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Dermatology - Summary
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Dermatology - Summary Table of all dermatology conditions organised by history findings, examination findings, investigation findings and management according to Australian guidelines.
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Inflammatory Skin ConditionsInfo History/RF Examination Investigation Management
Psoriasis Characterised by inflammation, vascular Pruritus Erythematous salmon pink Skin biopsy Lifestyle – education,
Chronic proliferation (erythema), epidermal +/- overlying silver scale – support, reassurance; Avoid
autoimmune, keratinocyte proliferation (thicker skin) Systemic – depression, variable size that are well Pathology triggers, sun exposure,
inflammatory Ax – genetic inheritance (polygenic) DM, arthritis, IBD, demarcated Hyperkeratosis/parakerotosis moisturise, BB can worsen
disease Triggers – infectious (beta-haemolytic lymphoma Nail – pitting, thickening, Neutrophils in stratum psoriatic plaques
strep, staph, HIV), mechanical irritation, onycholysis, dactylitis corneum Mild-Mod –
drugs (sausage fingers), yellow Epidermis thin over dermal corticosteroids, calcipotriol
Pathophys – disordered T cell activation → Location – extensor discolouration papillae (hence why it’s red) 0.05% 0 vit D analogue
cytokines → skin cell multiplication & surfaces Guttate – acute onset, post Acanthosis Severe – Phototherapy
capillary dilation – thickened and red, scaly Clinical Dx strep pharyngitis Dilated capillaries in dermal (UVB), methotrexate, oral
skin Rain-drop appearance w/ papillae steroids, monoclonal Abs
Epi – 2-4% of all people, onset ~15-25, deeper colour + silver scale Perivascular lymphohistiocytic Follow up – review w/
lifelong and fluctuating course Better prognosis infiltrate derm and psychosocial
supports
Eczema/Atopic Ax – genetic factors (polygenic Pruritus Erythema Allergy testing Lifestyle
Dermatitis inheritance) – inherited predisposition for Xerosis – dry skin Scaling/Flaking IgE levels A – Avoid Triggers – soap,
Inflammatory increased IgE formation and sensitisation Location – Vesicles, papules Skin biopsy over heating
skin condition Infants – face, scalp, Oozing/crusting B – Bathing (short,
driven by T- Pathophys – disturbance of epithelial knees, elbow (extensors) Ketosis pilaris Pathology lukewarm showers)
helper cells (t1 barrier (skin is drier, more permeable to Children – neck and Excoriations Spongiosis – Intracellular C – Clothing
hypersensitivity allergens/organisms); dysfunction of flexural surfaces (wrists, Lichenification (thickening) oedema between D – damage prevention I.e
reaction) – immune system (increased T helper antecubital fossa, popliteal Hypopigmentation keratinocytes bandages, regular
endogenous lymphocytes + IgE → increased response fossa) Acanthosis – thick skin in emollients, cut nails
to allergen); change in skin microbiome Adults – above + wrists, Not well demarcated chronic eczema
Known as hands, feet Parakeratosis – inflammatory Pharm
Atopic Triggers – env factors – hot, cold, Clinical Dx infiltrate Topical Corticosteroids –
Dermatitis sweating, frequent washing; allergens – Excoriation – signs of rubbing hydrocortisone cream
food, dust mites; stress, infection, clothing, Calcineurin inhibitors –
detergents, disinfectants, asthma or RF – allergic rhinitis, tacrolimus
allergic rhinitis asthma, age <5yrs, FHx of Treat infections – wet
eczema dressings to soak crusts,
Epi – common in infants, less common as Bactroban ointment, oral
we age Abx (fluclox)
Cx – psychiatric i.e depression, iatrogenic
(steroids → perioral dermatitis, DMARDs, Long-term
biologics), secondary bacterial infections Regular emollients, avoid
(staph, eczema herpticum) triggers, wet dressing,
dermatology + allergy
referrals
Infections
, Info History/RF Examination Investigation Management
Cellulitis/Abscess Ax – GABHS (strep pyogenes) – most Acute onset Orange peel appearance – Bedside – Non-pharm –
Infection of the common; staph aureus and Pasteurella Red, painful, hot, swollen cutaneous lymphatic ?Skin swab – causative Analgesia
epidermis, multocida (from dog/cat bites) is less skin oedema due to surrounding bacteria, but should swab Manage Ax (e.g wound)
dermis and common Spreads rapidly hair follicles only in open infective areas Elevate limb, keep area
subcutaneous May be well-demarcated Ascending lymphangitis (red only clean
tissue most often Pathophys – small skin lesion e.g or more diffuse border; proximal streaking from Outline to monitor
caused by interdigital tinea pedis; usually a defect in usually flat, ill defined infection of lymph vessels) erythema
streptococci or skin barrier e.g cut, insect bite Systemic Sx – Fever, chills, Bloods – Compression stockings
staph headache, malaise Toe-web abnormality – FBE (↑WBC)
Cx – severe cellulitis, bacteraemia, sepsis, fungal infection (tinea) may ↑ CRP/ESR Pharm – Abx
spread i.e endocarditis, osteomyelitis, RF – skin breach, reveal point of bacterial UEC 1st line – fluclox or
necrotising fasciitis, gas gangrene underlying condition, entry Blood culture + sensitivities cephalexin PO
vascular disease, Vesicles, blisters, bruising, 2nd line – fluclox or
immunosuppression, erosion/ulceration, abscess Imaging – cefazolin IV
obesity, diabetes, Lymphadenopathy Doppler US – rule out DVT Vanc if MRSA risk
DDx eczema/psoriasis, tinea
Unilateral – pedis, lymphoedema Location – lower limb, often Consider MRSA coverage if
erysipelas, unilateral swaps not back (e.g
necrotizing clindamycin, Bactrim,
fasciitis, DVT, Clinical Dx vanc)
septic arthritis, Erythema, well demarcated,
acute gout raised border, may become Abscess – incise and drain
Bilateral – bullous, purpuric or
chronic venous necrotic, pain and systemic Prevent future cellulitis –
insufficiency, Sx of infection address RF
lymphoedema
HPV Ax – double stranded, circular, non- Verruca vulgaris – common warts Endoscope – if upper resp No treatment for infection
Causes infection enveloped DNA virus with an icosahedral Lesions are plaques or papules – skin coloured or whitis, tract infection suspected itself; infection clears up
of skin and capsid usually firm, rough or scaly surface, cauliflower like Regular pap or acetic acid w/o any treatment
mucous Low risk types 6 and 11 cause anogenital appearance, on elbows, knees, fingers or palms; may tests of the cervix after 21 yr usually
membranes warts, mild cervical cell abnormalities, cause tenderness and pruritus can lead to bleeding olds
tumouts of nongenital mucosal membranes Mx for common warts
e.g resp tract, oral cavity, oesophagus, eye Verruca plantaris – plantar warts Definitive Dx cannot be Wait – usually skin warts
High risk types 16, 18, 31 and 33 cause Rough, hyperkeratotic lesions on the sole of the foot, made w/o molecular testing regress within 2 yrs
cervical Ca, high risk of anogenital, oral and often grow inwardly and cause pain while walking of biopsied cells for viral DNA
oropharyngeal SCC Verruca plana – flat warts or RNA Topical agents – salicylic
HPV types 1, 2 and 4 cause skin warts such Multiple small, flat patches or plaques, localised on the acid, cryotherapy or
as common warts – verruca vulgaris and face, hands and shins surgical interventions
plantar warts – myrmecias/verruca
plantaris
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