Git Pathology 2017
Git Pathology 2017
Git Pathology 2017
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
• 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
i) Intrinsic Innervation
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)
• 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
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)
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.
1.5 Physiology
• 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.
• 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
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• 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
• 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
• 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) Isotonic dehydration
2) Hypertonic (hypernatraemic) dehydration
3) Hypotonic (hyponatraemic) dehydration
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
3) Other features
• Dyspepsia; pain and discomfort; abdominal swelling; constipation; obstipation; dysphagia;
odynophagia; haematemesis; belching; malena stools; haematochazia
• 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.
4.0 OROPHARYNX
• The oesophagus produces limited symptoms of disease because of its simplicity in function. The common
complains include heart burn, dysphagia, odynophagia and hematemesis.
1. Agenesis
• Congenital absence of the oesophagus
• Rare and incompatible with life
4. Duplication of Oesophagus
• The is a double oesophagus
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
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
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
Introduction
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)
1.10 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
• 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)
Clinical Features
• Bleeding (upper GIT); Haematemesis
• 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
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
• Follows a number of opportunistic infections such as Candidiasis, Herpes, CMV and tuberculosis. This
occurs mainly when there is some defect in mucosal resistance
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
• 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
9.4. 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
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 •
• 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
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
• 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.
Clinical Features
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
3.1. 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)
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
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
• 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
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
• Comprises more than 90% of all gastric malignancies and leading cause of cancer related deaths
• 2nd commonest tumour
Mechanisms
• Metaplasia
• Dysplasia
Classification
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
• 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
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)
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.
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.
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
6.0 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
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
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
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)
• 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
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
4.0 Investigations
• 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.
Jejunoileal atresia
Features
• Vomit green bile within the first 24 hours of life
• Distended abdomen
• Reduced bowel movement
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2.2. MECKEL’S DIVERTICULUM
Features
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)
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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
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
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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
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
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
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Lesson 8: HERNIAS AND INTESTINAL OBSTRUCTION
Learning Objectives
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
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3.0 PREDISPOSITION
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
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
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
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
Diagnosis
1. Medical history
2. Physical examination of the groin.
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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
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4) Umbilical 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
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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
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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)
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
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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
8.0 DIAGNOSIS
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Lesson 9: DISORDERS OF THE LARGE INTESTINES
Learning Objectives
• 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).
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.
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
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
2.9 Staging
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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
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?
• 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
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
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
1.0 NORMAL STRUCTURE Describe the structure of the anus and rectum
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
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
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
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
8.1. 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).
• Connective tissue layer between the parietal peritoneum and the fascia lining of the abdominal and pelvic
walls
Peritoneal Cavity
• 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
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
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
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.
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%)
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Staging of Ascites
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
• 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
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
Pathophysiology
• Occurs through
i) Dissemination from the primary tumor
ii) Primary tumor of peritoneum
iii) Independent origins of the primary tumor and peritoneal implants
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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