Surgery Flashcards

1
Q

Head injury
- When do we CT head?

A

CT head within 1hours
- GCS <13 on initial assessment
- GCS <15 at 2h post-injury
- ?open or depressed skull #
- ?basal skull # (haemotympanum, panda eyes, CSF leak ear/nose, Battle sign)
- Post-traumatic seizure
- Focal neuro deficit
- >1 episode of vomiting

CT head within 8 hours
- age >65yo
- Bleeding/clotting disorder or anticoags
- Dangerous mechanism (struck by vehicle, ejected from vehicle, fall from >1m or >5 stairs)
- >30mins retrograde amnesia of events immediately prior to HI

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2
Q

Colorectal Cancer

Pathophysiology
Presentation
Investigation
Management

A

Pathophysiology
- Most develop from adenomatous polyps (10% of adenomas -> Ca)
- RFs: Adenomatous polyposis coli, Familial adenomatous polyposis, Hereditary nonpolyposis colorectal cancer (lynch syndrome), age, male, fm hx, IBD, low fibre diet, processed meat, smoking, alcohol

Screening
- FIT test 60-74yo every 2 years (1 in 10 w/ +ve result will be found to have Ca, 4 in 10 will have premalignant polyps)

Presentation
- Left sided: PE bleeding, change in bowel habit, tenesmus, palp mass LIF or on PR
- Right sided: IDA, abdo pain, palp mass RIF, often presents late

2ww Criteria
->40 w/ weight loss and Abdo pain
>50 w/ unexplained PR bleeding
>60 w/ IDA or change in bowel habit

also consider if rectal/abdo mass; unexplained anal mass or ulceration; <50 w/ rectal bleeding and abdo pain, change in bowel habit, weight loss, IDA

Investigations
- CEA (tumour marker) for monitoring
- Bloods - IDA
- Colonoscopy w/ biopsy
- CT for staging
- MRI rectum for rectal tumours to assess depth

Management
Surigcal options:
- Right Hemicolectomy/Extended Right Hemi - caecal or ascending colon (extended for transverse colon)
- Left Hemicolectomy (descending colon)
- Sigmoidectomy (sigmoid colon)
- Anterior Resection (high rectal >5cm from anus (leaves anal sphincter intact))
- AP Resection (low rectal, <5cm, leads to permanent coloscopy + lack of sphincters)
- Hartmann’s Procedure (emergency procedure eg. obstruction or performation)

Other: chemo, radiotherapy, palliative

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3
Q

Stomas
How to differentiate between ileostomy and colostomy

A

Ileostomy
- Location: RIF
- Spouted
- Liquid output
Colostomy
- Varying location (more likley left side)
- Flushed to skin
- Solid output

  • Loop = loop of bowel brought up to surface w/ two openings to stoma. Used to protect a more distal anastamosis. Can later be reversed.
  • End = bowel is brought up to the abdo walll. More permanent procedure.
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4
Q

PR Bleeding
Describe typical presentation and management of the following causes of PR bleeding

  • Haemorrhoids
  • Solitary Rectal Ulcer
  • Angiodysplasia
  • Anal Fissure

Other causes: Diverticulitis, UC (bloody diarrhoea), Gastroenteritis, Colorectal/Anal cancer

A

Haemorrhoids
- Pres: painless rectal bleeding, pruritis (pain if thrombosed)
- Types: external (below dentate line, prone to thrombosis), Internal (above dentate line, painless)
- Grading: I (NO prolapse), II (prolapse BUT spontaneous reduction), III (manually reduced), IV (NO reduction)
- Thrombosed - pain, purple, oedematous
- Management:
Most: conservative, soft stools, anusol
More: rudder band ligation
Thrombosed: if present in 72h -> excision. Otherwise conservative.

Solitary Rectal Ulcer
- Associated w/ chronic straining and constipation
- Histology -> mucosal thickening, lamina propria + smooth muscle

Angiodysplasia
- AV malformation. Common esp >60yo + in hereditary haemorrhagic telangiectasia
- –> Painless occult PR bleeding in most, 15% -> acute haemorrhage
- Diagnosed w/ colonscopy OR mesenteric angiography if acutely bleeding
- Mx: endoscopic cautery, tranexamic acid, eostrgoens

Anal Fissure
- <6/52 = acute, >6/52 = chronic
- RF: constipation, IBD, sexually transmitted infections (HIV, syphilis, herpes)
- Pres: painful, bright red, rectal bleeding
- N.B. 90% found on posterior midline (if not then ?Crohns or alternative path)
- Mx:
- Acute: soften stool, lubricants, topical anaesthetic + analgesia
- Chronic: GTN topical (if nil effect after 8/52 refer for ?surgery (sphincterotomy) or botulinum toxin

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5
Q

Preparation for surgery
- Which tests are done pre-op?
- PO fluids and fasting rules
- Drugs to stop pre-op
- Diabetes meds adjustment
- Steroids

A

Tests Pre-Op
- Bloods: FBC, U&E, LFTs, Clotting, G&S
- Urine analysis
- Pregnancy test
- Sickle Cell Test
- ECG/CXR

PO Fluids and Fasting Rules
PO fluids:
- clear fluids till 2h pre-op
- other stuff stopped 6h pre-op

Drugs to Stop Pre-op - CHOW
- Clopidogrel: stop 7d pre-op (aspirin can be continued)
- Hypoglycaemia (below)
- Oral contraceptives (COCP or HRT) - stop 4/52 pre-op
- Warfarin - stop 5d pre-op + start LMWH therapeutic dose (op only if <1.5 INR so can give PO vit K)

Diabetes meds adjustment
Oral hypoglycaemics
most managed by adjusting meds on day of surgery:
- Metformin - if BD take as normal, if TDS skip lunch dose
- Sulfonylureas: omit morning dose (+ afternoon dose if PM surgery)
- DPPIV inhibitors (gliptins) - take as normal
- GLP1 analgogues (tides) - take as normal
- SGLT2 inhibitor (flozins) - omit on day of surrgery
- Long-acting insulin - reduce dose by 20% day before + day of surgery

BD biphsasic or ultra-long-acting insulin - 1/2 normal morning dose
UNLESS >1 meal missed, poor glycaemic control, risk of renal injury —> VRII

If taking inuslin -> VRII

Steroids
- Continue. If cannot take PO then switch to IV.

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6
Q

Abdominal Aortic Aneurysm
Pathophysiology
Presentation
Investigation
Management

A

Pathophysiology
- Dilatation = >3cm
- RFs: marfans, ehlers danlos, infection, trauma, atherosclerosis, inflammatory (takayusus aortitis), smoking, HTN, fam hx, male, age, hyperlipidaemia
- (Diabetes if actually protective)
Presentation
- Symptomatic AAA: Abdo pain, back/loin pain, distal emboli, aortoenteric fistula
- Pulsatile mass
- Ruptured AAA: syncope, vomiting, haemodynamic compromise, Abdo tenderness, pulsatile mass
- Screening: men age 65 abdo USS
Investigation
1st:USS
once confirmed on USS then CT contrast if >5.5cm (to plan management)

Management

Elective Management
<5.5cm - monitor w/ duplex USS + risk factor management (yearly if <4.4cm, 3/12 if >4.5cm)

Surgery if:
- >5.5cm
- OR expanding >1cm/yr
- OR symptomatic

  • open or endovascular repair

Emergency Mx/Rupture
- Mx: O2, high flow IV access, Crossmatch
- Keep BP <100 (permissive hypotension)
- Transfer to vascular –> unstable -> open repair; Stable –> CT angio + open/endovasc repair

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7
Q

How do the following hernias present and what is done about them?

  • Inguinal
  • Femoral
  • Umbilicus
  • Paraumbilical
  • Epigastric
  • Incisional
  • Spigelian
  • Obturator
  • Richter

Childhood
- Inguinal
- Umbilical

A

Inguinal Hernia - superomedial to pubic tubercle. Direct (through posterior wall defect in inguinal canal); indirect (via inguinal canal). Mx - if symptomatic offer surgical management. Asymp - monitor. N.B. in children all are managed surgically as higher risk complications

Femoral Hernia - more in women. Inferolateral to pubic tubercle. High risk strangulation. Manage surgically within 2/52.

Umbilical Hernia - symettrical bulge under umbilicus. **In infancts tend to resolve by 4-5yo. Monitor. Complications rare. **

Paraumbilical Hernia - asymmetrical bulge above/below umbilicus

Epigastric - Lump in midline between umbilicus + xiphisternum. RFs: physical training, coughing, obesity.

Incisional Hernia - in 10% of abdo ops

Spigelian Hernia (aka lateral ventral hernia) - older patients. Surgically managed.

Obturator Hernia- through obturator foramen. More in women. Presents w/ bowel obstruction.

Richter Hernia - only the antimesenteric wall of the bowel herniates so -> strangulation without signs of obstruction

Complications
- Incarceration = irreducible
- Obstruction
- Strangulation = compromised blood supply - unwell, PR blood etc.

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7
Q

How do the following hernias present and what is done about them?

  • Inguinal
  • Femoral
  • Umbilicus
  • Paraumbilical
  • Epigastric
  • Incisional
  • Spigelian
  • Obturator
  • Richter

Childhood
- Inguinal
- Umbilical

A

Inguinal Hernia - superomedial to pubic tubercle. Direct (through posterior wall defect in inguinal canal); indirect (via inguinal canal). Mx - if symptomatic offer surgical management. Asymp - monitor. N.B. in children all are managed surgically as higher risk complications

Femoral Hernia - more in women. Inferolateral to pubic tubercle. High risk strangulation. Manage surgically within 2/52.

Umbilical Hernia - symettrical bulge under umbilicus. **In infancts tend to resolve by 4-5yo. Monitor. Complications rare. **

Paraumbilical Hernia - asymmetrical bulge above/below umbilicus

Epigastric - Lump in midline between umbilicus + xiphisternum. RFs: physical training, coughing, obesity.

Incisional Hernia - in 10% of abdo ops

Spigelian Hernia (aka lateral ventral hernia) - older patients. Surgically managed.

Obturator Hernia- through obturator foramen. More in women. Presents w/ bowel obstruction.

Richter Hernia - only the antimesenteric wall of the bowel herniates so -> strangulation without signs of obstruction

Complications
- Incarceration = irreducible
- Obstruction
- Strangulation = compromised blood supply - unwell, PR blood etc.

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8
Q

What are the following?

  • Peutz-Jegher Syndrome
  • Lynch Syndrome
  • Familial Adenomatous Polyposis
  • Gardners Syndrome
A

Peutz-Jeghers Syndrome
Path - autosomal dominant. Numerous hamartomatous polyps in GI tract; freckles on lips, face, palms + soles.
Pres -> Small bowel obstruction due to intussuception. GI bleeding. Pigmented lesions/freckles.
Mx: conservative
N.B. altho polyps are NOT pre-malignant 50% of pts will die from GI Ca by age 60yo

Familial Adenomatous Polyposis
Path- rare, autosomal dominant. Hundreds of polyps by 30-40yo –> Ca.
Mx: total colectomy + ileo-anal pouch formation in their 20s

Gardner’s Syndrome
Path - Autosomal dominant. variant of FAP w/ osteomas of skull, mandible, retinal pigmentation, thyroid Ca and epidermoid cysts of the skin
Mx: colectomy as per FAP

Lynch Syndrome (aka hereditary non-polyposis colorectal cancer)
Path - autosomal dominant -> increased risk of colorectal + endometrial Ca at young age (<50y) (other: stomach, ovarian, small bowel, pancreatic, prostate, urinary tract Ca)
- increased colorectal Ca risk without polyps

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9
Q

Abdominal Wound Dehisence

  • Pathophysiology
  • Presentation
  • Management
A

Pathophysiology
- Superficial = failure of skin wound
- Complete = failure of all layers w/ protrusion of viscera externally
- RFs: malnutrition, jaundice, steroid use, wound contamination, poor surgical technique, obesity, smoking

Presentation
- Visible wound opening (typically 5-7d post-op)
- Skin may be intact -> new bulging of the wound + seepage of pink serous or blood stained fluid (any increased wound discharge should be considered dehisence till proven otherwise)

Investigation
- Clinical diagnosis
- wound swab if concurrent infection

Management
- Analgesia
- Broad spectrum IV abx
- Cover the wound w/ saline soaked gauze + arrange urgent return to theatre for wound closure

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10
Q

Subarachnoid Haemorrhage

  • Pathophysiology
  • Presentation
  • Investigation
  • Management
A

Pathophysiology
- Traumatic or non-traumatic (spontaneous)
- Causes: ADPKD, AV malformation, Ehler’s Danlos, Pituitary apoplexy

Presentation
- Sudden onset, thunderclap headache, max intensity within 1 minute
- N+V, meningism, coma, seizures, sudden death
- ECG can show ST elevation

Investigation
- CT head (-ve in 7%)
- LP at 12h (xanthachromia) (opening pressure can be normal or raised)

Management
- Refer immediately to neurosurgery.
- They will CT intracranial angio to identify lesions + guide Mx
- Intracranial aneurysms –> Coiling within 24h (until treated keep pt on bed rest w/ well controlled BP + avoid straining)
- 21d course nimodipine (to prevent vasospasm)
- If hydrocephalus developed then external ventricular train or VP shunt used

Complications
- Vasospasm (21d of nimodipine to prevent)
- Hydrocephalus
- Seizures
- Hyponatraemia (SIADH)
- Re-bleeding (10%) - most common in 1st 12h. Repeat CT is suspected. High mortality.

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11
Q

What are the following?
- Ogilvie’s Syndrome
- Brain death
- Rectal Prolapse

A

Ogilvie’s Syndrome = acute colonic pseudoobstruction
- RFs: pelvic surgery, trauma, puerperium
- Presentation mimics mechanical obstruction
- Mx: neostigmine or colonic decompression

Brain Death
- Criteria for testing: Deep coma of known non-reversible cause, no sedation, normal electrolytes
- Testing done by 2 doctors on 2 separate occassions (both >5yr experience + 1 must be consultant, neither can be on transplant team)
- Look for: fixed pupils, no corneal, oculo-vestibular or gag reflect, no response to supraorbtal pressure. No resp effort when disconnected from ventilator+ pCO2 >6.0)

Rectal Prolapse
- Partial (rectal mucosa protrudes); complete (rectal wall)
- RFs: chronic training, vaginal deliveries
- Presents -> mucous discharge, faecal soiling, PR bright red blood on wiping, ulceration, rectal fullness/tenesmus
- Managed surgically in most

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12
Q

Superficial Thrombophlebitis

  • Pathophysiology
  • Presentation
  • Investigation
  • Management
A

Pathophysiology
- Inflammation of superficial veins (NOT infective, altho can get secondary infection -> septic thrombophlebitis)
- 20% have underlying DVT at presentation (esp if >5cm of vein affected)

Presentation
- Typically long saphenous vein
- Vein inflamed + painful

Investigation
- Doppler USS if proximal long saphenous vein affected to exclude concurrent DVT

Management
- Anti-embolism stockings (w/ ABPI first)
- LMWH prophylactic dose for 30 days OR fondaparinux or 45d (N.B. longer course of 6-12/52 if at sapheno-femoral junction)
- if LMWH contraindicated then 12 days of PO NSAIDs

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13
Q

Hiatus Hernia
- Pathophysiology
- Presentation
- Investigation
- Management

A

Pathophysiology - herniation of part of stomach above diaphragm
- Sliding (95%) - gastroesophageal junction moves above diaphragm
- Rolling (paraoesophageal): junction remains below but different bit of stomach herniates through oesophageal hiatus

RF: obesity, ascites, pregnancy

Presentation
- Heartburn, Dysphagia, Regurgitation, chest pain

Investigation
- Barium swallow most sensitive
- (altho many pts end up having endoscopy first to rule out ca etc)

Management
- Conservative: weight loss
- Medical: PPI
- Surgical: if not responding to above OR if complications (N.B. any signs obstruction, strangulation or volvulus needs NG decompression prior to surgery). Options: cruroplasty or nissens fundoplication.

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14
Q

General Anaesthetic Agents
What are they used for (induction vs maintenance), give typical side effects and advantages.

  • Volatile Liquid Anaesthetics (iso-, des-, sevo-flurane)
  • Nitrous Oxide
  • Propofol
  • Thiopental
  • Etomidate
  • Ketamin
A

Volatile Liquid Anaesthetics
- Induction + maintenance
- SEs: Myocardial depression, Malignant Hyperthermia

Nitrous Oxide
- For maintenance and analgesia
- SE: can diffuse into gas-filled body compartments so increasing their pressure (avoid in pneumothorax)

Propafol
- induction ALSO anti-emetic
- SE: pain on injection, hypotension

Thiopental
- SE: laryngospasm, hypotension

Etomidate
- SEs: adrenal supression + myoclonus
- BUT less hypotension than prop/thiopental so good in haemodynamic instability

Ketamine
- SEs: disorientation and hallucinations
- No BP drop so good in trauma

Malignant Hyperthermia
- Autosomal Dominant. Triggered by fluranes.
- Ca2+ released from sarcolemma –> muscle rigidity + hyperthermia
- Managed A-E plus dantrolene

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15
Q

Local Anaesthetic Agents
- Lignocaine
- Bupivacaine

When are they used? What is dosing? What about combining w/ adrenaline? What SEs can they cause?

A

Lignocaine
- Local anaesthetic
- SEs: Toxicity (if excess or IV administration) –> liver dysfunction, initial CNS overactivity + then depression, cardiac arrhythmias.
- Dose 3mg/kg OR 7mg/kg if combined w/ adrenaline (can’t use adrenaline if using MAOIs or TCAs)

Bupivacaine
- Longer duration than ligonaine. Good for wound infiltration post-op.
- SEs: cardiotoxic so contraindicated in regional blocks (in case tourniquet fails)
- Dose: 2mg/kg (adrenaline does NOT allow higher dose)

16
Q

Peripheral Arterial Disease
Pathophysiology
Presentation
Investigation
Management

A

Pathophysiology
- RFs same as general CVS. Acute ischaemic can be thrombus (more likley if pre-exising PVD) or embolic ( more likley if sudden onset or clear source e.g proximal aneurysm, AF)

Patterns of presentation:
- Intermittent claudication
- Critical Limb Ischaemic
- Acute Limb-Threatening Ischaemia

Presentation
Intermittent Claudication
- cramping in thigh, calf or buttock after fixed distance, relieved by rest +/- ischaemic rest pain

Critical Limb Ischaemia
- Rest pain >2 weeks needing opiates
- OR gangrene or ulceration
- OR ABPI <0.5

Acute Limb Threatening Ishcaemia = emergency 6Ps
- Pale, pulseless, painful, paralysed, paraesthetic, perishingly cold

Investigation
Intermittent Claudication + Critical Limb*
- Bueger’s Test (raise leg till pale, lower leg till colour returns, if <20 degrees then = severe)
- ABPI
Normal >0.9
Mild 0.8-0.9
Mod 0.5-0.8
Severe <0.5 (critical limb ischaemia)

Critical - Doppler USS
CT angio/MR angio for further imaging

(N.B. >1.2 ?calcification + falsely raised ABPI).

Acute Limb Threatening Ischaemia
- Handheld arterial doppler.
- If signal presents also get ABPI.

Management
Intermittent Claudication
- Liftstyle advice, statins
- Antiplatelets: 1st: Clopidogrel lifelong (2nd aspirin)

Critical Limb Ischaemia (or intermittent not responding to above)
- Surgery: angioplasty w/ stenting or bypass grafting

Acute Limb Threatening Ischaemia
- A-E, analgesia
- IV unfractionated heparin
- Vascular review
- Definitive: intra-arterial thrombolysis, embolectomy, angioplasty, bypass or amputation

17
Q

Small and Large Bowel Obstruction
Pathophysiology
Presentation
Investigation
Management

A

Pathophysiology
- Small: adhesions or hernia
- Large: malignancy, diverticular disease, volvulus

Presentation
- Abdo pain
- Vomiting (SBO)
- Abdo distension
- Absolute constipation (early in LBO)
- o/e distension, tinkling bowel sounds, tympanic percussion +/- focal tenderness/guarding (if ischaemic)

Investigations
- Bloods, VBG, G&S
- CT AP w/ contrast
- +/- initial AXR (SBO - valvulae conniventes; LBO (haustral lines (don’t completeley cross) + more peripheral))

Management
- Intitial: NBM, NG tube, IVI, catheter, analgesia/anti-emetics
- Surgery if suspicion of intestinal ischaemic, closed loop obstruction, strangulated hernia, tumour or failing to improve after 48h

18
Q

GI Perforation

  • Causes
  • Presentation
  • Initial Investigation
  • Management
A

Causes
- Upper GI: peptic ulcer, gastric/oesophageal Ca, FB (e.g. battery), Boerhaave
- Lower: Diverticulitis, colorectal Ca, appendicitis, Crohns, toxic megacolon (UC or C.diff)
- Other: endoscopy, trauma, mesenteric ischaemia, bowel obstruction

Presentation
- Unwell
- Abdo pain w/ localised or generalised pertonism
- Malaise, vomiting, lethargy + features of underlying cause

Investigation
- Bloods
- CT w/ contrast
- +/- initial erect CXR + AXR

Management
- Resus
- IV Abx, NBM, NG tube, IVI, analgesia
- Likely surgery (dependent on cause)

19
Q

Describe the following and their management

  • Volvulus
  • Pilonidal Sinus
A

Volvulus
- Path: torsion of colon around mesenteric axis. Mostly sigmoid (80%) or colon (20%)
- Associations: Sigmoid: older pt, chronic constipation, neuro e.g. PD, Duchenne muscular dystrophy, psych e.g. schizophrenia
- Features: Constipation, abdo bloating/pain, n+v
- Diag: AXR, Sigmoid volvulus (LBO + coffee bean sign), Caecal volvulus (SBO)
- *Mx: Sigmoid: rigid sigmoidoscopy + rectal tube insertion. Caecal: operative.

Pilonidal Sinus
RF: sweating, prolonged sitting, obesity, poor hygeine, local trauma
Pres: intermittent, red, painful + swollen mass in sacrococcygeal region w/ discharge +/- systemic signs of infection.
Ix: MRI may be needed if extensive
Mx: Some resolve over time (shave affected area, pluck hair from sinus, wash it out). Surgery: drain any abscess + excise the tract

20
Q

What is dumping syndrome?

  • Pathophysiology
  • Presentation
  • Investigation
  • Management
A

Pathophysiology
- When food moves too quickly to small bowel after eating eg post-gastrectomy, oesophagectomy etc.

Presentation
Early dumping:
- GI: abdo pain, diarrhoea, gurgling, bloating, nausea
- Vasomotor: flushing, palpitations, perspiration, tachycardia, hypotension, syncome

Late dumping:
- Hypoglycaemia
- Perspiration, palps, hunger, weakness, confusion, syncope, tremor

Investigation
- Oral Glucose Tolerance Test (dumping if HR increases 30mins after eating, 3% increase in haematocrit 30mins after eating or low blood glucose 1-3h after eating)
- Gastric emptying scan (scintigraphy)

Management
- Octreotide
- Surgery

21
Q

Breast Cancer
- Pathophysiology
- Presentation (including pre-malignant lesions)
- Investigation
- Management

A

Pathophysiology
Most = adenocarcinomas
- Invasive ductal (most common) (Ductal Ca = ‘No Special Type’, all others are ‘Special Type’)
- Ductal Carcinoma in Situ (DCIS)
- Invasive lobular carcinoma
- Lobular carcinoma in situ (LCIS)

Other Special Types:
- Medullary
- Mucinous/Colloid
- Tubular
- Adenoid Cystic Carcinoma
- Phyllodes
- Inflammatory
- Paget’s Disease of the nipple
(N..B. Pagets + Inflammatory may be associated w/ an underlying lesion or be on their own. Paget’s often has invasive underlying lesion)

Risk Factors:
- Early menarche, Late menopause, BRCA 1/2 mutations, Family Hx, Nulliparity, COCP, p53 mutations, ionising radiation, obesity, prev surgery for benign disease (most to do w/ oestrogen exposure)

Presentation
- Lump
- Nipple: inversion, discharge, bleeding
- Skin changes: eczmea, dimpling, ulceration
- Systemic: weight loss, fever, pain, lymphadenopathy

Other:
- Paget’s Disease (starts at nipple spreads out. Eczema tends to affect areola + spare nipple)
- Inflammatory

Investigation
- Screening: mammogram every 3yrs age 50-70

2ww Referral (definite)
- >30yo w/ unexplained breast lump +/- pain
- >50 w/ unilateral nipple sx

Consider in:
- skin changes suggestive of breast cancer
- >30yo w/ lump in axilla

When Referred:
- Examination
- USS: microcalcification, spiculated mass lesion (typical for carcinoma)
- Biopsy (tends to be core biopsy)

Management
*Surgery *(done in most)
- Wide-local Excision (solitary, peripheral, small lesions, DCIS <4cm)
- Mastectomy (multifocal, central, large, DCIS >4cm)
- +/- axillary node clearance
- Breast reconstruction offered to all

Radiotherapy
- All wide local excisions AND mastectomy w/ 4 or more +ve nodes

Hormonal Therapy (if +ve for oestrogen receptors)
- Pre- and Peri-Menopausal women = Tamoxifen (for 5 years post-diagnosis) (SE: endometrial Ca, VTE, menopausal sx. N.B. it protects against osteoporosis as although it is anti-oestrogen at the breast it is an oestrogen agonist in other tissues)
- Post-menopausal = Anastrazole (SEs: osteoporosis, hot flushes, arthralgia, insomnia)

Biologic Therapy (if HER2 +ve)
- Trastuzumab (Herceptin) (contraindicated in anyone w/ hx of heart disorders)

Chemotherapy
- Pre- or post-surgery

Pre-malignant
- Atypical Ductal/Lobular Hyperplasia - NOT actually pre-malignant BUT is a marker for increased risk of breast Ca in the future. Needs mammograms every 6-12/12

22
Q

Describe the presentation and management of the following benign breast disorders

  • Fibroadenoma
  • Intraductal Papilloma
  • Fibroadenosis (fibrocystic disease/benign mammary dysplasia)
  • Breast Abscess
  • Mammary duct ectasia
  • Fat Necrosis
  • Sclerosing Adenosis
  • Epithelial Hyperplasia
A

Fibroadenoma
- women of reproductive age, highly mobile, firm, smooth mass (breast mouse)
- No increased risk of malig. Over 2yrs 30% get smaller.
- If <3cm monitor. If >3cm excision.

Intraductal Papilloma
- 40-50yo, subareolar lesion. Can-> bloody/clear nipple discharge or mass.
- Imaging can look similar to carcinoma so needs biopsy.
- No increased malignancy risk.
- Treat w/ microdochectomy

Fibroadenosis
- Poorly defined lumpiness +/- pain. Worse prior to menstruation. Mostly middle-age women.

Breast Abscess
- Staph aureus most common in lactational women
- Erythema, pain, fluctuant swelling, swinging fever
- Incision + drainiage or needle aspiration + Abx

Mammary Duct Ectasia
- Dilation of breast ducts, mostly around menopause
- Tender lump around areolar +/- green nipple discharge + symmetrical slit-like nipple retraction
- Rupture can –> local inflammation/plasma cell mastitis
- Mammogram: dilated calcified ducts
- Mx: conservative. If unremitting discharge -> total or subtotal duct excision

Fat Necrosis
- 40% associated w/ trauma.
- Lump, discharge, skin dimpling, pain, nipple inversion (mimics Ca)
- USS - hyerechoic mass. If more developed mammogram can show irregular spiculated mass (needs biopsy)
- Mx: Self-limiting. Reassurance + analgesia.

Sclerosing Adenosis
- = radial scards + complex sclerosing lesions
- Lump or pain. Mammogram mimics carcinoma. Needs biopsy.
- No increased risk of malignancy. Conservative management.

Epithelial Hyperplasia
- Variable pres: generalised lumpiness or discrete lump
- If typical then conservative management
- If atypical or fam hx of breast Ca then greatly increased risk of breast Ca so needs monitoring +/- surgical resection