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6th Year > GI & Liver > Flashcards

GI & Liver Flashcards

1
Q

What is acute cholangitis & what are the common risk factors?

A

= inflammation & infection of the biliary tree which is a surgical emergency.
- Most common:
- Gallstones → obstructing bile outflow
- ERCP → infection introduced

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2
Q

What are the most common causative organisms for acute cholangitis?

A
  • E.coli
  • Klebsiella species
  • Enterococcus species
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3
Q

How does acute cholangitis present?

A
  • Charcot’s triad
    • Fever
    • RUQ pain
    • Jaundice
  • Pruritis
  • Pale stools
  • Dark urine
  • Nausea & vomiting
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4
Q

What imaging is done for suspected acute cholangitis?

A
  • Transabdominal USS → may show gallstones, common bile duct stones, and a dilated common bile duct.
  • CT abdomen → used if USS negative and high clinical suspicion.
    • Non-calcified stones will not be visible on CT
    • If secondary to malignancy can be useful for assessing tumour.
  • MRCP (Magnetic Resonance Cholangiopancreatography) → biliary specific MRI
  • ERCP (endoscopic retrograde cholangiopancreatography)
    • Gold standard investigation & intervention for acute cholangitis.
    • Invasive & high risk → acute pancreatitis & severe haemorrhage are important risks.
    • Several interventions can be done, including stone extraction and stent placement
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5
Q

What causes acute cholecystitis?

A
  • Gallstones -> obstruction of bile flow
  • Acalculous -> dysfunction of gallbladder emptying
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6
Q

How does acute cholecystitis present?

A
  • Right upper quadrant pain
    • Often begins as an attack of biliary colic, but it worsens over hours.
    • As the parietal peritoneum around the gallbladder becomes inflamed, the pain becomes sharper, more localised, and is exacerbated by movement.
    • Radiates to right shoulder → due to irritation of the phrenic nerve.
  • Fever
  • Nausea & vomiting
  • Murphy’s Sign → absence of this does not rule out acute cholecystitis
  • Tachycardic
  • Voluntary guarding
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7
Q

What are the changes seen on abdominal USS during acute cholecystitis?

A
  • Thick-walled gallbladder (>3mm)
  • Impacted gallstones
  • Pericholecystic fluid
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8
Q

How is acute cholecystitis managed?

A
  • Hospital admission
  • Conservative management
    • Nil by mouth → clear oral fluids
    • IV fluids
    • Antibiotics
    • Analgesia
  • Interventions
    • ERCP → if there are gallstones trapped in the common bile duct.
    • Emergency cholecystostomy → within 72hrs of symptom onset
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9
Q

What increases the risk of developing gallstones?

A
  • Increase in concentration of solutes
    • High cholesterol or bilirubin levels
    • Generalised overconcentration of bile due to dehydration
  • Bile stasis
    • Mechanical obstruction → stents, strictures, tumours
    • Functional impairment → oestrogen & progesterone impair gallbladder emptying
  • Infection causing bile pigment sludge
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10
Q

What is the gold-standard investigation for biliary colic, and what does it show?

A

Abdominal USS → gold standard, will show gallstones in a thin-walled gallbladder

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11
Q

How does biliary colic present?

A
  • Sudden onset, severe RUQ or epigastric pain → can radiate to lower chest, back, or right shoulder
    • Lasts about up to 6-8hrs
    • Dull & constant, occasional waves of more intense pain.
    • Triggered by fatty or spicy foods, with the pain starting a few hours after eating
  • Autonomic symptoms → nausea, vomiting, sweating, palpitations
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12
Q

What advise/management is given for biliary colic?

A
  • Self-limiting
  • Analgesia & follow-up USS
  • Sticking to clear fluids until symptoms resolve can reduce risk of spasms
  • Lifestyle changes → low-fat diet, gradual weight loss, avoidance of trigger foods
  • Elective laparoscopic cholecystectomy if severe or patient would like
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13
Q

What are the most common causes of chronic pancreatitis?

A
  • Chronic alcohol excess (key one to remember)
  • Cystic fibrosis
  • Pancreatic cancer
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14
Q

What are the symptoms of chronic pancreatitis?

A
  • Chronic epigastric pain → worse after eating fatty food (15-30mins after) and relieved by sitting forward.
  • Bloating
  • Weight loss
  • Symptoms of exocrine dysfunction → malabsorption, steatorrhoea
  • Symptoms of endocrine dysfunction → thirst, polyuria
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15
Q

How is chronic pancreatitis managed?

A

Conservative:

  • Stop drinking alcohol & smoking
  • Eat a healthy diet

Medical:

  • Analgesia
  • Replacement of pancreatic enzymes (Creon)
  • Subcutaneous insulin regimes to treat diabetes

Surgical:

  • ERCP with stenting
  • Surgery if severe
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16
Q

What are the 3 most common causes of acute pancreatitis?

A
  • gallstones
  • alcohol
  • post-ERCP
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17
Q

How does acute pancreatitis present?

A

Symptoms:

  • Epigastric pain → sudden, severe, may radiate to back
  • Nausea & vomiting
  • Decreased appetite
  • Abdominal tenderness
  • Systemically unwell → low-grade fever, tachycardia

Signs:

  • Epigastric tenderness
  • Abdominal distension
  • Reduced bowel sounds if an ileus has developed
  • Evidence of systemic inflammatory response.
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18
Q

How is acute pancreatitis managed?

A

Immediate:

  • Hospital admission
  • A-E assessment for initial resuscitation.
  • IV fluids
  • Nil by mouth until pain improves
  • Analgesia → IV paracetamol & opioids
  • Anti-emetics
  • Control of BMs

NB → do not routinely give antibiotics unless there is a specific indication.

Manage Underlying Cause:

  • Gallstones
    • ERCP
    • Cholecystectomy
  • Alcohol
    • Patients withdrawing from alcohol should be managed according to severity scores, such as CIWA.
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19
Q

What are the risk factors for peptic ulcers?

A
  • Disruption to mucus barrier
    • H.pylori
    • NSAIDs
  • Increase stomach acid
    • Stress
    • Alcohol
    • Caffeine
    • Smoking
    • Spicy foods
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20
Q

How does the pain differ on presentation of gastric vs duodenal ulcers?

A
  • Epigastric discomfort or pain
    • Gastric ulcers → pain worse on eating
    • Duodenal ulcers → pain improves on eating, followed by pain 2-3 hours later
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21
Q

How are peptic ulcers diagnosed?

A
  • Diagnosed on endoscopy
  • Rapid urease test can be performed to check for H.pylori.
  • Biopsy is considered to exclude malignancy
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22
Q

How does pancreatic cancer present?

A
  • Painless obstructive jaundice → usually due to a tumour in the head or neck of the pancreas compressing the common bile duct.
    • Yellowing of skin or sclera
    • Dark urine
    • Pale stools
    • Generalised itching
  • Non-specific upper abdominal or back pain
  • Unintentional weight loss
  • Change in bowel habit
  • New-onset diabetes or worsening of type 2 diabetes.
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23
Q

What is a specific blood test used for suspected pancreatic cancer?

A

CA19-9

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24
Q

How will hepatitis present on LFTs?

A
  • LFTs will show a hepatic picture
    • High transaminases → AST/ALT
    • Proportionately less of a rise in ALP
    • Bilirubin may rise due to inflammation of the liver cells.
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25
Q

What is Primary Biliary Cholangitis?

A

= an autoimmune condition where the intrahepatic bile ducts are attacked, resulting in obstructive jaundice & liver disease.

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26
Q

How does someone present with primary biliary cholangitis?

A
  • Typical patient is a caucasian woman aged 40-60 years.
  • Often patients are asymptomatic at diagnosis, and picked up on LFT testing.
  • Fatigue
  • Pruritis → accumulation of bile acids
  • GI symptoms & abdominal pain → due to lack of bile acids helping with fat digestion.
  • Jaundice
  • Pale, greasy stools → malabsorption of fat
  • Dark urine
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27
Q

What is the key investigation to remember when suspecting primary biliary cholangitis?

A

Anti-mitochondrial antibodies (AMA) are positive in >90% of individuals

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28
Q

How is primary biliary cholangitis managed?

A
  • Ursodeoxycholic acid → non-toxic, hydrophilic bile acid that protects cholangiocytes from inflammation and damage.
    • Slows disease progression & improves outcomes
    • Key treatment.
  • Colestyramine → for symptoms of pruritis, reduces intestinal absorption of bile acids
  • Immunosuppression in some patients.
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29
Q

What is primary sclerosing cholangitis?

A

= a condition where the intrahepatic & extrahepatic bile ducts become inflamed & damaged, developing strictures that obstruct bile flow out of the liver.

  • Chronic bile obstruction eventually leads to liver inflammation, fibrosis, and cirrhosis.
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30
Q

What are 4 risk factors for primary sclerosing cholangitis?

A
  • Male
  • Aged 30-40
  • Ulcerative colitis → strong association, with 70% of cases occuring in people with UC.
  • Family history
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31
Q

If symptomatic, how does primary sclerosing cholangitis present?

A
  • Abdominal pain in RUQ
  • Fatigue
  • Jaundice
  • Hepatomegaly
  • Splenomegaly
32
Q

What is the diagnostic investigation for primary sclerosing cholangitis?

What other investigations are done?

A
  • MRCP → diagnostic imaging investigation, shows bile duct strictures
  • LFTs cholestatic pattern → raised ALP
  • No autoantibodies are helpful for diagnosis.
  • Colonoscopy → should be performed for UC
  • Liver biopsy → not usually required, but useful if there is diagnostic uncertainty.
33
Q

How is primary sclerosing cholangitis managed?

A
  • No proven effective treatments.
  • ERCP → dilation of dominant strictures, and stents can be inserted.
  • Colestyramine → for pruritis
  • Replacement of fat-soluble vitamins
  • Liver transplant in advanced disease
  • Monitoring for complications → cholangiocarcinoma, cirrhosis, oesophageal varices.
34
Q

What are the risk factors for diverticulitis?

A
  • Older age
  • Low fibre diet
  • Smoking
  • Obesity
  • Medication → NSAIDs & opioids
35
Q

How is uncomplicated diverticulitis managed?

A
  • Oral co-amoxiclav
  • Analgesia
  • Only taking clear fluids until symptoms improve → usually in 2-3 days
  • Follow-up
36
Q

How is complicated diverticulitis managed?

A
  • Hospital admission
  • IV fluids
  • IV antibiotics
  • Nil by mouth
  • Analgesia
  • Urgent CT scan
  • If fistula or persistent abscess → laparoscopic resection
  • If faeculant peritonitis → colonic resection
37
Q

What are some causes of hernias?

A
  • Increased intra-abdominal pressure:
    • Chronic cough → COPD, bronchiectasis, cystic fibrosis
    • Abdominal distension → pregnancy, obesity
    • Straining → chronic constipation, heavy lifting during work or exercise
  • Weakened tissues
    • Trauma → such as surgery
    • Ageing
    • Chronic malnutrition
    • Collagen disorders
    • Congenital defects
38
Q

What are the two types of inguinal hernia?

A
  • Indirect → where bowel herniates through the inguinal canal
    • Normally after the testes descend through the inguinal canal, the deep inguinal ring closes, however sometimes this ring remains patent, leaving a tunnel.
  • Direct → due to weakness in the abdominal wall at Hesselbach’s triangle.
39
Q

How are the common hernias managed?

A

Inguinal, umbilical, epigastric - low risk of complications:
- If small & unbothersome then leave alone → low risk of obstruction or strangulation
- Mesh repair → gold standard.

Femoral:
- Always repaired due to high risk
- Laparoscopic mesh repair

40
Q

What is a hiatus hernia and how is it managed?

A

= herniation of the stomach up through the diaphragm.
- Medical → for GORD
- Surgical → laparoscopic fundoplication

41
Q

How does an anal fissure present?

A
  • Anal pain always occurs when passing stool
    • Severe, sharp, often followed by deep burning pain that lasts several hours.
  • Bleeding with defecation → seen on stool or toilet paper
  • Tearing sensation on passing stool
  • Can be acute or chronic
    • Acute → <6 weeks
    • Chronic → > 6 weeks
  • If presenting acutely with an abscess → rapid onset of perianal pain & swelling, often with systemic features such as fever or tachycardia.
42
Q

What is the most common type of colorectal cancer?

A

Adenocarcinoma

43
Q

How is suspected colorectal cancer investigated?

A
  • FIT
    • Faecal immunochemical tests
    • Looks for human Hb in the stool
    • Can be used as a test in primary care for those who do not meet the criteria for a 2 week referral.
    • Used in the bowel cancer screening programme.
  • CEA
    • Carcinoembryonic antigen
    • Not used for screening or testing, more for monitoring treatment & disease progression
  • Colonoscopy
    • Gold standard investigation
    • Any suspicious lesions are biopsied
  • CT colonography
    • CT scan with bowel prep & contrast to visualise the colon in more detail
    • Used if patient isn’t fit for colonoscopy but means you can’t biopsy any lesions.
  • Staging CT CAP
44
Q

How is Barrett’s Oesophagus managed?

A
  • Endoscopic surveillance for signs of progression.
  • PPIs → high dose, long term
  • Endoscopic ablation
45
Q

How does oesophageal cancer present?

A
  • Progressive dysphagia → initially for solids, later for liquids
    • Occurs when there is obstruction of 2/3s of the lumen
  • Hoarseness if local invasion of recurrent laryngeal nerve.
  • Appetite loss
  • Weight loss
  • Dyspepsia → treatment resistant
  • Reflux
  • Haematemesis
46
Q

What are the risk factors for oesophageal cancer?

A
  • Smoking
  • High alcohol intake
  • Obesity
  • GORD → Barrett’s Oesophagus
  • Achalasia
  • High intake of hot beverages
47
Q

What antibodies are tested for in coeliac disease?

A
  • Anti-tissue transglutaminase antibodies (Anti-TTG)
  • Total IgA level → to exclude IgA deficiency giving a false negative
48
Q

How does peritonitis present?

A
  • Severe abdominal pain → lying still as movement worsens the pain
  • Systemic signs of illness → fever, haemodynamic instability
  • Nausea & vomiting
  • Abdominal rigidity/involuntary abdominal guarding → involuntary tensing of abs in response to pressure on the abdomen
  • Rebound tenderness → pressure on the abdomen elicits less pain than releasing the hand
49
Q

What is the standard order in which laxatives are advised for constipation?

A
  1. Bulk-forming laxative
  2. Macrogol (laxido) → add or switch to if still symptomatic
  3. Stimulant laxative if stools are soft but difficult to pass, or feeling of incomplete emptying (short term use)
50
Q

What is the drug name of a bulking agent used for constipation? How does it work, and what are the contraindications?

A

Ispaghula husk.
- helpful in people unable to increase dietary fibre.
- need to increase fluid intake to reduce risk of obstruction.
- Increases faecal mass with soluble fibre, which stimulates peristalsis.
- Contraindicated: Faecal impaction, intestinal obstruction, reduced gut motility

51
Q

How do haemorrhoids present?

A
  • Painless, bright red bleeding → seen on toilet paper
    • Can become painful if the haemorrhoid thromboses.
  • Palpable lump in or around the anus
  • Peri-anal itch
  • Often with associated constipation & straining.
  • Tenesmus → feeling of fullness or incomplete defaecation
52
Q

What is Rigler’s Sign?

A

When gas is seen on both sides of the bowel wall on abdominal x-ray, indicating a pneumoperitoneum.

53
Q

What medication is given for diarrhoea in those with IBS?

A

Loperamide

54
Q

What medication is given for constipation in those with IBS?

A

Bulk-forming laxative - ispaghula husk

55
Q

How does an ileus present?

A

Symptoms:

  • Vomiting → green bilious vomiting
  • Abdominal distention
  • Absolute constipation & lack of flatulence

Signs

  • Absent bowel sounds → opposed to the tinkling bowel sounds of mechanical obstruction
  • Diffuse abdominal pain
56
Q

How is an ileus managed?

A
  • NBM or limiting sips of water
  • IV fluids
  • NG tube if vomiting
  • Mobilisation to help stimulate peristalsis
  • Use non-opioid analgesia
57
Q

What is liver cirrhosis?

A

= liver disease that is the result of chronic inflammation & damage to hepatocytes. There is widespread disruption of normal liver structure, which becomes distorted with regenerative nodules surrounded by diffuse fibrosis.

58
Q

What is decompensated liver cirrhosis?

A
  • the largely symptomatic phase of cirrhosis when the liver is damaged, affecting its function, with potentially life-threatening complications such as jaundice, ascites, hepatic encephalopathy, and variceal bleeding.
    • Due to portal hypertension and/or hepatocellular dysfunction.
59
Q

What are the 4 common causes of liver cirrhosis?

A
  • Alcohol-related liver disease
    • > 50 units of alcohol per week in men, >35 in women, for at least several months.
  • Non-alcoholic fatty liver disease
  • Hepatitis B
  • Hepatitis C
60
Q

What changes are seen in cirrhosis during a liver ultrasound scan?

A

nodularity of surface, corkscrew appearance of hepatic arteries (with increased flow as they compensate for reduced portal flow), enlarged portal vein, Ascites, Splenomegaly

61
Q

What are the complications of liver cirrhosis?

A
  • Malnutrition
  • Portal hypertension & varices
  • Ascites & spontaneous bacterial peritonitis
  • Hepatorenal syndrome
  • Hepatic encephalopathy
  • Hepatocellular carcinoma
62
Q

What is given prophylactically for oesophageal varices?

A
  • Propranolol → first line, non-selective beta-blocker
  • Variceal band ligation → if propranolol contraindicated
63
Q

How are bleeding oesophageal varices managed?

A
  • 2222, major haemorrhage protocol
  • Vasopressin analogue → terlipressin, causes vasoconstriction
  • Prophylactic broad spectrum antibiotics
  • Urgent endoscopy with variceal band ligation
  • Sengstaken-blackemore tube
  • Consider intubation & intensive care
64
Q

How are ascites due to liver cirrhosis managed?

A
  • Low sodium diet
  • Aldosterone antagonists → spironolactone
  • Paracentesis
  • Prophylactic antibiotics
65
Q

How is hepatic encephalopathy managed?

A
  • Lactulose → reduces the intestinal production & absorption of ammonia. Aim for 2-3 soft stools daily
  • Antibiotics → reduce the number of intestinal bacterial producing ammonia
  • Nutritional support
66
Q

What are the stages of alcohol-related liver disease?

A
  1. Hepatic Steatosis → drinking leads to the build up of fat in the liver. This is reversible with abstinence
  2. Alcoholic Hepatitis → drinking over a long period or binge drinking causes inflammation in the liver cells. Mild hepatitis is usually reversible with permanent abstinence.
  3. Cirrhosis → where functional liver tissue is replaced with scar tissue, this is irreversible. Abstinence can prevent further damage.
67
Q

What are the stages of NAFLD?

A
  1. Non-alcoholic fatty liver disease
  2. Non-alcoholic steatohepatitis
  3. Fibrosis
  4. Cirrhosis
68
Q

What are the key investigations in NAFLD?

A
  • Raised ALT → often the first indication that a patient has NAFLD
  • Liver USS → confirms diagnosis of hepatic steatosis, seen as increased echogenicity
  • Enhanced liver fibrosis blood test → first line investigation for assessing fibrosis in NAFLD
  • Liver biopsy- confirms diagnosis & excludes other causes of liver disease
69
Q

What does a coffee bean sign on abdominal x-ray indicate?

A

Sigmoid volvulus

70
Q

What are the 4 key symptoms in bowel obstruction?

A
  • Vomiting → green bilious
  • Abdominal distention
  • Diffuse abdominal pain → severe, colicky
  • Absolute constipation & lack of flatulence
71
Q

How is a volvulus managed?

A
  • NBM, NG tube, IV fluids
  • Conservative → endoscopic decompression
  • Surgical → laparotomy, Hartmann’s, hemicolectomy
72
Q

What are the 3 most common causes of bowel obstruction?

A
  • Adhesions
  • Hernias
  • Malignancy
73
Q

What are the differing features of UC & Crohns on endoscopy & histology

A

Crohns:
- Entire GI tract affected, most commonly in the terminal ileum.
- Skip lesions on endoscopy, transmural inflammation

Ulcerative Colitis:
- Limited to the colon & rectum
- Continuous inflammation, only affecting the superficial mucosa. Crypt abscess

74
Q

How is Crohn’s Disease managed?

A
  • Inducing remission
    • Steroids → prednisolone (1st line)
    • Enteral nutrition → particularly when there are concerns about steroids affecting growth.
    • If steroids inadequate, other medications can be considered → azathioprine, methotrexate
  • Maintaining remission
    • Azathioprine or mercaptopurine (1st line)
    • Methotrexate
    • Surgery → resection of distal ileum if disease isolated to this area, treat strictures & fistulas
75
Q
A

6th Year (11 decks)

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