Learning Outcomes
(for general perusal)
See picture

Summary of gastrointestinal function
List the main GI functions
- Gut motility propels and mixes food
-
Digestion: exocrine secretion
-
Absorption
Digestion: exocrine secretion
Absorption
Summary of gastrointestinal function
Give the details of the following GI functions
- Gut motility propels and mixes food
-
Digestion: exocrine secretion
-
Absorption
-
Circular and longitudinal smooth muscle, Sphincters
-
Breaks down complex molecules
Organic molecules (eg enzymes, bile salts, mucus)
HCl (stomach)/HCO3- (all other areas)
7-8 l secreted/re-absorbed each 24hrs
-
Large surface area: Mucosal folds, Villi, Microvilli
Specific absorption mechanisms: 2˚ active transport (Glucose, Galactose, Amino acids)
Facilitated diffusion (Fructose)
Diffusion/chylomicron formation/exocytosis: Lipids
Circular and longitudinal smooth muscle, Sphincters
Breaks down complex molecules
Organic molecules (eg enzymes, bile salts, mucus)
HCl (stomach)/HCO3- (all other areas)
7-8 l secreted/re-absorbed each 24hrs
Large surface area: Mucosal folds, Villi, Microvilli
Specific absorption mechanisms: 2˚ active transport (Glucose, Galactose, Amino acids)
Facilitated diffusion (Fructose)
Diffusion/chylomicron formation/exocytosis: Lipids
Symptoms/signs: gastrointestinal motility
-
Swallowing difficulties: dysphagia and choking
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GORD: heartburn (indigestion/dyspepsia), regurgitation
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Vomiting: nausea, haematemesis
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Obstruction: pain, nausea and vomiting, constipation
- Diarrhoea
- Constipation
- Faecal incontinence
Pathophysiology of Swallowing
(Tongue/soft palate/pharynx/larynx)
Outline the Neurological conditions affecting pharynx

- IX (sensory)
- X +XII (motor: somatic)
- bulbar palsy; (LMN defects IX, X+XII):
- sensory loss and lower motoneurone defects (or muscle weakness)
- reduced palatal sensation
- reduced gag reflex
- choking
- dysphonia (recurrent laryngeal n.)
- flaccid/wasted tongue
- pseudobulbar palsy; (UMN defects X + XII). As for bulbar palsy except:
- normal palatal sensation
- normal/increased gag reflex
- spastic tongue
- (maybe increased jaw jerk: motor Vth n.)
- sensory loss and lower motoneurone defects (or muscle weakness)
- reduced palatal sensation
- reduced gag reflex
- choking
- dysphonia (recurrent laryngeal n.)
- flaccid/wasted tongue
- normal palatal sensation
- normal/increased gag reflex
- spastic tongue
- (maybe increased jaw jerk: motor Vth n.)

Pathophysiology of Swallowing
- What does Lower oesophageal obstruction lead to?
- List the possible causes?

- dysphagia ± pain
-
- benign stricture
- peptic (GORD), corrosives
- oesophageal carcinoma
- achalasia
-
failure of peristalsis
-
poor relaxation of lower oesophageal sphincter
-
loss of inhibitory postganglionic nitrergic nerves (parasympathetic)
- peptic (GORD), corrosives
-
failure of peristalsis
-
poor relaxation of lower oesophageal sphincter
-
loss of inhibitory postganglionic nitrergic nerves (parasympathetic)
-

How can Achalasia be diagnosed?
With a barium swallow

Pathophysiology of gastro-oesophageal reflux disease (GORD)
- Outline the pathophysiology of GORD
- Failure of normal anti-reflux mechanisms:
- Transient relaxation of lower oesophageal sphincter between meals
- Loss of the flap valve effect of the intra-abdominal oesophagus/diaphragmatic constriction
- sliding hiatus hernia
- Failure of mucosal defence mechanisms
- mucus/HCO3-
- epithelial junctional complexes
- sliding hiatus hernia
- mucus/HCO3-
- epithelial junctional complexes

Pathophysiology of gastro-oesophageal reflux disease (GORD)
- What are the consequences of GORD?
- What is it aggravated by?
- What does long term-scarring lead to?
- Acid reflux leads to oesophagitis and heartburn, Regurgitation
- Aggravated by increases in intra-abdominal pressure
- Long term scarring leads to stricture/dysphagia

Pathophysiology of gastro-oesophageal reflux disease (GORD)
What are the principles of treatment of GORD?
- Weight loss
- Increase mucosal protection
- Alginates
- Antacids to neutralise pH
- Reduce gastric acid
- H2 receptor blockers
- Proton pump inhibitors
- Accelerate gastric emptying:
- Dopamine antagonists (metaclopramide)
- Alginates
- H2 receptor blockers
- Proton pump inhibitors
- Dopamine antagonists (metaclopramide)

Pathophysiology of vomiting
- Where is the vomiting centre?
- What are the stimuli for vomiting?
- What are the physiological changes that take place on vomiting?
- What does fluid loss lead to/cause?
- What does HCL loss cause?
- Medulla oblongata
- Emotion, motion, circulating chemicals, Pharyngeal stimulation, gastric/duodenal irritation/distention
-
Oesophageal sphincters relax, glottis closes, stomach relaxes, abdominal mm./diaphragm contracts, duodenum contracts
-
dehydration
-
hypochloraemic alkalosis
Oesophageal sphincters relax, glottis closes, stomach relaxes, abdominal mm./diaphragm contracts, duodenum contracts
dehydration
hypochloraemic alkalosis

Pathophysiology of bowel obstruction
Outline the symptoms arising from the small or large intestine?
What are the causes?
- Paralytic ileus or mechanical obstruction
- Colicky pain
- Nausea/vomiting/constipation
- Dehydration
- Abdominal distension
- Increased bowel sounds
- X-ray: dilated bowel loops and fluid levels
Causes:
- Lumen (eg foreign object)
- Wall (eg tumour)
- Outside wall (eg adhesions)
- Ileus (no bowel sounds ± pain)

Pathophysiology of diarrhoea
- Define
- What can cause increased motility?
- What can malabsorption be caused by?
- When can there be inflammation (blood diarrhoea)?
- What can increased secretions be brought about?
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Organic causes, stool weight >250 g/day
-
Viral gastroenteritis
Hyperthyroidism
Diabetic autonomic neuropathy
-
Osmotic diarrhoea
-
Infective, eg shigella, Inflammatory bowel disease
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Enterotoxins - Vibrio cholerae, E.coli, C.difficile
Organic causes, stool weight >250 g/day
Viral gastroenteritis
Hyperthyroidism
Diabetic autonomic neuropathy
Osmotic diarrhoea
Infective, eg shigella, Inflammatory bowel disease
Enterotoxins - Vibrio cholerae, E.coli, C.difficile
Bile salts and fatty acids (ileal resection)

Pathophysiology of constipation
- Define constipation?
-
What is Normal transit time?
-
What is Slow transit time?
- 2 or more of following for >12 weeks:
- <3 stools/week
- straining > 25%
- hard stools
- incomplete evacuation
- anorectal blockage by stools
2. <6 days: 60% cases, perception of constipation from straining and hard stools
3. >6 days: 15% - mainly young women, onset after puberty, often <1 stool/week
Pathophysiology of constipation
- What are defactory disorders?
- What is megacolon?
- What are the causes?
- Defecatory disorders: 25% - Contraction external anal sphincter during straining, Anterior rectocele, Rectal mucosal prolapse during straining
-
Dilated colon
-
Hirschprung’s disease - aganglionic segment rectum, failure of relaxation of internal sphincter
Dilated colon
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Hirschprung’s disease - aganglionic segment rectum, failure of relaxation of internal sphincter

Pathophysiology of constipation
How is constipation managed?
- Refer defecatory disorders
- Increase dietary fibre and fluid
- Laxatives in severe cases or for acute relief
- Bulk-forming
- Stimulant
- Osmotic
- Suppositories
- Enemas
- Bulk-forming
- Stimulant
- Osmotic
- Suppositories
- Enemas

Physiology of defecation
- Outline the Int. Anal Sphincter
- Outline the Ext. Anal Sphincter
- Smooth m., parasympathetic innervation
- Striated muscle, somatic innervation
See picture

Pathophysiology of faecal incontinence
Give examples of the following causes of faecal incontinence
- Neurological/Psychological
- Anal sphincter dysfunction
- Other causes
-
spinal trauma (S2-S4)
stroke
pudendal nerve damage
spina bifida
MS
dementia
-
sphincter damage, eg during childbirth
pudendal nerve damage
perineal descent
-
rectal prolapse
impaction with overflow
severe diarrhoea
spinal trauma (S2-S4)
stroke
pudendal nerve damage
spina bifida
MS
dementia
sphincter damage, eg during childbirth
pudendal nerve damage
perineal descent
rectal prolapse
impaction with overflow
severe diarrhoea
Pathophysiology of salivary glands
How can a dry mouth be caused?
- Sjögren’s syndrome
- drugs
- antimuscarinic
- antihistamines
- antiparkisonian
- tricyclics
- dehydration, shock
- Salivary duct obstruction
- Calculus
- antimuscarinic
- antihistamines
- antiparkisonian
- tricyclics
- Calculus

Physiology of gastric acid secretion
Outline the following
- Control of acid secretion
- mechanisms involved in acid secretion
See picture

Pathophysiology of peptic ulcer disease
- What is the main clinical feature?
- What are the complications?
- Break in the epithelial surface of the stomach or duodenum down to muscularis mucosae. Epigastric pain and nausea
- bleeding: haematemesis/melaena perforation

Pathophysiology of peptic ulcer disease
Outline the pathogenesis of the following...
- Duodenal ulcer
- Gastric Ulcer
3. Outline the treatment of PUD
- H. pylori plus increased acid, reduced bicarbonate, genetic susceptibility
- pan gastritis, decreased acid, reduced mucosal resistance
-
H. pylori eradication
antacids/alginates
reduce acid secretion
- PPI
- H2 receptor blocker
H. pylori eradication
antacids/alginates
reduce acid secretion
- PPI
- H2 receptor blocker

Pathophysiology of malabsorption
How can failure of DIGESTION come about?
-
deficiency of digestive enzymes
- pancreatic failure (lipase, amylase, protease, etc)
- cystic fibrosis
- chronic pancreatitis
- specific deficiencies
- lactose intolerance
-
bile salt deficiency
- failure of lipid digestion/absorption
- bile duct obstruction
- bacterial overgrowth
- ileal resection
- pancreatic failure (lipase, amylase, protease, etc)
- cystic fibrosis
- chronic pancreatitis
- specific deficiencies
- lactose intolerance
- failure of lipid digestion/absorption
- bile duct obstruction
- bacterial overgrowth
- ileal resection
Pathophysiology of malabsorption
How can failure of ABSORPTION come about?
- reduced surface area small intestine
- coeliac disease (gluten enteropathy)
- sub-total villous atrophy
- intestinal resection
- jejunal resection (limited effect)
-
ileal resection
-
reduced enterohepatic recirculation of bile salt
-
bile salt deficiency
-
bile salt diarrhoea
-
gallstones
- reduced B12 absorption
- coeliac disease (gluten enteropathy)
- sub-total villous atrophy
- jejunal resection (limited effect)
-
ileal resection
-
reduced enterohepatic recirculation of bile salt
-
bile salt deficiency
-
bile salt diarrhoea
-
gallstones
-
- reduced B12 absorption
-

Pathophysiology of malabsorption
What are the consequences of malabsorption?
- diarrhoea/steatorrhea
- weight loss/failure to thrive
- abdominal pain
-
micronutrient deficiencies:
- Fe2+-deficiency (microcytic anaemia)
- B12 deficiency (macrocytic anaemia)
- Fat soluble vitamin deficiency with fat malabsorption:
- Vit A: night blindness
- Vit D: osteomalacia
- Vit E: haemolysis, neurological deficit
- Vit K: clotting deficiency
- Fe2+-deficiency (microcytic anaemia)
- B12 deficiency (macrocytic anaemia)
- Fat soluble vitamin deficiency with fat malabsorption:
- Vit A: night blindness
- Vit D: osteomalacia
- Vit E: haemolysis, neurological deficit
- Vit K: clotting deficiency
Pathophysiology of malabsorption
Consequences of malabsorption
- diarrhoea/steatorrhea
- weight loss/failure to thrive
- abdominal pain
- micronutrient deficiencies
Outline the micronutrient deficiencies that can occur...
In particular, what do the following fat soluble vitamine deficiency with fat malabsorption cause?
- Vit A
- Vit D
- Vit E
- Vit K
- Fe2+-deficiency (microcytic anaemia)
- B12 deficiency (macrocytic anaemia)
- Fat soluble vitamin deficiency with fat malabsorption
- clotting deficiency
- haemolysis, neurological deficit
- osteomalacia
- night blindness
Pathophysiology of malabsorption
What are the principles of management of malabsorption?
- treat underlying disorder
- gluten exclusion
- treat bacterial overgrowth
- supplement deficient enzymes
- pancreatic deficiency
- limit fat intake with steatorrhoea
- treat micronutrient deficiencies
- B12, Fe2+, etc
- bypass digestion (elemental diet)
- bypass absorption (parenteral nutrition)
- gluten exclusion
- treat bacterial overgrowth
- pancreatic deficiency
- B12, Fe2+, etc
Pathophysiology of GIT bleeding
- What are the causes of upper GIT bleeding?
- What are the consequences of an acute upper GI bleed?
- Reflux oesophageus, Mallory - weiss syndrome, varices, gastric varices, Gastric and Duodenal Ulcer, Gastric carcinoma (uncommon), Haemorrhagic gastropathy and erosions, hereditary telangiectasia (uncommon)
-
haemetemesis (shock, CV collapse) and melaena (black, tarry stools)
