Surgery Flashcards
List the types of oesophageal cancer and associated risk factors
- Squamous cell carcinoma
- Adenocarcinoma
Risk factors: smoking, alcohol, hot beverages, GORD, Barrett’s, obesity, achalasia
Describe the signs and symptoms associated with oesophageal cancer
- Progressive dysphagia (solids then liquids)
- Weight loss
- Anaemia
- Less common – odynophagia, cough, hoarseness, haematemesis, melaena
List differential diagnoses for dysphagia
Within lumen
> Food bolus
> Foreign body
> Oesophageal candidiasis
Within wall
> Peptic/caustic stricture
> Schatzki ring
> Pharyngeal pouch
> Achalasia / oesophageal dysmotility
> Oesophageal web
> Oesophageal cancer
Outside oesophagus
> Mediastinal mass
> Lymphoma
> Thoracic aortic aneurysm
> Globus hystericus
Describe the treatment of oesophageal cancer
Curative intent – early cancers
> endoscopic mucosal resection (EMR) and endoscopic submucosal dissection (ESD)
> Endoscopic mucosal therapy – Barrett’s oesophagus with dysplasia
Tumours beyond mucosa +/- LN
> Neoadjuvant chemoradiation
> Surgery
> Ivor-Lewis oesophagectomy OR three stage (McKeown) operation
Describe the anatomy, blood supply, nerve supply and lymphatic drainage of the stomach
4 sections: cardia, fundus, body, pylorus
Blood supply
> Lesser curvature: left gastric artery (coeliac trunk branch)
> Greater curvature: left & right gastroepiploic arteries
> Fundus: short fastric artery (splenic branch)
> Pylorus: right gastric artery (common hepatic branch)
Venous drainage matches arterial supply
Nerve supply
> Parasympathetic: vagus nerve
> Sympathetic nerve: T6-T9 spinal cord segments
Lymphatics
> Lymph fluid drains into gastric and gastroomental lymph nodes found at curvatures
List risk factors for gastric cancer
Diet
> Processed meat
> Low fruit/veg intake
> High salt intake
> Nitrates / nitrites
Obesity
Smoking
H. pylori
Age > 50
Ethnicity – Asian and Pacific Islanders
Male gender
Heavy alcohol use
Describe the signs and symptoms of gastric cancer
Weight loss
Abdo pain
Nausea
Dysphagia
Melaena
Early satiety
Ulcer type pain
Occult GI bleeding more common than overt bleeding
Signs
- Palpable abdominal mass
- Palpable lymph node
> Left supraclavicular node (Virchow’s)
> Periumbilical (Sister Mary Joseph) - Ascites
Describe the different types of gastric cancer and their routes of spread
Primary
> Adenocarcinoma (94%)
> Tubular
> Papillary
> Mucinous
> Signet ring
> Lymphoma (4%)
> GI stromal tumour (GIST)
> Type of sarcoma, develops in the connective tissue
> Secondary
> Direct invasion from nearby organs
Routes of spread
> Haematogenous
> Peritoneal seeding
> Krukenberg tumours – ovarian metastasis
> Blumer’s shelf – metastasis in pouch of Douglas
> Lymphatic spread
> Direct – to adjacent organs
Describe the pathological classification of gastric cancer
Lauren classification
> Intestinal type
> Due to H. pylori
> Distal stomach
> Ulcerated growth
> Declining due to treatment of H. pylori
> Diffuse type
> Mainly affects cardia
> Younger age, worse prognosis
> No pre-cancerous lesions
> > Linitis plastica
> Diffuse type gastric cancer
> Tumour often infiltrates the submucosa and muscularis propria
> Superficial biopsies may be falsely negative
> “Leather bottle stomach”
Describe the investigations used in gastric cancer
Bloods
FBC – microcytic anaemia
LFTS – if deranged, possible mets
No reliable tumour markers but CEA, Ca125 and CA19-9 may be raised
Upper GI endoscopy
CT thorax, abdomen and pelvis – assess for metastatic disease
Staging laparoscopy to look for peritoneal metastases if considering resection
Describe the treatment of gastric cancer
> Peri-operative chemotherapy
> Proximal cancers – total gastrectomy
> Distal cancers (antrum or pylorus) - subtotal gastrectomy
> Very early T1 gastric cancers – endoscopic mucosal resection (EMR)
Advanced disease – palliative therapy
> Nutrition – enteral feed, build up drinks
> Treatment of infection
> Maintain lumen patency (stenting or endoscopic laser treatment)
> Palliative surgery (gastro-jejunostomy) to by-pass obstruction
List complications of total gastrectomy
Anastomotic leak
Dumping syndrome
> Sudden and large passage of hypertonic gastric contents into small intestine
> Results in an intraluminal fluid shift and subsequent intestinal distention
> Symptoms of nausea, vomiting, diarrhoea, hypovolaemia
Vitamin B12 deficiency – loss of secretion of intrinsic factor
MI / stroke / respiratory failure / DVT / PE
Describe the characteristics of Helicobacter pylori and its treatment
Gram negative helical bacterium produces urease enzyme
> Breaks down urea into CO2 and ammonia
> Ammonia neutralises stomach acid creating alkaline microenvironment
> Sets off cycle of repeated damage to epithelial cells, leading to inflammation, ulceration and ultimately gastric neoplasia
Eradication – triple therapy, 1 PPI + 2 antibiotics
> Omeprazole 20mg BD (PPI)
> Clarithromycin 500mg BD OR metronidazole
> Amoxicillin 1g BD
Describe the anatomy of the pancreas, including blood supply
- Head
- Neck
- Body
- Uncinate process
- Tail
Blood supply
- Gastroduodenal artery
- Superior & inferior pancreaticoduodenal artery
- Splenic artery - greater pancreatic artery
Describe the functions of the pancreas
Endocrine - islets of Langerhans
> Alpha cells: glucagon
> Beta cells: insulin + amylin (slows gastric emptying)
> Delta cells - somatostatin (regulates alpha & beta)
> Gamma cells: pancreatic polypeptide
> Epsilon cells: ghrelin (appetite)
Exocrine - acinar & duct tissue
- Proteases - trypsinogen and chymotrypsinogen
- Amylase: starch & maltose
- Lipase
- Others: elastase, ribonuclease…
Regulated by vagal innervation
> Acidic chime entering duodenum encourages S cells to release secretin which release alkaline pancreatic juices
> Fatty acids in duodenum release cholecystokinin, leads to secretion of digestive enzymes and bile from gallbladder
List risk factors for pancreatic cancer
Smoking, diabetes, high BMI, alcohol excess
Chronic and hereditary pancreatitis
Genetic familial syndromes e.g. Von-Hippel Lindau, MEN1
Medical conditions: peptic ulcer disease, IBD
Describe the signs and symptoms of pancreatic cancer
Obstructive jaundice (often painless) or pain radiating through to back
Cachexia, anorexia and unexplained weight loss
Pale stools and dark urine
loss of endocrine function - type 3c diabetes
Nausea / vomiting
Palpable gallbladder (Courvoisier’s sign)
Acute pancreatitis
Haematemesis, melaena, IDA
investigations
- high resolution CT scan
- ultrasound
- imaging may demonstrate double duct sign
> simultaneous dilatation of the common bile and pancreatic ducts
List types of pancreatic cancer
Solid non-endocrine
> Pancreatic ductal adenocarcinoma (PDAC)
> Adenosquamous
> Acinar cell
> Giant cell
> Pancreatoblastoma
Cystic non-endocrine
> Serous cystic
> Mucinous cystic
> Solid and cystic papillary
> Acinar cell cystadenocarcinoma
> IPMN – intraductal papillary mucinous neoplasm – malignant transformation possible
Neuroendocrine – functional v non-functional
> Gastrinoma - Zollinger-Ellison syndrome
> Increased levels of gastrin and stomach acid leading to ulcers and diarrhoea
> Insulinoma
> Slow growing, can present with hypoglycaemic coma
> Glucagonoma - High BMs
> VIPoma - Vener-Morrison syndrome
> Somatostatinoma
Describe the treatment for pancreatic cancers
Head of pancreas cancer
> Whipple’s procedure (pancreaticoduodenectomy) +/- pylorus sparing
Body / tail - distal pancreatectomy / total pancreatectomy
Neoadjuvant / adjuvant chemotherapy
Not for resection
> Palliative intent
> Relieve obstruction via biliary stent or duodenal stent if GOO
> Palliative chemotherapy
Describe Familial Adenomatous Polyposis (FAP)
APC gene (chromosome 5), AD inheritance
Gardner’s syndrome (subtype of FAP)
Numerous (>100) polyps
Almost 100% risk by age 40
Total colectomy performed in mid 20s
Still require endoscopic surveillance
List risk factors for CRC
Dietary – low fibre, high animal fat & red meat
Excess bile salts
Increasing age: majority >50 years age
Previous colon cancers or previous colorectal adenomas
Family history
IBD (UC > Crohn’s)
Familial conditions: FAP, HNPCC, juvenile polyps
Describe Lynch syndrome
Predominantly right-sided lesions
AD inheritance
Also increases risk of endometrial, breast, prostate and gastric cancer
most common inherited condition for CRC
Describe the adenoma-carcinoma sequence
Adenoma – benign neoplasm of large bowel glandular epithelium
Adenomas undergo dysplastic change to become carcinomas
Majority left-sided lesions
Describe the presentation of CRC
Change in bowel habit
> Bloods / mucus PR
> Lower abdo pain
> LBO / perforation
> Rectal pain / tenesmus
> Fistulate to adjacent structures
> Iron deficiency anaemia
> Weight loss
> Mass in RIF
> SBO or appendicitis in caecal lesions
30% present as an emergency
> Obstruction
> Perforation
How is the severity of ulcerative colitis (UC) classified?
Truelove and Witts Criteria
Moderate: 4-8 stool a day
Severe: 8 stools a day, may have fever or night sweats
Fulminant
>10 stools a day
Abdo pain, fever
Hypotension, tachycardia
Low Hb
Increased WCC &CRP, lowered albumin
Describe Duke’s classification for CRC
A – limited to bowel mucosa
B – infiltrating through muscle wall
C – local lymph node involvement
D – distant spread (lung, liver, bone)
Describe the management of ulcerative colitis (UC)
inducing remission
- Mild acute UC
> topical (rectal) mesalazine (aminosalicylate) - moderate acute UC
> topical (rectal) + oral mesalazine
> Prednisolone - Severe acute UC
> IV steroids e.g. hydrocortisone
> IV ciclosporin if steroids contraindicated
> if no improvement after 72h
» Infliximab
» Surgery
maintaining remission
- after mild/moderate flare: topical mesalazine OR topical + oral mesalazine
- following a severe relapse or if >=2 exacerbations in the past year: oral azathioprine or oral mercaptopurine
- Maintaining remission
> Aminosalicylate, azathioprine or mercaptopurine - Predfoam enemas for toxic megacolon
- Total panproctocolectomy is curative - patient will have a permanent ileostomy or an ileo-anal anastomosis (J-pouch)
> sub-total colectomy in acute flare due to risk of infection
List investigations for CRC
- Colonoscopy and biopsy
- Staging CT CAP
- Bloods, stool qFIT
- ECG - exclude ischaemic bowel from AF
- CEA marker - carcinoembryonic antigen
Describe the management of CRC
- Surgical resection
- Adjuvant chemoradiotherapy
- Palliative stenting for inoperable lesions; perform bypass surgery or colostomy to avoid obstruction
Which patients should be investigated for CRC?
Patients >50 with >6 week history of
- Change in bowel habit
- Rectal bleeding
- IDA
Describe the symptoms of anal cancer
Can be painful – constant pain suggests invasion into sphincter / sidewall
Blood and mucus on wiping
Tenesmus
Red flags – weight loss, anorexia, groin nodes
Name the most common type of anal cancer and its risk factors
Most commonly SSC, less commonly adenocarcinoma
Risk factors – HPV / anogenital warts or dysplasia / immunosuppression
List risks of blood transfusions
Transfusion reactions
> ABO & rhesus incompatible blood
> Unanticipated immunological reactions to correctly crossmatched blood
Transfusion transmitted infections
Poorer outcomes in surgical patients who are transfused
List complications of massive transfusion
Impaired oxygen delivery to tissues
Metabolic acidosis / hypocalcaemia
Coagulopathy – dilutional / consumptive
Hypothermia
Hyperkalaemia
Fluid overload
Transfusion related acute lung injury (TRALI)
List causes of perforated viscus
Upper GI (most common)
> DU/GU, gastric cancer, gallbladder, iatrogenic
Colonic (less common)
> CRC, diverticulum, stercoral, appendicitis, colitis
Small bowel (least common)
> Meckel’s diverticulum, ischaemia, Crohn’s, lymphoma
List risk factors for peptic ulcer disease
Infection – H. pylori
Neoplasia – gastric carcinoma
Vascular – inflammatory / autoimmune
Trauma – stab wounds
Iatrogenic – ERCP or OGD
Endocrine – Zollinger-Ellison syndrome: excessive gastrin
Drugs – NSAID use
Chemical – caustic substances/batteries
Define stercoral colitis
Stercoral colitis is an inflammatory colitis related to increased intraluminal pressure from impacted faecal material in the colon
Describe the management of a perforated ulcer
IV antibiotics + IV PPI
Perforated duodenal ulcer - oversew and omental patch
Gatric ulcer perforation - same or partial gastrectomy
Describe the clinical presentation of a small bowel obstruction
Faeculent vomiting
Absolute constipation
Colicky abdominal pain
Distended abdo with tinkling bowel sounds (BS)
List causes of small bowel obstruction
Intraluminal
> Foreign bodies
> Gallstones
> Meconium
Intramural
> Tumours
> Crohn’s – inflammatory strictures
Extrinsic
> Adhesions
> Hernias
> Cancer
Less common: gallstone ileus, intussusception, volvulus
Describe the pathophysiology of small bowel obstruction
Gas and fluid accumulate proximal to the site of the obstruction
Intestinal activity increases to overcome the obstruction > colicky pain
Ongoing gas and fluid accumulation > bowel distends > intraluminal pressure rises
Intestinal motility is reduced with fewer contractions
Intramural pressure becomes high, intestinal microvascular perfusion is impaired leading to intestinal ischaemia > necrosis
List investigations used in SBO
History and examination
Bloods
AXR +/- CT A/P
> AXR supine will show dilated small bowel loops >3cm, erect AXR will show air-fluid level
Describe the management of SBO
Drip and suck
> Pass NG tube, give IV fluids
> NG tube decompresses small bowel by draining content upwards
> IV fluids used to catch up with losses
Monitor UO – intake/output chart
Theatre after 48h
Trial of gastrografin if unsuccessful
Describe a sigmoid volvulus and AXR findings
Bowel twists on its mesentery and obstructs
Causes massive blockage at location and upstream
AXR:
> Coffee bean sign
> Points to LUQ
> Loop arising from LIF twists
> Dilated proximal large bowel + small bowel
List risk factors for volvulus
Common in patients with
Reduced mobility
Psychotropic medications, opiates, antidepressants
Chronic laxatives
Parkinson’s
Schizophrenia
Describe the management of sigmoid volvulus
Fluid and electrolyte replacement
Decompression using flexible sigmoidoscopy
Surgery if ischaemia or elective sigmoid colectomy for recurrent sigmoid volvulus.
Describe a caecal volvulus
Location is variable
Distended caecum, remainder of colon collapses
Obstruction is where volvulus is
Small bowel can be dilated depending on ileocaecal valve
Describe the presentation of LBO and list causes
Clinical presentation
> Absolute constipation and distension
+/- vomiting (depending on whether ileocaecal valve is open or closed)
Causes
> Stricture
> Malignant (CRC)
> Benign (diverticula, ischaemia, IBD)
> External compression; gynaecological malignancy
> Volvulus
> Adhesions
Describe the management of LBO
- IV fluids + NG tube
- Surgery
> If volvulus: flexible sigmoidoscopy decompression +/- flatus tube
> Laparotomy (caecal volvulus)
> Defunctioning colostomy / ileostomy
> Colonic stent
Closed-loop obstruction (competent ileocaecal valve not relieving pressure) - SURGICAL EMERGENCY
Describe the risk factors and presentation of ischaemic gut
Risk factors - Elderly / vasculopath / AF
- Small bowel
> Central abdominal pain, colicky then constant, pain out of keeping with abdominal findings
> Vomiting (possible altered blood) - Colon - ischaemic colitis
Colitis
> LIF pain
> Diarrhoea (may be bloody)
Describe investigations and management of ischaemic colitis
Initial investigations
> Very high WCC and CRP
> May have lactic acidosis on ABG
> AXR may look abnormal/obstructed
Management
> Initial resus and IV antibiotics
> Small bowel - laparotomy
> > Pan-ischaemia is fatal and non-resectable
> > Segmental ischaemic – resect
Colon
> Conservative treatment
> If perforates or deteriorating patient may need Hartmanns/colectomy
Describe the clinical presentation of appendicitis
clinical features
- periumbilical pain migrates to RIF with guarding, rigidity, rebound tenderness
> Max tender over McBurney’s point, 2/3 of the way along line between umbilicus and ASIS
- nausea and vomiting
- anorexia (common feature especially children)
- flatulence, bowel irregularity, diarrhoea
- pain on walking / speed bumps / potholes
- Rovsing’s sign – pain in RIF when LIF is palpated
- Psoas stretch sign
What is Valentino’s syndrome?
Perforated peptic ulcer
Chemical fluid from ulcer streams along right paracolic gutter to RIF
Causes peritoneal irritation and consequent chemical appendicitis
Describe the management of appendicitis
- Children: USS abdomen
- Young man – convincing clinically, proceed to lap/open appendicectomy
- Young woman – HCG to exclude ectopic, pelvis USS to exclude ovarian pathology, proceed to diagnostic lap +/- appendicectomy
- Older man/woman - CT A/P to exclude malignancy and confirm appendicitis
IV Abx pre-operatively
Define diverticula
Diverticula are acquired outpouchings of mucosa and submucosa, predominantly sigmoid colon
Describe the clinical presentation of diverticulitis
diverticula are outpouchings of the colonic mucosa through the muscular wall of the colon
the usual site is between the taenia coli where vessels pierce the muscle to supply the mucosa
- LIF pain (except Asian, more likely RIF pain)
- Fever
- Change in bowel habit
- Nausea, vomiting
- Urinary symptoms
- PR bleeding
List risk factors for diverticular disease
Low fibre
High fat
Red meat
Physical inactivity
Current smokers
Drugs – NSAIDs, steroids, opiates
List acute and chronic complications of diverticular disease
Acute
> Abscess, perforation, haemorrhage
> Perforation leads to generalised peritonitis, distended abdomen, diffuse tenderness/guarding
Chronic
> Stricture
Describe the management of diverticulitis
Initial management – IV antibiotics, fluids, analgesia
Non-improving patients or those with complications require intervention e.g. drainage of abscess, colonic resection if perforation or obstruction
Describe the composition of bile
Bilirubin - pigment - breakdown of haem products
Cholesterol - excreted in bile, requires lecithin and bile salts to solubilise
Bile salts - cholic & chenodeoxycholic acid conjugated to taurine and glycine; fat emulsifiers
Lecithin - fat emulsifier
Inorganic salts - NaCl, NaHCO3 - neutralisation of gastric acid
Water
Describe the pathophysiology of gallstones
Mixed stones
> Cholesterol supersaturation
> Gallbladder function (emptying/absorption)
> Reduced bile acid concentration (gut bugs, ileal resection/disease)
Pigment stones
> Accumulation of bilirubin e.g. due to haemolytic anaemia
> Bile stasis
> Biliary tract colonisation (deconjugation of bilirubin diglucuronide)
> Foreign body (stents, parasites)
List risk factors for gallstones
4 Fs - Female (oestrogen drives stone formation), fair, fertile, forties
Genetics
Low calorie diet, rapid weight loss
PPI use
Describe the clinical features and management of biliary colic
Clinical features
> Colicky RUQ / epigastric pain
> Acute onset, initiated by eating & drinking fatty foods
> Radiating to back
> Nausea and vomiting
> Dyspepsia, flatulence, food intolerance
Duration
> Lasts minutes to hours
> Settles spontaneously
> Well in between episodes
Blood results
> WCC, CRP – normal
> LFTs – normal
Management – analgesia and elective lap chole if severe
> If CBD is cut, hepatojejunostomy is performed; however, lifetime of recurrent biliary sepsis, gallstones
Describe the clinical features and management of acute cholecystitis
Obstruction of the cystic duct / Hartmann’s pouch
Pressure on/within GB increases
Leads to hypertrophy, relative ischaemia, peri-cholecystic oedema
Superadded infection
features
- Murphy’s sign +ve
- Boas siwn: hyperaesthesia beneath right scapula
Blood results
> WCC, CRP – raised
> LFTs – normal / mildly deranged
Management
> Standard initial Rx
» NBM – low fat diet
» Analgesia
> IV Antibiotics
> early laparoscopic cholecystectomy within 1 week of diagnosis
> Percutaneous cholecystostomy if gangrenous
List complications of cholecystitis
Gangrene
Chronic cholecystitis
Emphysema of GB
Mucocoele
Empyema of GB
Perforation
Mirizzi syndrome: GB stone impacted in Hartmann’s pouch leads to pressure and erosion of common hepatic duct
Gallstone ileus
> seen as small bowel obstruction + air in biliary tree on AXR
Carcinoma
Describe the causes, clinical presentation and management of ascending cholangitis
Clinical presentation
> Charcot’s triad
» Fevers / rigors
» Jaundice
» Pain
> Raynaud’s pentad
> Charcot’s
> CNS depression
> Shock
Causes: CBD stones, stricture, anastomotic stricture, post-ERCP
commonly caused by E. coli
Management
- Aggressive resus
- IV Abx - triple therapy - gent, amox, metro OR tazocin
- Urgent ERCP, sphincterotomy +/ stent
- Percutaneous transhepatic cholangiography
Describe gallstone ileus
In older individuals, long-term low-grade inflammation causes a fistula connecting duodenum & GB (sometimes stomach)
Presentation
> Presents as SBO
» Vomiting, distended abdomen, absolute constipation
» AXR may show stones & air in biliary tree
» Often impact at IC valve
Management
> Laparotomy
> Enterotomy and removal
> Leave GB alone
Describe the pathophysiology of acute pancreatitis
Pancreatic enzymes are prematurely activated leading to autodigestion
Triggered by injury to acinar cells or impairment of zymogen granules which store and package enzymes, or anything damaging duct epithelium
Important: conversion of trypsinogen to trypsin
Once cellular injury has been initiated, inflammatory process can lead to local oedema, haemorrhage and necrosis
Inflammatory mediators released into bloodstream lead to severe systemic complications including organ failure or death
List causes of acute pancreatitis
I GET SMASHED
Iatrogenic
Gallstones
Ethanol
Trauma
Steroids
Mumps / malignancy
Autoimmune (IgG4)
Scorpion stings
Hypercalcaemia / hypertrygliceridaemia
ERCP
Drugs
> azathioprine
> thiazides
> oestrogen
> mesalazine
Describe the investigations carried out in acute pancreatitis
Investigations
- Bloods including AMYLASE or lipase
Imaging
> Erect CXR to exclude pneumoperitoneum or LRTI
> USS abdo to exclude gallstones & determine CBD diameter
> > also demonstrates pancreatic head masses and pancreatic oedema
> MRCP - exclude biliary or pancreatic stones
> ERCP: especially with coexisting cholangitis in gallstone pancreatitis
> EUS: idiopathic pancreatitis
> CT with contrast
Describe CT findings in acute pancreatitis
Rule out peripancreatic collections, necrosis, abscesses and vascular complications of pancreatitis e.g. portal venous thrombus, pseudoaneurysms or haemorrhage
Areas of reduced parenchymal enhancement indicate necrosis
Interstitial oedematous pancreatitis
> Pancreas enlargement due to oedema
> Milder form
> Symptoms usually resolve within first week
> Acute interstitial pancreatitis
> Peripancreatic fat stranding centred on the head and body of the pancreas
> Pancreatic pseudocyst
> Well-defined fluid density cystic lesion
Necrotising pancreatitis
> Acute necrotic collection
» Ill-defined peripancreatic fat stranding with free fluid
> Early walled off necrosis
» Ill-defined peripancreatic collections that cross between anatomical compartments
» Become more organised with thick enhancing walls and heterogeneous internal debris
Describe severity scores for acute pancreatitis
Glasgow (Imrie) score >=3 within 48h of admission indicates severe, likely to develop complications
> Age, oxygen, WCC, urea, calcium, glucose, albumin, LDH, AST/ALT
Modified Glasgow / PANCREAS score
Revised Atlantic Classification
> Mild – no organ failure, no local/systemic complications
> Moderate – transient organ failure (<48h), local/systemic complications
> Severe – persistent organ failure (>48h)
CRP of >300mg/L 72h after onset of symptoms – necrosis likely