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rate of 60/min
<0.20 s
QRS complex:
R
ventricular activation
T wave:
P wave:
atrial
activation
P wave
<0.12 s
PR interval
SQP
QRS width
<0.10 s
ventricular
recovery
QT interval <0.42 sat
T
Fig. 9.6 Standard ECG recording during the timing
of various events in the cardiac cycle.
• A correctly positioned catheter should give a normal
venous pressure wave form (i.e. a, c, v waves).
• Measurement should be made aer ‘zeroing’ the transducer to the level of the right atrium.
• Isolated readings are of little use due to:
• individual variations in the condition of the heart
• some patients can compensate with a remarkable
degree of vasoconstriction in the presence of hypovolaemia, such that CVP may become transiently
elevated.
• Normal CVP ranges 5–12 mmHg.
• Low CVP indicates hypovolaemia.
• High CVP usually indicates uid overload.
CHAPTER 9 Cardiovascular System
211
• If there is disparity between function of the right and
le ventricles (e.g. right ventricular infarction, pulmonary embolism [PE], le ventricular disease), the lling
pressure of the right heart, i.e. CVP, may not reect the
lling pressure of the le heart. erefore CVP will not
be accurate and pulmonary capillary wedge pressure
measurement is required.
Pulmonary Capillary Wedge Pressure (Pulmonary
Artery Occlusion Pressure; PAOP)
• PAOP reects le atrial pressure as the resistance in the
pulmonary veins is low.
• A otation balloon catheter is passed through the right
heart into the pulmonary artery.
• Ination of the balloon excludes ow from the right side
of the heart, allowing a uid bridge to complete the connection to the le atrium.
• e pressure at the catheter tip equates to that in the le
atrium.
• e balloon is deated between readings to avoid pulmonary infarction.
• e normal pulmonary artery occlusion pressure (PAO)
is 6–12 mmHg. It should be kept below 15 mmHg to
minimize the risk of pulmonary oedema.
• e major advantage of the catheter is that it can be used
to measure CO.
Pulse Oximetry
• Measures the arterial oxygen saturation (SaO2).
• It relies on the measurement of the dierent absorption
of oxyhaemoglobin and deoxyhaemoglobin at dierent
wavelengths.
• e instrument pulses infrared light at wavelengths of
660–940 nm.
• e pulsation component of absorption is measured
and the constant background component not due to
arterial blood, i.e. absorption by skin, venous blood and
fat, is subtracted.
• Because oxygenated and deoxygenated Hb absorb differing amounts at the two wavelengths, pulse oximetry
is able to calculate a percentage of saturated Hb from the
ratio of the two.
• e problems with pulse oximetry include:
• delay: calculations are made from a number of pulses
and there is a 20 s delay between actual and displayed
values
• irregular pulse: atrial brillation
• venous pulsation (tricuspid incompetence)
• hypotension
• vasoconstriction
• abnormal Hb (carboxy-), and methaemoglobin
• bilirubin
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SECTION II Physiology
• methylene blue dye
• other factors: electrical interference (diathermy),
ickering lights, patient movement, shivering, nail
varnish (coloured or not).
Cardiac Output
• Useful as part of overall assessment of circulation.
• Once CO is known it is possible to derive values for
SVR, the amount of work the heart is performing, oxygen delivery and oxygen consumption.
• Specic pharmacological therapy can then be given to
optimize the circulation.
Urine Output
• Directly related to renal perfusion.
• Good indicator of overall uid balance.
Echocardiography
• Transthoracic echocardiography allows non-invasive
real-time imaging at the bedside.
• Provides information on cardiac structure, function and
haemodynamics.
Echo Doppler
• Measures blood ow in the aorta via an oesophageal probe.
• Gives indication of contractility and CO.
• Contraindicated with oesophageal pathology, e.g. stricture and varices.
Cardiovascular Support
• Ventilate.
• Infusion.
• Pump.
Ventilate
• Improves oxygenation and gas exchange.
• Controls acidosis (by CO2 control).
• Reduces oxygen demand by respiratory muscle.
Infusion
• Ensure adequate lling pressure.
• Fluid challenge with monitoring, e.g. CVP, PAOP.
Pump
• Maintain blood pressure.
• Monitor CO.
• Ensure organ blood ow.
• If SVR low, use vasopressor to improve perfusion pressure.
Pharmacological Support
• Inotropes: increase force of ventricular contraction,
usually β-eect.
• Vasopressor: constricts blood vessels, α-eect.
• Vasodilator: dilates blood vessels.
• Chronotrope: increased heart rate, β-eect.
Adrenaline
• Both α- and β-eects.
• Inotrope, vasopressor, chronotrope.
• β2-eect at low doses causes vasodilatation in skeletal
muscle, lowering SVR.
• α-vasoconstrictor eect at higher doses increases SVR
and myocardial oxygen demands, with adverse eect on
cardiac output.
Noradrenaline
• α-eect.
• Vasopressor.
• Indicated in septic shock when hypotension due to
peripheral vasodilatation persists despite adequate volume replacement.
Isoprenaline
• Exclusively β-eect.
• Inotrope, chronotrope.
• Vasodilatation in skeletal muscle; therefore reduces SVR.
• Tachycardia limits clinical use.
• Used to increase rate in heart block while awaiting pacing.
Dopamine
• Low dose dilates renal, cerebral, coronary and splanchnic
vessels, via D1 and D2 receptors and β1 receptors, resulting
in increased cardiac contractility and heart rate.
• High dose stimulates α-receptors, causing vasoconstriction.
Dobutamine
• β1 and β2.
• Inotrope, vasodilator.
• β1 eect increases heart rate and force of contraction.
• Mild β2 eect causes vasodilatation.
• First choice inotrope in cardiogenic shock due to le
ventricular dysfunction.
• Dobutamine and low-dose dopamine in conjunction
used in cardiogenic shock to increase BP via increased
cardiac contractility and urinary output (UO; via
increased renal perfusion).
Dopexamine
• β2 and D receptors.
• Inotrope, chronotrope.
• Peripheral vasodilatation, increased splanchnic blood
ow and increased renal perfusion (increased UO).
Vasodilators
• Nitrates: venodilators reducing preload.
• Nitroprusside: chiey arterial vasodilator with short
half-life given by infusion.
• Hydralazine: arterial vasodilator reduces aerload.
CHAPTER 9 Cardiovascular System
213
Phosphodiesterase Inhibitors
• Decrease the rate of breakdown of cAMP by phosphodiesterase III.
• Inotropic and vasodilator eect. Little chronotropic eect.
OSCE SCENARIOS
OSCE Scenario 9.1
An 80-year-old male is 5 days post-repair of abdominal
aortic aneurysm. He has suddenly developed a tachycardia
and become hypotensive. His ECG shows atrial brillation
with a rate of 140.
1. What are the causes of atrial brillation?
2. What are the physiological mechanisms which explain
the hypotension seen in fast atrial brillation?
3. How would you diagnose atrial brillation?
4. Describe your initial management of the patient.
OSCE Scenario 9.2
An 89-year-old male is 8 days post-laparotomy for repair
of a perforated duodenal ulcer. He has developed a
severe postoperative chest infection and is pyrexial and
hypotensive.
1. Describe your initial management of this patient.
2. Why does sepsis lead to hypotension?
3. Which inotrope is commonly used in sepsis and what is
its mode of action?
4. What is Starling’s law of the heart and how do inotropes
aect it?
OSCE Scenario 9.3
A 58-year-old male is admitted with severe interscapular
back pain. He is hypertensive with a BP of 200/140. A CT
angiogram shows a type B aortic dissection.
1. What is the dierence between a type A and B dissection?
2. How is a type A dissection managed?
3. How is an uncomplicated type B dissection managed?
• Increased myocardial contractility (increased CO) with
reduced PAOP and SVR.
• No signicant rise in heart rate or myocardial oxygen
consumption.
OSCE Scenario 9.4
A 72-year-old male patient underwent elective open
abdominal aortic aneurysm repair. An infra-renal aortic
cross clamp was required.
1. What are the physiological and cardiovascular changes
that result from aortic cross clamping?
2. What techniques would the anaesthetists use to reduce
these eects?
3. What are the physiological and cardiovascular changes
that result from releasing aortic cross clamp?
4. What techniques would the anaesthetists use to reduce
these eects?
OSCE Scenario 9.5
A 75-year-old female patient underwent dicult open
anterior resection. She has past medical history of hypertension, ischaemic heart disease and transient ischaemic
attack (TIA). e procedure was complicated with signicant blood loss that necessitated intraoperative blood
transfusion. Postoperatively, she was admitted to the highdependency unit as she required vasopressors support.
1. What methods can be utilised to monitor the cardiovas-
cular system?
2. What is the best indicator to assess adequate uid balance?
3. How does the pulse oximetry work?
4. What are the problems and pitfalls that can occur when
reading pulse oximetry?
5. What is a vasopressor? Give some examples used in
common clinical practice.
Answers in Appendix pages 449–451
Please check your eBook at https://studentconsult.inkling.com/ for more self-assessment questions. See inside cover for
registration details.
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Gastrointestinal System
FUNCTIONS
e functions of the various components of the gastrointestinal (GI) system are:
• Oral cavity: teeth crush and tear food; the tongue forms
a food bolus in preparation for swallowing; saliva secretion initiates carbohydrate digestion.
• Pharynx and oesophagus: conveys food from the oral
cavity to the stomach.
• Stomach: stores food; mechanically and chemically
digests food; regulates the passage of chyme into the
duodenum; secretes intrinsic factor.
• Small bowel: food passes from the stomach into the
small intestine; this is where the majority of food digestion and absorption occurs.
• Large bowel: water is removed from undigested food,
which is then stored in the rectum in preparation to be
excreted; vitamin K and some B vitamins are produced
by resident bacterial ora.
• Liver: an important site for carbohydrate, protein and
lipid metabolism; involved in the synthesis of several
plasma proteins and clotting factors; the primary site
for detoxication and elimination of body waste and
toxins.
• Gall bladder: stores and concentrates bile.
• Pancreas: has both exocrine and endocrine functions,
secreting the majority of digestive enzymes.
Nervous and Hormonal Regulation
Within the GI Tract
Nervous Regulation
e nervous system of the GI tract consists of:
• Intrinsic or enteric system.
• Extrinsic system:
• sympathetic
• parasympathetic.
• e intrinsic nervous system is found in the wall of the
GI tract and forms two well-dened plexuses:
• myenteric or Auerbach’s plexus: this lies between the
circular and longitudinal muscle layers; it is mainly
involved in motor function
• submucosal or Meissner’s plexus: this lies within the
submucosa; it is mainly sensory.
• e enteric nervous system responds to numerous
gut transmitters such as cholecystokinin, substance P,
vasoactive intestinal peptide (VIP) and somatostatin;
it is responsible for the majority of gut secretion and
motility.
• e enteric nervous system also receives input from the
autonomic (extrinsic) nervous system:
• Sympathetic: bres terminate in the submucosal and
myenteric plexuses; stimulation of the sympathetic
system leads to:
• blood vessels: vasoconstriction
• glandular tissue: inhibits secretion
• sphincters: contraction
• circular muscle of bowel: inhibits (↓ motility).
• Parasympathetic: bres terminate in the myenteric
plexus only; stimulation of the parasympathetic system leads to:
• glandular tissue: increases secretion
• sphincters: relaxation
• circular muscle of bowel: stimulates (↑ motility).
Hormones and Neurotransmitters
• Play an important role in regulating GI motility and
secretion; these include:
• gastrin
• secretin
• cholecystokinin (CCK)
• pancreatic polypeptide
• gastric inhibitory polypeptide (GIP)
• motilin
• enteroglucagons
• neurotensin.
• ese hormones and neurotransmitters will be discussed individually in the relevant sections.
214
CHAPTER 10 Gastrointestinal System
215
Oral Cavity, Pharynx and Oesophagus
Chewing
• Food is ingested through the mouth and is divided
between two regions:
• vestibule: space between the teeth, lips and cheeks
• oral cavity: inner area bound by the teeth.
• Chewing or mastication has a number of functions:
• teeth are able to cut, grind and tear food, allowing it
to be swallowed more easily
• mixes food with saliva and mucus; this lubricates it
in preparation for swallowing, and starts carbohydrate digestion with salivary amylase.
Saliva
• Saliva is secreted by a number of glands:
• parotid: watery secretion lacking mucus; accounts
for around 25% of saliva secretion; also contains salivary amylase and IgA
• submandibular: produces a more viscous saliva
(a mixed serous and mucosal saliva); accounts for
approximately 70% of saliva secretion
• sublingual: contains mucoproteins; accounts for only
5% of saliva secretion.
• Numerous saliva glands are present over the tongue and
palate.
• Saliva has a number of functions:
• lubrication to help swallowing: mucus
• speech
• taste
• antibacterial action: lysozyme and IgA
• starch digestion: amylase.
• Formation of saliva within the salivary glands is a twostage process:
1. Isotonic uid of similar composition to the extracellular
uid (ECF) is secreted by the acinar component of the
salivary gland.
2. e isotonic uid is modied as it moves along the duct;
Na+ and Cl− is removed and K+ and HCO
means of ATP transport proteins.
• During low rates of secretion the saliva is dilute as there
is plenty of time for ductal modication.
• During high rates of secretion the Na+, HCO
content increases and is thus more concentrated.
• Control of the secretion of saliva is via the autonomic
nervous system; this reex is stimulated by the salivary
nuclei in the medulla; secretion of saliva is stimulated by:
• stimulation of mechanoreceptors and chemorecep-
tors in the mouth
• higher centres in the CNS, i.e. smelling or thinking
about food.
−
are added by
3
−
and Cl−
3
• Parasympathetic impulses via cranial nerves VII and IX
stimulate saliva secretion; sympathetic impulses lead to
vasoconstriction and a decrease in saliva secretion.
Swallowing
Swallowing can be divided into a number of phases:
• Oral phase: voluntary; a food bolus is pushed against
the roof of the mouth by the tongue; this forces the food
into the oropharynx and then into the pharynx.
• Pharyngeal phase: involuntary; the superior constrictor raises the so palate (preventing food entering the
nasopharynx). In addition it initiates a wave of contraction (peristalsis) that pushes the food through the
upper oesophageal sphincter. At this stage respiration is
inhibited so as to prevent food entering the respiratory
system.
• Oesophageal phase: the wave of contraction, which was
initiated by the superior constrictor in the pharynx,
continues into the oesophagus. is wave of contraction
propels the food into the stomach. If the food fails to
enter the stomach then the resulting distension initiates
a secondary peristaltic wave.
Oesophageal Sphincter
• e oesophageal sphincter is an area of high pressure
(15–25 mmHg) in the region 2 cm above and 2 cm below
the diaphragm; it is a physiological sphincter as there are
no anatomical dierences to identify it as the sphincter.
• e oesophageal sphincter acts to prevent gastric juices
reuxing from the stomach into the oesophagus.
• In addition to the physiological sphincter there are a
number of other factors that assist in preventing reux:
• the right crus of the diaphragm compresses the oeso-
phagus as it passes through the oesophageal hiatus
• the acute angle at which the oesophagus enters the
stomach acts as a valve
• mucosal folds in the lower oesophagus act as a valve
• closure of the sphincter is under vagal control; how-
ever, the hormone gastrin causes the sphincter to
contract (secretin, CCK and glucagon cause it to
relax).
STOMACH
Gastric Mucosa
• e gastric mucosa contains a variety of secretory cells;
the mucosa is divided into:
• columnar epithelium: secretes a protective mucus layer
• gastric glands: intersperse the mucosa; they contain
a variety of secretory cells.
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SECTION II Physiology
• ese secretory cells include:
• mucus cells: secrete mucus and are situated at the
opening of the gastric gland
• peptic or chief cells: found at the base of the gastric
glands and secrete pepsinogen
• parietal or oxyntic cells: secrete hydrochloric acid
and intrinsic factor
• neuroendocrine cells: secrete a number of peptides
that regulate GI motility and secretion, i.e. gastrin.
• e predominant cell type in the gastric glands varies
throughout the various regions of the stomach:
• fundus and body: p eptic and parietal cells predominate
• antrum and pylorus: parietal cells are less common;
mucus and neuroendocrine (secreting gastrin) cells
predominate
• cardia: gastric glands are composed almost com-
pletely of mucus cells.
Gastric Secretion
Gastric Acid (Fig. 10.1)
• e stomach secretes approximately 2–3 L/day; it
contains:
• hydrochloric acid
• pepsinogen
• mucus
• intrinsic factor
• salt and water.
• Stomach acid has a pH of around 1–3; it plays a number
of roles:
• tissue breakdown
• converts pepsinogen to the active pepsin
• forms soluble salts with calcium and iron; this aids
their absorption
• acts as an immune defence mechanism by killing
micro-organisms.
• Gastric acid is secreted by the parietal cells; when activated, deep cles form in the apical membrane; these
canaliculi allow the acid to be secreted into the stomach.
• Chloride and hydrogen ions are pumped from the parietal cells; this process is energy dependent.
• H+ ions are pumped from the cell by the H+/K+ ATPase
system.
• Cl− ions are pumped from the cell by two routes: one is a
chloride channel, the other is a Cl−/K+ co-transport system (K+ is thus cycled into the cell via the H+/K+ ATPase
system and out via the Cl−/K+ system).
• H+ ions are produced by oxidative processes; this also
produces a hydroxyl ion; in a reaction catalysed by carbonic anhydrase this results in the formation of HCO
which is then exchanged for Cl− on the basolateral surface of the cell.
• e secretion of HCO
prevents the gastric acid from damaging the mucosa;
it is referred to as the ‘alkaline tide’; the production of
−
HCO
can be inuenced by prostaglandins.
3
−
is a protective mechanism that
3
−
3
,
G-cell
ACh
+
+
Parietal cell
+
K
CCK
+
Gastrin
+
+
H
–
D-cell
Somatostatin
–
–
Secretin
Duodenal
mucosa
chromaffin cells
–
GIP
Fig. 10.1 Regulation of acid secretion by the parietal cell. (From McGeown JG. Physiology, 2nd edn. Churchill
Livingstone, Edinburgh, 2002, with permission.)
Entero-
+
Histamine
+
CHAPTER 10 Gastrointestinal System
217
Pepsinogen Secretion
• e peptic cells produce pepsinogen, a proteolytic
enzyme that hydrolyses peptide bonds in proteins.
• e enzyme is secreted into the gastric glands in an
inactive form (pepsinogen); exposure to the acid environment in the stomach activates the enzyme (pepsin).
Mucus Secretion
• Mucus is secreted from cells at the neck of the gastric
glands; the secreted mucus forms a layer (mucosal barrier)
over the gastric epithelium and prevents the gastric acid
and secreted pepsins from digesting the stomach lining.
• e mucus is alkaline; this helps to neutralize gastric acid.
• Additional factors which protect the stomach from
digestion include:
• tight epithelial junctions prevent acid reaching deeper
tissues
• prostaglandin E secretion has a protective role by
increasing the thickness of the mucus layer, stimulating HCO
the mucosa (bringing nutrients to any damaged areas).
−
production and increasing blood ow in
3
Intrinsic Factor Secretion
• Secreted from parietal cells; the stimulus for excretion is
the same as for acid secretion.
• Intrinsic factor (IF) binds to vitamin B12; it is then
absorbed in complex with the IF via specialized receptors in the ileum (see below).
Regulation of Gastric Secretion
• Divided into three phases:
• cephalic
• gastric
• intestinal.
• Cephalic phase: sight, smell and even the anticipation
of food lead to impulses from the appetite centre in the
hypothalamus to the stomach; it contributes to almost
30% of gastric secretions. is descending input is parasympathetic and runs in the vagus; vagal activity stimulates gastric secretion in a number of ways:
• direct stimulation of the gastric glands via acetylcho-
line release
• release of gastrin from the neuroendocrine cells
(G-cells) in the antrum; gastrin stimulates acid and
pepsin secretion
• release of histamine from mast cells; this stimu-
lates parietal cells via H2 receptors, which leads to
acid production (gastrin also stimulates histamine
release).
• Gastric phase: food entering the stomach stimulates the
gastric phase; this is the primary stimulus to secretion and
accounts for around 60% of gastric secretion. Distension
of the stomach and the chemical composition of food
lead to acetylcholine release from the vagus.
• Intestinal phase: only accounts for 5% of gastric secretion; the stimulation is the presence of food in the duodenum; this results in the release of gastrin from G-cells
in the duodenal mucosa.
• ere are a number of other inuences on gastric
secretion:
• the secretion of gastrin is inhibited when the pH falls
to around 2–3
• somatostatin secreted from neuroendocrine cells
(D-cells) inhibits gastrin secretion
• secretin from the duodenal mucosa is released in
response to acid in the duodenum; it inhibits gastrin
release
• fatty food in the duodenum leads to the release of
CCK and GIP; both inhibit gastrin secretion.
• e action of hormones released in the duodenum is
referred to as the enterogastric reex.
Gastric Motility
• e main functions of the stomach are storage and mixing and propulsion of food into the intestine; the storage
area consists of the fundus and body, whereas the mixing and propulsion area is the antrum and pylorus.
Storage
• e stomach has a resting volume of around 50 mL and
an intragastric pressure of 5–6 mmHg; however, it is
able to accommodate signicantly greater volumes with
little change in pressure (approximately 1 L). As the
stomach is distended, parasympathetic input from the
vagus inhibits muscle contraction.
Mixing and Propulsion
• e stomach has three muscle layers: longitudinal, circular and oblique.
• Contractions in the stomach are more intense in the
more muscular pyloric area in comparison with the
gentle contractions in the storage area of the fundus.
• Peristaltic waves push food or chyme towards the pylorus;
as pressure increases the pyloric sphincter will open and a
small amount of food is allowed through to the duodenum.
• Parasympathetic impulses tend to increase motility
whereas sympathetic impulses decrease motility.
• e amount of food allowed in to the duodenum is carefully regulated by a number of factors:
• gastric volume:↑volume then more rapid emptying
• fatty food: CCK and GIP are released by the small
intestine in response to fatty foods; they increase
contractility of the pyloric sphincter
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SECTION II Physiology
• proteins: proteins and amino acids stimulate gastrin
release; gastrin increases contractility of the pyloric
sphincter
• acid: acid entering the duodenum results in a vagally
mediated delay in gastric emptying and also leads to
secretin release. Secretin inhibits antral contractions
and increases contractility in the pyloric sphincter.
Secretin also stimulates HCO
creas to neutralize the acid
−
release from the pan-
3
• hypertonic chyme: delays gastric emptying.
Clinical Physiology
Vomiting
• e reex action of ejecting the contents of the stomach
through the mouth.
• Prior to vomiting, autonomic symptoms such as salivation, pallor, sweating and dizziness oen occur.
• e events which occur during vomiting are:
• respiration is inhibited
• the larynx closes and the so palate rises
• the stomach and pyloric sphincter relax and the duo-
denum contracts, propelling intestinal contents into
the stomach
• the diaphragm and abdominal wall contracts →
intragastric pressure rises
• the gastro-oesophageal sphincter relaxes and the
pylorus closes
• stomach contents expelled through the mouth.
• e vomiting reex is co-ordinated by the vomiting
centre in the medulla; stimulation of the vomiting centre leads to motor impulses passing along cranial nerves
V, VII, IX and XII, and to the intercostals and abdominal muscles and diaphragm.
• Causes of vomiting include:
• stimulation of the posterior oropharynx
• excessive distension of the stomach or duodenum
• stimulation of the labyrinth, e.g. motion sickness
• severe pain
• raised intracranial pressure
• stimulation of the chemoreceptor trigger zone by
noxious chemicals
• bacterial irritation of the upper GI tract.
Treatment of Peptic Ulceration
• e treatment of peptic ulcer disease can be divided into
medical and surgical.
Medical treatment
• e choices for medical treatment are:
• reduce acid secretion
• mucosal protection
• antacids (pH increasers).
• ere are three groups of drugs used in the reduction of
acid secretion:
• histamine (H2-receptor) antagonists, e.g. cimeti-
dine and ranitidine: these drugs act by blocking
H2-receptors on parietal cells. Although these cells
also possess gastrin and muscarinic receptors, both
gastrin and acetylcholine mainly stimulate acid production indirectly by stimulating histamine release.
e blocking of H-receptors prevents the intracellular increase in cAMP, and thus acid production
• muscarinic antagonists, i.e. pirenzepine: this is only
of historical value, as this drug is no longer in clinical
use. Pirenzepine was a selective M1-receptor antagonist that was selective for the muscarinic receptors
on parietal cells but did not produce the unwanted
symptoms of blurred vision, dry mouth, etc.
• proton pump inhibitors (PPIs), e.g. omeprazole: this
group of drugs acts directly on the proton pump
(H+/K+ ATPase). It is inactive at neutral pH but is
activated by the acidic conditions in the stomach;
it then irreversibly binds to sulfydryl groups on the
proton pump.
• e mucosal protectants aim to support the mucus
layer that normally protects the gastric mucosa; there
are three types:
• sucralfate: formed from sulphated sucrose and alu-
minium hydroxide, it polymerizes at pH < 4 to form
a sticky layer that adheres to the base of the ulcer
• bismuth chelate: acts in a similar manner to sucral-
fate; in addition it has been shown to eradicate
Helicobacter pylori
• misoprostol: a synthetic analogue of prostaglandin
E2. is prostaglandin is thought to protect gastric
mucosa by stimulating the secretion of mucus and
bicarbonate, and increasing the mucosal blood ow.
• Antacids are a very simple treatment for peptic ulcers,
and simply consist of alkaline substances that increase
the pH within the stomach; examples include:
• sodium bicarbonate
• magnesium hydroxide and magnesium trisilicate
• aluminium hydroxide.
Surgical treatment
• With the advent of PPIs surgical treatment has become
much less common. Indications include:
• chronic unhealed ulcer
• failure to heal aer more than two courses of treatment
• possible malignancy
• complications, i.e. bleeding, perforation.
• e options for surgical treatment include (Fig. 10.2):
• Bilroth I partial gastrectomy
• Bilroth II partial gastrectomy
• truncal vagotomy and gastrojejunostomy
CHAPTER 10 Gastrointestinal System
Gastrojejunostomy
219
Upper 1/3
stomach
Duodenum
A
B
Upper 1/3
stomach
Duodenum
Pyloroplasty
C
E
D
F
Fig. 10.2 Surgical options for peptic ulceration. (A) Bilroth I. (B) Bilroth II or Polya. (C) Truncal vagotomy and
gastrojejunostomy. (D) Truncal vagotomy and pyloroplasty. (E) Selective vagotomy and pyloroplasty. (F) Highly
selective vagotomy (no drainage procedure needed). (From McGeown JG. Physiology, 2nd edn. Churchill
Livingstone, Edinburgh, 2002, with permission.)
220
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SECTION II Physiology
• truncal vagotomy and pyloroplasty
• selective vagotomy and pyloroplasty
• highly selective vagotomy (no drainage procedure
needed).
• e surgical treatment of peptic ulcers is associated
with a number of complications. ese can be divided
into post-gastrectomy syndromes and those that occur
post-vagotomy.
Post-gastrectomy syndromes
• Malnutrition: occurs due to small capacity stomach,
rapid gastric emptying and rapid intestinal transit.
• Deciency:
• iron deciency, as it is in the wrong ionic state for
absorption
• vitamin B12 deciency, due to a lack of intrinsic factor.
• Dumping syndromes: these can be early or late. Early
dumping occurs 30–45 min aer eating and is due to
rapid gastric emptying of a hyperosmolar meal into the
small bowel; this results in uid moving into the small
bowel by osmosis (third space loss) and results in dizziness, weakness and palpitations. Late dumping is due
to rapid swings in insulin secretion in response to the
glucose load in the small bowel; this leads to rebound
hypoglycaemia.
• Diarrhoea: due to early gastric emptying and passage of
hyperosmolar chyme attracting uid into the bowel.
• Bilious vomiting: the loss of the pylorus allows reux of
duodenal contents; this leads to bilious vomiting. e
reuxed bile can also lead to gastritis and further ulcer
development.
• Infection: there is a decreased ability to destroy bacteria,
particularly tuberculosis.
• Carcinoma: the duodenal reux increases the risk of
developing gastric cancer in the gastric remnant.
Effects of vagotomy
• Reduced gastric acid secretion.
• Delayed gastric emptying.
• Failure of the pylorus to relax prior to gastric peristaltic
wave.
• Reduced pancreatic exocrine secretions.
• Diarrhoea secondary to loss of vagal control of the small
bowel.
• Increased risk of large bowel cancer due to excessive bile
salts reaching the colon.
SMALL INTESTINE
Small Intestine Mucosa
• e primary function of the small bowel is the absorption of nutrients; a number of characteristics make it
particularly suited to this role:
• large surface area
• circular folds called plicae circulares, which cause
the chyme to spiral round, and thus increase the time
for absorption to take place
• the circular folds are covered with villi—nger-like
projections approximately 1 mm high; each of these
villi is further covered with microvilli (‘brush-border’).
ese serve to further increase the surface area.
• Interspersed among the villi are the crypts of Lieber kuhn.
ese are analogous to the gastric glands and contain
a number of dierent cell types:
• undierentiated cells that constantly replace
entero cytes
• D-cells: produce somatostatin
• S-cells: produce secretin
• N-cells: produce neurotensin
• Enterochroman cells: produce 5-hydroxytryptamine.
• e ‘brush-border’ secretes a number of enzymes
involved in digestion:
• disaccharidases: maltase, sucrase
• peptidases
• phosphatases
• enteropeptidase or enterokinase (activates pancre-
atic trypsinogen)
• lactase (under 4 years).
• e duodenum contains Brunner's glands, which secrete
mucus rich in bicarbonate (they are not present in the
jejunum or ileum).
Absorption (Table 10.1)
• e small intestine secretes 2–3 L/day of isotonic uid;
Cl− is transported to the bowel lumen and Na+ and water
follow. In addition, the bowel secretes a number of hormones (see above) and enzymes (see Pancreas section).
• e absorption of nutrients in the small bowel can be
divided into:
• carbohydrates
• fats
• proteins
• uids and electrolytes
• vitamins
• iron
• calcium.
Carbohydrates (Fig. 10.3)
Glucose and galactose are absorbed via a Na+-dependent process in which a Na+/K+ ATPase pumps out Na+. e glucose/
galactose are then absorbed with the Na+ via a cotransport
protein. A Na+-independent process absorbs fructose.
Fats (Fig. 10.4)
e absorption of fats is a complex multistage process:
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