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Y3 Surgery > General surgery > Flashcards

General surgery Flashcards

1
Q

Give 3 differentials for epigastric pain?

A
  • peptic ulcer disease
  • cholecystitis
  • pancreatitis
  • GORD
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2
Q

Give 3 differentials for periumbelical region pain

A
  • small or large bowel obstruction
  • appendicitis
  • AAA
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3
Q

Give 3 differentials for RUQ pain

A
  • cholecystitis
  • pyleonephritis
  • ureteric colic
  • hepatitis
  • pneumonia
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4
Q

Give 3 differentials for LUQ pain

A
  • gastric ulcer
  • pyelonephrosis
  • ureteric colic
  • pneumonia
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5
Q

Give 3 differentials for LLQ pain?

A
  • diverticulitis
  • ureteric colic
  • inguinal hernia
  • IBD
  • UTI
  • gynaecological (PID, ectopic)
  • testicular torsion
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6
Q

Give 3 differentials for RLQ pain?

A
  • appendicitis
  • ureteric colic
  • inguinal hernia
  • IBD
  • UTI
  • gynaecological
  • testicular torsion
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7
Q

Give 4 causes of GI haemorrhage, and the clinical features of each

A
  • ruptured AAA: central, back or loin pain w. syncope
  • ectopic pregnancy: uni or bilateral, dull, sharp or crampy pain in L or RLQ, amenorrhea, female, PV bleeding
  • bleeding gastric ulcer: epigastric or RUQ pain, haematemesis, malaena
  • Trauma
  • splenic rupture: trauma, hypovolaemic shock, LUQ pain radiating to left shoulder tip
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8
Q

Give 4 causes of perforated viscus, and the differential features of each?

A
  • peptic ulceration: epigastric or RUQ pain
  • small or large bowel obstruction: colicky or cramping pain, usually periumbelical + vomiting, absolute constipation, distension
  • perforated diverticular disease: LLQ pain, localised or generalised peritonitis, hx diverticulitis
  • inflammatory bowel disease
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9
Q

Give 3 causes of small bowel obstruction

A
  • adhesions
  • hernia
  • cancer
  • gall stone ileus
  • foreign body
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10
Q

Give 3 causes of large bowel obstruction

A
  • malignancy
  • diverticular disease
  • volvulus
  • faecal impaction
  • adhesions
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11
Q

Describe the clinical features of a perforated viscus

A
  • they lay very still and do not move the abdomen
  • appears very unwell
  • tachycardia and hypotension
  • rigid abdomen w/ percussion tenderness
  • involuntary guarding
  • absent or reduced bowel sounds suggest there is a paralytic ileus with it
  • signs of peritonitis
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12
Q

Give 5 risk factors for a large bowel volvulus

A
  • increasing age
  • neuropsych disorders
  • nursing home resident
  • chronic constipation
  • male
  • previous abdo operations
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13
Q

What are the 2 most common types of volvulus

A
  • sigmoid is most common

- caecal is 2nd

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14
Q

What are the 2 most common causes of ischaemic bowel? describe the differentiating features of each

A
  • voluvus: obstruction features such as colicky pain, vomiting, distension, absolute constipation
  • Mesenteric ischaemia: diffuse constant, out of proportion abdo pain, embolic sources such as AF, murmers, valve replacement
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15
Q

Describe the clinical features of ischaemic bowel?

A
  • severe pain out of proportion with clinical signs
  • metabolic acidosis and raised lactate
  • very raised wcc
  • pain diffuse and constant
  • unremarkable clinical examination
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16
Q

What are the most common causes of mesenteric ischaemia? (4 categories)

A
  • 50% embolic: AF, MI, prosthetic valve, abdo/ thoracic abdomen
  • 25% thrombosis due to atherosclerosis
  • 20% non occlusive (cardiogenic or hypovolaemic shock)
  • 10% mesenteric venous thrombosis (coagulopathy, malignancy, inflammatory disorders)
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17
Q

Give 6 causes of acute pancreatitis

A 
Gall stones
Ethanol
Trauma
Steroids
Mumps
Autoimmune (SLE)
Scorpion venom 
Hypercalcaemia 
ERCP
Drugs (azathioprine, NSAIDS, diuretics)
10-20% idiopathic
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18
Q

Describe the pathophysiology of pancreatitis

A

Premature release and activation of digestive enzymes, these digest fats resulting in fat necrosis (causing hypocalcaemia), blood vessles get eroded and bleed causing retroperitoneal haemorrhage and causes pancreatic necrosis

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19
Q

Describe the clinical features of acute pancreatitis

A
  • severe sudden onset epigastric pain radiating to the back
  • N+v
  • epigastric tenderness, soft abdomen and normal bowel sounds
  • if severe may get guarding and rigid abdomen due to peritonism or signs of hypovolaemic shock due to bleeding
  • grey turners sign (flank bruising) or cullens sign (umbelical bruising)
  • tetany due to hypocalcaemia
  • jaundice or cholangitis if gall stone is cause
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20
Q

What are grey turners an cullens signs and what do they indicate?

A

Grey turners= flank bruising
Cullens- umbelical brusing
Both indicate retroperitoneal bleeding due to acute pancreatitis, ruptured ectopic pregnancy, ruptured spleen, ruptured AAA

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21
Q

How should suspected acute pancreatitis be investigated?

A
  • amylase: will be 3x the upper limit of normal
  • LFTs: concurrent cholestatic element (ALT usually high)
  • Serum lipase: not available in all hospitals
  • ABG and routine bloods
  • abdo USS looking for stones
  • contrast enhanced CT if clinical assessment and blood are inconclusive or cause unknown
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22
Q

How should acute pancreatitis be managed?

A
  • A-E with high flow O2, IV access, IV fluid resus, NG tube, catheter
  • IV opioid analgesia
  • HDU or ITU admission
  • broad spectrum abx for prophylaxis against infection if pancreatic necrosis
  • treat cause: gall stone-> laproscopic cholecystectomy/ ERCP or withdraw alcohol/ drugs etc
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23
Q

Give 5 complications of acute pancreatitis

A
  • DIC
  • acute respiratory distress syndrome
  • hypovolaemia
  • hyperglycaemia
  • hypovolaemic shock and multiorgan failure
  • pancreatic necrosis
  • pancreatic pseudocyst
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24
Q

other than acute pancreatitis, what may cause a raised amylase?

A
  • bowel perforation
  • ectopic pregnancy
  • mesenteric ischaemia
  • DKA
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25
Q

How is pancreatic necrosis diagnosed and treated?

A
  • diagnosed with CT and fine needle aspirate

- needs pancreatic necrosectomy 3-5 weeks later

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26
Q

What is a pancreatic pseudocyst and what may they lead to?

A
  • cysts that form a weeks after the initial episode of pancreatitis
  • may cause biliary obstruction, gastric outlet obstruction, haemmorrhage or ruputre
  • 50% resolve spontaneously, some get surgical debridement
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27
Q

Describe the clinical features of peritonitis

A

pain starts in one place before localising to another area or becoming more generalised, signs of sepsis and involuntary guarding

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28
Q

Give 3 causes of peritonitis

A
  • appendicitis: periumbelical pain that moves to the RIF
  • perforated bowel: doesnt move, septic, guarding
  • peritoneal dialysis
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29
Q

How should an acute abdomen be investigated? (10)

A
  • urine dip: signs of infection, haematuria, cultures
  • pregnancy test: ectopic
  • ABG: useful in bleeding, bowel ischaemia, sepsis, to look for signs of tissue hypoperfusion and rapid Hb
  • routine bloods: fbc, u&e, lft, crp, amylase, calcium, group and save/ xmatch
  • blood cultures: if septic
  • ECG: excludes MI
  • USS: KUB if suspect renal tract pathology, biliary tree and liver if suspect gall stone, fallopian tubes if ectopic
  • erect CXR: if suspect perforation
  • AXR: if toxic megacolon, bowel obstruction or sigmoid volvulus suspected
  • abdo/ pelvis CT with contrast: covers perforation, bleeding, volvulus, obstruction, ectopic, mesenteric ischaemia
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30
Q

Describe the initial management of the acute abdomen?

A
  • A-E assessment
  • IV access
  • NBM
  • analgesia +/- antiemetics
  • imaging, urine sample, bloods
  • VTE prophylaxis
  • catheter and NG tube
  • IV fluids and monitor fluid balance
  • active major haemorrhage protocol or transfusions as appropriate
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31
Q

Describe the definitive management of a ruptured AAA

A
  • permissive hypotension
  • transfer to local vascular unit for open surgical repair
  • or for CT angio and endovascular repair if stable and suitable
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32
Q

Describe the definitive management of an ectopic pregnancy

A
  • laproscopy and salpingectomy if unstable and ruptured
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33
Q

Describe the definitive management of bleeding gastric ulcers

A
  • OGD, adrenaline injections and cauterisation of bleeding
  • high dose IV PPI and H. pylori eradication if necessary
  • angio- embolisation if active bleeding eg gastroduodenal artery erosions
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34
Q

Describe the definitive management of volvulus?

A
  • sigmoidoscope decompression and insertion of a flatus tube for upto 24hrs if sigmoid, flex sig if this is unsuccessful
  • laparotomy and hartmans procedure is indicated if colonic ischaemia or perforation, failed decompresson or necrotic bowel noted at endoscopy
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35
Q

Give 2 complications fo volvulus?

A
  • ischaemia
  • bowel perforation
  • 90% reoccur
  • stoma
  • death
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36
Q

Describe the definitive management of bowel obstruction (what is conservative management, when its used, when and what surgery is used)

A
  • if no ischaemia or strangulation-> NBM, decompress stomach by NG tube sucking, IV fluids to correct electrolyte disturbances
  • if adhesional and no ischaemia or perforation then do water soluable contrast study, if contrast reaches colon in 6hrs-> conservative, if not-> surgery
  • if closed loop obstruction, small bowel obstruction in virgin abdomen, obstructing tumour, strangulated hernia, evidence of ischaemia or 48hrs no improvement with conservative management then urgent laparotomy
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37
Q

Describe the definitive management of mesenteric ischaemia

A
  • laparotomy and excision of necrotic or non viable bowel with covering loop or end stoma which can be anastomosed later
  • revascularisation via radiological intervention depending on state of pt, bowel and angiographic appearance of mesenteric vessels
  • some pts can recover with fluids and supportive treatments, as it may have just been a temporary ischaemia so a period of monitoring to see if their bloods and clinical state improves or worsens may be opted for before an operation
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38
Q

Describe the definitive management of perforated bowel?

A
  • if not septic and no peritonitis it can be conservatively managed
  • oesphageal perforation needs endoscopically placed stent or just NG feeding
  • peptic ulcers need bowel rest and PPI
  • if unwell, peritonitis or failed conservative management they need surgery and thorough washout, repair of perforation or resection of area of disease with anastomosis or stoma
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39
Q

What is a closed loop bowel obstruction?

A

a second obstruction proximally (eg twist in bowel or competent ileocaecal valve) then the bowel will continue to distend until the wall becomes ischaemic and the wall will become ischaemic and perforate

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40
Q

Why does 3rd spacing occur in bowel obstruction

A

increased peristalsis of bowel to help move faeces past occluded segment + stagnation of faeces = secretion of large volumes of electrolyte rich fluid into the bowel

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41
Q

Describe the features of small bowel obstruction on an AXR

A
  • bowel >3cm diametes
  • central location
  • valvulae conniventes (lines completely crossing bowel)
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42
Q

Describe the features of large bowel obstruction on an AXR

A
  • bowel >6cm or 9cm at caecum
  • peripheral location
  • haustral lines (dont completely cross bowel)
  • coffee bean sign if sigmoid volvulus
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43
Q

List 4 complications of acute appendicitis

A
  • perforation
  • surgical site infection
  • appendix mass (oementum and small bowel adhere to appendix- conservatively managed)
  • pelvic abscess (fever, RIF mass, CT to confirm, abx and drainage, CT follow up)
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44
Q

What is barretts oesphagus? what causes it and how does it appear on endoscopy?

A
  • metaplasia of the strat squamous epithelium to simple columnar epithelium
  • mainly due to GORD
  • distal oesphagus appears red and velvety with some preserved pale squamous islands
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45
Q

How should barrettes oesophagus be managed? (for no dysplasia, low grade and high grade dysplasia)

A
  • high dose PPI BD
  • NSAIDS, smoking, alcohol, should be stopped
  • lifestyle advice: sit up after eating, avoid spicy food etc
  • no dysplasia-> monitor w/ endoscope every 2-5 years
  • if low grade dysplasia monitor every 6 months
  • high grade dysplasia and visible lesion present-> endoscopic ablation with mucosal resection or radiofrequency ablation
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46
Q

What are the two types of oesphageal cancer? what are each associated with?

A
  • squamous cell carcinoma: middle- upper oesphagus, associated with smoking and excessive alcohol
  • adenocarcinoma: lower oesphagus due to barretts oesphagus from reflux
  • leiomyosarcoma, rhabdomyosarcoma and lymphoma also occur but are rare
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47
Q

Describe the features of oesophageal cancer?

A
  • dysphagia: progressive, initially only to solids and then liquids later, all dysphagia is ca until proven otherwise
  • significant weight loss
  • odynophagia
  • hoarseness
  • dysphagia weight loss, upper abdo pain, dyspepsia or reflux qualify for 2WW for urgent endoscopy
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48
Q

Give 4 differentials for dysphagia?

A
  • mechanical: benign strictures, extrinsic compression, pharyngeal pouch, foreign body
  • neuromuscular: stroke, achalasia, oesophageal spasm, myasthenia gravis
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49
Q

How should suspected oesophageal cancer be investigated?

A
  • upper Gi endoscopy and biopsy for histology
  • CT CAP and PET CT to lok for mets
  • endoscopic USS to measure penetration into the oesophagus wall and assess biopsy mediastinal lymph nodes
  • laparoscopy is often used to look for intraperitoneal mets if the tumour has an intra- abdominal component
  • bronchoscopy may be warranted if hoarseness or haemoptysis
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50
Q

outline the management of oesphageal cancer?

A
  • 70% palliative as usually presents with advanced disease
  • palliative options inc oesophageal stents, radio and chemo, nutritional support and thickened fluids
  • SCC: chemoradiotherapy usually only choice as upper oesphagus is too complex to operate on, if lower usually get surgery + chemoradio
  • Adenocarcinoma: neoadjuvant chemoradio + oesophageal resection
  • the surgery is a large procedure and carries a 4% 30 day mortality rate and they need jejunostomy for feeding straight into the bowel, so pts need to be fit for it
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51
Q

What are the two major oesophageal motility disorders?

A

Achalasia and diffuse oesophageal spasm, rarer causes inc autoimmune (systemic sclerosis, polymyositis) and CT disorders may cause dysmotility

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52
Q

What is achalasia? what age group does it tend to affect?

A
  • failure of smooth muscle relaxation in the oesophagus
  • thought to be due to progressive destruction of ganglion cells in the myenteric plexus
  • mean age of diagnosis is 50
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53
Q

Describe the features of achalasia?

A
  • progressive dysphagia of solids and food boluses
  • feels as though they get stuck before entering stomach as LOS doesnt relax
  • may also get vomiting, cough, discomfort and poor nutritional status with it
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54
Q

How is achalasia investigated?

A
  • urgent endoscopy as could be cancer
  • oesophageal manometry is gold standard for diagnosis (pressure probe placed just above LOS, there will be no peristalsis an failure of the LOS to relax with high tone)
  • barium swallows are rarely performed now
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55
Q

How is achalasia managed?

A
  • conservative: many pillows when sleeping to reduce regurg, eat slowly and chew thoroughly, CCBs, botox and nitrate may provide short term relief
  • Surgical: endoscopic balloon dilation of LOS, 75% get good response, 5% get perforation OR laparscopic heller myotomy = division of fibre of LOS, 85% long term improvement and fewer side effects
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56
Q

What is diffuse oesophageal spasm?

A

mutlifocal high amplitude contractions of the oesophagus

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57
Q

How does diffuse oesophageal spasm present?

A
  • severe dysphagia to solids AND LIQUIDS
  • central chest pain exacerbated by eating foods
  • pain is often relieved by nitrates so is often mistaken for angina
58
Q

How is diffuse oesophageal spasm diagnosed and managed?

A
  • corkscrew appearance to oesophagus on barium swallow
  • manage with nitrates or CCB to relax the smooth muscle
  • with with associated hypertension of the LOS may benefit from pneymatic dilation myotomy but this is reserved for severe cases as its very invasive
59
Q

What is the name for a full thickness spontaneous rupture of the oesophageal wall?

A

boerhaaves syndrome

60
Q

What are the two most common causes of oesophageal tears and where do they most commonly occur?

A
  • iatrogenic (endoscopy) and severe forceful vomiting

- usually occur at left posteriolateral position just above the diaphragm

61
Q

Describe the features of oesophageal tears?

A

Sudden onset severe retrosternal chest pain, resp distress and subcut emphysema following severe vomiting or retching.
Perforation results in leakage of stomach contents into the mediastinum and pleural cavity which rapidly results in overwhelming inflammation causing multiorgan failure and death very quickly

62
Q

How should oesophageal tears be managed?

A
  • A-E
  • bloods inc x match
  • cxr (pneumomediastinum and intra thoracic air- fluid levels)
  • CT CAP with IV and oral contrast can diagnose but most are sent for urgent endoscopy off clinical suspicion alone
  • broad spectrum abx
  • on table ODG to find leak
  • thoracotomy + control leak + wash out
  • decompress oesphagus with NG tube and nutritional support vis NG tube
  • CT 10 days before starting oral intake to ensure no leak
63
Q

What is a mallory weiss tear?

A

Lacerations in the oesphageal mucosa at gastro- oesophageal junction, occurring due to profuse vomiting
Presents with short periods of haematemesis. Manage the same as any upper GI bleed, most managed conservatively as blood loss is limited.

64
Q

What is angiodysplasia?

A

AV malformations between previously healthy blood vessels (usually in caecum and ascending colon).
It is the 2nd most common cause of rectal bleeding and the most common cause of small bowel bleeding/

65
Q

How can angiodysplasia occur?

A
  • aquired: begins as reduced submucosal drainage due to chronic and intermittent contraction of the colon giving rise to dilated and tortious veins and so loss of capillary sphincter competency
  • congenital: hereditary haemorrhagic telangectasia or heydes syndrome
66
Q

Describe the clinical features of angiodysplasia

A

Rectal bleeding and anaemia are most common presentations. 10% picked up incidentally on colonoscopy. Upper GI lesions may present as haematemesis or malaena

67
Q

Give 3 differentials for rectal bleeding

A
  • colorectal cancer / polyps
  • diverticular disease
  • av malformation
  • haemorrhoids
  • coagulopathies
  • iron, b12 or folate deficiency if anaemia is presentation
68
Q

How should suspected angiodysplasia be investigated?

A
  • FBC, U&E, haematinics, LFTs, clotting, group and save if severe
  • upper GI endoscopy or colonoscopy depending on site of bleed
  • wireless capsule endoscopy to find small bowel lesions
69
Q

How is angiodysplasia managed?

A
  • 10% will present with major GI haemorrhage and so will need A-E resus + endoscopy and argon plasma coagulation or mesenteric angio and embolisation
  • smaller bleeds can be treated with bed rest, IV fluids +/- tranexaemic acid
  • bowel resections only needed if continuation of severe bleeding despite angio and endo interventions failed or multiple lesions which cannot be treated medically
70
Q

Give 3 non infective causes of gastroenteritis?

A
  • radiation colitis
  • ibd
  • microscopic colitis
  • chronic ischaemic colitis
71
Q

Give 3 complications of camplyobacter gastroenteritis

A
  • reactive arthritis
  • guillian barre
  • haemolytic uraemic syndrome
  • thrombotic thombocytopaenic pupura
72
Q

Describe the clinical features of haemolytic uraemic syndrome

A
  • initially bloody diarrhoea, fever, vomiting and weakness
  • then lathargy, reduced urine output and blood in their urine due to acute kidney failure, low rbc and low platelet count
  • usually caused by a strain of e.coli
73
Q

Describe the clinical features of neuroendocrine/ carcinoid tumours

A
  • vague abdo pain
  • N+V
  • abdo distension
  • bowel obstruction
  • unintentional weight loss
  • palpable abdo mass
  • carcinoid syndrome
74
Q

What is carcinoid syndrome?

A

The cells oversecrete serotonin (as well as prostaglandins and gastrin) which causes flushings (classically exacerbated by alcohol or coffee), abdo pain, diarrhoea, wheezing and palpitations

75
Q

How is a suspected neuroendocrine tumour investigated? what are the two specific tumour markers?

A
  • chromogranin A and 5 HIAA levels
  • routine bloods
  • genetic testing if fhx suspected
  • endoscopy for colorectal lesions
  • CT for small bowel lesions
  • whole body somatostatin receptor scintigraphy to look for mets
76
Q

How are neuroendocrine tumours managed? (if gastric, colonic, appendiceal, small intestine, colon and rectal)

A
  • Gastric NETs-> endoscopic resection and annual surveillance if low grade, partial or total gastrectomy +/- lymph node clearance if higher grade
  • small intestine NETs-> almst always malignant, lymph nodes always removed
  • appendiceal NETS-> appendectomy for lesions <2cm, right hemicolectomy for lesions >2cm
  • colonic NETs-> partial colectomy and regional lymph node clearance
  • Rectal NETs-> endoscopic resection if smaller, AP or low anterior resection if larger
77
Q

How are carcinoid crises (overwhelming hormone release from tumour causing resistant severe hypotension) avoided?

A
  • somatostatin analogues given pre and post op if the pt has carcinoid syndrome
78
Q

What can cause acute appendicitis?

A

luminal obstruction usually due to faecolith but may be due to lymphoid hyperplasia, impacted stool or rarely appendiceal or caecal tumours

79
Q

Give 4 risk factors for acute appendicitis

A
  • age 10-30
  • fhx
  • more common in Caucasians
  • ethnic minorities are more likley to perforate if they do get it
  • most common in summer apparently
80
Q

Describe the clinical features of acute appendicitis?

A
  • initially dull, poorly localised periumbelical pain which migrates to the RIF and becomes sharp in nature
  • anoerexia almost always present
  • usually also get nausea, diarrhoea or constipation
  • O/E: tachycardia, tachpnoea, rebound tenderness, percussion pain over mcburneys point, guarding, rovsings and psoas sign
81
Q

What are rovsings and psoas sign?

A
  • rovsings: RIF pain on palpation of LIF
  • psoas: RIF pain in extension of right hip
  • both indicate acute appendicitis
82
Q

How should acute appendicitis be managed?

A
  • USS or CT if diagnosis is uncertain
  • urgent laparoscopic appendectomy, with appendix sent to lab for histology to check for malignancy
  • rest of abdomen should be inspected while in there to check for other pathology like meckles diverticulum
83
Q

What type cancer are most colorectal cancers?

A
  • usually theyre adenocarcinomas, rarer ones inc lymphoma, carcinoid or sarcoma
  • most arise from adenoma carcinoma sequence
84
Q

What are the two hereditary conditions causing colorectal carcinoma?

A
  • Famillial adenomatous polyposis is caused by mutation of the adenomatous polyposis coli gene (a tumour suppressor)
  • Herediary non polyposis colorectal cancer: DNA mismatch repair gene mutation, commonly accounts for familial risk associated with colorectal cancer
85
Q

Give 3 risk factors for colorectal cancer

A
  • 75% have no risk factors

RFs inc: age >60, ibd, low fibre diet, high processed meat intake, smoking and alcohol intake

86
Q

Describe the clinical features of right and left sided colorectal cancer?

A
  • right sided: abdo pain, occult bleeding, mass in RIF
  • left sided: rectal bleeding, change in bowel habit, tenesemus, LIF mass
  • both may present with obstruction, change in bowel habit, rectal bleeding, weight loss, abdo pain and iron deficiency
  • age >40
  • weight loss only occurs if there are mets, unlike with upper GI malignancy
  • may just present with a microcytic anaemia
87
Q

give 3 differentials for colorectal cancer?

A
  • IBD: avg onset younger, bloody or mucusy diarrhoea
  • haemorrhoids: bright red blood covering surface of tool, rarely presents with abdo pain, altered bowel habit or weight loss
  • diverticulitis/ diverticular disease: can cause PR bleeding, abdo pain and change in bowel habit but unlikely to cause systemic inflammatory features
  • angiodysplasia: can cause PR bleeding, rarely causes change in bowel habit
88
Q

How should suspected colorectal cancer be investigated?

A
  • fbc, u&e, left, coag screen, haematinics
  • CEA: not for diagnosis but can be used for monitoring
  • colonoscopy with biopsy, flex sig or CT can be done if too frail
  • CT CAP for staging
  • MRI rectum and endo- anal USS if rectal ca
89
Q

What staging system is used for colorectal cancer?

A

Dukes staging

- A-D staging based on invasion into muscularis mucosa, regional lymph nodes or distant mets

90
Q

How should caecal or ascending colon tumours and transverse, descending and sigmoid colon tumours be managed?

A
  • caecal or ascending colong tumours-> right hemicolectomy with stoma or primary anastomosis
  • transverse-> extended right hemi
  • descending-> left hemi
  • sigmoid-> sigmoid colectomy
91
Q

How should high rectal and low rectal tumours be managed?

A
  • high rectal: >5cm from anus, managed with anterior resection (leaves rectal sphincter intact)
  • low rectal: abdominoperineal (AP) resection- excision of distal colon, rectum, anal sphincters, resulting in permanent colostomy
92
Q

What is a hartmanns procedure and when is it used?

A
  • resection of the recto- sigmoid colon with formation of endo colostomy and closure of rectal stump
  • used in emergencies such as bowel obstruction or perforation
93
Q

Are chemo or radiotherapy used or colorectal cancer?

A
  • chemo not used in metastatic disease

- neo adjuvant radio used in rectal cancer but not colon as risk of small bowel damage

94
Q

Describe the surgical management options for crohns

A
  • many with crohns have surgery at some point, but its only used after medical management failed or severe complications such as strictures or fistulas develop
  • most common procedure is ileocaecal resection- removal of terminal ileum and caecum and anastomosing ileum and ascending colon
  • bowel sparing approach should be taken to avoid short gut syndrome in later life
95
Q

Give 3 complications of crohns

A
  • fistula-> fistolutomy or seton to keep it open until it eventually heals over
  • stricture
  • perianal complications (abscesses, fistula)
  • GI malignancy
  • malabsorbtion
  • osteoporosis
96
Q

Describe the surgical management options for ulcerative colitis

A
  • 30% get surgery at some point
  • indications: failed medical management, toxic megacolon, bowel perforation or to reduce risk of carcinoma
  • total proctocolectomy is curative but pt left with ileostomy
  • many have subtotal colectomy with preservation of rectum initially
97
Q

How does toxic megacolon present? How is it managed?

A
  • severe abdo pain
  • distension
  • pyrexia
  • systemic toxicity
  • requires bowel decompression ASAP to reduce perforation risk
98
Q

What is a diverticulum and what part of the bowel is most commonly affected?

A

An outpouching of the bowel wall compromised of mucosa

They usually occur at the sigmoid colon

99
Q

give 3 complications of diverticular disease

A
  • diverticulitis
  • perforation
  • pericolic abscesses (need abx and bed rest, CT guided or laparoscopic drainage)
  • fistula (colovesicle, colovaginal- both need surgical repair)
  • stricture-> bowel obstruction
100
Q

Describe the clinical features of diverticular disease and diverticulitis

A
  • diverticular disease: lower abdo pain, usually colicky and relieved by defecation, altered bowel habit, nausea or flatulance
  • diverticulitis: abdo pain, localised tenderness in LIF, pyrexia, nausea, vomiting, PR bleeding, anorexia
  • may present with peritonitis due to perforation
  • if the pt is on steroids or immunosuppression symptoms of perforation or diverticulitis may be reduced/ masked
101
Q

how should suspected diverticular disease and diverticulitis be investigated?

A
  • routine bloods
  • Group and save
  • VBG
  • other sepsis investigations as appropriate
  • flex sig if suspect uncomplicated diverticular disease
  • ct if suspect diverticulitis (shows thickening of colonic wall, pericolonic fat stranding, abscesses, localised air bubbles, free air)
  • never do sigmoidoscopy or colonoscopy if suspect diverticulitis due to perforation
102
Q

How should diverticular disease be managed?

A
  • conservative: IV fluids, analgesia, tranfusion or embolisation if significant blood loss, should improve in 2-3 days
  • surgery: if perforation, overwhelming sepsis or failed conservative management
  • surgery is typically bowel resection via hartmanns procedure
  • elective segmental resection may be performed in recurrent disease
103
Q

What is a pseudo-obstruction? what causes it

A
  • dilation of colon due to adynamic bowel in abscence of mechanical obstruction, usually affecting caecum and ascending colon
  • thought to be due to interruption of autonomic nerve supply to colon due to electrolyte disturbance, endocrine disorders (hypothyroid)., meds (opioids, CCBS), recent surgery, illness, trauma, recent cardiac event or parkinsons disease
104
Q

What may untreated pseudo- obstruction lead to?

A

toxic megacolon, bowel ischaemia and perforation

105
Q

Describe the clinical features of a pseudo- obstruction?

A
  • generalised severe abdo pain
  • abdo distension
  • constipation
  • vomiting (late)
  • absent bowel sounds
  • focal tenderness
  • rebound tenderness
  • guarding
106
Q

How should suspected pseudo- obstruction be investigated?

A
  • bloods: fbc, u&e, lft, crp, ca2+. mg2+, tft
  • axr: bowel distension but cannot exclude mechanical obstruction
  • CT abdo pelvis with contrast: shows dilation of colon and can definitively exclude obstruction
107
Q

How is psuedo- obstruction managed?

A
  • most treated conservatively with NBM, IV fluids, NG tube decompression if vomiting
  • treat cause eg electrolyte imbalance
  • endoscopic decompression if it doesnt resolve within 24 hrs
  • IV neostigmine (anticholinesterase) can also be trialled
  • surgery only needed if ischaemia or perforation develops or it doesnt respond to conservative mangement
  • segmental resection + anastomosis, caecostomy or ileostomy can be used to decompress the bowel long term
108
Q

give 3 risk factors for gastric cancer

A
  • male
  • h pylori
  • increasing age
  • smoking
  • alcohol
109
Q

Describe the clinical features of gastric cancer

A
  • dyspepsia
  • dysphagia
  • nausea
  • vomiting
  • malaena
  • haematemesis
  • anorexia
  • weightloss
  • anaemia
110
Q

How should gastric cancer be investigated?

A
  • CAE used for disease monitoring
  • OGD for diagnosis and biopsy
  • HER2 and neu protein expression testing for monoclonal antibody therapy
  • CT CAP and staging laparoscopy needed for all
  • PET CT rarely used as they dont take up the tracer well
111
Q

How should proximal and distal gastric cancer be managed?

A

proximal- total gastrectomy
distal- subtotal gastrectomy
if pt is fit enough theyll get neoadjuvant and adjuvant chemo also
many pts only get palliative managemnet as they tend to present very late

112
Q

what is a hiatus hernia and what are the 2 types?

A
  • stomach herniates up into thorax
  • sliding (80%)= stomach slides up at gastro oesphageal junction
  • rolling/ paraoesphageal= upward movement of the gastric fundus creating a bubble of stomach into the thorax
113
Q

Give 3 risk factors for a hiatus hernia

A
  • age
  • chronic cough
  • pregnancy
  • obesity
  • ascites
114
Q

Describe the clinical features of hiatus hernia

A
  • dyspepsia and GORD symptoms
  • vomiting
  • weightloss
  • bleeding
  • hiccups
  • swallowing difficulties
115
Q

How is hiatus hernia diagnosed?

A

OGD

116
Q

How is a hiatus hernia managed?

A
  • PPI and weightloss, low fat and smaller meals, smoking cessation, reduce alcohol intake
  • surgery indicated when they remain symptomatic, theres a risk of strangulation or volvulus or nutritional failure due to gastric outlet obstruction
  • surgical management is with cruroplasty (push it back down and make hiatus smaller) or fundoplication
117
Q

How does a incarcerated/ strangulated hiatus hernia present?

A
  • severe epigastric pain
  • retching w/out vomiting
  • inability to pass and NG tube
  • this is called borchardts triad
118
Q

What is the most common type of anal cancer?

A
  • most are SCCs arising from below the pectinate line

- if arise from above the pectinate line- adenocarcinoma

119
Q

give 3 risk factors for anal cancer

A
  • HPV infection (leads to anal intraepithelial neoplasia (AIN) first)
  • HIV
  • increasing age
  • smoking
  • crohns
  • immunosurpressant
120
Q

Describe the clinical features of anal cancer

A
  • pain and rectal bleeding
  • anal discharge
  • pruritis
  • palpable masses
121
Q

Give 3 differentials for anal cancer

A
  • haemorrhoids
  • anal fissure
  • anal warts
  • skin cancer
122
Q

How should anal cancer be investigated

A
  • proctoscopy + biopsy under anaesthetic to assess tumour size and invasion
  • USS and FNA of palpable inguinal lymph nodes
  • CT CAP for mets
  • MRI pelvis for extent of local invasion
123
Q

How is anal cancer managed?

A
  • chemo and radiotherapy is 1st choice management
  • surgical management for advanced disease, very early T1N0 tumours or failure of chemo
  • surgery is usually an AP resection
124
Q

What is an anal fissure and what causes them

A

tear in the mucosal lining of the anal canal due to trauma from defecation or hard stool

125
Q

Describe the clinical features of an anal fissure

A
  • intense pain post defecation which can last for several hrs
  • PR bleeding on wiping and itching
126
Q

How can anal fissures be managed?

A
  • increased fibre diet and fluid intake
  • stool softening laxatives
  • GTN cream or dilitiazem cream can increase blood supply and relax the anal sphincter for better wound healing and reducing pain
  • if chronic and medical management fails: lacteral spincterotomy
127
Q

What can cause an anal fistula?

A
  • usually due to an anal abscess

- may also be IBD, systemic disease (TB, diabetes, HIV), trauma or previous radiation therapy

128
Q

Describe the clinical features of anal fistulae

A
  • intermittent or continuous discharge (mucus, blood, pus or faeces) onto the perineum
  • severe pain, swelling change in bowel habit
  • a fiberous tract may also be visible or felt on DRE
  • usually have a history of an abscess or ibd
129
Q

how should anal fistulae be investigated?

A
  • rigid sigmoidoscopy can be used to identify what type of fistula it is (extra sphinteric, supraspincteric, intersphincteric or submucosal)
130
Q

How are anal fistula managed?

A
  • if no symptoms= conservative management
  • fistulotomy= probe insert into tract and skin, subcut tissue and internal sphincter are separated to open the tract and let it heal by secondary intention
  • surgery not performed if there is an acute anorectal abscess
131
Q

What is thought to cause more anal abscesses?

A

Plugging of anal ducts (stuctures which drain the anal glands), this causes normal flora overgrowth which leads to e.coli or enterococcus infection

132
Q

What are the most common types of anal abscess?

A
  • commonest= perianal (superficial to internal sphincter)
  • intersphinceric
  • ischiorectal (deep to external sphincter)
  • supralevator
133
Q

Describe the clinical features of anal abscesses

A
  • perianal pain, exacerbated by sitting

- may also get swelling, itching, discharge, fever, rigors, malaise or even sepsis

134
Q

How should anal abscesses be investigated and managed?

A
  • superficial abscesses can be diagnosed on DRE, deeper and more complicated disease may need MRI
  • manage with abx and prompt surgical drainage under anaesthetic and leave open to allow to heal by secondary intention
135
Q

What is pilonidal sinus disease?

A

Formation of a sinus in the cleft of the buttocks due to a hair follicle in the intergluteal cleft becoming inflamed or infected, formation of a pit as the follilce is obstructed and then a cavity forms

136
Q

Describe the clinical features of a pilonidal sinus

A
  • intermittent red, painful and swollen mass in the sacrococcygeal region, often with discharge and systemic features of infection
  • usually affects males age 15-30
  • they open to the skin but dont continue into the anal canal like a fistula- this difference can be distinguished by a rigid sigmoidoscopy
137
Q

how should a pilonidal sinus be managed?

A
  • they usually ease with age and dont need surgery
  • shaving the area, washing it free of debris and plucking out embedded hair can help
  • abx can help if septic episode
  • asbcesses that form may need surgical drainage
  • if chronic you can remove by excision and laying the wound open
138
Q

what may cause a rectal prolapse?

A
  • chronic constipation
  • chronic cough
  • multiple vaginal deliveries
  • may be associated with haemorrhoids
139
Q

Describe the clinical features of rectal prolapse

A
  • rectal mucus discharge
  • faecal soiling
  • blood on wiping
  • tensesmus
  • a mass felt on sitting etc
140
Q

How should rectal prolapses be managed?

A
  • conservative: if unfit for surgery, minimal symptoms or due to vaginal delivery, consists of improving dietary fibre and fluid intake, reduce constipation and banding in clinic
  • surgery: involved removing the prolapsed mucosa and reinforcing the muscles of the rectum with placating stitches or where the rectum is mobilised and fixed to the sacral prominence

Y3 Surgery (7 decks)

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