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GI Flashcards

1
Q

What is the pathophysiology of cholelithiasis?

A

Excess hepatic cholesterol secretion relative to bile salts and lecithin (solubilizing agents) = supersaturated cholesterol which precipitates gallstone formation

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2
Q

Risk factors for cholesterol stones

A

“5F’s”:

  • Female
  • Fair
  • Forty
  • Fat
  • Fertile
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3
Q

What demographic also has a high incidence of cholelithiasis?

A

Pima Indians population

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4
Q

Risk factors for pigment stones

A
  1. Cirrhosis
  2. Chronic hemolysis
  3. Biliary stasis
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5
Q

Protective factors for cholelithiasis

A
  1. Statin
  2. Coffee
  3. Vitamin C
  4. Exercise
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6
Q

Symptoms of cholelithiasis

A
  1. Asymptomatic in 80%

2. Biliary colic (10-25%)

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7
Q

Treatment for cholelithiasis

A

Most don’t require treatment.

Consider cholecystectomy if risk of malignancy.

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8
Q

What conditions increase the risk of gallbladder malignancy/require cholecystectomy?

A
  1. Cholechondral cysts
  2. Caroli’s disease
  3. Porcelain gallbladder
  4. Sickle cell disease
  5. Pediatric patient
  6. Bariatric surgery
  7. Immunsuppression
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9
Q

Investigations for cholelithiasis

A
  1. Normal bloodwork (FBC, LFTs, bilirubin, lipase, amylase)
  2. USS diagnostic procedure of choice
  3. HIDA scan (cholescintigraphy) - rarely used
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10
Q

What is the radioisotope used in HIDA scan?

A

IV technetium-99 radioisotope

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11
Q

What causes biliary colic?

A

Gallstone transiently impacting cystic duct, no infection

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12
Q

Features of biliary colic

A
  • steady, dull RUQ/epigastric pain lasting minutes to hours (<6h)
  • crescendo-decrescendo pattern
  • Worse after fatty meal + at night, not after fasting
  • N/V
  • R shoulder tip pain, chest pain, scapular pain
  • No peritoneal/systemic signs
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13
Q

Investigations for biliary colic

A
  1. Normal bloodwork (FBC, U&Es, LFTs, bilirubin, amylase)

2. USS shows cholelithiasis, may show stone in cystic duct

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14
Q

Treatment for biliary colic

A
  1. Analgesia (paracetamol + NSAIDs for mild-moderate pain; IM diclofenac/opioid for severe pain)
  2. Rehydration during colic episode
  3. Elective laparoscopic cholecystectomy (95% success)
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15
Q

What are complications of elective laparoscopic cholecystectomy?

A
  1. CBD injury
  2. Hollow viscus injury
  3. Bile peritonitis
  4. Vessel injury leading to liver damage
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16
Q

Cause of acute cholecystitis

A
  • Inflammation of gallbladder resulting from sustained gallstone impaction in cystic duct or Hartmann’s pouch (postern-medial wall of gallbladder neck; normal variation)
  • No cholelithiasis in 5-10%
  • History of biliary colic
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17
Q

Features of acute cholecystitis

A
  1. Severe constant (>6h) epigastric/RUQ pain
  2. Anorexia
  3. N/V
  4. Low grade fever (>38.5)
  5. Focal peritoneal signs (Murphy’s sign, palpable/tender gallbladder; Boas’ sign - R sub-scapular pain)
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18
Q

Investigations for acute cholecystitis

A
  1. Bloods show high WBC + left shift, mildly elevated bilirubin (either stones or Mirizzi syndrome)
  2. USS (consider HIDA if USS negative)
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19
Q

What are the signs of acute cholecystitis on USS?

A
  1. Gallbladder wall thickening > 4mm
  2. Oedema (double-wall sign)
  3. Gallbladder sludge
  4. Cholelithiasis
  5. Pericholecystic fluid
  6. Sonographic Murphy’s sign
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20
Q

Complications of acute cholecystitis

A
  1. Gangrenous gallbladder (20%)
  2. Perforation (10% - abscess formation or local peritonitis)
  3. Mirizzi syndrome (extra-luminal compression of CBD/CHD due to large stone in cystic duct - associated with gallbladder cancer)
  4. Empyema of gallbladder (suppurative cholecystitis + sick pt)
  5. Emphysematous cholecystitis (bacterial gas present in gallbladder lumen, wall or pericholecystic space - risk in diabetic patient)
  6. Cholecystoenteric fistula (from repeated attacks of cholecystitis) –> gallstone illeus
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21
Q

What organisms are involved in emphysematous cholecystitis?

A
  1. C welchii
  2. E coli
  3. Klebsiella
  4. Anaerobic streptococci
  5. Enterococcus
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22
Q

Treatment for acute cholecystitis

A
  1. Admit, hydrate, NBM, NG tube, analgesia
  2. Antibiotics (cefazolin if uncomplicated cholecystitis)
  3. ERCP prior to surgery if CBD stones are present on USS (MRCP ± ERCP if CBD markedly dilated or CBD stones suspected)
  4. Cholecystectomy (within 72h preferred)
  5. Percutanoues cholecystostomy tube: critically ill or if general anaesthetic contraindicated
  6. Percutaneous stone extraction
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23
Q

What is acalculous cholecystitis?

A

Acute or chronic cholecystitis in the absence of stones

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24
Q

Causes of acalculous cholecystitis

A
  1. Gallbladder ischemia

2. Gallbladder stasis

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25
Q

Risk factors for acalculous cholecystitis

A
  1. ICU admission
  2. DM
  3. Immunosuppression
  4. Trauma patients
  5. TPN
  6. Sepsis
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26
Q

Features of acalculous cholecystitis

A

Occurs in 10% of acute cholecystitis cases with same features

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27
Q

Investigations for acalculous cholecystitis

A
  1. Bloods (FBC, U&Es, LFTs, liver enzymes, amylase, lipase)
  2. USS showing sludge in gallbladder, other USS features of cholecystitis
  3. CT/HIDA scan
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28
Q

Treatment for acalculous cholecystitis

A
  1. NBM, IV fluids, pain management
  2. IV broad-spectrum antibiotics
  3. Cholecystectomy
  4. If patient unstable –> percutaneous cholecystectomy
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29
Q

What is choledocholithiasis?

A

Stones in the common bile duct

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30
Q

Features of choledocholithiasis

A
  1. 50% asymptomatic, often having history of biliary colic
  2. Tenderness in RUQ/epigastrium
  3. Acholic stool, dark urine, fluctuating jaundice
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31
Q

What are pigment stones made of

A

Calcium bilirubinate

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32
Q

Causes of primary gallstone formation

A
  1. formed in bile duct

2. indicates bile duct pathology (benign biliary stricture, sclerosing cholangitis, choledochal cyst, cystic fibrosis)

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33
Q

Causes of secondary gallstone formation

A

Formed in the gallbladder (85% of cases)

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34
Q

Investigations for choledocholithiasis

A
  1. Bloods (FBC, leukocytosis suggests cholangitis; LFTs = increased AST, ALT early in disease, increased bilirubin/ALP/GGT later; Amylase/lipase to rule out gallstone pancreatitis)
  2. USS
  3. MRCP (visualization of ampullarf region, biliary + pancreatic anatomy) - non-invasive diagnostic test of choice
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35
Q

Treatment for choledocholithiasis

A
  1. ERCP: removal of stones + sphincterotomy

2. Percutaneous transhepatic cholangiography + biliary tree flushing with laparoscopic cholecystectomy if above fails

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36
Q

Complications of ERCP

A
  1. Retained stones
  2. ERCP pancreatitis (1-2%)
  3. Pancreatic/biliary sepsis
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37
Q

Complications of percutaneous transhepatic cholangiography + biliary tree flushing

A
  1. Cholangitis
  2. Pancreatitis
  3. Biliary stricture
  4. Biliary cirrhosis
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38
Q

What is acute/ascending cholangitis?

A

Obstruction of CBD leading to biliary stasis, bacterial overgrowth, suppuration, and biliary sepsis - may be life threatening especially in the elderly

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39
Q

Causes of ascending cholangitis

A
  1. Choledocholithiasis (60%)
  2. Stricture
  3. Neoplasm (pancreatic/biliary)
  4. Extrinsic compression (pancreatic pseudocyst, pancreatitis)
  5. Instrumentation of bile ducts
  6. Biliary stent
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40
Q

Organisms responsible for ascending cholangitis

A
  1. E coli
  2. Klebsiella
  3. Enterobacter
  4. Pseudomonas
  5. Enterococcus
  6. B fragilis
  7. Proteus
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41
Q

Clinical features of ascending cholangitis

A
  1. Charcot’s triad (RUQ pain, jaundice, fever)
  2. Reynold’s pentad (Charcot’s triad + confusion, shock)
  3. N/V, abdo distension, ileus, acholic stools, tea-coloured urine (elevated direct bilirubin)
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42
Q

Investigations for ascending cholangitis

A
  1. FBC (elevated WBC + left shift, may have positive blood cultures)
  2. LFTs (obstructive picture - elevated ALP/GGT + conjugated bilirubin, possible mild increase in AST/ALT)
  3. Amylase/lipase: rule out pancreatitis
  4. USS: duct dilatation
  5. CT: bile duct dilatation + can identify biliary stenosis
  6. MRCP when diagnosis unclear
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43
Q

Treatment of ascending cholangitis

A
  1. NBM, fluid + electrolyte resus, ± NG tube, IV antibiotics
    - Tazocin OR ampicillin + sulbactam
  2. Biliary decompression
    - ERCP + sphincterotomy
  3. Cholecystectomy
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44
Q

IV antibiotics to treat ascending cholangitis

A
  1. Ampicillin + sulbactam OR tazocin
  2. Metronidazole + ceftriaxone (3rd generation cephalosporin) OR fluoroquinolone (ciprofloxacin, levofloxacin)
  3. Carbapenem mono therapy (imipenem, meropenem)
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45
Q

Causes of gallstone ileus

A

Repeated inflammation causes a cholecystoenteric fistula (usually duodenal) = large gallstone enters the GI tract (impacting near the ileocecal valve) = mechanical bowel obstruction

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46
Q

Clinical features of gallstone ileus

A
  1. Crampy abdo pain
  2. N/V
  3. Constipation/obstipation
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47
Q

Investigations for gallstone ileus

A
  1. AXR: dilated small intestine, air fluid levels, may reveal radiopaque gallstone + air in biliary tree (pneumobilia)
  2. CT: biliary tract air, obstruction, gallstone in intestine
  3. Rigler’s Triad
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48
Q

What is Rigler’s triad

A
  1. Pneumobilia
  2. Small bowel obstruction
  3. Gallstone (usually in RIF)
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49
Q

Treatment for gallstone ileus

A
  1. Fluid resus, NG tube decompression
  2. Surgery: enterolithotomy + removal of stone, inspect small/large bowel for proximal stones
  3. Close fistula surgically or manage expectantly
    - Cholecystectomy generally NOT performed
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50
Q

What is Bouveret’s Syndrome?

A

Gastric outlet/duodenal obstruction caused by large gallstone passing thru a cholecystogastric or cholecystoduodenal fistula

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51
Q

Risk factors for carcinoma of the gallbladder

A
  1. Chronic symptomatic gallstones (70%)
  2. Old age
  3. Female
  4. Gallbladder polyps
  5. Porcelain gallbladder
  6. Chronic infection (H pylori, Salmonella)
  7. 1º sclerosing cholangitis
  8. Abnormal pancreaticobiliary duct function
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52
Q

Majority of carcinoma of gallbladder type

A

Adenocarcinoma

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53
Q

Clinical features of carcinoma of gallbladder

A
  • Local = non-specific RUQ pain ± palpable RUQ mass
  • Courvoisier’s gallbladder sign = enlarged gallbladder + painless jaundice due to obstruction of CBD, suggestive of gallbladder/pancreatic malignancy
  • Systemic: jaundice (50%), anorexia, N/V, weight loss, malaise
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54
Q

What is Courvoisier’s gallbladder sign?

A

Enlarged gallbladder + painless jaundice due to obstruction of CBD suggestive of gallbladder/pancreatic malignancy

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55
Q

Local extension sites of carcinoma of gallbladder

A
  1. Liver
  2. Peritoneum
  3. Stomach
  4. Duodenum
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56
Q

Early mets locations of carcinoma of gallbladder

A
  1. Lung
  2. Pleura
  3. Liver
  4. Bone
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57
Q

Investigations for carcinoma of gallbladder

A
  1. USS: mural thickening, calcification, loss of interface between gallbladder/liver, fixed mass
  2. Endoscopic USS: to distinguish benign vs malignant polyps
  3. Abdo CT: polypoid mass, mural thickening, liver invasion, nodal involvement + distal mets
  4. MRI/MRCP: distinguish benign vs malignant polyps
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58
Q

Treatment for carcinoma of the gallbladder

A
  1. Laparoscopic cholecystectomy (avoid open to prevent tumour seeding of the peritoneal cavity)
    - beyond mucosa = cholecystectomy, en bloc wedge resection of 3-5cm underlying liver, and dissection of hepatoduodenal lymph nodes
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59
Q

Prognosis for carcinoma of the gallbladder

A

5yr survival = 20% (detected late)

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60
Q

What is cholangiocarcinoma?

A

Malignancy of the epithelial cells of extra or intrahepatic bile ducts
- Majority adenocarcinoma

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61
Q

Risk factors for cholangiocarcinoma

A
  1. Age 50-70y
  2. Gallstones
  3. UC
  4. 1º sclerosing cholangitis
  5. Choledochal cyst
  6. Clonorchis sinensis
  7. Infection (liver fluke)
  8. Chronic intrahepatic stones (hepatolithiasis)
  9. Genetic disorders (Lynch syndrome, cystic fibrosis, multiple biliary papillomatosis, BAP1 tumour predisposition syndrome)
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62
Q

Clinical features of cholangiocarcinoma

A
  1. Jaundice
  2. Pruritis
  3. Dark urine + pale stools
  4. Anorexia/weight loss
  5. RUQ pain
  6. Courvoisier’s sign
  7. Hepatomegaly
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63
Q

Mets locations of cholangiocarcinoma

A
  • Early mets uncommon
  • tumour grows into portal vein or hepatic artery
  1. Peritoneum
  2. Lungs
  3. Pleura
  4. Liver
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64
Q

What is a Klatskin tumour?

A

Cholangiocarcinoma located at bifurcation of common hepatic duct

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65
Q

Investigations for cholangiocarcinoma

A
  1. LFTs: show obstructive picture, CA 19-9, CEA may be elevated
  2. USS, CT: bile ducts dilated
  3. ERCP, PTC: to determine respectability, for biopsies
  4. CXR, bone scan: mets workup
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66
Q

Treatment for cholangiocarcinoma

A
  1. Biliary drainage + wide excision margin (if resectable)
  2. Intrahepatic lesions: liver resection
    - if lower 1/3 = Whipple procedure
  3. Stent or choledochojejunostomy (surgical bypass) (if non-resectable)
  4. Chemotherapy ± radiotherapy
  5. Transplantation in patients with Klatskin tumours or NET with no evidence of extra hepatic disease + stability
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67
Q

Prognosis for cholangiocarcinoma

A

5yr survival:

  • 30% if localized
  • 24% if regional
  • 2% if distal
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68
Q

Organisms that live in the biliary tree

A

‘KEEPS’

  • Klebsiella
  • Enterobacter
  • Enterococcus, E. Coli
  • Proteus
  • Serratia
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69
Q

3 liver cysts that can cause RUQ mass

A
  1. Choledochal cyst
  2. Hydatid (cystic echinococcosis)
  3. Cystadenoma/Cystadenocarcinoma
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70
Q

Characteristics of choledochal cysts

A
  1. Congenital malformation of bile ducts
  2. High-risk of malignancy
  3. Majority present before 10y old
  4. Todani classification based on anatomical characteristics within biliary tree
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71
Q

Clinical features of choledochal cysts

A
  1. Recurrent abdo pain
  2. Intermittent jaundice
  3. RUQ mass
  4. Cholangitis
  5. Symptomatic gallstones
  6. Pancreatitis
  7. Portal HTN
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72
Q

Investigations for choledochal cysts

A
  1. LFT abnormalities
  2. USS
  3. CT
  4. Transhepatic cholangiography
  5. ERCP/MRCP
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73
Q

Treatment for choledochal cysts

A
  1. Complete excision of cysts

2. Liver resection or transplantation if cystic dilatation involves intrahepatic bile ducts (Caroli’s Disease)

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74
Q

Complications of choledochal cysts

A
  1. Biliary cirrhosis
  2. Portal HTN
  3. Cyst rupture
  4. Cholangiocarcinoma
  5. Increased risk of biliary malignancy
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75
Q

Description of hydatid (cystic echinococcosis)

A
  1. Infection with parasite Echinococcus granulosus
  2. Associated with exposure to dogs, sheep, horses, pigs, goats, camels + cattle in Southern Europe/Middle East/Australasia/South America
  3. Ingested parasitic eggs hatch in the small intestine, where larvae enter blood/lymphatic
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76
Q

Features of hydatid cyst

A
  1. Usually asymptomatic
  2. Palpable RUQ mass or hepatomegaly
  3. Chronic RUQ pain when symptomatic
  4. N/V, dyspepsia (non-specific symptoms)
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77
Q

Investigations of hydatid cyst

A
  1. Labs (anti-echinococcus antibody)
  2. USS
  3. CT: calcified cystic walls
  4. Needle biopsy
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78
Q

Treatment for hydatid cyst

A
  1. Systemic chemotherapy: Albendazole (anti-helminthic drug)

2. Surgical: total pericystectomy/partial hepatectomy/lobectomy/drainage

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79
Q

Complications of hydatid cyst

A
  1. IVC compression
  2. Cyst rupture which can cause fever, pruritus, eosinophilia, biliary colic, jaundice, cholangitis, pancreatitis or anaphylaxis
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80
Q

Description of cystadenoma/cystadenocarcinoma

A
  1. Rare cystic neoplasms arising from bile ducts
  2. Most common premalignant liver lesion
  3. Cystadenocarcinoma = invasive carcinoma
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81
Q

Features of cystadenoma

A
  1. Upper abdo mass
  2. Abdo pain
  3. Anorexia
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82
Q

Investigations for cystadenoma

A
  1. Labs: elevated LFTs, CEA, CA 19-9
  2. USS: anechoic mass with internal separations that are highly echogenic
  3. CT/MRI
  4. ERCP/MRCP
  5. Need histology for definite diagnosis
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83
Q

Treatment for cystadenoma

A

Excised because of malignancy risk

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84
Q

Complications of cystadenoma

A
  1. Cystadenocarcinoma may invade adjacent tissues and metastasize
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85
Q

List the 4 types of liver abscesses

A
  1. Pyogenic (bacterial): most common - E coli, Klebsiella, Proteus, Streptococcus, Staphylococcus, anaerobes
  2. Parasitic (amoebic): Entamoeba histolytic, Echinococcal cyst
  3. Fungal: Candida
  4. Sources: direct spread from biliary tract infection, portal spread from GI infection, systemic infection (i.e. endocarditis)
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86
Q

Clinical features of liver abscess

A
  1. Fever, malaise, chills, anorexia, weight loss, abdo pain, nausea
  2. RUQ tenderness, hepatomegaly, jaundice
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87
Q

Investigations for liver abscess

A
  1. FBC (anemia, leukocytosis)
  2. LFTs (elevated ALP + hypoalbuminemia, elevated transaminases + bilirubin variable)
  3. Blood cultures
  4. INR/PTT
  5. Stool cultures
  6. Serology (E histolytic + Echinococcus)
  7. USS, CXR (R basilar atelectasis/effusion), CT, MRI
  8. Cyst aspiration with C&S
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88
Q

Treatment for liver abscess

A
  1. Treat underlying cause
  2. Pyogenic abscesses treated with antibiotics (ceftriaxone + metronidazole OR tazocin)
  3. USS/CT-guided percutaneous drainage or surgical drainage
  4. Consider potential sources of sepsis (i.e. biliary source, infected tumour)
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89
Q

Prognosis of liver abscess

A

Mortality = 15%

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90
Q

Differential diagnoses for metastatic liver mass

A

‘Some GU Cancers Produce Bumpy Lumps’

  • Stomach
  • GU (kidney, ovary, uterus)
  • Colon
  • Pancreas
  • Breast
  • Lung
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91
Q

3 benign liver neoplasms

A
  1. Hemangioma (cavernous)
  2. Focal nodular hyperplasia
  3. Adenoma
92
Q

Description of hemangioma

A
  1. Most common benign hepatic tumour

2. Results from malformation + proliferation of vascular endothelial cells

93
Q

Clinical features of hemangioma

A
  1. Small + asymptomatic
  2. Those > 4cm = abdo pain
  3. Consumptive coagulopathy if huge (in kids)
94
Q

Investigations for hemangioma

A
  1. Contrast CT (Well-demarcated hypodense mass with peripheral enhancement on arterial phase with centripetal filling on delayed phases)
  2. USS (homogenous hyper echoic mass)
  3. MRI
  4. Avoid biopsy: may result in hemorrhage!!
95
Q

Treatment for hemangioma

A
  1. None if asymptomatic
  2. In symptomatic patients/mass effect = surgical resection
  3. Surgical resection = liver resection, hepatic artery ligation, enucleation, liver transplantation
  4. Non-surgical treatment = hepatic artery embolization, radiotherapy
96
Q

Description of focal nodular hyperplasia

A
  1. Hyperplastic response to vascular anomaly leading to disorganized growth of hepatocyte + bile ducts
97
Q

Clinical features of focal nodular hyperplasia

A
  1. . Rarely grows or bleeds
  2. No malignant potential
  3. Asymptomatic
98
Q

Investigations for focal nodular hyperplasia

A
  1. Central stellate scar surrounded by homogenous lesion on CT scan
  2. MRI
  3. Biopsy
99
Q

Treatment for focal nodular hyperplasia

A
  1. Difficult to distinguish from adenoma/fibrolamellar HCC (malignant potential)
  2. If confirmed to be FNH = no treatment required
100
Q

Description of hepatic adenoma

A

Benign abnormal growth of glandular epithelium

101
Q

Risk factors for hepatic adenoma

A
  1. Female
  2. Age 20-50
  3. Estrogen (OCP, pregnancy)
  4. Obesity
  5. Anabolic androgen use
  6. Type 1 glycogen storage disease
102
Q

Clinical features for hepatic adenoma

A
  1. Asymptomatic
  2. 25% RUQ pain/mass
  3. Bleeding
103
Q

Investigations for hepatic adenoma

A
  1. CT (well-demarcated masses, often heterogenous enhancement on arterial phase, isodense on venous phase without washout of contrast)
  2. USS
  3. MRI
  4. Biopsy (take bleeding risk into account)
104
Q

Treatment for hepatic adenoma

A
  1. Stop anabolic steroids or OCP

2. Excise due to risk of transformation to HCC and spontaneous rupture/hemorrhage

105
Q

List 5 primary malignant liver neoplasms

A
  1. Hepatocelllular carcinoma (most common)
  2. Cholangiocarcinoma
  3. Angiosarcoma
  4. Hepatoblastoma
  5. Hemangioendothelioma
106
Q

Risk factors for primary malignant liver neoplasms

A
  1. Chronic liver inflammation: cirrhosis, chronic hepatitis B/C, hemochromatosis, a1-antitrypsin deficiency, non-alcoholic steatohepatitis
  2. OCP (3x increased risk), steroids
  3. Smoking, alcohol, betel nuts
  4. Chemical carcinogens: aflatoxin, microcystin, vinyl choloride
107
Q

Clinical features of primary malignant liver neoplasms

A
  1. RUQ discomfort + R shoulder pain
  2. Jaundice, weakness, weight loss ± fever (if central tumour necrosis)
  3. Hepatomegaly, bruit, hepatic friction rub
  4. Ascites with blood (sudden intra-abdominal hemorrhage)
  5. Paraneoplastic syndromes: hypoglycaemia, hypercalcemia, erythrocytosis, watery diarrhea
  6. Metastasis: lung, intra-abdominal lymph nodes, bone, adrenal gland, brain, peritoneal seeding
108
Q

Where do primary malignant liver neoplasms spread to?

A
  1. Lung
  2. Intra-abdominal lymph nodes
  3. Bone
  4. Adrenal gland
  5. Brain
  6. Peritoneal seeding
109
Q

Investigations for primary malignant liver neoplasms

A
  1. INR + LFTs: AST, ALT, ALP, bilirubin, albumin
    - Elevated ALP, bilirubin, a-fetoprotein (80% of patients)
  2. USS (poorly-defined margins with internal echoes)
  3. Triphasic CT (enhancement on arterial + washout on portal venous phase)
  4. MRI
110
Q

Treatment for primary malignant liver neoplasms

A
  1. Surgical resection (except if cirrhosis due to decreased hepatic reserve)
  2. Liver transplant (except if extra hepatic disease + vascular invasion)
  3. Radiofrequency ablation, percutaneous ethanol injection, transcatheter arterial chemoembolization, chemotherapy + radiotherapy
111
Q

Prognosis for primary malignant liver neoplasms

A

5yr survival = 18% of patients

40-70% of patients undergo complete resection

112
Q

Description of secondary malignant liver neoplasms

A

Mets to the liver (most common malignant tumours found in the liver)

113
Q

What tumours metastasize to the liver?

A 
"Some GU Cancers Produce Bumpy Lumps"
- Stomach
- GU (ovary, uterus, kidney)
- Colon (colorectal - MOST COMMON)
- Pancreas, prostate
- Breast
- Lung
(- Gallbladder
- Melanoma)
114
Q

Treatment of secondary malignant liver neoplasms

A
  1. Chemotherapy
  2. Metastectomy thru surgical resection/local treatment
    - hepatic resection of met colorectal liver mets is standard of care + chemotherapy
    - prognosis 30-60% at 5yr for colorectal mets
115
Q

What is acute viral hepatitis?

A

Viral hepatitis < 6mo duration

116
Q

Clinical features of acute viral hepatitis

A
  1. Flu-like prodrome may precede jaundice by 1-2wks
    - N/V, anorexia, headaches, fatigue, myalgia, low-grade fever, arthralgia, urticaria (especially Hep B)
  2. Only some progress to icteric (clinical jaundice) phase, lasting days-weeks
    - Pale stools + dark urine 1-5d prior to icteric phase
    - Hepatomegaly + RUQ pain
    - Splenomegaly + cervical lymphadenopathy (10-20% of cases)
117
Q

Investigations for acute viral hepatitis

A
  1. AST + ALT (> 10-20x normal in hepatocellular necrosis)
  2. ALP minimally elevated
  3. Viral serology, particularly IgM antibody directed to virus (Anti-HAV IgM, HbsAg, anti-HCV)
118
Q

What are the 3 diagnostic tests for viral hepatitis?

A
  1. Anti-HAV IgM
  2. HBsAg
  3. Anti-HCV
119
Q

Differential diagnoses of hepatomegaly

A
  1. Congestive (R heart failure, Budd-Chiari syndrome)
  2. Infiltrative (malignant - 1º/2º, leukemia; benign - fatty liver, cysts, hemochromatosis, amyloid)
  3. Proliferative (infectious - viral, TB, abscess, echinococcus; inflammatory - granulomas/sarcoid, histiocytosis X)
120
Q

Treatment for acute viral hepatitis

A
  1. Supportive (hydration, diet)
  2. Usually resolves spontaneously but if severe HBV infection, treatment with antiviral (tenofovir). Antiviral treatment should be considered in HCV
  3. Indications for hospitalization = encephalopathy, coagulopathy, severe vomiting, hypoglycemia
121
Q

Poor prognosis markers for acute viral hepatitis

A
  1. Comorbidities
  2. Persistently high bilirubin (>340mmol)
  3. Increased INR
  4. Decreased albumin
  5. Hypoglycemia
122
Q

Major sources of ALP (4)

A
  1. Hepatobiliary tree
  2. Bone
  3. Placenta
  4. Intestine
123
Q

Differentials for hepatitis (5)

A
  1. Viral infection
  2. Alcohol
  3. Drugs
  4. Immune-mediated
  5. Toxins
124
Q

Complications of acute viral hepatitis

A
  1. Cholestasis (most commonly associated with HAV infection)

2. Hepatocellular necrosis: AST, ALT > 10-20x normal, ALP and bilirubin minimally increased, increased cholestasis

125
Q

Describe Hepatitis A Virus infection

A
  1. RNA virus
  2. Fecal-oral transmission, incubation period 4-6wk
  3. Diagnosed by elevated transaminases, positive anti-HAV IgM
  4. In kids = typically asymptomatic
  5. In adults = fatigue, nausea, arthralgia, fever, jaundice, hepatomegaly
  6. Can cause acute liver failure + death (< 5%)
  7. Can relapse (rarely), but never becomes chronic
  8. Treatment is supportive (disease often self-limiting)
126
Q

Hepatitis B serology for acute HBV

A
  1. HBsAG +
  2. HBeAg +
  3. Anti-HBc IgM +
127
Q

Hepatitis B serology for chronic HBV (high HBV DNA)

A
  1. HBsAg +
  2. HBeAg +
  3. Anti-HBc IgG +
  4. ALT/AST may or may not be elevated
128
Q

Hepatitis B serology for chronic HBV (low HBV DNA)

A
  1. HBsAg +
  2. Anti-HBe +
  3. ANti-HBc IgG +
  4. ALT/AST may or may not be elevated
129
Q

Hepatitis B serology for resolved infection

A
  1. HBsAg -
  2. Anti-HBs ±
  3. Anti-HBe ±
  4. Anti-HBc IgG +
130
Q

Hepatitis B serology for immunization

A
  1. HBsAg -
  2. Anti-HBs +
  3. Anti-HBc -
131
Q

4 Phases of Chronic Hepatitis B

A
  1. Immune tolerance: extremely high HBV-DNA, HBeAg positive, but normal ALT/AST
  2. Immune clearance (immunoactive): as above
  3. Inactive carrier (immune control): lower HBV-DNA, HBeAg negative, anti-hue positive, ALT/AST normal
  4. HBeAg-negative chronic hepatitis (immune escape): elevated HBV-DNA (>2000), HbeAg negative b/c core promoter gene mutation, anti-hue positive, ALT/AST high
132
Q

Treatment for Hepatitis B

A
  1. Counselling
  2. Hepatocellular carcinoma screening USS every 6mo as higher risk of liver fibrosis
  3. Reduce serum HBV-DNA to undetectable levels
  4. Treatment options: interferon, tenofovir, entecavir
  5. Vaccinate against HAV if serology negative (to prevent further liver damage)
  6. Follow blood + sexual precautions
  7. Vaccinate household contacts
133
Q

What is the significance of hepatitis B and D coinfection?

A
  • Acute hepatitis B + HDV coinfection = increase severity of hepatitis but NOT progression to chronic hepatitis
  • Chronic hepatitis B + HDV coinfection= increases risk of progression to cirrhosis
134
Q

Describe HDV infection

A
  • Defective RNA virus requiring HBsAg for entry into hepatocyte, therefore only infects patients with HBV; causes more aggressive disease than HBV alone
  • Coinfection = acquire HDV + HBV at same time
  • HDV can present as acute liver failure ± accelerate progression to cirrhosis
  • Treatment = low-dose interferon + liver transplant for end-stage disease
135
Q

4 causes of elevated serum transaminases (AST/ALT) in chronic hepatitis B

A
  1. Active hepatitis
  2. Reactivation
  3. Hepatitis D
  4. Other liver insult (fatty liver, alcohol, drugs, hepatitis A)
136
Q

Risk factors for contracting Hepatitis B

A
  1. Infants born to hepatitis B-infected parent
  2. Unprotected sex
  3. Needle sharing
  4. Travel to endemic regions
  5. Exposure to human blood, semen, other bodily fluids
137
Q

Describe HCV infection

A
  • RNA virus (genotype 1 is most common in North America)
  • Blood-borne transmission; sexual transmission is ‘inefficient’
  • Major risk factor = injection drug use
  • Other risk factors: blood transfusion, tattoos, intranasal cocaine use
  • Clinical manifestation develops 6-8wks post exposure
138
Q

Clinical features of HCV infection

A
  1. Mild + vague symptoms (fatigue, malaise, nausea)

- Not commonly diagnosed in acute stage as a result

139
Q

Diagnosis of HCV infection

A
  1. Suspected on basis of elevated ALT/AST and positive serum anti-HCV
  2. Diagnosis established by detectable HCV-RNA in serum
  3. Virus genotype may guide treatment decisions
  4. Normal hepatocellular enzymes don’t rule out active disease/presence of advanced fibrosis
140
Q

Treatment for HCV infection

A
  1. Vaccinate HAV and HBV if serology negative; avoid alcohol

2. Oral interferon-free regimens (sofosbuvir) have > 90% success rates

141
Q

Risk factors for progression of hepatitis infection to cirrhosis

A
  1. Alcohol
  2. HIV coinfection
  3. Old age at diagnosis
142
Q

Prognosis of HCV infection

A
  • 80% of acute hepatitis C become chronic (20% of these evolve to cirrhosis)
  • Risk of hepatocellular carcinoma increases if cirrhotic
  • Can cause cyroglobulinemia; associated with membranoproliferazive glomerulonephritis
143
Q

Description of alcoholic liver disease

A
  • Spectrum of diseases ranging from:
    1. Fatty liver (common among individuals with alcohol-use disorder) = reversible if alcohol stopped
  1. Alcoholic hepatitis (35% of alcohol-use disorders) = usually reversible of alcohol stopped
  2. Cirrhosis (10-15% of alcohol-use disorders) = potentially irreversible
144
Q

Pathophysiology of alcoholic liver disease

A
  1. Ethanol oxidation to acetaldehyde (NAD+ to NADH, increase NADH decreases ATP supply to liver, impairing lipolysis so fatty acids + triglycerides accumulate in liver; binds to hepatocytes = immune reaction)
  2. Alcohol increases gut permeability leading to increased bacterial translocation
  3. Alcohol metabolism causes: relative hypoxia in liver zone 3 (near central veins; poorly oxygenated) > zone 1 (around portal tracts, where oxygenated blood enters) = necrosis + hepatic vein sclerosis
  4. Histology of alcoholic hepatitis (swollen hepatocytes containing Mallory bodies, surrounded by neutrophils; large fat globules; fibrosis: space of Disse + perivenular)
145
Q

Clinical features of alcoholic liver disease

A
  1. Fatty liver (mildly tender hepatomegaly + jaundice rare)
  2. Mildly increased transaminases < 5x normal
  3. Alcoholic hepatitis (mild to fatal liver failure; stops drinking b/c feels unwell, resumes when feeling better - findings of hepatitis, mild jaundice, elevated INR; severe = low grade fever, RUQ discomfort, WCC high mimics R lower lobe pneumonia + cholecystitis)
146
Q

Investigations for alcoholic liver disease

A
  1. AST: ALT > 2:1 (both usually < 300)
  2. FBC: increased MCV, increased WBC
  3. Increased GGT
147
Q

Treatment for alcoholic liver disease

A
  1. Alcohol cessation (disulfiram, acamprosate, naltrexone)
  2. Multivitamin supplements (thiamine)
  3. Caution wit drugs metabolized by liver
  4. Prednisolone if severe alcoholic hepatitis
148
Q

GI complications of alcohol use

A
  1. Mallory-Weiss tear
  2. Esophageal varices (2º to portal hypertension)
  3. Alcoholic gastritis
  4. Acute/chronic pancreatitis
  5. Alcoholic hepatitis
  6. Fatty liver
  7. Cirrhosis
  8. Hepatic encephalopathy
  9. Portal HTN
  10. Ascites
  11. Hepatocellular carcinoma
149
Q

Risk factors for pancreatic cancer

A
  1. Increased age
  2. Smoking: 2-5x increased risk
  3. High fat/low fibre diets
  4. Heavy alcohol use
  5. Obesity
  6. DM, chronic pancreatitis
  7. Partial gastrectomy
  8. Cholecystectomy
  9. Chemicals: b-naphthylamine, benzidine
  10. African descent
150
Q

Clinical features of pancreatic cancer

A
  1. Abdo pain
  2. Jaundice
  3. Weight loss
  • Head of pancreas (70%) = painless jaundice, steatorrhea, weight loss, anorexia/cachexia, dark urine, hepatomegaly, recent onset DM, Courvoisier’s sign
  • Body/tail of pancreas (30%) = presents later/inoperable, weight loss + vague mid-epigastric pain, < 10% jaundiced
151
Q

Investigations for pancreatic cancer

A
  1. LFTs may show obstructive jaundice (elevated ALP + bilirubin)
  2. CA 19-9 most useful serum marker
  3. USS, CT ± ERCP, MRI, endoscopic USS
152
Q

Types of pancreatic cancer

A
  1. Ductal adenocarcinoma (most common type; exocrine pancreas)
  2. Intraductal papillary mutinous neoplasm (IPMN)
  3. Pancreatic neuroendocrine tumours (non-functional, insulinoma, gastronome, VIPoma, glucagonoma, somatostatinoma)
  4. Mucinous cystic neoplasm
  5. Acinar cell carcinoma
153
Q

Treatment for pancreatic cancer

A
  1. Resectable (10-20%)
  2. Whipple procedure (pancreaticoduodenectomy)
  3. Adjuvant chemotherapy recommended
  4. Non-resectable = palliative –> relieve pain, obstruction
154
Q

Prognosis for pancreatic cancer

A
  • 5yr survival for all patients is 1%

- Following surgical resection 20%

155
Q

What structures are removed in a Whipple procedure?

A
  1. CBD
  2. Gallbladder
  3. Duodenum
  4. Pancreatic head
  5. Distal stomach
156
Q

Characteristics of insulinoma

A
  1. Tumour that secretes insulin
  2. Most common pancreatic endocrine neoplasm
  3. 10% associated with MEN1 syndrome
157
Q

Clinical features of insulinoma

A
  1. Whipple’s triad (symptomatic fasting hypoglycaemia, serum glucose < 2.8mmol/L, relief of symptoms when glucose is administered)
  2. Palpitations, trembling, diaphoresis, confusion, seizure, personality changes
158
Q

What is Whipple’s triad

A
  1. Symptomatic fasting hypoglycemia
  2. Serum glucose < 2.8mmol/L
  3. Relief of symptoms when glucose is administered
    - Symptoms of insulinoma
159
Q

Investigations for insulinoma

A
  1. Bloods: decreased serum glucose + increased serum insulin + C-peptide, pro-insulin
  2. CT, endoscopic USS, MRI: insulinomas evenly distributed thruout pancreas
160
Q

Treatment for insulinoma

A
  1. Only 10% are malignant
  2. Enucleation of solitary insulinomas endoscopically
  3. Tumours > 2cm located close to the pancreatic duct may require pancreatectomy/pancreaticoduodenectomy
161
Q

Characteristics of gastrinoma

A
  1. Tumour secreting gastrin
  2. Cause of Zollinger-Ellison syndrome
  3. Associated with MEN1
162
Q

Clinical features of gastrinoma

A
  1. Abdo pain
  2. Peptic ulcer disease
  3. Severe esophagitis
  4. Multiple ulcers in atypical locations refractory to antacid therapy
163
Q

Investigations for gastrinoma

A
  1. Bloods: serum gastrin levels, secretin stimulation test
  2. Endoscopy: 90% of patients develop peptic ulcers
  3. CT, endoscopic USS, MRI
  4. Somatostatin receptor scintigraphy scan
164
Q

Treatment for gastrinoma

A
  1. 50% are malignant
  2. Surgical resection depending on location
  3. Non-surgical = high-dose PPI, octreotide (somatostatin analogs)
  4. Radiation therapy for nonsurgical candidates
165
Q

What is Zollinger-Ellison syndrome?

A
  1. Characterised by gastric acid hypersecretion caused by secretion of gastrin from gastrinomas
  2. Patient experiences diarrhea, abdo pain, peptic disease + reflux disease
166
Q

Characteristics of Vasoactive intestinal peptide (VIP)-secreting tumour

A
  1. Tumour secreting VIP
  2. Commonly located in distal pancreas
  3. Most are malignant when diagnosed
167
Q

Clinical features of VIPoma

A
  1. Severe watery diarrhea causing dehydration, anorexia, weakness, electrolyte disturbance (hypoK)
168
Q

Investigations for VIPoma

A
  1. Bloods: serum VIP levels

2. CT, MRI, endoscopic USS

169
Q

Treatment for VIPoma

A
  1. Repletion of fluid and electrolytes
  2. Somatostatin analogues (octreotide)
  3. Surgical resection/palliative debulking
170
Q

Most common intra-abdominal organ injury from blunt trauma

A

Splenic trauma

171
Q

What is Kehr’s sign

A
  1. L shoulder pain due to diaphragmatic irritation from splenic rupture
  2. Worse on inspiration
172
Q

Treatment for splenic trauma

A
  1. Non-operative
    - extended bed rest with serial hematocrit levels, close monitoring for 3-5d; hemostatic control; splenic artery embolization if pt stable + a complication
  2. Operative
    - Splenorrhaphy (suture of plea)
    - Partial splenectomy (rarely performed due to recurrent hemorrhage risk)
    - Total splenectomy if pt unstable/high-grade injury
173
Q

What are the indications for splenectomy?

A

‘SHIRTS’

  • Splenic abscess/splenomegaly
  • Hereditary spherocytosis
  • Immune thrombocytopenia purpura
  • Rupture of spleen
  • Thrombotic thrombocytopenia purpura
  • Splenic vein thrombosis
174
Q

Complications of splenectomy

A
  • Short-term:
    1. Injury to surrounding structures + vascular supply
    2. Postoperative thrombocytosis/leukocytosis
    3. Thrombosis of portal, splenic, mesenteric veins
    4. Subphrenic abscess
  • Long-term:
    1. Post-spelectomy sepsis
    2. Splenosis: intra-abdo seeding of splenic tissue during removal
    3. Increased risk of malignancy, DVT, PE
175
Q

Pathophysiology of splenic infarct

A
  1. Splenic artery occlusion/O2 delivery insufficiency leading to parenchymal schema + necrosis
  2. Occurs in sickle cell disease, thromboembolism, myelofibrosis, CML, hyper coagulable states
  3. Pt can be asymptomatic, have LUQ pain (70%), N/V, fever, chills, and Kehr’s sign
176
Q

Treatment of splenic infarct

A
  1. Non-operative: close follow-up, analgesia

2. Indications for splenectomy: rupture, abscess, persistent pseudocyst, bleeding, sepsis

177
Q

5 signs of metastatic gastric carcinoma

A
  1. Virchow’s node = L supraclavicular node
  2. Blumer’s Shelf = Mass in pouch of Douglas
  3. Krukenberg Tumour: Mets in ovary
  4. Sister Mary Joseph Node: Umbilical mets
  5. Irish’s Node: L axillary nodes
178
Q

Risk factors for gastric carcinoma

A
  • Compensatory epithelial cell proliferation via gastric atrophy from:
    1. H pylori, causing chronic atrophic gastritis
    2. Pernicious anemia associated with achlorhydria + chronic atrophic gastritis
    3. Previous partial gastrectomy (>10y post-gastrectomy)
  • Lifestyle + environmental factors:
    1. Salt/salt-preserved food
    2. Obesity
    3. Cigarette smoking
    4. EBV infection
    5. Abdo radiation therapy
  • Host-related factors:
    1. Blood type A (also associated with pernicious anemia)
    2. HNPCC, Hereditary diffuse gastric carcinoma
    3. Gastric adenomatous polyps
    4. Hypertrophic gastropathy
    5. Genetic syndromes: hereditary diffuse gastric cancer (CDH1 gene)
179
Q

Clinical features of gastric carcinoma

A
  1. Ulcer fails to heal/lesion on greater curvature of stomach or cardia
  2. Posprandial abdo fullness, pseudoachalasia, vague epigastric pain
  3. Anorexia/weight loss
  4. Belching, N/V, dyspepsia, dysphagia
  5. Hepatomegaly, epigastric mass (25%)
  6. Hematemesis, fecal occult blood, melena, iron-deficiency anemia
180
Q

Where do gastric carcinomas spread to?

A
  1. Peritoneum
  2. Ovary
  3. Liver
  4. Lung
  5. Brain
181
Q

Investigations for gastric carcinoma

A
  1. Upper GI endoscopy + biopsy

2. CT chest/abdo/pelvis

182
Q

Treatment for gastric carcinoma

A
  1. Total gastrectomy + Roux-en-Y esophagojejunostomy
  2. Chemotherapy/chemoradiotherapy
  3. If lymphoma = H pylori eradication, chemo±radiotherapy, surgery in limited cases
183
Q

Characteristics of GI stromal tumour

A
  1. Most common mesenchymal neoplasm of GI tract
  2. Derived from intestinal cells of Cajal (cells that have autonomous pacemaker function coordinating peristalsis)
  3. Associated with tyrosine kinase mutations (c-KIT)
  4. Most common in stomach + proximal small intestine, but can occur anywhere along GI tract
184
Q

Risk factors for GI stromal tumour

A
  1. Vague abdo mass
  2. Abdo fullness
  3. Bleeding + anemia
  4. Non-specific symptoms (bloating, early satiety, abdo pain/discomfort)
  5. 50% cause occult/overt GI bleeding
185
Q

Investigations for GI stromal tumour

A
  1. Contrast-enhanced CT

2. Preoperative biopsy via endoscopic USS

186
Q

Treatment for GI stromal tumours

A
  1. Surgical resection if > 2cm
  2. Consider adjuvant treatment with Imatinib if high-risk of relapse
  3. Advanced disease = palliative intent chemo with imatinib
187
Q

Characteristics of Crohn’s Disease

A
  1. Chronic transmural inflammation that can affect ‘gum to bum’
  2. More common in White people and Ashkenazi Jews
  3. Smoking makes Crohn’s worse
188
Q

Pathology of Crohn’s disease

A
  1. Most common location = ileum + R colon
  2. Linear ulcers leading to mucosal islands and ‘cobblestone’ appearance
  3. Granulomas found in 50%
189
Q

Clinical features of Crohn’s disease

A
  1. Recurrent episodes of abdo cramps, non-bloody diarrhea, weight loss
  2. Ileilitis = post-prandial pain, vomiting, RLQ mass; mimics acute appendicitis
  3. Fistulae, fissures, abscesses common
  4. Deep fissures with risk of perforation into contiguous viscera
  5. Enteric fistulae may communicate with skin, bladder, vagina, other parts of bowel
190
Q

Investigations for Crohn’s Disease

A
  1. Colonscopy with biopsy to visualize
  2. CT/MRI enterogrpahy to visualize small bowel
  3. CRP elevated in most new cases
  4. Bacterial cultures, O&P, C. difficile toxin to exclude other causes of inflammatory diarrhea
191
Q

Management of Crohn’s Disease

A
  1. Nutrition, symptomatic therapy (loperamide, acetaminophen)
  2. 5-ASA (mesalamine, sulfasalazine); Antibiotics (metronidazole, ciprofloxacin)
  3. Corticosteroids (predinosolone, budesonide, IV methylpredinosolone if severe)
  4. Immunosuppression (azathioprine, methotrexate)
  5. Immunomodulators (TNF-antagonists: infliximab, adalimumab)
  6. Experimental therapy or surgery
192
Q

Complications of Crohn’s Disease

A
  1. Intestinal obstruction/perforation
  2. Fistula formation
  3. Malignancy (lower risk compared to UC)
  • Surveillance colonoscopy same as UC if more than 1/3 colon involved *
193
Q

Pathophysiology findings of Crohn’s disease

A
  1. Cobblestoning on mucosal surface due to oedema and linear ulcerations
  2. Skip lesions: normal mucosa in between
  3. Creeping fat: mesentery infiltrated by fat
  4. Granulomas:25-30%
194
Q

3 Major patterns of Crohn’s presentations

A
  1. Ileocecal 40% (RLQ pain, fever, weight loss)
  2. Small intestine 30% (especially terminal ileum)
  3. Colon 25% (diarrhea)
195
Q

Causes of constipation

A

‘DOPED’

  • Drugs (narcotics, antidepressants)
  • Obstruction (L sided colon cancer, fecal impaction)
  • Pain
  • Endocrine dysfunction (DM, hypothyroidism, hypercalcemia, hypokalemia, uremia)
  • Depression
  • Neurological (intestinal pseodo-obstruction, PD, MS)
  • Collagen vascular disease (scleroderma)
  • Painful anal conditions (fissures)
196
Q

Clinical definition of constipation

A

< 3 bowel movements/week

197
Q

Investigations for constipation

A
  1. FBC, TSH, calcium, glucose
  2. Abdo XR
  3. Colon visualisation (colonoscopy) if concomitant symptoms such as rectal bleeding, weight loss, anemia, age > 50y
198
Q

Treatment for constipation (7)

A
  1. Dietary fibre (30g/d increase dose slowly)
  2. Surface-acting (decussate salts, mineral oils)
  3. Osmotic agents - effective in 2-3d (Movicol, lactulose, magnesium salts)
  4. Stimulants - effective in 24h (Senna, bisacodyl)
  5. Enemas + suppositories (phosphate enema)
  6. Prokinetic agents (prucalopride)
  7. Linaclotide (secretagogue, increases water secretion into intestinal lumen)
199
Q

Clinical features of appendicitis

A
  1. Low-grade fever, rises if perforation
  2. Abdo pain, then anorexia, then N/V
  3. Classic pattern = pain initially periumbilical, constant, dull, poorly localized, then well localized pain over McBurney’s point
200
Q

Signs of appendicitis

A
  1. McBurney’s sign (tenderness 1/3 the distance from ASIS to umbilicus on the R side)
  2. Rovsing’s sign (palpation pressure in LLQ causes McBurney’s point tendnerness)
  3. Psoas sign (pain on flexion of hip against resistance or passive hyperextension of hip)
  4. Obturator sign (flexion then external/internal rotation of R hip causes pain)
201
Q

Complications of appendicitis

A
  1. Perforation (esp if > 24h in duration)
  2. Abscess, phlegmon
  3. Sepsis
202
Q

Investigations for appendicitis

A
  1. Bloods (mild leukocytosis with L shift, higher leukocyte count with perforation, b-hCG to rule out ectopic pregnancy)
  2. Urinalysis
  3. USS
  4. CT scan
203
Q

Characteristics of intussusception

A
  1. Most common cause of bowel obstruction between 6-36mo

2. Telescoping of bowel into itself causing obstruction + vascular compromise

204
Q

Risk factors for intussusception

A
  1. Enlarged Peyer’s patches due to viral infection of GI tract
  2. MEckel’s diverticulum
  3. CF
  4. Lymphoma
  5. IBD
205
Q

Clinical features of intussusception

A
  1. Acute onset abdo pain, episodic ‘colicky’ pain
  2. Vomiting ± bilious
  3. Abdo mass (sausage shaped upper abdo mass)
  4. Currant-jelly stool suggests mucosal necrosis + sloughing
  5. Distended abdomen
  6. Localized peritonitis = transmural ischemia
206
Q

Investigations for intussusception

A
  1. AXR for signs of bowel obstruction/perforation

2. USS

207
Q

Treatment for intussusception

A
  1. If peritonitis = operative
  2. No peritonitis = reduction via air contrast enema
  3. Resection of involved colon if failure to reduce/bowel appears compromised
208
Q

2 familial colon cancer syndromes

A
  1. Familial adenomatous polyposis

2. Hereditary non-polyposis colorectal cancer (Lynch syndrome)

209
Q

Characteristics of familial adenomatous polyposis

A
  1. Autosomal dominant inheritance, mutation in APC gene
  2. 100-1000s of colorectal adenomas usually by age 20
  3. 100% lifetime risk of colon cancer (due to # of polyps)
210
Q

Clinical features of familial adenomatous polyposis

A
  1. Extracolonic manifestations:
    - Bile duct, pancreas, stomach, thyroid, adrenal glands, small bowel
  2. Variants
    - Gardner’s syndrome: FAP + extra-intestinal lesions
  3. Turcot syndrome: FAP + CNS tumours (childhood cerebellar medulloblastoma)
211
Q

Investigations for familial adenomatous polyposis

A
  1. Genetic testing
  2. If no polyposis found: annual flexible sigmoidoscopy from puberty to age 50, then routine screening
  3. If polyposis/APC gene mutation found: annual colonoscopy, consider surgery, consider upper endoscopy evaluating for periampullary tumours
212
Q

Treatment for familial adenomatous polyposis

A
  1. Surgery indicated by age 17-20
  2. Total proctocolectomy with ileostomy or total colectomy with ileorectal anastamosis
  3. Doxorubicin-based chemo
  4. NSAIDs for intra-abdominal desmoids
213
Q

Characteristics of HNPCC (Lynch syndrome)

A
  1. Autosomal dominant inheritance, mutation in DNA mismatch repair gene resulting in microsatellite genomic instability and subsequent mutations
  2. Microsatellite instability account for approx 15% of all colorectal cancers
214
Q

Clinical features of HNPCC

A
  1. Early age of onset, right > left colon, synchronous and metachronous lesions
  2. 70-80% lifetime risk of cancer
  • HNPCC 1 = hereditary site-specific colon cancer
  • HNPCC 2 = cancer family syndrome -> high rates of extracolonic tumours (endometrial, ovarian, hepatobiliary, small bowel)
215
Q

Diagnosis criteria of HNPCC

A
  1. Amsterdam Criteria (‘3-2-1 rule’)
    - 3 or more relatives with verified Lynch syndrome associated cancers, and 1 must be 1st degree relative of the other 2
    - 2 or more generations involved
    - 1 case must be diagnosed before 50y
  2. Genetic testing
  3. Colonoscopy (starting at age 20) annually
  4. Surveillance for exracolonic lesions
216
Q

Treatment for HNPCC

A

Total colectomy and ileorectal anastomosis with annual proctoscopy

217
Q

Risk factors for colorectal carcinoma

A
  1. Most have no specific risk factors
  2. Age > 50
  3. Genetic: FAP, HNPCC, family history of CRC
  4. Colonic conditions (adenomatous polyps, IBD - especially UC, previous CRC/gonadal/breast cancer)
  5. Diet (increased fat, red meat, decreased fibre)
  6. Smoking
  7. Diabetes + acromegaly (insulin + IGF1 are growth factors for colonic mucosal cells)
218
Q

Clinical features of colorectal carcinoma

A
  1. Hematochezia/melena
  2. Abdo pain
  3. Change in bowel habits
  4. Weakness, anemia, weight loss, palpable mass, obstruction
219
Q

Sites for colorectal carcinoma mets

A
  1. Liver (most common)
  2. Lung
  3. Bone
  4. Brain
  5. Tumour of distal rectum -> IVC -> lungs
  6. Peritoneal seeding: ovary + Blumer’s shelf (pelvic cul-de-sac)
220
Q

Clinical features of right colon CRC

A
  1. 25% of cases
  2. Weight loss, weakness, rarely obstruction
  3. Iron deficiency anemia, RLQ mass (10%)
  4. Exophytic lesions with occult bleeding
221
Q

Clinical features of left colon CRC

A
  1. 35% of cases
  2. Annular, invasive lesions
  3. Constipation ± overflow (alternating bowel patterns), abdo pain, decreased stool calibre, rectal bleeding
  4. Bright red blood per rectum, large bowel obstruction
222
Q

Clinical features of rectum CRC

A
  1. 30% of cases
  2. Ulcerating pathology
  3. Obstruction, tenesmus, rectal bleeding
  4. Palpable mass on DRE, BRBPR
223
Q

Investigations for colorectal carcinoma

A
  1. Colonoscopy (gold standard): look for synchronous lesions
  2. Bloods: FBC, urinalysis, LFTs, CEA (> 5ng/mL have worse prognosis)
  3. Staging: CT chest/abdo/pelvis, bone scan, CT head
  4. Rectal cancer: MRI or endorectal USS to stage
224
Q

Treatment for colorectal carcinoma

A
  1. Wide surgical resection of lesion according to vascular distribution and regional lymphatic drainage; usually colectomy with primary anastomosis
  2. Curative = wide resection of lesion (5cm margins) with nodes (>12) + mesentery
  3. Adjuvant chemotherapy (oxaliplatin-based) for stage 3 and select stage 2 patients
225
Q

What is follow up like for colorectal carcinoma

A

Stage 1 = mixed recommendations; either routine colonscopy or screening like stage 2+3

Stage 2+3: Regular follow-up every 3-6mo for 3yr; then every 6mo until 5yr, with regular measurement of serum CEA for at least 3yr. Annual CT abdo/pelvis/chest for at least 3yr; colonoscopy at 1, 3 and 5yr

Stage 4: no data on surveillance strategy

MCCQE Prep (4 decks)

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