produces a toxic molecule which prevents the proliferation of keratinocytes and inflammatory cells. Needless to say puva is carcinogenic.
  68. 68Ow does methotrexate work?Is a dihydrofolate reductase inhibitor. It works by interfering with folate metabolism and forming a false substrate for this enzyme
  69. 69Name some side effects of methotrexateHepatotoxicity, nephrotoxicity, immune suppression, increased cancer risk
  70. 70How should patients on methotrexate be monitored?Regular FBI, lfts and u and es
  71. 71What is the mech of action of cyclosporin?It is a calcineurin blocker, decreasing the T cell response.
  72. 72What are the main systemic agents used in psoriasis?Methotrexate, cyclosporin, systemic retinoids, biologics
  73. 73Side effects of systemic retinoids.Teratogenicity, musculoskeletal pain, mouth and eye dryness, elevated triglyceride levels
  74. 74What two main classes of biological are used in psoriasis?Tnf alpha blockers. Il 17 and il23 blockers
  75. 75What are the two pathological processes prominent in eczema?Immune system Is active, the skins barrier function is compromised.
  76. 76What are the three main eczema syndromes?Contact allergic, contact irritant, atopic
  77. 77Key questions to ask in a contact allergic dermatitis hx.Distribution consistent? Temporally consistent? Occ history, knowledge of hobbies?
  78. 78What is the investigation of choice for contact allergic dermatitis?Patch testing
  79. 79How does contact irritant eczema differ from contact allergic?nNo sensitisation period. More exposure leads to worse symptoms. Classic example is hand washing
  80. 80What 2 ways can we operationally define atopic?Family hx of atopic disease. Raised Ige levels in the blood, giving them increased chance of mounting a response
  81. 81What is ichthyosis vulgaris?It is a group of conditions caused by filaggrin mutations. Causes dryness and scaling of the skin without any major inflammation
  82. 82Differential diagnoses for atopic eczema.Fungal infection, primary staph infection, contact allergic dermatitis, scabies
  83. 83Signs of scratching?Excoriations, lichens fiction, modular prurigo
  84. 84Things to avoid in atopic eczemaSoaps, detergents, wool, hot environments, hot baths,
  85. 85What are the first line treatments in atopic eczema?Emollients, antiseptics, bandages and topical corticosteroids
  86. 86Who and where is corticosteroid absorption most evident?Children and in flexural regions
  87. 87Are there any alternatives to topical corticosteroids?Topical calcineurin inhibitors such as taro limbus can be used on areas such as the face. Good because it decreases side effects such as skin thinning. Has an immunosuppressive effect, so could theoretically increase skin cancer risk
  88. 88What are the main systemic immunosuppressives used in atopic eczema?Prednisolone, azathioprine, cyclosporin, methotrexate
  89. 89What three problems occur in acne?Abnormal keratinisation of the infundibulum, infection, increased sebum excretion
  90. 90In an open come done, what causes the black colour?Melanin
  91. 91How can a foreign body reaction develop in acne?Within the open comedone, there are vellus hairs. If these grow through the wall of the pyelosebaceous unit, they can set up a foreign body reaction
  92. 92What based make up should females be recommended to use to cover up acne?Water based, as oil based caused irritation and worsening of acne
  93. 93What are the main treatment modalities for acne?Topical agents - benzoyl peroxide and topical retinoids
    Antibiotics,
    Systemic retinoids
  94. 94How do topical retinoids work and in what acne are they thought to be best used first line?They are thought to work by altering keratinisation. It does this by inducing a mild inflammatory reaction. Best used in acne which is comedone dominant
  95. 95How does benzoyl peroxide work and when is it best used?Works by removing p acne bacterium. This in turn reduces the pro inflammatory fatty acids within the skin. Best used in acne where infection is prominent
  96. 96What antibiotics are best used in acne? How long should they be given for?Best antibiotics are tetracyclines and erythromycin. Have to be given long term. 6 months
  97. 97Which groups of patients should tetracycline not be given to and why?Teenagers - teeth staining and storage in bone.
    Pregnant women - teratogenic.
    Use erythromycin instead
  98. 98What tests should be carried out before starting someone on systemic retinoids?FBc, pregnancy test, lfts and lipids
  99. 99How long is it not safe to conceive for after stopping isoretinoid5weeks
  100. 100What are the clinical features of rosacea?Facial flushing, telangesctasia, papules pustules, hyperplasia of sebaceous glands, dermal fibrosis
  101. 101What food or drink tend to make acne rosacea worse?Alcohol and hot curries
  102. 102Differential diagnoses for rosacea?Acne, seborrhoeic dermatitis, peri oral dermatitis
  103. 103Topical treatment for rosacea?Metranidazole
  104. 104First line treatment for ocular rosacea?Tetracycline systemically
  105. 105Should topical corticosteroids be used in rosacea?No, they make it worse. Should never be used on the face unless you have a definitive diagnosis
  106. 106Are come domes seen in rosacea?No
  107. 107What is the distribution of the rash in seborrhoeic dermatitis?Lipid rich areas such as nasolabial folds, centre of chest, forehead, upper back
  108. 108In what specific subset may seborrhoeic dermatitis be particularly severe?Untreated aids
  109. 109How is an acute episode of urticaria treated?Non sedative h1 receptor blockade
  110. 110Name the 8 different types of urticaria.Acute, contact (immunological and non immunological), chronic auto-immune, dermographism, solar, cholinergic, cold, aquagenic
  111. 111What is the treatment algorithm for urticaria.1st line - non sedative h1 receptor blockade
    2nd line-another h1receptor blockade
    H2 receptor blockade
    Others - leukotriene inhibitors, puva and ciclosporin
  112. 112What are the commonest causes of angioedema?Wasp sting, bee sting, ace inhibitors
  113. 113What causes hereditary angioedema?C1 esterase deficiency
  114. 114What are the first line treatments for an acute attack of hereditary angioedema?C1 esterase concentrate or fresh frozen plasma in the first instance
  115. 115What is epidermolysis bullosa?An inherited blistering disease usually present at birth
  116. 116Name the three immunobullous disorders.Pemphigus, pemphigoid, dermatitis hepatiformis
  117. 117What are the two types of pemphigus?Pemphigus vulgaris - igg against desmoglein 3
    Pemphigus foliaceous- igg antibodies against desmoglein 1
  118. 118How can pemphigus vulgaris and foliaceous be differentiated?Foliaceous - superficial blistering. No mucosal involvement
    Vulgaris - mouth ulcers present, due to the involvement of desmoglein 3
  119. 119Clinical features of pemphigusBlisters (may be very superficial and so present as erosions)
    Mucosal involvement including eyes, pharynx, larynx, oesophagus, genitalia.
    Pemphigus foliaceous may be easily mistaken for seborrhoeic dermatitis
  120. 120How is pemphigus diagnosed?Biopsy of a new lesion
  121. 121How is pemphigus treated?1st line - systemic high dose corticosteroids and azathioprine
    2nd line-Iv immunoglobulin, anti cd20 or cyclophosphamide
  122. 122What do antibodies attack in pemphigoid?Hemidesmosomes which anchor keratinocytes to the basement membrane
  123. 123How do the blisters differ between pemphigus and pemphigoid?Pemphigoid blisters are more tense and durable than pemphigus
  124. 124What is seen on a diagnostic biopsy of a pemphigoid lesion?Igg staining along the basement membrane in a perilesional biopsy
  125. 125What is the treatment for pemphigoid?1. Potent topical corticosteroids
    2. To gain remission, systemic prednisolone is given, with/without azathioprine as a steroid sparing agent
  126. 126What is the patio physiology of dermatitis herpetiformis?Iga mediated, gluten intolerance, sometimes coeliac
  127. 127Clinical features of dermatitis herpetiformisIntense itch, small clusters of blisters on wrist, knees, elbows and sacrum, mucosal sparing
  128. 128What are the treatments for dermatitis herpetiformis ?Gluten free diet, dapsone ( monitoring required for the first several months)
  129. 129How do patients with erythema multiforme normally present?Classically a young/ middle aged male presenting with target lesions in an acral pattern, shortly after an episode of herpes simplex infection
  130. 130What is the acute and long term treatment for erythema multiforme?Acute - none/ topical steroids
    Long term- treatment of ebv with aciclovir
  131. 131What are the clinical features of SJS?Same as em, except with mucosal involvement, particularly the eyes and mouth. Adverse drug reactions account for more cases of SJS than em
  132. 132How is SJS treated?The more mucosal involvement, the sicker the patient. Usually managed as inpatient. Corticosteroids not routinely used. Ophthalmology may be required to deal with eyes.
  133. 133What drugs can cause toxic epidermal necrolysis and what is the peak for onset?Drugs include allopurinol, anti epileptics, ace inhibitors.
    Peak onset is between 7 and 28 days of start of drug regime
  134. 134What are the clinical features of toxic epidermal necrolysis?Sudden onset of erythema, positive nikolskys sign, target lesions may be present, skin wrinkling and lifting off, widespread mucosal involvement, intensely painful
  135. 135How is ten diagnosed pathologically?Full thickness punch biopsy, showing full thickness damage, allows differentiation from ssss where damage is just down to the granular layer
  136. 136What are the general treatments which should be undertaken in ten?Managed in HUD/ icu environment for fluid balance and analgesia purposes. Alternating pressure mattress, warm environment. Stop non essential drugs
  137. 137What causes ssss?Particular types of staphylococci produce a toxin against desmoglein 1. The same toxin is implicated in bulbous impetigo, however in this case it is circulating rather than local.
  138. 138Clinical features of ssssCommon in children under 5, but also seen in immunocompromised adults and those with renal failure. Staph infection occurs not in the skin. Child presents with scarlet fever like rsh. 48hours later, flaccid blisters develop and nikolskys sign is positive.
  139. 139Diagnosis of ssss with biopsy. Damage occurs down to the granular layer. How is it treated?Anti-staph treatment, normally with flucloxicilin. Supportive therapy and barrier nursing.
  140. 140Name four conditions to consider which may cause hirsutism.Pcos, cushings, congenital adrenal hyperplasia, adrenal tumours.
  141. 141What investigations may it be appropriate to carry out in hirsutism with a potentially endocrine origin?Testosterone, prolactin, dheas, sex hormone binding protein.
  142. 142What sex do hirsutism and hypertrichosis effect?Hirsutism affects women, hypertrichosis affects both sexes
  143. 143What conditions can hypertrichosis be seen in?Anorexia nervous, malnutrition, dermatomyositis.
  144. 144Why does male pattern alopecia occur?Occurs in 50%of males. Reaction to androgen which causes terminal hairs to become vellus hairs, and eventually fall out.
  145. 145What is telegenic effluvium, and what is the outcome?It is when a large number of hairs are forced to exit the anlagen phase into catagen after a stressful life event. A few months down the line, when they enter telegenic phase and fall out, widespread baldness is the result. The hair will grow back.
  146. 146What is alopecia areata?Characteristic, well demarcated coin shaped areas of hair loss, usually on the scalp or beard area. Exclamation mark hairs are seen. Area should regroup, maybe temporarily slightly darker or lighter thank original. Total loss of hair =alopecia totalis.
  147. 147Name 5 things which could cause chronic diffuse alopecia.Systemic malignancy,
    Renal/liver failure
    Pituitary/thyroid disease
    Iron deficiency
    Some drugs
  148. 148Name two common causes of scarring alopecia.Discoid lupus, lichen planus
  149. 149what is the dominant type of UVR in sunshine? which type causes sunburn?UVA most common, UVB causes sunburn
  150. 150xeroderma pigmentosum patients are principally sensitive to which type of radiation?UVR
  151. 151whats more common: BCC, SCC, AK?AK much more common than BCC, whichis much more common than SCC
  152. 152risk factors for NMSCpigmentation, ambient UV exposure, site, inherited syndromes, immunosuppression, PUVA
  153. 153what can IECs be confused with and why?psoriasis. found in patches on the lower leg. red scaly
  154. 154what does c + c stand for?currettage and cautery
  155. 155what problems do morphoeic BCCs present?they have an illdefined border. Mohs surgery required.
  156. 156are melanocytic naevi precursors to MM?it is thought that 50% of MMs develop from Melanocytic naevi
  157. 157Define Breslow thicknessThe distance in mm below the granular layer that an M has spread
  158. 158pyogenic granulomas are particularly common at which sight?fingers
  159. 159what is the link between sun exposure and BCC and SCC?SCC = cumulative sun exposure
    BCC - intermittent sun exposure

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Flashcards on Dermatology, created by Keith Allen on 08/09/2013.
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Keith Allen
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