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Git Pathology 2017

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MODULE: CLINICAL PATHOLOGY

UNIT: PATHOLOGY OF GASTROINTESTINAL SYSTEM


Carey Francis Okinda
March 2017
Outline
Topic Duration (Hrs)
1. Introduction to Pathology of Digestive System 2
2. Disorders of the Oral Cavity (TAKE AWAY ASSIGNMENT) 1
3. Disorders of the Oesophagus 1
4. Disorders of the stomach 1
5. PUD 1
6. GIT Bleeding 1
7. Disorders of the Small Intestines 3
8. Disorders of the Large Intestines 1
9. Disorders of the Rectum and Anus 1
10. Disorders of the peritoneum 2
TOTAL 14
Lesson 1: INTRODUCTION TO GIT PATHOLOGY
Learning Objectives

At the end of the lesson the learner will be able to: -


1) Describe the structure and function(s) of all the organs of the digestive tract
2) Explain the pathophysiology of GIT disorders
3) Investigate GIT disorders

1.0 INTRODUCTION

• GIT is the portal through which nutritive substances and fluid enter the body
• Digestion and absorption are the two major functions of the digestive system
• Primary function of the digestive system is to bring essential nutrients into the internal environment so that
they are available to each cell of the body

2.0 ORGANIZATION
• Comprises of the digestive tract and digestive glands (salivary glands, pancreases) and biliary system (liver,
gall bladder and bile ducts)
• Organs include – oral/buccal cavity, oesophagus, stomach, small intestine (duodenum, jejunum and ileum),
large intestine (ascending colon, transverse colon, descending colon and sigmoid), rectum and anal canal
• Accessory organs include teeth, tongue, salivary glands, liver, gall bladder, pancreas & vermiform appendix

3.0 STRUCTURE

• Alimentary canal (digestive tract) is a tubular approximately 9 m (30 ft) long


• Extends from the mouth to the anus
• Walls have 4 layers (mucosa, sub mucosa, muscularis and serosa) with different modifications at various
levels
Carey F. Okinda ©2017 1
Diagram 1.1: Layers of Alimentary Tract

4.0 GASTROINTESTINAL BLOOD FLOW

• Extensive splanchnic circulation which includes blood flow to the gut, spleen, pancreas and liver
• All the blood that passes through the gut, spleen, and pancreas then flows into the liver through the portal
vein and passes through the liver sinusoids and leaves via the hepatic veins to empty into the vena cava of
the general circulation

5.0 NERVE SUPPLY

• By the enteric nervous system

i) Intrinsic Innervation

• Enteric nervous system composes of two plexuses –


a) Myenteric (Auerbach’s) plexus
• Between longitudinal and circular muscle layers)
• Innervates longitudinal and circular smooth muscles layers (motor control of the GIT movements)
b) Sub-mucosal plexus (Meissner’s plexus)
• Lies in the sub mucosa
• Innervates glandular epithelium, intestinal endocrine cells and sub mucous blood vessels (control
GIT secretions and local blood flow)
• Plexuses are connected to the sympathetic and parasympathetic divisions of the autonomic nervous system
as well as to the prevertebral ganglia of the sympathetic nervous system, spinal cord and brain stem (via
the vagus nerve)
• Neurotransmitters of enteric neurones include acetylcholine and norepinephrine (most important) and
adenosine triphosphate, serotonin, dopamine, cholecystokinin, substance P, vasoactive intestinal
polypeptide and somatostatin.

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ii) Extrinsic Innervation

• Intestines receive dual extrinsic innervation from autonomic nervous system


a) Parasympathetic cholinergic activity
• Increases activity of intestinal smooth muscle
• Has cranial and sacral divisions
• Cranial division
▪ Via the vagus nerve except those for the mouth and pharynx
▪ Innervation to the oesophagus; stomach, pancreas and a less extend to the small intestine and
first half of the large intestine
• Sacral division
▪ Originate in the S2, S3 and S4 segments of the spinal cord and pass through the pelvic nerve to
the distal half of the large intestine
• Sigmoid, rectal and anal regions of the large intestine are considerably better supplied with
parasympathetic fibres than other intestinal areas.
b) Sympathetic adrenergic activity
• Reduces intestinal activity and contraction of sphincters
• Fibres to the GIT originate in the spinal cord between T5 and L2
• Innervate essentially all portions of the GIT rather than being more extensively supplied to the
portions nearest the oral cavity and anus as the parasympathetic fibres.

Sensory Nerves
• Many afferent nerve fibres arise in the gut
• Can be stimulated by irritation of the gut mucosa, excessive distension of the gut and presence specific
chemical substances.

Gastrointestinal Reflexes
• 3 gastrointestinal reflexes essential to gastrointestinal function control
i) Reflexes integrated entirely within the enteric nervous system control gastrointestinal secretion,
peristalsis, mixing contractions and local inhibitory effects.
ii) Reflexes from the gut to the pre-vertebral sympathetic ganglia and back to the GIT. They transmit
signals for long distances in the GIT e.g. gastro-colic reflex, entero-gastric reflexes and colono-ileal
reflex
iii) Reflexes from the gut to the spinal cord or brain and back to the GIT
a. From stomach and duodenum to the brain stem and back through the vagus nerve controls gastric
motor and sensory activity
b. Pain reflexes – cause general inhibition of the entire GIT
c. Defecation reflexes – from the colon and rectum to the spinal cord and back to produce powerful
colonic, rectal and abdominal contractions

6.0 FUNCTIONS
1) Break up food into smaller pieces
2) Transporting food through the GI tract (gastrointestinal)
3) Secreting digestive enzymes
4) Absorbing nutrients into the blood
5) Excreting solid waste products (waste)

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6) Immune system
7.0 DEFENCE MECHANISMS

Diagram 1.2: Defence Mechanisms


Non-Specific Resistance Specific Resistance
First line Second line Third line
• Intact skin • Phagocytic WBCs • Specialized lymphocytes B and T cells
• Mucous membranes • Inflammation • Antibodies
• Secretions • Fever
• Normal microbiota • Antimicrobial substances

Physical and Chemical


• Mucus membranes – layers of mucosal cells that line body cavities that open to the outside (digestive,
genitourinary and respiratory tracts). Mucus is produced by the mucosal cells contains antimicrobial
substance such as lysozymes, lactoferrin (sequester iron). Mucosal cells are rapidly dividing  flush out of
body along with attached bacteria
• Mouth and lower digestive tract – lots of bacteria (mostly anaerobes e.g. Bacteroides, anaerobic streptococci
[Streptococcus mutans in mouth] and Clostridium in colon)
• Saliva (contains lysozyme), bile (alkaline) in small intestine and stomach acids
• Defecation (faeces contains up to 50% bacteria)
• Mucus contain antibacterial agents, antibodies and immune cells called phagocytes

8.0 PATHOPHYSIOLOGY OF GIT DISORDERS

• Include trauma and physical damage; Genetic disorders; Congenital malformations; Disorders of blood
supply (ischaemia); Tumours; Poor diet and nutrition; Infections; Insufficient or excessive digestive acids;
Malfunction of the liver, pancreas or gallbladder; Immune system dysfunction

9.0 FEATURES OF GIT DISORDERS


Discussion:
• What are the features of GIT disorders?
• How do these features come about (pathophysiology)?

1) NAUSEA AND VOMITING


Discuss the causes and pathophysiology of nausea and vomiting
2) DIARRHOEA

1.1 Introduction
• Diarrhoeal disease is the second leading cause of death in children under five years old killing around 760
000 children every year.
• Globally, there are nearly 1.7 billion cases of diarrhoeal disease every year.
• Diarrhoea is a leading cause of malnutrition in children under five years old.

1.2 Definition
• Passage of three or more loose or liquid stools per day (or more frequent passage than is normal for the
individual)

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• Diarrhoea is an increase in the volume of stool or frequency of defecation
• Is the too rapid evacuation of too fluid stools more than 200 grams of stool in 24 hours
• Pseudo diarrhoea – more frequent bowel movement but less than 200 grams in 24 hours
• Incontinence – involuntary loss of stool due to anal sphincter dysfunction or neurologic impairment
• NOTE: Frequent passing of formed stools is not diarrhoea, nor is the passing of loose, "pasty" stools by
breastfed babies

1.3 Classification
• Acute diarrhoea – diarrhoea lasts less than 2 weeks
• Chronic diarrhoea – diarrhoea lasts more than 2 weeks
• Persistent diarrhoea lasting longer than two weeks but resolving within a month
• There are three clinical types of diarrhoea:
• Acute watery diarrhoea – lasts several hours or days, and includes cholera;
• Acute bloody diarrhoea – also called dysentery; and
• Persistent diarrhoea – lasts 14 days or longer.

1.4 Causes of Diarrhoea


Description Examples
1. Secretory diarrhoea Infectious (damage mucosal epithelium) e.g. Rota virus, Enteric adenoviruses;
Infectious (enterotoxin mediated injury) e.g. Vibrio cholera; E. coli, Clostridium
Neoplastic; Excess laxative use
2. Osmotic diarrhoea Antacids; lactose deficiencies; gastric lavage
3. Exudate diseases Infectious – damage to mucosal epithelium e.g. Shigella; Salmonella;
Campylobacter; E. histolytica
Idiopathic inflammatory bowel disease - Ulcerative colitis and Chron’s disease
4. Malabsorption Defective intraluminal digestion; Primary mucosal cell abnormalities
Reduced small intestinal surface area; Lymphatic obstruction; Infectious –
impaired mucosal cell absorption
5. Deranged Motility Decreased intestinal transit time e.g. surgical reduction of the gut length; Neural
dysfunction; Hyperthyroidism; Diabetic neuropathy; Carcinoid syndrome
Decreased motility (increased intestinal transit time) e.g. small intestinal
diverticula; surgical creation of a blind loop and bacterial overgrowth in the small
intestine

1.5 Physiology

Intestinal absorption of water and electrolytes


• Absorption of water from the small intestine is caused by osmotic gradients created when solutes
(particularly sodium) are actively absorbed from the bowel lumen by the villous epithelial cells through
several mechanisms
• To enter the epithelial cells, sodium is linked to the absorption of chloride, or absorbed directly as sodium
ion, or exchanged for hydrogen ion, or linked to the absorption of organic materials such as glucose or
certain amino acids
• Addition of glucose to an electrolyte solution can increase sodium absorption in the intestine as much as
threefold.
• After being absorbed, sodium is transported out of the epithelial cells by an ion pump (Na+K+ ATPase)
which transfers sodium into the extracellular fluid (ECF) elevating the osmolality that causes water and other
electrolytes to flow passively from the bowel lumen through intercellular channels and into the ECF
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• This process maintains an osmotic balance between fluid in the bowel and ECF in the intestinal tissue.

Diagram 1.3: Fluid Absorption

Intestinal secretion of water and electrolytes

• Normally occurs in the crypts of the small bowel epithelium where NaCl is transported from ECF into the
epithelial cell across its basolateral membrane
• Sodium is then pumped back into the ECF by Na+K+ ATPase
• At the same time, secretory stimuli increase the ability of chloride to pass through the luminal membrane of
the crypt cells, allowing that ion to enter the bowel lumen
• Movement of chloride ion creates an osmotic gradient that causes water and other electrolytes to flow
passively from the ECF into the bowel lumen through the intercellular channels.

1.6 Pathophysiology (Mechanisms of Diarrhoea)


• Two principal mechanisms include secretion and osmotic imbalance

Diagram 1.4: Mechanisms of Diarrhoea

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Secretory diarrhoea

• Caused by the abnormal secretion of fluid (water and salts) into the small bowel
• Secretion of water into the intestinal lumen exceeds absorption and the absorption of sodium by the villi is
impaired while the secretion of chloride in the crypts continues or is increased
• Net fluid secretion causes loss of water and salts from the body as watery stools causing dehydration
• Causes
o In infectious diarrhoea, changes result from the action of bacterial toxins or viruses on the bowel mucosa
a) Vibrio cholerae, produces a toxin, which activates adenylyl cyclase causing prolonged increase in
intracellular concentration of cAMP within crypt enterocytes resulting in prolonged opening of the
chloride channels that are instrumental in secretion of water from the crypts, allowing uncontrolled
secretion of water. Additionally, the toxin affects the enteric nervous system resulting in an
independent stimulus of secretion
b) Exposure to toxins from types of bacteria (e.g. E. coli heat-labile toxin) induce the same series of
steps and massive secretory diarrhoea that is often lethal unless the person or animal is
aggressively treated to maintain hydration
c) Other bacterial toxins and agents induce secretory diarrhoea by turning on the intestinal secretory
machinery including:
i. Some laxatives
ii. Hormones secreted by certain types of tumours
iii. Drugs (e.g. some types of asthma medications, antidepressants, cardiac drugs)
iv. Certain metals, organic toxins, and plant products (e.g. Arsenic, insecticides, mushroom
toxins, caffeine)
Osmotic diarrhoea

• Small bowel mucosa is a porous that allows water and salts to move across rapidly to maintain osmotic
balance between the bowel contents and the blood
• Diarrhoea can occur when a poorly absorbed, osmotically active substance is ingested
Carey F. Okinda ©2017 7
• If the substance is taken as an isotonic solution, the water and solute will simply pass through the gut
unabsorbed, causing diarrhoea.
• Causes
a) Purgatives, such as magnesium sulphate, work by this principle
b) Lactase deficiency or glucose malabsorption (occasional complications of enteric infections)
c) Ingestion of a poorly absorbed substrate - offending molecule is usually a carbohydrate or divalent ion.
Common examples include mannitol or sorbitol, epson salt (MgSO4) and some antacids (MgOH2).
d) Malabsorption: Inability to absorb certain carbohydrates is the most common deficit in this category of
diarrhoea, but it can result virtually any type of malabsorption

Inflammatory and Infectious Diarrhoea

• Epithelium of the digestive tube is protected by a number of mechanisms constituting the gastrointestinal
barrier
• Destruction of the epithelium results in exudation of serum and blood into the lumen and widespread
destruction of absorptive epithelium
• Water absorption occurs very inefficiently and diarrhoea results
• Pathogens frequently associated with infectious diarrhoea include - Bacteria: Salmonella, E. coli,
Campylobacter; Viruses: rotaviruses, coronaviruses, parvoviruses (canine and feline), Noro virus; Protozoa:
coccidia species, Cryptosporium, Giardia

Altered Intestinal Motility

• ENS contains many neurotransmitters including 5HT, substance P, VIP and CGRP
• ENS controls motility and secretory functions of the intestine
• ENS functions autonomously but may be modified by the sympathetic and parasympathetic nervous
systems
• Causes - autonomic diabetic neuropathy, after vagotomy (peptic ulcer surgery) and irritable bowel syndrome

1.7 Types of Dehydration

1) Isotonic dehydration
2) Hypertonic (hypernatraemic) dehydration
3) Hypotonic (hyponatraemic) dehydration

1.8 Effects of Diarrhoea

1) Dehydration
• Most dangerous because it can cause hypovolaemia, cardiovascular collapse, electrolyte imbalance
and death if not treated promptly.
2) Metabolic acidosis
• Due to loss of a large amount of bicarbonate may be lost in the stool
• If the kidneys continue to function normally, much of the lost bicarbonate is replaced by the kidneys and
a serious base deficit does not develop. However, this compensating mechanism fails when renal
function deteriorates, as happens when there is poor renal blood flow due to hypovolaemia. Then, base
deficit and acidosis develop rapidly
• Acidosis also results from excessive production of lactic acid when patients have hypovolaemic shock
• Features of base-deficit acidosis include

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i) Reduced serum bicarbonate concentration (<10 mmol/l)
ii) Arterial pH is reduced (< 7.10)
iii) Breathing becomes deep and rapid, which helps to raise arterial pH by causing a
compensating respiratory alkalosis
iv) Increased vomiting
3) Electrolyte imbalance - Potassium depletion
• Occur due to large faecal losses of this ion (losses are greatest in infants and malnourished children)
• Loss of potassium and bicarbonate together does not cause hypokalaemia because the metabolic
acidosis that results from the loss of bicarbonate causes potassium to move from ICF to ECF in
exchange for hydrogen ion, thus keeping the serum potassium level in a normal or even elevated range.
• Signs of hypokalaemia may include general muscular weakness, cardiac arrhythmias and paralytic ileus

3) Other features
• Dyspepsia; pain and discomfort; abdominal swelling; constipation; obstipation; dysphagia;
odynophagia; haematemesis; belching; malena stools; haematochazia

Carey F. Okinda ©2017 9


10.0 INVESTIGATIONS IN GIT DISORDERS

1) Stool examination (analysis)


a. Macroscopy
• Pus + blood - dysentery (rbc clumps – amoebic, discrete – bacillary
• Bulky - steatorrhoea
• Red streaks - fissure-in-ano, fresh – haemorrhoids/dysentery
• Black - malignancy/polyp, Fe, constipation
• Green - children – bacterial infection (pseudomonas)
• Rice water - cholera / viral diarrhoea
b. Microscopy
• Ova - tapeworm, roundworm, threadworm etc.
• Cysts – E. histolytica; E. coli, Giardiasis, Enterobius etc.
• Benzidine test (occult blood), benedicts (reducing sugars) and
• Stercobilinogen (haemolytic anaemia)
c. Bacteriological – stool culture

2) Endoscopy - oesophagostomy; gastroscopy; sigmoidoscopy; colonoscopy


3) Blood counts - Red and white blood cell counts
4) Blood cultures
5) H. pylori tests
a. Biopsy – culture and detection of urease enzyme activity by placing the biopsy specimen onto a
substrate containing urea and monitoring change in pH.
b. 13C-breath test - Helicobacter pylori is a bacterium that is capable of living in the low pH environment
of the stomach; adaptation to this hostile environment involves production of high levels of urease
(which can help raise the local pH).
6) Immunoassay for IgG antibody
7) Radiological and imaging - plain abdominal x-rays; Barium studies – meals, swallow, follow through,
enema; MRI; Ultrasound; CT scan
8) Biopsy
9) LFTs
10) Blood sugars
11) Tests of nonspecific biochemical abnormalities seen in malabsorption
• Serum calcium; serum albumin; serum alkaline phosphatase; serum proteins; serum urea nitrogen;
hypocholesterolaemia; The prothrombin time; The glucose tolerance curve; Vitamin A
12) Tests used in the evaluation of malabsorption/maldigestion
i) Carbohydrate malabsorption - D-xylose absorption test (decreased); Disaccharide test
(decreased); Breath hydrogen test (increased)
ii) Fat malabsorption - Faecal fat determination (elevated); 14C-triolein breath test (decreased)
iii) Bacterial overgrowth - 14C-Xylose breath test (increased)
iv) Specific disorders - Celiac disease (Endomysial antibody present); Pernicious anaemia (Schilling
test); Cystic fibrosis (sweat test)

Carey F. Okinda ©2017 10


Lesson 2: DISORDERS OF THE ORAL CAVITY
Learning Objectives

At the end of the lesson the learner will be able to: -


1) Describe the structure and function of all the organs in the oral cavity
2) Describe pathological conditions affecting the oral cavity

DISORDERS OF THE MOUTH

• Mouth cavity is the anterior opening of the digestive system which ingests food. It has a muscular tongue
on which are arranged the taste buds. There are two rows of teeth - upper and lower.

1.0 THE TEETH

2.0 ORAL MUCOSA

3.0 SALIVARY GLANDS

4.0 OROPHARYNX

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Lesson 3: DISORDERS OF THE OESOPHAGUS
Learning Objectives

At the end of the lesson the learner will be able to: -


1) Describe the structure and function oesophagus
2) Discuss the pathology of disorders of the oesophagus
3) Investigate disorders of the oesophagus

1.0 INTRODUCTION – ANATOMY AND PHYSIOLOGY

• The oesophagus produces limited symptoms of disease because of its simplicity in function. The common
complains include heart burn, dysphagia, odynophagia and hematemesis.

Diagram 3.1: The Oesophagus

2.0 CONGENITAL ABNORMALITIES

1. Agenesis
• Congenital absence of the oesophagus
• Rare and incompatible with life

2. Oesophageal atresia and tracheo-oesophageal fistula


• Most cases associated with trachea-oesophageal fistula
• Tracheo-oesophageal fistula is congenital disorder suggested in a new-born by copious salivation
associated with choking, coughing, and cyanosis on attempts at food intake.
• It occurs in three distinct variants
i)Communication between lower oesophagus-trachea (near bifurcation)- 90%
ii)A fistulous connection between the upper oesophagus and the trachea
iii)A fistulous connection between trachea and a completely patent oesophagus

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Diagram 3.2: Tracheo-Oesophageal Fistula

3. Oesophageal Stenosis and webs


• May occur as a developmental anomaly or following oesophagitis
• Involves fibrous thickening of the oesophageal wall and atrophy of the muscularis propria
• Frequently results from severe oesophageal injury with inflammatory scarring
• Usually develops in adulthood
• Presents with progressive dysphagia (solids – liquids)
• These anomalies have been classified histologically as follows:
Group I - Tracheobronchial rests (cartilage, respiratory mucus glands, ciliated epithelium)
Group II - Membranous diaphragm
Group III - Fibromuscular stenosis

4. Duplication of Oesophagus
• The is a double oesophagus

3.0 MUSCULAR DISORDERS

• There is motor dysfunction of the oesophagus and presents with dysphagia


• Include achalasia, hiatus hernia, oesophageal diverticula, webs and rings

3.1. Achalasia of Cardia (Cardiospasm)


• Achalasia means failure to relax
• A neuromuscular dysfunction in which the cardiac sphincter fails to relax during swallowing causing
progressive dysphagia and dilatation of the oesophagus (mega-oesophagus).
• The normal peristaltic wave initiated by swallowing dies before it reaches the cardiac sphincter.
Carey F. Okinda ©2017 13
Diagram 3.3: Achalasia of Cardia

Clinical Features
• Progressive dysphagia, nocturnal regurgitation and aspiration of undigested food

Differential Diagnosis
• Poliomyelitis, diabetic autonomic neuropathy and infiltrative disorders e.g. malignancy, amyloidosis

Complications
1. Oesophageal squamous cell carcinoma
2. Oesophagitis
3. Diverticula
4. Aspiration pneumonia
5. Airway obstruction

3.2. Oesophageal Diverticula


• A diverticulum is a pouch extending out from the normal wall of the swallowing channel.
• Diverticula (the plural of diverticulum) can develop in either the pharynx or oesophagus
• Small diverticula may not cause symptoms but larger diverticula can cause dysphagia for liquids and solids.
• Regurgitation of undigested food, often hours after ingestion is a characteristic symptom of patients with
diverticula

Diagram 3.4: Oesophageal Diverticula

Aetiology
• Congenital diverticula
• Acquired diverticula (Pulsion/Zenker’s and traction type)
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Features
Task: What are the features of oesophageal
Complications diverticula?
1) Obstruction
2) Infection
3) Perforation
4) Haemorrhage
5) Carcinoma
3.3. Hiatus Hernia

• Herniation or protrusion of the stomach though the oesophageal hiatus of the diaphragm due to defects in
muscle fibres that form the margin of the oesophageal hiatus
Diagram 3.4: Hiatus Hernia

Risk Factors
• Increased pressure within the abdomen caused by - heavy lifting or bending over, frequent or hard coughing,
hard sneezing, pregnancy and delivery, violent vomiting, straining with constipation, obesity and se of the
sitting position for defecation; heredity, smoking, drug use, stress and diaphragm weakness
Aetiology
1) Congenital
2) Acquired –
a) Fibrous scarring of the oesophagus due to degeneration (in aging)
b) Increased intra-abdominal pressure (pregnancy, tumours)
c) Oesophageal regurgitation and increased fatty tissue (obesity)
d) Permanent shortening of the oesophagus (perhaps caused by inflammation and scarring from the reflux
or regurgitation of stomach acid) which pulls the stomach up.

Clinical Features
• Heartburn
• Regurgitation of gastric juices
Types
i) Sliding(rolling) hernia - the junction between the oesophagus and the stomach as well as a portion of
the stomach itself, all of which are normally below the diaphragm, protrude above it

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ii) Paraesophageal hiatus hernia - the junction between the oesophagus and stomach is in its normal
place below the diaphragm, but a portion of the stomach is pushed above the diaphragm and lies
beside the oesophagus.
iii) Mixed – combination of sliding and paraoesophageal types

Diagram 3.5: Types of Hiatus Hernia

Diagnosis
1) Barium swallow — show outlines the oesophagus, fairly accurate at diagnosing paraesophageal hernias,
2) Endoscopy —check the inner lining of the stomach
3) Oesophageal manometry or motility studies —studies can measure how tightly the LES shuts, and they
can also check for abnormalities in oesophageal pressure and movement.
4) Cardiac evaluation — electrocardiogram and an exercise stress test to rule out heart disease.
5) Oesophageal pH monitoring —test uses electrodes to measure the pH (acid level) in the oesophagus,
usually over a 24-hour period.
6) Abdominal ultrasound — look for other abnormalities that account for your symptoms including gallbladder
problems.

Complications
1) Ulceration
2) Bleeding
3) Perforation
4) Strangulation
5) Obstruction
6) Reflux esophagitis

4.0 VASCULAR ABNORMALITIES

Out all the vascular abnormalities of the oesophagus

5.0 OESOPHAGEAL VARICES

Introduction

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• Variceal haemorrhage occurs from dilated veins (varices) at the junction between the portal and systemic
venous systems
• Tend to be in the distal oesophagus and/or the proximal stomach, isolated varices may be found in the distal
stomach, large and small intestine
• Majority of patients with variceal bleeding have chronic liver disease (bleeding is characteristically severe
and may be life-threatening)

Diagram 3.6: Oesophageal Varices

Causes

1) Pre-hepatic - Portal vein thrombosis, portal vein obstruction, congenital atresia/stenosis; increased portal
blood flow – fistula and increased splenic flow
2) Intrahepatic - cirrhosis, idiopathic portal hypertension (hepatoportal sclerosis), acute hepatitis (especially
alcoholic), schistosomiasis, congenital hepatic fibrosis
3) Post hepatic e.g. compression (e.g. from tumour); Budd-Chiari syndrome; Constrictive pericarditis (and
rarely right-sided heart failure)

1.9 Factors that increase the risk of variceal bleeding


• Same factors that increase the risk of portal hypertension e.g.: -decompensation of liver disease;
malnourishment; alcohol intake; physical exercise; increased intra-abdominal pressure; aspirin and Non-
steroidal anti-inflammatory drugs (NSAIDs); bacterial infection (cause of initial, and recurrence of, bleeding)

1.10 Presentation
Symptoms Haematemesis (most commonly), melena; abdominal pain; features of liver disease and
specific underlying condition; dysphagia/odynophagia (uncommon); confusion secondary to
encephalopathy (even coma)
Signs Peripherally shut down; pallor; hypotension and tachycardia (i.e. shock); reduced urine
output; melena; signs of chronic liver disease; reduced Glasgow Coma Scale; signs of sepsis
may also commonly be present; splenomegaly; haemorrhoids

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1.11 Investigations
1. Endoscopy
2. TBC - haemoglobin may be low; MCV may be high, normal or low; platelets may also be low
3. Renal function
4. LFTs
5. Group and cross-match
6. CXR - patients may have aspirated or have chest infection
7. Ascitic tap may be needed if bacterial peritonitis is suspected
8. Investigations as indication for the underlying cause of portal hypertension (see separate article Portal
Hypertension)

6.0 MALLORY-WEISS SYNDROME

• Longitudinal tears in the oesophagus at the gastroesophageal junction or gastric cardia as a consequence
of severe retching and vomiting
• Second most common cause stomach bleeding.
• Tear occurs as a result of excessive pressure or force on the stomach as a result of retching, vomiting,
chronic coughing and convulsions (these causes are usually persistent and extremely forceful in order for
the tear to occur)

Diagram 3.7: Mallory Weis Syndrome

Clinical Features
• Bleeding (upper GIT); Haematemesis

7.0 INFLAMMATORY LESIONS (OESOPHAGITIS)

1) Reflux (Peptic) Oesophagitis

• Most common
• Due to persistent regurgitation of gastric juice into the lower oesophagus
• Reflux normally prevented by tonal activity of the cardiac sphincter, constriction effect of the diaphragm and
acuteness of the cardio-oesophageal angle
• Predisposing factors are due to increased intra-abdominal pressure e.g. obesity, pregnancy
• Effects - high gastric acid levels damage oesophageal mucosa and reduce the tone of cardiac sphincter

Causes

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• Reduced efficacy of oesophageal anti-reflux mechanism
• Presence of sliding hiatus hernia
• Delayed gastric emptying
• Certain foods can relax the muscular ring at the lower end of the oesophagus, responsible for acid reflux.
Such foods include citrus fruit, tomatoes, garlic, chocolate, tea, coffee, alcohol, peppermints.
• Dishes high in fat and oil.
• Excess weight can cause extra pressure on the sphincter
• Certain medications, like aspirin.
• Stress, because this strain the nerves controlling the muscular ring.
• Smoking which stimulates stomach acid.

Diagram 3.8: Peptic Oesophagitis

Clinical Features
• Dysphagia; heartburn; hematemesis; melena; a painful burning sensation in the upper chest; sour and
burning taste of reflux when it reaches the mouth; hoarse voice from irritated larynx; difficulty breathing;
excessive belching; chronic coughing; wheezing and other asthma-like symptoms in adulthood

2) Barret’s Oesophagitis

• Consequence of reflux oesophagitis whereby the stratified squamous epithelium of the lower oesophagus
is replaced by columnar epithelium
• Metaplasia may lead to chronic peptic ulceration (risk of erosion and perforation), dysphagia and invasive
adenocarcinoma

Diagram 3.9: Berret’s Oesophagitis

Carey F. Okinda ©2017 19


Clinical Features - What are the clinical; features?
3) Infective oesophagitis

• Follows a number of opportunistic infections such as Candidiasis, Herpes, CMV and tuberculosis. This
occurs mainly when there is some defect in mucosal resistance

8.0 OESOPHAGEAL OBSTRUCTION

Causes
1. External compression e.g. mediastinal tumours e.g. bronchogenic carcinoma; mediastinal lymphadenopathy
e.g. tuberculosis; enlargement of the left atrium; vascular disorders e.g. aneurysms; pharyngeal pouch
2. Intrinsic lesions (strictures) - carcinoma; reflux oesophagitis; corrosive liquids; Chron’s disease
3. Oesophageal occlusion - foreign material/bodies and polypoid tumours
4. Functional obstruction – Achalasia; Kelly-Paterson (Plummer-Vinson) syndrome

9.0 NEOPLASMS

9.1. Classification
i) Benign Neoplasms - Are uncommon
ii) Malignant Neoplasms
• Two types originating from the epithelium
• Squamous cell carcinoma is related to diet and smoking
• Adenocarcinoma is increasing in incidence and commonly associated with Barret’s oesophagus
• Originate from the epithelium

9.2. Risk Factors

• Age; Gender; Oesophageal disorders (gastroesophageal reflux disease, Barrett's oesophagus, Achalasia,
oesophageal webs, injury, diverticula, Plummer-Vinson syndrome); Tobacco and alcohol; Obesity; Diet;
Workplace exposures to chemical fumes in certain workplaces; People who have had certain other cancers,
(lung cancer, mouth cancer, and throat cancer); Human papilloma virus; Family/genetic

9.3. Clinical Features and Pathology

• What are the clinical features of Ca Oesophagus?


• What are macroscopic and microscopic features of Ca oesophagus
• What are the radiological features of Ca oesophagus?

9.4. Spread

i) Local spread – stomach, hypopharynx, trachea (trachea-oesophageal fistula), larynx, mediastinum, lungs,
bronchi, pleura and aorta
ii) Lymphatic spread – cervical, paraoesophageal, trachea-bronchial, sub diaphragmatic nodes
iii) Haematogenous spread – lungs, liver and adrenals

9.5. Complications What are the complications of Ca oesophagus?

Carey F. Okinda ©2017 20


9.6. Investigations
What are the relevant investigations in Ca oesophagus?
9.7. Staging

The TNM stages of oesophageal cancer

Clinical Staging
Stage Substage Characteristics
0 CIN • High grade dysplasia (HGD) carcinoma in situ (CIS), Severely abnormal cells in the inner
lining of the oesophagus.
1 1A • In the submucosa - T1, N0, M0
1B • Grown into the muscle layer - T2, N0, M0.
2 2A • Membrane covering the outside of the oesophagus, but not spread to nearby lymph
nodes (T3, N0, M0)
2B • Within the muscle layer and 1 or 2 lymph nodes (T1 or T2, N1, M0)
• Has not spread to any other organs
3 3A • grown into the pleura, pericardium and diaphragm - (T4a, N0, M0), or adventitia and is
in 1 or 2 nearby lymph nodes (T3, N1, M0), or spread to 3 to 6 nearby lymph nodes (T1
or 2, N2, M0)
3B • adventitia and has spread to 3 to 6 lymph nodes but nowhere else (T3, N2, M0)
3C • Pleura, pericardium, diaphragm and is in up to 6 lymph nodes (T4a, N1 or 2, M0), or
trachea, vertebra or the aorta and has spread to any number of local lymph nodes (T4b,
any N, M0) or is any size and has spread to 7 or more nearby lymph nodes. But has not
spread to another part of the body (Any T, N3, M0)
4 4A • Cancer is advanced and has spread to other parts of the body, such as the liver or lungs
(any T, N, M1)
4B •

Carey F. Okinda ©2017 21


Lesson 4: DISORDERS OF THE STOMACH
Learning Objectives

At the end of the lesson the learner will be able to: -


1) Describe the structure and function of the stomach
2) Discuss the pathology of disorders of the stomach
3) Investigate disorders of the stomach

1.0 NORMAL STRUCTURE AND FUNCTION

• Has four layers - inner two layers (mucosa and the sub-mucosa) which produces mucus, muscle layer that
churns the contents of the stomach and outer membrane - the serosa, which holds the stomach together
• Food enters the stomach from the oesophagus through the connection between the stomach and the
oesophagus called the cardiac sphincter
• Cardiac sphincter prevents food from passing back to the oesophagus and the other end of the stomach
empties into duodenum
• The pyloric sphincter separates the stomach from the duodenum.
• Stomach has five anatomical parts that include the cardia, fundus, body (main part), pyloric antrum and the
pylorus
• Posterior relations of the stomach - the diaphragm, spleen, left suprarenal gland, left kidney, anterior surface
of the pancreas, left colic flexure, and the upper layer of the transverse mesocolon

Diagram 4.1: Structure of the Stomach

Diagram 4.2: Inner Structures of the stomach

Carey F. Okinda ©2017 22


Blood supply
• Coeliac artery and its branches (right and left gastric arteries and splenic artery)
• Spleenic artery gives off left gastroepiploic artery which anastomoses with the right gastroepiploic artery
• Venous - the portal vein

Nerve supply
• Sympathetic supply from coeliac plexus
• Parasympathetic supply from the vagus nerves

Functions
1) Temporary storage allowing time for the digestive enzymes, pepsins to act
2) Mechanical and chemical digestion
3) Absorption of water, alcohol and some lipid soluble drugs; Fe
4) Non-specific defence against microbes - by hydrochloric acid, vomiting
5) Production of intrinsic factor needed for absorption of vitamin B12
6) Controlled release of the stored contents into the duodenum

2.0 CONGENITAL ABNORMALITIES

2.1. PYLORIC STENOSIS

• Narrowing of the pylorus (opening from the stomach into the small intestine)
• Blockage is also referred to as a gastric outlet obstruction
• Normally, food passes easily from the stomach into the duodenum through a valve called the pylorus but in
pyloric stenosis, the muscles of the pylorus are abnormally thickened preventing the stomach from emptying
into the small intestine and food backs up into the oesophagus
• Cause of the thickening is unknown, although genetic factors may play a role
• Condition is usually diagnosed by the time a child is 6 months old.

Diagram 4.3: Pyloric Stenosis

Clinical Features

1) Vomiting is the first symptom in most children:


• May occur after every feeding or only after some feedings
• Usually starts around 3 weeks of age, but may start any time between 1 week and 5 months of age
• Is forceful (projectile) and the vomit itself is usually clear or has the appearance of partially digested
(curdled) milk.
Carey F. Okinda ©2017 23
2) The infant is hungry after vomiting and wants to feed again
3) Abdominal pain
4) Belching
5) Constant hunger
6) Dehydration (gets worse with the severity of the vomiting)
7) Failure to gain weight or weight loss
8) Wave-like motion of the abdomen shortly after feeding and just before vomiting occurs

Diagnosis
• Usually diagnosed before the baby is 6 months’ old
• A physical exam may reveal signs of dehydration
• An ultrasound of the abdomen may be the first imaging test performed
• A barium X-ray to show the shape of the stomach and pylorus

Complications
1) Malnutrition
2) Dehydration
3) Failure to thrive
4) Anaemia

3.0 INFLAMMATORY DISORDERS

3.1. GASTRITIS

• Condition in which the stomach lining - known as the mucosa - is inflamed


• May be acute or chronic.
• Sudden, severe inflammation of the stomach lining is called acute gastritis.
• Inflammation that lasts for a long time is called chronic gastritis

Causes

Non-erosive
1) Helicobacter pylori (H. pylori) infection causes most cases of chronic non-erosive gastritis. H. pylori are
bacteria that infect the stomach lining. H. pylori are primarily transmitted from person to person. In areas
with poor sanitation, H. pylori may be transmitted through contaminated food or water.
2) Autoimmune disorders in which the immune system attacks healthy cells in the stomach lining
3) some digestive diseases and disorders, such as Crohn's disease and pernicious anaemia
4) Viruses, parasites, fungi, and bacteria other than H. pylori

Erosive
1) Prolonged use of non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin and ibuprofen
2) Alcohol, cocaine,
3) Radiation
4) Traumatic injuries, critical illness, severe burns, and major surgery can also cause acute erosive gastritis.
This type of gastritis is called stress gastritis.

Features
• Upper abdominal discomfort or pain, nausea and vomiting (these symptoms are also called dyspepsia)

Carey F. Okinda ©2017 24


• Erosive gastritis may cause ulcers or erosions in the stomach lining that can bleed. Signs of bleeding in the
stomach include blood in vomit, black, tarry stools and red blood in the stool

Complications
1. Peptic ulcer disease
2. Gastric polyps
3. Benign and malignant gastric tumours
4. Atrophic gastritis – can lead to two types of cancer: gastric cancer and gastric mucosa-associated lymphoid
tissue (MALT) lymphoma.
Diagnosis
1. Endoscopy with a biopsy of the stomach.
2. Barium studies
3. Blood test - check for anaemia
4. Stool test - check for the presence of blood in the stool, another sign of bleeding in the stomach.
5. Tests for H. pylori infection

ACUTE GASTRITIS

• Is an acute mucosal inflammatory process usually of transient nature

Pathogenesis
• Deranged mucosal protection
• Frequently associated with heavy use of NSAIDS, excessive alcohol consumption, heavy smoking,
uraemia, severe stress, ischaemia and shock, suicidal attempts, gastric irritation and mechanical trauma

Clinical Features
• Epigastric pain, nausea and vomiting, haemorrhage, massive hematemesis, malena

Pathology
Macroscopy • Mucosa is oedematous, congested
• Superficial erosion (site of blood loss)
• Erosive – superficial epithelium is lost
Microscopy • Capillary congestion
• Leakage of RBCs into lamina propria
• H. pylori – neutrophilia

CHRONIC GASTRITIS
• Presence of chronic mucosal inflammatory changes leading to mucosal atrophy and intestinal metaplasia
usually in the absence of erosions

Causes
• Chronic infection by H. pylori
• Autoimmunity
• Toxic – alcohol and smoking
• Post-surgical
• Radiation

Carey F. Okinda ©2017 25


• Granulomatous conditions
Helicobacter associated

• Causes direct epithelial cell injury and excites vigorous immune responses leading to chronic inflammation
(duodenal and gastric ulcer)

Autoimmune
• Associated with B12 deficiency, macrocytic anaemia (pernicious anaemia)
• Circulating antibodies against gastric parietal cells
• Involves mainly the body
• Causes extensive intestinal metaplasia

Chemical
• Chemical injury
• Causes hyperplasia and proliferation of gastric pits

Clinical Features
• Nausea and vomiting
• Upper abdominal discomfort

4.0 GASTRIC NEOPLASMS

BENIGN TUMOURS

• The polyp is applied to nay nodule or mass that projects above the level of the surrounding mucosa
• Mucosal polyps are classified as neoplastic and non-neoplastic
• Include non-neoplastic polyps, adenomas and papilloma

Adenomas
• Also, called neoplastic polys
• Found in the antrum but rare
• Commonly associated with chronic gastritis

Stromal tumours
• Include lipomas, schwannomas and leiomyoma
• Appear as circumscribed nodules

MALIGNANT NEOPLASMS - ADENOCARCINOMA

• Comprises more than 90% of all gastric malignancies and leading cause of cancer related deaths
• 2nd commonest tumour

Causes/ Risk Factors


1. Age - most common around the age of 60 and rare under the age of 40.
2. Gender - men are around twice as likely to develop stomach cancer as women.
3. Environmental factors

Carey F. Okinda ©2017 26


a. Diet - diet high in salt and foods that are smoked or cured may increase the risk of stomach cancer.
Certain food preservative chemicals known as nitrosamines, which are found cured meats such as
bacon and ham, may increase your chance of developing stomach cancer.
b. Helicobacter pylori infection
4. Family history - some people inherit an increased risk of developing stomach cancer.
5. Type A blood group - people with type A blood are at higher risk of stomach cancer.
6. Smoking
7. Atrophic gastritis
8. Pernicious anaemia
9. Geographical factors
10. Racial factors

Mechanisms
• Metaplasia
• Dysplasia

Classification

a) Site of origin - antral (25%), fundic (15%) and cardiac (60%)


b) Macroscopic
i. Exophytic - Common in fundus and spreads through stomach wall to serosa causing ulceration and
fungating mass
ii. Ulcerative or infiltrative - common at antrum, presents as ulcers with rolled edges
iii. Diffuse pattern - affects entire gastric wall, presents with minimal ulceration with prominent mucosal
folds
c) Microscopic patterns
i. Gland forming neoplasm
• Resemble tumours of intestines
• Common in older individuals
ii. Diffuse adenocarcinomas
• Non-cohesive
• Infiltrate widely through the wall of the stomach
• 50% of gastric carcinoma
• Common in younger age group

Assessment
1. Patient presents with the same symptoms as gastric ulcer. Later, evaluation shows the lesion to be
malignant.
2. Gastric fullness (early satiety), dyspepsia lasting more than 4 weeks, progressive loss of appetite are initial
symptoms.
3. Stool samples are positive for occult blood.
4. Vomiting may occur and may have coffee-ground appearance.
5. Later manifestations include pain in black or epigastric area (often induced by eating, relieved by antacids
or vomiting); weight loss; haemorrhage; gastric obstruction.

Diagnostic Evaluation
1. Upper GI X-ray with contrast media may initially show suspicious ulceration that requires further
evaluation.
Carey F. Okinda ©2017 27
2. Endoscopy with biopsy and cytology confirms malignant disease.
3. Imaging studies (bone scan, liver scan, CT scan) helps determining metastasis.
4. Complete blood count (CBC) may indicate anaemia from blood loss.
CLINICAL FEATURES

• Persistent abdominal pain, gastric distension and vomiting, loss of weight (cachexia) and appetite
(anorexia), anaemia, weakness and malaise

TNM STAGING
T1 - to grow into the wall of the stomach
T1a - within the mucosa
T1b - mucosa and into submucosa.
T2 – involve the muscular layer
T3 - outer lining of the stomach.
T4 - through the outer lining of the stomach
T4a - broken through outer lining of stomach wall
T4b - other organs/structures nearby - liver, oesophagus or abdominal wall

SPREAD

1) Direct – local extension to the oesophagus, mucosal and submucosal lymphatic spread to duodenum,
draining LN and adjacent viscera e.g. liver
2) Distant
• Lymphatic – to supraclavicular node - Virchow’s node/Troisier’s sign
• Lungs (late)
• Haematogenous – liver, lungs, brain, bones, kidneys, adrenals
• Transcoelomic - Krukenberg tumour

Carey F. Okinda ©2017 28


Lesson 5: PEPTIC ULCER DISEASE
Objectives

At the end of the lesson the leaner will be able to: -


1) Explain the pathogenesis, pathophysiology and pathology of PUD
2) Investigate PUD
3) Describe the complications of PUD

1.0 Introduction and Definition


• An ulcer is a disruption of mucosal integrity of the stomach and/or duodenum leading to a local defect or
excavation due to active inflammation.
• Peptic ulcers are areas of degeneration and necrosis of gastrointestinal mucosa exposed to acid-peptic
secretions
• Mucosal erosions or ulcerations occur when damaging effects of aggressive factors such as acid, pepsin,
bile, NSAIDS and Helicobacter pylori overwhelm the G.I.T mucosal defence factors namely mucous and
bicarbonate secretion, prostaglandins, blood flow and the process of restitution and regeneration after
cellular injury.
• The gastric epithelium is under constant assault by several endogenous noxious factors such as HCl,
pepsinogen/pepsin and bile acids as well as exogenous substances such as medications, (NSAIDS),
alcohol and bacteria (H. pylori)
• A biological system which provides defence from mucosal injury and repairs any injury that may occur.
Mucosal resistance (protection) is provided by mucous in gastric juice in a soluble phase, insoluble
mucous gel which coats the mucosal surface of the stomach and mucosal prostaglandins.

Figure 5.1: Relevant Anatomy

2.0 Risk/Predisposing Factors

Discussion: What are the risk factors in acute PUD?

Carey F. Okinda ©2017 29


3.0 ACUTE PEPTIC (STRESS) ULCERS

• Are multiple, small mucosal erosions that involve mainly the stomach and occasionally the duodenum.
Aetiology
i) Psychological stress
ii) Physiological stress e.g. shock, severe trauma, septicaemia, intracranial lesions, drugs and local irritants
e.g. alcohol, smoking

Pathogenesis
• Mainly due to ischaemic hypoxic injury to the mucosal cells
• Depletion of the gastric mucosa barrier
• In most cases, gastric acid secretion is normal

Pathology
Macroscopy oval or circular multiple ulcers less than 1 cm in diameter common in stomach then
duodenum
Microscopy Shallow ulcers that do not invade the muscular layer; Inflammation at margins and base;
Heal with complete re-epithelialization

4.0 CHRONIC PEPTIC ULCERS (GU AND DU)

Risk/Predisposing Factors/Aetiology

• Helicobacter pylori; Acid-pepsin secretions; Reduced mucosal secretion; Gastritis; Local irritants; Dietary
factors; Psychological factors; Genetic factors; Hormonal factors; Miscellaneous (associated with other
conditions such as alcoholic cirrhosis, chronic renal failure, hyperparathyroidism, chronic pancreatitis)

Discussion: Explain how these factors predispose to chronic PUD

Pathogenesis
• Aetiopathogenesis is multifactorial
• Peptic ulcers are produced by an imbalance between the gastro-duodenal mucosal defense mechanisms
and damaging forces of gastric acid and pepsin, combined with superimposed injury from environmental
or immunologic agents
• Immediate cause of PUD is disturbance in normal protective mucosal barrier by acid-pepsin resulting in
digestion of the mucosa
• Defense mechanisms normally limit the injury
• Aggressive factors include acid secretion/gastric juice (including hydrochloric acid, pepsin, and bile salts
refluxed from the duodenum), H pylori, and NSAIDs. H. pylori, Pepsinogen Secretion, Cigarette smoking;
Corticosteroid use
• Defensive factors include mucus production, bicarbonate production, mucosal blood flow (more important
in the development of stress ulcer) high epithelial cell turnover prostaglandins (PGE2) - stimulate mucus
and bicarbonate production, and blood flow
• Key factors in peptic ulcer formation are exposure of the mucosa to gastric acid and pepsin secretions
and strong association with H. pylori infection.

Carey F. Okinda ©2017 30


Diagram 5.2: Factors Involved in Maintaining Acid Balance
PROTECTIVE AGGRESSIVE

Prostaglandins, mucous, Acid, pepsin, NSAIDS


Bicarbonate, mucosal blood flow Helicobacter pylori

Duodenal Ulcer
• Hyper-secretion of gastric acid into the fasting stomach at night under the influence of vagal stimulation
• Rapid emptying of the stomach (food buffers and neutralizes gastric acid)
• Helicobacter gastritis caused by H. pylori
• Usually associated with gastritis confined to the antrum

Gastric Ulcer
• Impaired gastric mucosal defences against acid-pepsin
• Increased serum gastrin levels
• Usually associated with pangastritis

Pathophysiology
Cause Mechanism
H. pylori H. pylori secretes urease (generates ammonia), protease (breaks down glycoprotein in the
gastric mucus) or phospholipases.
Bacterial lipopolysaccharide attracts inflammatory cells to the mucosa
Neutrophils release myeloperoxide.
A bacterial platelet-activating factor promotes thrombotic occlusion of surface capillaries.
Mucosal damage allows leakage of tissue nutrients in the surface microenvironment,
sustaining the bacillus. Damage of the protective mucosal layer
The epithelial cells are exposed to the damaging effect of acid-peptic digestion.

Carey F. Okinda ©2017 31


Cause Mechanism
Inflammation Chronically inflamed mucosa more susceptible to acid- peptic injury and prone to peptic
ulceration.
Ulcers occur at sites of chronic inflammation e.g. antrum, junction of antral and body- fundic
mucosa (division between the inflamed antral mucosa and normal acid secreting mucosa).
Pangastritis - When there is extensive gastritis, the ulcers are more proximally situated. In
elderly patients, gastric ulcers are more proximally situated as there is proximal migration
of the antral-body mucosal junction
Impaired The gastric acid and pepsin levels are normal and no H. pylori are present.
Defence Chronic use of NSAIDs (aspirin) causes suppression of mucosal prostaglandin and direct
irritative topical effect
Repeated use of corticosteroid in high dose.
Cigarette smoking impair healing and favour recurrences.
Alcoholic cirrhosis; Personality, psychological stress, ischemia.

Figure 5.3: Pathophysiology of PUD

5.0 Pathology
Macroscopy • Commonly solitary round and oval (punched out) ulcer of 1 – 2.5 cm in diameter
• Clean floor, thick firm base;
• Vary in depth from superficial (confined to mucosa) to deep ulcers (penetrating into
the muscular layer)
• Scarring
Microscopy • 4 histological layers – necrotic zone, superficial exudative zone, granulation tissue
zone and zone of cicatrisation

Carey F. Okinda ©2017 32


Diagram 5.4: PUD Pathology

6.0 Sites

Figure 5.5: Sites

7.0 Presentation
Discussion
• What are the clinical features of peptic ulcer (GU and DU)?
8.0 Differential Diagnosis • What are the similarities and differences between gastric and
duodenal ulcers?
1. Mesenteric ischemia
2. Angina pectoris
3. Biliary colic
4. Pancreatitis
5. Nonulcer dyspepsia (NUD) also known as functional dyspepsia or essential dyspepsia
6. Gallstone disease and its complications,
7. Gastroesophageal reflux disease,
8. Chronic pancreatitis,
9. Cancers of the stomach and pancreas,
10. Postgastrectomy gastritis
11. Diseases of the transverse colon
Carey F. Okinda ©2017 33
9.0 Investigations

1) Endoscopy -upper endoscopy, EGD (esophagogastroduodenoscopy), colonoscopy, sigmoidoscopy,


anoscopy
2) Barium x-rays (barium meal, swallow, enema, follow through)
3) Biopsies
4) Blood counts
5) Blood cultures
6) Stool examination

8.0 Complications
1) Healing and scarring – pyloric stenosis
2) Obstruction Explain how these
3) Haemorrhage complications occur.
4) Perforation
5) Penetration
6) Malignant transformation

DIFFERENCES
Feature Duodenal ulcer Gastric ulcer
1. Incidence • More common, 25 – 50 years • Less common, beyond 6th decade
2. Aetiology • H. pylori, hypersecretion of acid- • H. pylori
pepsin
3. Pathogenesis • Mucosal digestion; Damage of • Damage to mucous barrier
protective mucous barrier
4. Pathology • First part of duodenum; Solitary • as duodenal
• Composed of 4 layers
5. Complications • Haemorrhage; Perforation; • Perforation; Haemorrhage
Obstruction • Malignancy
6. Clinical Features • Pain-food-relief pattern • Pain-food pattern
• Night pain • No night pain
• No vomiting • Vomiting
• Melena > hematemesis • hematemesis > Melena
• No loss of weight • Significant loss of weight
• Deep tenderness in right • Deep tenderness in midline in
hypochondrium epigastrium
• Marked seasonal variation • No seasonal variation
• In people at greater stress • In labouring groups

Carey F. Okinda ©2017 34


Lesson 6: GIT BLEEDING
Objectives

At the end of the lesson the learner will be able to: -


1) Outline causes of GI bleeding
2) Explain the clinical features of GI bleeding
3) Investigate GI bleeding
4) Describe complications of GI bleeding

1.0 INTRODUCTION

• Massive lower GI bleeding is defined as passage of a large volume of red or maroon blood through the
rectum. Other features include hemodynamic instability and shock, initial decrease in haematocrit (Hct)
level of 6 g/dL or less, transfusion of at least 2 units of packed red blood cells (RBCs); Bleeding that
continues for 3 days or significant re-bleeding in 1 week
• Causes of GI bleeding are classified into upper or lower GIT bleeding

2.0 UPPER GIT BLEEDING

1.12 Causes
• Originates in the first part of the GI tract-the oesophagus, stomach, or duodenum
Part/organ Examples
1. Oesophagus • Inflammation - oesophagitis; oesophageal varices; tears - Mallory-Weiss syndrome;
ulcers; cancer and trauma
2. In the • Peptic ulcers (ulcers may enlarge and erode through a blood vessel, causing
Stomach bleeding; gastritis; cancer
3. In the Small • Duodenal ulcer; infections; inflammatory; cancer; gall-stones; Cushing’s ulcers;
Intestine Curling’s ulcers; diverticulum; duodenitis
4. Systemic • Bleeding disorders – Haemophilia, Von Willebrand’s disease, scurvy and
polycythaemia; Liver disease; anticoagulants; uraemia; DIC; pancreatitis
5. Miscellaneous • Aneurysm of the splenic/gastric artery/aorta; Amyloidosis; Polyarteritis nodosa;
hereditary haemorrhagic telangiectasia; Neurofibromatosis; Kaposi’s sarcoma;
Acute infections e.g. (yellow fever, scarlet fever, acute yellow atrophy, malaria,
septicaemia)

1.13 Clinical Features

1) Bright red blood, dark clots, or coffee ground-like material in vomit


2) Black, tar like stool
3) Symptoms of Passing only bright red blood, or passing blood mixed in stool
4) Bright red or maroon coloured blood in the stool
5) Acute bleeding - Weakness, shortness of breath, dizziness, rapid pulse, reduced urine flow, crampy
abdominal pain; cold, clammy hands and feet; faintness, diarrhoea, confusion, disorientation, sleepiness,
bright red blood coating the stool, dark blood mixed with the stool, black or tarry stool, bright red blood in
vomit; coffee-grounds appearance of vomit
6) Chronic bleeding - Weakness, fatigue, shortness of breath, pallor, chest pain, dizziness, lethargy,
faintness, bright red blood coating the stool, dark blood mixed with the stool, black or tarry stool, bright
red blood in vomit, coffee-grounds appearance of vomit
Carey F. Okinda ©2017 35
1.14 Differential Diagnosis
i) Peptic Ulcer Disease (PUD) >50% cases
ii) Gastritis/Duodenitis (15-30%), Subset due to NSAID use
iii) Varices from portal hypertension (10-20%)
iv) Mallory-Weiss tears at GE junction (5%)
v) Esophagitis (3-5%)
vi) Malignancy (3%)
vii) Nasopharyngeal bleed – swallowed blood
viii) Other- Aortoenteric fistula, angiodysplasia, Crohn’s, hemophilia, hemosuccus pancreaticus

3.0 LOWER GIT BLEEDING

• Originates in the portions of the GI tract further down the digestive system (parts of the small intestine
beyond the duodenum, large intestine, rectum, and anus).

1.15 Causes
1) In the Small intestines - tumours (adenocarcinoma, lymphoma); vascular ectasis; NSAIDS; Meckel’s
diverticulum; intussusception; Chron’s disease
2) In the Large Intestines - diverticulosis; inflammatory bowel disease - ulcerative colitis, Chron’s disease;
infections; polyps; Cancer
3) Rectum and anus – haemorrhoids, fissures; ulcerative colitis; polyps; cancer

Diagram 6.1: Causes of Lower GIT Bleeding

1.16 Clinical Features

History
• Bowel habits (going more or less often than usual)
• Stool colour (black or red) and consistency (looser or more firm)
• Pain or tenderness, and where it's located

Carey F. Okinda ©2017 36


Physical Examination

What will be the key findings on examination


of a patient with GI bleeding?

4.0 Investigations

1) Endoscopy -upper endoscopy, EGD (esophagogastroduodenoscopy), colonoscopy, sigmoidoscopy,


anoscopy
2) Barium x-rays (barium meal, swallow, enema, follow through)
3) Biopsies
4) Blood counts
5) Blood cultures
6) Stool examination
What are the complications of GI
5.0 Complications
BLEEDING?

Carey F. Okinda ©2017 37


Lesson 7: DISORDERS OF THE SMALL INTESTINES
Learning Objectives

At the end of the lesson the learner will be able to: -


1) Describe the structure and function of the small intestines
2) Discuss the pathology of disorders of the small intestines
3) Investigate disorders of the small intestines

1.0 NORMAL STRUCTURE AND FUNCTION

• Small intestine is 3-7 metres long and approximately 2.5-3 cm in diameter


• Intestinal villi are tiny finger-like outgrowths, in the lining of the small intestine
• Villi increase the surface area of the gut wall allowing for slower movement through the small intestine
and greater time for absorption of nutrients
• Each villus has a lacteal and capillary bit that picks up digested nutrients that are then transported by the
blood to all the cells of the body
• The wall of the small intestine consists of 4 layers – serosa, muscularis propria, sub mucosa and mucosa.

Diagram 7.1: Structure of the Small Intestine

2.0 CONGENITAL DISORDERS

2.1. INTESTINAL ATRESIA

• Congenital absence (complete occlusion) of the lumen commonly mainly the ileum or duodenum in which
the proximal segment has a blind end separated completely from the distal segment or joined by a fibrous
cord
• Presentation depends on the level of the obstruction
• Duodenal or jejunal atresia may cause polyhydramnios due to inability of the foetus to absorb swallowed
amniotic fluid

Features
• Vomiting and abdominal distension within 24 hours of birth, or these symptoms may be delayed somewhat
if the obstruction is more distal.
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Duodenal atresia

• Half of the infants with this condition are born prematurely and approximately two-thirds have associated
abnormalities of the heart, genitourinary, or intestinal tract
• Nearly 40% have Down syndrome
• Infants usually vomit within hours after birth, and may develop a distended abdomen
• Abdominal X-rays show a large dilated stomach and duodenum without gas in the remaining intestinal tract.

Diagram 7.2: Duodenal Atresia

Jejunoileal atresia

• Involves an obstruction of the jejunum or ileum)


• Segment of intestine just before the obstruction becomes massively enlarged (dilated), thus hindering its
ability to absorb nutrients and propel its contents through the digestive tract
• A number of infants also have abnormalities of intestinal rotation and fixation
• Cystic fibrosis is also an associated disorder (screen for cystic fibrosis)

Features
• Vomit green bile within the first 24 hours of life
• Distended abdomen
• Reduced bowel movement

2.2 INTESTINAL STENOSIS

• Congenital narrowing of the lumen affecting a segment of the small intestines


• The intestine above the level of obstruction is dilated while the segment below is collapsed

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2.2. MECKEL’S DIVERTICULUM

• A Meckel’s diverticulum is a small pouch of tissue on the intestine (bowel)


• One of the most common congenital abnormalities that occurs when the connection between the intestine
and the umbilical cord doesn't completely close off during foetal development resulting in a small out
pouching of the small intestine

Diagram 7.3: Meckel’s Diverticulum

Features

• Many people with a Meckel’s diverticulum never have symptoms


• Most common signs of a problem include:
i) Painless bleeding from the rectum
ii) Blood in stool (fresh or black/tarry)
iii) Anaemia (a health problem due to blood loss)
iv) Signs of infection (fever, chills, or pain or tenderness in the abdomen)

Diagnosis
i) Blood tests - check for signs of bleeding or infection
ii) Stool sample - check for blood
iii) Meckel’s scan - a special dye is injected into the child’s bloodstream through an IV (intravenous) line. This
dye may make the Meckel’s tissue show up on a scan.
iv) Ultrasound
v) Other tests - Imaging tests such as an x-ray or CT scan

Complications
i) Perforation
ii) Haemorrhage
iii) Diverticulitis (DDx – appendicitis)

2.3. INTESTINAL MALROTATION


• Developmental abnormality of the mid-gut which causes in failure of normal rotation of the mid-gut resulting
in exomphalos, misplacement of the caecum, appendix and ascending colon and mobile caecum

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Diagram 7.4: Intestinal Malrotation

3.0 INTUSSUSCEPTION
• An invagination of a proximal part of the bowel into a distal part of the bowel (one segment of the intestine
enfolds within another) or the telescoping of a segment of intestine into the segment below due to peristalsis
• Most common is the ileum passing into the cecum and colon through the ileocecal valve
• Telescoped segment is called the intussusceptum and the lower receiving segment is called intussuscipeins
• 95% of all intussusceptions occur in children
• Most common cause of intestinal obstruction in infants past the neonatal period

Diagram 7.5: Intussusception

Causes
• Idiopathic
• Complication of medical conditions such as viral infections (especially adenovirus), Meckel's diverticulum,
intestinal polyps, tumours, such as lymphosarcoma and neurofibroma, lymphoma, recent abdominal
surgery, inflammatory bowel disease and haemophilia

Features
• Abdominal pain (sudden, severe, colicky or cramping), vomiting (sometimes yellow or green tinged),
stools mixed with mucus and blood (often described as currant jelly), lethargy, poor feeding, diarrhoea,
shock, dehydration, fever

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Diagram 7.6: Effects of Intussusception

Complications
1) Bowel gangrene
2) Perforation of the intestinal wall
3) Peritonitis
4) Infection
5) Intestinal obstruction
4.0 VOLVULUS
• Condition in which the bowel twists on itself through 180o causing obstruction to the flow of material through
the bowel
• Can also lead to obstruction of the blood supply to the intestine itself causing ischaemia and necrosis
(gangrene)
• Most commonly due to a birth defect called malrotation (bowel becomes misaligned during foetal
development)
• Bowels do not have a normal attachment to the abdominal wall, which makes it possible for the bowels to
shift out of their normal position or to rotate.
• Volvulus can also occur in the absence of underlying malrotation

Diagram 7.7: Volvulus

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Clinical Features

• Abdominal tenderness, nausea or vomiting (green bile-looking material), bloody or dark red stool,
constipation or difficulty expelling stools, distended abdomen, shock

Investigations
• Stool sample test finds blood in the stool
• Upper GI X-ray with small bowel follow-through shows a malrotated bowel or midgut volvulus
• CT scan may show evidence of intestinal obstruction
• Barium enema often shows an abnormal position of the bowel, suggesting malrotation
• Blood tests to check the electrolytes may show abnormalities

5.0 MALABSORPTION

• Malabsorption syndrome (MAS) is characterized by defective or impaired intestinal absorption of nutrients

Aetiopathology
1) Primary MAS – due to primary deficiency of the absorptive mucosal surface and associated enzymes e.g.
Coeliac sprue, tropical sprue, Whipple’s disease
2) Secondary MAS – mucosal changes result for other factors such as disease, surgery, trauma and drugs
a) Impaired digestion
b) Impaired absorption
c) Impaired transport

Mechanisms of malabsorption
i) Inadequate digestion
ii) Intestinal damage
iii) Altered intestinal flora Using examples explain how these
iv) Biochemical abnormalities mechanisms bring about malabsorption
v) Lymphatic obstruction
vi) Inadequate absorptive surface
vii) Endocrine disturbances
viii) Circulatory disturbances

Clinical Features
• Passage of abnormally bulky, frothy, greasy, yellow or grey stools (steatorrhoea), chronic diarrhoea,
weight loss, anorexia, abdominal distension, borborygmic and flatulence, dehydration, hypotension,
muscle wasting
• Specific malnutrition and vitamin deficiencies

Complications
1) Alimentary tract - diarrhoea; flatus; weight loss; mucositis
2) Haemopoietic system - anaemia (iron, pyridoxine, folate, B12 deficiency, vitamin K deficiency); pellagra
3) Musculoskeletal - osteopenia; Tetany – low calcium and magnesium; Vitamin D deficiency
4) Endocrine - amenorrhea, impotence and infertility due to generalized malnutrition; Hyperparathyroidism –
from calcium and vitamin D deficiency
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5) Cardiovascular system
6) Immunodeficiency
7) Skin - purpura and petechie – vitamin K deficiency; Oedema – protein deficiency; Dermatitis and keratosis
– Vit A, zinc
8) Nervous system - peripheral neuropathy – Vit A, B6 and B12 deficiency; dementia

What investigations will be


relevant in malabsorption
syndrome?

6.0 INFECTIVE DISEASES

6.1. Bacterial

Explain the pathology of the following bacteria in terms of causative agent, pathogenesis,
pathophysiology, pathology, clinical features, diagnosis, investigations and complications: - Cholera,
TB, salmonellosis, shigellosis, clostridial infections, E. coli, Campylobacter, and Staphylococcal

6.2. Viral

Explain the pathology of the following viruses in terms of causative agent, pathogenesis,
pathophysiology, pathology, clinical features, diagnosis, investigations and complications: -
HIV/AIDS, Rota virus, Enteroviruses, Adenoviruses,

6.3. Parasitic
Explain the pathology of the following parasites in terms of causative agent, life cycle pathogenesis,
pathophysiology, pathology, clinical features, diagnosis, investigations and complications: - amoebiasis,
schistosomiasis, nematodes (ascariasis, strongyloides, hookworm, trichuris), cestodes (diphyllobothrium,
taenia solium and saginata), giardiasis

6.4. Fungal

Explain the pathology of the following fungi in terms of causative agent, pathogenesis, pathophysiology,
pathology, clinical features, diagnosis, investigations and complications: - candida

7.0 Neoplasms

Briefly discuss the pathology of neoplasms of


the small intestines.

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Lesson 8: HERNIAS AND INTESTINAL OBSTRUCTION
Learning Objectives

At the end of the lesson the learner should be to


1) Explain the causes and risk factors for hernias and intestinal obstruction
2) Discuss the pathology of hernias and intestinal obstruction

HERNIAS

1.0 INTRODUCTION

• A protrusion of a portion of a viscera through an abnormal opening in the wall of the containing cavity.
• A hernia is an abnormal protrusion from one anatomical space to another.
• 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 hernia sac
• Protrusion of a structure from its normal position to another through an opening that is either congenital or
acquired
• Abnormal protrusion of intra-abdominal tissue (a viscus or part of a viscus) through a fascial defect
(abnormal opening) in the abdominal wall.
• Most often, a hernial mass consists of covering tissues (skin, subcutaneous tissues, etc.), a peritoneal
sac, and any contained viscera
i) External hernia: Protrudes to the outside
ii) Internal hernia: Protrudes within the body
iii) Incisional hernia: Protrudes through a previous incision
iv) Reducible hernia: It is one where the contents of the sac may spontaneously or with pressure return to
the abdomen.
v) Irreducible (incarcerated) hernia: It is one whose contents cannot be returned to the abdomen.
vi) A strangulated hernia: It is one where there is compromise to the blood supply of the contents of the
sac leading to ischemia and gangrene.
vii) Hiatus hernia: Protrusion of the stomach above the diaphragm.

2.0 ANATOMY

Figure 8.1: Groin Anatomy

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3.0 PREDISPOSITION

• Children - poor nutrition and whooping cough


• Adults - chronic cough; straining – micturition/defecation; intra-abdominal malignancy; obesity – weakness,
aponeurosis (hiatus, paraumbilical, direct inguinal hernia); smoking; peritoneal dialysis; overexertion;
anything that causes an increase in pressure in the abdomen can then cause a hernia, including obesity,
lifting heavy objects, diarrhoea or constipation, or persistent coughing or sneezing.

4.0 PATHOGENESIS

• Caused by a combination of pressure and an opening or weakness of muscle or fascia; the pressure
pushes an organ or tissue through the opening or weak spot
• Pressure results from coughing, straining, obesity and intra-abdominal malignancy

Diagram 8.2: Hernia

5.0 COMPOSITION OF A HERNIA

1) Sac - diverticulum of peritoneum that consists of mouth, neck, body and fundus
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2) Coverings - derived from layers of the abdominal wall
3) Contents - omentum (omentocele); intestine (enterocele); portion of the circumference of the intestine
(Richter’s hernia); portion of the bladder; ovary with or without the Fallopian tubes; a Meckel’s diverticulum
(Littre’s hernia); fluid

5.1. Classification

1) Reducible - contents can be returned to the abdomen


2) Irreducible - contents cannot be returned
3) Obstructed - bowel in the hernia has good blood supply but it is obstructed
4) Strangulated - blood supply of bowel obstructed
5) Inflamed - contents of sac have become inflamed

6.0 CLINICAL FEATURES


Symptoms
i) Swelling or bulge beneath abdominal skin (may disappear when lying down)
ii) Pain or discomfort in the area of the bulge or the entire abdomen
• A burning, tearing, sharp, dull or pulling pain
• Due to stretching and tearing of tissues around the hernia with nerve endings
• Can cause localized pain or generalized pain when strangulation or incarceration occurs.
iii) Constipation or bloody stool
iv) Nauseas ness and/or vomiting
v) Urinary Difficulties

6 TYPES OF HERNIAS
1) Femoral Hernia
• Part of intestine, or other abdominal contents, is forced through a weakness in the femoral canal located
near the groin and below the inguinal ligament (crease between the lower abdomen and thigh)
• Common in males but are more likely to occur in females
• Predisposition - straining or coughing, overweight, constipation, pushing or carrying heavy things and
smoker's cough
Diagram 8.3: femoral Hernia

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Differential Diagnosis of Groin Swellings

1) Inguinal hernia – direct and indirect


2) Femoral hernia
3) Undescended testis
4) Inguinal lymphadenitis
5) Lipoma of spermatic cord
6) Excysted hydrocele
7) Saphena varix
8) Femoral artery aneurysm
9) Psoas abscess
10) Femoral nerve neuroma
2) Inguinal Hernia
• Occur when intestines (bowel), omentum or other abdominal organs protrude through the abdominal
ring within a processus vaginalis in the inguinal canal
• If the processus vaginalis does not remain patent an indirect hernia cannot develop
• Most common type of hernia
• Are typically a result of the testis descending from the abdomen into the scrotum, these types of hernias
are found in men more than women at a rate of about 10 to 1.

Diagram 8.4: Inguinal Hernia

Causes
• Congenital or present at birth
• Acquired as the result of sudden or repetitive strain, pressure or injury which weakens the abdominal wall.

Presentation
• Typically located in the inguinal area and unilateral or bilateral; direct or indirect
• Often present is a painless bulge in the groin area, more visible when straining or coughing and may
disappear when lying down
• May become incarcerated or strangulated
• Progressively increase in size and grow more and more uncomfortable with time

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Diagram 8.5: Types of Inguinal Hernia

Types of Indirect Inguinal Hernias


1) Congenital vaginal hernia
• The entire processus vaginalis remains patent and the contents of the hernia pass through it into the
scrotum
• Such a hernia is also called a complete hernia
2) Congenital funicular hernia
• A patent processus vaginalis is present in relation to the spermatic cord, but does not communicate with
the tunica vaginalis
• Hernial contents lie above the level of testis
3) Bubonocele
• The hernia is confined to the inguinal canal and does not protrude through the superficial inguinal ring

Diagnosis
1. Medical history
2. Physical examination of the groin.

Table 8.1: Direct and Indirect Hernias


Direct Inguinal Hernia Indirect Inguinal Hernia
1. Protrudes directly forwards when the patient Shows a more oblique route downwards towards
stands up the scrotum
2. Appears as a symmetric, circular swelling at the Indirect hernia is seen as an elliptical swelling
external ring, i.e. medial to the femoral artery
3. Reduced indirect hernia can be controlled by Direct hernia cannot
pressure over the internal ring, classically with a
single finger
4. On standing, the direct hernias appear Indirect hernia takes time to reach its full size
immediately
5. On lying down, direct hernias disappear There is a delay before the reducible indirect
immediately retracts fully

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Table 8.2: Differences between Femoral Hernia and Inguinal Hernia
Feature Inguinal Hernia Femoral Hernia
Sex Male Female
Defect Pass through inguinal canal Passes through the femoral canal
Site Above and medial to the pubic tubercle Below and lateral to the pubic tubercle
Strangulation Less common More common because of rigid neck-Ricter’s hernia
Treatment Can be treated without surgery Surgery is a must because of risk of strangulation
3) Incisional Hernia

• Occurs at the site of a previous incision in the abdominal wall as a result of the muscles of an old incision
breaking down.
• Often identifiable as a bulge at or near the area of prior incision
• Procedures that can result in an incisional hernia are intestinal surgery, vascular surgery, an appendectomy
or laparoscopy

What are the risk


factors for incisional
hernias?

Figure 8.6: Surgical Incisions

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4) Umbilical Hernia

• Occur in or around the naval, or umbilicus


• Abdominal lining, or any portion of abdominal organs, protrudes through a small hole in the abdominal wall
around the navel area
• Can be acquired as the result of a sudden or repetitive strain, pressure or injury which weakens the
abdominal wall or can also be congenital, or present since birth
• Caused at birth by a weakness in the navel area where the umbilical cord exited the infant, the umbilical
ring never quite heals.
• Signs and symptoms
o Vary from person to person, however
o Primary symptom - a small, soft bulge under or around the navel area, bulge may be visible, or it may
only be felt when pushed on, sometimes the umbilical hernia is accompanied by pain, or a burning
sensation, in the abdomen and may become more severe when lifting, coughing or sneezing. This area
may also become swollen and may appear red or a grey-blue on the surface
5) Epigastric Hernia

• Occur in the midline in the upper abdomen between the rib cage and the umbilicus
• Usually composed of fat and rarely containing abdominal organs.
• Can be congenital in origin or develop as a result of an increase in intra-abdominal pressure from lifting or
straining
• Epigastric hernias are usually asymptomatic but cause pain with straining
• May increase in size and may become strangulated or incarcerated
6) Ventral Hernia (Abdominal)

• Occur anywhere in the front of the abdominal wall usually appear in the midline
• Result from a tear or division in the muscles or fascia
• Composed of fat and rarely containing abdominal organs
• Can be congenital in origin or develop as a result of an increase in intra-abdominal pressure form lifting or
straining

Figure 8.7: Ventral Hernias

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INTESTINAL OBSTRUCTION
1.0 INTRODUCTION

• Is a partial or complete blockage of the bowel that results in the failure of the intestinal contents to pass
through
• A mechanical or functional obstruction of the intestines which prevents the normal movement of the
products of digestion
• Interferes with the propulsion of contents in the intestines

2.0 CLASSIFICATION

Table 8.3: Classification of Intestinal Obstruction


Classification Features
Dynamic or Dynamic: Peristalsis is working against Adynamic:
Adynamic a mechanical obstruction. The  This may occur in two forms.
obstructing lesion may be:  Peristalsis may be absent (e.g. paralytic ileus)
 Intraluminal (impacted faeces,  Or it may be present in a non-propulsive form
foreign bodies, bezoar, gallstones (e.g. mesenteric vascular occlusion or pseudo-
 Intramural (malignant or strictures) obstruction). In both types a mechanical
 Extramural (intraperitoneal bands element is absent
and adhesions, hernias, volvulus or
intussusception.
Mechanical or Mechanical Functional
functional  Caused by a physical blockage  Caused by paralysis of intestinal transit
obstruction  Complete arrest or serious  with certain exceptions, relies on conservative
impairment of the passage of management (and can be exacerbated by
intestinal contents caused by a operative intervention).
mechanical blockage
 often requires corrective surgery
Simple or  Simple  Strangulated
Strangulated  Blockage without interfering with  Arterial & venous flow of a bowel segment are
(presence or vascular supply cut off
absence of an  Closed loop obstruction - bowel obstructed at
adequate both the proximal & distal end
blood supply)  Requires more urgent operative correction
 Most commonly associated with hernia,
volvulus, intussusception, vascular occlusion
Complete or  Incomplete (partial)  complete
incomplete  abdominal pain, emesis  abdominal pain, emesis and obstipation
(level) (severe constipation).
Small Bowel  Small bowel obstruction  Large bowel obstruction
or Large  High: Early profuse vomiting, rapid  Early pronounced distension, mild pain,
Bowel dehydration vomiting, dehydration late e.g. carcinoma,
 Low: Predominant pain, and central diverticulitis or volvulus
distention, vomiting delayed, air-
fluid levels seen on AXR

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3.0 CAUSES Explain these
mechanisms
Table 8.4: Causes of Intestinal Obstruction
Class Description Site/mechanism Causes (examples)
peristalsis is Luminal gall stones; foreign bodies; faecoliths; round worms; tumours;
working bezoars; impaction; imperforate anus
Dynamic

against Intramural stricture e.g. Chron’s disease; Congenital stenosis and malignancy
mechanical Extramural adhesions and bands; strangulated hernia; intussusception; volvulus
obstruction and intra-abdominal tumour
peristalsis is Neurogenic paralytic ileus (paralysis of the muscularis of the intestine)
absent or obstruction
may be Vascular thrombosis, embolism and accidental ligation
present in a obstruction
non- Myopathies and Hirchsprung’s disease
Adynamic

propulsive neuropathies
form (pseudo
obstruction)

4.0 MECHANISMS OF OBSTRUCTION

• Volvulus; incarceration; obstruction; Intussusception; Impaired innervation

5.0 PATHOPHYSIOLOGY

• Dynamic obstruction
o Proximal intestine dilates and develops an altered motility
o Below the obstruction, the bowel has normal peristalsis and absorption until it becomes empty,
contracts and becomes immobile
o Initially the proximal peristalsis is increased in order to overcome the obstruction
o If the obstruction is not relieved the bowel distends resulting in reduced peristaltic force and eventually
flaccidity and paralysis
o Causes of proximal distention include gas (overgrowth of aerobic and anaerobic organisms which
produce gas) and fluid (accumulation of digestive juices with reduced absorption)
• Dynamics obstruction
o Peristalsis is affected
o Bowel distends

Figure 8.8: Pathophysiology of Intestinal Obstruction

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6.0 PRESENTATION

• Pain (sudden onset, severe colicky central abdominal); vomiting; constipation (absolute); dehydration;
hypokalaemia; pyrexia; abdominal distension and abdominal tenderness
• The four cardinal features of dynamic obstruction include colicky pain, distention, vomiting and absolute
constipation.
• The clinical features are also influenced by the site of obstruction whether small bowel or large bowel and
the onset of obstruction whether acute, chronic or acute on chronic

Table 8.5: Differences between Proximal and Distal Small Bowel Obstruction

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7.0 INVESTIGATIONS

• Abdominal ultrasound; plain abdominal x-ray (supine, erect – shows fluid levels; gas shadows; impacted
foreign material); Barium enema; CT scan; TBCs

Figure 8.9: X-Ray Findings

8.0 DIAGNOSIS

• Quartet of pain, distension, vomiting and absolute constipation

How would you make a diagnosis of IO?

What are the complications of intestinal obstruction?

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Lesson 9: DISORDERS OF THE LARGE INTESTINES
Learning Objectives

At the end of the lesson the learner will be able to: -


1) Describe the structure and function of the large intestine
2) Discuss the pathology of disorders of the large intestine
3) Investigate disorders of the large intestine

1.0 NORMAL STRUCTURE OF LARGE INTESTINES (COLON)

• Hollow tube - five to six feet (1.5 to 1.8 meters) long and up to five inches (12.7 cm) in diameter
• Divided up into segments - the first segment (the cecum) located in the lower right side of the abdomen;
second segment (ascending colon), third (transverse colon), and fourth segment (descending colon)
• Descending part of the colon leads down to the S-shaped portion of the bowel called the sigmoid, which
connects to the rectum
• Colon is made up of four different layers of tissue
i) Innermost mucosal layer (a thin layer, with specialized cells that are constantly dying and being
replenished and comes in direct contact with the faecal matter)
ii) Sub mucosal tissue (supports the mucosal layer)
iii) Muscular tissue (provides strength to the colon and causes contractions which push the faecal matter
through the large intestine)
iv) Outermost serosal layer (supports and protects the colon).

Diagram 9.1: The Large Intestine

2.0 ACUTE APPENDICITIS

2.1. Definition

• Inflammation of the inner lining of the vermiform appendix that subsequently spreads to its other parts

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2.2. Anatomy

• Definition

o This is a worm-like diverticulum arising from the posteromedial wall, of the caecum, about 2 cm
below the ileocaecal orifice
o It is a blind muscular tube with mucosal, submucosal, muscular and serosal layers.
• Dimensions
o The length varies from 2 to 20 cm with an average of 9 cm.
o The average length is between 7.5 and 10 cm
o It is longer in children than in adults.
o The diameter is about 5-10 mm.
o The lumen is quite narrow and may be obliterated after mid-adult life.

Diagram 9.2: Sites of the Appendix

2.3. Causes

1) Obstructive
a) Foreign bodies
i. Parasites – threadworms, roundworms, Enterobius vermicularis especially Oxyuris
vermicularis(pinworm)
ii. Vegetable – seeds, date stones
iii. ‘’Mineral’’ – faecoliths – commonest cause; found in 40% of cases of simple acute appendicitis,
65% of cases of gangrenous appendicitis without rupture, and 90% of cases of gangrenous
appendicitis with rupture. A faecolith is composed of inspissated faecal material/barium from
previous X-ray studies, calcium phosphates, bacteria and epithelial debris
b) Strictures and bands of a congenital nature
c) Tumour – obstruction of the appendiceal orifice by tumour, particularly carcinoma of the caecum, is
acute appendicitis in middle age and the elderly
d) Calculi
e) Sub mucous lymphoid tissue – diffuse lymphoid hyperplasia, especially in children

2) Non-Obstructive
a) Infection
b) Vascular occlusion
c) Inappropriate diet lacking roughage

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2.4. Pathophysiology

• Obstruction appendiceal lumen causes an increase in pressure within the lumen and increased continuous
secretion of fluids and mucus from the mucosa and the stagnation of this material
• Mucosal secretions continue to increase intraluminal pressure
• The pressure exceeds capillary perfusion pressure and venous and lymphatic drainage are obstructed
• There is vascular compromise which causes epithelial mucosa breaks down and bacterial invasion by bowel
flora occurs
• Increased pressure also leads to arterial stasis and tissue infarction
• Results in perforation and spillage of infected appendiceal contents into the peritoneum
• Intestinal bacteria multiply causing acute inflammation leading to the recruitment of white blood cells and
the formation of pus and subsequent higher intraluminal pressure
• If appendiceal obstruction persists, intraluminal pressure rises ultimately above that of the appendiceal
veins, leading to venous outflow obstruction which causes appendiceal wall ischemia resulting in a loss of
epithelial integrity and allowing bacterial invasion of the appendiceal wall.
• Within a few hours, this localized condition may worsen because of thrombosis of the appendicular artery
and veins, leading to perforation and gangrene of the appendix.
• Pelvic appendix may irritate the bladder or rectum causing suprapubic pain, pain with urination, or feeling
the need to defecate
• Multiple anatomic variations explain the difficulty in diagnosing appendicitis

2.5. Pathology
Gross (macroscopy) • Early stages – grossly oedematous with dilatation of serosal vessels
• Appendiceal wall is grossly thickened and the lumen is dilated
• Serosal exudate (fibrinous or fribropurulent)
Microscopy • Neutrophil infiltration

2.6. Clinical features

Symptoms
1. Periumbilical Colic
• Poorly localised colicky abdominal pain, central abdominal pain is usually his first symptom, and it may
be severe enough to wake him from sleep.
• The pain is moderately severe, and is steady, sometimes with intermittent cramping superimposed.
• Pain shifts to right iliac fossa after 1 – 12 hours average 4 – 6 hours.
2. Anorexia
3. Nausea and vomiting - caused both by neural stimulation and the presence of ileus
5. Vital Signs:
• Slight pyrexia (37.2-37.7oC) with corresponding increase in the pulse rate to 80 or 90 is usual
• If his pulse is raised, his appendix has possibly perforated.
• A steadily rising pulse is always serious
6. Distinction between obstructive & non-obstructive appendicitis:
• Nature of pain in obstructive type is colicky.
• In obstructive type - pain starts early in epigastrium.
• Vomiting more marked in obstructive type.
• Tenderness and rigidity – less in an early case of obstructive type
7. Bowel Function:
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• Most patients have obstipation beginning prior to the onset of abdominal pain, and many feel that
defecation would relieve their abdominal pain.
• Diarrhoea occurs in some patients, particularly children

Signs
• General – fever, tachycardia and dehydration
• Inspection – movement with respiration may be absent, distention
• Palpation
o Maximal tenderness at McBurney’s point
o RLQ tenderness and rebound tenderness
o Guarding; rigidity
• Auscultation - bowel sounds may be absent in perforated appendix-paralytic ileus or may be increased with
obstruction at the caecum
• The cardinal features are those of an unwell patient with low grade pyrexia, localized abdominal
tenderness, muscle guarding and rebound tenderness
• McBurney point: Gentle superficial palpation of the abdomen, beginning in the left iliac fossa moving
anticlockwise to the right iliac fossa, will detect muscle guarding over the point of maximum tenderness,
classically McBurney point.
• Pointing sign
o The patient is then asked to point to where the pain began and to where it moved
• Rovsing’s sign
o Deep palpation of the left iliac fossa may cause pain in the right iliac fossa, which is helpful in
supporting a clinical diagnosis of appendicitis. It is indicative of right-sided local peritoneal irritation
• Psoas sign
o Occasionally an inflamed appendix lies on the psoas muscle and the patient, often a young adult,
will lie with the right hip flexed for pain relief’
o Pain in the right lower quadrant brought on by extension of the right hip (iliopsoas sign), is
associated with a retrocecal appendix
o It suggests that an inflamed appendix is located along the course of the right psoas muscle
• Obturator test
o Spasm of the obturator internus is sometimes demonstrable when the hip is flexed and internally
rotated.
o If an inflamed appendix is in contact with the obturator internus, this manoeuvre will cause pain in
the hypogastrium (Zachary Cope).
o Pain with internal rotation of the hip (obturator sign) is associated with a pelvic appendix
o These signs are present in a minority of patients with acute appendicitis.
o Their absence never should be used to rule out appendiceal inflammation
• Dunphy's sign
o Sharp pain in the RLQ elicited by a voluntary cough.
o It may be helpful in making the clinical diagnosis of localized peritonitis.

2.7 Diagnosis
• The diagnosis of appendicitis rests more on thorough clinical examination of the abdomen than on any
aspect of the history or laboratory investigation.
• Similarly, RLQ pain in response to percussion of a remote quadrant of the abdomen, or to firm percussion
of the patient's heel, suggests peritoneal inflammation.
• Markle sign: Pain elicited in a certain area of the abdomen when the standing patient drops from standing
on toes to the heels with a jarring landing, is stated
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2.8 Differential Diagnosis

Table 9.1: Differential Diagnosis


System Differentials
1. Pancreatico-Biliary cholecystitis; Biliary colic; Pancreatitis
2. GIT gastroenteritis, enterocolitis; Meckel diverticulitis; Perforated duodenal ulcer; Crohn’s
disease, ulcerative colitis; Colon carcinoma, peri caecal abscess; Intussusception;
Mesenteric adenitis
3. Urinary system ureteric colic; Urinary tract infection (UTI); Pyelonephritis
4. Reproductive ovarian cyst torsion; Mittel Schmerz; ectopic pregnancy; pelvic inflammatory disease
(women) (PID); endometriosis; salpingitis
5. Respiratory Lobar pneumonia

Table 8.2: Differential Diagnosis


Age Differentials
1. Children Acute mesenteric adenitis/lymphadenitis; acute gastroenteritis; meckel’s diverticulitis;
intussusception; purpura; lobar pneumonia & pleurisy
2. Adults Ureteric colic/stone; right-sided acute pyelonephritis; perforated peptic ulcer; acute
pancreatitis; rectus sheath haematoma; disease of the male urogenital system (torsion of
the testis, acute epididymitis and seminal vasculitis); Crohn’s disease; primary peritonitis
3. Gynaecologic PID; Ruptured Graafian follicle/Mittelschmerz; Twisted ovarian cyst or tumour;
Disorders Endometriosis; Ruptured ectopic pregnancy
4. Elderly Sigmoid diverticulitis; Intestinal obstruction; Carcinoma of the caecum
5. Other Foreign-body perforations of the bowel; closed-loop intestinal obstruction; mesenteric
Diseases vascular occlusion; pleuritis of the right lower chest; acute cholecystitis; acute pancreatitis;
haematoma of the abdominal wall

2.9 Staging

Table 9.3: Staging of Appendicitis


Stage Description
1.0 Oedematous stage • Appendicitis may have spontaneous regression or may evolve to the 2nd stage
• Mesoappendix is commonly involved with inflammation
2.0 Purulent • Spontaneous regression occurs rarely
(phlegmonous) • Appendicitis usually evolves beyond perforation and rupture
stage • Peritonitis may be possible
3.0 Gangrenous stage • Spontaneous regression never occurs; Peritonitis is present

2.10 Scoring - MANTRELS or Alvarado Scoring

• Makes use of clinical signs, symptoms and laboratory findings


• Each of the alphabets represents a sign or symptom, and a score of 1 is award to each, where they exist,
except T and S that are scored 2 each

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Table 9.4: MANTREALS Staging of Appendicitis
Description Score interpretation
M Movement of pain to the RIF 1 Score Meaning
A Anorexia 1 9 - 10 Appendicitis highly likely
N Nausea and Vomiting 1 7-8 Indicative of appendicitis
T Tenderness in the RIF 2 5–6 Appendicitis likely
R Rebound tenderness 1 <5 Appendicitis unlikely
E Elevated temperature/pyrexia 1 A score of greater than 6 in children makes the
L Leucocytosis > 10,000/mm2 1 possibility of appendicitis up to 100% likely
S Shift in WBC count to the right 2
Total 10

The Paediatric Appendicitis Scoring (PAS) Scoring


• Designed for use in children between the ages of 4 – 15 years.
• It is more or less a modified Alvarado or MANTRELS scoring
• It uses 8 variables (laboratory findings as well as signs and symptoms), to which a score is of 1 or 2 is given
to each variable, where they exist.
• Maximum score that can be accumulated is 10.
• Presence of anorexia, pyrexia, nausea or vomiting, leucocytosis and high neutrophils are given a score of
1 each
• Tenderness on coughing, hopping or percussing the abdomen is given a score of 2.
• So too is the presence of tenderness in the right lower abdominal region.
• A Paediatric Appendicitis Score of 6 and above is highly indicative of appendicitis in children
2.11 Investigations

1) Full Haemogram - mild elevation of WBCs (i.e. >12,000/mL) especially neutrophilia (values greater than
17,000 cells indicate complicated appendicitis)
2) Urinalysis
• Differentiating appendicitis from urinary tract conditions
i) Mild pyuria may occur in patients with appendicitis because of the relationship of the appendix with
the right ureter
ii) Haematuria in ureteric colic
iii) Glycosuria in Diabetic ketoacidosis
iv) Urobilinogen in acute porphyria
3) Urea and Electrolytes - Detect any deranged electrolytes, R/o Renal Pyelonephritis and colic
4) C-reactive protein and ESR – raised
5) Liver and pancreatic function tests (e.g., Transaminases, bilirubin, alkaline phosphatase, serum lipase,
amylase) R/o Acute pancreatitis and cholecystitis
6) Pregnancy test-in females of childbearing age
7) CT scan for peri- appendiceal abscess and wall of appendix. May be used in obese patients where
ultrasonography may be hampered
8) Diagnostic laparoscopy

2.12 Complications

1. Perforation (Risk factors for perforation - extremes of age, immunosuppression, diabetes mellitus, faecolith
obstruction of the appendix lumen, pelvic appendix - free-lying, previous abdominal surgery which limits
the ability of the greater omentum to wall off the spread of peritoneal contamination)
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2. Peritonitis with paralytic ileus
3. Incisional hernia
4. Abscess formation – intra abdominal, diaphragmatic, liver abscess
5. Toxaemia
6. Wound infection
7. Dehydration
8. Adhesions → intestinal obstruction
9. Faecal fistula
10. Portal pyaemia/pylophlebitis
11. Mucocele

3.0 COLITIS
What are the causes and features of colitis?

4.0 IDIOPATHIC CHRONIC INFLAMMATORY BOWEL DISEASE

4.1. ULCERATIVE COLITIS

• Is an ulcero-inflammatory disease limited to the colon and affecting only the mucosa and submucosa except
in severe cases
• It begins in the rectum, and in continuity extends upwards into the sigmoid colon, descending colon,
transverse colon and sometimes the entire colon

Aetiology
• Unknown

Pathology
• Involves the rectum and extends proximally in retrograde fashion to involve the entire rectum
• Mucosa - extensive ulceration; slight reddening; granularity with friability; easy bleeding
• Regeneration causes pseudopolys
• Colon may swell and become gangrenous (toxic megacolon)

Clinical Features
• Depends on activity of the disease process
• Relapsing disorder; attacks precipitated by stress
• Bloody mucoid diarrhoea, bleeding, lower abdominal pain (relieved by defecation), abdominal cramps,
constipation (paradoxically due to disruption of normal peristalsis)

Complications
1) Local - blood and fluid loss; Cancer; Perfection; Malabsorption; Perianal fistula; Stricture; Toxic megacolon
(fulminant colitis)
2) Systemic - erythema nodosum; Pyoderma gangrenosum; Iritis; Arthritis; Chronic liver disease; Ankylosing
spondylitis

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4.2. CHRON’S DISEASE

• Is a chronic idiopathic bowel disease characterized by transmural non-caseating granulomatous


inflammation commonly affecting terminal ileum and/or colon
• May involve the duodenum, stomach, oesophagus

Aetiology

• Unknown but associated with genetic factors, immunological factors and exogenous factors (microbial
factors, psychosocial factors, smoking and oral contraceptives)

Pathology
• Multiple well demarcated segmental bowel involvement with intervening uninvolved (skipped areas/lesions)
• Affected segment is thick and hard (hose pipe)
• Lumen markedly narrowed
• Focal mucosal ulcers resembling canker sores (aphthous ulcers), oedema, and loss of normal mucosal
texture
• Mucosal inflammation (transmural)

Clinical Features
• Mild diarrhoea, fever, abdominal pain, attacks precipitated by physical and emotional stress, occult or overt
faecal blood loss, anaemia

Complications

1) Intestinal - malabsorption; Fistula formation; Stricture formation; Development of malignancy


2) Extra intestinal - migratory polyarthritis; Sarcoilitis; Ankylosing spondylitis; Finger clubbing; Erythema
nodosum

Table 8.5: Comparison of Main Features of Chron’s Disease and Ulcerative Colitis
Feature Chron’s Disease Ulcerative Colitis
1. Characteristics • Chronic relapsing inflammatory • Chronic relapsing inflammatory condition
condition of unknown aetiology of unknown Aetiology
2. Presentation • Abdominal pain or obstruction • Bloody diarrhoea
3. Sites • Anywhere in the GI tract • Confined to large bowel
• Commonest in distal ileum then • May be localized to rectum or in
colon continuity with any length of the colon
4. Inflammation • Transmural, patchy often partly • Mucosal, diffuse, non-granulomatous
granulomatous
5. Complications • Malabsorption; Fistula formation; • Blood loss; Electrolyte disturbances;
Anal lesions; Malignancy Toxic dilatation; Malignancy; Extra-
(adenocarcinoma); Amyloidosis colonic complications
• Perforation

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5.0 COLORECTAL CANCER
Risk Factors

• Family history and genetics; Age; Diet – red meat; Inflammatory bowel disease - ulcerative colitis and
Chron’s disease; Obesity; Smoking; Alcohol; Type 2 diabetes mellitus
Features
• Change in bowel habits – diarrhoea, constipation, narrowing of the stool that lasts more than a few days
• Urge to open bowels but not relieved by doing so
• Rectal bleeding (bright red or dark blood), chronic pain, bloating and/or fullness, decreased appetite,
anaemia, ulceration or growth, fatigue and weight loss
Investigations
• Total Blood counts
• Endoscopy – Colonoscopy and sigmoidoscopy
• Faecal occult blood test
• Barium enema
• Biopsy
• Imaging - X-rays, CT or CAT scan, Ultrasound, MRI
• Position emission tomography (PET) scan

Spread
• Metastasis to the liver and peritoneum
Staging

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Lesson 10: DISORDERS OF THE ANO-RECTAL REGION
Learning Objectives

At the end of the lesson the learner will be able to: -


1) Describe the structure and function of the anus, rectum and peritoneum
2) Discuss the pathology of disorders of the anus, rectum and peritoneum
3) Investigate disorders of the anus, rectum and peritoneum

1.0 NORMAL STRUCTURE Describe the structure of the anus and rectum

2.0 ANAL DISORDERS

3.0 FISSURE IN ANO

Introduction and Definition


• An anal fissure or rectal fissure is a break, cut or tear in the skin of the anal canal
• Common condition of the anus and anal canal
• Affect men and women equally and both the young and the old
• Usually cause pain during bowel movements that often is severe
• Most common cause of rectal bleeding in infancy

Anatomy

• Anal fissures occur in the specialized tissue that lines the anus and anal canal called anoderm at a line just
inside the anus (anal verge or inter-sphincteric groove)
• Unlike skin, anoderm has no hairs, sweat glands, or sebaceous (oil) glands and contains a larger number
of somatic sensory nerves that sense light touch and pain
• Abundance of nerves explains why anal fissures are so painful
• Hairless, gland-less, extremely sensitive anoderm continues for the entire length of anal canal until it meets
the demarcating line for the rectum, called the dentate line
• Most common location is the midline posteriorly in the anal canal (part of the anus nearest the spine)
because of the configuration of the muscle that surrounds the anus
• When fissures occur in locations other than the midline posteriorly or anteriorly trauma is the likely cause
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Diagram 10.1: Anatomy of the Rectum and Anus

Predisposing factors
• Infancy; Aging; Constipation; Childbirth; Crohn's disease

Causes of anal fissures


Class Examples
Traumatic • Bowel movement; Hard stool/constipation; Repeated episodes of diarrhoea; Insertion of a
rectal thermometer, enema tip, endoscope, or ultrasound probe; During childbirth
Non- • Anal cancer; Crohn's disease; Leukaemia; Infection - TB, viral infections (CMV or herpes),
traumatic syphilis, gonorrhoea, chlamydia, Chancroid, and HIV

Pathophysiology
• Most anal fissures are caused by stretching of the anal mucosa beyond its capability
• Pathophysiology depends on the causes

Clinical features
• Pain, sometimes severe, during bowel movements; Itching or irritation around the anus; A visible crack in
the skin around the anus; A small lump or skin tag on the skin near the anal fissure; Rectal bleeding

Complications
1. Failure to heal – failure to heal within six weeks is considered chronic. Poor blood supply contributes to the
poor healing
2. Recurrence
3. A tear that extends to surrounding muscles

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4.0 ANAL FISTULA (FISTULA IN ANO)

4.1. Introduction

• Fistula is an abnormal passage from one epithelial surface to another epithelial surface
• Fistulas occur spontaneously or secondary to perirectal abscess.
• Most fistulas originate in the anal crypts at the anorectal juncture

4.2. Classification
• Inter-sphincteric
• Trans-sphincteric
• Supra-sphincteric
• Extra-sphincteric
Etiology
• Erosion of anal canal
• Extension from infection from a tear in lining in anal canal
• Infecting organism is commonly Escherichia coli
• Fistulas usually arise spontaneously or occur secondary to drainage of a perirectal abscess.
• Predisposing causes include Crohn's disease and TB.
• Most fistulas originate in the anorectal crypts; others may result from diverticulitis, tumors, or trauma.
• Fistulas in infants are congenital and are more common in boys.
• Rectovaginal fistulas may be secondary to Crohn's disease, obstetric injuries, radiotherapy, or malignancy.

Risk factors:
• Injection of internal hemorrhoids, puncture wound from eggshells or fish bones, foreign objects, enema tip
injuries
• Ruptured anal hematoma
• Prolapsed internal hemorrhoid
• Acute appendicitis, salpingitis, diverticulitis
• Inflammatory bowel disease (chronic ulcerative colitis, Crohn disease)
• Previous perirectal abscess
• Radiation treatment to perineum/pelvis
Signs and symptoms
• Constant or intermittent drainage or discharge
• Firm tender perianal lump
• External anal sphincter pain during and after defecation
• Spasm of external anal sphincter during and after defecation
• Anal bleeding
• Discoloration of skin surrounding the fistula
• Fistulous opening frequently granulose or scarred
• Possible fever
• A fistula is suggested by the presence of a small external opening outside the anal verge draining mucus,
pus, or fecal matter.
• A fistula is confirmed by the demonstration of an internal opening within the anal canal.
• A history of recurrent abscess followed by intermittent or constant discharge is usual.
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• On inspection, one or more secondary openings can be seen, and a cordlike tract can often be palpated
Diagnostic procedures
• Proctoscopy
• Sigmoidoscopy
• Probe inserted into tract to determine its course
• Injection of dilute methylene blue into abscess cavity may be helpful in demonstrating fistula
Differential diagnosis
• Pilonidal sinus
• Perianal abscess
• Urethroperineal fistulas
• Ischiorectal abscess
• Submucous or high muscular abscess
• Pelvirectal abscess (rare)
• Rule out: Crohn disease; carcinoma; retrorectal tumors

5.0 PRURITUS ANI


Definition
• Intense chronic itching in the anal and perianal skin. Usual course – acute
Aetiology

1) Dermatologic disorders
• Allergies (soap, topical anesthetics, oral antibiotics); Fistulas; Fissures; Neoplasms; Psoriasis;
Eczema; Seborrheic dermatitis; Contact dermatitis

2) Infections
• Pinworms and other worms; Scabies; Pediculosis; Candidiasis; Tinea

3) Other
• Poor hygiene (fecal material allowed to dry on the skin); Diabetes mellitus; Chronic liver disease;
Diarrheic alkalotic irritation; Trauma from scented toilet paper
Risk factors
• Overweight
• Hairy, tendency to perspire a great deal
• Anxiety-itch-anxiety cycle
Signs and symptoms
• Primary - rectal itching and anal erythema
• Secondary- secondary infections with yeast, fungus, and/or bacteria are possible after prolonged
scratching, anal itching, anal fissures, maceration, lichenification and excoriations
Laboratory
1) Glycosuria
2) Hyperglycemia
3) Skin scraping, yeast
4) Stool - ova plus parasites
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6.0 ANORECTAL ABSCESS

Definition
• Anorectal abscess is an abscess adjacent to the anus
• Arises from an infection at one of the anal sinuses and soft tissues surrounding the anal canal, with formation
of a discrete abscess cavity

Diagram 10.2: Anorectal Abscess

Causes
• Infection - Common organisms include Escherichia coli, Enterococcus species, and Bacteroides species

Pathophysiology
• Anal glands normally function to lubricate the anal canal
• Obstruction of anal crypts results in stasis of glandular secretions and when subsequently infected,
suppuration and abscess formation within the anal gland results
• Anal abscess arises from an infection at one of the anal sinuses which leads to inflammation and abscess
formation
• Pathological effects depend on the cause of the anal abscess
• Abscess typically forms in the intersphincteric space and can spread along various potential spaces.

Predisposing factors
• Anal sex; Chemotherapy drugs used to treat cancer; Diabetes; Inflammatory bowel disease (Crohn's
disease and ulcerative colitis); Use of medications such as prednisone; Weakened immune system (such
as from HIV/AIDS)

Clinical features
• Classic locations - perianal (60%), ischiorectal (20%), intersphincteric (5%), supralevator (4%), and
submucosal (1%)
• Clinical presentation correlates with the anatomic location of the abscess

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Abscess Description
1. Perianal • Dull perianal discomfort (exacerbated by movement and increased perineal
abscess pressure from sitting or defecation) and pruritus
• O/E - a small, erythematous, well-defined, fluctuant, subcutaneous mass near the
anal orifice
2. Ischiorectal • Systemic fevers, chills, and severe perirectal pain
abscess • Fullness consistent with the more advanced nature of this process
• External signs are minimal and may include erythema, induration, or fluctuancy
• Digital rectal examination (DRE), a fluctuant, indurated mass may be encountered
• Optimal physical assessment of an ischiorectal abscess may require anaesthesia
to alleviate patient discomfort that would otherwise limit the extent of the
examination
3. Intersphincteric • Rectal pain; Exhibit localized tenderness on DRE
abscess • Physical examination may fail to identify an intersphincteric abscess
4. Supralevator • Present a similar diagnostic challenge
abscesses • As a result, clinical suspicion of an intersphincteric or supralevator abscess may
require confirmation through computed tomography (CT) scanning, magnetic
resonance imaging (MRI), or anal ultrasonography. Use of the last modality is
limited to confirming the presence of an intersphincteric abscess.

Investigations
1. Pelvic CT scan,
2. MRI or trans-rectal ultrasound

Differential Diagnosis
• Tuberculosis; Squamous cell carcinoma; Adenocarcinoma; Actinomycosis; lymphogranuloma venereum;
Crohn's disease; Trauma; Leukaemia; Lymphoma

Complications
• Anal fistula; Body-wide infection (sepsis); Fibrosis/scarring; Stricture; Anal incontinence; Recurrence

7.0 HAEMORRHOIDS
See: Cardiovascular System
See CVS unit Pathology

8.0 RECTAL PROLAPSE

8.1. Neoplasms

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Lesson 11: THE PERITONEUM
1.0 NORMAL STRUCTURE

• Peritoneum is the thin serous membrane that lines the walls of the abdominal and pelvic cavities and covers
the abdominal and pelvic viscera
• Largest serous membrane of human body and has a rather complex arrangement
• Possesses a certain degree of mobility on the extra peritoneal fat and can be stretched to certain degree
without tearing
• Composed of layer of mesothelium supported by a thin layer of connective tissue
• Has two parts
i) Parietal peritoneum (portion that lines the abdominal and pelvic cavities)
ii) Visceral peritoneum (covers the external surfaces of most abdominal organs, including the intestinal
tract).

Diagram 11.1: Structure of the Peritoneum

Extra peritoneal tissue

• Connective tissue layer between the parietal peritoneum and the fascia lining of the abdominal and pelvic
walls

Peritoneal Cavity

• Potential space between the parietal peritoneum and visceral peritoneum


• Largest cavity of human body with an enormous surface area
• Contains a small amount of serous fluid, but is otherwise empty
• Fluid lubricates the visceral peritoneum and allows the mobile viscera to glide freely on the abdominal wall
and each other within the limits dictated by their attachments.
• Entire peritoneal cavity can be divided into two parts
i) Greater Sac - main compartment, extends from the diaphragm down into the pelvis
ii) Lesser Sac – smaller compartment that lies behind the stomach. It is in free communication with the
greater sac through an oval window called the opening of the lesser sac

Abdominal structures in relation to peritoneum


i) Intraperitoneal organs
• Stomach, first part of duodenum, jejunum, ileum, cecum, appendix, transverse colon, sigmoid colon,
upper 1/3 of rectum, liver, spleen, uterus (females), Fallopian tubes (Females), ovaries (Females)
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ii) Retroperitoneal Organs
• Lie behind the peritoneum and are only partially covered with visceral peritoneum
• Include second and third parts of duodenum, ascending colon, descending colon, middle 1/3 of
Rectum, pancreas, kidneys, adrenal glands, proximal ureters, renal vessels, gonadal blood vessels,
inferior vena cave and aorta
iii) Infraperitoneal organs
• Lie inferior to the peritoneum in the pelvis and include the lower 1/3 of rectum, urinary bladder and
distal ureters

Peritoneal ligaments, omenta and mesenteries


i) Ligaments - falciform, coronary ligament, and Rt and Lt triangular ligaments
ii) Omenta
a. Greater omentum - connects greater curvature of stomach to transverse colon
b. Lesser omentum - suspends the lesser curvature of the stomach from the fissure of the ligamentum
venosum (fibrous remnant of the ductus venosus of foetal circulation) and porta hepatis
c. Gastrosplenic omentum - connects the stomach to the hilum of spleen
iii) Mesenteries - are two layered folds of peritoneum, which connect the parts of the intestine to the
posterior abdominal wall

Peritoneal pouches, recesses, and gutters

• Peritoneum is a highly-folded membrane resulting in formation of lots of pouches, recesses and gutters
• Some of the important of them are listed below:
i) Pouches - lesser sac and greater sac
ii) Recesses - duodenal recesses, ceacal recesses, intersigmoid recesses
iii) Spaces - subphrenic spaces
iv) Gutters - paracolic gutters

2.0 FUNCTIONS OF PERITONEUM

1) Ensures that the mobile viscera glide easily on one another


2) Seals off intraperitoneal infections localizing them
3) Suspend various organs within the abdominal cavity
4) Means of conveying blood vessels, lymphatics, and nerves to these organs

3.0 DISORDERS OF THE PERITONEUM

3.1. ASCITES

Introduction

• Ascites is the accumulation of excessive volume of fluid within the peritoneal cavity (Askitis is Greek word
meaning fluid filled bag)
• Occurs mainly due to a combination of portal hypertension and hepatocellular failure
• Usually associated with haemodilution, oedema and decreased urine output
• Presence of neutrophils suggests secondary infection and RBCs in ascitic fluid points to disseminated intra-
abdominal cancer

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Causes

1) Venous hypertension (congestion) –e.g.


• portal hypertension, cirrhosis, congestive cardiac failure (CCF), Constrictive pericarditis, Hepatic
venous outflow, obstruction (Budd-Chiarri syndrome/Veno-occlusive and portal vein block
2) Hypoalbuminaemia – Liver disease, Nephrotic syndrome, malnutrition, protein losing enteropathy
3) Malignant disease - secondary carcinomas, Lymphomas and leukaemia
4) Infections - TB peritonitis; fungal – candida, Cryptococcus; parasitic – strongyloides and entamoeba
5) Miscellaneous - Pancreatitis, Meig’s syndrome (ovarian tumour), Myxoedema, Systemic lupus
erythromatosus

Classification
Class Description Causes
Transudate • Ascites protein concentration Cirrhosis, portal hypertension, IVC or portal vein
ascites of < 25g/L thrombosis, portal nodes, RHF, hypoproteinaemia
• Serum ascites albumin (nephrotic syndrome, PLE, malnutrition), myxoedema,
gradient - >1.1 CCF pericarditis
Exudative • Ascites protein concentration - Malignancy (any intra-abdominal organ e.g. colon,
ascites > 25g/L stomach, pancreas, liver, kidney), infections especially
• Serum ascites albumin TB, pancreatitis, Budd-Chiari syndrome and
gradient - < 1.1 hypothyroidism

Pathogenesis
i) Under filling theory - compensatory renal retention of sodium and water secondary to splanchnic
vasodilatation.
ii) Overflow theory - primary retention of sodium and water

Diagram 10.2: Pathophysiology of Ascites

Cirrhosis

PROTEINS
Portal HTN Portal vein thrombosis Low serum albumin

LOW
Infection (acute or Hepatoma ; Malignant
chronic e.g. TB) tumours ; Benign tumours
ASCITES (ovary)

Cardiac failure
PROTEINS

Pancreatitis
HIGH

Constrictive pericarditis
Hepatic vein
obstruction
Pathophysiology IVC obstruction

i) Sinusoidal Hypertension
• Sinusoidal hypertension e.g. portal hypertension alters Starling’s forces which drives the fluid into the
space of Disse

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• Local HP exerted and there is increased hepatic and splanchnic production of lymph and transudation
into peritoneal cavity
• Fluid not adequately removed by hepatic lymphatics thus accumulates in the cavity

ii) Hypoalbuminaemia
• Reduced OP favours fluid exudation into the cavities and allows exudation of fluid into the peritoneum
across the osmotic gradient established.

iii) Percolation of Fluid


• Percolation of hepatic lymph into the peritoneal cavity occurs when normal flow of 800 – 1000 mls/day
is altered as seen in cirrhosis (20L/day) or there is distortion and obstruction of hepatic sinusoids
• Hepatic lymph is rich in proteins.

iv) Renal Sodium/water retention


• Sodium is retained due to impaired renal functional renal (inability to excrete sodium)
• Reduced effective systemic blood volume due to splanchnic pooling of blood triggers mechanisms
that enhance retention of fluid in the body.
• Ischemia activates the RAA system that facilitates retention of fluid in the body.
• Renal sympathetic system increases proximal convoluted tubules reabsorption of sodium and fluids.
• Increased plasma norepinephrine
• Increased ADH (AVP) due to failure of inhibition of vasopressin by prostaglandin E (from the collecting
ducts).

Signs
• When ascites fluid is < 1L abdominal distension and fullness in the flanks with distortion or eversion of the
umbilicus
• Hernia
• Abdominal striae
• Divarication/diastasis of the recti (separation of rectus abdominis muscles away from the midline)
• Meralgia paraethetica – tingling, formication, itching and other forms of paraesthesia in the outer side of
the lower part of the thigh in the area of distribution of the femoral cutaneous nerve
• Scrotal oedema
• Right sided pleural effusion (10%)

Methods of Detection of Ascites


1. Ultrasound
2. CAT
3. Diagnostic aspiration
4. Physical examination
a. Abdominal distension – bulging flanks that are dull to percussion with the umbilical region hyper-
resonant (due to floating bowel)
b. Fluid thrill
c. Shifting dullness
d. Positive Puddle sign

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Staging of Ascites

Stage I Ascites demonstrable by ultrasonography


Stage II Ascites demonstrable by a fluid wave (fluid thrill)
Stage III Marked distension, spider nevi, caput medusae and emaciation
Stage IV Tense, painful distension with marked wasting

OR
Stage 1 Fluid < 500 ml of ascites fluid, splashy, floppy abdomen with fullness in flanks
Stage 2 Fluid > 500 - 5000 ml, “U” shaped, dull percussion note and shifting dullness
Stage 3 Fluid more than 5000 ml, tense abdomen with a fluid thrill

Investigations
1. Ascitic tap (paracentesis – for microscopy, protein level); Ascitic neutrophils > 250/mm3 indicates
spontaneous bacterial peritonitis
2. Abdominal U/S
3. Laparoscopy
4. Liver function tests
5. Abdominal x-rays
6. CT scan

3.2. PERITONITIS

Definition and Introduction

• Peritonitis is the inflammation of the serosal membrane that lines the abdominal cavity and the organs
contained therein
• Peritoneal infections are classified as
o Primary (i.e., from haematogenous dissemination,
o Secondary (i.e., related to a pathologic process in a visceral organ, such as perforation or trauma,
including iatrogenic trauma)
o Tertiary (i.e., persistent or recurrent infection after adequate initial therapy)
• Primary peritonitis is most often spontaneous bacterial peritonitis (SBP) caused by chronic liver disease
• Infections in the peritoneum are further divided into generalized (peritonitis) and localized (intra-abdominal
abscess)

Risk Factors
• Peritoneal dialysis
• Medical conditions - cirrhosis, appendicitis, Crohn's disease, stomach ulcers, diverticulitis and pancreatitis.

Causes
• Depends on the type, as well as location, of peritonitis
1) Primary peritonitis - most common pathogens include Gram-negative (E coli, K pneumoniae,
Pseudomonas spp, Proteus spp, and Gram-positive (Streptococcus pneumoniae, Strep spp;
Staphylococcus sp
2) Secondary peritonitis - cirrhosis, pancreatitis, trauma, peptic ulcer
3) Tertiary peritonitis - immunosuppression

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4) Chemical peritonitis - may be caused by irritants such as bile, blood, barium, or other substances or
by transmural inflammation of visceral organs (e.g., Crohn’s disease) without bacterial inoculation of
the peritoneal cavity
5) Peritoneal abscess

Pathophysiology

• Infection, intra-abdominal sepsis, spillage of the contents trigger an inflammatory process


• Endotoxins produced by gram-negative bacteria lead to the release of cytokines that induce cellular and
humoral cascades, resulting in cellular damage, septic shock, and multiple organ dysfunction syndrome
(MODS)
• Peritonitis causes fluid to shift into the peritoneal cavity and bowel leading to severe dehydration and
electrolyte imbalance
• Adult respiratory distress syndrome can develop rapidly
• Renal failure, liver failure and DIC follow

Pathology
Macroscopy • Dull appearance
• Initially scarce serous fluid or slightly turbid fluid later on, the exudate becomes creamy
and evidently suppurative
• May be spread to the whole peritoneum, or be walled off by the omentum and viscera
Microscopy • Infiltration by neutrophils with fibrino-purulent exudation

Features
• Poor appetite and nausea
• Acute dull abdominal pain (that quickly turns into persistent, severe abdominal pain, worsened by any
movement), tenderness, and guarding, which are exacerbated by moving the peritoneum, e.g., coughing
(forced cough may be used as a test), flexing one's hips, or eliciting the Blumberg sign (rebound
tenderness)
• Chills and fever
• Fluid in the abdomen
• Extreme thirst
• Not passing any urine, or passing significantly less urine than usual
• Difficulty passing gas or having a bowel movement
• Vomiting
• Sinus tachycardia
• Development of ileus paralyticus (i.e., intestinal paralysis)

Investigations
1) Urinalysis
2) Imaging studies such as X-rays and computerized tomography (CT) scans
3) Exploratory surgery
4) Paracentesis
5) Total blood counts

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Complications
1. The complications of spontaneous peritonitis - hepatic encephalopathy; Hepato-renal syndrome; Sepsis
2. Complications of secondary peritonitis an abscess; Gangrenous bowel; Intraperitoneal adhesions; Septic
shock

3.3 PERITONEAL CANCER

• Peritoneal cancer is a rare cancer


• It develops in peritoneal cavity

Risks of Peritoneal Cancer


• Primary peritoneal cancer is more common in women than in men.
• BRCA1 and BRCA2 genetic mutations.
• Older age

Pathophysiology

• Occurs through
i) Dissemination from the primary tumor
ii) Primary tumor of peritoneum
iii) Independent origins of the primary tumor and peritoneal implants

Peritoneal Cancer Symptoms


• Abdominal discomfort or pain from gas, indigestion, pressure, swelling, bloating, or cramps
• Feeling of fullness, even after a light meal, nausea or diarrhea, constipation, frequent urination
• Loss of appetite
• Unexplained weight gain or loss
• Abnormal vaginal bleeding
• Rectal bleeding
• Shortness of breath

Investigation
1) Ultrasound - high-frequency sound waves produce a sonogram
2) CA-125 blood test
• Measures levels of a chemical in the blood called CA-125
• If levels are high, peritoneal or ovarian cancer is more likely present (can be high for other reasons)

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