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A case of abdominal pain Flashcards

1
Q

What is acute abdominal pain?

A

The rapid onset of severe symptoms that may indicate potentially life-threatening intra-abdominal pathology that requires urgent surgical intervention

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2
Q

Why was narcotic analgesia in undiagnosed patients with acute abdomen discouraged?

A

Because of concerns that the symptoms would be masked, examination hindered and therefore the correct diagnosis missed

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3
Q

Why is fentanyl a good narcotic analgesic to use?

A

Because of its potency and short half-life

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4
Q

Why are older people more at risk of severe disease?

A

Due to decreased immune function

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5
Q

How does the central and peripheral nervous system of older people affect their diagnosis?

A

CNS and PNS are reduced with ageing, PNS degradation can affect pain and temperature perception

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6
Q

Why is it difficult to localise abdominal pain in pregnant women?

A

Enlargement of the uterus displacing and compressing abdominal organs and the laxity of the abdominal wall makes it difficult to localise pain

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7
Q

What are the abdominal sources of acute abdomen?

A
  • Intestinal obstruction
  • Peritonitis secondary to infection
  • Haemorrhage
  • Ischaemia
  • Processes associated with contamination by GI contents
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8
Q

What’s an incarcerated hernia?

A

When the hernia formed becomes trapped in tissue and can’t escape

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9
Q

What are the main causes of abdominal obstruction?

A
  1. Adhesions
  2. Incarcerated hernias
  3. Volvulus, gallstones, intussusception
  4. Congenital anatomical abnormalities, GI neoplasm, IBD
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10
Q

What are the inflammatory causes of acute abdomen?

A

Cholecystitis, appendicitis, acute pancreatitis, acute diverticulitis and Meckel diverticulitis

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11
Q

What’s a hemoperitoneum?

A

The presence of blood in the peritoneal cavity

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12
Q

How would patients with a ruptured abdominal aortic aneurysm present?

A

Abdominal pain radiating through to the back and a pulsatile abdominal mass

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13
Q

What are the thoracic causes of epigastric pain?

A

Lower lobe pneumonias, MI, aortic dissection

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14
Q

Abdominal causes of epigastric pain?

A

Acute viral hepatitis, paracetamol overdose, cholecystitis, pancreatitis (radiating to the back), gastritis, peptic ulcer (perforated= acute pain), gastroenteritis (food poisoning), DKA, electrolyte abnormalities, led toxicity or other types of poisoning

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15
Q

Who should be informed if a patient contracts food poisoning?

A

Public health england

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16
Q

What is biliary colic?

A

Pain caused by gallbladder muscle contractions against a stone not big enough to cause obstruction that’s stuck in the neck of the gallbladder or in the cystic duct- there’s no inflammatory response

Bloods should be normal due to no inflammation or infection

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17
Q

What is cholecystitis?

A

Inflammation of the gall bladder

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18
Q

What is ascending cholangitis?

A

Biliary outflow obstruction with added infection

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19
Q

What are the symptoms of biliary colic?

A

Dull, upper right quadrant pain, nausia or vomiting, symptoms last for less than 6 hours- pain is constant

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20
Q

What are symptoms of biliary colic triggered by?

A

Fatty foods- fat stimulates cholecystokinin relase

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21
Q

What’s the function of cholecystokinin?

A

Induces the contraction of the gall bladder, relaxes the sphincter of oddi, increases bile acid production in the liver, delays gastric emptying and induces pancreatic enzyme production

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22
Q

What’s the sphincter of oddi?

A

The sphincter between the common bile duct and duodenum

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23
Q

What are the symptoms of cholecystitis?

A

Severe constant right hypochondriac or epigastric pain, nausia and vomiting, murphy’s sign (hand under the right costal margin- patient inspires and gall bladder hits the edge of fingers causing worsened patient pain), temperature and tachycardia

Bloods: raised WCC, raised CRP, normal LFTs

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24
Q

What are the symptoms of ascending cholangitis?

A

Severe pain, visibly jaundiced, fevers, tachycardia, hypotensive

Bloods: raised WCC, raised CRP, deranged LFTs, raised bilirubin (indicating jaundice)

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25
Q

What’s charcot’s triad?

A

Right upper quadrant pain, fever and jaundice (hallmarks of ascending cholangitis)

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26
Q

What’s primary biliary cholangitis?

A

An autoimmune condition affecting the common bile duct

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27
Q

What’s the investigation of choice for gall stones?

A

An ultrasound of the abdomen

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28
Q

How are gall stones formed?

A

Super saturation of bile- 80% of the time from crystallisation of cholesterol (cholesterol stones), 20% of the time from crystallisation of bilirubin breakdown products (pigment stones)

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29
Q

What are the risk factors for cholesterol stone formation?

A

Diet, obesity (increased cholesterol), age, ethnicity, hyperlipidemia, crohn’s (decreased absorption of bile salts), female, pregnancy, taking the combined oral-contraceptive pill

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30
Q

What is bile composed of?

A

98% water, bile salts, bilirubin (formed from breakdown of RBCs), cholesterol, regular plasma electrolytes

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31
Q

How do cholesterol stones manifest?

A

Light yellow- dark green/ brown, relatively large and found by themselves

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32
Q

How do pigment stones manifest?

A

Small, dark and numerous

33
Q

What are the risk factors for pigment stone formation?

A

Conditions that increase the breakdown rate of RBCs eg. haemolytic anaemia

34
Q

What are mixed stones?

A

A combination of cholesterol, bile pigments and bile salts

35
Q

Why does being female, pregnant or taking the oral-contraceptive pill increase risk of gall stones?

A

Because oestrogen increases biliary cholesterol production

36
Q

How can gallstones lead to pancreatitis?

A

Gall stones blocking the pancreatic duct which leads to inflammation of the pancreas due to build up of pancreatic juice

37
Q

How can gallstone pancreatitis be differentiated from other gallstone conditions?

A

Test the patient’s blood for amylase and lipase- increased in gallstone pancreatitis because there’s damage to the pancreatic cells leading to release of amylase and lipase

38
Q

What is ileus?

A

Absence of peristalsis

39
Q

What is gallstone ileus?

A

Small bowel obstruction secondary to gallstones, a large gallstone enters the duodenum and causes obstruction

40
Q

What’s the mechanism for gallstone ileus?

A

The walls of the gallbladder become inflamed and eroded, a fistula forms between the gallbladder and the duodenum and the gallstone enters, the gallstone becomes stuck at the ileocaecal valve (smallest part of the small bowel) causing small bowel obstruction

41
Q

How can gallstones lead to cholangiocarcinoma?

A

Any structure with chronic inflammation will lead to cancer, gallbladder is chronically inflamed therefore at risk of cancer

42
Q

What’s the treatment for symptomatic gallstones?

A

Laparoscopic cholecystectomy

43
Q

What are the criteria for gaining patient consent for a procedure?

A
  • Presume patients have capacity
  • Informed decision making- doctors should have a good knowledge of surgical procedure so should be able to answer any questions the patient has
  • Be able to explain the diagnosis and what treatments are available eg. alternative procedures
  • Be able to explain the purpose of the procedure and the benefits
  • Ensure the patient is aware of the risks
  • Allow the patient time to make their decisions
44
Q

What are the risks for laproscopic cholecystectomy?

A

General:
Complications inherent to any operation eg. bleeding, infection, poorly healed scar, pain won’t subside (chronic pain), increased risk of blood clots (paralysis of the muscles during procedure), risks associated with anaesthetics- anaphylaxis

Specific:
Damage surrounding structures, haemorrhage, leaking of urine etc, bile duct injury, surgery has to be converted into open surgery

Early:
Wound healing

Late:
Incisional hernias, scars not healing properly

45
Q

What does iatrogenic mean?

A

Illness caused by medical examination or treatment

46
Q

What’s the process of a laproscopic cholecystectomy?

A
  1. Incisions are made- two for the instruments, one for the surgical video camera
  2. Surgeon views the gallbladder and surrounding structures using the camera
  3. Surgeon removes the gallbladder
47
Q

What are cholesterol stones composed of?

A

Cholesterol (70%) in a matrix of bile pigments, calcium salts and glycoproteins

48
Q

What are brown pigment stones associated with?

A

Infection of the biliary tract (bacterial and helminthic deconjugation of bilirubin glucuronides), more frequent in Asia

49
Q

What do black pigment stones consist of?

A

Calcium bilirubinate, found in haemolytic anaemia or ineffective haematopoiesis and in patients with cystic fibrosis

50
Q

What are the three mechanisms involved in gallstone formation?

A
  1. Cholesterol supersaturation of bile
  2. Gallbladder hypomotility
  3. Kinetic, pro-nucleating protein factors
51
Q

What’s the main phospholipid in bile that allows cholesterol to be soluble in aqueous media?

A

Phosphatidylcholine

52
Q

When does precipitation of cholesterol occur?

A

When cholesterol solubility exceeds the cholesterol saturation index >1, cholesterol crystals occur at low phospholipid: cholesterol ratios, low phospholipid concentrations and high bile salt concentrations, multilammellar vesicles fuse and aggregate and solid crystals

53
Q

How does gallbladder hypomotility lead to gallstone formation?

A

Supersaturated bile is often found in healthy individuals therefore effective flushing from the gallbladder during postprandial contractions prevents gallstone formation, those with ineffective emptying had increased lipid concentrations

54
Q

What modulates the formation of microcrystals in supersaturated bile?

A

Kinetic protein factors

55
Q

What is the main crystallization promoting protein in the gallbladder?

A

Mucin, a glycoprotein mixture secreted by biliary epithelial cells

56
Q

What is nucleation?

A

The initial step in crystal formation where the atoms become re-arranged into a pattern characteristic of a crystalline solid

57
Q

What’s the function of biliary fluid?

A

Lipid digestion, cholesterol release, antimicrobial activity

58
Q

Which channels in the liver drain the bile produced in the hepatic lobules?

A

Canals of Hering, bile is drained in the opposite direction to the direction of blood flow drained by sinusoids

59
Q

What are the cells like in different layers of the gallbladder?

A

Innermost layer: columnar epithelial cells with microvilli- increase the surface area, useful for concentrating bile
Lamina propria layer beneath- smooth muscle
Outer serosal layer

60
Q

Which cells release cholecystokinin?

A

L-cells

61
Q

What are the two functions of cholecystokinin in relation to the gall bladder?

A
  1. To stimulate contraction of the smooth muscle in the gallbladder to release bile
  2. To signal the sphincter of oddi to relax
62
Q

What’s the difference between the sphincter of oddi and ampulla of vater?

A

The sphincter of oddi is the sphincter that controls the flow of bile through the ampulla of vater

63
Q

Which hormone stops the release of CCK?

A

Somatostatin

64
Q

How is unconjugated (insoluble in water) conjugated?

A

It’s taken up by the liver and conjugated by UDP-glucuronosyltransferase

65
Q

Why are x-rays not used for testing for gallstones?

A

Calcified gallstones are only seen in 10% of patients using x-rays

66
Q

What is the most sensitive and specific diagnostic test to confirm cholecystitis?

A

Hepatobiliary iminodiacetic acid scan (HIDA) aka. cholescintigraphy

67
Q

What is a HIDA scan?

A

A radionuclide scan where a tracer is given intravenously and is taken up by hepatocytes in the liver, tracer gathers in the gallbladder if the cystic duct is patent

68
Q

What can be administered to test for ejection fraction of the gallbladder?

A

CCK, EF< 35% abnormal

69
Q

How are bile acids produced?

A

In the liver via cholesterol precursors, rate limiting step is cholesterol 7alpha hydroxylase

70
Q

Why are bile salts important?

A

For emulsifying lipids in the intestine

71
Q

What are micelles made of?

A

Bile salts that acts as surfactants, free fatty acids and monoglycerides are contained in them

72
Q

How to bile salts keep lipids small and easy to digest?

A
  1. They form micelles with lipids at the centre which are amphipathic
  2. They hydrophilic portions are negatively charged repelling other micelles
73
Q

What is enterohepatic circulation involving bile salts?

A

When bile salts are reabsorbed in the distal ileum of the small intestine and recycled back to the liver

74
Q

Why does pancreatitis increase liver enzymes?

A

To compensate for the lack of pancreatic enzymes

75
Q

What is cholelithiasis?

A

Gallstones in the gallbladder

76
Q

What are pigmented stones (formed from bilirubin breakdown products) broken down into?

A

Brown and black stones

77
Q

Why can an obstructed bile duct lead to cholangitis?

A

Because the resulting bile stasis leads to bacterial overgrowth

78
Q

What’s the reynolds pentad?

A

The charcot triad + shock or altered mental state

CSI (2 decks)

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