Skin and Musculoskeletal Pathology Flashcards

Question

What is Atopic Eczema?

Answer 1

* Usually starts in childhood, occasionally adults * Often fam history * Associated with asthma & hayfever * Type 1 hypersensitivity reac to allergen

Answer 2

* Contact irritant dermatitis - direct skin injury by irritant (irritant too long on hands= reac) e.g. acid, alkali, strong detergent etc * Contact allergic dermatitis (need to develop reac)- nickel, dyes, rubber. Act as haptens which combine with epidermal protein to become immunogenic & cause reac (look at distrib in reac e.g. if on tummy could be from belt buckle, nickel in earrings if on ears)

Answer 3

Morphological subtypes: • Seborrhoeic dermatitis - affect areas rich in sebaceous glands: scalp, forehead, upper chest (ehere sebciuos galnds sit) • Nummular dermatitis - coin shaped lesions

Answer 4

* 1-2 % of population * Well defined, red oval plaques on extensor surfaces - (knees, elbows, sacrum). * Fine silvery scale (can be torn off- bleeding). Auspitz sign. Removal of scale causes small bleeding points. * +/- pitting nails. * +/- sero-negative arthritis (affecting small joints). * Can affect extensor surface on back of head Pathogenesis- clinical & microscopic features reflect massive cell turnover (too fast)

Answer 5

Psoriasiform hyperplasia" - distinct appearance: • i) Regular elongated club shaped rete ridges • ii)Thinning of epidermis over dermal papillae. • iii)Parakeratotic (contain nuclei) scale. • iv)Collections of neutrophils in scale (Munro microabscesses)

Answer 6

* Genetic factors. Some have fam history. Multiple loci [psoriasis Susceptibility/ PSORS genes] many in region of major histocompatibility complex on Chromosome 6p2 implicated. Same area involved in other autoimmune disorders eg IBD,MS * Env trigger factors,[ie Acquired factors] infec, stress, trauma, drugs e.g. may come into hospital for something else then causes psoriosis * Disregulation of immune system

Answer 7

* Arthropathy, 5-10% associated * Psychosocial effects * Cardiovascular disease, 2-3x risk.?inflammation, drugs. Stress, smoking * Cancer; Increased risk Non-melanoma skin cancer [eg BCC] ,Lymphoma disease or treatment effect (don’t know if lymphoma disease or treatment casuing the psoriassis)

Answer 8

* Discoid LE (DLE) - skin only (NOTHING else) * Systemic LE (SLE) - visceral disease, +/- involves skin. * Clinically look similar in skin- Red scaly patches on sun-exposed skin +/- scarring, scalp involvement causes alopecia. * SLE:- Butterfly rash on cheeks and nose. * Auto-imm disorder mainly affecting body’s connective tissues [CT disorder]. Auto antibodies directed at various tissues. * May affect any part of the body, but importantly kidneys * Autoantibodies against cells

Answer 9

* Thin atrophic epidermis. * Inflammation and destruction of adnexal structures. * IMF - LE band. IgG deposited in basement membrane. * Look for IgG in basement memb of skin (immunoflourescence) * LE- basement memb attacked by autoantibodies

Answer 10

• Autoantibody against skin • In Lupus Erythematous; o Have keratinocytes, antigens & basement memb o Deposition of antibodies in skin= attack antigen in basement memb o But antibody against it with fluorescent tag on it o LE immunoflouresence- fluorescent tags along basement memb (shows autoantibodies- can look for this in skin & kidneys)

Answer 11

* Inflamm of skin & proximal muscle * Peri-ocular oedema and erythema [Heliotropic rash- sun related; photosensitive distib] * Erythema in photosensitive distribution. * Myositis; proximal muscle weakness. * Can check for creatinine kinase in blood (from muscle). * In adults 25% associated with underlying visceral cancer (underlying malignancy- treat underlying cancer & rash will go away)

Answer 12

* Similar to L.E. * Often a lot of dermal mucin (connective tissues). * Negative IMF (immunoflouresence)

Answer 13

• Formation of fluid filled blisters in skin • 2 important conditions; pemphigus vs pemphigoid; o Both make blisters in skin o PemphigoiD- bullae Deeper o Proteins diff so makes slightly diff disease o PemphiguS- makes blister IN epidermis (S at end- superficial)

Answer 14

* Group of disorders characterised by loss of cohesion between keratinocytes resulting in an intraepidermal blister. * All types cause fragile blisters/bullae which rupture easily. * Can be extensive +/- involve mucous membranes. * Keratinocytes don’t stick together- fragile, easily rupture * Affect mucous membs- e.g. eyes Pathogenesis • Autoantibodies, directed against intercellular material. • Can be detected by immunofluorescence (IMF).

Answer 15

* Disease characterised by subepidermal blisters: * Elderly (70s & 80s often) with large tense bullae which do not rupture easily (often in lower legs) * Can be localised or extensive disease. * Pathogenesis: autoantibodies to glycoprotein in basement membrane. * Can be detected by IMF to make diagnosis

Answer 16

* Small intensely itchy blisters. Extensor surfaces * Often young patients. Associated with Coeliac disease. * Look for IgA deposition in dermal papillae on IMF (get neutrophil collections). * Histopathology; Neutrophil microabscesses in dermal papillae.

Answer 17

* Dermatomyositis and visceral cancer (if have one check for the other) * Dermatitis herpetiformis and Coeliac disease * Acanthosis Nigricans [dark warty lesions in armpits] and internal malignancy. * Necrobiosis Lipoidica [red + yellow plaque on legs] and Diabetes Mellitus * Erythema Nodosum [red tender nodules on shins] associated with infecs elsewhere esp.lung, drugs, and other diseases

Answer 18

• Very common • May arise from all elements of skin o Epidermis; BCC,SCC o Melanocytes; Naevi, Melanoma o Merkel cell tumour, rare but dangerous o Adnexal structures, sweat gland and hair follicle tumours and cysts. o Nerves and blood vessels; haemangioma, neuromas o Connective tissue; dermatofibroma (common tumour)

Answer 19

* Commonest skin tumour. Metastases very rare. * Aetiology; sun exposed site, especially face. Occasional secondary to radiotherapy * Pale skin that burns easily * Immunosuppression * Rare - Gorlin’s syndrome (inherited prob) * Can be on face- difficult to treat * Don’t leave them- treat early Clinically; • Early: nodule. • Late: ulcer (rodent ulcer). • Morphoeic BCC - ill defined (thickening & woodiness on skin) & infiltrative. Microscopically; tumours composed of islands of basaloid cells with peripheral palisade

Answer 20

* 2nd most commonest in skin * U.V. irradiation. Usually occurs in sun exposed sites. Increased risk in tropical countries. * -Radiotherapy. * -Hydrocarbon exposure - tars, mineral oils, soot. * Chronic scars/ulcers - SCC arises within these (Marjolins ulcer). * Immunosuppression - renal transplant patients at increased risk. * Drugs, some newer drugs for treating melanoma can cause SCC * (BRAF inhibitors) Clinically; nodule with ulcerated, crusted surface Microscopically; invasive islands & trabeculae of squamous cells showing cytological atypia * Metastases in 5% (lip, ear, perineum (genital ear)) * Other high risk features- > 2 cm, >4mm thick, high grade * Common on back of hand

Answer 21

* Pre-malignant disease; actinic [solar]keratosis. * Dysplasia to Squamous epithelium. * Very common on chronic sun exposed sites. * Scaly lesion with erythematous base * Only rarely progresses to invasive disease. * May spontaneously resolve (e.g. drop off) * Thick keratin layer (warty plaques)

Answer 22

``` • Constituent cell in epidermis • Melanocytes derive from neural crest • Function; to form melanin which is transferred to epidermal cells to protect the nucleus from UV radiation. • Give rise to tumours o Benign; naevi [moles]- ```

Answer 23

• Local benign collections of melanocytes • Several types; o Superficial; congenital or acquired o Deep in dermis; Blue naevi.[ mongolion spot- e.g. in lumbosacral area) • Atypical mole syndrome o Families with increased incidence of melanoma o Multiple clinically atypical moles o Histologically atypical/dysplastic naevi o Increased risk of developing melanoma. • Common naevus- collection of melanocytes (no atypia so is a nevus) • Giant congenital naevi o Atypical moles- atypical mole syndrome (lots of moles)

Answer 24

• Much rarer than BCC and SCC. • Incidence is rising rapidly. • Very dangerous malignancy which can metastasize widely. • Incidence increasing (since 1975) • Risk factors; o Sun exposure - especially short intermittent severe exposure. Australia has more melanomas. o Race - Celtic with red hair, blue eyes, fair complexions who tan poorly most at risk.Melanoma rare in dark skinned people (protected by melanin) o Fam history – Atypical mole syndrome - multiple large atypical moles Giant congenital naevi - small risk of turning malignant [<5%].

Answer 25

* Face, elderly people. * Slow growing, flat, pigmented patch. * Micro: Proliferation of atypical melanocytes along basal layer of epidermis. Skin also shows signs of chronic sun damage. * Late in disease, melanocytes may invade dermis (lentigo maligna melanoma) with potential to metastasise.

Answer 26

* Palms and soles, occasionally subungual (under nails). * Commonest form in afro-caribbeans (as areas where pigment not as strong). Forms enlarging pigmented patch. * Micro: Similar to lentigo maligna except no marked sun damage. * Need to do surgery to remove

Answer 27

* Commonest type in Britain. * Early: flat macule. Late: blue/black nodule. * Micro: Proliferation of atypical melanocytes which invade epidermis [pagetoid spread] and dermis. * Genetics; Often BRAF mutations Target for anticancer agents. Undergoing multiple clinical trials.

Answer 28

* Starts as pigmented nodule. +/- ulceration. Poor prognosis. * Micro: Invasive atypical melanocytes invade dermis to produce nodules of tumour cells

Answer 29

• Breslow thickness. Measure on microscope from granular layer of epidermis to base of tumour. • 5 year survival rates for primary melanoma • Thin melanoma- better prognosis • Need to catch it early Breslow Tumour Thickness 5yr Survival % <1 yumour Thickness= 91-95% 5yr Survival % 1-2=75-90, 2-4.00=60-75, >4.00= 45-60 • Site - BANS - back, arms (posterior upper), neck, scalp. All poorer prognosis • Ulceration • Satellites/ in-transits [cutaneous deposits that occur before first lymph node] e.g. melanoma on foremarm, will see dark specs of tumour going up arm whilst travelling to lymph nodes • Sentinel Node- lymph node which drains from melanoma first (Good indicator of prognosis) • Sentinal lymph node removed and if +ve, rest of lymph nodes in that anatomic area removed to try & halt disease progression.

Answer 30

Treatment • Surgery – excise primary and + lymph nodes if sentinel node positive • BRAF inhibitors- 60% melanoma’s have mutation in B-raf gene. Can use BRAF inhibitors

Answer 31

The Skin • Epidermis=dermis= subcutaneous tissue • Hair follicle between dermis & epidermis Functions • Physical barrier: chemicals, UV, micro-organisms • Homeostasis: thermoregulation, prevention of desiccation electrolyte loss • Immunological function: Ag presentation and phagocytosis (Langerhans cells, lymphocytes, mononuclear phagocytic cells) Microbiology • Heavily colonised • Coagulase-negative staphylococci, Staph. aureus, Propionibacterium, Corynebacterium spp. Pathogenesis • Localised infec o Inocluation  Penetrate skin with conyaminated object; accidental (e.g. rusty nail), deliberate (surgical procedure, injection drug uses)  Contamination of pre-existing breach in skin e.g. abrasion, athletes foot lesion o Other route of infec (that track to skin) e.g. neuronal migration in herpes simplex, meningococcal sespsis to skin • Systemic generalised infec e.g. chickenpox, meningococcal sepsis

Answer 32

Fungal Infecs of the Skin- Dermatophytosis Infections of the skin, hair, nails • SKIN: Tinea corporis (ring worm), tinea pedis (athletes foot), tiunea curis • NAILS: onchomycosis (causes nail destruc) • SCALP: Tinea CAPitis (scalp ringworm, kerion-boggy inflamm causing hair loss) • Causative agents- DERMATOPHYTE fungi; trichophyton spp. (e.g. T. rubrum), Microsporum spp. (e.g. M. canis) Pathogenesis • Dematophytes use keratin as nutritional substance (eat outer layers so restricted to outer layer) • Usually restricted to stratum corneum • Rarley penetrate living cells of epidermis Diagnosis- Skin scrapings- microscopy & cultre (PCR) Treatment- Topical or systemic antifungal agents • Depends on sit e & extent of infec • Skin infecs o Topical antifungal therapy- Clotrimazole, terbinafine o Scalp & nail infecs (systemic antifungal therapy)- terbinafine, itraconazole, griseofulvin

Answer 33

* Tinea versicolor, Dermatomycosis furfuracea * Causes hypo- or hyper- pigmentation of skin * Causative agent: MALASSEZIA SPECIES (M.furfur) Pathogenesis • Feeds on skin olis= forms acid • Azelaic acid bleaching of skin spots (spotys of depigmentation) Diagnosis- clinically, fungi fluorescence with woods lamp & skin scrapings microscopy (but difficult to grow so cultures don’t help)

Answer 34

* Small asymptomatic growths of skin (hands, genitals, feet, around nails, throat) * Causative agent: Human Papilloma Virus (HPV) * Pathogenesis: cause prolif & thickening of stratum corneum, granulosum & spinosum * Small asymptomatic growths of skin (hands, genitals, feet, around nails, throat) * Causative agent: Human Papilloma Virus (HPV) * Pathogenesis: cause proliferation and thickening of stratum corneum, granulosum and spinosum

Answer 35

* Cysts or abscesses in natal cleft * Caused by ingrowing hair * Contain hair and debris * Discharge to form sinus * Present with pain, swelling, pus * Recurrent * Treatment: Hot compress, analgesia, antibiotics, Surgical excision

Answer 36

Golden) Crusting, around nares or corners of mouth • Superficial skin • Causative organism: Staph aureus • Transmissible • Treatment: Topical antiseptics, Oral antibiotics

Answer 37

* Rash over face, raised, demarcated * Upper dermis * Can involve lymphatics- systemic * Causative organism: Strep pyogenes * Transmissible, recurrent * Treatment: Oral antibiotics

Answer 38

* Infec affecting inner layers of skin (dermis & subcutaneous fat, into lymphatics * Causative agent: Bacterial- Staph aureus, Group A Streptococci (Strep pyogenese), other B-haemolytic, Streptococci * Bacterial supra infec * Pathogenesis: bugs enter through break in skin e.g. via wound, insect bite, pre-existing condition eg. eczema, athletes foot, shingles (Zoster) etc. * Clinical presentation: Rubor (red), calor (heat), dolor (pain), tumor (swelling), Loss of skin creases (by swelling), blistering, pus/exudate, fever * Diagnosis: Clinical (unless septic cultures rarely helpful), Exclude other causes of red hot swollen leg (eg. DVT) * Treatment: Elevation (rasie legs to drain fluid away), rest, antibiotics, source control (drain pus)

Answer 39

* Infection of soft tissues around and behind eye * Pathogenesis:from skin or sinuses or haematogenous spread or trauma * Clinical presentation: Erythema, swelling with induration & pain on eye moving (irriataion of muscles moving eye)., bulging * Causative organism: S. aureus, S. pyogenes but also S. pneumioniae and H. influenzae * Treatment: IV antibiotics

Answer 40

* Skin infection caused by Pseudomonas aeruginosa * Rare, usually in immunosuppressed * Blood stream infection- blocking blood supply * Small patches of erythema- necrosis- ulceration- scar * Treatment: Treat underlying bloodstream infection

Answer 41

* Progressive necrosis of skin resulting in ulceration * Start as small papules then spread out * Non-infectious (likely inflammatory or auto-immune) * Can become secondarily infected * Assoc. with IBD, Arthritides, autoimmune conditions, haematological conditions * Differential diagnosis: infected ulcer (can be s=mistaken for ulcer) * Treatment: Steroids, antibiotics also if infec present

Answer 42

flesh-eating bug”, rapidly progressive, life threatening | • Tracking along fascia, cutting off blood supply to skin- areas of necrosis (get colonised with bacteria- infec)

Answer 43

• Type main types: – Type 1: Synergistic/poly-microbial, host impairment- gram negatives, Streps, anaerobes • Risk factors: DM, obesity, immunosuppression, alcohol, older age group- eg. Fournier gangrene (involves groin & scrotum- usually in old age where blood supply to tissues not optimal) – Type 2: Group A Strep (S. pyogenese) mediated • younger age group, associated with cut or injury – [Type 3: Vibrio vulnificus- sea water, coral; Type 4: fungal]

Answer 44

– Type 1 (pre-existing poor tisse- more an opportunistic infec): ischaemic tissue, colonisation then infection resulting in further ischaemia and necrosis Eg. Diverticulitis (bugs cross bowel wall & into tisse cauing infec), Fournier – Type 2 (more to do with virulence & pathogeicity of group a strep): infection, toxin release- disruption in blood supply-necrosis

Answer 45

– Swelling, erythema (non confluent- as cellulitis preads all the way but fascitis has red patches), pain (out of context- e.g. screaming in agony but minor patches) – Crepatus (or gas under tissues), sepsis/toxaemia, necrosis (balck areas), “dish water” exudate (dirty water looking exudate rather than pus)

Answer 46

Surgical emergency- debridement (all necrotic material removed), antibiotics

Answer 47

• Necrosis caused by inadequate of blood supply • Risk factors: Atherosclerosis (narrowing blood vessels)- smoking, DM; auto-immune e.g. vasculitis • “Dry” (ischaemia) vs. “Wet” Gangrene (when ischaemia becomes infected) vs. “Gas” Gangrene (progression to infec & necrotising fascitis & crepitius • Pathogenesis: – Poor blood flow- tissue necrosis- colonisation- infection- synergistic infection- further necrosis (which can progress to wet gangerene) • Clinical presentation: – Dry- “mummified”, auto-amputate – Wet- boggy, swollen “dactylitis”, exudate, surrounding erythema – Gas- as above but with gas in tissue- crepitus • Causative agents: – Skin (Staphs, Streps); Enteric (GNB, Anaerobes inc. Clostridium) • Treatment: – Surgical: source control (debridement), revascularisation; Antibiotics

Answer 48

• Spectrum of disease from superficial through to deep bone infection in patients with Diabetes • Portal of entry usually damage • Pathogenesis: – Damage to blood vessels- Local ischaemia, impaired immunity and poor wound healing (damaged tissues don’t get better) – Damage to nerves- Neuropathy (desensate- get damage to feet without knoeing about it), trauma – High blood sugars- prone to bacterial infection • Causative organisms: – Superficial- skin flora: Staph aureus, Streps, Corynebacterium – Deeper- skin and enteric flora: above + GNB (more gram –ves as get deeper down), anerobes • Clinical presentation • Treatment: – Surgical debridement of dead material – revascularisation – Antibiotics – off-loading (need weight to be taken off area for it to heal) – Diabetic control

Answer 49

Infection of bone (e.g. skin infec tracking right down to bone) • Pathogenesis: – Mechanism: • Contiguous: eg. Diabetic foot infection • Haematogenous: bugs in bloodstream to bone • Penetrating (introduced via operations to patients): peri-prosthetic, traumatic – Acute vs. Chronic • Acute- assoc. with inflammatory reaction, fulminant, sepsis • Chronic- present for >1 month, smouldering, acute flares • Infection results in bone death (sequestrum) (that bacteria can live in) and new bone formation (involucrum) • Causative organisms: – Haem- (children): S. aureus, Strep, Kingella, Haemophilus – Contiguous: Skin (Staph, Streps) enteric (GNB, anaerobes) – Penetrating: surgical- skin flora, open fracture- skin, environment e.g. motorbike accident & landed in ditch – Sickle cell: Salmonella sp. • Clinical Presentation: – Acute pain, swelling, erythema, sinus, pathological fracture (formation of dead bone & new bone formation- weakens bone) – Imaging, microbiology (blood, tissue/bone) • Treatment: – Antibiotics (prolonged treatment- 4-6 weeks) alone (haematogenous) – Surgical debridement and stabilisation (if dead bone present)

Answer 50

• Infection of the joint (usually bacterial but can also be cause by viruses, mycobacterium and fungi) • Pathogenesis: • Haematogenous: blood stream infection • Local spread: soft tissue, bone, bursitis • Penetrating injury: joint injections, surgery, trauma • Causative organisms: • S. aureus, Streps, Haemphilus, N. gonorrhoeae, E.coli • Clinical presentation: Pain, swelling, erythema, reduced range of movement (unable to weightbear), Sepsis • Diagnosis: Clinical, confirmed by joint aspiration of synovial fluid(MCS) • Treatment: – Antibiotics (guided by cultures)- 4 to 6 weeks – Surgical source control: Joint washout (remove as much of bacteria as they can)

Answer 51

• “PERI-prosthetic joint infection”- infection of tissue and bone surrounding a prosthetic joint • Pathogenesis: – Bugs get onto surface of foreign body (metal ware)- immune system cannot reach- bugs establish biofilm (slime), then start to loosen joint – Early infecs: Implanted at time of surgery or shortly after (via wound) – Late infecs: Haematogenous spread by blood but can be late presenting Early infections • Causative organisms: bacterial (occasionally fungal) – Early (e.g. from surgery) : Staph aureus, Staph epidermidis, Propionibacterium – Late E.g. from a bacteremia): Above and E. coli (e.g. from UTI), B Haem Streps, Viridans Streps (e.g. from dental care) • Clinical presentation: – Pain, instability, swelling/erythema, sinus formation- pus – Treatment (from least to most helpful): – Antibiotics alone (not very helpful as antibiotics can’t get through the slime) – Antibiotics with debridement – Single-stage revision • remove infected joint and replace with new one at same operation – Two- Stage revision (as involves 2 operations) • Remove old joint, given 6 weeks of antibiotics, insert new joint when sure all infection settled

Answer 52

* Sexually Transmitted Infection (STI) or congenital * Caused by the spirochete, Treponema pallidum * How sytemic infec can manifest through skin * Can pass from mum to child * 3 stages to disease: * Primary; chancre (painless, firm non-itchy ulcer), at the point of contact (usually genitals), usually solitary, lasts 3-6wks, lymphodenopathy * Secondary; 4 -10 weeks after chancre, Rash- symmetrical, red/pink, non-itchy, Rash everywhere, inc. soles/palms/mucous membs. Maculo-papular or pustular, Rash contains Treponema (so if biopsy it will be able to i.d. bug), Assoc. with other systemic symptoms * Tertiary; 3 to 15 years after initial infection, 3 forms: Gummatous (skin manifestation), Neuro & Cardiovascular, Gummatous (Late Benign):Chronic Gummas (large inflammatory swellings of skin, bone and liver)- inflamm from body’s immune * Treatment: Antibiotics- Penicillin