Skin and soft tissue Flashcards
What are the stages of skin graft taking?
Adherence
- fibrin bonds form
- fibroblasts replace fibrin with collagen
Imbibition (osmotoic diffusion)
- graft absorbs fluid 48-72 hrs
- fluid contains nutrition to keep graft viable
Inosculation with direct connection to wound bed vessels & neovascularisation with angiogenesis.
- begins after 72hrs
Remodelling
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What is this and how is it treated?
Felons are subcutaneous abscesses of the fingertip pulp.
Diagnosis is made clinically by assessing for tenderness, erythema and fluctuance of the fingertip pulp.
Treatment is usually I&D and IV antibiotics.
*I&D incision doesn’t cross DIPJ crease. mid lateral approach is ulnar side in digits 2-4 and radial in thumb and digit 5.
What are the common pathogens in necrotising skin and soft tissue infections?
There are clostridial (gas gangrene) and non clostridial organisms.
Of the non clostridial infections there are 4 types:
Type 1= polymicrobial (75%)
Type 2= Group A strep (most common monomicrobial)
Type 3= marine bacteria e.g. vibrio (3 in the sea)
Type 4= fungal e.g. mucormycedes
How do necrotising soft tissue infections usually present?
These patients are usually systemically unwell with fever and sepsis
-the affected area has pain out of proportion to visual changes seen.
- Ecchymoses,
- bullae,
- cellulitis with ill defined margins,
- crepitus (from anaerobic production of nitrogen and hydrogen not readily absorbed),
- skin necrosis and
- hypoaesthesia (from small blood vessel thrombosis and superficial nerve destruction) is late sign.
During operation:
- murky grey ‘dishwater fluid’ on incising tissue.
- tissue planes fall apart as running fingers through it.
- fat dull and grey, muscle doesn’t twitch and dulled, and skin doesn’t bleed much.
What is sarcoma, how is it diagnosed and how is it managed?
Overview
Soft tissue sarcomas are malignant tumors of mesenchymal origin, affecting soft tissues such as muscles, fat, and connective tissues.
Classification
The WHO classifies soft tissue sarcomas into over 70 subtypes based on tissue origin, using immunohistochemical markers to guide treatment and predict outcomes.
Risk Factors
Risk factors for soft tissue sarcomas include environmental and chemical exposures, radiation, genetic predispositions like Li-Fraumeni syndrome, Neurofibramatosis 1&2, gardners syndrome and chronic lymphedema leading to angiosarcoma.
Clinical Features
Slow-growing, painless mass; physical examination shows a palpable, encapsulated mass, with the assessment of fascial involvement and lymph nodes being critical for prognosis.
Diagnosis
The evaluation of suspected soft tissue sarcomas involves specialised imaging, biopsy techniques, rigorous pathological assessment per 2020 WHO guidelines, and staging via the AJCC system.
Management
Management of soft tissue sarcomas involves surgical excision, radiotherapy to reduce recurrence, and selective use of chemotherapy for high-grade or aggressive tumours.
Specific Soft Tissue Sarcomas
- Undifferentiated pleomorphic sarcoma, - rhabdomyosarcoma, and Dermatofibrosarcoma protuberans are among the commonest soft tissue sarcomas seen in clinical practice.
What are the stages of wound healing?
- Haemostasis (immediate - hrs)
- clot formation
- vasoconstriction
- platelet aggregation
- release of growth factors e.g. PDGF and TGFbeta
- release of cytokines and chemokines
- fibrin matrix to act as a scaffold and stabilises wound - Inflammation (days to weeks)
- vasodilation
- vascular permeability
- cellular recruitment of neutrophils, macrophages then lymphocytes
- growth factor elaboration
- seen as oedema - Proliferation (days to weeks)
- Phases (AGE)- Angiogenesis
- Granulation
- Epithelialisation (barrier to bacteria but thin, vulnerable)
- fibroblast proliferation
- contractile proteins and myofibroblasts
- ground substance and collagen deposition
- Remodelling (weeks to months)
- wound contraction
- cross linking of collagen and change from type III to type I
- apoptosis of cells no longer required
- repigmentation
- 80% of tensile strength by 6 weeks
What are factors that impede wound healing?
Patient factors:
- prev radiation site
- medications steroids (systemic), NSAIDs
- diabetes
- peripheral artery disease
- chronic venous insufficiency
- immunosuppression
- smoker
- age
- malnutrition & vitamin deficiencies
- chemo or radiotherapy
Disease factors:
- foreign bodies
- infection
- neoplasm
- dirty wound
- ischaemia
- location e.g. lower legs
Surgical factors:
- secondary intention
How do you classify wound contamination?
I use the National Healthcare Safety Network (NHSN) classification: (% risk of infection)
Clean = uninfected (1-5%)
Clean-contaminated = entry into the respiratory, GIT, urinary or genital tracts. (3-11%)
Contaminated = traumatic wounds, break in sterile technique (10-17%)
Dirty = infected (>27%)
What is a surgical site infection
Defined by the United States Centres for Disease Control and Prevention as an infection related to an operative procedure that occurs near the surgical site within 30 days of the procedure or within 90 days of implanted prosthetic material at time of surgery.
Superficial: Limited to Skin or Subcutaneous Tissue
Deep: Involves Muscle or Fascia
Organ/Space: Involves Body Cavity or Organ
What is an ulcer?
Destruction of the epidermal surface down to underlying subcutaneous fat or deeper tissues.
How does negative pressure wound therapy work?
- reduces excess exudate
- pulls wound edges together/helps with contraction of wound
- barrier to bacteria
- reduces number of dressing changes and therefore disruption of new fragile epithelisation with daily dressing changes.
- stimulates growth factors, promotes angiogenesis and granulation tissue formation, proliferation of fibroblasts, increases collagen formation.
What are some known defects in collagen and their associated sequelae?
Genetic Defects in Collagen
I-I: Type I in Imperfecta (bone deformities, grey sclera)
Al-Four-t: Type IV in Alport (GN, may need renal transplant)
“ED Happens to All Men”: All Types in ED (joint laxity, dislocations, stretchy skin)
Fib-Fan: Fibrillin in Marfan’s (aortic dissection, tall etc)
What are the most common organisms in surgical site infections?
Majority are From Native Flora (Skin, Mucous Membranes or Hollow Viscera)
Most Common Organism: Staphylococcus aureus
Most Common GNR: Escherichia coli
Most Common Anaerobe: Bacillus fragilis
What is the pathogenesis of keloid and hypertrophic scars?
Both are an excess of collagen deposition in the healing process excess is laid down in proliferation and remodelling phases.
Hypertrophic = tissue stays within the margin of the wound edges. Usually regresses with time. No genetic predisposition. Composed of organised type III collagen.
Keloid = tissue extends beyond the original scar and usually does not regress with time. Composed of disorganised Type III & Type I collagen. Genetic predisposition autosomal dominant.
How do you treat hypertrophic or keloid scars?
Initial Treatment: Intralesional Steroid Injection
May Consider Silicone Gel & Pressure Therapy for Hypertrophic Scars First
Triamcinolone Acetonide 10-40 mg/mL
If Fails: Surgical Excision
High Recurrence Rate but Hypertrophic Scar Responds Better
Lowest Recurrence: “Triple Keloid Therapy”
Z-Plasty, Then Steroid Injection & Silicone Sheet Application
Describe different methods of debridement.
Surgical - sharp excision. preferred for large areas or if concurrent infection
Chemical - through enzymatic digestion of devitalised tissue using collagenase, papain etc in dressings
Irrigation - dilution is solution to pollution and as hydrodissection. Generally use warm isotonic saline in pulsed fashion with low pressure.
Biological - maggots applied to wound bed secrete proteolytic enzymes to digest necrotic tissue which they then ingest. Leaves behind healthy tissue only.
Define different wound closure approaches.
Primary intention/closure - closure of the wound edges immediately.
Secondary intention - wound edges left open and allows for reepithelisation over time.
Tertiary intention - close skin after 3-4 days (also known as delayed primary intention)
Higher level - e.g. skin grafts, flaps
What are contraindications to Negative pressure wound therapy?
Exposed organs/ blood vessels or vascular grafts
Infection
Malignancy
Ischaemia or devitalised tissue.
Describe the different types of wound dressings and their applications.
Can be classified as open, semi-occlusive and occlusive.
Open = Both air and liquid can penetrate. e.g. 4x4 gauze or rolls. Used to physically debride tissue by sticking to it as it dries and pulling the tissue off at dressing change. Can be painful.
Semi-occlusive = Air can penetrate but not liquid. Good for dry wounds/minimal exudate.
- hydrogels = synthetic polymer with high water count e.g. Intrasite gel.
- hydrocolloids = inner layer moistens wound bed, outer layer film/foam protects wound. Best for low- moderate exudative wounds e.g. duoderm.
- foams = nonadherent semipermeable polyurethane. Good for mod-high exudative wounds. Can be impregnated with various agents e.g. silver, honey. Requires another adhesive dressing above. e.g. mepilex.
- Alginates - complex polysaccharides produced by algae. Insoluble to water but exchange calcium for sodium. The Na rich wound fluid forms gel. Mod - high exuding wounds. Omits unpleasant odour.
Occlusive:
- films - thin clear adhesive dressings e.g. tegaderm. allows visualisation of underlying wound. holds in moisture with minimal absorptive capacity. Used for IVLs and catheters etc.
How does dermabond work?
It is a topical cyanoacrylate skin adhesive. It is an acrylic monomer than polymerises to form a strong plastic covering. Dries after a few mins and peels off after 1-2 weeks.
What is the pathogenesis of ingrown toenail?
Ingrown toenails, also known as onychocryptosis, occur when the edge of a toenail grows into the skin, causing pain and inflammation. The pathogenesis of ingrown toenails is multifactorial, with many possible causes, including:
- Nail trimming: Cutting toenails too short or rounding the edges can cause the nail to spike and traumatise the surrounding tissue.
- Shoes: Wearing shoes that are too tight can compress the nail bed and cause the nail to turn into a cutting surface.
- Foot hygiene: Poor foot hygiene can contribute to ingrown toenails.
- Sweaty feet: Having very sweaty feet can increase the likelihood of an ingrown toenail.
- Nail shape: Certain nail shapes, such as “pincer” toenails, can increase the risk of ingrown toenails.
Other conditions: - Conditions like diabetes, heart or kidney failure, and chronic venous insufficiency can increase the risk of ingrown toenails. - Medications: Some medications, such as epidermal growth factor receptor inhibitors (gefitinib, cetuximab), can increase the risk of ingrown toenails.
What % phenol do you use for ingrown toenail wedge resection and what are some contraindications to its use and alternatives.
88%
contraindicated in pregnancy and breastfeeding patients and in those with PVD.
Alternative is cautery with the diathermy.
What are each of these terms referring to?
1. onychocryptosis
2. onychogryphosis
3. onchomycosis
Ingrown toenail.
Ram’s horn nails/thickened curled nails due to overgrowth.
Fungal infection of nails.
What are the 3 treatment options for ingrown toenail?
Simple removal of the toenail
This is performed either as a primary treatment or if the nail is
infected. The nail will usually grow again, and the chances of
the nail causing further problems is about 50%.
Wedge Excision
This is removal of part of the toenail and sometimes treatment
of part of the nail root, by excision or with application of
phenol, to prevent regrowth. Some patients will develop
further problems with regrowth and infection. Wedge excision
results in a slightly thinner nail.
Zadek’s Procedure
This is where the toenail and the nail bed are removed, usually
for recurrent ingrowing toenails. As the nail root contains the
cells from which the nail develops, removing the nail root as well stops nail from regrowing. Cannot be performed when infected.
Describe how you would advise a patient to eradicate MRSA.
The protocol for eradicating Methicillin-Resistant Staphylococcus aureus (MRSA) in New Zealand includes:
Decolonization
A regimen that typically includes:
- Topical application: Apply an antibiotic ointment like mupirocin or povidone-iodine to the nostrils twice a day for 3–5 days.
- Body wash: Use a body wash containing triclosan 1% or chlorhexidine gluconate 4% daily for 5 days.
- Dentures: Soak dentures overnight in a denture cleaning product.
- Mouthwash: Gargle twice a day with a 0.2% chlorhexidine-based mouthwash if you have a known throat carriage.
Antibiotics
- Take an oral antibiotic like trimethoprim-sulfamethoxazole, clindamycin, minocycline, linezolid, or doxycycline for 7–10 days.
Hygiene
- Wash clothes, bedding, and towels in hot water with laundry detergent. If washed in cold water, iron them with a steam iron, dry them in the sun, or put them in a dry, uncontaminated place for 10–14 days.
Contact Infection Prevention and Control
If you are MRSA positive, being considered for suppression while an inpatient, or have an invasive MRSA infection, you should isolate and involve Infection Prevention and Control
How are pressure injuries classified?
Describe the pathogenesis of pressure injuries.
Inciting factor e.g.
Pressure, Shearing Force or Friction
>
Applied Pressure Greater than Arteriolar Pressure (32 mmHg) Causes Ischemia & Reperfusion Injury
- Direct Cell Membrane Damage
- ECM Protein Damage
- Reactive Oxygen Species – Increase Proinflammatory Markers & Proteolytic Enzymes
Most Severely Affected Tissues are Deep Near the Bone
Pressure Over a Bony Prominence Produces a Cone-Shaped Distribution
Unseen Extent of Injury is Often Greater than Superficial Ulcer May Show (“Tip of the Iceberg”)
Spot diagnosis What is it? What are some differentials? How is it diagnosed?
Pyoderma gangrenosum.
Differentials;
- malignancy
- pressure injuries
- infections
- calciphylaxis.
Diagnosed using Delphi Criteria:
Require the Major Criteria & Four Minor Criteria
Major Criteria:
- Biopsy of Ulcer Edge Showing Neutrophilic Infiltration
Minor Criteria:
- Exclusion of Infection
- Pathergy
- Personal History of IBD or Inflammatory Arthritis
- History of Papule, Pustule or Vesicle that Rapidly Ulcerated
- Peripheral Erythema,
- Undermining Border & Tenderness at Site of Ulceration
- Multiple Ulcerations (At Least One on the Anterior Lower Leg)
- Cribriform or “Wrinkled Paper” Scars
- Decreased Ulcer Size within One Month of Starting Immunosuppressive Therapy
What are the treatments of pyoderma gangrenosum?
Treat Underlying Systemic Disease
Immunosuppressive Therapy:
Limited Disease: Topical Steroids or Calcineurin Inhibitors (Tacrolimus)
Extensive/Rapidly Progressing: Systemic Steroids or Cyclosporine
Prevention: May Consider Prophylactic Immunosuppressive Therapy Prior to Other Surgeries (Not Proven)
Surgical Debridement
Controversial & Done Only with Caution – Can Incite Pathergy
Only Debride Clearly Necrotic Tissue
Attempt to Limit Surgery to Periods of Good Disease Control
Other Therapies:
Infliximab (TNF-Alpha Inhibitor)
Mycophenolate
Methotrexate
Azathioprine
Intravenous Immunoglobulin (IVIG)
What are the typical pathogens involved in human bite wounds? What antibiotics would you use to cover these?
Skin Flora (Staphylococcus & Streptococcus)
Oral Flora (Eikenella corrodens, Prevotella, Fusobacterium & Porphyromonas)
First-Line: Amoxicillin/Clavulanate (Augmentin)
Second-Line (Penicillin Allergy): Should Cover Eikenella & Anaerobes
Eikenella Coverage:
- Trimethoprim-Sulfamethoxazole (TMP-SMX/Bactrim)
- Doxycycline
- Ciprofloxacin
Anaerobic Coverage:
- Metronidazole (Flagyl)
- Clindamycin
ABCDeF
(A = augmentin 1st line, Bactrim/Cipro/Doxy AND Flagyl/Clinda)
What are the typical pathogens involved in dog/cat bite wounds? What antibiotics would you use to cover these?
Most Common Organisms: Streptococci (#1) & Staphylococci (#2)
Other Organisms:
Pasteurella multocida
Bartonella henselae – From Cats
Capnocytophaga
Anaerobes
First-Line: Amoxicillin/Clavulanate (Augmentin)
Second-Line (Penicillin Allergy): Should Cover Pasteurella & Anaerobes
Pasteurella Coverage:
- Trimethoprim-Sulfamethoxazole (TMP-SMX/Bactrim)
- Doxycycline
- Ciprofloxacin
Anaerobic Coverage:
- Metronidazole (Flagyl)
- Clindamycin
ABCDeF
(A = augmentin 1st line, Bactrim/Cipro/Doxy AND Flagyl/Clinda)
Spot diagnosis. What are the cardinal signs of this condition? How is it managed?
Pyogenic Flexor Tenosynovitis
Presentation (Kanavel Cardinal Signs)
- Uniform, Symmetric Swelling of the Affected Digit
- Digit Held in Partial Flexion at Rest
- Severe Tenderness Along the Entire Course of the Flexor Tendon Sheath (Generally Not Just Localised to the Tip)
- Pain Along the Tendon Sheath with Passive Extension – Most Common Symptom
- Treat emergently with incision and drainage and antibiotics.
Spot diagnosis. How do they present? Treatment?
Glomus tumour. (Modified Smooth Muscle Tumor of Glomus Bodies which are – AV Shunts Surrounded by Connective Tissue Involved in Temperature Regulation)
- Benign
- Associated with Neurofibromatosis Type 1
Present with pin point tenderness extreme exacerbation with pressure by pencil tip (Love test) and pain relieved by proximal torniquet (Hildreth sign). Cold sensitivity. Blue/purplish mass usually subungal or deep dermis of palm, wrist, forearm, or foot.
Excise.
Spot diagnosis. Risk factors.
Skin tag (Acrochordon).
Risk factors:
- areas of high friction e.g. axilla, neck, skin folds in people with;
- obesity
- diabetes
- pregnancy
- elderly
- Crohns if perianal skin tags.
Spot diagnosis. Differentials. Treatment options.
Keratoacanthoma (benign proliferation of pilosebaceous infandibulum).
Most commonly difficult to distinguish from SCC
Other differentials include BCC
Actinic keratosis.
Observe
- most have rapid proliferation phase 6-8 weeks then maturation phase appear stable for weeks - months then spontaneously involute to an atrophic scar.
Topical
- 5 flurouracil
- imiquimod
Intralesional
- 5 flurouracil
- methotrexate
Surgical
- excision biopsy to r/o SCC.
Spot diagnosis.
Associations. Treatment
Xanthoma
(lipid deposits in tissue, macrophages ingest and become foam cells).
Associated with hyperlipidaemia hypercholesterolaemia.
Treat underlying cause. Can consider cryotherapy, topical trichloroacetic acid, electrodessication.
Spot diagnosis.
Differentials.
Dermatofibroma
Differential - in transit met/ subcutaneous melanoma.
Spot diagnosis.
Treatment.
This is a ganglion cyst i.e. herniation of the connective tissue from joint capsules, tendon sheathes or bursae.
Treatment
- asx - oberve
- sx - aspirate >50% recur
- excise and ligated the pedicle.
Spot diagnosis.
Associated condition.
What other signs might this condition have?
Neurofibromas (benign proliferation of nerve sheath, contains schwann cells, fibroblasts, perineual cells and mast cells.
Neurofibramatosis 1
Cafe au lait and axillary freckling.
What is it?
How do they present?
What are risk factors?
How are they worked up?
What is the treatment?
Merkel cell
- very aggressive neuroendocrine tumour with early spread.
Often asymptomatic until very late.
- pink/red, raised firm ulcerated nodule.
Risk factors include; elderly, sun exposure, immunocompromised and polyomavirus.
WIll usually get PET and MRI/CT preop to stage them given early spread.
Excise with 1-2cm radial margins, SLNB and XRT. Will stain positive for CK20 and TFF1 (Thyroid transcription factor).
Treatment;
WLE with 1-2cm radial margins and SNB + XRT. If positive SNB then completion dissection +/- XRT.
How do you stage sarcoma?
TNM and grade contributes to stage. (Not used for GIST, Osteosaarcoma or Kaposi sarcoma these have their own system).
Grade 1 – Stage 1
Grade 2-3 – Stage 2-3
N – Stage 4 (Trunk/Extremity) or Stage 3B (Retroperitoneum)
What is the diagnosis?
What are some differentials?
Retroperitoneal liposarcoma.
Differentials;
Other sarcomas
TB
Actinomyces infection
What cell lines are each of these subtypes of sarcoma originating from?
1. Liposarcoma
2. Leiomyosarcoma
3. Rhabdomyosarcoma
4. Dermatofibrosarcoma Protuberans
- Adiopcytes
- Smooth muscle
- Skeletal muscle (pictured)
- Cutaneous
What is the likely diagnosis and what are some differentials?
Dermatofibrosarcoma protuberans (locally aggressive cutaneous sarcoma).
Differentials
- melanoma
- merkel cell
- radiation-induced angiosarcoma
What is the TNM staging for melanoma?
What are some dermatoscopic appearances suggestive of melanoma?
Chaos and clues.
Chaos =assymmetry of structure or colour
Clues include =
1 Grey or Blue Structures
2. Eccentric Structureless Area
3. Thick Lines Reticular or Branched
4. Black Dots or Clods, Peripheral
5. Lines Radial or Pseudopods, Segmental
6. White Lines
7. Polymorphous Vessels
8. Lines Parallel, Ridges (Palms or Soles) or Chaotic (Nails)
9. Polygons’
What are the stages of hidradenitis suppurativa?
Hurley stages divides into 3;
Stage 1 = abscess’/nodules without sinuses or scarring
Stage 2 = above with sinuses or scarring but with normal skin inbetween.
Stage 3 = its continuous diffuse sinuses and scarring with multiple. interconnecting tracts.
What branch is given off the median nerve just before the carpel tunnel and what does it supply?
What is given off after entering the carpel tunnel and what does it supply?
Before entering the carpal tunnel, the median nerve gives off the palmar sensory branch for the palm. Inside the carpal tunnel, it divides into:
Recurrent Motor Branch: LOAF muscles—1st and 2nd lumbricals, opponens pollicis, abductor pollicis brevis, and flexor pollicis brevis. This branch varies in its pattern.
Sensory Branch: radial volar half of the hand.
What are the symptoms and signs of carpel tunnel syndrome?
Symptoms:
- tingling
- numbness
- pain
(thumb through to half ring finger)
- weakness especially on opening jars or gripping objects.
- symptoms usually worst at night
Signs:
- inspect - muscle wasting of thenar eminence, lumbricals
- power - thumb opposition, flexion, inability to perform ‘ok’ symbol.
- Phalens test - wrist flexion to maximum for 60secs (get both hands dorsums up against each other)- symptoms reproduced.
- Tinels test - tapping over extended wrist at the carpel tunnel reproduces the symptoms.
Describe the anatomy of the carpel tunnel.
What is this? What are risk factors for it? How is it treated?
Dupytrens contractures of the right hand.
Definition
Dupuytren’s disease is a benign fibroproliferative disorder affecting the fascia of the palm and fingers.
Epidemiology
More common in older men of Northern European descent and is linked to family history, alcoholism, diabetes, epilepsy, & manual labour.
Pathoanatomy
Normal fascial anatomy becomes diseased with the formation of cords and nodules causing progressive contracture, usually on the ulnar hand. Cleland’s ligaments are not affected by the disease process.
Clinical Assessment
A progressive history and clinically palpable disease with a fixed flexion deformity. It is a clinical diagnosis.
Management
Treatment aims to release contractures using non-operative methods like Collagenase injections and needle aponeurotomy, or surgical release such as fasciotomy or fasciectomy.
What is cubital tunnel syndrome, what is the anatomy that makes up the cubital tunnel and how is it treated?
Definition of Cubital Tunnel Syndrome
Cubital Tunnel Syndrome arises from ulnar nerve compression within the cubital tunnel, leading to motor and sensory deficits.
Anatomy of the Cubital Tunnel
The ulnar nerve originates from C8-T1. The tunnel is formed by FCU fascia, Osborne’s ligament, medial epicondyle and olecranon.
Diagnosis of Cubital Tunnel Syndrome
Little & ulnar-sided ring finger paresthesia, reduced grip strength, clawing & Fromen sign. Tinel’s and elbow flexion tests positive.
Investigations of Cubital Tunnel Syndrome
Diagnosis is clinical, supported by nerve conduction studies. In specific cases, ultrasound, MRI, or X-rays might be needed.
Treatment of Cubital Tunnel Syndrome
Involves therapy, analgesics, and surgical options: simple decompression, anterior transposition, and medial epicondylectomy. Non-surgical approaches are effective in mild cases.
Common sites of compression are:
FCU Fascia: forms the arcuate ligament with Osborne Ligament.
Ligament of Osborne: roof of the cubital tunnel.
Arcade of Struthers: band from intermuscular septum to medial triceps.
Medial Intermuscle Septum
Epicondyle
