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CHAPTER 10 Gastrointestinal System
B
A
221
TABLE 10.1 Summary of the Absorption
Micelles
and Secretion of Fluid Within the GI Tract
Secreted/
Absorbed
Ingested
Mouth Nothing 2–3 L fluid
ingested 1.5 L
saliva secreted
Stomach Lipid-soluble
compounds,
2–3 L gastric
juices secreted
e.g. alcohol
Gallbladder Absorbs water and
concentrates bile
500 mL bile
secreted
Pancreas Nothing 1.5 L pancreatic
juices secreted
Small bowel 8–9 L fluid
absorbed
Large bowel 1 L of fluid
absorbed
Secondary active
transport
Glucose
+
Galactose
Na
1.5 L intestinal
secretions
100 mL excreted
in faeces
‘Facilitated’
diffusion
Fructose
Fig. 10.4 Lipids are absorbed by diffusion as mono-
glycerides and fatty acids. Inside the cell they are
reconstituted to triglycerides, packaged as chylomicrons, and then enter the lymphatic channels (lacteals).
(From McGeown JG. Physiology, 2nd edn. Churchill
Livingstone, Edinburgh, 2002, with permission.)
• fats form globules in the stomach
Monoglycerides
Fatty acids
Triglycerides
Chylomicrons
Lacteals
• globules are coated with bile salts in the duodenum
• the bile salts disperse these globules into smaller drop-
Primary active
ATP
transport
+
K
Fructose
+
Na
Glucose
Galactose
lets; this increases the surface area exposed to pancreatic enzymes
• fatty droplets are broken down by pancreatic lipases to
monoglycerides and free fatty acids (FFA)
• the monoglycerides and FFAs combine with bile salts to
form micelles
• micelles have a hydrophilic outer layer and are able to
diuse into the enterocytes; the bile salt stays in the
Capillary
Capillary
bowel lumen
• in the enterocytes, the smooth endoplasmic reticulum
reforms triglycerides from the absorbed monoglycer-
Key
ATP
Movement against concentration gradient
Diffusion down concentration gradient
Carrier molecule
ATP dependent pump
ides and FFAs
• the reformed triglycerides are formed into particles of
fat called chylomicrons, which are released from the
basal layer of the enterocyte to diuse into the lacteals
within the villi; from here they enter the lymphatic circulation and then into the venous circulation.
Fig. 10.3 Carbohydrate absorption mechanism. (A)
Glucose and galactose are absorbed by an active transport mechanism using Na+ as a cotransport. (B) Fructose
absorption is passive, but utilizes a carrier molecule.
(From McGeown JG. Physiology, 2nd edn. Churchill
Livingstone, Edinburgh, 2002, with permission.)
Protein (Fig. 10.5)
• Proteins are broken down into amino acids by the proteolytic enzymes released from the stomach (pepsin)
and pancreas (see below).
• A Na+-dependent cotransport mechanism absorbs amino
acids.
222
Amino
Secondary active
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SECTION II Physiology
+
acid
Na
+
Na
Amino
acid
Capillary
Fig. 10.5 Amino acids are absorbed using a Na+
cotransport system. (From McGeown JG. Physiology,
2nd edn. Churchill Livingstone, Edinburgh, 2002, with
permission.)
ATP
transport
Primary active
transport
K
+
• ere are four transporters:
• neutral amino acids
• basic amino acids
• acidic amino acids
• proline and hydroxyproline.
• e majority of amino acids are absorbed in the upper
small intestine; any that enter the large bowel are metabolized by the resident bacterial ora.
Fluids and Electrolytes
• Approximately 2–3 L of uid is ingested each day;
another 8–9 L is secreted into the GI tract, but only
100–200 mL is excreted in the faeces.
• Na+ absorption is coupled with the absorption of glucose and amino acids; active absorption is stimulated
by aldosterone.
• K+ is absorbed along a concentration gradient (caused
by water absorption); a small amount is secreted in
mucus.
• Anions such as Cl− are generally absorbed by electrochemical gradients created by Na+ absorption.
• e absorption of water is a result of the osmotic gradient established by the absorption of nutrients and
electrolytes.
Vitamins
• Vitamins are divided into fat-soluble and water-soluble;
this classication refers to the method of absorption.
• Fat-soluble vitamins (A, D, E and K) are absorbed
within the micelles created during fat absorption.
• Water-soluble vitamins (C and B) are absorbed by more
specic mechanisms:
• vitamin C is absorbed by a Na+-dependent mecha-
nism in the jejunum
• vitamin B12 is absorbed in the ileum aer intrinsic
factor (secreted in the stomach) binds to its specic
receptor. e IF–vitamin B12 complex is then taken
up into the cell
• the remaining B vitamins diuse freely across the
enterocyte cell membrane.
Iron
• Iron is absorbed in the duodenum and jejunum in the
ferrous (Fe2+) and not the ferric (Fe3+) form; gastric acid
is responsible for converting iron to the ferrous form.
Absorption is then via the transport protein transferrin.
is binds iron and links to a membrane-bound receptor, and is then taken into the cell via endocytosis; it
is then transferred to the plasma and binds to plasma
transferrin.
Calcium
• Absorption is dependent on a calcium-binding protein
in intestinal cells; these receptors can be increased by
vitamin D, and thus the rate of calcium absorption can
be increased when plasma levels fall.
Small Intestinal Motility
• ere are three types of movement in the small bowel:
• segmentation (feeding)
• peristalsis (feeding)
• migrating motility complex (MMC) (fasting).
• Segmentation is a movement that facilitates mixing of
chyme; the circular muscle layer contracts and relaxes
in adjacent segments; this results in circular movements
of the chyme.
• Peristalsis is a propulsion movement that is triggered by
distension. e longitudinal muscle contracts; midway
through contraction of the longitudinal muscle the circular muscle also contracts. is pattern of contraction
is repeated and moves food through the bowel.
• Peristaltic contractions eventually reach the ileocaecal
valve and cause it to relax, thus allowing food to enter
the large bowel.
• Peristaltic contractions last a few seconds and only
propel the food a few centimetres; the MMC leads to
contraction along the full length of the small bowel and
lasts several hours. eir purpose is to push any remaining food debris into the colon. e stimulation for the
MMC is not fully understood, but may involve the hormone motilin.
CHAPTER 10 Gastrointestinal System
223
• e movements of segmentation and peristalsis are
intrinsic and result from the basal electrical rhythm in
the intestine. It can be inuenced by extrinsic nervous
input:
• parasympathetic: increases rate of contraction
• sympathetic: decreases rate of contraction.
• In addition to the autonomic input, there are several
reexes which also inuence intestinal contractility:
• ileogastric reex: distension of the ileum decreases
gastric motility
• gastroileal reex: increase in gastric secretion or con-
tractility increases ileal motility.
Clinical Physiology
Physiological Effects of Duodenal Resection
Removal of the duodenum (duodenectomy) leads to a
range of physiological abnormalities, including:
• Ulceration of small bowel: the duodenum is able to
withstand gastric acid better than small bowel; this is
due to HCO
from the pancreas—allowing the neutralization of gastric acid within the chyme. Following duodenal resection, surgical reconstruction of bowel continuity oen
involves small bowel; the rerouted gastric acid causes
peptic ulceration in the small bowel.
• Malabsorption: Fe2+, Ca2+ and PO
impaired fat emulsication.
• Dumping: loss of control over gastric emptying leads
to uncontrolled passage of chyme into the small bowel,
resulting in dumping.
Physiological Effects of Terminal Ileal Resection
Removal of the terminal ileum (ilectomy) leads to a range
of physiological abnormalities, including:
• Bile salt reabsorption: the terminal ileum is the site of
bile salt absorption; loss of this mechanism leads to:
• bile salts in the colon; this alters the bacterial ora
and stool consistency, and can lead to an increased
risk of colonic malignancy
• due to the loss of enterohepatic circulation, there is a
decrease in bile salt pool; this predisposes to cholesterol gallstones.
• Vitamin B12 deciency: receptor-mediated reabsorption in conjunction with intrinsic factor occurs in the
terminal ileum; resection of the ileum will result in
deciency of B12 and cause a macrocytic anaemia and
degeneration of the spinal cord if not corrected.
• Water reabsorption: the ileum plays an important role
in the absorption of water from bowel contents (especially in the elderly); this leads to diarrhoea and an
increase in stool frequency.
−
secreted from the Brunner's glands and
3
−
malabsorption and
4
PANCREAS
Exocrine Secretions
Fluid Component
• e pancreas secretes approximately 1.5 L of uid per day;
it contains a variety of enzymes and is rich in bicarbonate.
• e epithelial cells that line the ducts form the uid
component of pancreatic juice; HCO
into the lumen in exchange for Cl− and directly via a
luminal channel. Sodium and potassium are exchanged
for H+ formed by the reaction catalysed by carbonic
anhydrase. Na+ follows HCO
chemical neutrality and water follows by the osmotic
gradient created by the movement of Na+ and HCO
Enzyme Component
• e enzymes secreted by the pancreas can be divided into:
• proteolytic
• amylase
• lipolytic.
Proteolytic enzymes
• ese enzymes are secreted in an inactive form, called
zymogen granules, from pancreatic acinar cells. e key
event in the activation of these enzymes is activation of
trypsinogen to trypsin. Activation of trypsinogen is by
an enzyme secreted by the duodenum (enterokinase)
and the alkaline environment.
• Trypsin then activates the other enzymes:
• chymotrypsinogen: chymotrypsin (cleaves peptide
bonds)
• proelastase: elastase (cleaves peptide bonds)
• trypsinogen: trypsin (cleaves peptide bonds)
• procarboxypeptidase: carboxypeptidase (cleaves pep-
tides at the C-terminus).
Amylase
• Responsible for the majority of starch digestion; it splits
α-1,4-glycosidic bonds; the brush-border enzymes of
the small bowel digest the resulting oligosaccharides.
Lipolytic enzymes
• As with proteolytic enzymes, the lipolytic enzymes are
excreted in an inactive form; they are all activated by
trypsin. ese enzymes include:
• lipase: cleaves triglycerides to FFAs and glycerol
• co-lipase: helps bind lipase to the lipids
• phospholipase A2: cleaves FFAs from phospholipids
• cholesterol esterase.
Regulation of Exocrine Secretions
• As with gastric secretion, regulation of pancreatic juice
secretion is divided into three phases:
• cephalic: vagal
• gastric: vagal
• intestinal: CCK and secretin.
−
is transported
3
−
to maintain electro-
3
−
.
3
224
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SECTION II Physiology
Cephalic
• During the cephalic phase the sight, smell and taste of
food cause vagal (parasympathetic) stimulation and the
release of acetylcholine (ACh) and VIP. ese activate
the acinar and ductal cells as well as increasing blood
ow via vasodilatation. A small stimulus also comes
from gastrin released from the gastric antrum cells.
Gastric
• Accounts for a relatively small stimulus to secretion;
gastrin secretion and distension (vagal gastropancreatic
reex) stimulate pancreatic secretion.
Intestinal
• Accounts for 60–70% of the stimulus for pancreatic
secretions; two main hormones are responsible for stimulating pancreatic secretions:
• cholecystokinin (CCK): release of a uid rich in
enzymes from acinar cells
• secretin: release of a bicarbonate-rich uid.
• Factors that promote secretion of these hormones (from
the duodenal mucosa) include:
• lipids (CCK)
• peptides and amino acids (CCK)
• acid (secretin).
Endocrine Secretions
See Chapter 12.
Clinical Physiology
Physiological Effects of Pancreatic Resection
Removal of the pancreas (pancreatectomy) leads to a range
of physiological abnormalities, including:
• Malnutrition: inadequate digestion of protein and lipids due to the loss of proteolytic and lipolytic enzymes.
e inadequate breakdown of protein leads to progressive weight loss and inadequate fat digestion; this leads
to fatty stools and atus (due to bacterial overgrowth).
e absorption of fat-soluble vitamins (A, D, E and K)
is reduced, and leads to progressive deciencies.
• Malabsorption: loss of alkaline pancreatic secretions
leads to failure to neutralize gastric chyme and leads to
Fe2+, Ca2+ and PO
to anaemia and osteoporosis.
−
malabsorption; this eventually leads
4
• Diabetes mellitus: loss of the pancreas leads to an absolute deciency of insulin.
LIVER AND GALL BLADDER
Liver
Bile Production (Fig. 10.6)
• Hepatocytes secrete uid into the canaliculi; this uid is
very similar to plasma with reference to its ion composition; however, it also contains:
• bile acids: cholic acid and chendeoxycholic acid
• bile salts: formed by linking the amino acids glycine
and taurine to bile acids. Bile salts have a hydrophobic
and hydrophilic region (amphipathic); this enables
them to form an emulsion of lipids in the intestinal
uid. e emulsion produces a large surface area for
pancreatic enzymes to act upon; in addition bile salts
form smaller collections of FFAs and monoglycerides
(micelles) to facilitate absorption into enterocytes.
e bile salts are not absorbed during this process,
and remain in the bowel lumen until the distal ileum,
where they are absorbed (see below)
• bile pigments: these are produced by the breakdown
of the haem unit of haemoglobin; it gives bile its
green/yellow colour. e destruction of ageing red
blood cells (RBCs) takes place in the spleen; in this
process bilirubin is released into the circulation; it is
poorly soluble and is transported to the liver bound
to albumin. e bilirubin is conjugated to glucuronic
acid in the hepatocytes, producing a water-soluble
compound that is excreted in bile. In the intestine
bacteria convert these pigments to:
• urobilinogen: some is reabsorbed in the intestine
and secreted back into the bile or excreted in the
urine
• stercobilin and urobilin: give faeces brown colour
• cholesterol
• lecithin
• mucus.
• ere are two factors that govern bile secretion; one is
dependent on bile acid recirculation (enterohepatic circulation), and the other is independent of this:
• enterohepatic circulation: >90% of secreted bile acids
are reabsorbed from the intestine (distal ileum) and
returned to the liver via the portal vein; the remaining 5–10% of bile acids are altered by bacterial ora
and become insoluble, and are thus excreted. e
rate at which bile acids are returned to the liver will
inuence the rate at which they are secreted into the
canaliculi
• the remaining components of bile (water, Na+,
−
HCO
) are secreted into the canaliculi indepen-
3
dently of bile acid recirculation. HCO
both actively pumped into the lumen; water follows
−
and Na+ are
3
due to the resulting osmotic gradient. Secretion of
the bicarbonate-rich uid is stimulated by secretin,
gastrin and glucagon.
• Regulation of secretion: CCK stimulates the contraction of the gall bladder and the release of bile into the
duodenum.
Metabolic Functions
e liver is responsible for the handling of dietary carbohydrate, protein and lipids.
Haemoglobin
Globin
Haem
Liver
CHAPTER 10 Gastrointestinal System
225
2+
Fe
Liver
Stercobilinogen
(= urobilinogen)
A
Porphyrin
Plasma
albumin
intestine
Small
Bilirubin
Bilirubin
glucuronide
Urobilinogen
Absorbed
Kidney
Urobilinogen
Reabsorbed
B
Fig. 10.6 (A) Summary of bile pigment metabolism. (B) Enterohepatic circulation of bile salts.
Carbohydrate metabolism
• Following a meal the digested components are delivered
to the liver via the portal vein; the absorbed glucose is
then converted to glycogen (the principal form of stored
carbohydrate; glycogenesis). At times of low blood glu-
starvation these stores are released, providing fatty
acids (provides energy as ATP for gluconeogenesis)
and glycerol (acts as a non-carbohydrate substrate
for gluconeogenesis)
• synthesizes lipoproteins and cholesterol.
cose or high energy demand the glycogen within the
liver is converted back to glucose (glycogenolysis).
Protein metabolism
• e liver has a number of roles related to protein
metabolism:
Protein Synthesis
• As mentioned above, the liver synthesizes all the plasma
proteins (other than immunoglobulins), all the nonessential amino acids and many of the clotting factors.
• able to produce glucose from amino acids and other
non-carbohydrate substances (gluconeogenesis);
this becomes particularly important in times of prolonged exercise and depletion of glycogen stores during starvation
• involved with synthesis of many of the plasma pro-
Vitamin D Activation
• Activation of vitamin D is a two-stage hydroxylation
process. e liver performs the rst hydroxylation to
give 25-hydroxycholecalciferol, and the kidney performs the second to give 1,25-hydroxycholecalciferol.
teins, such as albumin and clotting factors
• also handles the degradation products of amino
acid metabolism. Use of amino acids throughout the
body results in the production of ammonia, which is
converted to urea.
Lipid metabolism
• e liver is involved with several facets of lipid metabolism:
• glucose is converted to FFAs; this is then transported to adipose tissue. It is then combined
with glycerol and stored as triglycerides. During
Detoxification
• e liver detoxies a number of substances:
• peptide hormones: insulin, Anti-Diuretic Hormone
(ADH), growth hormone
• steroid hormones: testosterone, oestrogen, adrenal
cortex hormones
• catecholamines
• drugs
• toxins.
Bile
salts
Secreted
in bile
Small
intestine
226
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SECTION II Physiology
• e detoxication process involves two stages:
• stage 1: increase in the water solubility of the substrate (i.e. the cytochrome p450 system)
• stage 2: reduction in biological activity and toxic
activity.
Vitamin and Mineral Storage
• e liver stores a number of substances; in addition to
glycogen and fats, it also stores:
• iron
• copper
• vitamin A, D, E, K and B12.
Phagocytosis
• Kuper cells in the hepatic sinusoids remove bacteria,
debris and old RBCs.
Haemopoiesis
• In the embryo the liver is involved in haemopoiesis;
in adults it only plays a role in disease states such as
chronic haemolysis (extramedullary haemopoiesis).
Clinical Physiology
Jaundice
• Dened as the yellow pigmentation of the skin and eyes
as a result of excess bilirubin in the circulation; this
usually becomes clinically detectable at plasma levels
>40µmol/L (normal range is <22 µmol/L).
• Jaundice can be classied in three ways:
• prehepatic (haemolytic)
• hepatic (parenchymal)
• post-hepatic (cholestatic).
• is classication refers to the site of the obstruction or
abnormality aecting normal bilirubin metabolism.
• e following is a summary of bilirubin metabolism:
• RBCs are broken down in the spleen and release bili-
rubin, a breakdown product of the porphyrin ring of
haemoglobin; at this stage bilirubin is unconjugated
• unconjugated bilirubin is not water-soluble and
binds to albumin; it is in this form that it is transported to the liver
• in the liver the bilirubin is conjugated to glucuro-
nide; conjugated bilirubin is water-soluble
• bilirubin is then stored in the gall bladder and
excreted in the bile
• once the bilirubin enters the bowel, intestinal bacte-
ria convert it to urobilinogen. e urobilinogen may
be absorbed and recirculated back into the bile; some
is excreted in the urine, the remaining urobilinogen
that is not absorbed is excreted in the faeces; it gives
the faeces their brown colour. e urobilinogen that
is excreted in the faeces is further altered by bacterial
ora and is referred to as stercobilinogen.
Prehepatic jaundice
• is is caused by disorders that result in excessive
destruction of RBCs (haemolysis); the liver is overwhelmed by the bilirubin that is being produced and
is unable to conjugate it. e jaundice is thus referred
to as being an unconjugated hyperbilirubinaemia. is
nding is highly suggestive of a prehepatic cause for the
jaundice. Other laboratory ndings associated with prehepatic jaundice include:
• no bilirubin in the urine (unconjugated bilirubin is
not water-soluble)
• ↑urobilinogen in the urine (as a result of more biliru-
bin being broken down in the intestine)
• reticulocytosis: in response to the need to replace
destroyed blood cells
• anaemia
• ↑lactate dehydrogenase (LDH)
• ↓haptoglobin: protein that binds free haemoglobin
and transfers it to the liver.
• Common causes of prehepatic jaundice include:
• inherited:
• red cell membrane defects, e.g. hereditary sphero cytosis
• haemoglobin abnormalities, e.g. sickle cell disease
• metabolic defects, e.g. G6PD deciency
• acquired:
• immune, e.g. transfusion reactions
• mechanical, e.g. heart valves
• acquired membrane defects, e.g. paroxysmal nocturnal haemoglobinuria (PNH)
• infections
• drugs
• burns.
• In addition to the haemolytic causes of prehepatic jaundice, there are a group of disorders known as congenital
hyperbilirubinaemias; these include:
• unconjugated hyperbilirubinaemia:
• Gilbert’s syndrome: due to an abnormality in bilirubin uptake
• Crigler–Najjar syndrome: due to the absence of
glucuronyl-transferase
• conjugated hyperbilirubinaemia:
• Dubin–Johnson and Rotor’s syndrome: defects in
the handling of bilirubin.
Hepatocellular jaundice
• is is caused by a variety of conditions that interfere
with hepatocyte function. ere is usually an element
of cholestasis as hepatocytes swell and obstruct the ow
of bile. e hyperbilirubinaemia is a combination of
conjugated and unconjugated, reecting the impaired
CHAPTER 10 Gastrointestinal System
227
hepatocyte function and partial obstruction. Laboratory
tests demonstrate the following:
• liver enzymes, i.e. ↑ aspartate amino transferase
(AST) and ↑ alanine amino transferase (ALT); this
reects liver damage and thus release of these enzymes from hepatocytes
• ↑alkaline phosphatase: reects the partial cholestasis
• abnormal clotting tests reect the impaired hepatocyte function.
• Causes of hepatocellular jaundice include:
• viruses, e.g. hepatitis A, B, C and E; Epstein–Barr
virus (EBV)
• autoimmune disorders, e.g. chronic hepatitis
• drugs, e.g. paracetamol overdose
• cirrhosis
• liver tumours and metastasis.
Cholestatic jaundice
• is is due to obstruction of the biliary system and can
be further divided into intrahepatic or extrahepatic
obstruction:
• intrahepatic cholestasis is similar to hepatocellular
jaundice, as the obstruction is usually due to hepatocyte swelling; causes include:
• hepatitis
• drugs
• cirrhosis
• primary biliary cirrhosis
• extrahepatic cholestasis occurs due to obstruction of the
large bile ducts distal to the canaliculi; causes include:
• gallstones
• biliary stricture
• carcinoma: head of pancreas, ampulla, bile duct
(cholangiocarcinoma), malignant lymph nodes at
the porta hepatis
• pancreatitis
• sclerosing cholangitis.
• Laboratory tests demonstrate the following:
• bilirubin in the urine (characteristic dark colouration); this occurs as the bilirubin is conjugated and
thus water-soluble
• no urobilinogen in the urine; due to the obstruction, no bilirubin enters the bowel to be converted to
urobilinogen
• ↑canalicular enzymes: alkaline phosphatase and
γ-Glutamyl Transferase (GT)
• ↑liver enzymes ALT and AST; not as signicant as
seen in hepatocellular causes, but biliary backpressure inevitably leads to mild hepatocyte damage.
Gall Bladder
• e gall bladder stores bile; the bile from the liver is
diverted into the gall bladder due to the high tone in the
sphincter of Oddi. e bile is then concentrated by the
absorption of Na+, HCO
• e bile is released into the duodenum when the gall
bladder contracts; the major stimulus is the release of
CCK from the duodenum in response to fats and acid.
A small amount of gall bladder contraction is mediated
by the vagus when a fatty meal enters the stomach.
• CCK also stimulates pancreatic secretions and reduces
the tone within the sphincter of Oddi.
−
, Cl− and water.
3
Clinical Physiology
Physiological Effects of Cholecystectomy
• e removal of the gall bladder (cholecystectomy) is
usually well tolerated, but does have several physiological consequences that may lead to symptoms:
• the loss of the concentrating action of the gall blad-
der can lead to increased ow of bile, leading to
reux and biliary gastritis
• the formation of micelles during fat absorption is
disturbed, and can lead to fat intolerance and malabsorption; this can produce abdominal pain and
diarrhoea.
Water Absorption
• e colon is the last site for water reabsorption; it
absorbs up to 1 L of water per day. Na+ is transported
from the lumen under the inuence of aldosterone;
water follows along the osmotic gradient.
• Failure of uid absorption in the colon leads to diarrhoea (see below).
Colonic Flora
• e colon has a huge population of both aerobic and
anaerobic bacteria; these perform a number of roles:
• fermentation of indigestible carbohydrate: produces
fatty acids that the colonic mucosa is able to use as an
energy source and a variety of gases, such as carbon
dioxide and methane; these are released as atus
• degradation of bilirubin to urobilin, urobilinogen
and stercobilin
• synthesis of vitamins K, B12, thiamine and riboavin.
Large Intestinal Motility
• Food traverses the small intestine in approximately 5 h;
colonic movements are considerably slower, taking up
to 20 h or more before defecation.
• e colon has a number of movements:
• mixing or retrograde peristalsis: the circular mus-
cle contracts and narrows the lumen, the longitudinal muscle is incomplete in the colon and forms
bands called taenia coli. Contraction of the taenia
228
Pathways to
External anal
sphincter
Sacral
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SECTION II Physiology
coli appears to cause faecal matter to roll, and thus
increase its exposure for absorption (occurs predominantly in the right colon)
• peristalsis and mass movements: these are more
common in the transverse and distal colon, and
move faecal matter towards the anus. More prolonged contractions of the colon (mass movements)
serve to empty the colon, and invariably produce the
desire to defecate as faeces are pushed into the rectum and anus. Mass movements are initiated by distension of the stomach and duodenum (gastrocolic
and duodenocolic reexes).
• Vagal stimulation increases colonic motility and sympathetic stimulation decreases it.
• e colon is able to inuence gastric motility by releasing enteroglucagon (also released from the distal ileum).
is hormone is released in response to glucose and fat
in the ileum and colon, and inhibits gastric and small
bowel motility.
Defecation
• Mass movements lead to distension of the rectum as
faeces are pushed along; this leads to the sensation of
needing to defecate.
• e control of defecation (continence) is by sympathetic and parasympathetic input, but is also under
somatic control. e nervous input supplies two
sphincters:
• internal sphincter: smooth muscle under involun-
tary control; sympathetic impulses lead to contraction of the sphincter and para-sympathetic impulses
lead to relaxation
• external sphincter: composed of skeletal muscle and
allows voluntary control of defecation.
• e reex arc that initiates defecation is (Fig. 10.7):
• rectal distension: when faecal material enters the
rectum and causes distension, impulses from stretch
receptors in the rectum travel via parasympathetic
bres (S2, 3, 4) in the sacral nerves
• conscious awareness: as a result of rectal distension
there is activation of ascending sensory pathways
that allow dierentiation of solid faecal matter
and atus. Impulses also travel along the pudendal
nerve; this results in contraction of the external
sphincter
• parasympathetic impulse: leads to an increase in
the tone of the colon and relaxation of the internal
sphincter
• not convenient to defecate: voluntary contraction of
the external sphincter; the urge to defecate oen subsides at this point. If the distension on the rectum is
due to solid faecal matter then descending impulses
reinforce contraction of the external sphincter to
maintain continence
Pathways from
motor cortex
spinal
cord
Somatic motor
nerves
sensory cortex
distension
Parasympathetic
motor nerves
Rectal
Parasympathetic
motor nerves
Mass
movement
Sigmoid
colon
(contracts)
Rectum
Internal anal
sphincter
Anus
Fig. 10.7 Summary of the defecation reflex.
• convenient to defecate: the external sphincter relaxes,
allowing faeces through the anus; this is oen aided
by the contraction of abdominal muscles.
Clinical Physiology
Diarrhoea
• Dened as more frequent evacuation or the passage of
liquid/so faeces.
• e pathophysiological mechanisms responsible for the
diarrhoea can be classied as follows.
Osmotic
• Fluid enters the bowel if there are large amounts of
hypertonic substances in the lumen, e.g. purgatives,
malabsorption leading to high glucose levels. e diarrhoea reduces if the patient stops eating.
Secretory
• ere is active secretion and decreased absorption of
uids from the lumen. Causes include:
• enterotoxins, e.g. cholera
• hormones, e.g. VIP from a VIPoma
• bile: following ileal resection
• fats: following ileal resection
• laxatives.
• In secretory diarrhoea stopping food has no eect.
Inflammatory
• Diarrhoea occurs due to mucosal damage and thus
reduced absorption, i.e. infective diarrhoea or inammatory bowel disease.
Abnormal motility
• Causes include diabetic neuropathy, post-vagotomy
syndrome, carcinoid, thyrotoxicosis, irritable bowel
syndrome (IBS) and bowel resection.
CHAPTER 10 Gastrointestinal System
229
Constipation (Box 10.1)
• Dened as the infrequent or dicult passage of abnormally hard/rm faeces.
• Causes are oen divided into medical and surgical.
NUTRITION
Requirements
• e energy requirements of a normal adult are around
2000–2500 kcal/day.
• Carbohydrates, proteins and fats supply this energy.
• In addition, the body needs vitamins, minerals and trace
elements; deciency can result in ill health.
• Carbohydrates: present in numerous foods, provide a
rapidly used energy source, but are also converted to
glycogen in the liver, and if ingested in excess quantities
BOX 10.1 Summary of the medical and
surgical causes of constipation
Medical Surgical
Diet Anal fissure
Lifestyle Carcinoma of the rectum/anus
IBS Carcinoma of the colon
2+
↑Ca
Hypothyroidism Pelvic masses
Drugs, i.e.
opiates, tricyclic
antidepressants
Foreign body
Post-operative immobility
Hirschsprung’s disease (rare
in adults)
will be converted to fat and laid down in adipose tissue.
Carbohydrates provide 4.1 kcal/g of energy.
• Protein: broken down to amino acids which then form
hormones, enzymes, etc. Of the 20 dierent amino acids,
12 can be synthesized in the liver, but 8 are referred to
as essential amino acids as they cannot be synthesized
(isoleucine, leucine, lysine, methionine, phenylalanine,
threonine, tryptophan, valine). Proteins provide 5.3
kcal/g of energy.
• Fats: can be saturated (found in meats, sh and dairy
products) or unsaturated (vegetable); three fatty acids
are referred to as essential as the body is unable to synthesize them (linolenic, linoleic and arachidonic acid).
Fats have numerous roles throughout the body:
• support of other tissues, e.g. fat around kidneys
• stores fat-soluble vitamins
• forms part of the nerve sheaths
• forms part of cell membranes
• provides 9.3 kcal/g of energy.
• Minerals: include sodium, potassium, calcium, phosphorus, iron and iodine. ey are involved in numerous
cellular processes (Box 10.2).
• Vitamins: required in small amounts but deciency
can lead to a variety of clinical conditions (Box 10.3).
Divided into fat-soluble (A, D, E and K) and watersoluble (C and B).
• Trace elements: include zinc, copper, manganese, chromium, cobalt, selenium and molybdenum.
Regulation
• Regulation of eating and food intake is under the control of two centres in the hypothalamus:
• hunger or feeding centre: lateral hypothalamus
• satiety centre: ventromedial hypothalamus.
BOX 10.2 Summary of the Roles of Minerals in Physiological Processes
Mineral Role
Sodium Main extracellular ion, and is involved in fluid regulation, muscle contraction and nerve conduction
Potassium Main intracellular ion, and is involved in many cellular processes
Calcium Mineralization of bone, muscle contraction and blood clotting
Magnesium Necessary for muscle and nerve function, also needed for normal parathyroid hormone secretion
Iron Formation of haem and oxidation of carbohydrates
Iodine Synthesis of thyroid hormones
Selenium Part of the enzyme glutathione peroxidase and also responsible for converting thyroxine to tri-
iodothyronine in liver microsomes
Zinc Involved in numerous metabolic pathways as a cofactor for enzymes, and vital for the synthesis of
RNA and DNA
Phosphorus Forms complexes with calcium to form bone and is essential in energy-requiring processes as part of ATP
Chromium Facilitates the action of insulin
Copper Required for synthesis of haemoglobin and is a component of coenzymes in the electron transport chain
230
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SECTION II Physiology
BOX 10.3 Summary of the Various Disorders Caused by Vitamin Deficiencies
Vitamin Deficiency Syndrome
Vitamin A Night blindness, epithelial
atrophy and infections
Vitamin D Rickets (child) and osteomalacia
(adults)
Vitamin E Haemolytic anaemia
Vitamin K Clotting disorders
Vitamin B
Vitamin B
1
2
Beriberi
Dermatitis and light sensitivity
Vitamin Deficiency Syndrome
Vitamin B
Vitamin B
Pantothenic acid Neuropathy
Biotin Muscle pains and skin lesions
Vitamin B
Folic acid Anaemia
Vitamin C Scurvy
3
6
12
Pellagra
Convulsions, anaemia, vomiting
and skin lesions
Pernicious anaemia
• Aer a meal when the blood glucose is high and the
stomach is distended the satiety centre is stimulated,
and this inhibits feeding. When blood glucose falls the
activity within the satiety centre decreases and allows
impulses from the hunger centre to predominate.
OSCE SCENARIOS
OSCE Scenario 10.1
A 40-year-old male presents with recurrent attacks of right
upper quadrant pain exacerbated by fatty food. His only
signicant past medical history is a right hemicolectomy
ve years previously for acute regional ileitis (Crohn’s
disease). Investigations reveal normal liver function tests
but FBC reveals anaemia with a raised Mean Corpuscular
Volume (MCV). Abdominal ultrasound scan demonstrates
gallstones.
1. Explain the pathophysiology underlying the develop-
ment of gallstones in this patient.
2. What is the cause of the patient’s anaemia?
3. What would be the eects of failing to treat the anaemia?
4. How would you treat the anaemia?
OSCE Scenario 10.2
A 32-year-old female is admitted with jaundice and right
upper quadrant pain. Liver function tests reveal a bilirubin
of 112µmol/L, a markedly raised alkaline phosphatase and
gamma GT. Liver enzymes are normal.
1. What is jaundice?
2. At what level of bilirubin is jaundice clinically apparent?
3. Classify the types of jaundice.
4. What is the most likely cause in this case?
5. Describe the dierent types of gallstone.
6. List the complications of gallstones.
• Lesions in the hunger centre lead to a lack of food intake
(aphagia).
• Lesions in the satiety centre lead to increased food
intake (hyperphagia).
OSCE Scenario 10.3
A 63-year-old male is admitted with central abdominal
pain radiating through to his back. He is hypotensive with
a BP of 90/60 mmHg and tachycardic. e results of blood
investigations are shown below:
WBC 19 × 109/L
Glucose 8 mmol/L
AST 390 U/L
LDH 500 U/L
Amylase 2235 U/L
1. e raised amylase suggests acute pancreatitis. What are
the common causes of acute pancreatitis?
2. What is the patient’s initial Ranson score?
3. What are the criteria measured at 48 h for the Ranson
score?
4. What pancreas-related complications can occur with
acute pancreatitis?
OSCE Scenario 10.4
A 50-year-old male patient presented to Accident and
Emer gency with epigastric pain aer starting a course of
NSAIDs 2 weeks ago for a are up of arthritis. His pain was
getting worse over the last 24 h. Abdominal examination
revealed peritonism with guarding. His HR is 130/min,
temperature 38.5°C and BP 130/70. You suspect perforated
peptic ulcer.
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