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Phase 2- GI > Week 2 > Flashcards

Week 2 Flashcards

1
Q

What are the functions of the liver?

A

Amino acid, carbohydrate and lipid metabolism; plasma protein and enzyme synthesis; production of bile; detoxification; storage of proteins, glycogen, vitamins and metals; and immune functions

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2
Q

How is the liver connective tissue matrix arranged?

A

As portal tracts and parenchyma

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3
Q

What is the vasculature of the liver?

A

Hepatic artery supplies 30-40% of the blood supply (2/3rd of the oxygen), portal vein supplies 60-70% (1/3rd of the oxygen) and the hepatic vein drains the liver.

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4
Q

What is the portal triad made up of?

A

Bile ducts, and the portal vein in the portal tracts

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5
Q

Where does the portal vein enter the liver?

A

Porta hepatis

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6
Q

What enters and leaves the liver at the porta hepatis?

A

The hepatic artery and portal vein enters, and the bile duct leaves

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7
Q

How are hepatocytes arranged?

A

Hepatocytes lie in plates and cords. They exchange material with blood at sinusoidal surface; there are three types of surface: sinusoidal, intercellular and canalicular

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8
Q

What are the different liver cells?

A

Hepatocytes, endothelial cells, Kupffer cells (macrophages), perisinusoidal (fat-storing) cells and liver-associated lymphocytes

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9
Q

What is the connective tissue in the liver?

A

Liver capsule, portal tracts and parenchymal reticulin

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10
Q

What structures make up the biliary system?

A

Bile canaliculi, bile ductules and bile ducts. The bile system runs in the opposite direction to the blood

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11
Q

What structures make up the biliary tree?

A

The right and left hepatic ducts join to form the common hepatic duct. This joins the cystic duct from the gallbladder to form the common bile duct.

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12
Q

What is cholestasis?

A

Bile stasis; caused by impaired bile synthesis or secretion or obstruction to flow

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13
Q

What are some common abnormal liver function tests?

A

Bilirubin: increased in cholestasis
Alkaline Phosphatase: increased in cholestasis
GGT: increased in cholestasis or enzyme induction
AST/ALT: increased in hepatocyte damage
Albumin: decreased in long-term impaired synthesis
PTT: increased in short-term impaired synthesis

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14
Q

What are the LFT changes in pre-hepatic jaundice?

A 
Total bilirubin: increased
Conjugated bilirubin: normal
Unconjugated bilirubin: increased
Urobilinogen: normal or increased
Urine colour: normal (urobilinogen, no bilirubin)
Stool colour: normal
Alk Phos: normal
ALT and AST: normal
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15
Q

What are the LFT changes in hepatic jaundice?

A 
Total Bil: increased
Conj. Bil: increased
Unconj. Bil: increased
Urine colour: dark (urobilinogen + conj. bil
Stool colour: normal
Alk Phos: increased
ALT and AST: very increased
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16
Q

What are the LFT changes in post-hepatic jaundice?

A 
Total Bil: very increased
Conj. Bil: very increased
Unconj. Bil: normal
Urobilinogen: decreased
Urine colour: dark (conjugated bilirubin)
Stool colour: pale
Alk Phos: very increased
ALT and AST: increased
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17
Q

What is the three-fold definition of cirrhosis?

A

Diffuse process with fibrosis and nodule formation

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18
Q

What is cirrhosis?

A

End-stage liver disease, result of chronic inflammation over many years

  • persistence of injury causing agent
  • (fibrous) scarring and hepatocyte regeneration (leads to nodules)
  • eventually irreversible and cirrhosis develops
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19
Q

What is the pathogenesis of cirrhosis?

A

Hepatocyte injury leads to progressive liver cell loss, which causes chronic inflammation, and hepatocyte regeneration. Chronic inflammation causes fibrosis, and hepatocyte regeneration causes hyperplastic nodules. Both of these cause architectural abnormality in the liver, leading to ischaemia which causes further liver cell loss.

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20
Q

What are the common causes of cirrhosis?

A 
Alcohol or alcohol-like: 60-70%
Hepatitis (including viral): 10% or more
Biliary disease: 5%
Unknown: 10-15%
Haemochromatosis: 5%
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21
Q

What are the complications of cirrhosis?

A

Portal hypertension: cirrhosis increases resistance to blood flow through the liver, thus increasing pressure in the portal circulation, causing; portal-systemic shunts and varies, ascites, and splenomegaly. Other complications include liver failure, hepatocellular (liver) cancer

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22
Q

What secretory protein production is impaired in liver failure?

A

Albumin, transport proteins, coagulation and fibrinolysis (e.g. factors II, V, VII-XIII), complement and protease inhibitors

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23
Q

What are the systemic effects of liver failure?

A

Jaundice, coagulation disorders, altered intermediary metabolism (e.g. impaired synthesis of urea and glycogen), altered xenobiotic metabolism (e.g. drugs), immune, circulatory and endocrine disturbances

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24
Q

What are acini?

A 
A micro-circulatory unit in the liver, which is made up of three zones:
Zone 1- closer to the afferent arteriole
- respiratory chain
- citric acid cycle
- fatty acid oxidation
- gluconeogenesis
- urea synthesis
- production and bile excretion
Zone 2- ill-defined intermediate area
Zone 3- closer to the terminal hepatic veins
- glycolysis
- glutamine synthesis
- xenobiotic metabolism

Oxidative functions tend to be carries out in the zone 1, while metabolic processes requiring lower O2 are handled in zone 3

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25
Q

How does carbohydrate metabolism occur in the liver?

A

Storage as glycogen and release via glycogenolysis. Gluconeogenesis, the synthesis of glucose from other sources e.g. lactate, pyruvate, glycerol and alanine. Glucose as an energy substrate (glycolysis, citric acid cycle, synthesis of FA and TG). Conversion of fructose and galactose to glucose phosphates

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26
Q

How does lipid metabolism occur in the liver?

A

Mitochondrial beta oxidation of short chain fatty acids, and synthesis of FA, TG, cholesterol, phospholipids, and lipoproteins

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27
Q

How does protein metabolism occur in the liver?

A

Most circulating proteins are synthesis wholly or largely by the liver and used as a measure of hepatic synthetic function: albumin and glycoproteins. Glycation of protein also occurs in the liver

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28
Q

How are amino-acids metabolised in the liver, and how is urea disposed of?

A

Nitrogen is converted into urea in the liver and excreted by the kidneys. Ammonia is produced and cleared in the liver (very complicated)

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29
Q

How do biotransformation and excretion occur in the liver?

A

These processes are usually used for detoxification, but can generate toxic or carcinogenic metabolites. Phase 1 reactions in the smooth ER are mediated by cytochrome P450 to produce hydroxylated or carboxylated compounds. Phase 2 reactions: subsequent conjugation with glucaronic acid, acetyl or methyl radicals or glycine, taurine or sulphate

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30
Q

What is the composition of bile?

A

Water, electrolytes, phospholipids, bile salts or acids, bile pigments, cholesterol, heme waste products, and other substances from blood.

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31
Q

What is the function of bile?

A

Bile acids are needed for fat absorption- mechanism to remove cholesterol and waste

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32
Q

How is Hb broken down?

A

Around 126 days, RBCs are phagocytosed and Hb is released. Hb is broken down into: haeme (converted into bilirubin), globins (broken into amino acids and recycled), and iron (bound to transferrin and returned to iron stores in the liver or bone marrow.

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33
Q

How is bilirubin metabolised in the intestine?

A

Intestinal bacteria degrade conjugated bilirubin to form urobilinogen:

  • 80% of urobilinogen formed is oxidised to stercobilin and excreted in faeces, giving stool its brown colour
  • 20% of urobilinogen formed is:
    • absorbed by the extra-hepatic circulation to be recycled through the liver and re-excreted
    • enters systemic circulation to be filtered by the kidney and excreted in the urine
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34
Q

How is bilirubin metabolised in the liver?

A

Bilirubin is bound by albumin and taken to the liver (unconjugated bilirubin); it is water insoluble and cannot be removed from the body. Once at the liver, unconjugated bilirubin flows into sinusoidal tissue and is released from albumin. Ligandin picks up the unconjugated bilirubin, and presents it to glucaronic acid. In the liver, it becomes conjugated with the help of UDP-glucoronyl transferase (water soluble, and combines with gallbladder secretions and is expelled into the intestines)

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35
Q

What are the metabolic functions of the liver disturbed by?

A

Congenital deficiency of enzymes, nutritional deficiency/excess of substrate, toxic/chemical damage to organelles, hypoxic/ischaemic insult or secondary to metabolic effects of a disease

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36
Q

What is the effect of mitochondrial damage in the liver?

A

Inhibition of beta oxygenation of fatty acids; leads to micro-vesicular steatosis
Interference with oxidative phosphorylation; leads to insufficient ATP generation
Impairment of the respiratory chain; leads to excess ROS with lipid peroxidation
Increase in permeability transition; leads to cell death (apoptosis)

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37
Q

What can cause toxic damage to the liver?

A

Mitochondrial damage can be caused by drugs (antivirals, salicylate, valproate, tetracycline) and toxins (hypoglycin, atractyloside). Endothelial damage to hepatic veins can be caused by cytotoxic drugs, and toxins (senecio, aflatoxin, pyrrolizidine). Glutathione depletion and cell death can be caused by drugs (paracetamol) and hypoxic ischaemia

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38
Q

What are the mechanisms of centrilobular necrosis?

A

Sepsis, shock induces ischaemia, congestive heart failure, toxicity from drugs and poisons; made worse by malnutrition, infection, fasting and exercise

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39
Q

What are the pathological manifestations of metabolic disease of the liver?

A

No structural abnormalities evident, but severe functional disturbance. Hepatocyte injury leading to apoptosis, necrosis, cirrhosis or tumours. Storage of lipid, glycogen or other products manifesting as hepatomegaly

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40
Q

What are the main components of bile?

A

Bicarbonate, cholesterol, phospholipids, bile pigments and bile salts

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41
Q

What are bile pigments generated from?

A

Breakdown of haeme group from Hb in macrophages of the recticulo-endothelial (RE) system in the spleen/bone marrow/liver

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42
Q

What is haemoglobin composed of?

A

4 globin monomers and 4 haeme groups (Fe2+ and a porphyrin ring)

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43
Q

What are the four globin monomers broken down into?

A

Constituent AAs, and recycled

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44
Q

What happens to the haeme group after breakdown of Hb?

A

The iron ion is recycled, and the porphyrin ring is converted to bilirubin for transport to the liver; for modification and excretion

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45
Q

How is haem broken down into bilirubin?

A

Haem is converted to biliverdin by haem oxygenase, and biliverdin is converted to (unconjugated) bilirubin by biliverdin reductase

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46
Q

How does bilirubin conjugation occur in the liver?

A

Unconjugated bilirubin, bound to albumin in the blood is transported over a sinusoidal bilirubin transporter into the hepatocyte, when it loses albumin. UDP glucoronyl transferase conjugate bilirubin, by adding glucuronic acid. Bile can now be transported out of hepatocytes into bile canaliculi for accumulation in bile

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47
Q

How is bilirubin metabolised in the intestines?

A

Conjugated bilirubin is converted to u-bilirubin by beta-glucoronidase in the small intestine. Intestinal microflora converts u-bilirubin into 3 urobilinogens: mesobilinogen, stercobilinogen and urobilinogen. In the large intestine, these are converted to mesobilin and stercobilin (excreted in the faeces, causing its brown colour), and urobilin by intestine microflora.

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48
Q

What happens to urobilin?

A

It is taken up by the portal vein, and is excreted by the kidneys (via the liver) in urine.

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49
Q

What is the function of bile salts?

A

To act as biological emulsifiers.

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50
Q

What are bile salts/acids synthesis from?

A

Cholesterol, plus an amino acids (either glycine or taurine) to form glycholic acid or taurocholic acid

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51
Q

How does the process of emulsification occur?

A

Emulsification is the breakdown of large lipid droplets into small, uniformly distributed droplets. The hydrophobic portion binds to and disperses large triglyceride lipid droplets. Hydrophilic portion prevents large droplets reforming. This increases the surface area on which triglyceride lipase can act

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52
Q

How do bile salts promote micelle formation?

A

A micelle is a very small lipid aggregate with hydrophilic head groups on the outside and hydrophobic tails pointing in. They are made of bile salts, fatty acids, monoglycerides, phospholipids, cholesterol and fat soluble vitamins. Micelles continuously breakdown and reform- each time the contents are released and some diffuse across the intestinal lining. TAGs reform in the epithelial cells and are packaged into chylomicrons which enter the blood via the lymph.

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53
Q

Summarise bile salt action in the intestine:

A
  1. Bile salts emulsify the fat globules in the intestines
  2. Bile salts form micelles with FFA produced
  3. The absorbed FFAs form TGs and are packaged into chylomicrons for secretion in lacteals
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54
Q

How is bile secretion regulated?

A

Between meals the sphincter of Oddi is contracted. Pressure increased in the common bile duct, and bile flows into the gallbladder- epithelial cells reabsorb water and electrolytes, thus concentrating the bile. FAs and AAs entering the duodenum (after a meal) stimulate endocrine cells to release CCK, which stimulates contraction of the smooth muscle in the gallbladder, and relaxes the sphincter of Oddi. Acidic chyme in the duodenum stimulates other endocrine cells to release secretin; stimulating duct cells in the liver to release bicarbonate into the bile, as well as stimulating bile production

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55
Q

How are bile salts recycled?

A

As bile salts in the body are not enough to fully process the fats in a typical meal, they must be recycled by the enterohepatic circulation. Transporters move bile salts from the digestive tract to the intestinal capillaries, where they are transported to the liver via the hepatic portal vein. Hepatocytes take up bile salts from the blood and increase bile salt secretion into bile canaliculi. 95% of released bile salts are recycled via the enterohepatic circulation; 5% are lost in faeces.

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56
Q

What are the three classifications of jaundice?

A

Pre-hepatic (elevated haemolysis), hepatic (liver damage) or post-hepatic (blockage of bile ducts).

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57
Q

How can the different types of jaundice be distinguished?

A

Proportion of unconjugated:conjugated bilirubin

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58
Q

How does pre-hepatic jaundice occur?

A

Present in several conditions associated with elevated haemolysis- liver cannot cope with increased levels of unconjugated bilirubin.

  • more RBC breakdown
  • more haemoglobin
  • more bilirubin produced
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59
Q

How does neonatal jaundice occur?

A

At birth, new-borns must destroy foetal haemoglobin and replace with adult Hb- RBCs have a short lifespan. With an undeveloped liver (lack of glucuronyl transferase) there is insufficient capacity to cope with elevated haemolysis.

60
Q

How can haemolytic disease of the newborn cause neonatal jaundice?

A

Rh incompatibility between mother and foetus may also cause haemolysis; maternal Rh- blood sensitised by previous pregnancy with Rh+ foetus or Rh+ blood transfusion. Can cause very high bilirubin concentration. At risk of kerniecterus- bilirubin crosses immature blood brain barrier, deposition of bilirubin in basal ganglia and brainstem nuclei, resulting in brain damage if untreated

61
Q

How does hepatic jaundice occur?

A

Liver takes up unconjugated bilirubin, conjugates it and exports it to the gallbladder.
Hepatic jaundice can occur at any point in the system:
a. impaired uptake of unconjugated bilirubin
b. impaired conjugation of bilirubin
c. impaired transport of conjugated bilirubin into bile canaliculi
- e.g. primary biliary cholangitis (autoimmune destruction of small bile ducts)
- present in conditions that result in liver damage causing cholestasis due to swelling and oedema resulting from inflammation

62
Q

How does post-hepatic jaundice occur?

A

Present in conditions associated with obstruction of hepatic, cystic or common bile duct. Prevents bile from being released into the small intestine = cholestasis. Gallstones (small pebbles of cholesterol) that move from gallbladder to block ducts- arise if capacity of bile salts and phospholipids to solubilise cholesterol is exceeded.
Pancreatitis: acute or chronic inflammation of the pancreas following infection or damage. Swelling can block bile flow.
Pancreatic tumours: tumour growth can block bile flow

63
Q

What does the severity of gallstone-related symptoms depend on?

A

Location of gallstones

64
Q

What symptoms are associated with stones in the cystic bile duct?

A

Painful contractions

65
Q

What symptoms are associated with stones in the common bile duct?

A

No bile secretion into the gut, steatorrhea (fatty faeces as no bile salts), grey faeces (absence of bile pigments) and post-hepatic jaundice (reduced excretion of bilirubin)

66
Q

What symptoms are associated with stones in the duodenal papilla?

A

No bile or pancreatic secretions into the gut, malnutrition (no digestion of chyme), acute pancreatitis

67
Q

What are the implications for surgery in post-hepatic jaundice?

A

Bile salts are required for efficient digestion and absorption of lipids and lipid-soluble vitamins (A, D, E and K). Vitamin K is a co-factor of the liver for gamma-glutamyl carboxylase (GGCX), which is required to make active coagulation factors II, VII, IX and X. A course of VitK is administered parenterally to post-hepatic jaundice patients prior to surgery to prevent haemorrhage

68
Q

How is conjugated bilirubin measured in serum?

A
  1. Add diazo reagent to serum
  2. Conjugated bilirubin converted to blue/purple diazo derivative of bilirubin (azobilirubin)
  3. Measurement of absorbance at 530-545 nm proportional to conjugated bilirubin (not unconjugated)
  4. Compare to known standards to calculate concentration
69
Q

How is total bilirubin measured in serum?

A
  1. Add diazo reagent with caffeine to serum
  2. Caffeine displaces unconjugated bilirubin from albumin
    • free unconjugated bilirubin can now react with the diazo reagent
  3. Both conjugated and unconjugated bilirubin converted to blue/purple diazo derivative of bilirubin
  4. Measurement of absorbance at 530-545 nm proportional to both conjugated and unconjugated bilirubin
  5. Compare to known standards to calculate concentration
70
Q

How is bilirubin measured in urine?

A

Test area impregnated with diazide that forms a tan coloured dye in the presence of excess conjugated bilirubin (unconjugated Br is not water soluble so not filtered by the kidney). Hyperbilirubinuria is always pathological as it means conjugated Br has leaked back into the blood stream (hepatic or post-hepatic jaundice)

71
Q

How is urobilinogen measured in urine?

A

Test area is impregnated with p-dimethylaminobenzaldehyde- forms a pink azo dye in the presence of urobilinogen. Normally present in low concentrations: high concentrations indicate increased haemolysis or liver disease (pre/ hepatic jaundice). Absence of raised urobilinogen in a jaundiced patient can indicate biliary obstruction (post-hepatic jaundice)

72
Q

Are bile pigments measured in faeces?

A

Not done- waste of time/money. Visual inspection easy and free- absence of stercobilin is obvious

73
Q

How are blood gas analysers used to detect jaundice?

A

On some NICU wards blood gas analysers are used for early detection and monitoring of jaundice severity/treatment: based on absorbance (at 450 nm) of whole blood sample

74
Q

What do transcutaneous measurements of bilirubin measure?

A

Yellowness of skin due to bilirubin; measured at multiple wavelengths to correct for variations in Hb, melanin and skin thickness. Forehead or sternum measurements correlate best with serum bilirubin concentration

75
Q

What areas are under voluntary control in the GI system?

A

Upper oesophageal sphincter (swallowing), and external anal sphincter (defecation)

76
Q

What innervates the intestines?

A

Auerbach’s (myenteric plexus)

77
Q

What do the interstitial cells of Cajal do?

A

Mediate enteric neurotransmission from enteric neurones to smooth muscle cells

78
Q

Describe the enteric nervous system:

A
  • Mediates reflex activity in the absence of CNS input (interprandial period)
  • Influenced by extrinsic factors:
    • vagal control: excitatory to non-sphincteric muscle
    • sympathetic control: inhibitory to non-sphincteric muscle, excitatory to sphincteric muscle
  • Other neurohormonal influences:
    • 5 hydroxy-tryptamine
    • motilin
    • opioid receptors
79
Q

What two things can be measured to gauge motility function?

A 
Pressure (circular muscle function)
Transit: 
- radio labelled isotopes
   scintigraphy
   breath tests
- dynamic contrast radiology
80
Q

Where does the sympathetic neural supply for the oesophagus come from?

A

The sympathetic trunk

81
Q

Where does the parasympathetic innervation of the oesophagus come from?

A

The vagus nerve

82
Q

What is the muscular structure of the oesophagus?

A

The upper part of the oesophagus is striated muscle, and the lower part is smooth muscle. There is an inner circular layer, and an outer longitudinal layer

83
Q

How can oesophageal function be measured?

A

High resonance manometry

84
Q

What changes in achalasia?

A

LOS does not relax, no peristaltic activity (sometimes), bolus gets stuck in oesophagus, frequent regurgitation during meal

85
Q

How is achalasia treated?

A

Rigiflex balloon dilatation, laparoscopic heller’s myotomy and per oral endoscopic myotomy

86
Q

What are the features of oesophagus in scerloderma?

A

Weak LOS, absent peristalsis, severe oesophagitis (treated with PPIs, surgery creates achalasia)

87
Q

What are the features of nutcracker oesophagus?

A

Associated with pain on swallowing, no evident therapies, functional swallow; benign prognosis

88
Q

Describe the interprandial (fasting) period, and the migrating motor complex:

A 
Cyclic contraction sequence
Occurs every 90 minutes
4 phases:
1. prolonged period of quiesence
2. increased frequency of contractility
3. a few minutes of peak electrical and mechanical activity
4. declining activity merging to next phase 1
Regulated by motilin 
Acts to cleanse stomach
89
Q

What is motilin?

A

Polypeptide hormone, produced by M cells in the small intestine. Secreted at 90 minute intervals; housekeeper of the gut- cleanses in time for next meal. Stimulates contraction of gastric fundus and enhances gastric emptying
Erythromycin is a motilin agonist

90
Q

What are the three phases of meal related motility?

A

Cephalic, gastric and intestinal

91
Q

Describe the cephalic phase:

A

Secretory phase, vaguely mediated. Sight/smell of food leads to increased gastric secretion. 20% of gastric secretion in this phase

92
Q

Describe the gastric phase:

A

Proximal gastric tone reduces and fundus expands to accommodate meal. Stomach expands without increase in pressure- MMC is replaced by contractions of variable amplitude and frequency, allowing mixing and digestion. Frequency and direction of gastric muscular contractions controlled by ‘gastric pacemaker’ zone within the proximal gastric body. Pacemaker generates rhythmic depolarisations at a frequency of 3 cycles per minute, which only trigger gastric smooth muscle contractions with additional neurohumoral input. Liquids leave the stomach earlier than solids- emptying time for inert liquid is 20 minutes. Solids undergo mixing and churning; digestible food particles leave stomach when size is reduced to 2mm- solids empty completely over 3-4 hours

93
Q

Describe gastric emptying:

A

Liquids empty faster than solids. Nutrient content slows down gastric emptying; fatty meals take longer to leave the stomach, for liquid foods 200kCal/r is delivered to the duodenum

94
Q

What are features of disorders of accelerated gastric emptying?

A

Dumping syndrome and diarrhoea

95
Q

What are features of disorders of delayed gastric emptying (gastroparesis)?

A

?Abdominal pain, vomiting, poorly controlled GORD, malnutrition

96
Q

What are some causes of gastroparesis?

A

Idiopathic, longstanding diabetes with microvascular disease, drugs- opiates, post viral

97
Q

What are some symptoms of gastroparesis?

A

Abdominal pain, nausea and (often delayed) vomiting, weight loss

98
Q

How is gastroparesis managed?

A

Dietary: small meals frequently, liquid food tolerated better than solid, nutritional support (post-pyloric feeding)
Attention to underlying cause: limit use of opiate/codeine or other trigger medication, post-viral (may improve over time), diabetes (improve diabetic control). PEG tube??

99
Q

What medications can be used to manage gastroparesis?

A

Pro-kinetics: 5HT4 agonists, D2 antagonists, motilin agonist, botulinum toxin injection to pyloric sphincter

100
Q

How can gastric electrical stimulation be used to manage gastroparesis?

A

2 electrodes sit 1 cm apart, 9 cm from the pylorus in greater curve of the stomach- high frequency low amplitude contractions. Gastric electrical stimulation does not improve gastric emptying, but improves nausea and vomiting and is more effective in diabetic aetiology

101
Q

How does small intestinal transit occur in fasting conditions?

A

Via the MMC

102
Q

Describe small intestine transit:

A

Small intestine transports solids and liquids at the same rate, however liquids transported to caecum more rapidly due to faster gastric emptying; head of liquids column reaches caecum after 30 minutes; 150 minutes for half of chyme to transverse small bowel; chyme moves from ileum to colon intermittently in boluses, with bolus movement due to “prolonged propagated contraction”

103
Q

Describe chronic intestinal pseudo-obstruction:

A

Signs of mechanical obstruction without mechanical occlusion of the gut; chronic abdominal pain, constipation, vomiting, weight loss. Neuropathic or myopathic aetiology.

104
Q

Describe acute post-operative ileus:

A
  • Constipation and intolerance of oral intake in the absence of mechanical obstruction after surgery
  • Physiological ileus lasts 0-24 hours in small intestine, 24-48 hours in stomach and 48-72 hours in colon
  • Risk factors for prolonged ileus:
    • open surgery (vs laproscopic)
    • prolonged abdominal or pelvic surgery
    • delayed enteric nutrition
    • peri-operative complications
    • peri-operative opiate analgesia
105
Q

Describe acute colonic pseudobstruction (Ogilvie’s syndrome)

A
  • Large bowel parasympathetic dysfunction
  • Commonest after cardiothoracic or spinal surgery
  • Risk of caecal perforation
106
Q

How is acute colonic pseudobstruction managed?

A

Gut rest, IV fluids, nasogastric decompression; IV neostigmine (AChesterase inhibitor); colonoscopic decompression; surgery

107
Q

What are myopathic causes of chronic intestinal pseudo-obstruction?

A

Scleroderma, amyloidosis

108
Q

What are neuropathic causes of chronic intestinal pseudo-obstruction?

A

Parkinson’s disease

109
Q

What are endocrine causes of chronic intestinal pseudo-obstruction?

A

Diabetes mellitus, severe hypothyroidism

110
Q

What are pharmacological causes of chronic intestinal pseudo-obstruction?

A

Phenothiazines, anti-parkinsonian drugs

111
Q

How are disorders of small bowel transit managed?

A

Nutritional: enteral feeding, parenteral feeding
Antibiotics for small bowel bacterial overgrowth
In refractory cases, small bowel transplantation

112
Q

Describe colonic motility:

A

No typical pacemaker activity. Colon must:
- mix material without propulsion (for water absorption)
- act as a storage site
- cause aboral movement of content
- expel faeces
Mixture of short duration and long duration contractions

113
Q

Describe colonic motility in response to a meal:

A

Marked increases in colonic activity (gastrocolic reflex). Transit from caecum to rectum takes 1-2 days (shorter duration in men tannin women, therefore increased faecal weight in men (higher water content)), transit slowest though the caecum

114
Q

Which drugs reduce colonic motility?

A

Opiates (via Mu receptor)
Anticholinergics
Loperamide:
- gut selective opiate Mu receptor agonist, decreases tone and activity of myenteric plexus, slows colonic transit leading to increased water absorption, used for symptomatic management of diarrhoea

115
Q

Which drugs increase colonic motility?

A

Stimulant laxatives, increase gut motility, alter gut electrolyte transport.
Prucalopride, gut selective 5HT4 receptor agonist- increases colonic (and other gut motility)
Linaclotide- minimally absorbed guanylate C receptor agonist; increases secretion and HCO3 into lumen (increases intestinal fluid, speeds colonic transit)

116
Q

Describe the internal anal sphincter:

A

Smooth muscle, involuntary control, in resting conditions this provides greatest component of contraction

117
Q

Describe the external anal sphincter:

A

Started muscle, voluntary control, recruited in reflex reaction to coughing/sneezing

118
Q

How does anal incontinence occur?

A 
Excessive rectal distension:
- acute or chronic diarrhoeal illness
- chronic constipation
Anal sphincter weakness:
- muscle damage
- damage to pudendal nerve
119
Q

What causes anorectal constipation?

A

Hirschsprung’s disease (children), obstructive defecation (paradoxical contraction of puborectalis and external sphincter during defecation), rectocele, anal fissure (associated pain on defecation)

120
Q

What happens to the colon spinal cord injury (T12 or above)?

A

Injury to T12 or above:

  • “reflex bowel”
  • damage to upper motor neurones
  • reflex arc intact
  • tonic anal sphincter
  • bowel open spontaneously but without control
  • reflex can be initiated by rectal stimulation (e.g. suppository)
121
Q

What happens to the colon spinal cord injury (injury to sacral nerve roots)?

A
  • lower motor neurone injury
  • “flaccid bowel”
  • no reflex arc
  • slow stool propulsion through colon
  • flaccid anal sphincter leads to incontinence
  • management based on manual evacuation of stool
122
Q

Why would LFTs be requested?

A

Well person screening, to investigate unexplained symptoms, to investigate symptoms and signs suggestive of liver disease, for pre-operative baseline assessment and to monitor the progress of established liver disease and assess the response to treatment

123
Q

What are the two aminotransferases measured in LFTs?

A

Aspartate and alanine aminotransferase

124
Q

What are ALT and AST involved in?

A

They participate in gluconeogenesis by catalysis the transfer of amino groups from aspartic acid or alanine to ketoglutaric acid to produce oxaloacetic acid and pyruvic acid respectively

125
Q

What are ALT and AST markers of?

A

Hepato-cellular injury

126
Q

Is AST or ALT more specific for liver disease?

A

ALT

127
Q

What is AST and where is it found?

A

Present in cytosolic and mitochondrial isoenzymes; present in liver, cardiac and skeletal muscle, kidneys, brain, pancreas, lungs, leukocytes and red cells

128
Q

What is ALT and where is it found?

A

Cytosolic enzyme, found in the same places as AST, but much lower activity in extra-hepatic tissues

129
Q

What is GGT and where is it found?

A

Microsomal enzyme, present throughout the liver and hepatobiliary tree and other organs (heart, kidneys, lungs, pancreas and seminal vesicles) but plasma activity is mostly related to the liver isoenzyme

130
Q

What is GGT useful for?

A

Poor specificity for liver disease, but useful to either identify raised alkaline phosphatase of liver origin or chronic alcohol consumption

131
Q

What does GGT do?

A

Responsible for the transfer of glutamyl groups from gamma-glutamyl peptides to other peptides or amino acids

132
Q

How does GGT change with excess alcohol consumption?

A

In people who have chronic liver disease the absolute plasma activity of GGT is higher- may be due to the indiction of the enzyme by alcohol and/or liver damage.

133
Q

When does GGT give a false positive, and a false negative?

A

False positive n people taking enzyme inducing drugs (e.g. phenytoin, carbamazepine, and barbiturates) and a false negative in those who do not have liver disease

134
Q

What is alkaline phosphatase?

A

A group of enzymes that hydrolyse phosphate esters in alkaline solutions (physiological substrate is not known)

135
Q

What genes encode ALP?

A

Chromosome 1: tissue non-specific ALP (widely expressed being present on osteoblasts, hepatocytes and other cells)
Chromosome 2: intestinal, placental and germ cell

136
Q

Where is the liver derived ALP isoenzyme?

A

Located on the exterior surface of the bile canalicular membrane and probably enters the bloodstream via the paracellular pathway

137
Q

When is ALP raised?

A

In bile duct obstruction- not related to failure to clear ALP or release from damaged hepatocytes, but more likely by stimulated synthesis

138
Q

What does the prothrombin time reflect and measure?

A

PT measures the rate of conversion of prothrombin to thrombin, and reflects a vital synthetic function of the liver

139
Q

What are the steps in the evaluation of patients with abnormal LFTs?

A

Clinical history: presenting and duration of symptoms, exposure to hepatotoxins, family history, exposure to viruses, physical examination, interpretation of initial screening, pattern of abnormality, other tests SEE LECTURE for diagram

140
Q

What is the hepatocellular pattern in LFT results?

A

ALT or AST >150 U/L ALP <200 U/L
Serology:
- viral serology hepatitis
- autoantibodies
- ferritin/iron studies, copper, caeruloplasmic, alpha-1-antitrypsin concentration and phenotype (to investigate inherited liver disease)
Liver biopsy:
- if serology unhelpful and persistent LFT elevation
- to further assess a serological diagnosis

141
Q

What is the cholestatic pattern in LFT results?

A

ALP >180 U/L, ALT <150 U/L, GGT >100 U/L, Br < 50 umol/L
Ultrasound abdomen
If dilated ducts consider MRCP/ERCP
- if norma biliary tree then anti-mitochondrial antibody (AMA)
- if AMA negative, persistent elevation and further investigation appropriate then consider MRCP/ERCP and liver biopsy

142
Q

What can bilirubin, as bio-product of haemoglobin catabolism, elevation indicate?

A

Excess production following haemolysis of trauma, reduced level of conjugation, hepatocyte failure, biliary obstruction

143
Q

What is isolated rise in ALP with normal GGT likely to relate to?

A

Bone disease (fractures, Paget’s disease, osteomalacia, bony metastasis)

144
Q

Which of the chemical is released into the bile by the liver and plays a role in digestion in the small intestine?

A

Taurocholic acid

145
Q

At what intervals does MMC activity occur during the inter-digestive phase?

A

Every 90-120 minutes

146
Q

What test should be carried out to confirm Gilbert’s syndrome?

A

Unconjugated bilirubin

147
Q

Where does the porta hepatis lie?

A

Inferior to the caudate lobe, and superior to the quadrate lobe

Phase 2- GI (5 decks)

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