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Intro: An abscess is a localised collection of pus (comprised of neutrophils, necrotic tissue, proteinaceous exudate as well as other organisms) that can develop within the dermis or subcutaneous space, it is walled off by a zone of acute inflammation. It is caused when WBCs release cytokines, oxygen free radicals and other inflammatory mediators leading to formation of granulation tissue (macrophages, angiogenesis and fibroblasts) as well as collagen deposition.

Aetiology: Most commonly caused by pyogenic organisms, particularly those with resistance to phagocytosis and lysosomal destruction. 75% of cases are caused by Staph Aureus, others include Strep. pyogenes, E. coli, Coliforms, Bacteroides. It can also be caused by local tissue necrosis or foreign bodies (e.g. splinters). Most abscesses relating to surgical wounds form 7-10 days after surgery, 75% of surgical site infections occur after the patient has left the hospital.

Presentation:
· Heat, pain, swelling, redness, loss of function, rigors
· Swinging pyrexia (wide swings in temperature à very indicative of abscess)
· Leucocytosis (>80% neutrophils), elevated CRP

Clinical Course:
· Without treatment, "point" towards epithelial surfaces (e.g. skin, gut, bronchus, etc.) and discharge contents
· Deep seated abscesses will progressively enlarge and cause tissue damage
· Complications arise at a local (cellulitis) and systemic (sepsis) level, even small abscesses can lead to 'bacterial showers' causing bacteraemia. This is cleared by hepatic and splenic macrophages, it is what causes the swinging pyrexia
· Incomplete treatment à chronic abscess à sinus or fistula formation

Management:
· Treatment with prophylactic antibiotics may help to clear some organisms prior to abscess formation however once abscess has formed they are unable to penetrate the abscess and are therefore useless. Without draining, antibiotic treatment will lead to a sterile abscess (antibioma). Antibiotics are helpful if the infection has spread (e.g. cellulitis or sepsis)
· Abscess needs drainage by incision or aspiration, guided needle aspiration can use CT or ultrasound as required. Healing by secondary intention is recommended (leaving the wound open to heal on its own)
Coronary heart disease (coronary artery insufficiency) is a mismatch between myocardial oxygen supply and demand. Most common cause is atherosclerosis leading to lumen narrowing and reduced blood/oxygen. Rarer causes include vasospasm, embolism and trauma.

Revascularisation used when medical/lifestyle management have satisfactorily improved angina symptoms or to improve mortality in patients with severe coronary artery disease.

Percutaneous Coronary Intervention (PCI):
· Under local anaesthetic a catheter is placed in the femoral or radial artery with a guidewire à it is then taken to the coronary artery of interest
· Balloon passed into the artery and inflated to compress the atherosclerosis à increased lumen, most times a stent will then be put in (made of stainless steel or drug eluting)
· A drug eluting stent will slowly release immunosuppressant drugs to prevent restenosis, there is a much lower chance of restenosis (5-10%) compared to bare metal stents (10-30%)

Coronary Artery Bypass Grafting (CABG):
· Under general anaesthetic, coronary vessels are anastomosed together to bypass occluded vessels using autologous (from the same person) vessels
· Arterial graft: internal thoracic artery (i.e. internal mammary artery) remains attached to subclavian and anastomosed
· Venous graft: great saphenous vein attached proximally to the ascending aorta
· Only for significant, symptomatic stenosis requiring long term treatment (PCI way more chill and easy à preferred for simpler cases)
15-30% of chest wall traumas will require surgery, most penetrating injuries can be managed conservatively with serial chest x-rays and simple tube thoracotomies.

Approach:
· Primary survey & resuscitation: prehospital trauma care and preliminary trauma care in the hospital
· Emergency assessment of the hemodynamically unstable patients to rule out life threatening conditions (aortic injury, tension pneumothorax, cardiac tamponade and haemothorax)
· Rapid diagnostic evaluation:
o CXR
o FAST scan
o ABG
o Ultrasound - haemopericardium, haemothorax, intraperitoneal fluid
o Echo & ECG
o Others: CT, transoesophageal echo, bronchoscopy, angiography

Cases where surgery is required:
· Cardiac tamponade (compression of the heart due to accumulation of fluid in the pericardial space):
o Presentation: distended neck veins, muffled heart sounds, hypotension
o Diagnosed with a FAST (focused assessment with sonography for trauma à bedside ultrasound) scan
o Immediate management: cardiocentesis & placement of catheter
o Definitive management: thoracotomy or pericardial window to release tamponade and control haemorrhage
· Haemothorax:
o Presentation: dyspnoea, diminished/absent breath sounds, decreased tactile fremitus (palpable vibration), chest pain, flat neck veins
o Diagnosed by CXR
o Treatment: chest tube drainage of more than 1.5L initially or more than 200mL/hr for 2 hours (or persistent hypotension) suggests major vascular injury and needs surgical repair
o Likely to be intercostal vessels or internal thoracic
· Massive air leak (tracheobronchial injury)/pneumothorax:
o Presentation: dyspnoea, hoarseness, dysphonia, treatment resistant pneumothorax
o Air leaks through all stages of respiration, preventing full expansion of the lung
o Needs surgical exploration
· Aortic injury/rupture (or laceration of any major vessels):
o Presentation: chest pain, dyspnoea, haemorrhagic shock (tachycardia/hypotension) if rupture
· Myocardial rupture:
o Presentation: hypotension, muffled heart sounds, look at wound, neck vessel distension
· Impaled objects (foreign bodies)
· Intraabdominal haemorrhage: diaphragm, oesophagus, thoracic duct
Adjuvant therapy: given after primary treatment to lower risk of recurrence (primary treatment in breast cancer in surgery). Should be a discussion with a multidisciplinary team.

Local therapy:
Radiotherapy:
· Aimed at achieving local disease control
· Treats neoplasm through the cell-damaging effect of ionising radiation à kills cells in direct line of fire
· Should be used in all patients who have breast conserving therapy or if mastectomy with high rate of recurrence/lymph node involvement

Systemic Therapy:
Chemotherapy:
· Systemic effect on body
· Drugs with cytotoxic properties used to inhibit proliferation of rapidly growing cells (do not need to specifically target an area)
· Agents: anthracycline and taxane
· Indications: high risk patient (triple negative, tumour size >2 cm, positive lymph nodes, aggressive tumour histology)
· Many adverse effects

Hormonal therapy:
· Systemic effect on body
· Bind to cell receptors to prevent cells from dividing
· Indicated in positive hormone receptors
· In ER & PR positive cancer
· SERM (tamoxifen) if pre-menopausal:
· Inhibits growth of breast cancer cells by competitive antagonism of ER
· In breast they antagonise, in ovaries/bone/endometrium they are agonists
· Aromatase inhibitors in post-menopausal:
· Decrease oestrogen levels in body through inhibiting aromatase (required for peripheral conversion of androgens to oestrogens) à decrease ability of cancer cells to grow
· Not useful in pre-menopausal women because still producing oestrogen from ovaries - do not need peripheral conversion
· Main side effects: menopausal symptoms & bone weakening
· HER-2 receptor positive: Herceptin - e.g. trastuzumab (monoclonal antibody)
· ER - possibility of oophorectomy or pharmacological ovarian ablation
Mastectomy:
· Indicated for patients who aren't candidates for BCS or those who prefer mastectomy
· Types:
o Simple mastectomy: removal of all breast tissue + nipple/areola complex, no dissection of the axilla apart from the tail holding a few lymph nodes (standard procedure for invasive breast cancer)
o Modified radical mastectomy: above + all axillary lymph nodes + pec minor removal
o Radical mastectomy: above + pec major (no longer indicated due to higher morbidity without survival benefit)
· Advantages:
o No post-op radiation therapy unless high risk cancer
o No follow up imaging required
o Lower rates of recurrence + better psychological benefits
o Better for small breasts as lumpectomy gives poor cosmetic results
o Can have reconstructive surgery
· Disadvantages:
o Longer operation
o Poorer cosmetics
o Psychological impact on appearance and sexual dysfunction

Breast conserving surgery (lumpectomy):
· Attempts to provide equal survival rates to mastectomy, a cosmetically acceptable breast and low rate of recurrence
· Types:
o Wide local excision: aims to remove tumour with 1cm macroscopic margin of normal breast tissue
§ Skin not normal excised unless it is tethered
o Quadrantectomy: removal of anatomical quadrant of breast tissue
· Advantages:
o Similar survival benefits
o Preservation of breast shape/skin
o Shorter operation
o Psychological advantage of appearance
· Disadvantages:
o Need post-op radiation therapy
o Higher rates of local recurrence
o May need reoperation for margins
o Quadrantectomy has poor cosmetic outcome
· Contraindications:
o Large tumour to breast ratio
o Multifocal tumours
o Fixation to chest wall
o Involvement of skin or nipple
o History of chest radiation
Most common differential in adolescents is fibroadenoma. Presents typically asymptomatically, may be painful a few days prior to menstruation. Mostly right upper quadrant, it's mobile, rubbery and well-circumscribed. In this case might be nice to reassure the patient that most breast lumps are benign.
· Fibroadenoma on ultrasound with have reflective pieces with curves of white in a sea of black - "speculated"

Triple assessment: clinical assessment (history/examination), imaging (mammogram/ultrasound) and tissue biopsy

History:
· Duration - when and how was the lump first noticed
· Change - bigger/smaller, change with menstrual cycle
· Lump - mobile, consistency, pain
· Changes to skin/nipple - erythema, skin puckering, nipple inversion, distortion
· Discharge
· Relation to menstrual cycle/OCP
· Trauma
· Risk factors - previous breast lesions, family history, hormonal risk factors, pregnancy history, lifestyle (smoking, alcohol, occupational)
· Constitutional symptoms: weight loss, fever, night sweats, back pain, neurological changes, SOB, cough

Examination (with a chaperone present):
· Inspection and palpitation of the breast with hands by side and above head
· Breast contour
· Skin changes: erythema, dimpling, puckering, peau d'orange
· Nipple changes: inversion, distortion, eczema, nodules, ulcers, discharge
· Palpitation of the four quadrants with systemic approach, nipple, axillary tail, lymph nodes (axillary and supraclavicular)
o Size, shape, consistency, tenderness

Investigations:
· Watch and wait (with specific notes describing the lesions) à if lesion hasn't resolved after 2-3 menstrual cycles à ultrasound with a potential non-excisional biopsy (FNA or Core)
Conservative Treatment (generally first line due to risk of incontinence):
· Aim is to relax sphincter à improved blood flow à promotion of healing
· High fibre + high fluid diet
· Stool softeners/avoid straining
· Sitz bath (relaxing somatoanal reflex)
· Anti-inflammatory, analgesic creams and/or suppositories
· Local anaesthetic injection
· Topical vasodilator therapy
o Glycerol trinitrate ointment (improve perfusion & reduce anal sphincter pressure)
§ Risk of dilating intracranial vessels à headache
o Diltiazem (calcium channel blocker)
· Botox injection into the internal anal sphincter
o Second line treatment before/instead of surgery
o Indicated in patients with a high risk of faecal incontinence and do not undergo surgery
o Induces relaxation of hypertonic anal sphincter by inhibiting the release of Ach

Surgical management:
· Should be done after >8 weeks of conservative management and endoscopy to exclude IBD
· Risk of faecal incontinence determines surgical treatment (risk high in multiparous [many births] and elderly patients)
o Low risk: lateral internal sphincterotomy
§ Dividing the internal sphincter to lower the resting pressure without destroying the effect of the sphincter (loosens the sphincter a little bit à aim to relieve spasm and increase blood flow)
§ Gold standard
§ Risk of anal dilation à incontinence of stool/flatulence (moreso flatulence), risk of recurrence
§ Local anaesthetic & adrenaline injected between internal & external sphincter
o High risk: anal advancement flap, fissurectomy (excision of fissure)
Differentials (*=important):
· Upper GI bleed:
o Symptoms: melena, haematemesis
o Causes:
§ Erosive/inflammatory: *gastroduodenal ulcers (most common), erosive gastritis/duodenitis, oesophagitis
§ Vascular: oesophageal variceal haemorrhage (most common especially with liver cirrhosis/hypertension), *angiodysplasia (degenerative disease of GI blood vessels causing bleeding stomach - colon)
§ Neoplastic: oesophageal/gastric carcinoma
§ Traumatic/iatrogenic: Mallory-Weiss tear (post forceful vomiting), post endoscopic intervention
§ Other: portal hypertension gastropathy
· Lower GI bleed:
o Symptoms: haematochezia or melena (depending how high up it is)
o Causes:
§ Erosive/inflammatory: *diverticulosis (30%), IBD, infectious diarrhoea
§ Vascular: haemorrhoids, ischemia, rectal varices, *angiodysplasia
§ Neoplastic: *colorectal/anal carcinoma, colon polyps
§ Traumatic/iatrogenic: following colonoscopy/polypectomy/biopsy, post-surgery anastomotic bleeding
§ Other: Anal fissures

Management:
· Perform a primary survey using an ABCDE approach, focusing on haemodynamic stability
· History:
o Duration of bleeding, progression, precipitating events
o Changes in bowel habits: colour of stool, how much blood, colour of blood, mixed in/separate (only on toilet paper?)
o Associated symptoms:
§ Ischaemic/infectious/inflammatory: abdominal pain, haematochezia, diarrhoea
§ Malignancy: weight loss, constipation, tenesmus (feeling like you need to poo after you've already done it)
§ Pain, vomiting, vomiting blood
§ Constitutional symptoms
o Past medical history: GORD, medications, liver cirrhosis, clotting disorder
o Family history: colorectal cancer, bowel diseases
o Lifestyle: smoking, travel history
· Examination:
o Vitals, signs of shock
o Abdominal exam: tenderness, masses, hepatomegaly, Virchow's lymphadenopathy, ascites
o Rectal exam: inspection (fissures, haemorrhoids, fistula), palpable masses, blood on glove
· Investigation:
o Tests:
§ Bloods: FBC (haematocrit/WBC/platelets), UEC, LFT, coags, G&H, CRP, VBG
§ Stool: culture, WBC
o Imaging:
§ Proctoscopy/sigmoidoscopy/colonoscopy/gastroscopy
§ CT angiography/mesenteric angiography
§ Tagged radionucleotide RBC scintigraphy (adding radiographic tracer to blood and injecting into vein - then scan abdomen to track where bleeding is) if colonoscopy not diagnostic
Most likely a polyp - any localised lesion protruding from the bowel mucosa into the lumen.
· Commonly found in those >50yrs, can be seen in younger individuals (e.g. familial adenomatous polyps)
· 70% are adenomas, can be pedunculated or sessile in shape
o Adenomas have the potential for malignant change, however it typically takes 5-10 years to progress to invasive cancer (as a general rule >polyp = >chance of malignancy)
· Other polyps: hyperplastic, inflammatory "pseudo" polyps
· Mostly asymptomatic, may cause altered bowel habits, blood/mucous in stools or iron deficiency anaemia

Large (>2cm) or malignant polyps required surgical resection using an endoscopic snare.

Classification of colonic adenomas:
· Tubular adenomas (pedunculated or sessile):
o Retain the normal tubular form of the colonic mucosa
o Least potential for malignant transformation
· Villous adenomas (sessile or pappiliferous [frond like]):
o Tend to secrete more mucous
o More dysplastic than tubular adenoma à more malignant potential
· Tubular-villous adenoma (mostly pedunculated):
o Majority of polyps
o Intermediate between tubular and villous adenomas

Follow up:
· Amount of polyps
· Size of polyps
· Histology of polyps
· Reason for scopes in first place
· FHx
· PMHx
· Can undergo malignant changes
· Summary:
o 5 year low risk adenomatous polyps (<3, <10mm, no high grade features)
o 3 year high risk adenomatous polyps (>3, >10mm, villous or high grade dysplasia)
o 1 year very high risk adenomatous polyps (5-10 adenomas)
o <1year extremely high risk adenomatous polyps (>10 adenomas or possible incomplete excision of adenoma)
All lumps of the lateral neck in an adult (>40yrs) are malignant until proven otherwise (particularly in absence of inflammation). Most commonly lymphadenopathy due to metastatic carcinoma (usually SCC).

Differentials:
· Bacterial infection (uncommon)
o Develops within a few days/weeks of URTI, dental infection, trauma or travel
o Signs of swelling (erythema, etc.), Rhinorrhoea, odynophagia (painful swallowing), otalgia, odontalgia or other symptoms of a head/neck infection
o Treat with broad spectrum antibiotics - follow up in two weeks
· Benign growth

History:
· Characteristics of mass (onset, progression):
o Rapid expansion - infectious, lymphoma
o Little change - benign neoplasm
o Fluctuant with time - congenital cysts
· Discharge
· Other symptoms - pain, voice change, hoarseness, dysphagia, otalgia
· Symptoms of thyroid disorder
· Systemic symptoms: infection + constitutional
· Any other lumps?
· Recent infection
· Past med/fam history of head and neck cancer
· Social history - smoking/alcohol, recent travel

Examination:
· Vitals & general inspection
· Location of mass - superficial/deep, anterior or posterior triangle?
§ Anterior triangle borders: inferior ramus of the mandible, anterior border of SCM (down to clavicle), midline of anterior neck
§ Posterior triangle borders: posterior border of SCM, lateral border of trapezius muscle, middle third of clavicle
· Inspection and palpation - size, shape, consistency, tenderness, mobility, colour, pulsatile
o Malignant - rock hard, fixed, matted
o Infected - isolated, asymmetric, tender, warm, erythematous, possibly fluctuant
o Congenital cystic - soft, ballotable, mobile
o Vascular - bruits, pulsatile
o Thyroid - immobile midline, elevates with swallowing
· Bruits
· Movement with tongue protrusion & swallowing
· Lymphadenopathy
o Posterior lymph nodes = nasopharyngeal cancer
o Supraclavicular lymph nodes = lung, gynae and GIT
· Examination of oral cavity, oropharynx, ears, nasopharynx, thyroid and skin
· CN exam
· Cardiorespiratory/Abdo exam

Investigations:
· Bloods: FBC, CRP/ESR, blood culture (if infection suspected)
· Imaging:
o Contrast CT should be initial study of choice
o FNA
Inguinal hernias arise above the inguinal ligament, femoral hernias arise below the inguinal ligament.

Inguinal hernias:
· Direct: medial to inferior epigastric vessels, occurs due to weakening of transversalis fascia
o Often protrudes through Hesselbach's triangle
· Medial border = lateral border of rectus abdominis muscle
· Lateral = inferior epigastric vessels
· Inferior = inguinal ligament

· Indirect: lateral to epigastric vessels, enters through deep ring
o More likely (although rarely gets into scrotum) to protrude through superficial ring and enter scrotum/labia majora
o Usually congenital due to incomplete obliteration of the processus vaginalis
o Inguinal canal borders:
§ Anterior: external oblique aponeurosis, lacunar ligament
§ Inferior: inguinal ligament, lacunar ligament
§ Superior: transversus abdominis muscle, internal oblique
§ Posterior: transversalis fascia laterally, conjoint tendon (meeting point of transversus abdominus & internal oblique)


Femoral hernia:
· Femoral canal purpose: allow for expansion of femoral vein in order to increase venous return
· Located in the anterior thigh in the femoral triangle
o Borders:
§ Medial border = lacunar ligament
§ Lateral border = femoral vein
§ Anterior border = inguinal ligament
§ Posterior border = pectineal ligament, superior ramus of pubic bone and pectineus muscle
o Opening to the femoral canal is located at its superior border (the femoral ring)
§ Ring closed by a layer of connective tissue (femoral septum), which is pierced by lymphatic vessels exiting the canal
· Primary survey
o Vitals/signs of shock
o Supplemental O2
o Insert two large bore cannulas:
§ IV crystalloids
§ Bloods: FBC (haematocrit/WBC/platelets), UEC, LFT, coags, G&H, CRP, VBG
o Consider need for transfusion & correction of coagulopathy
o IDC & fluid balance chart
o NBM
o Early contact with gastroenterology/anaesthetics/general surgery as appropriate

· History:
o Duration of bleeding, progression, precipitating events
o Changes in bowel habits: colour of stool, how much blood, colour of blood, mixed in/separate (only on toilet paper?)
o Associated symptoms:
§ Ischaemic/infectious/inflammatory: abdominal pain, haematochezia, diarrhoea
§ Malignancy: weight loss, constipation, tenesmus (feeling like you need to poo after you've already done it)
§ Pain, vomiting, vomiting blood
§ Constitutional symptoms
o Past medical history: GORD, medications, liver cirrhosis, clotting disorder
o Family history: colorectal cancer, bowel diseases
o Lifestyle: smoking, travel history

· Examination:
o Abdominal exam: tenderness, masses, hepatomegaly, Virchow's lymphadenopathy, ascites
o Rectal exam: inspection (fissures, haemorrhoids, fistula), palpable masses, blood on glove

· Investigation (considerations depending on severity of bleeding):
o Tests:
§ Stool: culture, WBC
o Imaging:
§Proctoscopy/sigmoidoscopy/colonoscopy/gastroscopy
§ CT angiography/mesenteric angiography (can be therapeutic & diagnostic)
· Femoral artery à catheter up to aorta à dye injected into aorta à bleed located à diagnosis complete, can treat by manipulating scope down into bleed and embolising
· Embolisation: Gel foam sandwich - gel foam with titanium coils within it
§ Tagged radionucleotide RBC scintigraphy (adding radiographic tracer to blood and injecting into vein - then scan abdomen to track where bleeding is) if colonoscopy not diagnostic

· Management:
o Surgical excision of bleeding site if endoscopy/angiography don't stop bleed, patient continues to be haemodynamically unstable despite aggressive resuscitation or if they're a good surgical candidate with recurrent bleeds
§ Can be done laparoscopically
§ Can see a "blush" on abdo CT with contrast à active pooling of contrast material within or around the spleen
§ Angiography should be done & fix before surgery
· Primary survey
o Vitals/signs of shock
o Supplemental O2
o Insert two large bore cannulas:
§ IV crystalloids
§ Bloods: FBC (haematocrit/WBC/platelets), UEC, LFT, coags, G&H, CRP, VBG
o Consider need for transfusion & correction of coagulopathy
o IDC & fluid balance chart
o NBM
o Early contact with gastroenterology/anaesthetics/general surgery as appropriate

· History:
o Duration of bleeding, progression, precipitating events
o Changes in bowel habits: colour of stool, how much blood, colour of blood, mixed in/separate (only on toilet paper?)
o Associated symptoms:
§ Ischaemic/infectious/inflammatory: abdominal pain, haematochezia, diarrhoea
§ Pain, vomiting, vomiting blood
§ Constitutional symptoms
o Past medical history: varices, peptic ulcer disease, alcoholism, varices, chronic liver disease, haematological disease, GORD/oesophagitis, AAA repair, recent copious vomiting
o Family history of above
o Lifestyle: smoking, travel history

· Examination:
o Abdominal exam: tenderness, masses, hepatomegaly, Virchow's lymphadenopathy, ascites
o Rectal exam: inspection (fissures, haemorrhoids, fistula), palpable masses, blood on glove

· Investigation (considerations depending on severity of bleeding):
o Tests:
§ Stool/vomit: culture, WBC
o Imaging:
§ Colonoscopy/gastroscopy
§ CT angiography
§ Tagged radionucleotide RBC scintigraphy (adding radiographic tracer to blood and injecting into vein - then scan abdomen to track where bleeding is) if colonoscopy not diagnostic

· Management:
o Endoscopy: adrenaline injection, cautery, banding of varices, thermal coagulation
o Emergency laparotomy if endoscopic treatment fails
Basal cell carcinoma
· Definition: locally invasive keratinocyte cancer from basal cells (stem cells) of the epidermis
· Epidemiology: most common cancer in humans, more common in men
· Aetiology: sun/UV exposure, mutations of PTCH tumour suppressor gene
· Clinical presentation:
o Slow growing plaque/nodule
o Skin coloured, pink or pigmented
o Varying size
o Spontaneous bleeding/ulceration
o Shiny/pearly appearance
o Rolled edges
o Telangiectasia
o Rarely metastasise, but highly invasive (may have perineural involvement)
· Management:
o Excision biopsy
o Cryotherapy
o Radiotherapy

Squamous cell carcinoma
· Definition: invasive cancer of the keratinocytes form the epidermis
· Epidemiology: more common in men
· Aetiology: sun/UV exposure, mutation of p53 tumour suppressor gene
· Clinical presentation:
o Enlarging crusty or scaly lumps
o Grow over weeks-months
o May ulcerate
o Often tender or painful
o Often in sun-exposed areas
o Can metastasise to regional lymph nodes and invade deeper structures
· Management:
o Excision biopsy
o Cryotherapy (aggressive)
o Radiotherapy

Melanoma
· Definition: invasive cancer of melanocytes
· Epidemiology: 3rd most common cancer (excluding non-melanoma skin cancers) in Australia
· Aetiology: repeated intense sun/UV exposure (lots of sunburns/blistering) & genetic factors
· Clinical presentation:
o Variety of colours
o Change in shape, size, colour,
o large diameter, inflammation,
o Oozing, change in sensation
o ABCDE (next question)
o Metastatic potential depending on depth
· Management (look two questions down):
o Excision biopsy
o Lymph nodes may be biopsies and/or excised
o Immunotherapy may be used
o Patient education - self-examination, sun safety and regular check-ups
All lumps of the lateral neck in an adult (>40yrs) are malignant until proven otherwise (particularly in absence of inflammation). Most commonly lymphadenopathy due to metastatic carcinoma (usually SCC).

History:
· Characteristics of mass (onset, progression):
o Rapid expansion - infectious, lymphoma
o Little change - benign neoplasm
o Fluctuant with time - congenital cysts
· Discharge
· Other symptoms - pain, voice change, hoarseness, dysphagia, otalgia
· Symptoms of thyroid disorder
· Systemic symptoms: infection + constitutional
· Any other lumps?
· Recent infection
· Past med/fam history of head and neck cancer
· Social history - smoking/alcohol, recent travel

Examination:
· Vitals & general inspection
· Location of mass - superficial/deep, anterior or posterior triangle?
§ Anterior triangle borders: inferior ramus of the mandible, anterior border of SCM (down to clavicle), midline of anterior neck
§ Posterior triangle borders: posterior border of SCM, lateral border of trapezius muscle, middle third of clavicle
· Inspection and palpation - size, shape, consistency, tenderness, mobility, colour, pulsatile
o Malignant - rock hard, fixed, matted
o Infected - isolated, asymmetric, tender, warm, erythematous, possibly fluctuant
o Congenital cystic - soft, ballotable, mobile
o Vascular - bruits, pulsatile
o Thyroid - immobile midline, elevates with swallowing
· Bruits
· Movement with tongue protrusion & swallowing
· Lymphadenopathy
o Posterior lymph nodes = nasopharyngeal cancer
o Supraclavicular lymph nodes = lung, gynae and GIT
· Examination of oral cavity, oropharynx, ears, nasopharynx, thyroid and skin
· CN exam
· Cardiorespiratory/Abdo exam

Investigations:
· Bloods: FBC, CRP/ESR, blood culture (if infection suspected)
· Imaging:
o Contrast CT should be initial study of choice
o FNA
Choledocholithiasis:
· Bloods: ↑ ALP, ↑ GGT, ↑ total and direct bilirubin, ↑AST & ALT, possible pancreatic inflammation (↑ lipase & amylase)
· Transabdominal US: dilated common bile duct

Approach to therapy (supportive therapy à remove stone à prevention of recurrence):
· Supportive therapy:
o Spasmolytic (dicyclomine)
o NSAIDs (opioids if contraindicated or insufficient)
· Removal of obstruction:
o Endoscopic Retrograde Cholangiopancreatography (ERCP) - diagnostic and therapeutic
§ Uses a side viewing endoscope to visualise the duodenal papilla à a small cannula is introduced into the biliary system & radiographic contrast is used to view the anatomy with fluoroscopy
§ Other interventions can also be used:
· Sphincterotomy/papillotomy: cutting the superficial papillary sphincter & sphincter of Oddi with electrocautery
· Papillary balloon dilation: inflation of balloon catheter in the ampulla to enlarge the opening
· Stone collection:
o Balloon retrieval: for single stones/undilated duct
§ Deflated balloon inflated past the stone, then inflated and withdrawn (pulling the stone with it as it is pulled out)
o Basket retrieval: for multiple stones, dilated duct or if balloon is unsuccessful
§ The basket is inserted past the stone, expanded and withdrawn (collecting the stones as it goes past)
· Lithotripsy:
o Designed to break stones that could not be extracted using normal methods
o Stones first captured with a basket à broken down by via mechanical, laser or electrohydraulic lithotripsy devices
o Can do intra-operative common bile duct exploration (uncommon)
o Extracorporeal shock wave lithotripsy (rarely used) - after localising the common bile duct with US from outside the body, focused US shock waves break apart the stone(s)
· Prevention of recurrence:
o Elective laparoscopic cholecystectomy (after ERCP)
§ Indications: concurrent cholelithiasis, acute cholecystitis
§ Recommended within 72h of ERCP
Varicose veins become enlarged/twisted due to venous insufficiency. This occurs in superficial and deep veins, visible varicose veins are the superficial veins (deep veins back up into superficial veins).

Aetiology: poor muscle pump function/incompetent venous valves (reflux)/venous thrombus/obstruction à elevated venous pressure à venous dilatation à varicose veins

Q1. What two significant venous abnormalities are visible on this picture?
Just say whatever is on the photo. (* marks visible symptoms)

Clinical features:
· *Visible dilated and tortuous vessels (most often great saphenous vein)
· *Reticular veins (smaller, visibly coloured vessels)/telangiectasia (red lines on skin due to dilated vessels)
· Leg heaviness and restlessness
· Exercise intolerance
· *Oedema
· *Ulcers & hyperpigmentation (due to RBC breakdown à hemosiderin [iron storage complex] release à accumulation in the dermis à skin pigmentation)
· Lipodermatosclerosis - inflammation of the subcutaneous tissue resulting in "champagne legs"
o
o Unknown cause but associated with venous insufficiency and obesity
· Paraesthesia
· Pruritis

Q2. How should this patient be investigated?
· Doppler ultrasound:
o Assess venous incompetence and in some cases exclude DVT
o Presence of venous reflux confirms diagnosis of chronic venous insufficiency
· Other:
o Duplex USS with colour-flow
o Venous refill time (plethysmography)
o Muscle pump ejection fraction (plethysmography)

Q3. What are the complications if the venous hypertension goes untreated.
· Symptoms (e.g. leg heaviness, pain, pruritis, etc.) worsen
· Damage to skin and subcutaneous tissue à ulceration (chronic skin defect that doesn't heal spontaneously)
o Typically just above ankle
· Generalised pain, DVT

Q4 What is the mainstay of treatment for this condition.
Conservative:
· Compression stockings
· Elevation of limb when sitting
· Avoid periods of long standing
· Regular exercise
Surgical:
· Inadequate response to 3 months of conservative treatment
· Endovenous treatment:
o Sclerotherapy - direct salt solution into vein causing collapse and clotting
o Ablation - laser or radiofrequency to cauterise effected veins
· Surgical excision:
o Ligation
Vein stripping
Q1: What is the common presentation of this problem?
· Constant, severe, perianal pain à local tenderness/induration
· Low grade fever
· Tachycardia
· Potential bowel habit changes or rectal bleeding
· Erythematous, fluctuant mass with indurated (hard) skin

Q2: What is the first line of management?
· Examination under anaesthesia
· Surgical drainage (without damaging anal sphincters)
o Aim: to stop further infection & tissue damage which may impair sphincter function, promote fistula formation or predispose to systemic infection
· Antibiotics if spreading/immunocompromised
· Pus MCS to determine skin/GIT cause

Q3: What bacteria are usually cultured?
· Commonly polymicrobial
· Aerobic:
o Staph aureus (skin cause)
o Strep pyogenes (skin cause)
o E. coli (GIT cause)
· Anaerobic:
o Bacteroides fragilis (GIT cause)

Q4: What is the usual cause of this?
· Typically from infected anal crypt gland
o Anal canal has 6-14 glands that lie between the internal and external anal sphincter à ducts from these glands drain at the dentate line
· Abscess develops when an anal crypt gland becomes obstructed with food matter, oedema from trauma (e.g. hard stools/foreign body) or an adjacent inflammatory process (e.g. Chron's)
o Obstruction permits bacterial growth and abscess formation
· Some abscess traverse distally in the intersphincteric groove into the perianal skin, which they present as a tender fluctuant mass (perianal abscess) à path of least resistance
· Associated with repetitive trauma: Chron's, fistula, haemorrhoids, malignancy, STIs