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Dermatology
Fichas del conjunto (159)
- 1What are the layers of the epidermis from deep to superficial?Basal layer
Spindle cell layer
Granular layer
Stratum corneum - 2What are the three major proteins produced in the epidermis?Keratinise
Filaggrins
Involucrins - 3If drugs are to be delivered transdermally, what 2 properties must they have?Lipid soluble and small
- 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. - 5What are the two main types of melanin and what colour are they?Eumelanin - brown/black
Pheomelanin - red/yellow - 6What is the key enzyme involved in melanin synthesis?Tyrosinase
- 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
- 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
- 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
- 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
- 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 - 12What is the bulk of the dermis made up of?Collagen
- 13What is the dominant cell type in the dermis?The fibroblast
- 14What are the two layers of the dermis?The superficial papillary dermis and the deeper reticular dermis
- 15What causes helpers danlos syndrome?Collagen mutation
- 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)
- 17What vitamin is essential for collagen synthesis?Vitamin c. In scurvy, dermatological features such as corkscrew hairs, peri follicular haemorrhages and gingivitis are present.
- 18A mutation in the fibrillation gene causes which diseasemarfans
- 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
- 20What is the clinical lesion seen as a result of mast cell degranulation?Weal. Widespread weals is called urticaria
- 21How good is the blood supply to the skin?Larger than the blood supply to the brain
- 22What is the nervous supply of eccrine sweat glandsCholinergic post ganglionic fibres of the sympathetic nervous system
- 23What two functions does sweat serve in man?Cooling
Functional grip on palms and soles in fight or flight response - 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
- 25What type of cell are eccrine, apocrine and sebaceous glads derived from?Keratinocyte
- 26What are the two main types of post natal hair?Vellus (short, white and thin) or terminal (thick, black, long)
- 27How are sexual hairs formed?These are formed by the action of androgens on vellum hairs
- 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 - 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
- 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
- 31What are type 2 hypersensitivity reactions?They are gig mediated cytotoxic reactions. Examples include pemphigus, pemphigoid and systemic vascularises involving ANCA
- 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
- 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.
- 34Name three types on common type 1 hypersensitivity reactionPeanut, latex, penicillin
- 35What is acanthosis?Thickening in the epidermis due to an increase in the number of keratinocytes. Also called hyperplasia, may be caused by
Scratching - 36What is acantholysis?It is a defect in the adhesion between keratinocytes. Seen in pemphigus, where cells float free from one another
- 37What is a crust?Crust is dried exudate. It is seen in conditions such as eczema and impetigo
- 38What is erythema?Increased redness of the skin due to an increase in intravascular blood
- 39What is hyper keratosis?Increased thickness of the striatum corneum where there are more layers of corner yes than there should be.
- 40What is parakeratosis?Cells in the striatum corneum are normally anucleate. In diseases such as psoriasis, they have nuclei, this is called parakeratosis
- 41What is necrobiosis?A degeneration of collagen normally found within palisading granulomas
- 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
- 43Name 2 common conditions where onycholysis is seenpsoriasis
Dermatophyte nail infections - 44What is panniculitis?Inflammation of the subcutaneous fat e.g. Erythema nodosum
- 45When would you see sterile and non sterile pustules?Sterile - psoriasis
Non sterile - impetigo - 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
- 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
- 48What is spongiosis?Intracellular oedema within the epidermis
- 49What is an ulcer.A full thickness break in the dermis and epidermis
- 50What is a weal?An area of focal dermal oedema. Fluid is deeper than in a blister
- 51What are the two peaks in psoriasis incidence?- type 1: late teenage, early adulthood. Associated with Hla
- type 2: 5th and 6th decade - 52What drugs are thought to worsen psoriasis?Beta-blockers, lithium, interferon alpha, choloquine
- 53What Hla type is associated with psoriasis?Hla cw6
- 54What are the 2 cardinal histology cal features of psoriasisEpidermal hyperproliferation
Pronounced inflammatory infiltrate - 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
- 56Koebner phenomenonWhen psoriasis is active, trauma to the skin results in psoriasis developing at that area
- 57Name the 7 descriptive terms for types of psoriasisStable plaque psoriasis, guttate psoriasis, flexural psoriasis, erythrodermic, pustular, palmoplantar, nail
- 58What does guttate psoriasis usually proceed?A streptococcal sore throat by 2-3 weeks
- 59What are the two main forms of pustular psoriasis?Palmoplantar and generalised
- 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.
- 61What three classic nail changes are seen in psoriasis?Pitting, onycholysis and oily spots
- 62What are the differential diagnoses for erythroderma?Eczema, drug reaction, lymphoma, idiopathic
- 63What precipitating factors can be removed in the management of psoriasis?Few environmental factors can be managed. HIV, drugs, heavy drinking
- 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) - 65Why use emollients in psoriasis?Renders plaques less visible. If scalicylic acid is added, it helps to break up plaques
- 66Hat are the 4 main topical options for psoriasis treament?Emollients, corticosteroids, vitamin d analogues, tar
- 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.
- 68Ow does methotrexate work?Is a dihydrofolate reductase inhibitor. It works by interfering with folate metabolism and forming a false substrate for this enzyme
- 69Name some side effects of methotrexateHepatotoxicity, nephrotoxicity, immune suppression, increased cancer risk
- 70How should patients on methotrexate be monitored?Regular FBI, lfts and u and es
- 71What is the mech of action of cyclosporin?It is a calcineurin blocker, decreasing the T cell response.
- 72What are the main systemic agents used in psoriasis?Methotrexate, cyclosporin, systemic retinoids, biologics
- 73Side effects of systemic retinoids.Teratogenicity, musculoskeletal pain, mouth and eye dryness, elevated triglyceride levels
- 74What two main classes of biological are used in psoriasis?Tnf alpha blockers. Il 17 and il23 blockers
- 75What are the two pathological processes prominent in eczema?Immune system Is active, the skins barrier function is compromised.
- 76What are the three main eczema syndromes?Contact allergic, contact irritant, atopic
- 77Key questions to ask in a contact allergic dermatitis hx.Distribution consistent? Temporally consistent? Occ history, knowledge of hobbies?
- 78What is the investigation of choice for contact allergic dermatitis?Patch testing
- 79How does contact irritant eczema differ from contact allergic?nNo sensitisation period. More exposure leads to worse symptoms. Classic example is hand washing
- 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
- 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
- 82Differential diagnoses for atopic eczema.Fungal infection, primary staph infection, contact allergic dermatitis, scabies
- 83Signs of scratching?Excoriations, lichens fiction, modular prurigo
- 84Things to avoid in atopic eczemaSoaps, detergents, wool, hot environments, hot baths,
- 85What are the first line treatments in atopic eczema?Emollients, antiseptics, bandages and topical corticosteroids
- 86Who and where is corticosteroid absorption most evident?Children and in flexural regions
- 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
- 88What are the main systemic immunosuppressives used in atopic eczema?Prednisolone, azathioprine, cyclosporin, methotrexate
- 89What three problems occur in acne?Abnormal keratinisation of the infundibulum, infection, increased sebum excretion
- 90In an open come done, what causes the black colour?Melanin
- 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
- 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
- 93What are the main treatment modalities for acne?Topical agents - benzoyl peroxide and topical retinoids
Antibiotics,
Systemic retinoids - 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
- 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
- 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
- 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 - 98What tests should be carried out before starting someone on systemic retinoids?FBc, pregnancy test, lfts and lipids
- 99How long is it not safe to conceive for after stopping isoretinoid5weeks
- 100What are the clinical features of rosacea?Facial flushing, telangesctasia, papules pustules, hyperplasia of sebaceous glands, dermal fibrosis
- 101What food or drink tend to make acne rosacea worse?Alcohol and hot curries
- 102Differential diagnoses for rosacea?Acne, seborrhoeic dermatitis, peri oral dermatitis
- 103Topical treatment for rosacea?Metranidazole
- 104First line treatment for ocular rosacea?Tetracycline systemically
- 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
- 106Are come domes seen in rosacea?No
- 107What is the distribution of the rash in seborrhoeic dermatitis?Lipid rich areas such as nasolabial folds, centre of chest, forehead, upper back
- 108In what specific subset may seborrhoeic dermatitis be particularly severe?Untreated aids
- 109How is an acute episode of urticaria treated?Non sedative h1 receptor blockade
- 110Name the 8 different types of urticaria.Acute, contact (immunological and non immunological), chronic auto-immune, dermographism, solar, cholinergic, cold, aquagenic
- 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 - 112What are the commonest causes of angioedema?Wasp sting, bee sting, ace inhibitors
- 113What causes hereditary angioedema?C1 esterase deficiency
- 114What are the first line treatments for an acute attack of hereditary angioedema?C1 esterase concentrate or fresh frozen plasma in the first instance
- 115What is epidermolysis bullosa?An inherited blistering disease usually present at birth
- 116Name the three immunobullous disorders.Pemphigus, pemphigoid, dermatitis hepatiformis
- 117What are the two types of pemphigus?Pemphigus vulgaris - igg against desmoglein 3
Pemphigus foliaceous- igg antibodies against desmoglein 1 - 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 - 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 - 120How is pemphigus diagnosed?Biopsy of a new lesion
- 121How is pemphigus treated?1st line - systemic high dose corticosteroids and azathioprine
2nd line-Iv immunoglobulin, anti cd20 or cyclophosphamide - 122What do antibodies attack in pemphigoid?Hemidesmosomes which anchor keratinocytes to the basement membrane
- 123How do the blisters differ between pemphigus and pemphigoid?Pemphigoid blisters are more tense and durable than pemphigus
- 124What is seen on a diagnostic biopsy of a pemphigoid lesion?Igg staining along the basement membrane in a perilesional biopsy
- 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 - 126What is the patio physiology of dermatitis herpetiformis?Iga mediated, gluten intolerance, sometimes coeliac
- 127Clinical features of dermatitis herpetiformisIntense itch, small clusters of blisters on wrist, knees, elbows and sacrum, mucosal sparing
- 128What are the treatments for dermatitis herpetiformis ?Gluten free diet, dapsone ( monitoring required for the first several months)
- 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
- 130What is the acute and long term treatment for erythema multiforme?Acute - none/ topical steroids
Long term- treatment of ebv with aciclovir - 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
- 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.
- 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 - 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
- 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
- 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
- 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.
- 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.
- 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.
- 140Name four conditions to consider which may cause hirsutism.Pcos, cushings, congenital adrenal hyperplasia, adrenal tumours.
- 141What investigations may it be appropriate to carry out in hirsutism with a potentially endocrine origin?Testosterone, prolactin, dheas, sex hormone binding protein.
- 142What sex do hirsutism and hypertrichosis effect?Hirsutism affects women, hypertrichosis affects both sexes
- 143What conditions can hypertrichosis be seen in?Anorexia nervous, malnutrition, dermatomyositis.
- 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.
- 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.
- 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.
- 147Name 5 things which could cause chronic diffuse alopecia.Systemic malignancy,
Renal/liver failure
Pituitary/thyroid disease
Iron deficiency
Some drugs - 148Name two common causes of scarring alopecia.Discoid lupus, lichen planus
- 149what is the dominant type of UVR in sunshine? which type causes sunburn?UVA most common, UVB causes sunburn
- 150xeroderma pigmentosum patients are principally sensitive to which type of radiation?UVR
- 151whats more common: BCC, SCC, AK?AK much more common than BCC, whichis much more common than SCC
- 152risk factors for NMSCpigmentation, ambient UV exposure, site, inherited syndromes, immunosuppression, PUVA
- 153what can IECs be confused with and why?psoriasis. found in patches on the lower leg. red scaly
- 154what does c + c stand for?currettage and cautery
- 155what problems do morphoeic BCCs present?they have an illdefined border. Mohs surgery required.
- 156are melanocytic naevi precursors to MM?it is thought that 50% of MMs develop from Melanocytic naevi
- 157Define Breslow thicknessThe distance in mm below the granular layer that an M has spread
- 158pyogenic granulomas are particularly common at which sight?fingers
- 159what is the link between sun exposure and BCC and SCC?SCC = cumulative sun exposure
BCC - intermittent sun exposure
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- Fichas sobre Dermatology, creado por Keith Allen el 08/09/2013.
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- Keith Allen
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