Gastrointestinal I

Question 1

Oesophageal sphincters

Answer 1

The upper oesophageal sphincter at the junction between pharynx and oesophagus (pharyngo-oesophageal) prevents the entry of air into the oesophagus. The upper oesophageal sphincter is formed by a circular layer of striated muscle, i.e. the cricopharyngeus.

The lower oesophageal sphincter prevents the entry of gastric contents into the oesophagus. The lower oesophageal sphincter is not an anatomical entity, but the lower 4 cm of the oesophagus functions as a sphincter.

Sphincteric competence is aided by the normal intra-abdominal location of the terminal part of the oesophagus. The lower oesophageal sphincter opens when the wave of peristalsis begins in the upper oesophagus. Opening is vagally mediated. In the absence of oesophageal peristalsis the sphincter remains tightly closed to prevent reflux of gastric contents.

Question 2

Swallowing phases

Answer 2

Oral or voluntary stage

Pharyngeal stage

Oesophageal stage.

Swallowing can be initially voluntary, but thereafter it is almost entirely under reflex control.

Question 3

Swallowing: Oral

Answer 3

The tongue propels the bolus of food into the pharynx, where it stimulates tactile receptors that initiate the swallowing reflex. Sensory impulses from these receptors are transmitted to the swallowing centre in the medulla via the fifth, ninth, and tenth nerves. After integration in the medulla, efferent impulses are transmitted via the twelfth, seventh, fifth and tenth nerves to the muscles involved in the process of swallowing.

Question 4

Swallowing: Pharyngeal

Answer 4

1) The soft palate is pulled upwards and the palatopharyngeal folds move inwards towards one another, preventing reflux of food into the nasopharynx.
2) The vocal cords are approximated, the epiglottis covers the opening of the larynx, and the larynx moves upwards against the epiglottis. Food is thus prevented from entering the trachea.
3) The upper oesophageal sphincter relaxes and the superior constrictor of the pharynx contracts to force the bolus onwards.
4) The bolus is then propelled onwards by sequential contraction of the superior, middle and inferior constrictors of the pharynx. This produces a peristaltic wave pushing the bolus towards the upper end of the oesophagus.
5) During the pharyngeal stage, respiration is reflexively inhibited.

Question 5

Swallowing: Oesophageal

Answer 5

1) After passing the upper oesophageal sphincter, the latter reflexively constricts.
2) The bolus is propelled downwards by the primary peristaltic wave caused by impulses originating in the swallowing centre and conducted via the tenth nerve to the myenteric plexus of the oesophagus.
3) This wave pushes the bolus ahead of it at 2–4cm/s, i.e. the entire oesophagus is traversed in approximately 10 s.
4) If the primary peristaltic wave is insufficient to clear the oesophagus of food, the distension of the oesophagus initiates another peristaltic wave that begins at the site of dis- tension and moves downwards. This is known as secondary peristalsis.
5) Tertiary contractions may occur. These are stationary, non-propulsive contractions that may occur anywhere in the oesophagus. They are considered abnormal, but are frequently present in the elderly who have no symptoms of oesophageal disease.

Question 6

Lower oesophageal sphincter competence

Answer 6

1) At the lower end of the oesophagus is a high pressure zone where the pressure averages 15–25 mmHg.
2) It extends from approximately 2 cm above the diaphragm to 2 cm below.
3) It is purely a physiological sphincter, as it cannot be identified anatomically.
4) The competence of this sphincter is necessary to prevent reflux of gastric juices from the stomach into the oesophagus.

Question 7

Lower oesophageal sphincter competence: other mechanisms

Answer 7

1) The oesophagus is compressed by muscle fibres of the right crus of the diaphragm as it passes through the oesophageal hiatus.
2) The acute angle of entry of the oesophagus into the stomach produces a valve-like effect.
3) Mucosal folds at the gastro-oesophageal junction act as a valve.
4) The intra-abdominal portion of the oesophagus is subjected to intra-abdominal pressure which compresses the walls of the intra-abdominal segment of the oesophagus.
5) The hormone gastrin causes contraction of the muscle at the lower end of the oesophagus.

Question 8

Functions of the stomach

Answer 8

1) It acts as a reservoir allowing the ingestion of large meals.
2) It mixes food with gastric secretions, producing chyme which is then delivered to the small intestine for further digestion and absorption to occur.
3) It produces gastric juices which contain hydrochloric acid, pepsin, intrinsic factors, and mucus secretions.
4) The pyloric glands produce the hormone gastrin (G cells)

Question 9

Gastric secretions

Answer 9

2–3 L of gastric juice are secreted each day. This contains: 
1)	Water and ions
2)	Hydrochloric acid
3)	Mucus
4)	Pepsin
5)	Gastric lipase
6)	Intrinsic factor 
HCl is required for the activation of pepsinogen to pepsin. HCl is formed by active secretion from stimulated parietal cells. Control of gastric secretion is under neural and hormonal control. The control of gastric secretion is divided into three phases: cephalic, gastric and intestinal.

Question 10

Hydrochloric acid (see acid secretion diagram)

Answer 10

1) Needed for the activation and optimum activity of pepsin.
2) It is secreted by the parietal cells of the body and fundus of the stomach.
3) It activates pepsinogen to pepsin.
4) It allows conversion of ferric iron in the diet to the ferrous form and provides an acid environment in the duodenum to facilitate iron and calcium absorption.
5) The presence of acid in the duodenum stimulates the release of secretin.
6) HCl is also responsible for killing a number of ingested bacteria.

Question 11

Pepsin

Answer 11

1) Pepsin is secreted as the inactive precursor pepsinogen by the chief cells of the gastric glands.
2) Pepsinogen is activated to pepsin by the presence of HCl.
3) Pepsin breaks down food proteins into smaller peptides and polypeptides, digesting as much as 20% of protein of an average meal.
4) When the duodenal contents are neutralised, pepsin is irreversibly inactivated.

Question 12

Mucus

Answer 12

Gastric mucus is produced by the superficial cells of the gastric mucosa, the mucous-neck cells and the mucous cells of the pyloric glands. It is a thick, sticky, glycoprotein material which adheres to the gastric mucosa. It acts as a lubricant and also protects the underlying mucosa from digestion by acid and pepsin.

Question 13

Intrinsic factor

Answer 13

1) Intrinsic factor is a glycoprotein secreted by the parietal cells. It is required for the normal intestinal absorption of vitamin B12.
2) Vitamin B12 binds to intrinsic factor and passes to the terminal ileum, where receptors in the ileal mucosa bind the complex and B12 is absorbed by the ileal mucosal epithelial cells.
3) Intrinsic factor is released by the same stimuli that cause secretion of acid from parietal cells, i.e. vagal, gastrin and histamine.
4) Lack of intrinsic factor may arise from deficient production by parietal cells due to antiparietal cell antibodies, in pernicious anaemia, or following loss of parietal cells, i.e. following gastrectomy.
5) In the absence of intrinsic factor, vitamin B12 will not be absorbed in the terminal ileum, and megaloblastic anaemia will result.
6) Removal of more than 1 m of the terminal ileum, e.g. resection in Crohn’s disease, will also result in megaloblastic anaemia.

Question 14

Acid secretion: Cephalic phase

Answer 14

1) This is initiated by the site, smell and taste of food, and occasionally by the thought of food.
2) The effect is vagally mediated and is abolished by vagotomy.
3) Cholinergic vagal fibres are the mediators of the cephalic phase.
4) Acetylcholine released directly stimulates the parietal cells to produce acid.
5) It also stimulates acid secretion indirectly by releasing gastrin from G cells and histamine from enterochromaffin-like cells in the gastric mucosa.

Question 15

Acid secretion: Gastric phase

Answer 15

1) The presence of food in the stomach releases gastrin by both a mechanical and chemical stimulation.
2) Products of protein digestion are the chemical stimulators. Amino acids in the antrum cause gastrin release directly by stimulation of receptors on G cells.
3) Distension of the body or antrum are the mechanical mediators. The presence of food in the stomach excites vagal reflexes, impulses passing to the brain via vagal afferents and returning via efferents to stimulate the parietal cells.
4) Distension of the pyloric area enhances gastrin release through a local intramural cholinergic reflex.
5) Gastrin then stimulates the parietal cells via its release into the circulation, rein- forcing direct parietal cell stimulation. Once the buffering capacity of the gastric contents is saturated, the gastric pH falls rapidly and inhibits further acid release.
6) Gastric secretion is also directly stimulated by calcium ions, caffeine and alcohol.

Question 16

Acid secretion: Intestinal phase

Answer 16

1) During this phase, gastric secretion is brought about by duodenal distension and the presence of protein digestion products, i.e. peptides and amino acids.
2) The effect is mediated by endocrine mechanisms, largely via G cells in the duodenum and proximal jejunum. Other mechanisms operating during the intestinal phase inhibit gastric secretions.
3) These include the presence of acid, fat digestion products and hyper- tonicity in the duodenum and proximal jejunum. Acid in the duodenum causes the release of secretin into the circulation.
4) Secretin inhibits gastrin released by G cells and inhibits the response of parietal cells to gastrin.

5) Fatty acids in the duodenum inhibit gastric
secretion by releasing two hormones: cholecystokinin and gastric inhibitory peptide (GIP).

6) GIP suppresses gastrin release and also directly inhibits acid secretion by parietal cells. Cholecystokinin inhibits acid secretion by parietal cells.

Question 17

Gastric mucosa protection

Answer 17

Prostaglandin E2 is a gastro-protective mediator with the following actions:
• Inhibition of acid secretion
• Promotion of secretion of protective mucus
• Vasodilatation of submucosal blood vessels.
Gastric and duodenal mucosa is protected against acid-pepsin by a layer of mucus into which bicarbonate is secreted. If the gastric mucosa is damaged and the protective layer of mucus is lost, acid diffuses into the stomach wall, initiating or perpetuating peptic ulceration.
Vasodilatation of the submucosal blood vessels allows the hydrogen ions which have diffused into the stomach wall more opportunity to diffuse back into the blood vessels and into the circulation, where they are buffered.
Aspirin, alcohol and bile impair the protective function of the mucus layer.

Question 18

GI Hormones

Answer 18

The gastrointestinal hormones are peptides produced by enterochromaffin cells in the gastrointestinal mucosa. They are involved in the control of gastrointestinal secretions and motility. The cells producing these hormones are sometimes referred to as APUD cells (amine precursor uptake and decarboxylation). The major hormones are:

1) Gastrin
2) Cholecystokinin (CCK)
3) Secretin
4) Somatostatin

Question 19

Gastrin

Answer 19

1) Gastrin is produced by the G cells contained in the antral mucosa and in the upper small intestine.
2) Factors responsible for gastrin release are:
a. (i) stimulation by the products of digestion, caffeine and alcohol
b. (ii) extrinsic nerve stimulation during the cephalic phase of gastric secretion
c. (iii) antral distension, where the release is mediated by local intrinsic nerve reflexes.
Gastrin release is inhibited by
1) Increasing gastric acidity
2) Secretin
3) Somatostatin.
Gastrin is carried in the blood stream and stimulates gastric secretion of hydrochloric acid, pepsinogen and intrinsic factor. It also enhances gastric motility and may increase the tone of the lower oesophageal sphincter.
Gastrin may be produced by gastrinomas in the gastrointestinal tract, and this can result in increased production of acid, causing peptic ulceration (Zollinger–Ellison syndrome).

Question 20

Cholecystokinin

Answer 20

1) Cholecystokinin is produced by cells found in the mucosa lining the duodenum and the jejunum.
2) It is released into the blood stream in response to the products of digestion, especially fatty acids, peptides and amino acids.
3) The presence of these in duodenum and jejunum acts either directly on the cells or through local intrinsic nerve reflexes.
4) CCK delays gastric emptying
5) CCK stimulates an enzyme rich secretion from the acinar cells of the pancreas.
6) CCK also causes contraction of the gall bladder and relaxation of the sphincter of Oddi.

Question 21

Secretin

Answer 21

1) Secretin is produced by cells lying in the mucosa of the duodenum and jejunum.
2) It is released into the blood stream following increased acidity of the duodenum and jejunum and also by the presence of fatty acids.
3) It causes increased secretion of HCO3 by stimulating the duct cells of the pancreas and also of the liver.
4) It also reduces gastric acid secretion by direct action on oxyntic cells and by inhibition of gastrin release.

Question 22

Somatostatin

Answer 22

1) Produced by the D cells in the intestine and pancreatic islets in response to glucose, fats and bile salts in the intestinal lumen.
2) It has an inhibitory effect on
a. Pancreatic enzymes secretion
b. Insulin and glucagon release
c. Gastric acid
d. Pepsin secretion
e. Gastrin release.

Question 23

Antacids action

Answer 23

1) Neutralisation of gastric acid;
2) Reduction of delivery of acid into the duodenum 
following a meal; and
3) Inactivation of proteolytic enzymes by raising the 
gastric pH above 4–5
Antacids include sodium bicarbonate, calcium car- bonate, magnesium salts and aluminium hydroxide. Magnesium salts tend to cause diarrhoea; aluminium salts tend to cause constipation. A combination of the two is often used to offset the diarrhoea caused by one and the constipation caused by the other.

Question 24

H2-receptor antagonists

Answer 24

H2-receptor antagonists in clinical use include ranitidine and cimetidine.

1) Ranitidine may be preferable in young males who need a prolonged course as there is a lower reported incidence of gynaecomastia and impotence.
2) Ranitidine may be more appropriate in the elderly as cimetidine is known to cause confusion.
3) Ranitidine has a lower affinity for cytochrome P450 than cimetidine and does not inhibit the metabolism of warfarin, phenytoin and theophylline to a significant degree as compared with cimetidine.

Question 25

Proton-pump inhibitors

Answer 25

These include omeprazole, lansoprazole and pantoprazole. They inhibit gastric secretion by blocking the H+/K+ ATPase enzyme system (the proton-pump) of the gastric parietal cells.
Indications for proton-pump inhibitors include:
1) Peptic ulcer disease
2) NSAID-associated peptic ulcer and gastric erosions
3) Gastro-oesophageal reflux disease (GORD)
4) In combination with antibiotics for eradication of
a. H. pylori
b. Oesophagitis
c. Zollinger–Ellison syndrome

Question 26

Small bowel

Answer 26

The following substances are either digested or absorbed: Carbohydrate, fat, protein, vitamin B12, folate, iron, calcium, water and electrolytes.
Even following extensive resection of small bowel it is possible to survive with approximately 80cm without the need for total parenteral nutrition.
Active transport mechanisms occur for the absorption of many substances.

Question 27

Vitamin B12

Answer 27

1. Vitamin B12 is present in animal food sources, e.g. liver, meat, cheese, milk, eggs. It does not occur in plant sources.
2. It combines with gastric intrinsic factor produced by the parietal cells of the stomach.
3. The B12- intrinsic-factor complex passes to the terminal ileum where the vitamin B12 is absorbed.

Question 28

Reduced B12 absorption

Answer 28

1) Lack of intrinsic factor, e.g. pernicious anaemia, gastric resection
2) Resection of the terminal ileum
3) Diseases of the terminal ileum, e.g. Crohn’s and blind loop syndrome – bacteria compete with the 
patient for vitamin B12.

Question 29

Folic acid

Answer 29

1) 
Folic acid is present in foods, vegetables, fish and liver.
2) It is absorbed in the jejunum.
3) Malabsorption occurs in diseases involved in the jejunal mucosa, e.g. coeliac disease and following jejunal resection.
4) Patients on epanutin, an anti-epileptic drug, may become folate deficient because of the inhibition of a mucosal enzyme system and consequent prevention of folate leaving the mucosal cells. 


Question 30

Iron

Answer 30

1) 
Iron is absorbed by active transport in the duodenum and the jejunum.
2) Iron is found in meat, liver, eggs and green vegetables.
3) Most of the dietary intake is in the ferric form, but is converted in the presence of hydro- chloric acid in the stomach to the ferrous form for absorption in the duodenum and upper jejunum.

Question 31


Calcium 


Answer 31

1) Calcium is absorbed by active transport from the upper small intestine, chiefly the duodenum.
2) Absorption is regulated by requirements. Most of the calcium in the diet is in the form of calcium phosphate and is derived from milk and other dairy products.
3) A fall in serum calcium level in the plasma leads to an increased output of parathyroid hormone. This acts on bone, the kidney and indirectly on the gastrointestinal tract through the active form of vitamin D to return the serum calcium to normal.
4) Acidity increases calcium absorption from the gut lumen.
5) Factors influencing calcium absorption include:
a. (i) increased dietary oxalates, phytates and phosphates, which chelate calcium and reduce its absorption
b. (ii) vagotomy and gastrectomy, which reduce acid secretion and, therefore, reduce absorp- tion
c. (iii) steroids (glucocorticoids) which antagonise the effects of vitamin D on the gastrointestinal tract and reduce absorption.

Question 32

Malabsorption: Causes

Answer 32

1) Defects of mixing of food and digestive juices
2) Defective production of enzymes
3) Defective production of enzymes
4) Abnormal luminal conditions
5) Loss of enterocyte mass (reduction of absorptive area)

Question 33

Malabsorption: Defective production of enzymes

Answer 33

This may occur with abnormalities of the pancreas, e.g. chronic pancreatitis, cystic fibrosis, or carcinoma of
the head of the pancreas.
Lack of pancreatic enzymes reduce absorption of fats, proteins and carbohydrates.

Question 34

Malabsorption: Defective production of bile

Answer 34

1) This may occur because of blockage of the bile duct by stone, tumour or inflammation. Bile can not enter the duodenum, preventing digestion and absorption of fats with consequent steatorrhoea and malabsorption of fat soluble vitamins.
2) Bile salt reabsorption is impaired by terminal ileal disease, e.g. Crohn’s disease, or resection, resulting in defective enterohepatic circulation and consequent reduction in bile salt concentrations in the duodenum.

Question 35

Malabsorption: Abnormal luminal conditions

Answer 35

1) This may result from increased intraluminal pH as a result of reduced gastric secretion, e.g. after vagotomy
 or gastrectomy. This would result in decreased absorption of iron and calcium.
2) Blind loop syndrome (bacterial overgrowth in areas of stasis) may cause malabsorption. Bacteria may compete with the host for dietary vitamin B12, resulting in megaloblastic anaemia.


Question 36

Malabsorption: Loss of enterocyte mass (reduction of absorptive area)

Answer 36

This usually results from surgical resection, e.g. Crohn’s disease, mesenteric infarction, or trauma. The effects depend on the extent of resection as well as the site, proximal or distal.

Question 37

Small bowel resection: Jejunum

Answer 37

1) After resection of a length of jejunum the ileum can take over some of the functions. However, the reverse is not true, the jejunum being incapable of absorbing bile salts and vitamin B12.
2) Following loss of most of the jejunum, absorption of fat, protein and carbohydrates is severely curtailed because of loss of the large absorptive area. Severe diarrhoea occurs with add- itional loss of water and electrolytes.
3) After a few weeks, ileal adaptation takes place and diarrhoea abates. Loss of body weight and reduced folate and iron absorption occur in the early phase after resection.

Question 38

Small bowel resection: ileum

Answer 38

1) With resection of more than 1 m of terminal ileum, absorption of vitamin B12 and bile salts is reduced.
2) Malabsorption of vitamin B12 results in megaloblastic anaemia. However, with normal stores prior to resection it can take 3–6 years for this to develop. Vitamin B12 supplements will then be required parenterally.
3) With loss of the terminal ileum there is a reduced absorption of bile salts and the bile salt pool declines. As the pool normally circulates 6–8 times/day the liver cannot replenish this loss.
4) Reduction in the bile salts leads to an increased tendency to gall stone formation and poorer emulsification and absorption of fats in the small intestine leading to steatorrhoea and decreased absorption of vitamins A, D, E and K. Calcium deficiency may also occur as a result of decreased absorption of vitamin D.
5) Decreased absorption of bile salts results in more entering the colon resulting in diarrhoea.

Question 39

High vs Low output fistulae

Answer 39

High output fistulae occur in the upper small bowel e.g. duodenal fistula, and low output in the ileum.

Question 40

High output fistulae

Answer 40

1) Approximately 3–4L of fluid is lost per day. This is derived from gastric juice, bile, pancreatic juice and duodenal secretions.
2) This requires replacement with isotonic saline, as the juices lost are mostly isotonic.
3) Loss of alkaline pancreatic juice and bile gives rise to a metabolic acidosis. Any oral intake of food passes out through the fistula; in some cases it is virtually unchanged and, unless replaced by intravenous feeding, would result in starvation.
4) Skin protection is required with external fistulae because activated pancreatic trypsin will digest the keratin of the skin, causing excoriation.
5) Treatment of high output fistulae requires intravenous administration of water and electrolytes commensurate with losses, together with total parenteral nutrition until the fistula closes or is surgically closed.

Question 41

Low output fistulae

Answer 41

1) A low small bowel fistula may initially put out up to 1500mL daily.
2) A low output small bowel fistula is similar to an ileostomy. The proximal ileum can gradually adapt to the loss of any colonic surface distal to it, and more fluid and electrolytes are absorbed.
3) Fluid loss is lower in low fistulae because there is still a large proximal surface area to deal with fluid absorption.
4) Also, loss of nutrients is less because most have already been absorbed in the proximal small bowel. In the initial stages, fluid and electrolyte management is important but nutrition may be maintained by elemental diets.

Question 42

Large bowel functions

Answer 42

The primary functions of the colon are:

1) Absorption
2) Secretion
3) Motility
4) Storage

Question 43

Large bowel: absorption

Answer 43

1) Water and electrolytes are absorbed in the colon. Approximately 1–2 L of ileal contents containing 90% water reach the colon daily.
2) Water is absorbed during transit such that only 100–200mL of water are lost in the faeces.
3) Some amino acids, fatty acids and vitamins, e.g. vitamin K, may be absorbed in the colon, but only a small amount of these normally reaches the colon, having been absorbed in the small intestine.
4) A proportion of ingested starch reaches the colon, where bacterial action converts it to short chain fatty acids which are absorbed.
5) Sodium is actively absorbed, being potentiated by the action of aldosterone.

Question 44

Large bowel: secretion

Answer 44

1) Potassium is secreted into the intestinal lumen.
2) Aldosterone increases potassium secretion.
3) Potassium is also secreted in mucus, and hypokalaemia may result if large amounts of mucus are lost, e.g. from a large vil- lous adenoma.
4) Bicarbonate is also secreted by colonic cells. It neutralises any acidity of the faeces which may result from bacterial fermentation of carbohydrate.
5) Mucus is secreted by the goblet cells and lubricates the passage of faeces.

Question 45

Large bowel: Motility

Answer 45

1) Retrograde peristalsis (antiperistalsis) These are annular contractions moving against flow and occur chiefly in the right colon.
a. This churns the contents, confining them to the caecum and ascending colon.

2) Segmentation This occurs chiefly in the transverse and descending colon.
a. Contraction rings occur in the smooth muscle over lengths of approximately 2.5cm.
b. These occur at different points along the bowel, dividing it into segments of contracted and relaxed areas.
c. Faeces are propelled over short distances in both directions.

3) Mass movement This represents a strong peristaltic wave which covers a large distance in the transverse and descending colon, pushing faeces distally.
a. Mass movement occurs only 3–4 times daily, usually after food. Some of the material entering the caecum may pass by faeces remaining from earlier periods.
b. In most people the unabsorbed part of a meal reaches the caecum in approximately 4h and the descending colon in 24h.
c. However, because of the complex and variable movements of the colon, approximately 25% of the residue of a meal can remain in the rectum at 72 h. Mass movement occurs following entry of food into the stomach, i.e. the gastrocolic reflex.

Question 46

Large bowel: Storage

Answer 46

1) The colon stores faeces until the time for defaecation is appropriate.
2) The primary site of storage is the transverse colon.
3) Gas is also stored in the colon. Colonic gas is largely nitrogen but also contains oxygen, carbon dioxide, methane and some hydrogen sulphide.
4) Mannitol has been used in the past to prepare the bowel for surgical procedures. Colonic bacteria ferment mannitol to produce hydrogen. Hence, mannitol should be avoided in bowel preparation.
5) Excessive colonic gas is usually due to hydrogen. Avoidance of lactose, beans and wheat in the diet is appropriate in avoiding excessive colonic gas.

Question 47

Defaecation

Answer 47

1) The lining of the anal canal contains sensory nerve endings which are sensitive to tactile, thermal and painful stimuli.
2) Somatic sensation classically ceases at the dentate line, but often it may extend more proximally.
3) The nerve endings in the anal canal relay information into the CNS, identifying the luminal contents, i.e. whether solid or gas.
4) When faecal material enters the rectum, causing the pressure to increase above 18 mmHg, a desire to defaecate occurs. This is due to stimulation of receptors within the rectal wall.
5) Afferent impulses pass via the pelvic nerves to sacral segments 2, 3, 4, i.e. the defaecation centre.
6) Efferent impulses then pass back to the rectum to the myenteric plexus where postganglionic parasympathetic nerves are activated. These cause contraction of the rectum, pushing faeces distally. The internal sphincter also relaxes.
7) Afferent impulses from the rectum also activate ascending sensory pathways providing conscious awareness of rectal distension.
8) When faecal material enters the upper anal canal, sensory receptors are stimulated which send impulses to S2, 3, 4 segments of the cord.
9) The effect of these impulses is two-fold:
a. (i) there is reflex activation of the pudendal nerve which sends impulses to the external sphincter to increase its contraction and maintain continence
b. (ii) there is activation of ascending pathways to the sensory cortex, which differentiates between solid and gas.
c. If it is solid, efferent impulses pass down the cord to reinforce contraction of the external sphinc- ter and maintain continence.
d. If it is gas the sphincter relaxes and flatus is passed.

Question 48

Involuntary defaecation

Answer 48

Overdistension of the rectum with a pressure of greater than 55mmHg causes involuntary defaecation.

This involuntary mechanism occurs in patients with spinal cord transection above S2, 3, 4. Immediately after transection, spinal shock occurs and there is no reflex activity, with retention of faeces. When reflex activity returns, reflex defaecation occurs although the patient is unaware that the rectum is filling.