Gall bladder disease
Dom LO Title LO Detail
BCS Anatomy of portal 1. To describe the anatomy of the portal venous system.
venous system 2. To outline the changes that occur to the portal venous system with portal hypertension
BCS Hepatobiliary 1. To describe the pathology of hepatobiliary diseases, including cirrhosis and liver
2. To describe the vascular and biliary causes of hepatobiliary disease.
3. To list infective and toxic causes of hepatobiliary disease.
4. To outline the principles of management of common liver diseases
5. To describe the underlying principles and be able to interpret results from liver function
BCS Upper GI bleeding 1. To outline the causes of upper gastrointestinal bleeding.
2. To describe the principles of its medical, endoscopic and surgical management
3. To be able to explain the risks of blood transfusion
EPPD Stereotyping 1. Recognise and avoid stereotyping and judgmental behaviour.
ICCP Clinical reasoning 1. Assessment of haemodynamic status and resuscitation
ICCP Examination skills 1. Demonstrate proficiency in clinical examination of the patient with liver disease
ICCP Assessment of 1. Demonstrate basic proficiency in the assessment of substance dependence
ICCP Laboratory 1. Demonstrate proficiency in the interpretation of liver function tests
PPH Alcohol (Public 1. Describe the range of morbidity (bio-psycho-social) associated with hazardous and
Health) harmful levels of alcohol intake at the individual, family and population levels.
2. What public health strategies are in place in Australia to reduce alcohol-related
PPH Viral hepatitis Describe:
(Public Health) 1. The notifiable disease process and its objectives;
2. The burden of disease caused by viral hepatitis;
3. Risk factors for acquiring viral hepatitis; and
4. Population approaches to the primary and secondary prevention of morbidity
associated with Hepatitis A, B and C infection.
PPH Treatment and 1. Using hepatitis as an example, demonstrate skills in finding and appraising studies of
prognosis (EBM) treatment and prognosis, and applying the results to individual management through a
weighing up of individualised absolute benefits and risks.
Another Hard Day At The Office
THE PORTAL VENOUS SYSTEM
1. Describe the anatomy of the portal venous system.
Collects blood from the abdominal part of the GIT, gallbladder, pancreas,
Carries blood to liver and branches into expanded capillaries: sinusoids.
The blood is then collected by the hepatic veins that drain into the IVC.
Carries blood from three major veins: superior and inferior mesenteric veins
and the splenic vein.
Forms posterior to the neck of the pancreas by the union of the splenic and
superior mesenteric veins.
Inferior mesenteric vein ends posterior to the pancreas by joining the splenic
vein (it may join the portal vein or even the superior mesenteric vein).
The portal vein ascends to the liver in the free margin of the lesser
omentum, posterior to the bile duct and hepatic artery.
The portal vein divides into right and left branches at the porta hepatis.
The branches then empty into hepatic sinusoids.
Portal Systemic Anastomoses.
The portal venous system communicates with the systemic venous system.
When the portal circulation is obstructed, blood from the GIT can still reach
the right side of the heart through the IVC via collateral routes.
As the portal vein has no valves, blood can flow from the liver to the IVC
via three alternate routes.
In portal hypertension, venous pressure in the portal venous system is
increased, consequently some blood in the portal venous system may
reverse its direction and pass through the portal-systemic anastomoses into
the systemic venous system.
This causes the veins in the portal-systemic anastomotic areas to dilate and
The main portal-systemic anastomotic areas:
a. Gastroesophageal region.
Oesophageal tributaries of the left gastric vein
anastomose with the oesophageal veins, which
empty into the azygos vein.
b. Anorectal region.
The superior rectal vein anastomoses with the
middle and inferior rectal veins, which are
tributaries of the internal iliac and internal
pudendal veins, respectively.
c. Paraumbilical region.
The paraumbilical veins in the falciform ligament
anastomose with subcutaneous veins in the
anterior abdominal wall.
d. Retroperitoneal region.
Tributaries of the splenic and pancreatic veins
anastomose with the left renal vein. Short veins
also connect the splenic and colic veins to the
lumbar veins of the posterior abdominal wall.
The veins of the bare area of the liver also
communicate with the veins of the diaphragm
and the right internal thoracic vein.
2. Describe the changes that occur with portal hypertension.
Splenomegaly: Splenic enlargement is caused by passive venous congestion.
Development of Portosystemic Venous Anastomoses, Bypassing the Obstructed
Portal Circulation: Venous anastomoses occur wherever the portal and systemic
venous drainages commingle, resulting in dilated, tortuous veins at the following
In the lower oesophagus and stomach (gastro-oesophageal varices) – these
frequently rupture, causing severe upper gastrointestinal bleeding
In the rectum (haemorrhoids);
Around the umbilicus, where the collateral veins radiate outward in the
abdominal wall (“caput medusae”).
Entry of portal venous blood into the systemic circulation through these collateral
channels may result in hepatic encephalopathy because blood bypassing the liver
eludes detoxification. Portacaval anastomoses created surgically to relieve portal
hypertension may have the same effect.
Ascites: Ascites is due to increased transudation fluid across the peritoneal
membrane, particularly over the surface of the liver. The major factor leading to
severe ascites in chronic liver disease is a decrease in serum albumin level, with
portal hypertension playing only a contributory role.
Transudation of fluid decreases blood volume and initiates the normal
neurohormonal release of renin. This stimulates the formation of AT 2 which
in turn stimulates the release of aldosterone. Aldosterone stimulates the
retention of salt and water, and helps to normalise blood volume.
There is also impairment of hepatic lymphatic drainage
1. Describe the pathology of cirrhosis and the causes and complications of chronic liver
An accumulation in the liver of connective tissue resulting from an
imbalance between production and degradation of the extracellular matrix
and accentuated by the collapse and condensation of pre-existing fibers.
The normal liver is made up of hepatocytes and sinusoids distributed within
an extracellular matrix composed of collagen (predominantly types I, III and
IV) and non-collagen proteins, including glycoproteins (e.g. fibronectin,
laminin) and several proteoglycans (e.g. heparan sulphate, chondroitin
sulphate, dermatan sulphate, hyaluronate). Fibroblasts, normally found only
in the portal tracts, can produce collagen, large glycoproteins, and
Other liver cells (particularly hepatocytes and fat-storing Ito cells, Kupffer
cells and endothelial cells) also can produce extracellular matrix
components. Fat-storing cells, located beneath the sinusoidal endothelium
in the space of Disse, are precursors of fibroblasts, capable of proliferating
and producing an excess of extracellular matrix. The development of
fibrosis from active deposition of collagen is a consequence of liver cell
injury, particularly necrosis, and inflammatory cells. The precise factors
released from these cells is not known, but one or more cytokines or
products of lipid peroxidation are likely. Kuppfer cells and activated
macrophages produce inflammatory cytokines. New fibroblasts form
around necrotic liver cells; increased collagen synthesis leads to scarring.
Fibrosis may derive from active fibrogenesis and from impaired degradation
of normal or altered collagen. Fat-storing cells, Kupffer cells, and
endothelial cells are important in the clearance of type I collagen, several
proteoglycans, and denatured collagens. Changes in these cells’ activities
may modify the extent of fibrosis. For the histopathologist, fibrous tissue
may become more apparent from passive collapse and condensation of pre-
Thus, increased synthesis or reduced degradation of collagen results in
active deposition of excessive connective tissue, which affects hepatic
1. Pericellular fibrosis impairs cellular nutrition and results in
2. Within the space of Disse, fibrous tissue accumulates around the
sinusoids and obstructs the free passage of substances from the
blood to the hepatocytes.
3. Fibrosis around hepatic venules and the portal tracts disturbs
hepatic blood flow.
Venous resistance across the liver increases from portal vein branches to
sinusoids and finally to hepatic veins. All three routes can be involved.
The fibrous bands that link portal tracts with central veins also promote
anastomotic channels: Arterial blood, bypassing the normal hepatocytes, is
shunted to efferent hepatic veins, which further impairs hepatic function and
can accentuate hepatocellular necrosis. The extent to which these processes
are present determines the magnitude of hepatic dysfunction: e.g. in
congenital hepatic fibrosis, large fibrous bands involve predominantly the
portal regions but usually spare the hepatic parenchyma. Congenital hepatic
fibrosis thus presents as portal hypertension with preserved hepatocellular
Diffuse disorganization of normal hepatic structure by regenerative nodules
that are surrounded by fibrotic tissue.
Cirrhosis is the end stage of many forms of liver injury characterized
initially by fibrosis. The progression from fibrosis to cirrhosis and the
morphology of the cirrhosis depend on the extent of injury, the presence of
continuing damage, and the response of the liver to damage. Cirrhosis is
related not so much to the injurious agents as to the kind of injury and the
liver’s response to it. The liver may be injured acutely and severely (as in
sub-massive necrosis with hepatitis), moderately over months or years (as in
biliary tract obstruction and chronic active hepatitis), or moderately but
continuously (as in alcohol abuse). Cytokines and hepatic growth factors
(e.g. epidermal growth factor) are presumably responsible for the response
to injury: fibrosis plus regenerating nodules.
During the repair process, new vessels form within the fibrous sheath that
surrounds the surviving nodules of liver cells; these “bridges” connect the
hepatic artery and portal vein to the hepatic venules, restoring the
intrahepatic circulatory pathway. Such interconnecting vessels receive
blood from the sinusoids and provide relatively low-volume, high-pressure
drainage that is less efficient than normal and results in increased portal vein
pressure (portal hypertension). Disordered blood flow to the nodules and
compression of hepatic venules by regenerating nodules also contribute to
Cirrhosis is not static; its features depend on the disease activity and stage.
Morphologic classification does little to reveal its cause.
Micronodular cirrhosis is characterized by uniformly small nodules (< 3
mm in diameter) and regular bands of connective tissue. Typically, nodule
lack portal organization; terminal (central) hepatic venules or portal tracts
are difficult to identify.
Macronodular cirrhosis is characterized by nodules that vary in size (3
mm to 5 cm in diameter) and contain some normal lobular structure (portal
tracts, terminal hepatic venules). Broad fibrous bands of varying thickness
surround the large nodules. Collapse of the normal liver architecture is
suggested by the concentration of portal tracts within the fibrous scars.
Mixed cirrhosis (incomplete septal cirrhosis) combines elements of
micronodular and macronodular cirrhosis. Regeneration in micronodular
cirrhosis can result in macronodular or mixed cirrhosis. Conversion from
micronodular to macronodular cirrhosis takes 2 years.
Toxins and drugs, e.g. alcholic (60 – 70%), methyldopa, methotrexate,
Infections, e.g. viral hepatitis (10%).
Autoimmune diseases, e.g. chronic active hepatitis, primary biliary cirrhosis
(5 – 10%).
Metabolic disorders, e.g.
1. Wilson’s disease (due to defective biliary Copper excretion) (rare)
2. Haemochromatosis (due to excessive iron absorption) (5%)
3. 1-antitrypsin deficiency (look for concomitant respiratory
4. Glycogen storage diseases – history of failure to thrive, exercise
intolerance, BSL abnormalities.
Vascular disorders, e.g. hepatic venous outflow obstruction (Budd-Chiari
syndrome – associated with thrombotic states – OCP, pregnancy), veno-
occlusive disease, congestive heart failure.
Cryptogenic cirrhosis (10 – 15%).
Many severe complications of cirrhosis are secondary to portal hypertension
because hypertension leads to the development of collateral flow from the
portal venous system to the systemic circulation. Portal hypertension is
associated with splenomegaly and hence hypersplenism; the development of
collateral vessels lining the oesophagus and stomach produce varices.
Oesophageal varices and, less often, gastric varices are particularly prone to
bleeding, which is often massive massive haematemesis and often death.
Another complication is hypoxemia with reduced arterial O2 saturation,
secondary to pulmonary shunting, ventilation-perfusion mismatch, and
reduced O2 diffusing capacity.
In addition, jaundice, ascites, renal failure, and hepatic encephalopathy may
develop because of portal hypertension, portal-systemic shunting, other
circulatory disturbances, and impaired hepatic metabolic function.
Lastly, hepatocellular carcinoma frequently complicates cirrhosis associated
with chronic hepatitis B and C viruses, hemochromatosis, and long-standing
glycogen storage disease.
2. What are the principles of management of common liver diseases?
Management of cirrhotic patients includes:
Withdrawal of the causative agent (e.g. alcohol).
Where possible, treatment of the underlying causes – hepatitis and
Treatment of manifestations of hepatic failure, e.g. jaundice, ascites,
peripheral oedema, hepatic encephalopathy, coagulopathy, renal failure and
Withdrawal of offending agent:
Once identified, the causative agent should be withdrawn indefinitely.
Venesections for hemochromatosis – 1mg Fe2+ per mL of blood removed
Oral corticosteroids for chronic active hepatitis.
D-penicillamine for Wilson’s disease.
Ascites and peripheral oedema:
Dietary salt and fluid restriction.
Therapeutic paracentesis with IV fluid support.
Search for precipitating factors, e.g. dehydration, electrolyte imbalance,
infection, occult GI bleeding.
Dietary protein restriction.
Antibiotics e.g. neomycin.
Occasionally, dexamethasone to reduce cerebral oedema.
IM vitamin K given for three days.
If no improvement, maybe fresh frozen plasma or platelet infusion.
Cultures of blood, urine, ascitic fluid etc.
Treatment with a broad spectrum antibacterial agent.
May be due to dehydration, ATN or the hepatorenal syndrome.
1.Hepatorenal syndrome – appearance of renal failure in patients
with hepatic disease – unknown aetiology - renal perfusion with
renal vasoconstriction. Oliguria with low sodium, no protein.
Withdrawal of diuretics.
Patient made euvolaemic with appropriate intravenous fluids.
Institution of a high caloric diet.
Nasogastric or parenteral feeding may be necessary if caloric deficiencies
cannot be corrected with oral feeding.
Upper gastrointestinal bleeding:
Blood volume replacement.
Endoscopic sclerosis of varices.
IV vasopressin or octreotide.
Sclerotherapy – varices injected with sclerosing agent
Advanced cirrhosis < 65 years old.
CI in patients with active alcoholism, sepsis, CRF and malignancy.
70 to 80% survival rate at 12 months (greater in paediatric patients).
Major physical and emotional stress – pre-transplantation psychiatric
assessment is essential.
Require life-long immunosuppressive drugs.
1. Outline the causes of upper gastrointestinal bleeding.
Chronic peptic ulcer (40%), gastric ulcer (20%).
Acute peptic ulcer (erosions) (30%).
Portal hypertensive gastropathy.
Oesophageal and/or gastric varices.
Drugs: NSAIDs, steroids, thrombolytics, anticoagulants.
Nose bleeds (swallowed blood).
Erosive or ulcerative esophagitis.
Angiodysplasia – Dieulafoy Malformation.
Ehlers-Danlos or Peutz-Jeghers’ syndrome.
Aorto-enteric fistulas (in those with an aortic graft).
2. Describe the principles of its medical, endoscopic and surgical management.
Management of oesophageal varices
The object of therapy is to stop acute bleeding as soon as possible and manage
persistent varices with medical and procedural therapies. Bleeding must be
controlled quickly to prevent shock.
In endoscopic therapy, an endoscope (a device with a light that can look inside of a
body cavity) is used. The health care provider may directly inject the varices with a
clotting agent, or may place a rubber band around the bleeding veins. This procedure
is used in acute bleeding episodes and as prophylactic (preventative) therapy.
Acute bleeding may also be treated by a balloon tamponade – a tube that is inserted
through the nose into the stomach and inflated with air to produce pressure against
the bleeding veins.
In transjugular intrahepatic portosystemic shunting, a catheter is extended through
the vein into the liver where it connects the portal system to the systemic venous
system and decreases portal venous pressure.
Vasopressin is a medication that may be used to decrease portal blood flow and slow
Emergency surgery for patients refractory to medical treatment may be necessary.
Portocaval shunts (that pass blood to the vena cava from the portal vein by a graft) or
resection of part of the oesophagus are two treatment options, but these procedures
have a high death rate.
Medical management of all upper GI bleeds
While waiting for endoscopy or if not indicated:
1) Decide if a central line is indicated (shock; significant co-morbidity; re-
bleed; poor peripheral access).
2) Monitor vital signs hourly until stable, then 4 hourly – you are watching for
3) Daily U&E; clotting studies if >4 units blood needed (keep 2 units in
1. Describe the assessment of haemodynamic status and principles of resuscitation.
Bleeding as a cause of acute illness should be considered in a number of groups of
Recent surgery or invasive procedures.
Altered coagulation states.
History of upper gastrointestinal symptoms.
Postural hypotension (i.e. significant fall in systolic BP > 10 mmHg when patient
moves from supine to erect position) is only certain to be present after more than
15% of blood volume (70 ml/kg) is lost.
There are several causes of postural hypotension other than hypovolaemia, viz:
Drugs – narcotics, vasodilators.
Autonomic neuropathies (diabetes).
Prolonged blood rest.
Spinal cord injuries.
Symptoms and signs of acute blood loss
Blood loss Systolic blood pressure Symptoms and signs
(% of blood (mmHg)
10 – 15 Normal Postural hypotension
15 – 30 Slight fall Tachycardia
30 – 40 60 – 80 Pallor
> 40 40 – 60 Anuria
Management of blood loss
The urgency of volume replacement and the rate of resuscitation are both functions
of the amount and rate of loss. The initial assessment will suggest how much
replacement is needed. If after this replacement is given the patient is still not stable,
then it should be assumed that there is on-going, unrecognized bleeding.
In the initial phase of resuscitation in the emergency department cross-matched blood
is usually not available. It is appropriate to use a colloid initially and then to use a
mixture of packed red cells and clotting factors later as they become available. Since
the patient usually has no oral intake in this situation it is important to consider
maintenance fluid requirements as well.
Attend to the priorities of intravascular volume and tissue perfusion. Don’t
wait for blood to be available – start volume replacement with colloid.
Determine the required rate of replacement (slow onset of haemorrhage
allows some compensation).
Titrate to an appropriate patient end-point.
Correct ½ the abnormality and then re-evaluate.
Cover continuing losses.
Massive blood loss
When 50% of the circulating blood volume has been lost in a short period the
optimal fluid for replacement is fresh whole blood, but volume replacement with
colloid must commence while determining the patient’s blood group. Blood cross-
matching takes time and group-specific uncross-matched blood is very safe
serologically, and if available can be given until fresh cross matched blood is
A review of the priorities in management of massive bleeding:
Cardiopulmonary resuscitation (CPR).
First-aid control of haemorrhage.
Restitution of circulating volume.
Restitution of oxygen carrying capacity.
Medical and surgical hemostasis.
Management of specific injuries.
2. Explain the risks of blood transfusion.
Haemolytic Transfusion Reactions:
The most dreaded complication and can be fatal.
The most severe reactions are those involving mismatches in the ABO
Hemolysis is rapid and intravascular, releasing free haemoglobin into the
Severity depends on the dose of RBCs given.
Anesthetized surgical patients have the most severe reactions, as they are
unable to give early warning signs of myalgias and chills.
Also backache and headache and in severe reactions, dyspnea, hypotension
and vascular collapse.
The transfusion must be stopped immediately. Hydration to prevent acute
tubular necrosis if haemoglobinemia is present.
Most transfusion reactions are not haemolytic but represent reactions to
antigens present on WBCs in patients who have been sensitized to the
antigens through previous transfusions or pregnancy.
Chills and fever within 12 hours of transfusion.
Severe cases show cough, dyspnea and transient pulmonary infiltrates on X-
Respond to acetominophen and diphenhydramine and corticosteroids.
Rarely, patients will develop hives or bronchospasm.
These reactions mostly due to plasma proteins (not WBCs).
Patients who are IgA-deficient may develop these reactions due to
antibodies to IgA.
Future reactions may be avoided using washed or frozen RBCs.
Rarely, blood is contaminated with gram-negative bacteria.
Transfusion can lead to septicaemia and shock from endotoxin.
Antibiotics as indicated.
Diseases Transmitted Through Transfusion:
All blood products can transmit viral diseases (RBCs, platelets, plasma,
Donors are screened to detect those at high risk of transmitting diseases.
All blood is routinely screened for HBV, HCV and HIV.
Risk of post-transfusion hepatitis B is 1:200,000.
Risk of post-transfusion HIV is 1:250,000.
Risk of post-transfusion HCV is 1:3,300.
1. Recognize the professional and domestic effects of alcoholism.
Alcohol is a significant co-factor in disease. It is very obvious to practitioners that
alcohol abuse lowers inhibitions, and is often associated with exposure to venereal
diseases and to HIV infections. The chronic alcoholic’s lifestyle, malnutrition, and
often bleak living conditions greatly enhance the chance for acquisition of such
chronic diseases, both viral and tubercular. Further, in such patients, compliance
therapy is a significant problem, contributing to the growing problem of M.
tuberculosis drug resistance.
Low frustration tolerance.
Poor quality sleep.
Fatty liver – hepatic steatosis.
Alcohol use/abuse has been estimated to effect as much as 10-15% of physicians.
Historically, drug abuse has been linked to physicians because of their close
proximity to mind-altering drugs, narcotics, and drugs that elevated the mood, often
initiated during long arduous hours of training as interns or residents.
The AMA’s definition of “impairment” is “inability to practice medicine with
reasonable skill and safety to patients” because of a physician’s illness (illness or
illnesses including alcohol or drug dependence). These individuals provide a risk in
care for their patients.
Much of the susceptibility relates to the physicians personality. Their premorbid
compulsive personalities, rigid life schedule, excessively long hours and subsequent
fatigue often result in mood-altering drug experimentation as a release from stress.
2. Explain the public health aspects of chronic viral infections.
Chronic persistent viral hepatitis
A more common clinical syndrome due to infection with hepatitis B and C viruses.
The patient usually has mild symptoms or only slight abnormalities in LFTs lasting
for 6 months or more (an arbitrarily defined period).
A benign self-limited disease that may last for several years but does not progress to
Represents the chronic carrier state – hepatitis B or C virus is present in the blood,
and the patient is infective.
Occurs frequently in immunocompromised patients (chronic renal failure and
Also in vertical transmission, common in SE Asia and Africa, where the carrier rate
for hepatitis B is 10-15%.
Histologically, increased numbers of lymphocytes and plasma cells confined to the
portal tracts, and the limiting plate of hepatocyte is intact. There is no active necrosis
of liver cells. In hepatitis B, liver cells stain positive for HBsAg.
Chronic active viral hepatitis
Caused by hepatitis B, C and delta agent (delta requires B). An identical syndrome
occurs as a toxic reaction to certain drugs (oxyphenisatin, methyldopa, isoniazid) or
with alpha-1-antitrypsin deficiency, Wilson’s disease, and autoimmune chronic viral
Diagnosis of the specific virus involved is by serologic tests. Antinuclear auto-
antibodies are present in the serum of patients with autoimmune chronic active
hepatitis, in whom viral serology is negative.
Clinically, it is characterized by a chronic illness associated with marked elevation of
liver enzymes (AST, ALT, GGT). Episodes of acute hepatitis may be superimposed,
and portal hypertension may develop.
Progresses to cirrhosis and chronic liver failure. It has a bad prognosis.
Histologically, the hallmark is continuing focal necrosis of liver cells. The portal
tracts show widening due to lymphocytic and plasma infiltration and fibrosis. The
inflammation extents into the liver lobule, disrupting the limiting membranes of
hepatocytes, with entrapment and necrosis of liver cells in the periphery of the lobule
Patients with chronic hepatitis B and C have an increased incidence of hepatocellular
Prevention of viral hepatitis
Preventative measures may be necessary for:
Individuals with known exposure to hepatitis A virus-contaminated food or
Hospital employees exposed to blood products that are at risk of developing
hepatitis B or C.
Patients receiving transfused blood and blood products, again at risk for
hepatitis B and C.
Hepatitis A: hyperimmune gamma globulin provides passive protection against
hepatitis A and can be used to prevent a clinical attack after exposure to the virus.
There is also a vaccine available that provides lifelong immunity.
Hepatitis B: a recombinant DNA vaccine is effective in preventing infection and has
been recommended for high-risk groups such as hospital employees who have
contact with patients’ blood and tissues.
Blood transfusions: screening of blood donors for hepatitis B and C has virtually
eradicated transmission of viral hepatitis via blood transfusion.
Needle exchanges: prevention of IVDU re-using non sterile needles, sharing of
needles is important to reduce the transmission of HCV.
3. Discuss the recognition and avoidance of stereotyping and judgmental behavior.
Deeply held attitudes may create resistance to assessing alcohol use fully. For
example, the problems faced by patients with alcohol problems can be viewed in a
judgmental manner as self-inflicted, the implication being that they are less worthy
in some way of further assistance than other groups of patients. The reality of
contemporary medical practice however reflects hospitals being full of patients who
are ill because of the lifestyles they have led whether the primary agents involved in
their illnesses are diet, poor exercise, smoking or alcohol.
Other attitudes frequently expressed about patients with alcohol problems reflect the
futility of conducting assessments given that such patients will lie about the extent of
their consumption or deny that they have a problem. While proponents of the disease
model have placed much emphasis on alcohol denial, empirical examination of this
issue through correlating patient self-reports with those of spouses or biochemical
indices of drinking indicate that the vast majority of patients report alcohol
consumption and negative consequences of drinking relatively accurately.
1. Describe the clinical examination of the patient with liver disease.
There may be no symptoms or signs. In compensated disease there may be
Dupuytren’s contracture (fibrous thickening of the palmar fascia, with digital
contracture), parotid enlargement (alcohol abuse, not cirrhosis per se), hepatomegaly
(but a small, hard liver in advanced cirrhosis), palmar erythema, gynaecomastia,
testicular atrophy (all attributed to oestrogen levels), clubbing, xanthelasmata,
xanthomata, and spider naevi. These consist of a central arteriole with leg-like
branches, which blanch on central pressure and are usually confined to skin drained
by the SVC (face, neck, upper chest and back). Ascites (shifting dullness); abnormal
abdominal veins; bleeding varices; splenomegaly. Jaundice; scratch marks; hepatic
encephalopathy (e.g. hepatic flap) and if there is hypoalbuminaemia, leuconychia and
pitting oedema. Altered vitamin D metabolism may cause osteomalacia.
Congestive heart failure.
Secondary carcinomatous deposits.
Cirrhosis (usually alcoholic).
Also infections - glandular fever, infectious hepatitis; leukaemia and
reticuloendothelial disorders; tumors (primary hepatoma, amoebic and
hydatid cysts); amyloid, sarcoid and storage diseases; primary biliary
cirrhosis (large regular liver in women with jaundice and xanthelasmata);
haemachromatosis (look for pigmentation).
Cirrhosis with portal hypertension.
Reticuloendothelial disease, e.g. Hodgkin’s disease and chronic lymphatic
Intra-abdominal neoplasms (remember gynaecological lesions).
Hepatic cirrhosis with portal hypertension (relatively late in the disease).
Congestive heart failure and rarely constrictive pericarditis.
Nephritic syndrome (and other low albumin states).
Acute viral hepatitis.
Bile duct obstruction.
Multiple secondary deposits of carcinoma in the liver.
Gilbert’s syndrome / Crigler-Najjar syndrome.
Also haemolytic anaemia, congenital hyperbilirubinaemia, stricture or
carcinoma of the major bile ducts or ampulla.
2. Outline the assessment of substance dependence.
Narrowing of the drinking repertoire.
Do you tend to drink the same amount of alcohol each day of the week?
Stereotyped pattern of drinking should be deduced from the drinking
Salience of drinking (primary over other activities).
Do you skip meals because you are drinking?
Have you failed to do what was expected of you because of drinking?
Also refers to primacy over activities previously enjoyed and preferred to
Subjective awareness of compulsion to drink.
Have you experienced that you were not able to stop drinking once you had
Enquiries about “loss of control” considered to be a classical early warning
indicator of evolving dependence.
Increased tolerance to alcohol.
Have you needed more alcohol than previously to get the desired effect?
One of the more difficult elements to enquire specifically about in a single
question. Often best inferred from speed of drinking and ability to drink
large amounts of alcohol without becoming intoxicated.
Repeated withdrawal symptoms.
Do your hands shake a lot in the morning after drinking?
Tremor and nausea occasionally after drinking do not necessarily imply
Relief or avoidance of withdrawal symptoms by further drinking.
Have you needed a first drink to settle you down the morning after
A slightly disguised question such as this is useful before asking specific
questions on relief of morning tremor, sweating and nausea.
Reinstatement after abstinence.
Think back to when you restarted drinking after having none for a few days
or weeks. How long does it take you until you are drinking as heavily as
Reinstatement means the rapid return to the pre-abstinence level of drinking
and dependence symptomatology if and when the person resumes drinking.
Usually inferred from the longitudinal drinking history.
Are you or others CONCERNED about the level of your drinking?
Do you or others get ANGRY when confronted about your drinking?
Do you ever feel GUILTY about drinking?
Do you ever have an EYE-OPENER in the morning?
Answering YES to 2 or more is highly suggestive of a substance abuse problem.
3. Discuss the interpretation of liver function tests.
Functions of the liver
Detoxification – bilirubin, drugs
Protein synthesis – coagulation, serum proteins
Metabolism – glucose control, fat
Alanine aminotransferase (ALT).
ALT is an enzyme produced in hepatocytes, the major cell type in the liver.
ALT is often inaccurately referred to as a liver function test, however, its
level in the blood tells little about the function of the liver. The level of
ALT in the blood (actually enzyme activity is measured in the clinical
laboratory) is increased in conditions in which hepatocytes are damaged or
die. As cells are damaged, ALT leaks out into the bloodstream. All types of
hepatitis (viral, alcoholic, drug-induced etc.) cause hepatocyte damage that
can lead to elevations in the serum ALT activity. The ALT level is also
increased in cases of liver cell death resulting from other causes such as
shock or drug toxicity. The level of ALT may correlate roughly with the
degree of cell death or inflammation; however, this is not always the case.
An accurate estimate of inflammatory activity or the amount of cell death
can only be made by liver biopsy.
Aspartate aminotransferase (AST).
AST is an enzyme similar to ALT but less specific for liver disease as it is
also produced in muscle and can be elevated in other conditions (for
example, early in the course of a heart attack). Many physicians also
inaccurately refer to AST as a liver function test. In many cases of liver
inflammation, the ALT and AST activities are elevated roughly in a 1:1
ratio. In some conditions, such as alcoholic hepatitis or shock liver, the
elevation in the serum AST level may be higher than the elevation in the
serum ALT level.
Alkaline phosphatase is an enzyme, or more precisely a family of related
enzymes, produced in the bile ducts, intestine, kidney, placenta and bone.
An elevation in the level of serum alkaline phosphatase (actually enzyme
activity is measured in the clinical laboratory), especially in the setting of
normal or only modestly elevated ALT and AST activities, suggest disease
of the bile ducts. Serum alkaline phosphatase activity can be markedly
elevated in bile duct obstruction or in bile duct diseases such as primary
biliary cirrhosis or primary sclerosing cholangitis. Alkaline phosphatase is
also produced in bone and blood activity can be increased in some bone
An enzyme produced in the bile ducts that, like alkaline phosphatase, may
be elevated in the serum of patients with bile duct diseases. Elevations in
serum GGT, especially with elevations in alkaline phosphatase, suggest bile
duct disease. Measurement of GGT is an extremely sensitive test, however,
and it may be elevated in virtually any liver disease and even sometimes in
normal individuals. GGT is also induced by many drugs, including alcohol,
and its serum activity may be increased in heavy drinkers even in the
absence of liver damage or inflammation.
Bilirubin is the major breakdown product that results from the destruction of
old red blood cells (as well as some other sources). It is removed from the
blood by the liver, chemically modified by a process called conjugation,
secreted into the bile, passed into the intestine and to some extent
reabsorbed from the intestine. Bilirubin concentrations are elevated in the
blood either by increased production, decreased uptake by the liver,
decreased conjugation, decreased secretion from the liver or blockage of the
bile ducts. In cases of increased production, decreased liver uptake or
decreased conjugation, the unconjugated or so-called indirect bilirubin will
be primarily elevated. In cases of decreased secretion from the liver or bile
duct obstruction, the conjugated or so-called direct bilirubin will be
primarily elevated. Many different liver diseases, as well as conditions
other than liver diseases (e.g. increased production by enhanced red blood
cell destruction), can cause the serum bilirubin concentration to be elevated.
Most adult acquired liver diseases cause impairment in bilirubin secretion
from liver cells that cause the direct bilirubin to be elevated in the blood. In
chronic, acquired liver diseases, the serum bilirubin concentration is usually
normal until a significant amount of liver damage has occurred and cirrhosis
is present. In acute liver disease, the bilirubin is usually increases relative to
the severity of the acute process. In bile duct obstruction, or diseases of the
bile ducts such as primary biliary cirrhosis or sclerosing cholangitis, the
alkaline phosphatase and GGT activities are often elevated along with the
direct bilirubin concentration.
Albumin is the major protein that circulates in the bloodstream. Albumin is
synthesized by the liver and secreted into the blood. Low serum albumin
concentrations indicate poor liver function. The serum albumin
concentration is usually normal in chronic liver diseases until cirrhosis and
significant liver damage is present. Albumin levels can be low in conditions
other than liver diseases including malnutrition, some kidney diseases and
other rare conditions. Albumin has a half life of days-weeks and thus
disease of the liver must be present for a long time before significant
alterations in albumin will be evident.
Prothrombin time (PT).
Many factors necessary for blood clotting are made in the liver. When liver
function is severely abnormal, their synthesis and secretion into the blood is
decreased. The prothrombin time is a type of blood clotting test performed
in the laboratory and it is prolonged when the blood concentrations of some
of the clotting factors made by the liver are low. In chronic liver diseases,
the prothrombin time is usually not elevated until cirrhosis is present and the
liver damage is fairly significant. In acute liver diseases, the prothrombin
time can be prolonged with severe liver damage and return to normal as the
patient recovers. Prothrombin time can also be prolonged in cases of
vitamin K deficiency, by drugs (warfarin, used therapeutically as an anti-
coagulant, prolongs the prothrombin time) and in non-liver disorders.
Platelets are the smallest of the blood cells (actually fragments of larger
cells known as megakaryocytes) that are involved in clotting. In some
individuals with liver disease, the spleen becomes enlarged as blood flow
through the liver is impeded. This can lead to platelets being sequestered in
the enlarged spleen. In chronic liver diseases, the platelet count usually falls
only after cirrhosis has developed. The platelet count can be abnormal in
many conditions other than liver diseases.
Serum protein electrophoresis.
In this test, the major proteins in the serum are separated in an electric field
and their concentrations determined. The four major types of serum
proteins whose concentrations are measured in this test are albumin, alpha-
globulins, beta-globulins and gamma-globulins. Serum protein
electrophoresis is a useful test in patients with liver diseases as it can
provide clues to several diagnostic possibilities. In cirrhosis, the albumin
may be decreased and the gamma-globulin elevated. Gamma-globulin can
be significantly elevated in some types of autoimmune hepatitis. The alpha-
globulins can be low in alpha-1-antitrypsin deficiency.
Dom LO Title LO Detail
BCS Normal anatomy and 1. To describe anatomy of the large intestine and of the anorectal area
physiology 2. To list the main functions of the terminal ileum
3. To outline the anatomical and physiological factors affecting fluid exchange in the
BCS Causes and treatment 1. To list the principle microbiological causes of gastroenteritis and dysentery and to
of diarrhoea recognise their major pathological manifestations
2. To describe the different pathophysiological processes that are responsible for
3. Discuss how the choice of therapy for diarrhoea depends upon the underlying
cause of the disease.
BCS Pathology and 1. To describe the pathology of ulcerative colitis and Crohn’s disease and other
treatment of IBD diseases of the large intestine
2. To be able to distinguish between the clinical features of ulcerative colitis and
3. To describe the principles of the management of IBD and outline the
pharmacology of drugs used in its management
4. To outline the genetic aspects of large bowel disease
EPPD Clinical trials 1. Be aware of the related psychological, ethical and doctor-patient issues
concerning the enrolment of patients in clinical trials.
ICCP Psychological impact of 1. Describe the psychological impact of chronic disease
ICCP Examination skills 1. To develop basic skills in rectal examination and proctoscopy
PPH Per rectal bleeding 1. How does the prevalence of the conditions responsible for per rectal bleeding vary
(Public Health) according to patient age and gender?
2. Discuss the pros and cons of screening for colorectal cancer.
3. Who should and who shouldn’t be screened?
4. What are the recommended screening guidelines for colorectal cancer?
PPH Chronic illness (Social Using inflammatory bowel disease as an example, discuss:
Sciences) 1. the range of responses to the diagnosis of a chronic disease;
2. the life-style and psychosocial implications of chronic disease;
3. strategies to assist patients to accept and optimally manage their chronic illness;
4. the role of community organisations in assisting persons with chronic diseases;
5. the importance of a strong partnership between patient, general practitioner,
specialists and other health professionals in the holistic management of people with
It Returns To Haunt Me
ANATOMY AND PHYSIOLOGY OF THE LARGE INTESTINE
1. Outline the anatomical and physiological factors affecting fluid exchange in the gastro-
Daily water turnover (mL) in the gastrointestinal tract
Endogenous secretions 7000
Salivary glands 1500
Total input 9000
Balance in stool 200
Secretions of the small intestine
Mucus by Brunner’s glands:
Located in the first few centimeters of the duodenum.
Secrete an alkaline mucus in response to (1) tactile stimuli or irritating
stimuli of the overlying mucosa; (2) vagal stimulation, which causes
secretion concurrently with increase in stomach secretion; and (3)
gastrointestinal hormones, especially secretin.
Protects the duodenal wall from digestion by the gastric juice.
Contains a large excess of bicarbonate ions.
Inhibited by sympathetic stimulation.
Intestinal digestive juices by the Crypts of Lieberkühn:
Located on the entire surface of the small intestine.
Lie between the intestinal villi.
Crypts and villi covered by an epithelium composed of two cell types: (1) a
moderate number of goblet cells, which secrete mucus the lubricates and
protects the intestinal surfaces, and (2) a large number of enterocytes, which
in the crypts secrete large quantities of water and electrolytes and, over the
surfaces of the villi, reabsorb the water and electrolytes along with the end
products of digestion.
Secretions of the large intestine
Mucosa has many Crypts of Lieberkühn, but there are no villi.
Consists mainly of mucous cells that secrete only mucus.
Contains large amounts of bicarbonate ions.
Rate of secreted regulated by direct, tactile stimulation of the mucous cells
and by local nervous reflexes. Also stimulation of the pelvic nerces, which
carry the parasympathetic innervation to the distal one half to two thirds of
the large intestine, also causes marked increase in the secretion of mucus
(associated with increased motility).
Mucus protects from wall against excoriation and it provides the adherent
medium for holding fecal material together. Furthermore, it protects the
wall from bacterial activity and provides a barrier to acid.
Secretion of water and electrolytes in response to irritation:
Rampant bacterial infection (as in enteritis) causes irritation which results in
the mucosa secreting large amounts of water and electrolytes in addition to
the normal viscid solution of alkaline mucus.
Dilutes the irritating factors and causes rapid movement of the feces toward
Diarrhea, results in loss of large quantities of water and electrolytes.
Also washes away the irritant factor, which promotes earlier recovery than
would otherwise occur.
Anatomical basis of absorption
Absorptive surface of the intestinal mucosa – the villi:
Absorptive surface of the intestinal mucosa has many folds called valvulae
conniventes (or folds of Kerckring), which increase the surface area of the
absorptive mucosa about threefold.
Located over the entire surface of the small intestine are literally millions of
small villi. These enhance the absorptive area another 10-fold.
A brush border consisting of as many as 1000 microvilli characterizes each
intestinal epithelial cell. This increases the surface area exposed to the
intestinal materials at least another 20-fold.
Combination of the folds of Kerckring, the villi, and the microvilli increases
the absorptive area of the mucosa perhaps 1000-fold.
Within the villi, the arrangement of the vascular system for the absorption of
fluid and dissolved material into the portal blood and the central lacteal for
lymph is especially advantageous – prevents a build-up of digestive
products and hence ensures a favourable concentration gradient for
Absorption in the small intestine
Absorption of water:
Isosmotic absorption: water is transported through the intestinal membrane
entirely by diffusion.
As ions and nutrients are absorbed, so also is an isosmotic equivalent of
Absorption of ions:
Active transport of sodium:
Small intestine must absorb 25 to 35 grams of sodium each day (20
to 30 grams in endogenous secretions, 5 to 8 grams orally).
Sodium plays an important role in the absorption of sugars and
amino acids (co-transport).
Active transport of sodium from inside the epithelial cells through
the basolateral walls into the paracellular spaces.
Part of the sodium is absorbed with chloride ions.
Part of the sodium is absorbed while potassium or hydrogen ions
are transported in the opposite direction.
Sodium moves down a steep electrochemical gradient from the
chyme through the brush border of the epithelial cell into the
epithelial cell cytoplasm.
Osmosis of water creates a flow of fluid into and through the
paracellular space and, finally, into the circulating blood of the
Aldosterone greatly enhances sodium absorption:
Dehydration causes large amounts of aldosterone to be secreted by
the adrenal glands.
Enhances all the enzyme and transport mechanisms for all aspects
of sodium absorption by the intestinal epithelial cells.
Secondary increases in absorption of chloride ions, water and some
Action also on kidney to retain Na
Secretion of bicarbonate ions in the ileum and large intestine – simultaneous
absorption of chloride ions:
Provides alkaline bicarbonate ions to buffer acidic products formed by
bacteria, especially in the large intestine.
An exchange protein in the luminal membrane exchanges bicarbonate ions
formed inside the cell for chloride ions in the intestinal lumen.
The excess chloride is transported by facilitated diffusion through the
Extreme secretion in Cholera and other types of diarrhoea:
Normally, immature epithelial cells deep within the Crypts of Lieberkühn
secrete small quantities of sodium chloride and water into the intestinal
lumen. This secretion is normally reabsorbed by the older epithelial cells
outside the crypts, thus providing a watery solution for absorbing intestinal
Toxins of cholera and some other types of diarrheal bacteria can stimulate
the crypt secretion so greatly that this secretion inundates the reabsorption.
The toxin stimulates the formation of excess cAMP, which opens
tremendous numbers of chloride channels, allowing chloride to flow into the
crypts. In turn, this activates a sodium pump. All this excess sodium
chloride causes extreme osmosis of water into the crypts as well.
Characteristic “rice-water diarrhoea”
Absorption of glucose:
Glucose is basically transported by a sodium co-transport mechanism – the
transport protein will not transport the sodium to the interior until it also
combines with some other substance such as glucose.
The initial active transport of sodium through the basolateral membrane
provides the eventual motive force for moving glucose through the
enterocyte to the paracellular space.
Transport of glucose causes a high osmotic pressure in the paracellular
space, which causes water to be absorbed osmotically through the cell
junctions. At high concentrations, the osmotic flow increases and carries
with it anything dissolved in the fluid (“solvent drag” mechanism).
Absorption in the large intestine
Absorption and secretion of electrolytes and water:
High capacity for active absorption of sodium, and the electrical potential
created causes chloride absorption as well.
The tight junctions are much tighter, preventing back-diffusion of ions,
allowing the mucosa to absorb sodium ions against a much higher
The mucosa secretes bicarbonate ions while it simultaneously absorbs
chloride ions. The bicarbonate helps neutralize the acidic end products of
bacterial action in the colon.
The absorption of sodium and chloride ions creates an osmotic gradient
across the large intestinal mucosa, which in turn causes absorption of water.
Maximum absorption capacity:
Able to absorb a maximum of about 5 to 7 litres of fluid and electrolytes
When the total quantity exceeds this amount (by way of the ileocecal valve
or by large intestinal secretions), the excess appears in the feces as
2. Describe the function of the terminal ileum.
In the terminal ileum, Na+ is cotransported with bile salts.
Vitamin B12 absorption from food involves a series of steps in which B12 is released
from food, binds to R factors from saliva, and forms a complex with intrinsic factor
in the stomach that is absorbed by specific receptors in the terminal ileum.
Resorption of bile salts
Absorption of Vitamin B12
3. Describe the surgical anatomy of the large intestine and of the anorectal area.
Location: lies below the junction of the ileum with the large intestine. It is a blind-
ended pouch in the right iliac fossa about 6 cm long.
Anteriorly: small intestine, sometimes the greater omentum, and the
anterior abdominal wall in the right iliac region.
Posteriorly: psoas and iliacus muscles, femoral nerve, lateral cutaneous
nerve of the thigh, the appendix.
Medially: the appendix.
Arteries: from the anterior and posterior caecal arteries, which are
branches of the ileocolic artery, a branch of the superior mesenteric artery.
Veins: the ileocolic vein, a tributary of the superior mesenteric vein which
then unites with the splenic vein to form the portal vein.
Lymph drainage: pass to lymph nodes in the mesoappendix and to ileocolic lymph
nodes that lie along the ileocolic artery. Efferent lymph vessels pass to the superior
mesenteric lymph nodes.
Nerve supply: branches from the sympathetic and parasympathetic (vagus) nerves
from the superior mesenteric plexus.
Location: varies from 8-13cm long, the base is attached to the posteromedial surface
of the cecum about 2.5cm below the ileocecal junction. The appendix lies in the
right iliac fossa, its base is situated one-third of the way up the line joining the right
anterior superior iliac spine to the umbilicus (McBurney’s point). Internally, the base
is found by identifying the teniae coli and tracing them back to where they converge
to form a continuous longitudinal muscle coat.
Arteries: the appendicular artery, a branch of the posterior cecal artery.
Veins: the appendicular vein joins the posterior cecal vein.
Lymph drainage: the lymph vessels drain into nodes lying in the mesoappendix, then
passes through a number of mesenteric nodes to reach the superior mesenteric nodes.
Nerve supply: from sympathetic and parasympathetic (vagus) nerves from the
superior mesenteric plexus. Afferent nerve fibers concerned with the conduction of
visceral pain from the appendix accompany the sympathetic nerves and enter the
spinal cord at the level of T10.
Location: about 13 cm long and lies in the right lower quadrant. At the inferior
surface of the right lobe of the liver, it turns left, forming the right colic flexure.
Anteriorly: coils of small intestine, the greater omentum, anterior
Posteriorly: the iliacus, the iliac crest, the quadratus lumborum, the origin
of the transverse abdominis muscle, lower pole of the right kidney,
iliohypogastric and the ilioinguinal nerves.
Arteries: from the ileocolic and right colic arteries, branches of the
superior mesenteric artery.
Veins: the ileocolic and right colic veins, tributaries of the superior
Lymph drainage: lymph vessels pass to the paracolic and epicolic lymph nodes and
from them to the superior mesenteric lymph nodes.
Nerve supply: derived from the coeliac and superior mesenteric ganglia.
Location: about 38 cm long and occupies the umbilical region, suspended by the
transverse mesocolon. The left colic flexure is higher than the right colic flexure and
is suspended form the diaphragm by the phrenicocolic ligament.
Anteriorly: the greater omentum, anterior abdominal wall.
Posteriorly: duodenum, head of the pancreas, coils of the jejunum and
Blood supply: proximal two-thirds by the middle colic artery, a branch of the
superior mesenteric artery; distal third by the left colic artery, a branch of the
inferior mesenteric artery.
Lymph drainage: proximal two-thirds drain into the superior mesenteric nodes;
distal third drains into the inferior mesenteric nodes.
Nerve supply: proximal two-thirds innervated by sympathetic and vagal nerves
through the superior mesenteric plexus; distal third innervated by sympathetic and
parasympathetic pelvic splanchnic nerves through the inferior mesenteric plexus.
Location: about 25 cm long and lies in the left upper and lower quadrants. From the
left colic flexure to the pelvic brim, where it becomes continuous with the sigmoid
Anteriorly: coils of small intestine, the greater omentum, anterior
Posteriorly: lateral border of the left kidney, origin f the transverses
abdominis muscle, quadratus lumborum, iliac crest, the iliacus, the left
psoas. The iliohypogastric and the ilioinguinal nerves, the lateral cutaneous
nerve of the thigh, and the femoral nerve.
Arteries: the left colic and the superior sigmoid arteries of the inferior
Veins: drained by the inferior mesenteric vein.
Lymph drainage: lymph vessels pass to the intermediate colic lymph nodes, then to
the inferior mesenteric lymph nodes. Those from the left colic flexure also drain to
the superior mesenteric lymph nodes.
Nerve supply: sympathetic supply from the lumbar part of the sympathetic trunk and
the superior hypogastric plexus. The parasympathetic supply is derived from the
pelvic splanchnic nerves.
Location: about 25-38 cm long and is a continuation of the descending colon. At the
level of S3 it becomes continuous with the rectum.
Anteriorly: in the male, urinary bladder; in the female, the posterior surface
of the uterus and upper part of the vagina.
Posteriorly: the rectum and the sacrum, also the terminal ileum.
Arteries: from the sigmoid branches of the inferior mesenteric artery.
Veins: the inferior mesenteric vein returns blood from the sigmoid colon.
Lymph drainage: to the inferior colic lymph nodes on the branches of the left colic
arteries, and from them to the inferior mesenteric lymph nodes around the inferior
Nerve supply: sympathetic supply from the lumbar part of the sympathetic trunk and
the superior hypogastric plexus by means of the plexuses on the branches of the
inferior mesenteric artery. The parasympathetic supply is derived from the pelvic
Location: about 13 cm long and begins in front of the third sacral vertebrae. It ends
2.5 cm in front of the coccyx by piercing the pelvic diaphragm and becoming
continuous with the anal canal.
Posteriorly: the sacrum and coccyx; piriformis, coccygeus, and levatores
ani muscles; the sacral plexus; the sympathetic trunks.
Anteriorly: in the male, sigmoid colon and coils of ileum in the rectovesical
pouch, the posterior surface of the bladder, the termination of the vas
deferens and the seminal vesicles on each side, the prostate; in the female,
sigmoid colon and coild of ileum that occupy the rectouterine pouch (Pouch
of Douglas), posterior surface of the vagina.
Arteries: from the superior, middle, and inferior rectal arteries. Superior
rectal artery is a direct continuation of the inferior mesenteric artery.
Middle rectal artery is a small branch of the internal iliac artery. Inferior
rectal artery is a branch of the internal pudendal artery.
Veins: the superior, middle, and inferior rectal veins.
Lymph drainage: drain into the pararectal lymph nodes. Lymph vessels draining the
upper half accompany the superior rectal artery to the inferior mesenteric nodes.
Lymph vessels from the lower part follow the middle rectal artery to the internal iliac
Nerve supply: the middle rectal plexus is an offshoot of the inferior hypogastric
plexus. The parasympathetic nerves are derived from S2, S3, and S4 nerves and run
with the pelvic splanchnic nerves to join the inferior hypogastric plexus. The sensory
fibers follow the path of the parasympathetic nerves; their fibers are stimulated by
distention of the rectum.
COMPLAINT ASSOCIATED CLINICAL INCUBATION EPIDEMIOLOGICAL ORGANISMS FIRST LINE
FEATURES PERIOD FEATURES TREATMENT
ACUTE Vomiting Sever dehydration 24-72 hours Infants and young Rotavirus Rehydration therapy
WATERY Fever in some
Common world-wide in all
Peak in colder seasons in
Nausea Fever 6-72 hours Infants and young children in Enterotoxigenic Rehydration therapy
Vomiting Malaise developing countries Escherichia coli
The stool takes the Abdominal Severe dehydration Traveler’s diarrhea in adults
shape of the pain
container Nausea Malaise 8-36 hours Children Non-typhoid Rehydration therapy
Vomiting Common world-wide Salmonellae
Fever Food-borne outbreaks (animal
Abdominal Warmer seasons
Abdominal Chills 3-5 days World-wide distribution Campylobacter Rehydration therapy
pain Blood and pus in In developed countries may Erythromycin in severe
Fever the stools be food-borne (animal cases
Malaise products) or transmitted by
handling of animals
Vomiting Severe dehydration 1-3 days Children in endemic areas Vibrio cholerae Rehydration therapy
Abdominal Circulatory Adults in newly affected areas Tetracycline
pain collapse, “shock” Not found in Latin America
Nausea Fever 6-72 hours Nursery outbreaks in Enterpathogenic Rehydration therapy
Vomiting developed countries Escherichia coli
Uncertain in developing
DYSENTRY Fever Malaise 36-72 hours Children Shigellae Rehydration therapy
The stool is soft Abdominal Vomiting Poor hygiene Ampicillin or
and watery with pain Urgency to Malnutrition Trimethoprim-
blood and/or pus defaecate Institutions Sulfamethoxazole
Painful spasm on Warmer seasons
PROLONGED Abdominal 2-6 weeks All age groups Entamoeba Metronidazole
DIARRHEA (or discomfort World-wide distribution histolytica*
DYSENTRY) Abdominal Anorexia 1-3 weeks Young children Giardia lambia* Metronidazole
For at least 7 days, distention Nausea Some travelers
stools have been Flatulence Malabsorption Poor hygiene
more frequent or of Frothy stools World-wide distribution
(with or without
blood or pus)
* Can be identified on examination of stools with a light microscope.
Blood and pus from Shigellae and Campylobacter can also be identified.
1. Outline the main microbiological causes of gastroenteritis and dysentery.
Rotavirus (group A): 70-nm dsDNA virus, person-to-person transmission via food
and water, affects 6- to 24-month-old infants. Worldwide, 140 million cases and 1
million deaths occur per year. Minimal infective inoculum is 10 particles. Outbreaks
Detect using the rotavirus latex agglutination test.
Enteric adenoviruses: 80-nm dsDNA virus, person-to-person transmission, children
younger than 2 years.
Astroviruses: ssRNA viruses affecting children; person-to-person transmission via
water, cold foods, and raw shellfish.
Small round structured viruses, of which Norwalk virus is the prototype, classified
in the family Caliciviridae: 27-nm ssRNA viruses; person-to-person transmission
via cold food, water, and raw shellfish; affects school-age children to adults.
Outbreaks are common after exposure to a common food source.
Morphology: the small intestine exhibits modestly shortened villi, lamina propria
inflammation, and damage to surface cells.
Clinical findings: incubation periods range from hours to several days; acute illness
occurs from 1 to 7 or more days. In addition to diarrhea, anorexia, headache, and
fever may develop.
Mechanisms of bacterial illness are as follows:
Ingestion of preformed toxin in contaminated food (food poisoning):
Staphylococcus aureus, Vibrios, Clostridium perfringens. Botulism is
neurotoxic, nor diarrheogenic.
Infection by toxigenic organisms, which proliferate in gut lumen and
elaborate an enterotoxin.
Infection by enteroinvasive organisms, which proliferate, invade, and
destroy mucosal epithelial cells.
The key bacterial properties by which disease can be produced are:
Bacterial adhesion and replication: to produce disease, ingested organisms
must adhere to the mucosal epithelial cells; otherwise, they are swept away.
Adherence depends on plasmid-encoded adhesions; proteins are expressed
on the bacterial surface.
Peristalsis, diarrhoeal tide
Bacterial enterotoxins: these are polypeptides that cause diarrhea. Two
Secretagogues (e.g. cholera toxin from Vibrio cholerae), which
stimulate fluid secretion by activation of endogenous secretion
Cytotoxins (e.g. Shiga toxin), which cause direct tissue damage
through epithelial cell necrosis.
E. coli produce both forms of toxins.
Bacterial invasion: microbe-stimulated endocytosis permits intracellular
proliferation, cell lysis, cell-to-cell spread, and spread to circulation. This is
typical of enteroinvasive E. coli, Shigella, Salmonella, and Yersinia
Morphology: morphologic manifestations are extremely variable. Nonspecific
features include damage to surface epithelium, increased mitotic rate, lamina propria
hyperemia and edema, and neutrophilic infiltration of lamina propria and epithelium.
Salmonella: ileum and colon with Peyer patch involvement, S. typhimurium
causes typhoid fever (bacteremia and dissemination to biliary tree, joints,
bones, and meninges).
Shigella: colonic inflammation, erosion, and exudates.
Campylobacter jejuni and other species: small intestine, appendix, colon,
ulcers, inflammation, and exudates.
Y. enterocolitica and Y. pseudotuberculosis: ileum Peyer patches,
appendix, colon, and mesenteric lymph nodes with necrotizing granulomas
and systemic spread.
V. cholerae: essentially normal small intestine.
Clostridium perfringens: usually mild; some strains cause severe
necrotizing enterocolitis (pigbel).
E. coli: enterotoxigenic E. coli produce cholera-like toxin;
enterohemorrhagic produce shiga-like toxin; enteropathogenic attach and
efface epithelium but do not invade; enteroinvasive are like shigellosis. All
cause traveller’s diarrhea.
Ingestion of preformed toxins: explosive diarrhea and abdominal pain
Infection with enteric pathogens: incubation period of hours to days,
followed by diarrhea and dehydration or dysentery, depending on the
Insidious infection: Yersinial and mycobacterial infection. All
enteroinvasive organisms can mimic (or coexist with) acute onset of
inflammatory bowel disease.
2. Summarize the different mechanisms that cause diarrhea and how they relate to choice
Associated with cAMP increase:
Enterotoxin of Vibrio cholerae.
Enterotoxin of Escherichia coli.
Vasoactive intestinal polypeptide (from pancreatic islet cell
Not associated with cAMP:
Enterotoxin of Staphylococcus aureus.
Enterotoxin of Clostridium perfringens.
Some laxatives (bisacodyl, phenolphthalein).
AIDS (unknown mechanism).
Infections: viral and Salmonella gastroenteritis, Shigella, E. coli,
Inflammatory bowel disease.
Carcinoid syndrome (serotonin, prostaglandins).
Disaccharidase deficiency (lactose or sucrose intolerance).
Laxatives (lactulose, magnesium salts).
Irritable bowel syndrome.
Autonomic neuropathy (diabetes mellitus).
Failure of colonic water absorption:
Total colectomy – surface area
Irritable bowel syndrome.
Deficiency of pancreatic enzymes (chronic pancreatitis, cystic
fibrosis, pancreatic resection).
Zollinger-Ellison syndrome (high acid inhibits lipase).
Deficient bile salt concentration:
Bacterial overgrowth leading to bile salt deconjugation (stasis in
blind loops, diverticula, fistulas, hypomotility states e.g. diabetes,
scleroderma, visceral myopathy).
Interrupted enterohepatic circulation of bile salts (terminal ileal
resection, Crohn’s disease).
Precipitation of bile salts (neomycin, cholestyramine (therapeutic
Primary mucosal abnormalities:
Inadequate small intestine:
Intestinal resection (Crohn’s disease, mesenteric vascular disease
In the younger patient, maintenance of hydration is particularly important.
The aim of treatment is to keep patients functioning while minimizing
symptoms. Antiemetics and antidiarrheal agents constitute practical
Avoid antimicrobial drugs. They are usually not indicated and can mask or
delay a diagnosis where stool cultures are not carried out.
Aim for a documented diagnosis.
Endoscopic diagnosis is much simpler than in the past and should be used
Realize that some patients may never be “diagnosed”. Symptom relief may
be the best that can be achieved.
Oral (clear liquids, sodium and glucose-containing oral rehydration
solutions). (One teaspoon salt, 5 teaspoons of glucose/L)
Intravenous (normal saline or lactated Ringer’s solution, especially
if severely dehydrated or patient has intractable vomiting).
Absorbents (Kaopectate, aluminium hydroxide): These do not alter the
course of the disease or reduce fluid loss but allow the patient more control
over the timing of defecation. Other medications should be taken ½ hour
before or 2 hours after absorbents are used.
Antisecretory agents such as bismuth subsalicylate (Pepto-Bismol). Usual
dose is 30 ml every 30 minutes for 8 doses.
Antiperistaltics, such as opiate derivatives. Do not use in patients with
fever, systemic toxicity, or bloody diarrhea. Discontinue if no improvement
or if patient deteriorates.
Diphenoxylate with atropine (Lomotil). Available in tablets (2.5
mg of diphenoxylate) and liquid (2.5 mg of diphenoxylate/5 ml).
The initial dose for adults is two tablets QID (20 mg/day). For
children the dose is 0.1 mg/kg/dose QID. The dose is tapered as
diarrhea improves. It is not indicated for diarrhea caused by
pseudomembranous colitis or enterotoxin-producing or invasive
bacteria. Lomotil should not be used in ulcerative colitis or in
children under 2 years of age.
Loperamide (Imodium). Available over the counter in 2 mg
capsules and liquid (1 mg/5 ml). It increases the intestinal
absorption of electrolytes and water and decreases intestinal
motility and secretion. The dose in adults is 4 mg initially,
followed by 2 mg after each diarrhea stool, not to exceed 16 mg in
one 24-hour period. In children the dose is based on age, with 2 to
5 year olds receiving 1 mg TID, 6 to 8 year olds 2 mg BID, and 9
to 12 year olds 2 mg TID on the first day of treatment. Thereafter
0.1 mg/kg is administered after each diarrhea stool, not to exceed
the total daily dose recommended for the first day of therapy.
Loperamide is safe and decreases the number of unformed stools
and the duration of diarrhea in patients with Shigella-induced
dysentery who are treated with ciprofloxicin.
Antibiotics. Not necessary for most episodes of diarrhea but should be
directed against known or strongly suspected pathogens. Once cultures are
done, empiric with an agent that covers Shigella and Campylobacter is
reasonable in those with severe diarrhea with systemic signs. A 3-day
course of a fluoroquinolone (ciprofloxacin 500 mg PO BID or norfloxacin
400 mg PO BID) is the first-line therapy. TMP/SMP (Pactrim DS 2 tab PO
QD) is an alternative therapy, but resistant organisms are common in the
tropics. If the diarrhea is caused by seafood ingestion, infection with either
Vibrio cholerae or Vibrio parahaemolyticus is possible and can be treated
with either a fluoroquinolone or with doxycycline 100 mg PO BID.
Traveler’s diarrhea. Prophylaxis not routinely recommended because of
the risk of adverse effects from the drugs (rash, anaphylaxis, vaginal
candidiasis) and the development of resistant gut flora. Possible regimens
for prophylaxis include bismuth subsalicylate (Pepto-Bismol) 524 mg PO
BID with meals and QHS, doxycycline 100 mg PO QD (resistance
documented in many areas of the world), TMP/SMX 160 mg/800 mg (1
double strength tablet) PO QD, or norfloxacin 400 mg PO QD
(fluoroquinolones should not be prescribed to children or pregnant women).
No significant resistance to fluoroquinolones has yet been reported in high-
risk areas, and they are the most effective antibiotics in regions where
susceptibilities are not known. Loperamide can be added to the
fluoroquinolones or TMP/SMX when treating traveler’s diarrhea. These
medications should be continued for 1 or 2 days after patient returns home.
Fluid repletion. A simple oral rehydration solution may be composed of 1
level teaspoon of salt and 4 heaping teaspoons of sugar added to 1 liter of
water. Bottled flavored mineral water with saltine crackers is an acceptable
INFLAMMATORY BOWEL DISEASE
Ulcerative Colitis Crohn’s Disease
Rectal involvement Over 90% Rectum spared in > 50%
Distribution of lesions Continuous Skip lesions
Mucosal appearance Friable, purulent, diffusely Aphthous, linear ulcers with
Associated ileal disease 10%, mild, terminal ileal 50% have combined ileal and
inflammation colonic involvement
Perianal abscess, fistulas Rare Common
Intestinal strictures and Not seen Common
Intestinal fistulas Not seen Common
Fissures (radiologic) Not seen Common
Intestinal perforation Rare Rare
Intestinal hemorrhage Common Rare
Toxic megacolon Rare Very rare
Sclerosing pericholangitis Common Rare
Uveitis or arthritis Common Common
Pyoderma gangrenosum Rare Not seen
Depth of inflammation Mucosal (submucosal rarely) Transmural
Creeping mesenteric fat Not seen Common
Fibrous thickening of wall Not seen Common (“lead pipe”)
Crypt abscesses Common Common
Pseudopolyps Common Common
Granulomas (epitheloid, Not seen Common
Fissures (microscopic) Not seen Common
Dysplasia Common Rare
Carcinoma 10% Rare
1. Describe the clinical features of inflammatory bowel disease.
The major symptoms of UC are bloody diarrhea and abdominal pain, often with fever
and weight loss in more severe cases. With mild disease, there may be one or two
semiformed stools per day, containing little blood, and there may be no systemic
manifestations. In contrast, the patient with severe disease may have frequent liquid
stools containing blood and pus, complain of severe cramps, and demonstrate
symptoms and signs of dehydration, anemia, fever and weight loss. With
predominantly rectal involvement, constipation rather than diarrhea may be present,
and tenesmus (ineffective straining at stool) may be a major complaint. On occasion,
intestinal symptoms may be overshadowed by fever, weight loss, or one of the
extracolonic manifestations of the disease.
Complications of acute disease include toxic dilatation of the colon, perforation and
The risk of carcinoma of the colon is increased in patients with disease of more than
seven to ten years duration.
The clinical features of Crohn’s disease depend largely upon the site of involvement.
Abdominal pain is the predominant symptom in patients with ileal disease, and they
may present with an illness indistinguishable from acute appendicitis.
Patients with colitis develop diarrhea, but with rectal bleeding in only 50%. Patients
with both colonic and ileal disease have a combination of symptoms.
Fever, weight loss and malaise are common. Anemia and nutritional impairment
occur more often than in ulcerative colitis.
The disorder may be complicated by stricture formation, fistulae and perianal
Growth retardation is an important manifestation in children.
2. Distinguish and describe the pathology of ulcerative colitis and Crohn’s disease and
other diseases of the large intestine.
Congenital aganglionic megacolon – Hirschsprung disease
Failure of development of ganglion cells in the myenteric and submucosal plexuses
of the colon.
Results in failure of peristalsis in the affected segment – remains narrow and spastic
and represents a zone of functional intestinal obstruction.
Rectum is always affected; proximal involvement is more variable.
Proximal colon dilates – often massively – leading to abdominal distention.
Collagenous and lymphocytic colitis
Chronic watery diarrhea in middle-aged and older women.
Benign clinical course.
Collagenous colitis: patches of band-like collagen under the surface epithelium.
Lymphocytic colitis: prominent intraepithelial infiltrate of lymphocytes and is
associated with autoimmune diseases and celiac sprue.
Ischaemic bowel disease:
Transmural infarction: sudden and total occlusion of a major vessel,
infarction of all bowel layers. Bowel segment is haemorrhagic as a result of
blood reflow into damaged area. Bowel appears rubbery and dusky,
bacteria produce gangrene, and perforation develops within days. Imparts
50 to 75% death rate.
Mural and mucosal infarction: incomplete necrosis or necrosis of mucosa
only. Mucosa appears haemorrhagic, but serosa may be normal.
Distribution is frequently patchy; inflammation depends on duration of
injury. Ischemic changes may be due to any cause (occlusive or
Chronic ischaemia: causes mucosal inflammation, ulceration, fibrosis, and
stricture. Ischemia has a segmental patchy distribution.
Nonspecific abdominal complaints, easily confused with acute and chronic
Tortuous, abnormal dilations of submucosal veins that extend into the
lamina propria, cecum, and ascending colon and tend to bleed. They range
from small, focal ectasias to large, dilated, tortuous formations.
Acquired ectasias are attributed to partial, intermittent occlusion of
submucosal veins in the cecum and ascending colon, the site of maximal
wall tension because of its greater diameter.
Variceal dilation of anal and perianal submucosal venous plexuses.
Associated with constipation, venous stasis of pregnancy, and cirrhosis (and
other causes of portal hypertension).
Ectasia of the inferior hemorrhoidal plexus below the anorectal line
(external haemorrhoids) is seen as well as in superior hemorrhoidal plexus
(internal haemorrhoids). Secondary thrombosis (with recanalization),
strangulation, or ulceration with fissure formation may develop.
Colonic diverticular (diverticulosis) are uncommon in patients younger than age 30
but present in 50% of adults older than age 60 in Western populations.
Multiple flask-like outpouchings 0.5 cm to 1 cm in diameter are seen,
usually in distal colon.
Occur alongside teniae coli and dissect into appendices epiploicae.
The thin wall is lined by mucosa and submucosa and an attenuated-to-absent
Muscularis of intervening bowel wall is hypertrophic.
Pathogenesis includes the following mechanisms:
Focal weakness in bowel wall at sites of penetrating blood vessels (vasa
Increased intraluminal pressure resulting from exaggerated peristaltic
contractions, possibly the result of decreased bulk in diet (low fibre diet).
Diverticulitis – inflammation of diverticulum after obstruction or perforation.
May lead to pericolic abscesses, sinus tracts, and peritonitis.
Tumors of the colon and rectum
Non-neoplastic polyps: polyps resulting from abnormal mucosal maturation,
inflammation, or architecture; no malignant potential.
Arise as a result of epithelial proliferative dysplasia; adenocarcinoma
generally arises from adenomas.
Three histologic appearances are characteristic:
Tubular adenoma: tubular glands, smooth surface.
Villous adenoma: villous frondlike projections.
Tubulovillous adenoma: a mixture of the first two.
Risk of coexistent malignancy is correlated with three interdependent
Severity of dysplasia.
Adenomas are slow growing; doubling time is approximately 10 years.
Most adenomas are in the colon (90%).
All adenomas exhibit dysplastic epithelium (tall, hyperchromatic disorderly
cells with increased nuclear-cytoplasmic ratio, cigar-shaped nuclei).
Smooth contoured bumps in the mucosa involving only a few
With growth, they become bulky neoplasms (up to 4 cm diameter)
and protrude into the lumen – traction creates a submucosal stalk
lined by normal mucosa.
Branching dysplastic glands are embedded in lamina propria.
Larger when discovered and may carpet up to 10 cm of colonic
Finger-like projections are lined by dysplastic epithelium with a
lamina propria core.
Intermediate in size, with likelihood of having a stalk, and mixture
The only adequate treatment for any adenoma is resection, regardless of
whether carcinoma is present. Any residual adenomatous tissue is still a
premalignant lesion or may yet harbor invasive adenocarcinoma.
Familial adenomatous polyposis coli is the archetype of autosomal
dominant polyposis syndromes.
Innumerable adenomatous polyps in colon (and elsewhere in the gut); risk
of progression to adenocarcinoma is 100%.
Minimum of 100 colon adenomas required for diagnosis.
Prophylactic colectomy is curative for colonic risk of cancer; adenomas
elsewhere create continued problems.
Average age of onset is teens to twenties. Progression to cancer occurs in
10 to 15 more years without surgery.
Defect in APC gene and interactions with cadherins.
Also non-APC familial colon cancer – associated with satellite repair genes.
98% are adenocarcinomas.
Peak incidence occurs at age 60 to 79 years except in young adults with
Most arise in polypoid adenomas, also a hereditary nonpolyposis colorectal
cancer syndrome exists.
Diet may be important; risk is associated with low fiber intake, high content
of refined carbohydrates, high intake of red meat, decreased intake of
protected micronutrients (vitamins A, C, E).
Caecum/ascending colon, 38%; transverse colon, 18%; descending colon,
8%; rectosigmoid, 35%; multiple sites at presentation, 1%.
Polypoid, fungating masses (especially in capacious cecum and right colon)
or annular, encircling masses with napkin-ring obstruction (characteristic of
distal colorectum). Both forms penetrate bowel wall over years.
Microscopically, tall, columnar cells resembling neoplastic epithelium of
adenomas but now invasive as glands or cell clusters into submucosa and
muscularis propria; carcinoma also may be poorly differentiated.
Tumors incite a desmoplastic stromal response: inflammation and fibrosis of
A minority of tumors produces copious mucin; less commonly, foci of
neuroendocrine differentiation, signet-ring features, or squamous
differentiation are apparent.
Clinically, fatigue, weakness, iron deficiency anemia, abdominal
discomfort, progressive bowel obstruction, and liver enlargement
(metastases) eventually occur.
Abdominal X-ray shows “apple core” sign
Prognosis is based on extent of invasion at diagnosis (100% for lesions
limited to the mucosa; 25% for extensively invasive tumors). Surgery is the
only hope for cure.
Tumor of gut endocrine cells.
Peak incidence is in the fifties.
Ileal, gastric, and colonic carcinoids are frequently aggressive.
Many elaborate bioactive products (e.g., amines or peptides).
Intramural or submucosal masses are seen – small, firm and yellow-tan.
Rectum, masses tend to be solitary; elsewhere, there tend to be multiple
Nodules may cause kinking and obstruction of intestine.
Microscopically, discrete islands, trabeculae, glands, or sheets of
monotonous uniform cells with scant, pink, granular cytoplasm and oval,
stippled nuclei are seen, separated by a fibrous stroma.
Clinically, carcinoid tumors are usually asymptomatic; local symptoms
occur from obstruction and bleeding.
Inconstant secretory products include gastrin, ACTH, insulin and others.
Ectopic ACTH Cushing’s syndrome
Rectal carcinoids are always innocuous.
Five-year survival rate for other carcinoids is 90%.
Primary GI lymphomas occur more frequently in chronic sprue-like
malabsorption syndromes, natives of Mediterranean region, congenital
immunodeficiency states, HIV infection, and after organ transplantation
B-cell lymphomas also may rise from MALT.
Adults are affected.
Stomach, 55 to 60%; small intestine, 25 to 30%; colon, 20 to 25%.
Younger individuals (30 to 40 years of age), after long duration oof
malabsorptive disorder; usually T-cell lymphoma.
Prognosis is poor.
B-cell lymphoma in children and adults of Mediterranean ancestry;
background of chronic diffuse mucosal plasmacytosis.
Also called immunoproliferative small intestinal disease.
Prognosis is poor.
Early lesions, plaque-like expansions of mucosa and submucosa.
Advanced lesions, full-thickness mural lesions or polypoid, fungating
masses protruding into the lumen.
Microscopically, atypical lymphocytes infiltrate mucosa and wall, replacing
normal structure. Extreme numbers of lymphocytes may populate the
epithelium (lymphoepithelial lesion). B-cell lesions (95%) may be low or
high grade; T-cell lesions are all high grade.
Clinically, sporadic lymphomas are amenable to surgical resection and are
chemoresponsive. Outcome depends on size, grade, and invasiveness of
tumor at time of resection.
Small intestine masses risk of intussusception (telescoping of bowel –
produces gut obstruction)
3. Outline the natural history of inflammatory bowel disease (IBD).
The clinical course is variable.
Most patients suffer a relapse within 1 year of the first attack, reflecting the recurrent
nature of the disease. There may, however, be prolonged periods of remission with
only minimal symptoms.
The severity of symptoms reflects the extent of colonic involvement and the intensity
of the inflammation.
Patients who present with limited involvement of the rectum (ulcerative proctitis) or
rectum and sigmoid (ulcerative proctosigmoiditis). Their disease is usually mild,
with minimal systemic or extracolonic manifestations, although ulcerative proctitis is
sometimes difficult to treat, exhibiting protracted bleeding and tenesmus. The major
symptoms are rectal bleeding and tenesmus. Most of these patients, especially those
with only rectal involvement, do not develop more extensive disease. In the
remainder, the disease may extend proximally with variable involvement.
Perhaps 85% of patients with UC have mild to moderate disease of an intermittent
nature and can be managed without hospitalization.
In approximately 15% of patients, the disease becomes more fulminant, involves the
entire colon, and presents with severe bloody diarrhea and systemic signs and
symptoms. These patients are at risk of developing toxic dilation and perforation of
the colon and represent a medical emergency.
Mortality appears greatest early in the disease.
Extraintestinal manifestations (arthritis, uveitis, skin lesions and sclerosing
Prognosis for CD is not as favorable as for UC (except acute regional enteritis; this
has an excellent prognosis).
In the majority of patients with CD, the course is chronic and intermittent regardless
of the site of involvement.
Responds less well to medical therapy with time.
Two-thirds of patients develop complications requiring surgery at some point.
Mortality rate increases with the duration of the diseases and probably ranges from 5
to 10 percent.
Most deaths occur from peritonitis and sepsis.
Following surgery, patients often have recurrence and relapses.
Therapy will result in reasonably stable and productive lives for most CD patients.
Intestinal obstruction or fistula.
Extraintestinal manifestations (arthritis and uveitis).
Complications of IBD
Fistulas: forms between involved loops of bowel and adjacent viscera.
Ileum and colon: malabsorption due to bacterial colonization.
Ileal loops: short circuit the bowel, resulting in malabsorption.
Enterovesical: UTI and passage of gas and feces with urine.
Enterovaginal: fecal vaginal discharge.
Malabsorption syndromes: a complication of disease involving the terminal ileum, in
which there may be failure to absorb vitamin B12 and bile acids, resulting in
macrocytic anemia and fat malabsorption.
May be iatrogenic – post-surgical resection
Need to ensure adequate nutrition – IM B12 supplements
Perforations: can occur in severe UC since with extensive ulceration of the bowel
wall may become extremely thin. Clinical features include acute peritonitis with
signs of peritoneal inflammation and the demonstration of free air under the
diaphragm on upright film of the abdomen.
Phlegmon formation – perforation leading to localised sepsis. Rapidly
enveloped by the omentum and infection is sequestered. The gut is
inflamed, oedematous and painful – treated conservatively with antibiotics.
Can be treated surgically but there is a risk of creating a “short-gut
syndrome”. Phlegmon is bypassed – proximal normal gut is anastomosed
distally, affected gut can then heal in situ and the gut re-joined later.
Toxic dilatation: may occur in CD but is more common in UC. Can be considered a
severe form of UC with the additional feature of colonic dilatation. The
neuromuscular tone of the bowel is affected by the severe inflammation, resulting in
Carcinoma: increased incidence of carcinoma in patients with chronic IBD,
especially in those who have more extensive mucosal involvement (i.e., pancolitis)
and those who have had their disease for extended periods of time. In colitis patients,
the tumors are more often multiple, flat, and infiltrating and appear to have a higher
grade of malignancy. Early warning signs (i.e., rectal bleeding, change in bowel
habits) will be difficult to interpret in the setting of colitis.
Extraintestinal manifestations: their cause is currently unknown.
Joint manifestations occur in 25% of patients. May range from arthralgia
only to an acute arthritis with painful, swollen joints. The non-deforming
arthritis is mono- or polyarticular and often migratory. Knees, ankles and
wrists are most commonly involved, but any joint may be affected.
Skin manifestations are more common with colonic disease. Occur in
about 15% of patients, and when present, severity correlates with activity of
the bowel disease.
Erythema nodosum may be seen and heals without scarring.
Pyoderma gangrenosum an ulcerating lesion often occurring on the
trunk, is relatively painless and may heal without scarring.
Aphthous ulcers resemble “canker sores” of the mouth, and in
approximately 5 to 10% of patients they are present during periods
of active disease and then resolve.
Ocular manifestations such as episcleritis, recurrent iritis, and uveitis occur
in approximately 5% of patients and may represent a severe manifestation of
the disease. Activity parallels the course of the bowel disease, and the
lesions may respond dramatically when colectomy is done.
Sclerosing cholangitis, a chronic inflammation of unknown cause
involving the extrahepatic and intrahepatic bile ducts that may
produce varying degrees of extrahepatic biliary obstruction.
Corticosteroids and immunosuppressive therapy are not beneficial
while results after colectomy are inconsistent.
Cholangiocarcinoma, arising in the extrahepatic biliary tree, has an
increased incidence in patients with UC. Biliary obstruction must
be distinguished from sclerosing cholangitis.
Chronic active hepatitis which may progress to cirrhosis may be
seen in IBD although the relationship between these disorders is
unknown. Colectomy does not influence the course of this form of
4. Describe the principles of the management of IBD and outline the pharmacology of
drugs used in its management.
The treatment of an acute exacerbation of ulcerative colitis or Crohn’s disease
The severity of the attack.
The extent of the disease.
Mild attacks can usually be managed out of hospital. Severe episodes require
In severe disease, attention must be paid to fluid and electrolyte balance, correction
of anaemia and maintenance of nutrition. Clinical status and vital signs must be
carefully monitored looking for early evidence of toxic dilatation and deterioration.
5-Aminosalicylic acid (5-ASA) derivatives are effective in acute ulcerative colitis
and in Crohn’s disease affecting the colon. They are also able to reduce the risk of
relapse in ulcerative colitis approximately four-fold when taken long-term, and this
effect does not diminish with time.
Sulfasalazine consists of 5-ASA linked by an azo bond to sulfapyridine, a
sulfonamide. 5-ASA is the active component, whereas sulfapyridine acts as
a carrier molecule preventing absorption in the small intestine. The latter is
responsible for most of the side effects of headache, nausea, vomiting and
malaise, which can be managed by reintroduction at a lower dose; and non-
dose related effects, e.g. fever, rash and agranulocytosis, which require
withdrawal of the drug. Reversible reduction in fertility occurs in a small
proportion of male patients.
Olsalazine (azodisalicylate sodium) is a dimmer of 5-ASA, and does not
contain a sulfonamide component. It may produce a secretory diarrhea in
up to 10% of patients, but this can be minimized by titrating the dose and
taking it after meals.
Mesalazine (5-ASA) is available in an oral, polymer coated form which is
designed to be released at the pH of the terminal ileum (i.e. pH 6). It has a
low incidence of adverse effects. At present, mesalazine and olsalazine are
only approved for use in patients who are allergic to sulfonamides or
intolerant of sulfasalazine.
Corticosteroids may be used topically, orally or parenterally. Topical preparations
include suppositories, retention enemas or rectal foam. The latter is easier to retain
than the enema form. The usual oral corticosteroids given are prednisone and
prednisolone. Side effects are usually not troublesome because these agents are
mostly used for short periods in reducing doses. However, care needs to be taken in
patients with diabetes, hypertension or heart disease, or if they are to be used long-
Immunosuppressive drugs, e.g. azathioprine and its active metabolite 6-
mercaptopurine (6-MP), are indicated:
In chronic active disease not responding to more conventional therapy.
In patients who require continuous low dose corticosteroids to maintain
In an attempt to lower the corticosteroid dose in those who develop side
In the treatment of fistulae in Crohn’s disease.
During therapy with these drugs, the white cell count must be monitored for possible bone marrow
toxicity, although this is uncommon with the low doses used (1 to 2 mg/kg/day). Other possible side
effects include pancreatitis, cholestasis and potential for neoplasia.
Methotrexate is also used – DHFR inhibitor folate impaired pyrimidine synthesis
Antibiotics: metronidazole is used in perianal Crohn’s disease and also in some
patients with Crohn’s colitis. The most common side effect of this agent is
gastrointestinal upset. Peripheral neuropathy, first manifested by paraesthesias, can
occur with long-term use and may be irreversible; if it occurs, the drug must be
No benefit has been shown for broad spectrum antibiotics per se in either
ulcerative colitis or Crohn’s disease.
5. Outline the genetic aspects of large bowel disease.
Inflammatory bowel disease
While the causes of ulcerative colitis and Crohn’s disease remain unknown, certain
features of these diseases have suggested several areas of possible importance. These
include familial or genetic, infectious, immunologic, and psychological factors.
These diseases are more common in whites than in blacks or Asians, and Jews have
an incidence three to six times greater than that of non-Jews.
The increased incidence of IBD in whites and in Jews and the occurrence of familial
clustering suggest a genetic predisposition to the development of the disease. An
increased incidence of CD in monozygotic twins also is strong evidence for a genetic
A search for genetic markers that might be of value in identifying susceptible
individuals has not identified any single marker (i.e., a histocompatibility antigen) in
patients with IBD.
Adenomas and colon carcinomas
Familial adenomatous polyposis and Gardner syndrome patients exhibit a somatic
mutation in the tumor-suppressor APC gene (adenomatous polyposis coli).
Mutations occur in the tissue of sporadic cancers as well.
Inherited mutations in DNA mismatch repair genes occur in a hereditary
nonpolyposis colorectal cancer syndrome. This leads to faulty DNA proofreading,
widespread alterations in the genome, and predisposition to cancer. Sporadic cancers
can exhibit the same defect.
DNA methylation: loss of DNA methyl groups occurs early in colonic adenomas.
K-ras gene and other oncogenes are mutated with increasing frequency as adenoma
size increases and in carcinomas.
Allelic loss on 18q is common in colon cancer at the DCC locus (deleted in colon
cancer). This is a cell adhesion protein.
Losses at 17p (site of p53 gene) are common in cancers.
Telomerase is an enzyme that maintains chromosome telomere length and cell
replicative ability; it is expressed in cancers but not in adenomas.
Cumulative alterations in the genome appear to lead to progressive increases in size,
level of dysplasia, and invasive potential of neoplastic lesions. No single event or
sequence of events is requisite, but a multihit genetic mechanism appears to be
1. Describe the psychological impact of chronic disease.
Chronically ill patients experience more depressive symptoms, more anxiety, less
self-esteem, and a lower ability to control many aspects of their lives than people
without any disease.
Disorders of psychological functioning may be caused by biological factors, such as
structural and neurochemical changes in the brain (stroke and Parkinsonism) or
aberrations of immune system functioning (in rheumatoid arthritis), as well as by
changed psychosocial factors as a consequence of the disease. Examples of the latter
are loss of function and role (family, social, financial), negative body image and
sense of identity, loss of independence, promoted sense of helplessness and effects on
Functional impairment: Increased levels of both depressive and anxiety symptoms
among people with functional impairment. As functionally disabled people
encounter difficulties that are relatively unresponsive to problem-solving efforts, a
sense of mastery may also be particularly difficult to achieve and maintain. Patients
with diseases involving more functional impairment, e.g. arthritis or stroke, have a
less favorable psychological status than patients with diseases involving relatively
little functional impairment, such as diabetes or lung disease. Additional losses, such
as the loss of function, role, and body image and a more negative view of themselves,
their future, and their world, may lead to more feelings of depression and anxiety.
Illness controllability: In contrast to cardiac disease and diabetes, which are quite
responsive to self-administered diet and medication, cancer and arthritis offer few
opportunities for personal and medical control and, therefore, these patients may be
more at risk for low feelings of mastery and for depressive and anxiety feelings.
Degree of life threat: Patients with an uncertain prognosis, e.g. recently diagnosed
cancer patients, may have a higher risk of being psychologically distressed, because
they are uncertain about their chance of remission or cure.
Demographics: More psychological dysfunction for women, for people of low
education, and for people without a partner. For anxiety, the association with age
becomes negative, possibly because older people are more likely than younger people
to have developed effective coping strategies for dealing with life events because
these are more common and normative in old age.
2. Discuss the skills in managing uncertainty and adverse outcomes.
3. Discuss the issues relating to the shared care management of patients.
Integrated care for health disorders, particularly chronic diseases, is a long-term and
complex challenge, particularly because of the involvement of many individuals with
different beliefs, attitudes, assumptions and reward structures. Two basic conceptual
models of disease - the biomedical and psychosocial - underlie many of these
The biomedical model views humans as the sum of multiple individual 'subsystems,'
and disease represents dysfunction of one or more of these subsystems. This model is
'reductionist' and 'individualistic' in nature in that if 'THE' defective subsystem can be
identified, studied and improved, it is assumed that health would return. The
biomedical model focuses primarily on the individual with ill-health and has added
greatly to our basic understanding of disease processes.
The psychosocial model is 'interactive' and dynamic, and sees the 'whole' as more
than the sum of its parts. This model values elements outside of the individual, e.g.
work and home environment, as important in maintaining or establishing health.
Because of fundamental differences between these 2 models of health and disease,
conflicts, e.g. efficacy vs. exposure; role of individual vs. environment; etc., may
exist among varying professionals regarding the nature, purpose, targets, structure,
and consequences of integrated care programs. These fundamental conflicts, if
unrecognized and ignored, can significantly attenuate the benefits of well-intentioned
prevention and treatment integrated care programs.
PHYSICAL EXAMINATION OF THE LOWER GI TRACT
1. Outline the fundamentals of the rectal examination and proctoscopy.
Method of exam
Have the patient stand and lean forward, resting his hands on the examination table.
Place a small amount of lubricant on your gloved index finger.
Place your finger at the anus and wait for reflex sphincter relaxation.
Gently insert your finger and examine as much of the rectal wall as possible.
Sequentially examine the right lateral, posterior and left lateral surfaces felling for
Evaluate the prostate gland in men along anterior wall.
Examine the anterior surface of the prostate.
Evaluate the lateral lobes and the sulcus.
Note the size, shape, consistency and tenderness.
Note the rectal contents.
Remove the finger and evaluate the faeces on the gloved finger and save it for Guaic
The rectal exam can also be done in the left lateral decubitus.
Rectal exam is unpleasant.
The sphincter has sufficient tone to grasp your finger.
Soft stools may be felt.
The prostate gland is about 2.5 cm in length, with a medial sulcus, is firm and non-
Stools can be seen on the gloved finger and retain it for Guaic testing.
Sphincter: loss of tone and patulous (Cauda equina syndrome).
Contents: hard impacted stools, foreign body.
Rectal wall: pelvic masses (ovary, uterus) in women.
Mucous membrane: irregular, mass (cancer).
Prostate in men:
Smooth, large, firm and non-tender (benign enlargement).
Hard, irregular nodule or fixed hard mass (cancer, stone, chronic prostatitis).
Large, boggy and tender (acute prostatitis).
Bloody (hemorrhoids, bleeding rectal lesion).
Black (upper GI bleed, iron, some antacids).
ISSUES IN CLINICAL TRIALS
1. Discuss the related psychological, ethical and doctor-patient issues concerning the
enrolment of patients in clinical trials.
Defining management options of future patients vs. safeguarding the patient’s best
Utilitarianism: In the absence of RCT, it is not possible to be certain that a new drug
or clinical intervention is actually beneficial to patients with a particular disease or
condition, compared either to a “standard” (accepted or approved) therapeutic
strategy or to no treatment at all (an untreated control population).
Kantian philosophy: The individual physician’s principal ethical responsibility is to
the individual patient that he or she is treating, and not to future patients who may
benefit from the potentially important information gained through a well-designed
and well-conducted randomized trial.
Beneficence and non-malificence
If it is the physician’s best judgment – based on his or her interpretation of this data,
personal experience, and knowledge of the individual patient’s specific medical
condition – that one regimen would be preferred over the other(s), then the physician
should not recommend that the patient participate in this trial, no matter how
important the information gained may be to society.
If the physician has no opinion about whether the new treatment is acceptable, then
random assignment is ethically acceptable, but such lack of enthusiasm does not
augur well for either the patient or the study.
When the physician believes that the severity and likelihood of harm and good are
evenly balanced, randomization may be ethically acceptable.
If the patient has no preference for either treatment, then randomization is acceptable.
If, however, he or she believes that the new treatment may be either more or less
successful or more or less toxic, the use of randomization is not consistent with
fidelity to the patient.
New agents not FDA-approved (available only to clinical trials): A physician who
believes, based on previously reported clinical data (usually from phase 2 drug trials),
that a new drug is potentially superior to the standard therapy has no choice but to
recommend that the patient participate in the trial. The patient would have a 50%
chance of receiving the new therapy (and a 50% chance of being placed in the control
group), compared to a 0% chance if he or she does not participate in the study.
Informed consent issues
An individual gives a genuinely informed consent to some medical intervention when
he both understands the risks and possible benefits of the treatment.
It is quite unlikely that any patient-subject can see himself accurately within the
broad context of the situation, to weigh the inconveniences and hazards that he will
have to undergo against the improvements that the research project may bring to the
management of his disease and to his own particular case.
It would be impractical and probably unethical for the investigator to present the
nearly endless list of all possible contingencies; in fact, he may not himself be aware
of every untoward thing that might happen.
Patient-subjects who are incapacitated and hospitalized because of illness, frightened
by strange and impersonal routines, and fearful for his health and perhaps life are far
from exercising a free power of choice when the person to whom he anchors all his
hopes asks him to volunteer for a clinical trial.
When a man or woman agrees to act as an experimental subject, his or her consent is
marked by neither adequate understanding nor total freedom of choice.
Subjects have a legal right to “discontinue participation at any time without penalty
Largely due to the frailty inherent in human nature – carelessness, despair of getting
better, or adverse reactions.
Lying: Participants lie to get into studies (often with the help of their own physicians)
and, once enrolled, lie about their medical condition and level of compliance. They
could be taking a place that could have been taken by someone else just as needy
who also fits the required medical profile, thus constituting an injustice to them.
Breaking promises: frustrate the use of placebos by dropping out if randomized to
the placebo arm or by analyzing the drugs they receive or by pooling drugs, which
ensures they receive some portion of the active substance – thereby playing havoc
with assigned dosage levels.
Researchers may forbid subjects from taking prophylactic drugs that might confound
the effects of experimental agents.
The approval of desperately needed effective therapies could be slowed or side-
tracked forever, while many initially promising but unacceptably toxic drugs could
command center stage for years before their true effects are revealed.
By delaying the successful and timely completion of vitally important clinical trials,
noncompliance thus threatens to deprive present and future sufferers of effective
palliative, curative, and preventative measures.
Coercion or enticement?
Participants may see themselves as having “no real choice” but to accept the
researcher’s offer – back against the wall.
Their circumstances may constrain their will and vitiate the validity of their consent.
Researchers are offering participants the prospect of improving their baseline
situation; and most potential subjects are more than happy to move from what might
be called their “pre-proposal baselines” to the situation created by the proposal to
participate (“If you play by the rules, we will give you access (or at least the
possibility of access) to promising new drugs”).
Significant gaps in knowledge about diseases due to overrepresentation of white men
in research populations.
Physicians now frequently lack adequate evidence on whether women and people of
color will be harmed, helped, or not affected at all by numerous therapies now
endorsed as promoting “human health”.
Gender and racial inequality is unethical.
Maternal-fetal protection: in the name of potential protection for potentially
pregnant women and their fetuses, all women have lost opportunities to improve and
extend their lives. This does not apply to the potential damages to sperm, thereby
creating the possibility of birth defects.
Diseases disproportionately affecting females and people of color are given low
funding priority, knowledge that could alter current ineffective or detrimental routine
medical care is never produced.
Extrapolating results from white males to everyone else can be dangerous due to
numerous factors like physiological differences.
Dom LO Title LO Detail
BCS Anatomy of upper GI 1. Recognise the main anatomical features of the oesophago-gastric junction
2. Describe the anatomy of the biliary tract
BCS Physiology of the upper GI 1. Outline the major physiological factors that control the oesophago-gastric
2. Describe the process of bile secretion
3. Describe the physiological processes involved in GI motility and secretion.
BCS Pathology and treatment of 1. Describe the underlying pathology of major diseases of the upper GI tract
upper GI disease (including mouth, salivary glands, oesophagus and stomach) and biliary tree.
2. Discuss how bile secretion is deranged in cholelithiasis and outline the
complications of this condition
3. Discuss the mechanism of action of drugs that control GI motility and
EPPD Decision-making 1. Understand the risks and benefits of common GI procedures and operations
and how these influence patient/doctor decision making
ICCP History taking 1. To understand the importance of history in determining the cause of
ICCP Clinical reasoning 1. To make the clinical distinction between functional and structural GI disorders
ICCP Laboratory investigations 1. Describe the selection and interpretation of GI investigations for common
upper GI symptoms
ICCP Managing uncertainty 1. Describe strategies that assist in coping with clinical situations in which there
are high levels of uncertainty, iatrogenic morbidity, and undesired outcomes
PPH Upper abdominal pain 1. What is the prevalence of upper abdominal pain in the community?
(Public Health) 2. Outline the distribution and determinants of conditions causing upper
abdominal pain in the community. How does this vary according to age and
3. Discuss the psychosocial aspects of functional gastrointestinal disease.
PPH Opportunistic health 1. Be aware of the importance of opportunistic health promotion in medical
promotion (Public Health) consultations.
2. List those evidence-based health promotional activities recommended for
females in the following broad age categories: 20-40, 40-60, > 60.
It's All in Your Mind!
Know the main anatomical and physiological factors which control the oesophago-gastric junction and how this is
deranged in gastro-oesophageal reflux. BCS
The oesophagus descends through the posterior mediastinum and pierces the diaphragm just left of the
median plane (at the level of T10), travels about 1cm in the abdomen forming a groove in the left lobe
of the liver anteriorly and entering the stomach at the cardiac orifice. At this point, the oeophagus is
covered anteriorly and laterally by peritoneum and encircled by the oesophageal plexus of nerves. At
the inferior end of the oesophagus, the oesophagogastric junction, there is a physiological mechanism
known as the oesophageal sphincter, which contracts and relaxes. Food normally pauses momentarily
here and the sphincter is usually quite efficient at preventing reflux of gastric contents superiorly.
Physiologically, the pressure exerted by the contracted LOS is greater than either the intraoesophageal
pressure or the intragastric pressure. Gastric contents therefore do not normally reflux into the
The normal anti-reflux mechanisms consist of the Lower Oesophageal Sphincter (LOS) and the
anatomic configuration of the gastroesophageal junction. Reflux occurs only when the gradient of
pressure between the LOS and the stomach is lost. It can be caused by increased intragastric pressure or
by a transient or sustained decrease in LOS tone. The decrease in sphincter tone may be due to muscle
weakness or to inappropriate sphincter relaxation mediated by inhibitory nerves. Abnormal activity of
the diaphragmatic crural muscle also predisposes to gastroesophageal reflux. Normally the crura of the
diaphragm act as a “pinch-cock” mechanism.
Review and examine in more detail, the anatomy of the biliary tract, the physiology of bile secretion, and how this
is deranged in cholelithiasis and its complications. BCS
Bile is secreted by hepatocytes into minute channels called bile canaliculi, which drain into the the
hepatic duct. When food is not being digested, bile is diverted by way of the cystic duct into the
gallbladder. Following a meal, bile is moved through the common bile duct and the sphincter of Oddi
into the small intestine where it plays a role in digestion and the absorption of fat. Bile consists of bile
salts (glycocholic and taurocholic acids) (important in digestion and absorption of fat through
facilitation of emulsification), bile pigments (from the breakdown of Hb, excreted in faeces), cholestrol
lecithin, Na+, Cl- and HCO3-. The sphincter of oddi, a ring of smooth muscle surrounding the common
bile duct in the region where the duct enters the duodenum, prevents bile from entering the small
intestine between meals. When food enters the upper small intestine, fat and protein digestion products
stimulate the release of CCK from the duodenal mucosa into the blood, permitting relaxation of the
sphincter of oddi and contraction of the gallbladder.
While in the gallbladder, bile is concentrated by the active removal of Na + from the lumen to the blood,
and the consequent (passive) movement of Cl- and HCO3-. The gallbladder mucosa is a simple
columnar absorptive epithelium. This results in concentration of the contents of the gallbladder, as the
organic constituents are not absorbed. The water insoluble lipid components of the bile usually remain
in solution, but sometimes this doesn't occur, resulting in the precipitation of gallstones.
Bile salts are synthesised by hepatocytes and actively transported by these cells into the bile canaliculi.
These bile salts enter the small intestine, play an essential role in the digestion and absorption of fat,
traverse most of the small intestine and are absorbed from the terminal ileum. They are returned to the
blood, then removed from the blood by the liver, then secreted back into the bile where the recycling
process starts again. This is called the enterohepatic circulation of bile salts, which is not 100%
efficient, as some salts are lost in the faeces, but the capacity for the liver to resynthesise these
molecules from cholesterol far exceeds the loss.
Bile salts are the main stimuli for the secretion of bile. Portal blood concentrations of bile salts are
greatest, and thus bile flow is at its highest level when food is being digested, at which time bile salts
are being circulated between the liver and the small intestine. Between meals, when the concentration
of bile salts in the portal blood is low and bile salts are being stored in the gallbladder, the liver bile
flow is low.
Secretin also stimulates the secretion of bile, but the secreted fluid is a basic HCO 3--rich fluid from the
epithelium of the bile ducts that plays a part in neutralising the acid that enters the small intestine from
Cholesterol salts yellow
Pigment salts (bilirubin complexed with Ca2+) black
There are 4 conditions that must be met to produce gallstones:
1. The bile must be supersaturated with cholesterol
2. The gallbladder motility is reduced crystal formation
3. Cholesterol nucleation is accelerated
need focus or nidus to seed crystal growth
4. Mucous hypersecretion traps crystals so they can coalesce into stones
Female (M:F = 1:2)
i. Stasis will produce calculi (gall bladder, urinary bladder)
i. RBC breakdown
Ileal disease (resection or bypass)
i. Impaired bile salt resorption bile salt recycling synthesis
Understand the importance of history in determining the cause of abdominal pain. DC
The correct interpretation of acute abdominal pain is one of the most challenging demands made of any
physician. Few other clinical situations demand greater experience and judgment, because the most
catastrophic of events may be forecast by the subtlest of symptoms and signs.
There are few abdominal conditions that require such urgent operative intervention that an orderly
approach need be abandoned, no matter how ill the patient. Nothing will supplant an orderly,
painstakingly detailed history, which is far more valuable than any laboratory or radiological
examination. This kind of history is laborious and time-consuming, making it unpopular, even though a
reasonably accurate diagnosis can be made on the basis of the history alone in the majority of cases. In
cases of acute abdominal pain, a diagnosis is readily established in most instances, whereas success is
not so frequently achieved in patients with chronic pain. Since the irritable bowel syndrome is one of
the most common causes of abdominal pain, the possibility of this diagnosis must always be kept in
mind. The chronological sequence of events in the patient's history is often more important than
emphasis on the location of pain. If the examiner is sufficiently open-minded and unhurried, asks the
proper questions, and listens, the patient will usually provide the diagnosis. Careful attention should be
paid to the extraabdominal regions that may be responsible for abdominal pain. An accurate menstrual
history in a female patient is essential.
As in history taking, there is no substitute for sufficient time spent in the examination. It is important to
remember that abdominal signs may be minimal but nevertheless, if accompanied by consistent
symptoms, may be exceptionally meaningful.
Some Points on History:
A frequent misconception is that pain associated with intraabdominal vascular
disturbances is sudden and catastrophic in nature. The pain of embolism or thrombosis of
the superior mesenteric artery or that of impending rupture of an AAA certainly may be
severe and diffuse. Yet, just as frequently, the patient with occlusion of the superior
mesenteric artery has only mild continuous diffuse pain for 2 or 3 days before vascular
collapse or findings of peritoneal inflammation appear. Abdominal pain with radiation to
the sacral region, flank, or genitalia should always signal the possible presence of a
rupturing AAA. This pain may persist over a period of several days before rupture and
Pain arising from the abdominal wall is usually constant and aching. Movement,
prolonged standing, and pressure accentuate the discomfort and muscle spasm.
Pain referred to the abdomen from the thorax, spine, or genitalia may prove a vexing
diagnostic problem, because diseases of the upper part of the abdominal cavity such as
acute cholecystitis or perforated ulcer are frequently associated with intrathoracic
complications. A most important, yet often forgotten dictum is that the possibility of
intrathoracic disease must be considered in every patient with abdominal pain, especially
if the pain is in the upper part of the abdomen. Diaphragmatic pleuritis resulting from
pneumonia or pulmonary infarction may cause pain in the right upper quadrant and pain
in the supraclavicular area, the latter radiation to be sharply distinguished from the
referred subscapular pain caused by acute distention of the extrahepatic biliary tree.
The ultimate decision as to the origin of abdominal pain may require deliberate and
planned observation over a period of several hours, during which time repeated
questioning and examination will provide the proper explanation. Whenever the cause of
abdominal pain is obscure, a metabolic origin always must be considered.
The problem of DDx is often not readily resolved. The pain of porphyria and of lead colic
usually is difficult to distinguish from that of intestinal obstruction, because severe
hyperperistalsis is a prominent feature of both. The pain of uremia or diabetes is
nonspecific, and the pain and tenderness frequently shift in location and intensity.
Diabetic ketoacidosis may be precipitated by acute appendicitis or intestinal obstruction,
so if prompt resolution of the abdominal pain does not result from correction of the
metabolic abnormalities, an underlying organic problem should be strongly suspected.
Causalgic pain may occur in diseases that injure nerves of sensory type. Pain arising from
spinal nerves or roots comes and goes suddenly and is of a lancinating type. Severe
muscle spasm is common but is either relieved or is not accentuated by abdominal
palpation. Psychogenic pain conforms to none of the aforementioned patterns of disease,
varying enormously in type and location but usually has no relation to meals. It is often at
its onset markedly accentuated during the night. Nausea and vomiting are rarely observed,
although occasionally the patient reports these symptoms. Spasm is seldom induced in the
abdominal musculature and, if present, does not persist, especially if the attention of the
patient can be distracted.
Understand the psycho-social aspects of functional bowel disease. DC
Higher rates of psychiatric comorbidity as well as more impaired psychosocial adjustment occur with
the functional bowel disorders and are particularly high in self-selected referral patients compared with
community populations. Reciprocally, some studies show higher rates of functional bowel disturbances
in patients with psychiatric diagnoses.
Remaining alert for and addressing coexisting psychiatric illness will enhance treatment outcome
(increased patient compliance, functioning, and satisfaction). Additionally, psychological factors affect
the clinical expression of structural disease. Resetting treatment goals from cure to coping with chronic
illness and setting personal limits are important.
Understand the risks and benefits of common GI procedures and operations and how these influence
patient/doctor decision making. EPPD/BCS
To help diagnose treatable conditions.
The more laparoscopic or laparotomy procedures, the more chance of adhesions
Procedural costs and following up false negatives.
Anaphylactic reaction to barium or contrast dyes.
Inadvertent spread of tumour – along biopsy track.
When managing uncertainty in clinical situations, it must be remembered that:
Clinical diagnosis is an inexact science.
Harmful investigations must be balanced with missing diagnoses.
Strategies must be used to best combine these factors - what is the degree of necessity?
Influences on clinical decision-making:
Doctor's role Clinical Patient
as Decision values,
gatekeeper concerns and
to medical expectations
tests Doctor's concern of
Why do we need certainty?
Management is dependent on certainty.
To exclude life (or life-style) threatening diseases.
To be sure that we use treatment that is available to reverse the threat of disease.
Patients want their disease to be labeled.
Make probability diagnosis.
But serious disorders are not to be missed.
Remember, the pitfalls diagnoses are often missed, as are the seven masquerades.
Always ask is the patient trying to tell me something?
The seven masquerades are;
Thyroid disease ( or )
Recognise the importance and high frequency of functional disturbances as a cause of GI symptoms.
Functional disturbances are the most common presenting conditions to general practitioners,
accounting for 50% of consultations for digestive complaints and 10% of all consultations. Functional
disturbances occur where there is no clear defined organic lesion. However, most involve motor
dysfunction of the stomach, SI, colon or anorectum.
Irritable bowel syndrome (IBS)
Most common functional GIT disorder.
Chronic disorder characterised by disordered motor and/or secretory function of the GIT
(particularly small and large intestines) in the absence of identifiable disease.
Ratio of women:men = 2:1 with most presentations before the age of 40 years, however
any age is possible.
Numerous factors have been postulated to affect GIT sensorimotor function. Abnormalities in
fasting and stimulated motility in both the small intestine and the large intestine have been
Primary phenomenon may be sensitisation of afferent neural pathways from gut to CNS, producing
heightened perception of normal gut distension & contraction (this heightened perception may then
reflexly trigger disordered motor activity)
Cost to the community in terms of absenteeism from work, unnecessary investigations, etc
IBS patients are usually more neurotic, anxious and depressed than normal population and those
with organic GIT disorders.
No uniformity, with some foods causing diarrhoea in an idiosyncratic, probably
non-immunogenic fashion (intolerance).
Low fibre might be important if constipation is important.
Sugars (lactose in milk or fructose and sorbitol in fruits and some confectionery)
can cause diarrhoea, flatulence & bloating.
Attack of IBS can be preceded by infectious diarrhoea (damage to ENS by pathogen) and symptoms
can last for months or years.
1. Abdominal pain or discomfort felt in 1 or both iliac fossae, often relieved by
defecation or flatus passage
2. Distension or bloating
3. Disordered bowel habits, intermittent or continuous diarrhoea or constipation
or both. Morning rush syndrome is common – patients have the urge to defecate
These symptoms can be in various combinations with exacerbations and remissions.
The presence of blood in the stool requires investigation and should not be ascribed to IBS
The big question: How far to investigate, and how much to leave the diagnosis
up to exclusion factors.
In young people, perform a sigmoidoscopy, ESR and FBC.
In people older than 40 years, with recent change in bowel habits FOB,
colonoscopy (looking for colon CA)
Severe diarrhoea (consider infection stool culture)
In IBD (rectal biopsy) and malabsorption (faecal fats) before IBS diagnosis
inflammatory bowel disease
PID & endometriosis
check for food intolerance
IBS is troublesome GIT symptoms with no recognizable organic pathology.
Affects women more than men.
Diagnosis by exclusion (no structural pathology, no test & no cure).
Lifetime prevalence >20%
Experience different forms of abdominal pain, distension and altered bowel
habits and potentially other associated GIT/systemic symptoms (dysphagia,
nausea, dyspareunia, urinary frequency, etc)
Pathophysiology includes abnormal smooth muscle activity and heightened
awareness of bowel movement
Understand the pharmacology and physiology of drugs affecting GI motility and secretion.
Inhibit prostaglandin synthesis, which is crucial in stimulation of secretion of mucous and
bicarbonate from the gastric mucosa.
Therefore, NSAIDs will decrease the protective effect of the barrier accounting for the
observation that these agents have a tendency to cause gastric ulceration and bleeding.
These drugs competitively inhibit histamine actions at all H2-receptors, the clinically
important part of which is their inhibition of gastric acid secretion.
Cause inhibition of histamine-stimulated and gastrin-stimulated acid secretion and
decrease ACh-stimulated acid secretion.
Cimetidine - Cimehexal, Cimetimax, magicul, SBPA Cimetidine, Sigmetadine,
Tagamet. Oral, IM or IV. Half-life is shorter than ranitidine. Has been noted to
occasionally cause gynaecomastia in men and a decrease in sexual function.
Binds androgen receptors and inhibits CYP450 and therefore decrease the
metabolism of numerous drugs. May cause confusion in the elderly. Reduces
renal tubular secretion of basic drugs. Unwanted effects of diarrhoea, dizziness,
muscle pains, transient rashes and hypergastrinaemia have been reported. Single
daily doses are sufficient.
Ranitidine - DBL Ranitidine, Rani 2, Zantac, Zantac 75. Oral, IM or IV. Less
effect on CYP450 and androgen receptors than Cimetidine. Reduces renal
tubular secretion of basic drugs. Unwanted effects of diarrhoea, dizziness,
muscle pains, transient rashes and hypergastrinaemia have been reported. Single
daily doses are sufficient.
Nizatidine - Tazac. Oral. Unwanted effects of diarrhoea, dizziness, muscle pains,
transient rashes and hypergastrinaemia have been reported. Single daily doses
Famotidine - Amfamox, Pepcid, Pepcidine. Oral. Unwanted effects of diarrhoea,
dizziness, muscle pains, transient rashes and hypergastrinaemia have been
reported. Single daily doses are sufficient.
Act by irreversibly blocking H +/K+-ATPase which is the terminal step in the acid
secretory pathway, thereby markedly inibiting both basal and stimulated gastric acid
Omeprazole - Acimax, Losec Tablets, Losec Capsules, Losec Intravenous,
Maxor. Works preferentially at low pH, so that accumulation occurs in the
secretory canaliculi of the gastric parietal cells. Half-life is about an hour, but the
effects last for 2-3 days. Unwanted effects are not common, but include
headache, diarrhoea, rashes, dizziness, somnolence, mental confusion,
impotence, gynaecomastia, myalgias and arthralgias.
Pantoprazol - Somac.
Lansoprazol - Zoton.
The main effect of stimulating muscarinic-receptors in the GIT is an increase in secretion
and an increase in motility. Therefore, antagonism will produce, amongst other effects,
Pirenzipine. Acts at M1-receptor found in parasympathetic ganglia and possibly
also on the histamine secreting cell and the gastric parietal cell. It reduces basal
and stimulated gastric acid secretion and has minimal extra-gastric effects, but
those that do occur can be more disturbing than that of the other anti-secretory
drugs. It is given orally.
Act by neutralising gastric acid secretion and therefore raising gastric pH, thus inhibiting
peptic activity, which practically ceases above pH 5. There is also thought to be
enhancement of prostaglandin synthesis and reduction of Helicobacter pylori replication,
both of which help in the healing of ulcers.
Antacids in common use are salts of Aluminium or Magnesium. Magnesium salts
cause diarrhoea, Aluminium salts cause constipation, therefore mixtures of the two are
used to preserve normal bowel function.
Magnesium hydroxide - insoluble powder that forms MgCl2 in the stomach, but
does not cause metabolic alkalosis since Mg++ is poorly absorbed.
Magnesium trisilicate - insoluble powder which reacts slowly with gastric juice
forming MgCl2 and colloidal silica. Has a prolonged antacid effect.
Aluminum Hydroxide gel - forms AlCl3 in the stomach, then releases Cl- in the
stomach where it is reabsorbed. Has prolonged effects.
Sodium bicarbonate acts rapidly and is said to raise the pH of the gastric juice to
about 7.4. Carbon dioxide gas is liberated, however the increased carbon dioxide
tension stimulates gastric secretion and can result in a secondary rise in acid
secretion. Sodium bicarbonate can be absorbed by the intestine, frequent
administration may cause metabolic alkalosis.
These are Methylcellulose, Sterculia, Agar, Bran and Ispaghula Husk.
These agents are all polysaccharide polymers that are not broken down in the normal
processes of digestion in the upper GIT and act by virtue of their capacity to retain water
in the gut lumen, and thereby promote peristalsis.
They take a couple of days to start working, but have no serious unwanted effects – may
help to prevent diverticular disease
These consist of poorly absorbed solutes - the Saline Purgatives and Lactulose.
These maintain an increased volume of fluid in the lumen of the bowel by osmosis, which
accelerates the transfer of the gut contents through the small intestine, transfers a large amount of
fluid into the large intestine, which causes purgation shortly afterwards.
The main salts used are magnesium sulphate and magnesium hydroxide.
Lactulose is a semi-synthetic disaccharide of fructose and galactose, which are converted to lactic
and acetic acid by bacteria. It may take 2-3 days to act and can causes excessive flatulence,
cramps, diarrhoea and electrolyte disturbances.
These are agents that stimulate the mucosa of the gut and thereby increase peristalsis. The
important purgatives in this group are:
Bisacodyl - stimulates sensory nerve endings in the colon, resulting in peristaltic
activity and defecation within 15-30 minutes.
Sodium picosulphate - stimulates sensory nerve endings in the colon, resulting in
peristaltic activity and defecation within 15-30 minutes.
Preparations of senna - has laxative effect because it contains derivatives
anthracene. The drug passes unchanged into the colon where bacteria hydrolyse
the glycoside bond, releasing free anthracene derivatives which are absorbed and
have a direct stimulatory effect on the myenteric plexus. This stimulation leads
to smooth muscle activity and defecation.
These agents can cause abdominal cramps and prolonged use can lead to
deterioration of intestinal function.
Used as an anti-emetic and is also effective in increasing gastrointestinal motility.
Domperidone - thought to enhance motility by blocking -adrenoceptors, and
decreasing their relaxant effect. Also increases LOS pressure (thus inhibiting
gastrooesophageal reflux), increases gastric emptying and enhances duodenal
peristalsis. Useful in disorders of gastric emptying and in chronic gastric reflux
Metoclopramide – acts centrally as an anti-emetic. Also has a local effect on
gastric motility, causing marked acceleration of gastric emptying with increased
gastric acid secretion. Useful in GOR and in disorders of gastric emptying.
Cisapride – stimulates ACh release in the myenteric plexus in the upper GIT.
Raises oesophageal sphincter pressure and increases gut motility. Used in reflux
oesophagitis and in disorders of gastric emptying. No anti-emetic action. May
cause life-threatening arrhythmias when interactions occur.
Agents in this class are generally employed as primary therapy for diarrhoea.
Morphine – tone, rhythmic contractions of the intestine,
propulsive action. Overall effect is constipating. The sphincters (anal,
pyloric, ileocolic) contract and the tone of the colon is increased.
Codeine – tone, rhythmic contractions of the intestine, propulsive
action, secretion. Overall effect is constipating. The sphincters (anal,
pyloric, ileocolic) contract and the tone of the colon is increased.
Diphenoxylate – tone, rhythmic contractions of the intestine,
propulsive action. Overall effect is constipating. The sphincters (anal,
pyloric, ileocolic) contract and the tone of the colon is increased.
Loperamide – tone, rhythmic contractions of the intestine,
propulsive action, secretion. Overall effect is constipating. The
sphincters (anal, pyloric, ileocolic) contract and the tone of the colon is
increased. Loperamide passage of faeces and duration of traveller’s
Side-effects include include nausea, vomiting, abdominal cramps,
drowsiness and dizziness
Muscarinic receptor antagonists – seldom used against diarrhoea specifically,
because of the widespread systemic effects, however small doses of atropine are
used in combination with diphenoxylate.
Used extensively to treat diarrhoea:
Fluid and Electrolyte Transport Modifiers (secretory agents):
Inhibits calmodulin, and reduces secretion of water and electrolytes. Effective in
Not clinically available
Inhibit prostaglandin synthesis, and so have significant antidiarrhoeal actions.
Other mechanisms may be involved.
Isotonic solutions of NaCl plus glucose or starch-based cereal (important in infants)
Be able to describe the pathology of major diseases of the upper GI tract and biliary tree. BCS
Atresia and fistulas:
Uncommon. Must be repaired early to maintain life.
An atresia is a non-canalised cord instead of the oesophagus, with blind pouches
connected to the lower part of the pharynx and the upper part of the stomach.
A fistula may attach any part of the oesophagus to the trachea or a bronchus.
Other congenital abnormalities are generally present concurrently.
Stenosis, webs and rings:
Non-neoplastic constrictions are most often acquired.
Stenosis: fibrous thickening of the oesophageal wall, particularly of the
submucosa with atrophy of the muscularis propria. Thin, ulcerated epithelium.
Results from severe oesophageal injury with inflammatory scarring, such as
following GOR. Usually manifest by dysphagia.
Mucosal Webs: Uncommon, ledgelike semicircumferential protrusions of the
mucosa into the lumen. In the upper oesophagus they are denoted webs, in the
lower oesophagus, schatzki rings.
Partial or incomplete relaxation of the Lower Oesophageal Sphincter
Increased resting tone of the Lower Oesophageal Sphincter.
Pathogenesis is not well understood, but thought to involve intrinsic and
extrinsic (vagus and dorsal motor nucleus of the vagus) degeneration or
destruction of neural innervation.
Manifest by progressive dysphagia.
Separation of the diaphragmatic crura and widening of the space
between the muscular crura and the oesophageal wall.
The two types of hiatus hernia are sliding (95% cases - protrusion of the
stomach above the diaphragm creates a bell shaped dilation) and
paraoesophageal (= rolling) (5% cases - a separate portion of the
stomach enters the thorax through the widened foramen).
Aeitiology is unknown, but gastro-oesophageal reflux is commonly
seen in association with hiatal hernia, thought it is thought to be a
result, not a cause.
Outpouching of the ailimentary tract that contains all visceral layers. They
develop in three regions:
Zenker diverticulum - immediately above the upper oseophageal
sphincter. Disordered cricopharyngeal motor dysfunction is implicated
in the genesis of this disorder.
Traction diverticulum - near the midpoint of the oesophagus. Traction
may be caused by scarring resulting from mediastinal lymphadenitis or
motor dysfunction or a congenital lesion.
Epiphrenic diverticulum - immediately above the lower oesophageal
sphincter. This is thought to be caused by dyscoordination of peristalsis
and Lower Oesophageal Sphincter relaxation
Mallory-Weiss Syndrome - lacerations:
Longitudinal tears in the oesophagus at the oesophagogastric junction are called
mallory-weiss tears. They are believed to be the consequence of severe retching,
and morphologically usually cross the oseophagogastric junction.
Encountered most commonly in alcoholics due to refluxing of gastric contents in
the setting of an alcoholic stupor, but may be associated with hiatal hernias.
May be a cause of massive haematemesis, but tends to resolve with supportive
Injury to the oesophageal mucosa with subsequent inflammation.
Reflux of the gastric contents into the lower oesophagus is the first and
foremost cause of oesophagitis.
Some causative factors are:
Decreased effectiveness of the anti-reflux mechanisms such as
decreased tone of the lower oesophageal sphincter, which itself
may be caused by CNS depression, alcohol, tobacco,
hyothyroidism or pregnancy.
Presence of a sliding hiatal hernia.
Inadequate or slowed clearance of refluxed material.
Delayed gastric emptying and increased gastric volume
thereby increasing the volume of refluxed material.
Complication of long-standing gastrooesophageal reflux.
Distal squamous mucosa is replaced by metastatic columnar
eptithelium, as a response to prolonged injury. In order for the
diagnosis of Barrett’s Oesophagus there must be histological evidence
of colonic mucosa (with goblet cells) not gastric mucosa, although the
two may coexist.
Inflammation and ulceration followed by ingrowth of pluripotent stem
cells, then differentiation to columnar epithelium which is more
resistant to the peptic effects of gastric acid is the proposed aetiology.
Looks hyperaemic and velvety on endoscopy.
Barrett's mucosa is a known risk factor for the development of
adenocarcinoma (30 times risk).
Infectious and Chemical Oesophagitis:
Oesophageal inflammation may have other origins, such as: ingestion
of mucosal irritants (alcohol, corrosive acids, heavy smoking, etc),
cytotoxic therapy and infection.
Sufficiently prolonged or severe portal hypertension induced the formation of
collateral bypass channels wherever the portal and caval systems communicate,
those in the region of the lower oesophagus cause varices.
Portal blood flow is diverted through the coronary veins of the stomach
plexus of oesophageal mucosa submucosal veins of oesophagus azygous
veins systemic circulation.
Symptomless until rupture causing massive haematemesis, shock etc.
Greater than 90% of cirrhotic patients have varices - these are most often
associated with alcoholic cirrhosis.
Mostly mesenchymal in origin and lie within the oesophageal wall.
Most common: leiomyomas. Fibromas, lipomas, hemangiomas,
neurofibromas and lymphangiomas may also occur.
Mucosal polyps are usually composed of a combination of fibrous,
vascular or adipose tissue covered by an intact mucosa, called
fibrovascular polyps or pedunculated lipomas depending on
composition. Squamous papillomas are sessile lesions with a central
core of connective tissue and a hyperplastic papilliform squamous
Generally asymptomatic throughout development.
Generally arise from the epithelial layer. There are rare exceptions.
Squamous cell carcinoma:
Dietary and environmental factors are involved in the
aetiology of this cancer. Alcohol and tobacco are thought to be
involved due to polycyclic hydrocarbon content.
SCC of the oesophagus begin as in situ lesions. Early lesions
appear as small, grey-white plaque-like thickenings or
elevations of the mucosa.
Morphology may be protruded (polypoid exophytic), flat
(diffuse, infiltrative tending to spread within the wall of the
oesophagus, narrowing lumen and causing mural thickening
and rigidity) or excavated (necrotic cancerous ulceration that
excavates deeply into surrounding structures.
Metastasis to cervical, middle third mediastinal, paratracheal,
tracheobronchial, gastric and coeliac lymph nodes occurs
Highly correlated with Barrett mucosa - point mutations in p53
are evident in dysplastic foci allowing clonal progression to
Usually in the distal oesophagus, arising from Barrett's
mucosa, may invade the adjacent gastric cardia, initially
appearing as flat or raised sections of an otherwise intact
mucosa. Progress to large nodular masses that are diffusely
infiltrative or deeply ulcerative.
Pancreatic heterotopia - nodules of essentially normal pancreatic tissue may be
present in the gastric or intestinal submucosa, muscle or subserosa.
Gastric heterotopia - small patches of ectopic gastric mucosa in the duodenum or
in more distal sites may present as perplexing sources of bleeding.
Diaphragmatic hernia may result from congenital absences of regions of the
diaphragm, usually on the left side.
Congenital hypertrophic pyloric stenosis. Familial occurrence indicates a
multifactorial pattern of inheritence.
Clinically present with regurgitation and persistent projectile non-bilious
vomiting. Usually visible peristalsis and palpable mass in region of pylorus.
May be acquired in adults after chronic antral gastritis or pyloric peptic ulcers.
Carcinoma may be a more sinister cause.
Inflammation of the gastric mucosa, being acute with neutrophilic infiltration or
chronic, with lymphocytes, plasma cells or both.
Acute mucosal inflammatory process, usually of a transient nature. May
be accompanied by haemorrhage into the mucosa, and in severe erosive
form may be a cause of acute GI bleeds.
Aetiology includes heavy use of NSAIDs, excessive alcohol
consumption, heavy smoking, Rx with chemotherapeutics, uraemia,
systemic infection. The mechanism by which these operate is thought to
be increased acid production, decreased production of bicarbonate,
reduced blood flow and disruption of the mucosal protective layer.
Chronic gastritis, including Helicobacter infections:
Chronic gastritis is the presence of chronic mucosal inflammatory
changes leading eventually to mucosal atrophy and epithelial
metaplasia, usually in the absence of erosions. Epithelial changes may
become dysplastic and constitute a background for the development of
Aetiology: chronic infection by Helicobacter pylori, autoimmune
(pernicious anaemia – anti-intrinstic factor Ab target parietal cells),
toxic (alcohol, smoking), post-surgical, obstruction, radiation,
Peptic ulcer disease:
Ulcers are defined as a breach in the mucosa of the alimentary tract, which
extends through the muscularis mucosa into the submucosa or deeper.
Chronic, most often solitary, lesions that occur in any portion of the
gastrointestinal tract exposed to the aggressive action of acid-peptic
juices. Both the acid and the pepsin are critical, but production is a
result of the imbalance between gastroduodenal defence mechanisms
and the damaging forces.
May come and go, heal then recur. Propensity to recur remains. Men
are more affected than women, but less so after menopause.
Helicobacter pylori is very important in the pathogenesis of peptic
ulcers - present in all duodenal ulcers and 70% gastric ulcers. Secretes
urease than generates ammonia and proteases which breakdown gastric
mucous. Causes inflammatory reactions that make the cells more liable
to acid injury. Causes damage to the mucosa that permits the leakage of
tissue nutrients into the surface microenvironment thereby sustaining
Zollinger-Ellison Syndrome exhibits multiple peptic ulcerations in the
stomach, duodenum and jejunum, owing to excess gastrin secretion by
a tumour and hence excess gastric acid production (similar
classification to carcinoids).
NSAIDs suppress mucosal prostaglandin synthesis and therefore
mucosal protection, asprin is a direct irritant, cigarette smoking impairs
blood flow, any cause of hypercalcaemia stimulates gastric production
and therefore acid release.
Most peptic ulcers are in the anterior wall of the first part of the
duodenum. Morphologically they are usually round-to-oval, sharply
punched-out defect with relatively straight walls. Histological picture
may vary from active necrosis to chronic inflammation and scarring to
healing. Malignant transformation is unknown in duodenal ulcers and
rare in gastric ulcers.
Acute gastric ulceration:
Focal, acutely developing gastric mucosal defects are a known
complication of NSAID therapy and physiological stress.
Multiple lesions located in the stomach and possibly the duodenum,
ranging from erosions (shedding of superficial endotehlium) to deep
ulcerations (deeper lesions - complete mucosal thickness).
Commonly encountered in patients with shock, extensive burns, sepsis,
severe trauma and any cause of ICP (stimulation of CNX).
May arise from gastric outlet obstruction or functional atony of the
stomach and intestines (paralytic ileus from generalised peritonitis) or
hairball (trichobezoar) or fibrous material collections (phytobezoar).
May contain up to 15 litres of fluid and lead to catastrophic rupture.
Group of uncommon conditions characterised by giant cerebriform
enlargement of the rugal folds of the gastric mucosa by hyperplasia.
Three variants: Ménétrier disease, Hypertrophic-hypersecretory
gastropathy and Gastric gland hyperplasia secondary to excessive
Great risk of peptic ulceration due to increased acid production. These
conditions may be mistaken for infiltrative carcinoma or lymphoma of
the stomach radiologically.
Tumours arising from the mucosa are more common than mesenchymal and
In the alimentary tract, the term polyp is applied to any nodule or mass
that projects above the level of the surrounding mucosa. Polypoid
lesions include more layers than just the mucosa.
Most polyps are non-neoplastic, appearing to be of a hyperplastic
nature. Seen frequently on a back-ground of chronic gastritis.
Most frequent malignant tumour - 90%. Less common in UK, USA,
Canada, Australia. More common in men. More common in lower
socioeconomic groups. Diet and environmental factors are highly
implicated as risk factors.
Can be divided into two histologic subtypes - intestinal morphology
(formation of bulky, glandular tumours - neoplastic intestinal glands)
and diffuse morphology (infiltrative growth of poorly differentiated
discohesive malignant cells - neoplastic gastric type mucous cells).
Dysplasia of the gastric mucosa represents the final common pathway
by which intestinal type gastric cancers arise. The diffuse type appears
to arise de novo without evolution through dysplasia.
Allelic genetic losses in the intestinal type of gastric cancer show
similarities to colon cancer, however disparities in mutation point to
unique pathogenic pathways.
Favoured location is the lesser curvature of the anteropyloric region.
Classification is made on the basis of depth of invasion, macroscopic
growth pattern and histologic subtype. Early gastric carcinoma is
confined to the mucosa and submucosa, irrespective of lymph nodal
involvement. Carcinoma-in-situ is confined to the surface epithelial
layer. Advanced gastric carcinoma is a neoplasm that has extended
below the submucosa into the muscular wall.
Macroscopic growth patterns are exophytic (protrusion), flat or
depressed (extensive malignancy or metastasis linitis plastica) or
Prognosis is poor. Few signs (weight loss, abdominal pain, anorexia,
vomiting) till late in course.
Less common gastric tumours:
Gastric lymphomas - 5% of gastric malignancies.
Gastric neuroendocrine cell (carcinoid) tumours are rare.
Smooth muscle mesenchymal tumours - leiomyoma (benign) and
Metastatic involvement of the stomach is rare.
Small and Large Intestines:
Duplication, malrotation, omphalocoele (abdominal musculature fails to form - abdominal
contents herniate) and gastroschisis (portion of abdominal wall fails to form completely -
abdominal contents extrude) are congenital abnormalities.
Atresia and stenosis:
Congenital intestinal obstruction is uncommon - duodenal atresia is most
common - may be imperforate mucosal diaphragm or stringlike segment of
bowel connecting proximal and distal segments.
Stenosis is less common - may be due to narrowed intestinal segment or
diaphragm with a narrow central opening.
Failure of the cloacal membrane to rupture leads to an imperforate anus.
Failure of the involution of the vitelline duct, which connects the lumen of the
developing gut to the yolk sac, produces a Meckel diverticulum.
Usually 2 inches long, 2 feet from the ileocaecal valve. Contains all three layers
of the normal bowel wall: mucosa, submucosa and muscularis propria. May have
heterotopic rests of pancreatic or gastric tissue.
Congenital aganglionic megacolon - Hirschprung disease:
Characterised by the absence of ganglion cells in the large bowel functional
obstruction and colonic dilation proximally.
Can be sporadic, but familial cases occur and gene defect is thought to be in
genes controlling migration and survival of neuroblasts and neurogenesis.
Rectum is always affected. Commonly occurs with other wide-spread serious
Diarrhoea and dysentry:
Precise definitions are elusive, but an increase in stool mass, stool
frequency or stool fluidity is perceived as diarrhoea by most patients.
Usually >250g containing 70-95% water.
Dysentery is low-volume, painful, bloody diarrhoea.
Secretory Diarrhoea: Net intestinal fluid secretion leads to output of
greater than 500mL of fluid stool per day, which is isotonic with plasma
and persists during fasting.
Osmotic Diarrhoea: excessive osmotic forces exerted by luminal
solutes lead to output of greater than 500mL of stool per day which
abates on fasting. Stool osmolality exceeds electrolyte concentration by
Exudative Diseases: mucosal destruction leads to output of purulent,
bloody stools which persists on fasting. Stools are frequent, but may be
small or large volume.
Malabsorption: Improper absorption of gut nutrients produces
voluminous, bulky stools with increased osmolarity combined with
steatorrhoea. Usually abates on fasting.
Deranged Motility: Improper gut neuromuscular function may produce
highly variable patterns of increased stool volume. This is usually a
diagnosis of exclusion.
Intestinal diseases of microbial origin are marked principally by
diarrhoea and sometime ulceroinflammatory changes.
E. coli is a common pathogen, but the spectrum varies with age,
nutrition, immune status, environment. Commonly not isolated.
Caused by a distinct group of viruses - Rotavirus is the most common.
Clinical syndrome: incubation period of 2 days followed by several
days of watery diarrhoea.
Morphologic changes consist of shortening and blunting of the villi and
infiltration of the lamina propria by lymphocytes.
Diarrhoeal illness of bacterial form is caused by several pathogenic
Ingestion of preformed toxin, present in contaminated food
(major offenders are Staphylococcus aureus, Vibrio cholerae
and Clostridium perfringens)
Infection by toxigenic organisms, which proliferate within the
gut lumen and elaborate an enterotoxin.
Infection by enteroinvasive organisms, which proliferate,
invade and destroy mucosal epithelial cells.
Bacteria must have the ability to adhere to the mucosal epithelial cells
(so they don't get swept away) and replicate, the ability to elaborate
eneterotoxins (polypeptides that cause diarrhoea) and the capacity to
invade. Bacterial invasion is followed by intracellular proliferation, cell
lysis and cell-to-cell spread.
Pathologic manifestations may be insignificant, despite dramatic or
lethal diarrhoea. Most bacterial infections exhibit a general non-specific
pattern of damage to the surface epithelium, decreased epithelial cell
maturation, increased mitotic rate, hyperaemia and oedema of the
Clinical picture will depend on the pathophysiology of the organism -
can be severe complications when there is massive fluid loss or
destruction of the intestinal mucosal barrier and resultant dehydration,
sepsis and perforation or minor where there is extreme discomfort.
Enteroinvasive organisms may mimic acute onset IBD.
An acute, necrotising inflammation of the small and large intestine and
is the most common acquired GIT emergency of neonates.
Causes: Immaturity of the GIT, Intestinal mucosa cytokine release on
initiation of solid foods, bacterial colinisation of the gut on onset of oral
feeding, mucosal injury, deranged intestinal blood flow.
Usually affects the terminal ileum and the ascending colon, but may
incorporate all of both intestines. Full thickness of bowel wall becomes
haemorrhagic, inflamed and gangrenous.
Varies in presentations depending on stage and severity of the disease.
Antibiotic associated colitis or pseudomembranous colitis:
Acute colitis characterised by formation of an adherent inflammatory
exudate (pseudomembrane) overlying sites of mucosal injury, usually
caused by protein exotoxins of Clostridium difficile – Type A and Type
B toxins – usually only Type A is assessed in the laboratory.
Occurs primarily in adults as an acute or chronic diarrhoeal illness,
although it has been recorded as a spontaneous infection in young
adults without predisposing influences.
Collagenous and lymphocytic colitis:
Collagenous colitis is characterised by chronic watery diarrhoea and
patches of band-like collagen deposits directly under the surface
Lymphocytic colitis is characterised by chronic watery diarrhoea and a
prominent intraepithelial infiltrate of lymphocytes.
Collagenous colitis is more in middle-aged and older women,
lymphocytic occurs in men and women equally. Mucosa is normal
despite 3-20 watery non-bloody motions per day.
Miscellaneous intestinal inflammatory disorders
Parasites and protozoa:
Entamoeba histolytica is a dysentry-causing protozoan parasite spread
by the faecal-oral route. Amoebae invade the colonic crypts and lamina
propria then make flask-shaped ulcers. These parasites may penetrate
portal vessels, embolise the liver and produce multiple hepatic
abscesses. May also occur in lung, heart kidneys and brain.
Giardia lamblia is an intestinal protozoan spread by faecal
contaminated water. It attached to the intestinal mucosa, but does not
appear to invade. Villi range from normal to marked blunting with a
mixed inflammatory infiltrate of the lamina propria. Clinically, this
produces a malabsorptive diarrhoea.
Some patients exhibit a malabsorptive syndrome with small intestine
villius atrophy or a colitic syndrome resembling ulcerative colitis, in the
absence of demonstrable pathogens. Often infected with opportunistic
infections Cryptosporidium parvum
Diarrhoea is a significant complication of bone marrow transplantation.
Pre-transplant conditioning may cause direct toxic injury - villus
blunting and degeneration of crypts in small intetsinal mucosa.
Severe watery diarrhoea is a feature of acute graft-versus-host disease -
there will be focal crypt cell necrosis, eventually leading to total
sloughing of mucosa, causing life threatening derangement of
electrolytes and possibly leading to sepsis and intestinal haemorrhage.
Drug-induced intestinal injury:
Focal ulceration may occur if a pill adheres to the mucosa and releases
all of its contents locally (such as when no water is used).
The small and large intestines are susceptible to drug-induced
enterocolitis, commonly associated with the use of NSAIDs.
Malabsorption may result after a non-specific inflammation.
Ulceration and stricture may occur. This must always be a DDx when
abdominal illness is encountered.
Abdominal irradiation may severely impair the normal proliferative
activity of the small intestine and colonic mucosal epithelium.
Acute radiation enteritis manifests as anorexia, abdominal cramps and
malabsorptive diarrhoea. Chronic radiation enteritis or colitis may
exhibit more indolent symptoms.
May be perpetuated by radiation induced vascular injury leading to
ischaemic fibrosis and strictures.
Malabsorption is characterised by suboptimal absorption of fats, fat-soluble and
other vitamins, proteins, carbohydrates, electrolytes, minerals and water. It is the
result of disturbance of intraluminal digestion, terminal digestion or
transepithelial transport. There may be many clinical presentations in various
systems as a result of malabsorption:
Stools may be abnormally bulky, frothy, greasy, yellow or grey (steatorrhoea).
Bacterial overgrowth within the intestines may occur, futher damaging epithelial
cells and impairing absorption. Diarrhoea is usually osmotic, due to increase
undigested intraluminal intestinal contents.
Alimentary tract - Diarrhoea, flatus, abdominal pain, weight loss.
Haematopoietic system - anaemia from iron, pyridoxine, folate of
Vitamin B12 deficiency and bleeding from Vitamin K deficiency.
Musculoskeletal system - osteopenia and tetany from calcium,
magnesium, vitamin D and protein malabsorption.
Endocrine system - amenorrhoea, impotence, infertility and
Epidermis - purpura, petechiae, oedema, dermatitis, hyperkeratosis.
Nervous system - peripheral neuropathy from vitamin A and B 12
Also called celiac disease, it is characterised by mucosal lesions of the
small intestine and impaired nutrient absorption which improves on
withdrawal of wheat gliadins and related grain proteins from the diet.
Sensitivity to gluten is thought to be the pathogenic factor and cell-
mediated immunity appears to be important. Cytokines released during
the immunological interactions damages the enterocytes.
Mucosa may be flat or scalloped with marked atrophy or total loss of
villi. Crypts are elonged, hyperplastic and tortuous. Lamina propria has
an overall increase in plasma cells, lymphocytes, macrophages,
eosinophils and mast cells.
Tropical or post-infectious sprue:
Celiac-like disease that occurs almost exclusively in people living in or
visiting the tropics. No specific causal agent has ever been identified,
but bacterial overgrowth (E. coli) has been implicated.
Morphologically variable - near-normal to severe diffuse enteritis.
Rare systemic condition - can involve any organ, but principally the
intestine, CNS and joints. Causative organism is a gram positive
actinomycete, Tropheryma whippelii.
Small intestinal mucosa is laden with distended macrophages in the
lamina propria. Shaggy gross appearance. Inflammation is essentially
Lymphadenopathy and hyperpigmentation may occur.
Disaccharidase (lactase) deficiency:
Lactase remains in the intestinal lumen as it is not broken down
properly - causes an osmotic diarrhoea.
Malabsorption usually becomes clinically obvious with the initiation of
milk feeding - explosive, watery, frothy diarrhoea with abdominal
distension. No visible micro- or macroscopic pathology.
Characterised by a defect in the synthesis and export of lipoproteins
from the intestinal mucosa - FFA and monoglycerides resulting from
hydrolysis of dietary fat enter the epithelial cells are re-esterified but
can't be turned into chylomicrons.
TGs are therefore stored within the cells causing lipid vacuolation and
there is complete absence from plasma any lipoprotein containing
apolipoprotein B - VLDL, LDL and chylomicrons.
Idiopathic inflammatory bowel disease:
Crohn and UC - known as inflammatory bowel diseases. They are chronic, relapsing inflammatory
disorders of unknown origin. Crohn disease is a granulomatous disease that may affect any portion
of the GIT from oesophagus to anus but most often involves the small intestine and colon.
Ulcerative colitis is a non-granulomatous disease limited to the colon. Both exhibit extra-intestinal
Is a perturbation in the state of physiological inflammation that is the normal steady-state of the
intestine, a mix between inflammation due to microbes, dietary antigens, etc and mucosal
There is no clear Mendelian inheritance pattern, but 15% patients have IBD affected first degree
Causes may be stimulation of host mucosal immunity that then fails to down-regulate. Clinical
manifestations of IBD and the diagnostic pathology are ultimately the result of activation of
inflammatory cells whose products cause non-specific tissue injury. Neutrophils are the most
important contributor of these mediators, then eosinophils and mast cells.
Crohn disease is characterised pathologically by:
Sharply delimited and typically transmural involvement of the bowel by an
inflammatory process with mucosal damage
The presence of non-caseating granulomas.
Fissuring with formation of fistulas.
Affects 40% small intestine alone, 30% both small and large and 30% large alone.
Serosa is dull, mesenteric fat wraps around the intestine (creeping fat). The intestinal wall
is rubbery and thick from oedema, inflammation, fibrosis and hypertrophy of the
There is sharp demarcation of diseased bowel segments from adjacent uninvolved
segments. When multiple segments are involved, the intervening bowel is essentially
normal (skip lesions).
Chronic mucosal damage with architectural distortion is manifest in the small intestine as
variable villus blunting and in the colon as crypts exhibit irregularity and branching.
Mucosa may undergo metaplasia. Granulomas have been documented throughout the
length of the alimentary tract, but absence does not preclude diagnosis.
May be marked loss of albumin, generalised malabsoroption, malabsorption of bile salts,
migratory polyarthritis, ankylosing spondylitis, clubbing of the fingertips.
Ulceroinflammatory disease limited to the colon and affecting only the mucosa and
submucosa. Ulcerative colitis extends in a continuous fashion proximally from the
rectum. If it involves the entire colon, it is a pancolitis. Well formed granulomas are
May have skin lesions, sacroiliitis, migratory polyarthritis, ankylosing
spondylitis, pericholangitis and hepatic involvement.
Mucosa may exhibit slight reddening and granularity with friability and
easy bleeding. Pseudopolyps may appear - islands of regenerating
mucosa. Mural thickening does not occur in ulcerative colitis and the
serosal surface is usually completely normal.
Toxic damage to the muscularis propria and the neural plexuses may
lead to complete neuromuscular shutdown in most severe cases (the
colon swells and becomes gangrenous). This condition is called toxic
Lamina propria has a mononuclear inflammatory infiltrate.
When patients are having an attack, there is stringy mucus in bloody
diarrhoea with lower abdominal pain and cramps.
Long-term complication is cancer as underlying inflammatory disease
can mask the symptoms and signs. The rate of progression to dysplasia
and carcinoma is in fact quite low provided that initial examinations are
negative for dysplasia.
Ischaemic bowel disease:
Are restricted to the distribution of the affected vessel(s). Rich
anastomotic connections may render single vessel occlusions harmless
but blockage of coeliac, superior or inferior mesenteric arteries may
infarct metres of intestine.
Ranges of injury:
Transmural infarction - all visceral laeyrs.
Mural infarction - mucosa and submucosa.
Mucosal infarction - no deeper than muscularis mucosae.
Predisposing conditions for ischaemia:
Arterial thrombus from atherosclerosis, systemic vasculitis,
dissecting aneurysm, angiographic proceedures and
Arterial embolism from cardiac vegetations, angiographic
proceedures and aortic atheroembolism.
Venous thrombosis from hypercoagulable states, OCP,
antithrombin III deficiency, intraperitoneal sepsis,
postoperative state, neoplasia and cirrhosis.
Non-occlusive ischaemia from cardiac failure, shock
dehydration and vasoconstrictive drugs.
Radiation injuries, volvulus, herniation and stricture.
Infarctions appear haemorrhagic (whether arterial or venous) because of the blood reflow back into
the affected area. Arterial occlusions show sharp demarcations, venous occlusions do not.
Both acute and chronic mucosal ischaemia are notoriously segmental and patchy, on a micro- and
Tortuous dilations of submucosal and mucosal blood vessels are seen most often in the
caecum and right colon and account for 30% of significant lower intestinal bleeding;
intestinal haemorrhage may be chronic and intermittent or acute and massive.
The vascular channels may only be separated from the inteswtinal lumen by the vascular
wall and a layer of attenuated epithelial cells, explaining the propensity toward bleeding.
Thought to be caused by vascular degeneration and mural tension due to lumenal
pressure and large diameter.
Variceal dilations of the anal and peri-anal plexuses that develop secondary to
persistently elevated venous pressure within the haemorrhoidal plexus.
Most frequent predisposing factor is constipation with straining at stool and the venous
stasis of pregnancy. May also develop as collateral anastomotic channels resulting from
A diverticulum is a blind pouch leading off the alimentary tract, lined by mucosa that
communicates with the lumen of the gut. Discounting Meckel's, they tend to be acquired
and either lack or have attenuated muscularis propria. Unless specified, diverticular
disease refers to acquired outpouchings of the colonic mucosa and submucosa.
Most are small, spherical or flask-like outpouchings of the sigmoid colon, descending or
entire colon, tending to occur alongside taeniae coli.
Two factors are important in their pathogenesis - focal weakness in the colonic wall and
increased intraluminal pressure.
Only 20% of those affected ever develop manifestations such as intermittent cramps,
continuous lower abdominal discomfort, constipation.
Occurs most commonly in the small intestine due to its small lumen.
80% of obstructions are caused by hernias, intestinal adhesions, intussusception and
volvulus. This leads to abdominal pain, distension, vomiting, obstipation and failure to
A weakness or defect in the wall of the peritoneal cavity may permit protrusion of a
pouch-like, serosa-lined sac of peritoneum called a hernial sac, usually occur at inguinal
and femoral canals, umbilicus, surgical scars and occasionally retroperitoneally at the
ligament of trietz.
Hernias are of concern chiefly because segments of viscera frequently protrude and
become trapped in them (external herniation)
Inguinal hernias have small orifices, large sacs and may consume small bowel loops
(often), omentum or large bowel.
If venous return is compromised, trapped viscus may swell and prohibit removal, called
incarceration. The consequent compromise of arterial and venous supply (strangulation)
leads to infarction.
Develop post-peritonitis, i.e. after surgical procedures, infection (PID), endometriosis, as
healing is taking place.
Adhesions can develop between bowel segments, abdominal wall and operative site
creating fibrous bridges and loops through which other viscera may slide and become
trapped (internal herniation).
Occurs when one segment of the small intestine, constricted by a wave of peristalsis
suddenly becomes telescoped into the immediately distal segment of bowel. This segment
continues to propagate by peristalsis, dragging its mesentery with it.
Usually a suspicious cause in adults at the point of traction. Intestinal obstruction ensues
and trapping of mesenteric vessels leads to infarction.
Complete twisting of a loop of bowel about its mesenteric base of attachment produces
obstruction and infarction.
Occurs most often in large redundant loops of sigmoid, followed in frequency by the
caecum, small bowel, stomach or rarely transverse colon.
Tumors of the small intestine:
75% of the length of the GIT only 3-6% of the GIT tumours.
Account for 25% of the benign small intestinal tumours, with
leiomyomas, lipoma and neuromatous lesions following in frequency.
Most occur in the region of the ampulla of vater.
The large majority of these occur in the duodenum and jejunum. They
grow in a napkin ring encircling pattern or as polypoid fungating
Tumors in the duodenum, around the ampulla of vater may present with
obstructive jaundice early in their course. Also cramping pain, nausea,
vomiting and weight loss.
Many have penetrated bowel wall, invaded mesentery and spread to
regional nodes, possible liver metastasis.
Tumours of the colon and rectum
Adenocarcinomas constitute the vast majority of colorectal cancers and represent
70% of all malignancies arising in the GIT.
A polyp is a tumourous mass that protrudes into the lumen of the gut.
Begin sessile (flat) and progress to pedunculated. May be formed as the
result of abnormal mucosal maturation, inflammation or architecture.
They are non-neoplastic and do not have malignant potential per se.
Occur sporadically, particularly in the colon, occur in greater frequency
with age and represent 90% of all epithelial polyps.
Hyperplastic polyps can arise at any age, but they usually have no
Epithelial polyps that arise as the result of proliferation and dysplasia
are termed adenomatous polyps or adenomas - these are true neoplastic
lesions (new growth) and are carcinoma precursors.
Three subtypes, based on epithelial architecture: tubular adenomas,
villous adenomas and tubulovillous adenomas.
All adenomatous lesions arise as the result of epithelial proliferative
dysplasia, which may range from mild to so severe as to constitute
carcinoma in situ. There is strong evidence that adenomas are a
precursor lesion for invasive colorectal adenocarcinoma.
Malignant risk is correlated with polyp size, histologic architecture and
severity of epithelial dysplasia. It is rare in tubular adenoma smaller
than 1 cm in diameter., it is high in sessile villous adenomas greater
than 4 cm in diameter and severe dysplasia is often found in villous
Disorders of the gallbladder
Disorders of the extrahepatic bile ducts
Choledocholithiasis and ascending cholangitis
Carcinoma of the gallbladder
Carcinoma of the extrahepatic bile ducts.
Ability to cope with clinical situations in which there are high levels of uncertainty, iatrogenic morbidity, and
undesired outcomes. ICSCRP/EPPD
Health care workers have a moral obligation to ensure, wherever possible, that their intervention will
result in a net benefit to the patient. This means that any associated treatment risks and probabilities
must be taken into account when determining potential harms and benefits. The division between
beneficence and non-maleficence is not clear and the best ethical approach requires speculation and
In these sort of clinical situations, one must stick to a diagnostic strategy. Based on the evidence, a
probability diagnosis has to be made. However, it should be ensured that serious disorders not to be
missed. Special consideration must be given to the pitfalls, which are diagnosis that are often missed.
The Seven Masquarades are seven diseases that present themselves in atypical ways or don't have a
typical presentation and must be considered in unclear situations. These are:
As part of this diagnostic strategy, always ask the question: Is the patient trying to tell me something?
Inherent in the concept that probabilities can guide decision making is the assumption that one can
arrive at a reasonable threshold by knowing the relative risks and benefits of various options and
deciding at what probability this ratio changes to favor an alternative strategy. In performing any
decision analysis, the relevant probabilities must be known or estimated, a process that sometimes
requires guesswork. A major practical limitation of decision analysis is the subjective judgment often
required to estimate utilities. If the conclusions of an analysis were altered by relatively minor changes
in the assumptions on which it was based, the analysis would not be sufficiently reliable to become the
basis for decision making.
Decision analysis sometimes demonstrates a clear and dramatic advantage with one particular option.
In other circumstances, there may be little difference between two options. Either option may be
reasonable, or secondary issues that cannot be taken into account in the formal analysis (Patient's
feelings about risks; recent local experience with particular interventions) should be the final
determinants in the decision. Even when the outcome of the analysis seems clear, the physician or the
patient may believe that the situation in question is an exception to the rule. Other reasonable
alternatives must also be considered. Furthermore, even the best analyses, like all clinical intuition, are
based on assumptions that may be open to debate.
Making clinical distinctions between functional and structural GI disorders. ICSCRP
Functional gastrointestinal disorders are somatic complaints relating to the gastrointestinal tract that are
manifestations of psychosocial factors. The primary symptoms of functional gastrointestinal disease
may be dyspepsia, intermittent diarrhoea or constipation. Structural or organic gastrointestinal disease
may have symptoms of weight loss,
Abdominal pain may be structural or functional
Selection and interpretation of GI investigations. ICSCRP
Dom LO Title LO Detail
BCS Fluid and electrolyte balance 1. To detect fluid and electrolyte imbalance and understand its
BCS Pain management 1. To revise the physiological mechanisms of pain and describe, in principle,
how pain is managed.
BCS Anatomy 1. To describe the embryology and anatomy of the inguinal canal
2. To describe the anatomy of the femoral canal
BCS Gut obstruction 1. Describe the major pathology of the small intestine
2 .To describe the pathophysiology of gut obstruction including:
(a) differences in consequences between pyloric, high intestinal and low
intestinal obstruction and strangulation;
(b) relationship between pathophysiology and clinical course of different
types of obstruction;
(c) relationship of pathophysiological mechanisms to planning of treatment
3. To outline the principles of operative management of strangulated hernia
with gangrenous gut
ICCP Clinical reasoning 1. To list the appropriate investigations in the patient with an acute abdomen
and how to interpret them
ICCP Clinical and radiological features 1. Describe and be able to demonstrate the clinical and radiological features
of small bowel obstruction of small bowel obstruction.
ICCP Procedural skills 1. Be able to perform nasogastric tube insertion, intravenous cannulation
and fluid administration
ICCP Decision making in emergencies 1. Describe the rationale that underlies decision making in the emergency
PPH Patient values and concept of 1. Demonstrate an ability to determine and integrate patients’ values and lay
illness (Social Sciences) concepts of illness and health care activities, into clinical management.
ANATOMY OF INGUINAL REGION
1. Describe the embryology and anatomy of the inguinal canal.
Development of the inguinal canal
Prior to the descent of the testis and the ovary from their site of origin high in the
posterior abdominal wall (L1), a peritoneal diverticulum call the processus vaginalis
is formed. The processus vaginalis passes through the layers of the lower part of the
anterior abdominal wall and, as it does so, acquires a tubular covering from each
layer. It traverses the fascia transversalis at the deep inguinal ring and acquires a
tubular, the internal spermatic fascia. As it passes through the lower part of the
internal oblique muscle, it takes with it some of its lowest fibres, which form the
cremaster muscle. The muscle fibres are embedded in fascia, and thus the second
tubular sheath is known as the cremasteric fascia. The processus vaginalis passes
under the arching fibres of the transversus abdominis muscle and therefore does not
acquire a covering from this abdominal layer. On reaching the aponeurosis of the
external oblique, it evaginates this to form the superficial inguinal ring and acquires a
third tubular fascial coat, the external spermatic fascia. It is in this manner that the
inguinal canal is formed in both sexes. (In the female the term “spermatic” fascia
should be replaced by the covering of the round ligament of the uterus.)
Meanwhile, a band of mesenchyme, extending from the lower pole of the developing
gonad through the inguinal canal to the labioscrotal swelling, has condensed to form
In the male the testis descends through the pelvis and inguinal canal during the
seventh and eighth months of foetal life. The normal stimulus for the descent of the
testis is testosterone, which is secreted by the foetal testes. The testis follows the
gubernaculum and descends behind the peritoneum on the posterior abdominal wall.
The testis then passes behind the processus vaginalis and pulls down its duct, blood
vessels, nerves, and lymph vessels. The testis takes up its final position in the
developing scrotum by the end of the eighth month.
Since the testis and its accompanying vessels, ducts, and so on follow the course
previously taken by the processus vaginalis, they acquire the same three coverings as
they pass down the inguinal canal. Thus, the spermatic cord is covered by three
concentric layers of fascia: the external spermatic fascia, the cremasteric fascia, and
the internal spermatic fascia.
In the female the ovary descends into the pelvis following the gubernaculum. The
gubernaculum becomes attached to the side of the developing uterus, and the gonad
descends no further. That part of the gubernaculum becomes attached to the side of
the developing uterus, and the gonads descends no further. That part of the
gubernaculum extending from the uterus into the developing labium majus persists as
the round ligament of the uterus. Thus, in the female only the structures that pass
through the inguinal canal from the abdominal cavity are the round ligament of the
uterus and a few lymph vessels. The lymph vessels convey a small amount of lymph
from the body of the uterus to the superficial inguinal nodes.
The inguinal canal is an oblique passage through the lower part of the anterior
abdominal wall and is present in both sexes. It allows structure to pass to and from
the testis to the abdomen in males. In females it permits the passage of the round
ligament of the uterus from the uterus to the labium majus. In addition, it transmits
the ilioinguinal nerve in both sexes.
The canal is about 4 cm long in the adult and extends from the deep inguinal ring, a
hole in the fascia transversalis, downward and medially to the superficial inguinal
ring, a hole in the aponeurosis of the external oblique muscle. It lies parallel to and
immediately above the inguinal ligament. In the newborn child, the deep ring lies
almost directly posterior to the superficial ring, so that the canal is considerably
shorter at this age. Later, as the result of growth, the deep ring moves laterally.
Deep inguinal ring: an oval opening in the fascia transversalis, lies about 1.3 cm
above the inguinal ligament midway between the anterior superior iliac spine and the
symphysis pubis. Related to it medially are the inferior epigastric vessels, which
pass upward from the external iliac vessels. The margins of the ring give origin to
the internal spermatic fascia (or the internal covering of the round ligament of the
Superficial inguinal ring: a triangular-shaped defect in the aponeurosis of the
external oblique muscle and lies immediately above and medial to the tubercle. The
margins of the ring, sometimes called the crura, give origin to the external
Anterior wall of the canal: is formed along its entire length by the aponeurosis of the
external oblique muscle. It is reinforced in its lateral third by the fibres of origin of
the internal oblique. This wall is therefore strongest where it lies opposite the
weakest part of the posterior wall, namely the deep inguinal ring.
Posterior wall of the canal: is formed along its entire length by the fascial
transversalis. It is reinforced in its medial third by the conjoint tendon, the common
tendon of insertion of the internal oblique and transversus, which is attached to the
pubic crest and pectineal line. This wall is therefore strongest where it lies opposite
the weakest part of the anterior wall, namely, the superficial inguinal ring.
Inferior wall or floor of the canal: is formed by the rolled-under inferior edge of the
aponeurosis of the external oblique muscle, namely, the inguinal ligament and, at its
medial end, the lacunar ligament.
Superior wall or roof of the canal: is formed by the arching lowest fibres of the
internal oblique and transversus abdominis muscles.
2. Describe the anatomy of the femoral canal.
This short, conical medial compartment of the femoral sheath lies between the medial
edge of the femoral sheath and the femoral vein. This space allows the femoral vein
to expand during times of increased venous return from the lower limb. It contains a
few lymph vessels, sometimes a deep inguinal lymph node, loose connective tissue,
and fat. It is also the route by which the efferent lymph vessels from the deep
inguinal lymph nodes pass to the external iliac lymph nodes. The canal is widest at
its abdominal end, the femoral ring, and extends distally to the level of the proximal
end of the saphenous opening.
Femoral ring: is the small superior end or mouth of he femoral canal. It is about 1
cm wide and is closed by extraperitoneal fatty tissue called the femoral septum,
which is pierced by the lymph vessels connecting the inguinal and external iliac
lymph nodes. The four boundaries of the femoral ring are: laterally, the partition
between the femoral ring and the femoral vein; posteriorly, the superior ramus of the
pubis covered by the pectineus muscle and its fascia; medially, the lacunar ligament
and conjoint tendon; and anteriorly, the medial part of the inguinal ligament.
PATHOPHYSIOLOGY OF GUT OBSTRUCTION
1. Describe the differences in consequences between pyloric, high intestinal and low
intestinal obstruction and strangulation.
General consequences of obstruction of a hollow tube
Hypertrophy (long term).
Mucosal necrosis, with distension.
Retention of secretions.
In general, the higher the site of the obstruction within the intestinal tract, the more severe the symptoms.
Dilation of the stomach and active peristalsis, which may be visible.
Severe vomiting with hypochloraemic/hypokalaemic alkalosis results.
Pyloric stenosis may occur as a congenital anomaly or may be associated with PUD
or gastric neoplasms, mainly carcinoma.
High intestinal obstruction
Small bowel obstruction:
Auscultation may reveal high-pitched rushes or tinkles that coincide with
episodes of cramping.
Pain is epigastric or periumbilical.
Frequent non-bilious vomiting is prominent if the obstruction is proximal to
the ampulla of Vater.
Colicky pain occurs at frequent intervals (2-5 mins).
Constipation may not occur until later, and distension is minimal or absent.
Vomiting is bilious and less frequent.
The vomiting may be feculent if the obstruction has been long-standing.
Colicky pain occurs at intervals of 10 minutes or more, and it is less intense.
A dull ache may persist between cramps.
Distension increases gradually.
Low intestinal obstruction
Colon cancer 60-70% of cases.
Diverticulitis and volvulus 30% of cases.
Milder attacks of pain often occur in the weeks preceding the acute episode.
Colic is perceived in the lower abdomen or supra-pubically, and
constipation and distension are characteristic.
Nausea is common, and vomiting may occur.
Tenderness is usually mild in uncomplicated colonic obstruction.
Rectal exam or sigmoidoscopy may detect the obstructing lesion.
Colonic pseudo-obstruction (Ogilvie’s syndrome):
Elderly, bedridden or institutionalised individual, often after recent cardiac,
abdominal or orthopaedic surgery.
Constant pain, fever, tachycardia, peritoneal signs, a tender abdominal mass,
2. Describe the relationship between pathophysiology and clinical course of different types
Acute small bowel obstruction
Obstruction may occur at any level – most common in small intestine.
Tumours and infarction are the most serious, but only ~10-15%.
Four main causes (80%):
Most obstructions result in simple occlusion of intestinal lumen, resulting in
distension and enormous loss of fluid into the gut.
Causes outside the wall (extramural):
Adhesions – post-PID, post-OP.
Hernia (internal or external).
Causes inside the wall (intramural):
Inflammation e.g., diverticulitis (colon).
Strictures (ischaemic, congenital).
Causes inside lumen (luminal):
Obstructive gallstones, fecaliths, foreign bodies.
Paralytic ileus (e.g. post-operative).
Vascular – bowel infarction.
Myopathies and neuropathies (e.g., Hirschsprung’s)
Congenital absence of myenteric plexus ganglion cells
Weakness or defect in peritoneal wall protrusion of pouch-like hernial sac (lined
Inguinal and femoral canals.
Retroperitoneal (usually at ligament of Treitz).
Main concern is that segments of viscera (usu. small intestine) protrude through and
become trapped (external herniation), particularly inguinal hernias.
Incarceration: particularly at neck of pouch venous drainage of trapped viscus
stasis and oedema and permanent trapping (no cough reflex).
Strangulation: compromise of arterial supply and venous drainage infarction.
Surgery, infection, endometriosis (may be congenital) peritonitis which may heal
with adhesions between bowel segments/anterior abdominal wall and segment
May create closed loops through which other viscera may slide/be trapped (internal
herniation) incarceration OR strangulation (as in external herniation).
One segment constricted by peristalsis is telescoped into distal segment of bowel.
Usually no underlying lesion in kids (adults - signifies intraluminal mass/tumour at
point of traction) mechanical obstruction and trapping of mesenteric vessels, can
Infection hypertrophic enlargement of Peyer’s patches forms a solid
Children have larger Peyer’s patches
Complete twisting of loop of bowel about its mesenteric base of attachment
mechanical obstruction and infarction.
Most common in sigmoid, then caecum, small intestine, stomach or transverse colon
Clinical course of obstruction
Dilation, oedema and interference with neurovascular supply.
Stranglation intervention to relieve obstruction.
More congestion, oedematous.
Necrosis – death of a group of cells or of tissue usually in a localized area.
Gangrene – cell and tissue death on a widespread basis, resulting from loss of
nutritive supply and by bacterial infection.
Perforation – non-viable wall is friable and easily perforated.
Peritonitis and sepsis.
3. Describe the relationship of pathophysiological mechanisms to planning of treatment.
Treatment of mechanical obstruction consists in relieving the obstruction surgically
at the earliest time consistent with safety of the patient.
The distension must be corrected by suction-decompression (NGT)
Fluid-electrolyte-blood deficits repaired (IV saline).
Operation should be done as soon as possible when the patient is in satisfactory
condition and before ischaemic necrosis develops.
Strangulation of the bowel is a dangerous complication which is the cause of most
deaths from obstruction. When blood supply is compromised, the involved segments
become necrotic, perforate easily with diffuse soiling of the peritoneal cavity, and
resection of the gangrenous bowel will be required.
Hypovolaemic shock caused by plasma loss
Intestinal obstruction is often a cause of severely reduced plasma volume. The
distention of the intestine in obstruction partly blocks venous blood flow in the
intestinal circulation, which increases intestinal capillary pressure. This in turn
causes fluid to leak from the capillaries into the intestinal walls and intestinal lumen.
Also, the lost fluid has a high content of protein, thereby reducing the total plasma
protein as well as the plasma volume.
Pain of obstruction
Pain is felt if the bowel or any other hollow viscus is distended or if its
muscle coat goes into spasm.
The cause of visceral pain is tension in the muscle fibres produced by
stretching of the wall, spasm of the muscle or stretching of the capsule of
Violent peristaltic contractions occur in an attempt to force luminal contents
through an obstruction.
Colic: described as severe and cramping in nature, but intermittent, with
Gives rise to pain because the gut loses motility and becomes distended.
Visceral pain of ischaemic origin is caused most often by strangulation of
the bowel in hernia or volvulus.
Narcotics: except in a case of severe prostrating pain, narcotics should not be used
until diagnosis is established because they may mask important clinical features of
PATHOLOGY OF THE SMALL INTESTINES
1. Describe the major pathology of the small intestine.
Rare disorder – failure of development of lumen in one part of the intestine.
Jejunum and ileum are most commonly affected.
Multiple bowel segments may be affected.
Present with intestinal obstruction in the first week of life.
Surgery is curative.
Diverticulum: a blind pouch leading off the alimentary tract, lined by
mucosa that communicates with the lumen of the gut.
Persistence of the omphalomesenteric duct (connects yolk sac with gut
lumen) leaves solitary diverticulum 30cm from the ileocecal valve,
A pouch of mucosa.
40% of cases have heterotopic gastric or pancreatic mucosa.
Gastric mucosa may present with peptic ulceration.
Bleeding from an ulcerated Meckel’s diverticulum causes
chronic intestinal blood loss, resulting in iron deficiency
Diverticula may intussuscept, incarcerate, or perforate.
Infection (Meckel’s diverticulitis) presents very similar to acute
Present in 2% of the normal population and are usually asymptomatic.
Acute small intestine infarction:
Arterial thrombosis: atherosclerosis, vasculitis, dissecting
aneurysm, angiography, surgery, and hypercoagulable states.
Arterial embolism: cardiac vegetations, angiography, aortic
Venous thrombosis: hypercoagulable states, cirrhosis, sepsis,
surgery and abdominal trauma, neoplasms.
Nonocclusive ischaemia: cardiac failure, shock, dehydration,
Miscellaneous: radiation, volvulus, stricture, herniation.
Transmural infarction: sudden and total occlusion of a major
vessel, infarction of all bowel layers. Bowel segment is
haemorrhagic as a result of blood reflow into damaged area.
Bowel appears rubbery and dusky, bacteria produce gangrene, and
perforation develops within days. More common in the small
bowel (completely dependent on mesenteric blood supply).
Mural and mucosal infarction: incomplete necrosis or necrosis of
mucosa only. Mucosa appears haemorrhagic, but serosa may be
normal. Distribution is frequently patchy; inflammation depends
on duration of injury. Ischaemic changes may be due to any cause
(occlusive or nonocclusive). Large bowel has posterior abdominal
Chronic ischaemia: causes mucosal inflammation, ulceration,
fibrosis, and stricture. Ischaemia has a segmental patchy
Total infarction imparts 50 to 70% death rate. It usually occurs in
severely ill patients and features severe abdominal pain and
tenderness, blood diarrhoea or gross malaena, nausea, vomiting,
bloating, and abdominal wall rigidity.
With incomplete infarction, there are non-specific abdominal
complaints, easily confused with acute and chronic inflammatory
A sensitivity to gluten, which contains the gliadin protein
component, shared by wheat, oat, barley, and rye, is present.
Genetic susceptibility: Familial clustering; 90 to 95% of patients
express the DQw2 (and HLA B8) histocompatibility antigen.
Immune-mediated injury: Serum antibodies to gliadin and potential
cross-reactivity to type 12 adenovirus.
Diffuse enteritis is present with flattened (atrophic) villi, elongated
regenerative crypts, surface epithelial damage with intraepithelial
lymphocytes, and robust lamina propria inflammation
(lymphocytes, plasma cells, macrophages). Severity decreases in
proximal-to-distal intestine and reverts to near-normal upon
withdrawal of dietary gluten.
Symptoms: diarrhoea, flatulence, weight loss, fatigue. Celiac sprue
present in infants up to mid adult life. Other causes must be
excluded; disease responds to withdrawal of dietary gluten.
Complications: iron and vitamin deficiencies, 10 to 15% risk of
gastrointestinal lymphoma, usually T-cell.
Almost exclusively in people living in or visiting the tropics.
Cause is unknown; enterotoxigenic E. coli is a possibility.
Responds to long-term broad-spectrum antibiotic therapy.
Extremely variable intestinal changes are seen, ranging from
normal to resembling celiac disease.
In contrast to celiac disease, the brunt of injury is distal.
Lamina propria has abundant lymphocytes and more eosinophils
than celiac disease.
A rare, systemic condition principally involving intestine, central
nervous system, and joints.
Attributed to infection by Tropheryma whippelii, a gram-positive
Small intestinal mucosa is laden with distended macrophages in
lamina propria, which contain rod-shaped bacilli by electron
Similar macrophages are present in lymphatics, lymph nodes,
joints, and brain.
Inflammation is essentially absent.
Malabsorption occurs with diarrhoea, steatorrhoea, abdominal
cramps, distension, fever, and weight loss; migratory arthritis and
heart disease may be presenting problems.
Usually whites 30s-40s are affected; the male-female ratio is 10:1.
Whipple disease usually responds to antibiotic therapy.
Protrusion of a sac of peritoneum through a defect or weakness in the
Through the internal inguinal ring (indirect inguinal hernia).
Through the posterior wall of the inguinal canal (direct inguinal
Into the femoral canal (femoral hernia).
Around the umbilicus (periumbilical hernia).
Through areas weakened by surgical scars (incisional hernia).
In the posterior abdominal wall (lumbar hernia).
Through the diaphragm (diaphragmatic hernia).
The peritoneal sac of a hernia may contain a variety of abdominal tissues,
commonly omentum and intestine and more rarely bladder.
When intestine constitutes part of the contents, intestinal obstruction
(“obstructed hernia”) may occur as well as strangulation – occlusion of
venous drainage and arterial supply to the segment because of constriction
at the neck, causing infarction and gangrene.
Localised peritoneal inflammation (peritonitis) after surgery, infection,
endometriosis, or radiation.
Healing leads to fibrous bands between viscera.
Complications include internal herniation (within peritoneal cavity),
obstruction, and strangulation of viscera.
Adhesions may be congenital.
Refers to telescoping of one segment of intestine into the immediately distal
segment, usually small bowel.
In infants, intussusception is spontaneous and reversible.
During weaning, exposure to new antigens or infectious agents is
believed to cause hypertrophy of lymphoid follicles in the terminal
Hypertrophied follicles are pushed into the lumen as the apex of an
In adults, point of traction is usually a tumour.
Causes intestinal obstruction, haemorrhagic infarction and gangrene.
Complete twisting of a bowel loop about is mesenteric base or around an
abnormal fibrous band (i.e., adhesions).
Leads to intestinal obstruction and often strangulation of the vascular
supply, causing infarction.
Volvulus commonly occurs in the sigmoid colon in elderly individuals.
Caecal volvulus occurs in younger people who have developmental
malrotation of the bowel.
Frequently occur in the region of the ampulla of Vater, especially in patients
with polyposis syndromes.
Silent, unless they obstruct the intestinal lumen or common bile duct.
Usually present with obstruction (cramping pain, nausea, vomiting), weight
loss, and bleeding.
Spread to mesentery, regional lymph nodes, and liver is as with colonic
Five-year survival is 70% with wide en bloc excision.
FLUID AND ELECTROLYTE BALANCE
1. Explain the detection of fluid and electrolyte imbalance and its correction/prevention.
Clinical estimation of fluid loss
Mild (<2 litres in adult):
Moderate (2-3 litres in adult):
As above, plus:
Oliguria (<400 ml/day).
Postural hypotension > 20 mmHg systolic.
Severe (> 3 litres in adult):
As above, plus:
Systolic BP < 100 mmHg.
Tachycardia (not elderly), low pulse volume.
Cold extremities, poor capillary return.
Reduced skin turgor (“doughy”).
Normal serum reference ranges
Sodium 137 – 147 mmol/L.
Potassium 3.5 – 5.0 mmol/L.
Chloride 96 – 109 mmol/L.
Bicarbonate 25 – 33 mmol/L.
Glucose (fasting) 3.0 – 5.0 mmol/L.
Urea (age dep.) 2.0 – 8.5 mmol/L.
Creatinine (age dep.) 0.04 – 0.14 mmol/L.
Resuscitation in hypovolaemic shock
Use the largest veins with which you are familiar, i.e., antecubital fossa – otherwise
do a cutdown or ventral venous cannulation. Rate of flow is inversely proportional to
length of cannula, and CVP lines are long. Cutdowns are rarely used, but if you
forget about them entirely, you stand to lose the occasional life.
Use 2 large-bore cannular (14G or 16G): it takes 20 mins to infuse 1 litre through a
18G cannula, but only 3 mins through one of 14G.
Raise the drip stand and squeeze the bag, or use an inflatable pressure device to
Estimate and anticipate the fluid loss.
Crystalloid (e.g., Hartmann’s solution) has intravascular t½ of only 30-60 mins and
must be given in three times the volume to that lost; colloid (e.g., Haemaccel) lasts
several hours and is replaced 1:1 with blood lost. Consider blood if haemorrhage and
over 15% volume lost (adult blood volume = 70 mL/kg; child = 80-90 mL/kg) –
crossmatched blood is ideal, but time-consuming; group compatible is a compromise,
only takes 10 mins to prepare and is preferable to O Rh – ve.
Give fluid rapidly; slow only when pulse falls, BP rises and urine flows (> 30 mL/hr
adult and >1 mL/kg/hr child). Catheterise the bladder. Consider CVP line to
monitor progress. A satisfactory response might be a 2cm rise after IV infusion of
250mL colloid over 15 mins.
Don’t forget to give O2 (at 12L/min via tight-fitting face mask with reservoir in all
trauma, unless strong contraindication).
Monitor pulse, BP, and ECG continuously. Remain at bedside.
GI obstruction: 0.9 % saline until BP rises.
1. List the appropriate investigations in the patient with an acute abdomen and how to
Urgency of acute abdominal conditions usually precludes prolonged investigation.
There are only a few specific tests or examinations which may be relied upon to give
clear-cut answers to the exact cause of the acute condition.
Urine and blood should be examined routinely.
Pus or blood in the urine suggest disease of the urinary tract and can also
result form an inflamed appendix lying in proximity to the ureter or bladder.
In dehydration, the specific gravity of the urine may be increased – urine is
In dehydration, the red cell and haemoglobin levels increased as a result of
The total leukocyte count and percentage of polymorphonuclear cells are
usually elevated in acute inflammatory conditions, whereas early in the
course of intestinal obstruction there may be no significant alterations.
Conditions in which tissue necrosis occurs, as in a strangulated intestinal
obstruction, are generally associated with a marked polymononuclear
leukocytosis. With acute appendicitis, the leukocytosis isn’t great unless
you already have a perforated appendix.
The serum amylase test is essential when the possibility of acute pancreatitis
exists. This possibility should be kept in mind in all patients with acute
severe upper abdominal pain.
Certain tests are indicated when extra-abdominal conditions are suspected as
the cause of an acute abdomen. These include:
Blood and urine sugar determinations in diabetic ketoacidosis.
Haemoglobin electrophoresis in possible sickle cell crisis.
Chest X-ray in pneumonia.
ECG in coronary artery disease.
Lead levels in children with pica and anaemia chronic lead v
Serum electrolytes to determine the degree of dehydration and electrolyte
imbalance should be done when fluid loss has been significant.
Plain X-ray films of the abdomen in the supine and upright positions can
often provide immediate information which helps to confirm a diagnosis or
exclude certain diagnoses which have been considered.
Gas below the diaphragm in the upright film is almost pathognomonic or
perforation of a hollow viscus, usually a ruptured peptic ulcer or a traumatic
In mechanical small bowel obstruction, plain films in the upright position
reveal dilated distended loops of gut with fluid levels above the obstruction,
and absence of gas below the obstruction, i.e., terminal ileum and colon.
Generalised distention of large and small bowel occurs in paralytic ileus.
Usually upper GI barium studies are contraindicated because of the
possibility of barium leakage into the peritoneal cavity when perforation is
impending or perforation exists.
Barium enema is an important diagnostic aid in intussusception in infants
and children, and sometimes is used therapeutically under low pressure to
reduce the intussusception. May also be helpful in diverticulosis of the
colon and in large bowel neoplasms, where sigmoidoscopy and biopsy may
When acute cholecystitis is suspected, IV cholangiography is useful for
2. Recognize the clinical and radiological features of small bowel obstruction.
Acute obstruction of the small bowel in adults is caused most commonly either by
incarcerated hernia or by post-operative adhesions within the peritoneal cavities.
Age has a significant influence upon the cause of small bowel obstruction.
In newborns, congenital problems such as atresia and meconium ileus are
important causes of obstruction.
In young children, intussusception is encountered with frequency.
In general, the higher the site of the obstruction within the intestinal tract, the more
severe the symptoms.
Pain is usually sudden in onset, severe, and spasmodic in nature because it results
from vigorous peristaltic activity of the bowel as it attempts to propel the intestinal
contents through the site of obstruction. The patient will often double up with pain
during cramping distress and then a brief period of freedom from distress.
Copious vomiting occurs early in high intestinal obstruction. Initially the vomitus
contains gastric contents, followed by small intestinal contents later, usually bile
coloured. If persistent vomiting occurs, and if the obstruction is in the lower part of
the small bowel, the vomitus becomes faecal in character (feculent vomitus).
Usually with established intestinal obstruction the patient is unable to pass flatus or
stools spontaneously. Bowel contents beyond the obstruction may be passed,
however, and in children with intussusception, this material contains blood mucous
which gives it the characteristic “currant jelly” appearance.
In the early stages, temperature, pulse rate and respiratory rate are normal, as is the
Increased temperature with elevated white cell count suggests that strangulation-
obstruction is developing.
On examination, inspection will reveal the presence or absence of surgical scars or
evidence of inguinal or femoral hernia.
Palpation is usually not revealing but with intussusception, a sausage-shaped mass
may be felt in the right abdomen. This mass is the invaginated segment of the small
Progressive distention occurs.
Tenderness and muscle rigidity in the presence of intestinal obstruction are
suggestive of peritoneal inflammation and strangulation-obstruction.
Auscultation will reveal increased bowel sounds. During episodes of pain, loud high-
pitched peristaltic rushes occur.
As distention progresses, interference with neurogenic and vascular elements of the
bowel develop, motility is reduced and bowel sounds are decreased.
Vomiting with high intestinal obstruction is associated with significant loss of fluid
and electrolytes, and dehydration and electrolyte imbalance ensue rapidly unless the
obstruction is relieved.
Circulatory impairment leads to ischaemia and necrosis of the gut wall and
progressive reduction in all bowel functions.
Plain X-ray films are often diagnostic.
The bowel loops above the obstruction are distended with gas and fluid with absence
of gas seen below the level of obstruction.
In the upright film, fluid levels are found in the dilated loops.
Proximal jejunal obstruction may not cause dilatation.
Distal obstruction is characterised by a ladder pattern of dilated loops of bowel in the
The conditions most likely to be confused with bowel obstruction are those in which
colicky pain in a smooth muscle organ is the outstanding symptom; thus diseases of
the gall bladder, the urinary tract, and the female pelvic organs may resemble an
Paralytic ileus or functional intestinal obstruction must also be considered. Surgery
is not indicated for paralytic ileus and may adversely affect its course.
Examination of the abdomen with a stethoscope is most helpful. Bowel sounds in
paralytic ileus are hypoactive to absent, in contrast to the hyperactive sounds
associated with mechanical obstruction.
MANAGEMENT OF OBSTRUCTION
1. Outline the principles of pain management.
Selection of drug:
Patient’s allergies/side effects.
Duration of action.
Mode of administration.
Aspirin and NSAIDs:
May provide relief equivalent to oral codeine; in some instances are
equivalent to parenteral morphine.
If relief of pain is insufficient, may be combined with:
Orally effective morphine-like agents, e.g., codeine.
Because of differing MOAs, combinations can achieve an analgesic effect
that would otherwise require a higher dosage of opioid, but with fewer side
Major drug for moderate-to-severe pain.
Subcutaneous or IM for moderate-to-severe pain.
Doses need to be tailored to the patient based on individual
sensitivity to the drug and the pain-sparing needs of the individual.
IV for severe pain – continuous infusion or intermittent dosing.
Patient-controlled analgesia (PCA) – valuable post-operatively.
Epidurally and intrathecally in selected situations.
Orally, subjected to first pass metabolism – two to six-fold less
potent than parenterally.
May be used with aspirin or Panadol for additive actions.
Opioid with amphetamine: reduce sedative effects.
Opioid with antidepressants: enhance analgesia.
Opioid and antihistamine, anticonvulsant and glucocorticoids.
2. Demonstrate nasogastric tube insertion and intravenous cannulation insertion.
When the patient is acutely ill, investigation and supportive treatment should proceed
concurrently, if a specific diagnosis is not immediately apparent.
Diagnose a type of disorder.
Relieve accumulated digestive secretions and gas.
To empty the tract to allow healing.
Process of removing gaseous and liquid substances form the GIT.
Attempt to relieve pressure caused by an accumulation of gas and intestinal
contents because of a lack of GIT motility or an obstruction.
Process of applying pressure internally, using a specifically designed tube
placed at a specific site.
Most commonly, applying pressure on haemorrhagic oesophageal varices at
the gastro-oesophageal junction.
Gastric feeding is an artificial method of giving patients fluid and nutrients
via an NGT, when oral intake is inadequate or impossible.
Wash out the stomach.
Used frequently as an emergency treatment in gastric dilatation and
Also used to cleanse the stomach prior to gastric surgery.
Laboratory examination of the contents of a fasting stomach and is
important in the diagnosis of gastric pathology.
Increase in gastric acidity usually coincides with presence of duodenal
Decreased gastric acidity indicates possible carcinoma or pernicious
Normal fasting contents of the stomach are clear and watery.
Gastric contents that are tinged green may indicate a combination of bile
and hydrochloric acid.
Golden yellow contents may indicate achlorhydria (absence of free
hydrochloric acid in the gastric juice).
Acquire knowledge of patient’s history.
Decreasing the risk of aspiration.
Evaluating clinical status.
Write an order/check for order.
Explain to the patient.
Establish a distress signal.
Routine hand wash.
Position the patient.
Assess patient nares.
Determine length of tubing to be used.
Lubricate the tube.
Insert the tube.
If resistance is felt ask the patient to take a deep breath in.
Never force the tube.
Instruct the patient to lower their chin to their chest.
The tube should be advanced as your patient swallows.
The tube should be tested for location:
Aspirating the stomach contents and testing for acidity with blue
Auscultating the left upper quadrant of the patient’s abdomen with
injecting 10-20 mls of air into the tube.
Secure the tube to the patient.
Close the end of the tube with a spigot or attach to a drainage bag.
Dispose of equipment.
Routine hand wash.
Document the procedure.
3. Outline the principles of operative management of strangulated hernia with gangrenous
Strangulation requires urgent surgery (within 1 hr), as does large bowel obstruction
with gross dilatation (>8 cm) and tenderness over the caecum – as perforation is
At surgery, dead bowel must be removed. Revascularization may be attempted but is
difficult and often necessitates a second laparotomy.
Bowel can last 3-4 hours without perfusion.
Recovery – 5 mins in warm, moist packs to restore blood flow.
If still ischaemic, no contraction on poking then its gangrenous and resected
with end-to-end anastomosis.
Usually large volumes of IV fluid must be given.
1. Discuss issues in decision making in the emergency situation
Surgical vs non-surgical acute abdomen
Severe abdominal pain in patients who have been fairly well, and which persists as
long as six hours.
Persistent localised tenderness with muscle spasm, indicative of localised peritoneal
inflammation. The tenderness may be best determined by rectal or pelvic exam.
Characteristic, severe, intermittent cramping, colicky pain, with obstruction of a
Markedly hyperactive bowel sounds with small intestinal obstruction, or decreased to
absent bowel sounds with paralytic ileus. Paralytic ileus not secondary to other
abdominal pathology is treated non-surgically. Paralytic ileus as an end-result of
mechanical small bowel obstruction or perforated duodenal ulcer requires surgical
intervention to relieve the underlying pathology.
Repeated vomiting of copious amounts of bile-stained or faecal material – in small
Palpation of a mass. In RLQ or RUQ – with intussusception. Adnexal mass by
pelvic exam – ectopic pregnancy. Tender and thickened adnexae by pelvic in PID.
An irreducible incarcerated inguinal hernia. A tender RLQ mass by abdominal
palpation or rectal exam – appendiceal abscess.
Certain tests when associated with characteristic clinical features:
Markedly elevated serum amylase levels – acute pancreatitis.
Free air under diaphragm in an upright X-ray film perforation of a hollow
viscus – usually duodenal ulcer.
Distended loops of small bowel above the level of obstruction in small
bowel obstruction with absence of gas below by X-ray; generalised
distention of large and small bowel – paralytic ileus.
Priority I indicates catastrophic events, such as perforation of a viscus, massive
haemorrhage, sudden arterial occlusion with extensive tissue necrosis, all of which
are characterised by sudden onset of severe prostating continuous pain, moderate to
extreme abdominal tenderness and muscle spasm, and rapid development of shock.
There is marked tissue damage and fluid loss from traumatic chemical or vascular
insult. Immediate institution of supportive and resuscitative measures (i.e.,
intravenous correction of fluid and electrolyte imbalance, blood replacement, gastric
suction, vasopressor agents, oxygen, narcotics) is imperative. Emergency operation
as soon as the patient’s condition permits must be done to repair a perforated viscus,
to restore blood supply by relief of strangulation-obstruction, or to control
haemorrhage in a ruptured ectopic pregnancy, ruptured spleen and (hopefully when
condition permit) a dissecting aneurysm.
Acute pancreatitis, which may have a sudden catastrophic onset, is treated non-
operatively with supportive and resuscitative measures, as outlined above, with
nasogastric suction to control or prevent paralytic ileus, and with antibiotics to
control or prevent infection. The pathophysiology of acute pancreatitis involves
intrapancreatic activation of digestive enzymes and autodigestion of the pancreas
with oedema, haemorrhage and necrosis of the gland. Surgical treatment for acute
pancreatitis is no longer strictly taboo due to better fluid and electrolyte management.
It may be difficult to differentiate acute pancreatitis from other catastrophic
conditions. The clinical picture and markedly elevated serum amylase with be
helpful. Differentiation of an acute myocardial infarction is ordinarily not a difficult
diagnostic problem and the ECG will be helpful. An acute dissecting aneurysm may
progress with such rapidity that there may be little or no time for diagnosis or
In this catastrophic group, emergency treatment is imperative. Without treatment,
rapid and progressive deterioration of the patient occurs, and the prognosis is very
Priority II includes conditions associated with vigorous smooth muscle contractions
in an attempt to propel luminal contents past an obstruction. This is the so-called
colic group, which is characterised by severe intermittent recurrent cramping pain
and serious disturbance in gastrointestinal function when the obstruction is in the
Marked systemic reactions are not generally encountered in the early stages of gut
obstruction, but become severe as the process advances. In bowel obstruction the
need for surgical treatment is urgent to prevent ischaemic necrosis of the gut, but not
as critical as in the catastrophic category. There is more time for studies and
preparation of the patient. Diagnosis can usually be established by careful clinical
evaluation of the patient, characteristic hyperactive bowel sounds, and demonstration
by X-ray of distended loops of gut above the level of obstruction. Fluid and
electrolyte imbalance must be corrected and distention relieved by nasogastric
suction before operation. The prognosis is good in cases seen early but much more
serious when ischaemic necrosis of gut occurs and resection of gangrenous bowel is
Biliary and renal colic are treated conservatively with use of meperidine (Demerol)
for relief of pain and relaxation of smooth muscle spasm to facilitate passage of the
calculus. Both renal and biliary colic are treated medically with diet, fluids and
narcotics, and surgery is usually not required, at least for the acute episode of colic.
At times a marked gastroenteritis or a faecal impaction may cause severe colicky
pain, but history, physical examination, and the benign course will obviate any
serious consideration of ill-advised surgery.
Priority III, the lowest category of urgency, includes inflammatory conditions
associated with abdominal pain and a possible acute abdomen. The progression of
inflammation changes occurs over a period of several hours to a few days. Initially
the systemic and abdominal manifestations are not severe and there is considerably
more time to observe and evaluation the patient. With progression of inflammation
and infection, pain and tenderness increase, become more localised, and fever and
leukocytosis increase. Without treatment, there is further tissue damage, and
perforation and peritonitis may occur. Clinical diagnosis is usually possible on the
basis of clinical features and tests.
Until a diagnosis or a decision to operate is made, narcotic analgesics should not be
used lest they mask the pain which is an important diagnostic feature of the disease.
Similarly, antibiotics may alter the course and they should be deferred until diagnosis
is established. Operative and non-operative measures should be instituted, according
to the diagnosis and indications, and the prognosis is generally favourable.
Acute appendicitis is prototypic of the acute inflammatory group. Diagnosis is
clinical and early operation is indicated before suppuration and perforation occur.
Diverticulitis is an inflammatory process occurring in diverticulosis of the colon in
older adults. It is usually treated medically with antispasmodics, intestinal antibiotics
and diet. Colostomy or colectomy may become necessary for patients with repeated
attacks who fail to respond to medical therapy. When the lumen of a diverticulum
becomes obstructed, inflammation occurs within the diverticulum and spreads to
adjacent bowel wall. The most common complication is perforation with localised
peritoneal inflammation. This causes the so-called LLQ appendicitis for which
surgery is required.
Acute cholecystitis is generally a complication of chronic cholecystitis and occurs
when the gall bladder outlet is suddenly and completely occluded, usually by a stone.
Plain film of the abdomen may reveal radio-opaque stones and gall bladder studies
with contrast media show a non-functioning gall bladder. When the patient is in
good condition and the acute attack is of short duration, cholecystectomy is the
treatment of choice. In more seriously ill patients with more chronic infection,
operation may be deferred 6 weeks, until the acute process has subsided due to
medical treatment. The important non-operative measures include gastrointestinal
decompression, parenteral fluids, antibiotics and close observation of the patient for
evidence of progression of disease or impending rupture.
Nonsurgical diseases in the inflammatory category include the following:
A child who has moderately high fever, with abdominal pain, and RLQ
tenderness (although it may be LLQ or bilateral) will have acute mesenteric
adenitis 80% of the time, rather than appendicitis. Mesenteric adenitis is
associated with an acute pharyngitis, often with leukocytosis and surgical
intervention is not required. Sometimes the diagnosis cannot be made with
certainty except at operation. When the danger of laparotomy is
considerably less than that of a possible perforated appendix, operation is
justified, and 4 out of 5 is a pretty good batting average.
Regional enteritis is a chronic granulomatous inflammation of the terminal
ileum, characterised by chronicity, weight loss and bouts of infection,
diarrhoea, and cramping abdominal pain. Occasionally acute exacerbations
may mimic an acute abdomen. Barium study of the small intestine give a
characteristic “string” appearance in the involved segment. Medical
treatment is symptomatic and supportive.
Acute pelvic inflammatory disease can be readily diagnosed by its clinical
features and by culture of cervical discharge. Treatment is medical and
includes vigorous appropriate antibiotic therapy along with general
2. Demonstrate an ability to determine and integrate into clinical management patients’
values and lay concepts of illness and health care activities.
3. Be skilled at finding, appraising studies of prognosis and treatment, and applying the
results to individual management through a weighing up of individualized absolute
benefits and risks.