Skin Flashcards
Definitions of and organisms causing cellulitis and erysipelas
Infective spreading inflammation of skin and subcut tissue resulting in pain, erythema, oedema and warmth
- Cellulitis involves deeper dermis & subcut fat.
- Erysipelas involves upper dermis & superficial lymphatics.
Organisms
- Cellulitis = beta-haemolytic strep most commonly grp A strep (pyogenes), also S. aureus; gram neg aerobic bacilli in minority
- violaceous colour and bullae suggests strep infection
- Erysipelas = most commonly beta-haemolytic strep
- Abscess = most commonly S. aureus, either methicillin-susceptible or MRSA
Contributing factors for cellulitis & abscess: diabetes, immunosufficiency, venous stasis, lymphoedema, obesity, pre-existing skin conditions eg psoriasis/eczema, tinea pedis
Describe the pathophysiology and treatment of ingrown toenails.
Ingrown toenails (or onychocryptosis) occur when a spicule of the lateral nail plate pierces the lateral nail fold and penetrates into the skin, with subsequent foreign-body inflammatory reaction and secondary infection. The lateral great toenail is most commonly affected.
Characteristic signs and symptoms include pain, edema, exudate, and granulation tissue.
Predisposing factors include poorly fitting shoes, excessive trimming of the lateral nail plate, pincer nail deformity, and trauma.
Treatment options range from conservative (salt bath, re-direction, podiatry) to surgical excision and thermo-chemical ablation. Antibiotics have no proven role.
Describe the pathophysiology of frostbite.
Following exposure to subfreezing temperatures, ice crystals form extracellularly. If freezing is rapid, ice crystals may also form inside cells. Fluid and electrolyte fluxes cause lysis of cell membranes with subsequent cell death. An inflammatory process ensues mediated by thromboxane A2, prostaglandin F2-alpha, bradykinins, and histamine. This leads to tissue ischemia and necrosis.
Discuss wound healing, include molecular mediators in your answer.
- Reactive
- Haemostasis (coagulation pathways, PAF)
- Inflammation (IL-1, IL-2, IL-8)
- Chemotaxis (LB4, C5<u><strong>a</strong></u>, Chemokines)
- Epithelial migration (macrophages)
- Regenerative
- Proliferation (VEGFR, PDGF, TGF-b, IFN-y)
- Maturation
- Remodelling
- Contraction (Fibroblasts, MMPs)
- Scarring (Fibroblasts, MMPs)
- Remodelling of scar (Fibroblasts, MMPs)
- Type III collagen replaced by Type I
What is atypical mole syndrome?
Three or more of the following characteristics:
- Two or more clinically atypical naevi
- >100 naevi >2 mm diameter or >50 naevi if <20 or >50 years of age
- Naevi abnormally distributed (buttocks or dorsum of foot)
- Naevi in the anterior scalp
- Iris pigmented lesion(s)
AMS predisposes to melanoma; RR of 3-20 in the presence of atypical naevi so higher at the AMS end of the spectrum. May suggest a mutation in the MAPK pathway or heterozygosity of the CDKN2A gene.
What is Familial Atypical Multiple Mole and Melanoma syndrome?
Familial Atypical Multiple Mole and Melanoma syndrome is an familial condition diagnosed by:
- Melanoma in 2 or more first or second degree relatives
- Many atypical naevi (usually more than 50)
Subsequent genetic research has demonstrated that many of these patients have an AD inherited condition characterised genetically by mutations in the CDKN2A gene, which codes for a series of checkpoint regulators.
What are the suggested excision margins for melanoma according to
NZ and Australian Guidelines?
The evidence?
Evidence
- No benefit seen for margins >2cm regardless of size
- For in situ disease histologically complete resection rates are slightly higher with 9mm margins cf 5mm
- For lesions >2mm 1cm is worse than 3cm
- For lesions 1-2mm trend for 1cm worse than 3cm
SO
- Try and get 1cm for in situ disease
- Where feasible get 2cm for any lesion deeper than 1mm.
Describe the pathophysiology of necrotizing soft tissue infection.
The infection usually begins via a break in the muco-cutaneous barrier; usually the skin.
Bacteria, aided by pathogenic factors such as hyaluronidase, lipase, collagenase (many sp.), streptokinase, and M-proteins (GAS), and alpha-toxin (clostridial sp.) spread throughout the layers of the skin.
Local inflammatory change also promotes microvascular occlusion which facilitates further spread of the infection.
M protein is an important virulence determinant of GAS; necrotising infection caused by GAS strains w M types 1&3 = assoc w strep toxic shock syndrome in ~50% cases. GAS strains of these & other serotypes can produce pyrogenic exotoxins, which induce cytotoxins –> contribute to shock, tissue destruction, organ failure. GAS infection is more often assoc w septic shock requiring tx w inotropes/vasopressors.
What is Hydradenitis Suppurativa?
What areas are commonly affected?
What are the common symptoms?
- Hidradenitis suppurativa is a chronic, inflammatory skin disorder of the folliculopilosebaceous units characterized by the development of inflammatory nodules, pustules, sinus tracts, and scars, primarily in intertriginous areas (groin & axillae, also inframammary, perineal & perianal areas)
- Traditionally been considered the result of occlusion of apocrine glands by keratotic debris –> leads to bacterial proliferation, suppuration & spread of inflammation to surrounding subcut tissues –> subcut tracts & pits develop; infected tissues ultimately become fibrotic & thickened
- Physical pain, odor, chronic drainage, and disfigurement are common features of this disorder.
What is your management of hydradenitis suppurativa?
Multimodality therapy
- Lifestyle changes:
- Stop smoking
- Dietary restrictions
- Medical therapy:
- Antibiotics; Doxycycline 100mg PO BD 14 days
- Steroids for severe disease
- Tailored surgery:
- For acute disease, mainstay = I&D
- Punch biopsy for smaller lesions
- De-roofing taking only the affected folliculopilosebaceous units - PICO for dressing
- Wide local excision and grafting
- Liberal biopsies to exlcude malignancy
- NB 50% recurrence rate after WLE
What is Merkel Cell Cancer?
How is it managed?
Merkel cell carcinoma is a rare, aggressive cutaneous malignancy that predominantly affected older, fair skinned adults, especially those who are immune-suppressed. It has a predilection for local recurrence and local lymph node metastases.
Although rare, New Zealand and Australia have some of the highest reported rates in the world, at ~1 per 100,000 in NZ. Risk factors for MCC include older age (18 per 100,000 in those above 85), light skin, and immune suppression, especially with mTOR drugs.
Merkel cell carcinoma (MCC) has been traditionally believed to arise from Merkel cells, which are located in the basal layer of the epidermis and hair follicles and are associated with skin mechanoreceptors. However, this hypothesis is controversial. An alternative hypothesis is that these tumours originate from an immature totipotential stem cell that acquires neuroendocrine features during malignant transformation. Recent data suggests they are linked to Merkel Cell Polyomavirus, a ubiquitous dsDNA virus.
(AEIOU) Diagnosis is difficult as the majority of patients are asymptomatic (88%) so a high level of suspicion is required. Most have a rapidly expanding lesion (63%), a minority are on immune suppression (~10%). Almost all patients are older than 50 (90%). UV exposure is present in 90%.
Staging is based on size (2cm) and whether the lesion has metastasised to regional or distant nodes. The 5 year survivals are 50%, 35%, and 15% respectively.
Wide local excision (1-2cm) and SNB are recommended for early disease, though SNB is less studies in this group. Many surgeons would not perform SNB for MCC larger than 2cm as adjuvant radiotherapy will be given any way. Locally advanced disease can be treated with surgery for the primary and lymphadenectomy for the nodal basin. Radiotherapy may be used in frail patients for both the primary and lymph nodes. Systemic treatment with biological therapy e.g. PD-L1 inhibitors are being studies but no high quality date exists yet.
What is the role of topical therapy for cutaneous malignancy?
- Fluorouracil and imiquimod creams are topical treatments that may be used to treat some non-melanoma skin cancers, usually second-line to surgical excision
- These medicines work by destroying cancerous cells in the skin, resulting in a local reaction including erythema and erosion, followed by re-epithelisation of the skin
- Fluorouracil and imiquimod may be appropriate for the treatment of actinic keratoses, superficial BCC and SCC in situ
- Treatment regimens vary depending on the type of lesion, but fluorouracil and imiquimod creams are typically applied twice daily for up to 6-10 weeks, with an expected reaction after 1-2 weeks of treatment
What is Kaposi’s sarcoma?
- Kaposi sarcoma (KS) is an angioproliferative disorder that requires infection with human herpes virus 8 (HHV-8), also known as Kaposi sarcoma-associated Herpes virus (KSHV), for its development
- KS is classified into four types based upon the clinical circumstances in which it develops:
- Classic (the type originally described by Kaposi, which typically presents in middle or old age)
- Endemic (several forms described in Sub-Saharan indigenous African populations)
- Iatrogenic (typically seen in renal allograft recipients)
- AIDS-associated (epidemic KS)
- Treatment involves optimal care for the underlying pathology (AIDS, Immune suppression) and then control of symptoms as HHV-8 cannot be eradicated; this may be with:
- Surgery
- Radiation therapy
- Cryotherapy
- Chemotherapy
- Immunomodulation with IFN-a
What is an ulcer?
- A breach in the epithelium of a tissue
- A dimished ability of the tissue to heal
- Acute and chronic inflammation
Provide an overview of commonly used anti-thrombotic medications.
- Warfarin
- Vitamin-K reductase inhibitor
- Affects II, VII, IX, X, Prot-C, Prot-S
- Not safe in pregnancy
- INR to measure
- Heparin
- Binds to, and potentiates, Antithrombin III
- Inactivates Thrombin, Xa, and other proteases
- Large molecule
- Measured with aPTT
- LMWH
- More anti-Xa activity than anti-thrombin activity
- 100% bioavailability subcut
- Safe in pregnancy
- Direct thrombin inhibitors
- “Dabigatran” Rivaroxiban”
- Recombinant derivative of leech saliva (hirudin)
- Dabigatran is reversible and dialysable
- Thrombin time to measure
What is the differential for a cystic lesion of the dermis/epidermis?
Sebaceous/Epidermal cyst
Dermoid cyst
Trichilemmal csyt
Think about:
Dermatofibroma
Dermatofibrosarcoma protuberans
How are wounds classified with regard to infection risk?
Clean
- 2% infection risk
- Elective, non-traumatic, primarily closed, no inflammation, no break in technique, body tracts not entered.
Clean-contaminated
- <10% infection risk
- Urgent or emergency case that is otherwise clean, elective opening of body tracts with minimal spillage and no infected fluids, minor technique break.
Contaminated
- 10-20%
- Non-purulent inflammation, gross intestinal spillage, infected tract entered, major break in technique, penetrating trauma <4 hours old, chronic open wounds
Dirty
- 20-40%
- Purulent inflammation, pre-operative perforation of infected tract, penetrating trauma >4 hours old.
How are burns classified?
The traditional classification of burns as first, second, third, or fourth degree was replaced by a system reflecting the need for surgical intervention. Current designations of burn depth are superficial, superficial partial-thickness, deep partial-thickness, and full-thickness.
How is frostbite or cold injury classified?
First degree
- Hyperaemia and oedema without skin necrosis
Second degree
- Large clear vesicle formation accompanies hyperaemia and oedema with partial thickness skin necrosis
Third degree
- Full thickness and s/c tissue necrosis occurs, commonly with haemorrhage vesicle formation
Fourth degree
- Full thickness skin necrosis including muscle and bone gangrene
How are soft tissue sarcomas staged?
With difficulty…
The AJCC combine their TNM system with the French grading system (better than the NCI system) for grade to complete staging.
- T-staging
- 5cm or less
- 5-10cm
- 10-20cm
- Greater than 20cm
- N-staging / M-staging
- Nodes or mets negative/positive.
Grade calculated by accounting for tumor differentiation, mitotic grade, and degree of necrosis.
Note that the tumour biology imparts far more prognostic information, so that STSs are now being indivdually graded such as GISTs, Kaposi sarcoma, dermatofibrosarcoma all have different systems.
How are soft tissue sarcomas classified?
Briefly describe the lesions that characteristically make up each of these classes.
The most traditional classification for this histologically diverse group is:
- Extremity/trunk versus
- Retroperitoneal/visceral
Extremity/trunk:
- More common
- Malignant peripheral nerve sheath tumours, schwannomas, angiosarcomas, DFSP, and desmoids make up the bulk of these tumours.
- Amputation is becoming less common, mostly as a result of management through MDM
- Multi-modality therapy appears to be more effective for treatment; the optimum timing and nature of this is unclear. This includes the use of isoltated-limb-perfusion.
- Desmoids are increasingly being surveilled, consider Tamoxifen for adjuvant therapy.
Retroperitoneal/visceral:
- 15% are retroperitoneal
- Liposarcoma, Leiomyosarcoma, and MFH (undiff. pleomorphic sarcoma) make up the bulk of the retroperitoneal lesions.
- 75% of patients require visceral resection to complete negative margins.
- Data not as encouraging re multi-modality therapy.
- GIST makes up most visceral STS (stomach>SB>rectum).
- Leiomyosarcoma typically affects the retroperitoneum and uterus.
Which melanoma patients should be discussed at MDM?
Patients with the following should be discussed at a MDM:
complex reconstruction cases, including MIS
- stages II (B and C) cases if management decisions
are not straightforward
- stages III and IV cutaneous melanoma cases
- desmoplastic melanoma
- melanoma in people under 25 years of age
- non-cutaneous melanoma.