GI revision lecture notes
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Dyspepsia: an epigastric pain
Important foregut structures: Oesophagus, stomach, duodenum to second part,
pancreas, liver.
Some causes: Non ulcer (functional) dyspepsia (60%), GORD (15-25%), Peptic ulcer,
gastric ulcer, oesophageal cancer, gastric cancer.
Associated symptoms: heartburn (GORD), fullness, bloating, nausea, vomiting
Red Flags: Weight loss, anorexia, persistant vomiting, haematemesis (frank blood or
‘coffee grounds’), fatigue, anaemia (esp if elderly), epigastric mass, dysphagia, previous
gastric surgery, melaena.
Investigations:
FBC (anaemia)
Endoscopy
Management:
Lifestyle changes – alcohol, smoking etc. Eliminate NSAIDs
In order: antacid, H2 receptor antagonist, proton pump inhibitor
Dysphagia: a difficulty in swallowing
Causes of obstruction:
 Inside oesophageal lumen: Foreign body (e.g. false teeth!), tumour
 Within wall: stricture, achalasia
 Outside oesophagus: lymphoma, Lung cancer
An alternative way of remembering them
 Motor causes: achalasia
 Mechanical causes: tumour, stricture or foreign body.
 Neurological: bulbar palsy, myasthenia gravis.
Achalasia is a disease in which there is a loss of peristalsis in the oesophagus and a loss
of the ability of the lower oesophageal sphincter to relax to let food into the stomach. It
is diagnosed by a barium swallow.
The cause of achalasia is damage to the myenteric plexus – a nerve plexus running
between the longitudinal and circular layers of muscle in the oesophagus.
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The phases of Swallowing:
Oral
 Bolus molding
Pharyngeal
 Glottis closes
 Larynx elevates
 Food is deposited into
the oesophagus
Oesophageal

Peristaltic wave
takes bolus downwards

Glottis opens
The nerves involved in swallowing are:
 CN IX (glossopharyngeal)
 CN X (vagus)
 CN XII (hypoglossal)
Brief anatomy of the oesophagus:
There are four layers from lumen outwards
 Mucosa – stratified squamous epithelium
 Submucosa
 Muscle: the upper third is skeletal muscle, the lower third is smooth muscle and the
middle third is mixed. There are two layers of skeletal muscle – one is arranged
circumferentially and one is longitudinal.
 Adventitia
The narrowest part of the oesophagus are as the pharynx becomes the oesophagus and as
the oesophagus enters the stomach.
Anteriorly lie the left bronchus, trachea and arch of the aorta.
Another cause of dysphagia is oesophageal atresia – failure of the oesophagus to
recanalise in foetal development.
The liver
Arteries
Hepatic artery – delivers
about 30% of the liver’s
blood
Veins
Hepatic veins (right, left
and middle – formed by
union of central veins of
live. Open into IVC just
inferior to diaphragm. Their
attachment to IVC helps
keep liver in position.
Portal venous system
The SMV and the splenic
vein merge to form the
portal vein. Delivers about
70% of liver’s blood.
The IMV is not involved
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The blood supply from the gut passes through the portal vein into the liver before going
anywhere else (through the portal vein). This allows the processing of food,
detoxification of drugs and the removal of bacteria by way of Kuppfer cells.
The liver is split into units for easy of
explanation. The lobule is an anatomical unit
while the acinus is a physiologic unit
emphasising the metabolic activity of the liver
 Zone 1 is the periportal zone – this is the
most oxygenated and most susceptible to
damage from toxins
 Zone 2 is the mid zone
 Zone 3 is the centrilobar zone– this is the
least oxygenated and most susceptible to
ischaemic damage.
Classic Lobule
Functions of the liver (a few examples)
Metabolic:
 Storage of fat soluble vitamins
 Bilirubin
 Carbohydrate metabolism
 Fatty acid metabolism
Synthesis:
 Albumin – without this the oncotic
pressure of blood would drop and oedema
would result.
 Clotting factors – II, III, VII and IX
 C reactive proteins
 Bile
Immunity:
Phagocytosis of bacteria by kuppfer cells
Biochemical tests – tests for markers that change in disease.
First three are included in liver function tests:
 Bilirubin: 3-22 mol/l (>50 is noticeable as jaundice)
 Alanine aminotransferase (ALT): 3-55 U/l
 Alkaline phosphatase (ALP): 80-280 U/l
 Albumin: 40-52 g/l
 Lactate dehydrogenase (LDH): rarely of much use
Portal Lobule
Acinus
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Bile:
Haemoglobin (and to a lesser extent myoglobin) is extracted from broken down
erythrocytes within the reticuloendothelial system (mostly the spleen). It is bound to
albumin and transported to the liver where it is released from albumin and conjugated
(made water soluble) to become a constituant of bile which enters the duodenum via the
ampulla vata in the second (descending) part of the duodenum. Most of this is reabsorbed
in the terminal ileum but some passes on to the large bowel where it is metabolised by
bacteria into urobilogen (unconjugated). Some of this exits the body as stercobilen in
the faeces while the rest is absorbed by the gut wall, passes into the kidneys and is
excreted in urine.
Jaundice
Not noticeable until bilirubin > 50 mol/l. Normal levels are 3-22 mol/l.
Jaundice can be divided into three types
 Prehepatic jaundice occurs due to events before bilirubin enters the liver
 Hepatic jaundice occurs because of problems within hepatocytes
 Posthepatic jaundice occurs due to a problem after bile leaves the hepatocytes
Some examples of these are:
Prehepatic
Hepatic
Posthepatic
Haemolytic disease (e.g.
Viral
Gallstone
sickle cell). This results in
Drug (e.g. paracetamol OD) Tumour (e.g. head of
overloading of the
Cirrhosis
pancreas, ampulla vata,
hepatocytes – a high
hepatic)
proportion of the bilirubin is
unconjugated
Typical presentation of liver disease
 Oedema – due to decreased albumin formation – decreased oncotic force within the
vessels allows fluid to leave and enter the tissues.
 Ascites – due to oedema or portal hypertension
 Testicular atrophy or gyenacomastia – from failure to break down hormones
 Palmar erythema (pale palm with red on each side)
 Clubbing
 ‘Liver flap’ – due to encephalopathy
 Spider naevi (from nipple area upwards)
 Coagulopathy (failure of coagulatio) – non production of clotting factors
Inadequate synthesis of
Albumin – oedema and ascites
Clotting factors – purpura and bleeding
Bilirubin - jaundice
Inadequate elimination of
Nitrogenous waste – encephalopathy
Hormones – hyper oestrogen
Bacteria via Kupffer cells - sepsis
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Cirrhosis
‘An irreversable diffuse process characterised by destruction of hepatocytes, fibrosis,
and nodular regeneration’
Fibrosis interferes with the vascular architecture resulting in a haphazard blood flow – the
end result is an inefficient liver prone to failure.
Causes include: alcohol, hepatitis B & C viruses, gallstones and an overload of iron
(haemochromatosis).
Portal hypertension
A rise in pressure within the portal vein and its tributaries.
Resultant from increased resistance to portal blood flow caused by cirrhosis:
perisinusoidal collagen deposition, perivenular fibrosis, expansion of nodules
Portasystemic anastamoses
Communications between the portal veins and the systemic veins – these become
important in portal hypertension
Between systemic and portal veins
oesophageal vein and left gastric vein
Oesophageal varices*
rectal/inferior rectal veins and superior rectal vein
Haemorroids
small epigastric v of anterior abdo wall and paraumbilical
Caput medusae
*Bleeding from this site may occur through the rupture of delicate engorged vessels by
eating – this may result in haematemesis, melaena or death.
Other results of portal hypertension:
 Ascites (can also be caused by congestive heart failure, malignancy or trauma)
- Transudate vs Exudate: A transudate contains <25 g/L protein while an exudate
contains >25 g/L protein. The distinction is clinically useful as the two have largely
different causes (see below).
 Splenomegaly (via back pressure). Hypersplenism is common resulting in increased
erythrocyte destruction (and macrocytic anaemia)
 Encephalopathy (toxins, especially ammonia, are being routed around the liver and
so are not being detoxified before reaching the brain). Symptoms include tremors,
behaviour change, delirium, drowsiness and coma as well as a ‘liver flap’. Can be
treated by a low protein diet (causes kwashiorkor through low production of
albumin).
Transudates
•Cardiac failure
•Hypoproteinaemia
•Constrictive pericarditis
•Ovarian tumours, e.g. Meig's syndrome.
Exudates
•malignant disease
•pyogenic infection
•tuberculosis
•pancreatitis
•lymphoedema
•myxoedema
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Treatment of portal hyperstension
A portacaval anastomosis or portastsytemic shunt can be created surgically – links the
portal vein to the inferior vena cava where the pass close, behind the liver.
Peptic ulcers
These are either gastric or duodenal ulcers. The most common sites for these ulcers are
the lesser curvature and antrum of the stomach and the anterior and posterior wall of the
duodenum. Ulcers basically result from acid overcoming the acid defences.
Acid production in the stomach – this is by parietal cells (which also make intrinsic
factor). Acid secretion is controlled by histamine, gastrin and ACh from the vagus nerve.
About 3 litres of gastric juice is made per day but not all of this is acid.
The primary protection against acid is mucus – this is made by mucus neck cells in the
stomach and Bruners glands in the duodenum.
Causes: 90% of duodenal and 75% of gastric ulcers are caused by Helicobacter pylori
with other causes being NSAIDs, Crohns disease, malignancy and smoking.
Complications may be remembered by the mnemonic HOP: haemorrhage, obstruction
(via stricture formation) and perforation. Perforation may lead to haemorrhage of nearby
blood vessels with possibly fatal results. With gastric ulcers this is most likely to be the
splenic artery and with duodenal ulcers it is most likely the gastroduodenal artery.
Mechanism of action for H. pylori: The bacteria produces ammonia by way of a
urease. This stimulates gastrin which in turn stimulates acid production by parietal
cells. The extra acid secretion may overload the defences of the stomach wall and result
in an ulcer. Elimination of H. pylori can be curative in ulcers. This is achieved by a
combination of a proton pump inhibitor (to reduce acidity) plus two antibiotics e.g.
omeprazole (PPI) + amoxicillin and clarithromycin.
Mechanism of action for NSAIDs and Aspirin. These are cyclooxagenase (COX)
inhibitors. This enzyme is vital for the production of prostaglandins which, in turn are
required for mucus production therefore mucus production (the primary defensive mech)
falls.
Acute appendicitis
The anatomical landmark for the appendix is McBurney’s point – this is 1/3rd up an
imaginary line extending from the anterior superior ileac spine to the umbilicus. When
accessing this area surgically it is necessary to cut through the layers of the abdominal
wall. These are (from outside in):
1. Skin
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2. Superficial fascia: fatty layer
(camper’s) overlies membranous
layer (Scarpas)
3. External oblique
4. Internal oblique
5.
6.
7.
8.
Transversus abdominis
Transversalis fascia
Endoabdominal fat
Peritoneum
Pain from acute appendicitis has a changing pattern: it starts in the visceral peritoneum
and as such is referred to the umbilical region (T10). Later it moves to the right iliac fossa
when parietal peritoneum becomes involved. Pain may radiate to the back.
Appendicitis is caused by obstruction of the appendix, usually by a faecolith. This results
in ischaemic injury, necrosis and possibly a superimposed infection.
Dangers include peritonitis, rupture and shock
Shock:
Pancreatitis
The pancreas has both endocrine and exocrine functions:
Endocrine
 cells: glucagons
 cells: insulin
 cells: somatostatin
P cells: polypeptide
Exocrine
 amylase:
Lipase:
Stimulants to secrete digestive enzymes include
 Food in the stomach  vagus activated  gastrin released
 CCK
 Secretin from the duodenum
Causes include: (most important ones in bold)
I GET SMASHED
 Iatrogenic
 Gallstones
 Ethanol
 Trauma
 Steroids






Mumps (and some other viruses)
A
Scorpion venom!
H
ERCP
Diuretics
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Cystic fibrosis
Signs and symptoms:
 Pain is retroperitoneal – it radiates to the back and may be relived by sitting forwards.
 There may be weight loss due to a decrease in lipase resulting in decreased digestion
of fats and a decreased uptake of fat soluble vitamins.
 Faecal changes include steattorrhoea – stools that are malodorous and hard to flush.
A significal cause of both pancreatitis and cirrhosis is alcohol abuse. This is particularly
important as it is a modifiable risk factor.
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Inflammatory bowel disease
Crohns disease
From mouth to anus esp. terminal ileum
(usually spares rectum).
All layers of gut wall
Skip lesions
Chronic granulomatous (macrophage)
Can result in fistulas
Can result in malabsorption
Rarely toxic megacolon
Ulcerative colitis
Only affects the colon
Can result in skin lesions (rarely) and
gallstones
Can result in skin lesions, liver disease and
polyarthritis
Superficial ulcers
A more common cause of toxic m-colon.
The layers of wall in small and large intestine:
 Mucosa
 Submucosa
 Muscularis
 Aventitia
Functions of the small bowel:
 Digestion and absorption of food, mixing and propulsion of contents
Functions of the large bowel:
 Absorption of salt and water
 Mucus secretion
 Production of vitamins (e.g. vit K) through endogenous bacteria.
Diarrhoea: this results primarily in loss of potassium
Vomiting: this results in loss of sodium, chloride, and hydrogen ions.
Groin Herniae
85% of groin hernias are inguinal and 60% are indirect with indirect hernia, abdominal
viscera penetrates the superficial inguinal ring and travels a variable distance down the
inguinal canal, possibly ending up in the scrotum (in males). With direct hernia (25% of
groin herniae), the viscera protrudes through an area of relative weakness in the
transversalis fascia. Direct herniae rarely obstruct of strangulate.
The inguinal canal
The inguinal canal lies parallel to and superior to the medial part of the inguinal ligament.
It contains blood vessels and lymphatic vessels as well as the ileiolingual nerve and the
spermatic cord (in males) or round ligament (in females).
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The deep inguinal ring is the site of an outpouching of transversalis fascia 1.25 cm
superior to middle of inguinal ligament and lateral to the inferior epigastric artery.
The superficial inguinal ring is a slit-like opening between diagonal fibres of the
external oblique. Superolateral to pubic tubercle.
Mesh repair of
groin hernias seen
from inside with
anatomical
relationships.
A: Direct
B: Indirect
C: Femoral
The inguinal
canal has two
walls, a roof and
a floor:
Anterior wall:
mainly
aponeurosis of
external oblique.
Lateral part
reinforced by
fibres of internal
oblique.
Posterior wall:
Mainly by
transversalis
fascia – medial
part reinforced
by conjoint tendon.
Roof: arching fibres of internal oblique and transversus abdominis.
Floor: superior surface of in-curving inguinal ligament
The conjoint tendon is the merging of the pubic attachments of internal oblique and
tranversus abdominis aponeurosis into a common tendon
Also important are femoral hernias (15% of groin herniae), these are protrusion of
viscera through the femoral ring and into the femoral canal – from here it may progress
through the sapphenous opening into the loose connective tissue of the thigh allowing it
to become much larger though it cannot travel downwards due to the fascia lata of the
thigh.
Femoral herniae are often small and easy to miss but are prone to obstruction and
strangulation.
GI revision lecture notes
Other herniae
Epigastric
Umbilical
Paraumbilical
Incisional
Description
Extraperitoneal fat protrudes through
a congenital defect in the linea alba
above the level of the umbilicus
Occurs in infants – protrusion
through the umbilicus esp when
child cries
In adults – herniation through a
weakened linea alba near the
umbilicus.
Herniation though a surgical scar –
follows 2-5% of all abdominal
surgery
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Treatment
Non-absorbable suture
95% close spontaneously in
first 3 years of life.
Overlapping layers and
suture.
Overlapping suture or mesh
Complications of herniae:
Irreducibility: contents cannot be manipulated back into abdominal cavity (fibrosis,
adhesions, distension of contained bowel)
Obstruction: intestinal obstruction in irreducible hernia results in pain, vomiting and
distension.
Strangulation: compromised blood supply followed by gangrene – organisms and toxins
may pass through bowel wall to cause peritonitis.
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Test Questions
What arteries supply the liver, what is their origin?
What veins form the portal veinous sytem, how much of the livers blood do these bring?
What veins drain the liver (not portal system – these supply the liver)?
List 4 metabolic functions of the liver, 4 synthetic and 1 immune.
List 3 biochemical tests that may indicate liver problems
What is the process by which bile produced from haemoglobin and myoglobin?
Most bile is reabsorbed – where does this occur?
In what forms is bile excreted?
What are normal levels of bilirubin, at what level does jaundice become noticeable?
Give an example of prehepatic jaundice
Give an example of hepatic jaundice
Give an example of posthepatic jaundice
List at least 5 clinical signs of liver disease (and causes if known)
Define cirrhosis
What is the mechanism of damage to the liver
List four possible causes
What is portal hypertension and what is its cause?
List the sites of three of the portasystemic anastomoses.
What condition arises at each of these sites?
Which one is most likely to result in dangerous bleeding? What symptoms may be seen?
What are three other results of portal hypertension? What problems does each cause?
What other things can result in ascites?
What is the treatment for portal hypertension?
What is dysphagia and list some causes?
What is achalasia and what causes it?
What are the four layers of the oesophagus?
Where does the myenteric plexus lie?
What structures lie anterior to the oesophagus?
What is oesophageal atresia?
Gastric and duodenal ulcers are collectively known as peptic ulcers
Where are each type most often found?
What is the basic cause of peptic ulcers?
What cells produce acid (and intrinsic factor) in the stomach?
What mechanisms control this production?
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What is the primary protection against acid and what cells are responsible in the stomach
and duodenum?
What are the main contributing factors to peptic ulcers?
What are the main complications of peptic ulcers (mnemonic: HOP)?
What vessels are most likely to haemorrhage with gastric and duodenal ulcers?
How does H. pylori cause ulcers?
How do aspirin and NSAIDs cause ulcers?
The surface landmark for the position of the appendix is McBurney’s point – where is
this located?
What are the layers of the anterolateral abdominal wall?
Describe the changing pattern of pain (and why this happens) that occurs in acute
appendicitis.
Crohns disease and Ulcerative colitis are both inflammatory bowel diseases - describe the
differences between them.
List the layers of the small and large bowel.
List functions of the small bowel.
List functions of the large bowel.
What electrolyte is primarily lost in diarrhoea?
What electrolytes are primarily lost in vomiting?
Describe direct and indirect inguinal herniae
Where is the inguinal ligament and what does it contain?
What forms the deep inguinal ring and where does it lie?
What forms the superficial inguinal ring and where does it lie?
What forms the anterior wall of the inguinal canal?
What forms the posterior wall of the inguinal canal?
What forms the roof of the inguinal canal?
What forms the floor of the inguinal canal?
What is the conjoint tendon?
Describe femoral herniae
Describe epigastric herniae
Describe umbilical herniae
Describe paraumbilical herniae
Describe incisional herniae
What are the complications of herniae?