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Some causes: Non ulcer (functional) dyspepsia (60%), GORD (15-25%), Peptic ulcer,
gastric ulcer, oesophageal cancer, gastric cancer.
Causes of obstruction:
• Inside oesophageal lumen: Foreign body (e.g. false teeth!), tumour
• Within wall: stricture, achalasia
• Outside oesophagus: lymphoma, Lung cancer
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.
GI revision lecture notes 2
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.
The liver
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 Classic Lobule Portal Lobule Acinus
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.
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
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 µ mol/l. Normal levels are 3-22 µ 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
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.
Transudates Exudates
•Cardiac failure •malignant disease
•Hypoproteinaemia •pyogenic infection
•Constrictive pericarditis •tuberculosis
•Ovarian tumours, e.g. Meig's syndrome. •pancreatitis
•lymphoedema
•myxoedema
GI revision lecture notes 6
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.
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
GI revision lecture notes 7
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.
Shock:
Pancreatitis
Endocrine Exocrine
α cells: glucagons α amylase:
β cells: insulin Lipase:
δ cells: somatostatin
P cells: polypeptide
Cystic fibrosis
A significal cause of both pancreatitis and cirrhosis is alcohol abuse. This is particularly
important as it is a modifiable risk factor.
GI revision lecture notes 9
Can result in skin lesions (rarely) and Can result in skin lesions, liver disease and
gallstones polyarthritis
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 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 11
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.
GI revision lecture notes 12
Test Questions
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
Define cirrhosis
What is the mechanism of damage to the liver
List four possible causes
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?