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SURGERY - Gen Surg > GI > Flashcards

GI Flashcards

1
Q

How would a patient with appendicitis present?

A
  • periumbilical poorly localised pain that then migrates to RIF where it is localised and sharp
  • vomiting, anorexia, nausea, diarrhoea, constipation
  • Tachycardia, Tachypnoiea, Pyrexia
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2
Q

How would a patient with appendicitis present on examination?

A

Rebound tenderness on examination

Pain over McBurney’s point

Guarding

Roysing’s sign = RIF pain on palpation of LIF

Psoas sign = RIF pain with extension of right hip

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3
Q

What investigations would you do for suspected appendicitis?

A
  • urinalysis to exclude UTI, renal, urological
  • Pregnancy test to exclude ectopic (bhgc)
  • Bloods (FBC, CRP, Group and Save, anticoagulation, U&Es)
  • Trans abdo US (gold standard)
  • CT
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4
Q

How would you manage appendicitis?

A

Laparoscopic appendectomy

Potentially conservative antibiotic therapy

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5
Q

What are some causes of acute pancreatitis?

A

G - gallstones

E - ethanol

T - trauma

S - steroids

M - mumps

A - autoimmune disease eg. SLE

S - scorpion venom

H - Hypercalcaemia

E - Endoscopic Retrograde Cholangiopancreatography (ERCP)

D - Drugs eg. azathiprine, NSAIDs, diuretics

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6
Q

What is the pathophysiology of acute pancreatitis?

A
  • GET SMASHED causes inflammatory response in the pancrease
  • Results in activation of digestive enzymes in the pancreas
  • enzymes are released into systemic circulation
  • Causes autodigestion of fats (fat necrosis) and blood vessels (haemorrhage)
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7
Q

How would acute pancreatitis present?

A
  • severe epigastric pain radiating to the back (better on leaning forward)
  • nausea and vomiting
  • Grey Turners (bruising on flanks)
  • Cullen’s sign (bruising around umbilicus = retroperitoneal haemorrhage)
  • Not so much epigastric tenderness on exam as it is retroperitoneal
  • Tetany due to hypocalcaemia secondary to fat necrosis
  • Gallstone pathology = jaundice + cholangitis picture
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8
Q

How would you investigate potential acute pancreatitis?

A
  • serum amylase x3 above normal limit
  • LFTs (ALP raised in gallstone picture)
  • Serum lipase raised
  • Modified Glasgow criteria used to assess severity in first 48 hours
  • Abdo US for gallstone
  • AXR shows sentinel loop sign sometimes indicating localised ileus
  • Contrast CT shows pancreatic oedema and swelling
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9
Q

How would you manage acute pancreatitis?

A

SUPPORTIVE

  • high flow o2
  • fluids
  • NG tube is vomiting
  • opioid analgesia (although some studies saying it can cause spasm of sphincter of Oddi)
  • broad spectrum antibiotics eg. imipenem (incase of pancreatic necrosis)
  • Treat underlying eg. ERCP and sphincterotomy OR Cholecystectomy if gallstones
  • avoid alcohol
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10
Q

What is angiodysplasia?

A
  • Degenerative vascular malformation of the GI tract.
  • Fragile leaky blood vessels causing GI bleeding and anaemia.
  • Commonly presents as clusters of dilated vessels in mucosa/submucosa of caecum and ascending colon.
  • High prevalence in R colon due to high intraluminal pressures in right colon obstructing submucosal venous blood flow.
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11
Q

How does angiodysplasia present?

A
  • Chronic, painless, intermittent GI bleed
  • Fresh rectal bleeding in lower GI
  • Melaena in upper GI
  • Usually over >60 years old
  • Anaemia due to the bleeding
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12
Q

How would you investigate suspected angiodysplasia?

A
  • FBC (low hb, microcytosis, hypochromia)
  • group and save, U&Es, etc
  • OGD to rule out upper GI bleed
    • Selective mesenteric angiography if bleeding is too severe to see a lesion
  • Colonoscopy for lower GI
    • Selective mesenteric angiography if bleeding is too severe
  • Faecal occult blood
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13
Q

How would you manage angiodysplasia?

(Haemodynamically stable)

A
  • they generally tend to stop spontaneously
  • Colonoscopy/OGD to identify bleeding site
    • If you can’t find anything but the bleeding continues, use mesenteric angiogram
    • Or do a wireless capsule enteroscopy
  • Electrocautery/ Adrenaline injection/ Photocoagulation/ Clips
  • Oestrogen, thalidomide, Octreotide are used interchangeably if contraindicated for surgery
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14
Q

How would you manage angiodysplasia?

(Haemodynamically unstable)

A
  • colonoscopy/ogd/mesenteric angiogram to identify lesion
  • If huge lifethreatening haemorrhage, do enteroscopy to localise bleeding
  • Blind Sub-total colectomy
  • (Recurrent bleeding is common after right hemi-colectomy as unidentified lesions can still be present)
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15
Q

How does an anorectal abscess happen?

A

Blockage of the anal ducts results in fluid stasis which leads to infection.

(Commonly E.Coli, Bacteriodes spp, Enterococcus spp)

Anal glands are in the intersphincteric space (between internal and external sphincters) so infection can spread to adjacent areas.

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16
Q

How are anorectal abscesses classified?

A

By where they occur:

Perianal, Ischiorectal, Intersphincteric, Supralevator

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17
Q

How would an anorectal abscess present?

A
  • Pain in perianal region exacerbated by sitting down
  • Localised swelling, itching, discharge
  • Systemic eg. fevers, rigors, malaise, sepsis
  • Erythematous, fluctuant, tender perianal mass (potentially purulent)
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18
Q

How would you investigate and manage an anorectal abscess?

A

DRE or chronic disease may need CT/MRI

Management:

  • antibiotoic therapy (trust protocol)
  • analgesia
  • incision and drainage under general anaesthetic
    • heal by secondary intention
    • proctoscopy should be performed after drainage to look for fistula-in-ano
    • Insertion of seton if fistula is identified
  • Post-op antibiotics following drainage can lower risk of fistula formation
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19
Q

What is it called when there is a second obstruction proximal to the first?

A

Closed loop obstruction

A surgical emergency!!

Bowel will continue to distend until bowel becomes ischaemic and perforates.

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20
Q

What are the most common causes of small and large bowel obstruction?

A

Small bowel = adhesions, herniae

Large bowel = malignancy, diverticular disease, volvulus

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21
Q

What are the XRAY findings of bowel obstruction?

A

Small bowel:

dilated >3cm, central abdo, plicae circulares visible completely crossing bowel

Large bowel:

dilated >6cm (caecum >9cm), peripheral, haustra lines do not completely cross the bowel

erect chest xray may show air under the diaphragm if there is perforation! (Pneumoperitoneum)

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22
Q

Where are cholangiocarcinomas most commonly found?

A

Biliary system cancers are most commonly found in the bifurcation of the right and left hepatic ducts

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23
Q

What are some risk factors for cholangiocarcinoma?

A
  • PSC
  • UC
  • Infective (HIV, hepatitis, liver flukes)
  • Toxins (rubber and aircraft chemicals)
  • congenital (caroli’s disease, choledochal cyst)
  • alcohol excess
  • DM
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24
Q

How would a cholangiocarcinoma present?

A

Generally asymptomatic until later

  • post hepatic jaundice
  • pruritis
  • pale stools, dark urine
  • RUQ pain
  • early satiety, weight loss, anorexia, malaise
  • Jaundice and cachexia on observation
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25
Q

How would you investigate for a cholangiocarcinoma?

A
  • elevated ALP, bilirubin, etc to confirm obstructive jaundice
  • MRCP to diagnose cholangiocarcinoma
  • ERCP to determine site of obstruction
  • CT imaging for staging
    *
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26
Q

How would you manage a cholangiocarcinoma?

A

SURGICAL

  • complete surgical resection if theyre operable
  • Intrahepatic or Klatskin tumours = partial hepatectomy and reconstruction of biliary tree
  • Distal CBD tumours = pancreaticoduodenectomy (Whipples)

PALLIATIVE

  • ERCP to stent bile duct and relieve obstruction symptoms
  • Surgical bypass of obstructio not relieved by stenting
  • Palliative radiotherapy to slow tumour growth
    • Cisplatin + gemcitabine
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27
Q

What are some causes of cholangitis (infection of the biliary tract)?

A
  • Gallstones
  • ERCP
  • Cholangiocarcinoma
  • pancreatitis
  • primary sclerosing cholangitis
  • infections eg. E.Coli, Klebsiella species, Enterococcus
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28
Q

How would cholangitis present?

A
  • Charcot’s triad = Jaundice, Fever, RUQ Pain
  • Pruritus
  • Pale stools and dark urine (obstructive jaundice)
  • maybe Hypotension and Tachycardia
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29
Q

How would you investigate a cholangitis?

A
  • FBC
  • LFTs (ALP high)
  • Blood cultures
  • US of biliary tract shows bile duct dilation and potentially a gallstone
  • ERCP = gold standard
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30
Q

How would you manage a cholangitis?

A
  • Sepsis 6 if needed!
  • ERCP to clear obstruction
  • If cannot tolerate an ERCP, do a percutaneous transhepatic cholangiography
  • Cholecystectomy if gallstones are the underlying cause
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31
Q

What puts you at increased risk of colorectal cancer?

A
  • mutations eg. Adenomatous Polyposis Coli (APC), Hereditary nonpolyposis colorectal cancer (HNPCC)
  • Old age
  • IBD
    Low fibre diet
  • High processed meat intake
  • Smoking
  • High alcohol intake
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32
Q

How would a colorectal caner present?

A
  • change in bowel habit
  • rectal bleeding
  • weight loss
  • abdo pain
  • iron-deficiency anaemia
  • Right sided = occult (not visible) bleeding, anaemia, mass in RIF, late presentation
  • Left sided = rectal bleeding, change in bowels, tenesmus, mass in LIF or on DRE
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33
Q

How would you investigate a colorectal cancer?

A
  • FBC (microscopic anaemia), LFTs, clotting, group and save
  • CEA tumour marker
  • Colonoscopy + Biopsy = Gold standard
    • if the patient is frail, do a flexi sigmoidoscopy or CT colonography to diagnose
  • CT chest abdo pelvis for staging
  • MRI rectum for rectal cancers to assess depth of invasion and need for pre-op chemo
  • Endo-anal US for early rectal cancers to assess need for trans-anal resection
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34
Q

How would you manage a colorectal cancer?

A

SURGERY = curative

  • regional colectomy to remove primary tumour + ensure adequate margins, followed by primary anastomosis and formation of stoma
    • Caecal or ascending colon = R hemicolectomy
    • Descending colon tumours = L Hemicolectomy
    • High rectal tumours = anterior resection
    • Low rectal tumours = abdominoperineal resection
  • Hartmann’s if bowel obstruction/perforation = Emergency!!!

Conservative

  • Chemi for advanced = FOLFOX (Folinic acid, Fluorouracil, oxaliplatin)
  • Radio for rectal cancer as neo-adjuvant
  • Endoluminal stenting to relieve acute bowel obstruction in L sided tumours
    • SE of stents = perforation, migration, incontinence
  • Stoma formation for those with acute obstruction
  • Resection of secondaries for any liver mets
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35
Q

Crohns and UC i have put with medicine revision

A

refer to teach me surgery if want more info on procedures?

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36
Q

What are the different kinds of diverticular disease?

A

Diverticulum = outpouching of the bowel most commonly found in the sigmoid colon

Diverticulosis = Presence of diverticula

Diverticular disease = symptomatic diverticula

Diverticulitis = inflammation of the diverticula

Diverticular bleed = diverticulum erodes into a vessel and causes a large vol painless bleed

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37
Q

How do diveritcular occur?

A
  • increased intraluminal pressure caused by stool in an aging/weakened bowel
  • causes outpouching of mucosa through areas of weakness in the bowel wall (eg. where blood vessels penetrate)
  • Bacteria can overgrow in the outpouchings and lead to inflammation of the diverticulum, which can perforate
  • sometimes fistulae can also form
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38
Q

How does diverticular disease present?

A
  • Diverticular pain = intermittent lower abdo colicky pain, relieved by defaecation
    • altered bowel habits, nausea, flatulence
  • Diverticulitis = acute, sharp, localised LIF pain worsened by movement, localised tenderness
    • systemic eg. decreased appetite, pyrexia, nausea
  • Perforated diverticulum = localised peritonism or generalised peritonitis
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39
Q

How would you investigate diverticular disease?

A
  • Routine bloods, CRP, etc
  • Urine dipstick
  • Group and Save and VBG for Diverticulitis
  • Flexi sigmoidoscopy
  • CT Abdo/Pelvis scan for Diverticulitis
    • thickening of colonic wall
    • pericolonic fat stranding
    • abscesses
    • localised air bubbles or free air
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40
Q

How would you manage diverticular disease?

A
  • simple anaglesia and fluids

Conservative

  • Diverticulitis = IV antibiotics, IV fluids, bowel rest (only clear fluids orally), analgesia
  • Diverticular bleeds = embolisation or surgical resection if conservative doesn’t work

Surgical

  • Hartmann’s procedure (in those with perforation with faecal peritonitis or overwhelming sepsis)
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41
Q

What is a femoral hernia and who’s more at risk of it?

A

When abdo viscera or omentum passes through the femoral ring and into the potential space of the femoral canal.

High risk of strangulation due to rigid borders of the femoral ring.

Epidemiology:

  • women due to wider female bony pelvis
  • Pregnancy
  • Raised intra-abdo pressure eg. heavy lifting, chronic constipation
  • Increasing age
42
Q

How would a femoral hernia present and be investigated?

A
  • lump in the groin (infero-lateral to the pubic tubercle)

You would do an US, CT abdo-pelvis scan, Surgical exploration

43
Q

What are the 3 complications of a hernia?

A

Incarceration

Obstruction

Strangulation

44
Q

How would you manage a femoral hernia?

A

manage surgically within 2 weeks of presentation due to high risk of strangulation!!

45
Q

What is biliary colic?

A

Pain that occurs due to a gallstone being impacted in the gallbladder neck.

There is no inflammatory response, but pain is caused by the gallbladder contracting against the occluded neck.

46
Q

What is the epidemiology of gallstone disease?

A

5 Fs

  • Fat
  • Female
  • Fertile
  • Forty
  • Family history
  • Oral contraeptives (oestrogen causes more cholesterol to be secreted into bile)
  • Pregnancy
47
Q

What is the pathophysiology of gallstone disease?

A
  • bile is made from cholesterol, phospholipids and bile pigments
  • stored in the gallbladder and passes into the duodenum through the ampulla of vater
  • gallstones are formed due to supersaturation of bile

Stones

  • cholesterol stones = completely from cholesterol due to excess cholesterol production
  • Pigment stones = completely from bile pigments from excess bile pigments production (seen in haemolytic anaemia)
  • Mixed stones = composed of cholesterol and bile pigments
48
Q

How would people with gallstone pathology present?

A
  • Biliary colic
    • sudden pain that is dull and “colicky” - more episodic than colicy… as it’s happening, the pain is pretty constant
    • RUQ radiates to epigastrium or back
    • nausea/vomiting
    • precipitated by eating fatty foods (fatty foods stimulates CCK release)
  • Acute cholecystitis!!!
    • pain is not helped by pain relief
    • signs of inflammation (fever, high WCC)
    • derangement of liver function tests
    • tender in RUQ
    • Murphy’s sign
49
Q

How would you investigate gallstone pathology?

A

The usual… bloods, urinalysis, U&Es, CRP, pregnancy test

  • LFTs (raised ALP)
  • amylase to rule out pancreatitis
  • Trans-abdo US for gallstone, thickened gallbladder wall, bile duct dilation
  • Magnetic Resonance Cholangiopancreatography = Gold standard
50
Q

How would you manage biliary colic?

A
  • Analgesia (NSAIDs and PRN opioids)
    • if these don’t work, consider cholecystitis!
  • Antiemetic
  • Lifestyle factors eg. low fat diet, weightloss
  • Elective laparoscopic cholecystectomy if there is a high chance of recurrence
51
Q

How would you manage acute cholecystitis?

A
  • IV antibiotics (co-amoxi +/- metronidazole)
  • Fluid resuscitation therapy
  • Sepsis 6 if needed
  • NG tube if patient is vomiting
  • US and nil by mouth (US more sensitive in absence of bowel gas)
  • Antiemetics
  • Laparoscopic cholecystectomy within 1 week OR Percutaneous Cholecystostomy to drain infection if patient is not fit for surgery
52
Q

What puts you at risk for getting gastric cancer?

A
  • Male
  • H-Pylori infection
    • G-ve helical bacterium produces urease, breaking down urea into CO2 and ammonia
    • Ammonia neutralises stomach acid
    • Damages epithelial cells resulting in inflammation, ulceration, gastric neoplasia
  • Old age
  • Smoking
  • Alcohol
  • Salty diet
  • Family history
  • Pernicious anaemia
53
Q

How would gastric cancer present?

A
  • anorexia, weight loss, anaemia, etc
  • Dyspepsia
  • Dysphagia
  • Early satiety
  • Vomiting
  • Melaena
  • Epigastric mass on exam
54
Q

How would you investigate a gastric cancer?

A
  • Bloods, fbc, lft, u&es, group and save, coagulation
    • always ask for these when there is haematemesis or melaena
  • Upper GI endoscopy + biopsy
    • send for histology, CLO test (H Pylori), HER2/neu protein expression
  • CT chest/abdo/pelvis for staging
  • Staging laparoscopy for peritoneal mets
  • TNM staging
55
Q

How would you manage gastric cancer and what are some SEs?

A
  • Ensure adequate nutrition
  • nutritional support (NG tube or radiologically inserted gastrostomy tube)

Surgery

  • Peri-op chemo (3 cycles neoadjuvant, 3 cycles adjuvant)
  • Proximal gastric cancer = total gastrectomy
  • Distal = subtotal gastrectomy
  • Tumours confined to muscularis mucosa = Endoscopic Mucosal Resection

SE of gastrectomy = anastomotic leak, re-operation, dumping syndrome, vit b12 deficiency

Conservative

  • Palliative chemo if really late disease presentation
  • Stenting for those with gastric outlet obstruction due to obstructing cancer
  • Sometimes palliative surgery (distal gastrectomy or bypass)
56
Q

What are some comon causes of haematemesis?

A
  • Oesophageal varices
  • Gastric Ulcers (commonly on lesser curve of stomach or posterior duodenum)
  • Mallory Weiss (bleeding starts after vomiting)
  • Oesophagitis
  • Bourhaves (rare)
57
Q

How would you manage haematemesis?

A

A-E

Peptic Ulcer

  • adrenaline injection and cauterisation of bleeding
  • high dose IV PPI (eg. 40mg omeprazole)
  • H Pylori eradication therapy if necessary

Oesophageal varices

  • Endoscopic banding
  • prophylactic antibiotic therapy
  • somatostatin analogues (eg. octreotide) or vasopressors (eg. terlipressin) started
  • Long term beta-blocker therapy
58
Q

What is a haemorrhoid?

A

Abnormal swelling or enlargement of anal vascular cushions.

(there are 3 cushions, at 3/7/11 oclock)

They can prolapse, thrombose and become very painful.

Caused by excess straining (eg. chronic constipation), old age, increased intra abdo pressure (obese, pregnant, ascites, etc), family history, portal hypertension, cardiac failure.

59
Q

What are the different degrees of a haemorrhoid?

A

1st degree = Remain in the Rectum

2nd degree = Prolapse through the anus on defecation but spontaneously reduce

3rd degree = prolapse through the anus on defecation but require digital reduction

4th degree = Remain persistently prolapsed

60
Q

How would haemorrhoids present?

A
  • painless red rectal bleeding commonly after defaecation (seen on paper or surface of stool, not mixed in)
  • pruritus due to chronic mucus discharge and irritation
  • rectal fullness or an anal lump
  • soiling due to impaired continence or mucus discharge
  • pain if thrombosed haemorrhoids
    • thrombosed prolapsed haemorrhoids = purple/blue, oedematous, tense, tender perianal mass
61
Q

How would you investigate haemorrhoids?

A
  • Proctoscopy
  • Flexi sigmoidoscopy or colonoscopy to exclude malignancy
  • DRE
62
Q

How would you manage haemorrhoids?

A

Conservative

  • increase fibre and fluid
  • prescribe laxatives
  • topical analgesia (lignocaine gel)

Non-Surgical

  • rubber band ligation for 1st-2nd degree haemorrhoids
  • infrared coagulation or photocoagulation
  • bipolar diathermy
  • direct-current electrotherapy
  • haemorrhoidal artery ligation therapy

Surgical

  • Stapled Haemorrhoidectomy OR Milligan Morgan Haemorrhoidectomy
    • if still symptomatic, not responding to conservative therapies, and unsuitable for banding
    • used for 3rd-4th degree
63
Q

What is a hiatus hernia?

A

A hernia is a protrusion of an organ/part of an organ through the wall of the cavity that contains it, into an abnormal position.

Hiatus hernia = protrusion of an organ from the abdo cavity into the thorax, through the oesophageal hiatus

Usually due to increased intra-abdo pressure eg. pregnancy, obesity, ascites.

Or old age due to loss of diaphragmatic tone

64
Q

What are the 2 pathophysiologies of a hiatus hernia?

A

Sliding hiatus hernia

  • GOJ, abdo, part of oesophagus, stomach cardia all slide through diaphragmatic hiatus into thorax

Rolling hiatus hernia

  • Gastric fundus moves up to lie by the Gastro-Oesophageal Junction creating a stomach bubble in the thorax
65
Q

How does a hiatus hernia present?

A
  • gastrooesophageal reflux symptoms eg. burning epigastric pain worse when lying flat, etc
  • Vomiting
  • Weightloss
  • Bleeding or anaemia secondary to oesphageal ulceration
  • Hiccups or palpitations
  • swallowing difficulties
66
Q

How would you investigate a hiatus hernia?

A

Oesophagogastroduodenoscopy (OGD)

CT or MRI

67
Q

What is the management of a hiatus hernia?

A

Medical

  • proton pump inhibitor eg. omeprazole
  • weightloss
  • alterations in diet (low fat, small portions)
  • sleep with increased pillows
  • smoking cessation
  • reduced alcohol

Surgical

  • if patient presents with risks of strangulation, volvulus, or remains symptomatic after medicine
  • Cruroplasty
  • Fundoplication (gastric fundus wrapped around lower oesophagus and stitched)
68
Q

What are the complications of a hiatus hernia and its management?

A

Hiatus Hernia

  • rolling = more prone to incarceration and strangulation
  • gastric volvulus (stomach twists by 180 degrees and can block gastric passage and cause tissue necrosis)
    • can present with Borchard’s triad = epigastric pain, retching but no vomiting, inability to pass NG tube

Surgery complications

  • recurrence of hernia
  • abdo bloating due to inability to burp due to improved anti-reflux mechanism
  • dysphagia if fundoplication is too tight
  • fundal necrosis if blood supply is disrupted
69
Q

What is an inguinal hernia?

A

When abdo cavity contents enter the inguinal canal.

Due to old age, increased abdo pressure, obesity, male

70
Q

What are the 2 different pathophysiologies of an inguinal hernia?

A

Direct inguinal hernia

  • bowel enters inguinal canal through Hesselbach’s triangle (area of weakness in posterior wall of canal)
  • commonly in older patients, secondary to abdo wall laxity or an increase in abdo pressure

Indirect inguinal hernia (80%)

  • bowel enters inguinal canal via deep inguinal ring lateral to inferior epigastric vessels
  • occur due to incomplete closure of processus vaginalis
71
Q

How would an inguinal hernia present?

A
  • As a lump in the groin
  • discomfort worse with activity or standing
  • if incarcerated = painful, tender, erythematous
  • Sometimes features of bowel obstruction
  • Sometimes features of strangulation if blood supply compromised (pain out of proportion, tender)
72
Q

How would you manage an inguinal hernia?

A
  • open repair (Lichenstein technique)
  • laparoscopic repair (preferred for recurrent or bilatearl inguinal hernias)
73
Q

What are 3 complications of inguinal hernias and the management?

A
  • Incarceration (contents of hernia unable to return to original cavity)
  • Obstruction (bowel lumen obstructed)
  • Strangulation (compression of hernia leading to compromised blood supply leading to bowel becoming ischaemic)

Post-op complications

  • pain, bruising, haematoma
  • recurrence
  • chronic pain persisting 3 months after hernia repair
  • damage to vas deferens or testicular vessels leading to ischaemic orchitis
74
Q

What are some risk factors for hepatocellular carcinoma?

A
  • viral hepatitis B and C
  • high alcohol intake
  • smoking
  • age >70
  • aflatoxin exposure (found in cereal and nuts)
  • fam history of liver disease
  • hereditary haemochromatosis
  • Primary Biliary Cirrhosis
    *
75
Q
A
76
Q

How would liver cancer present?

A
  • cirrhosis = fatigue, fever, weight loss, lethargy
  • dull ache in right upper abdo
  • worsening ascites or jaundice
  • SIGNS OF CHRONIC LIVER DISEASE
  • enlarged craggy irregular liver on exam
  • raised alpha fetoprotein (AFP)
  • US = diagnostic if there is a mass >2cm
    • confirm with CT
  • MRI liver scan demonstrates a mass with arterial hypervascularisation
  • Biopsy or percutaneous fine needle aspiration to confirm
77
Q

What staging systems do you use to stage liver cancer and to predict the potential of a liver transplant?

A

Barcelona Clinic Liver Cancer staging system

Child-Pugh and MELD scores (for liver transplant potential)

78
Q

How would you manage a hepatocellular carcinoma?

A

SURGERY

  • surgical resection if no cirrhosis
  • transplant for patients that fulfil Milan criteria
    • one lesion <5cm or 3 lesions <3cm
    • No extrahepatic manifestations
    • No vascular infiltrations

Non-SURGICAL

  • image guided ablation if early Hepatocellular Carcinoma
  • Transarterial chemoembolisation (TACE) for large multinodular tumours
    • high conc of chemo drugs injected into hepatic artery and embolising agent added to induce ischaemia
79
Q

What is meckel’s diverticulum?

A

Congenital malformation of the small bowel.

Results from failure of the vitelline duct to obliterate during the 5th week of fetal development.
Results in bleeding, obstruction, inflammation, perforation

(no cards on it, if you want more info read notes)

80
Q

What is melena?

A

Black tarry stools due to upper GI bleeding.

Usually offensive smelling due to alteration of blood by intestinal enzymes

81
Q

How would you investigate melena?

A
  • PR exam
  • full abdo exam to assess for epigastric tenderness, pritonism, hepatomegaly, etc
  • Routine bloods, U&Es, LFTs, clotting
  • Group and save
  • ABG for lactate
  • OGD
  • CT abdo with IV contrast
82
Q

What are the two main kinds of oesophageal cancer and what are the risk factors of both?

A

Squamous cell carcinoma Risk factors

  • smoking
  • alcohol
  • chronic achalasia
  • low vit a levels
  • iron deficiency

Adenocarcinoma (lower 3rd of oesophagus) Risk factors

  • long standing GORD
  • obesity
  • high dietary fat intake
83
Q

what is the pathophysiology of oesophageal adenocarcinoma?

A
  • arises due to metaplastic epithelium (Barrett’s)
  • progresses to dysplasia to malignancy
84
Q

How does oesophageal cancer present?

A
  • dysphagia (initally to solids then progresses to liquids)
  • significant weight loss
  • odonyphagia or hoarseness
  • upper abdo pain
  • dyspepsia or reflux
  • On exam = recent unintentional weightloss, cachexia, dehydration, supraclavicular lymphadenopathy, other signs of mets eg. jaundice
85
Q

How would you investigate an oesophageal cancer?

A
  • Urgent OGD within 2 weeks
    • biopsy any findings
  • CT chest/abdo/pelvis for staging
  • staging laparoscopy for intra-peritoneal mets
  • Palpable lymph nodes investigated via fine needle aspiration biopsy
  • Bronchoscopy for hoarseness or haemoptysis
86
Q

How would you manage oesophageal cancer?

A

SURGERY

  • oesophagectomy (remove tumour, top of stomach, surrounding lymph nodes)
    • SCC of upper oesophagus = definitive chemo-radio therapy
    • SCC of middle or lower = neoadjuvant CRT then surgery
    • Adenocarcinomas = neoadjuvant chemo or chemo-radio
      • then oesophageal resection

SE of surgery = anatomotic leak, re-op, pneumonia, death, need to insert a feeding jejunostomy after as reservoir function of stomach is lost.

PALLIATIVE

  • oesophgeal stent if difficulty swallowing
  • radiotherapy/chemotherapy to improve symptoms
  • photodynamic therapy
  • nutritional support/ supplements
  • radiologically inserted gastrostomy tube to bypass obstruction when dysphagia becomes too bad
87
Q

What are some risk factors for developing pancreatic cancer?

A
  • smoking
  • chronic pancreatitis
  • recent onset of DM
  • family history
  • late onset diabetes >50 years old
88
Q

How would pancreatic cancer present?

A
  • late, vague non-specific presentation (80% are unresectable at diagnosis)

Head of pancreas

  • obstructive jaundice (compression of CBD)
  • abdo pain radiating to back
  • weight loss
  • acute pancreatitis
  • thrombophlebitis migrans

Cancer of tail = asymptomatic until late

Exam = look cachetic, malnourished, jaundiced, abdo mass in epigastric region, enlarged gallbladder

89
Q

How would you investigate pancreatic cancer?

A
  • FBC, U&Es, LFTs (raised bilirubin, ALP, gamma-GT show obstructive jaundice)
  • Ca19.9 tumour marker
  • Abdo ultrasound to shwo pancreatic mass or dilated biliary tree
  • Pancreatic protocol CT scan to diagnose
    • then chest, abdo, pelvis CT
  • Endoscopic ultrasound guided fine needle aspiration biopsy
90
Q

How would you manage a pancreatic cancer?

A

SURGERY

  • radical resection
    • head = Whipples
    • Tail/body = distal pancreatectomy
  • Contraindications = peritoneal, liver, distant mets
  • SE = pancreatic fistula, delayed gastric emptying, pancreatic insufficiency

CHEMO

  • adjuvant chemo (5-flourouracil) after surgery
  • Folfirinox regime for metastatic regime
    • Gemcitabine therapy for those who can’t tolerate folfirinox

PALLIATIVE

  • insert biliary stent via ERCP or percutaneously to relieve obstructive jaundice
  • palliative chemo (gemcitabine based)
  • Treat exocrine insufficiency (and consequent malaborption +steatorrhoea)
    • enzyme replacements and lipases eg. Creon
91
Q

What are some exampels of endocrine tumours of the pancreas?

A

G cells secrete gastrin = gastrinoma

  • stimulates gastric acid release
  • results in zollinger-ellison syndrome

A cells secrete glucagon = glucagonoma

  • increases blood glucose conc
  • results in hyperglycaemia, DM

B cells secrete insulin = insulinoma

  • decrease blood glucose conc
  • results in symptomatic hypoglycaemia eg. sweating, changed mental state

Somatostatinomas

  • results in DM, gallstones (inhibition of cholecystikinin), weightloss, achlorhydria (gastrin inhibition)
92
Q

Whhat is Ogilvie syndrome/ pseudo-obstruction?

A

Interruption of autonomic nervous supply to the colon, resulting in absence of smooth muscle action in the bowel wall.

This results in dilation of the colon due to the adynamic bowel (in the absence of mechanical obstruction).

If untreated results in increasing colonic diameter = toxic megacolon, bowel ischaemia, perforation.

Can be due to: electrolyte imbalance, medications (opioids, CCB, antidepressants), recent surgery, severe illness or trauma (eg. cardiac ischaemia), neuro disease (eg. MS, parkinsons, Hirschsprungs)

93
Q

How would you manage pseudo-obstruction?

A

Conservative

  • NBM and fluids
  • NG tube if vomiting
  • endoscopic decompression if it does not resolve in 24-48 hours
    • insert flatus tube
  • IV neostigmine can be trialled if there is limited resolution
  • Nutritional support

Surgical

  • segmental resection +/- anastomosis
    • must remove all affected areas for this to be curative
  • Caecostomy or ileostomy to decompress bowel long term
94
Q

What is septic shock?

A

Sepsis with hypotension despite adequate fluid resus

OR

requiring inotropic agents to maintain normal systolic BP

95
Q

What is the criteria for sepsis?

A
  • Presence of a known or suspected infection
  • clinical features of organ dysfunction (SOFA score >/= 2 means sepsis)
  • qSOFA is shortened version of SOFA for rapid assessment
    • Resp rate >22, altered mental state, systolic BP >100
96
Q

What is a volvulus?

A

Twisting of a loop of intestine around its mesenteric attachment, resulting in a closed loop bowel obstruction.

Bowel can become ischaemic due to compromsied blood supply = necrosis and perforation

97
Q

What are the risk factors of a volvulus?

A
  • old age
  • neuropsychiatric disorders
  • chronic constipation or laxative use
  • male
  • previous abdo operations

Typically occurs in sigmoid colon as the long mesentery of the sigmoid colon makes it prone to twisting on its mesenteric base.

98
Q

How would a volvulus present?

A
  • clinical features of large bowel obstruction
  • sigmoid colon is distal so vomiting is a late sign
  • colicky pain
  • abdo distension
  • absolute constipation
  • rapid onset!!! (over a few hours)
  • abdo is tympanic to percussion (examine for peritonism)
    *
99
Q

How would you investigate a volvulus?

A
  • Bloods, etc
  • Electrolytes, Ca2+, TFTs to exclude pseudo-obstruction
  • CT abdo/pelvis shows dilated sigmoid colon with “whirl sign”
  • Abdo XRay shows “coffee bean” sign in LIF
100
Q

How would you manage a volvulus?

A

Conservative

  • decompression with sigmoidoscope
  • insertion of flatus tube

Surgical

  • indicated if colonic ischaemia/perforation, repeated failed atttempts at decompression, necrotic bowel found in endoscopy
  • Sigmoid volvulus = Laparotomy or Hartmann’s
  • Caecal volvulus = Laparotomy and ileocaecal resection
101
Q
A

SURGERY - Gen Surg (3 decks)

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