Pathology – Session 27 Pathological basis of GIT diseases

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Lecture Notes

Session 27: Pathological basis of GIT diseases

Felician Sikujua (MD)

Learning tasks

At the end of this session, students are expected to be able to:

Explain gastrointestinal tract immune system.

Explain gastrointestinal pathologies.

Explain gastrointestinal bleeding.

Describe disorders of gastrointestinal motility.

Explain features of gastrointestinal pathologies.

Explain functional gastrointestinal disorders.

Gastrointestinal immune system

The system incorporates a number of defense mechanisms, which include prominent aggregations of lymphoid tissue, known as the gut-associated lymphoid system (GALT).

Distributed throughout the tract.

Gastrointestinal tract immune system consists of

Luminal and epithelial barrier defences.

Cellular components such as T and B cells.

Non-cellular inflammatory mediators.

The GI immune system plays a role in systemic autoimmune disorders and immune tolerance.

Gastrointestinal immune system cont…

The enteric nervous system, which is composed of a complex array of neurons and ganglia organized around the myenteric (auerbach) and submucosal (meissner) plexus.

Although it is an independent nervous system, complex interactions with the autonomic and central nervous systems are necessary for normal function.

Abnormal interactions among the enteric, autonomic, and central nervous systems in the development and continuation of symptoms in functional bowel disorders such as irritable bowel syndrome.

Presenting features of Gastrointestinal pathologies

Abdominal pain.

GI bleeding.

Diarrhoea.

Steatorrhea.

Constipation.

Nausea and vomiting.

Dysphagia.

Odynophagia.

Gastroesophageal reflux.

Anorexia.

Weight loss.

Abdominal pain

Complex interaction of sensory neuroreceptors in the abdominal organs and transmission of these impulses through autonomic nervous system.

Abdominal pain originates from

Tissue injury.

Distention.

Contraction.

Inflammation.

Direct chemical injury.

Types of abdominal pain according to localization

Visceral pain.

Somatoparietal pain.

Referred pain.

Refer to Handout 27.1 for additional information on types of abdominal pain according to localization.

Acute abdominal pain(Acute abdomen)

Acute pain in the abdomen is usually due to the following mechanisms

Luminal obstruction.

e.g. Intestinal obstruction).

Inﬂammation.

e.g. Appendicitis, cholecystitis, pancreatitis etc.).

Perforation.

e.g. Rupture of viscus/ visceral organs causing peritonitis).

Volvulus or torsion.

Intestinal ischemia.

Causes of acute abdominal pain (Acute abdomen)

Peptic ulcer disease.

Acute pancreatitis.

Acute cholecystitis.

Acute appendicitis.

Acute hepatitis.

Acute pyelonephritis.

Diverticulitis.

Intestinal obstruction.

Strangulated hernia.

Intestinal ischemia.

Gastroesophageal reflux disease (GERD).

Rupture viscus (visceral organs) and peritonitis

Ruptured appendix.

Ruptured ectopic pregnancy.

Ruptured abdominal aortic aneurysm.

Ruptured ovarian cyst.

Abdominal abscess.

Ovarian cyst/ ovarian torsion.

Causes of chronic (or recurrent) abdominal pain

Inflammatory or infectious enterocolitis.

Chronic pancreatitis.

Irritable bowel syndrome.

Nonulcer dyspepsia.

Abdominal malignancy.

Gastrointestinal bleeding

GI bleeding can be

Acute or chronic.

Massive or occult.

Acute GI bleeding implies a temporally circumscribed event that occurred in the past 24 to 48 hours .

Hemodynamic instability may result depending on quantity and rapidity of bleeding also with patient’s cardiovascular status.

Gastrointestinal bleeding cont…

GI bleeding may be classified due to location of bleeding

Upper GI bleeding.

Proximal to (above) ligament of treitz.

Lower GI bleeding.

Distal to (below) the ileocecal valve.

Middle GI bleeding.

In between upper and lower.

Upper gastrointestinal bleeding

It may present/manifest as

Hematemesis.

Vomiting blood/coffee ground vomiting.

Melena.

Passing black tarry stool.

Hematochezia.

Passing fresh blood in the stool.

May be divided into

Variceal bleeding e.g. in Esophageal varices

Non variceal bleeding e.g. in PUD, Mallory-Weiss tear.

Middle gastrointestinal bleeding

Acute GI bleeding from the small intestine (middle GI bleeding) distal to the duodenum is rare.

Lower gastrointestinal bleeding

Small intestine causes

Intussusception.

Ischemic bowel diseases.

Crohn disease.

Meckel diverticulum.

Colorectal causes

Diverticulosis.

Internal hemorrhoids.

Ischemic colitis.

Rectal ulcers.

Polyp/cancer.

Post- polypectomy ulcer.

Other colitis.

Tumors.

Chronic gastrointestinal bleeding

It presents/manifests as

Hemoccult-positive stools.

Anaemia (Iron deficiency).

Causes

Malignancy of the GI tract (most worrisome).

Inflammatory bowel diseases (Crohn’s disease and Ulcerative colitis).

Hemorrhoids.

Diarrhoea

An increased number or fluidity of stools.

Classification

According to content (i.e. watery or blood diarrhea).

According to duration (i.e. acute or persistent).

According to severity (i.e. No dehydration, some dehydration and severe dehydration).

It may be acute (e.g. due to viral gastroenteritis) or chronic (e.g. in malabsorption).

Diarrhoea cont…

Can result from increase in secretion of water into lumen or decreased absorption or both.

Osmotic diarrhoea ceases when patient takes nil per oral while secretory diarrhea continues.

Large volume diarrhoea generally originates from the small intestine.

Small volume diarrhoea generally originates from the colon.

Bloody diarrhoea (dysentery ) occurs with mucosal inflammation or erosions or ulcerations secondary to infectious, inflammatory, or ischemic enterocolitis.

Steatorrhoea

Fatty stools that arises from disruption of fat solubilisation, digestion, or absorption in the small intestine.

Maldigestion or inadequate luminal breakdown of fats occurs with pancreatic exocrine deficiency or lack of bile.

Malabsorption, occurs with mucosal diseases such as celiac sprue or during impaired lymphatic transport.

Constipation

Commonly in the elderly.

It is often used to describe more than one symptom including

Infrequent stools.

Difficult passage of stool.

A sense of incomplete evacuation.

Abdominal bloating or discomfort.

Constipation cont…

Causes include

Inadequate stool water or faecal material.

Decreased colonic motility.

Reduced mobility.

Chronic illness.

Medication use.

Psychological factors.

Functional outlet obstruction.

Treatment plans vary, starting point is to increase the patient's daily fibres and fluid intake.

Nausea and Vomiting

Nausea is the unpleasant sensation of the desire to vomit.

Vomiting is a forcefully ejecting gastric content out of the mouth.

Nausea and vomiting may lead to

Fluid and electrolyte imbalances.

Nutritional deficiencies.

Aspiration pneumonia.

Oesophageal rupture.

Causes of nausea and vomiting

Acute causes

Acute obstruction.

Inflammation.

Ischemia.

Acute infections.

Medications,

Pregnancy.

Head trauma.

Chronic causes

Pregnancy.

Medications.

Motility disorders e.g. diabetic gastroparesis, partial obstruction.

Intracranial diseases.

Psychogenic disorders.

Metabolic or endocrine disturbance.

Dysphagia

It is a difficult in swallowing.

The sensation of solids or liquids not passing from the mouth to the stomach, is a common symptom.

There are two (2) types of dysphagia

Oropharyngeal dysphagia.

Oesophageal dysphagia.

Oropharyngeal dysphagia

Oropharyngeal dysphagia may be caused by

Neuromuscular diseases to structures involved in swallowing.

Mechanical obstruction to structures involved in swallowing.

Skeletal muscle disorders to structures involved in swallowing.

Depression.

Dementia.

Patients are unable to propel their food from the hypopharynx into the upper esophagus.

Coughing or aspiration during meals indicates that food has passed into the tracheobronchial tree.

Oesophageal dysphagia

Oesophageal dysphagia is caused by

A motility disorder such as achalasia.

Diffuse oesophageal spasm.

Scleroderma.

Mechanical esophageal obstruction such as

Benign stricture.

Oesophageal ring.

Oesophageal neoplasm.

Odynophagia

Odynophagia is pain during swallowing.

It reflects oesophageal mucosal inflammation secondary to

Infectious causes.

Pill-induced oesophagitis.

Irradiation.

Ingestion of caustic substances.

Gastroesophageal reflux disease (GERD)

GERD is a sensory-motor disorder develops when acidic gastric contents reflux into the oesophagus and remain there long enough to overcome the resistance of the oesophageal epithelium.

Patients with GERD fall into three (3) categories

Nonerosive reﬂux disease (NERD).

Erosive esophagitis.

Barrett’s esophagus.

Extra-oesophageal manifestations of GERD include laryngitis, asthma, and chronic cough.

Anorexia

Anorexia is loss of the desire to eat.

Anorexia may be

Acute ( e.g. in inflammatory GI processes).

Chronic (e.g. in depression, malignancy) causing weight loss.

Anorexia must be distinguished from the fear of eating because of associated discomfort.

The underlying mechanism of anorexia is complex

It includes endocrine and neural regulation in the GIT and hypothalamus, peptides (e.g. cholecystokinin), and cytokines (e.g. tumour necrosis factor).

Early satiety

Sensation of early gratification of appetite such that individual consumes less than caloric requirements.

Early satiety may be acute or chronic, but it is usually insidious in onset.

Common causes include

Delayed gastric emptying such as occurs in long-term diabetes mellitus.

Decreased gastric distention secondary to gastric malignancy.

Gastric outlet obstruction caused by peptic ulcer disease.

Patients not hungry at meal time, must often ‘force’ to eat, yet still eat far less than they had in the past.

Weight loss

May be 'physiological' due to dieting, exercise, starvation.

Alternatively, weight loss may signify disease.

Loss of more than 3 kg over 6 months is significant.

Pathological weight loss can be due to

Psychiatric illness e.g. Eating & mood disorders,

Systemic disease e.g. Chronic infections: HIV, TB.

Gastrointestinal causes e.g. Dysphagia, Malignancy, Malabsorption.

Advanced disease of any specific organ system.

Disorders of gastrointestinal motility

Motility disorders result from impaired control of the neuromuscular apparatus of the gastrointestinal tract i.e. neuropathies and myopathies.

Combined disorders (neuropathies and myopathies) occur in systemic sclerosis, amyloidosis and mitochondrial cytopathy.

Symptoms

Recurrent or chronic nausea and vomiting.

Bloating and abdominal discomfort.

Constipation or diarrhoea in the absence of intestinal obstruction.

Causes of disorders of gastrointestinal motility

Genetic defects that result in congenital dysmotilities e.g. Hirschsprung's disease.

Spinal cord injury above the level of the sacral segments.

Extrinsic neuropathic processes such as trauma.

Damage to the autonomic nerves by trauma, infection, neuropathy and neurodegeneration.

Disorders of the enteric nervous system.

Refer to Handout 27.2 for additional information on causes of disorders of gastrointestinal motility.

Functional gastrointestinal disorders

Disorders in which signiﬁcant GIT symptoms are not associated with organic disease.

Chronic or recurrent gastrointestinal symptoms without a structural or biochemical explanation identified by routine diagnostic tests.

It does not imply a psychiatric disturbance or absence of disease but rather a known or suspected underlying disorder of gut function.

Functional gastrointestinal disorders cont…

Examples of functional GI disorders are

Irritable bowel syndrome (IBS).

Functional (or non-ulcer) dyspepsia.

Functional (or non-cardiac) chest pain.

Functional abdominal pain syndrome.

Functional feacal incontinence.

Irritable Bowel Syndrome (IBS)

Characterized by chronic or recurrent abdominal pain or discomfort and an erratic disturbance in defecation.

Bloating is also common.

Basal colonic motility is normal in IBS.

Abnormally responsive colon to meals, drugs, gut hormones (e.g. cholecystokinin) and stress.

The motility of the distal end of the colon after meals (the gastrocolonic response) is augmented.

This may explain why postprandial cramps or discomfort is common.

Functional (or non ulcer) dyspepsia

Deﬁned as presence of early satiation, post-prandial fullness or epigastric pain or burning, in the absence of organic disease that readily explains the symptoms.

A link between Helicobacter pylori and functional dyspepsia has been established.

Chronic use of coffee, aspirin and other NSAIDs cause functional dyspepsia.

Smoking and alcohol are not important risk factors for functional dyspepsia.

The prevalence of gastric motility disturbances in patients with functional dyspepsia.

Functional (or non ulcer) dyspepsia cont…

Patients with functional dyspepsia may have a stiff fundus that does not relax postprandially.

Cause fullness and an inability to finish a normal meal (early satiation).

Patients with functional dyspepsia are more anxious and depressed.

Acute stress may result in decreased gastric contractility.

Functional dyspepsia can be subdivided into

Ulcer-like dyspepsia.

Dysmotility-like dyspepsia.

Reflux-like dyspepsia.

Key points

GIT immune system comprise of luminal and epithelial barriers, T and B cells and inflammatory mediators.

Abdominal pain originates from tissue injury, distention, contraction, inflammation, and direct chemical injury.

Chronic GI bleeding manifests as hemoccult stool and anemia .

Motility disorders result from impaired control of the neuromuscular apparatus of the GIT.

In functional GIT disorders, most patients will have no structural cause for their symptoms.

Review questions

How does acute gastrointestinal bleeding presents?

What is steatorrhoea?

Explain four (4) causes of pathological weight loss.

What is functional dyspepsia?

List five (5) causes of disorders of gastrointestinal motility.

References

Boon N. A. ; Colledge N. R; Walker B. R..;(2006): Davidson’s Principles and Practice of Medicine (20th Ed.) Churchill Livingstone, USA. Pg. 864-876.

Hawkey C. J.; Bosch J.; Richter J. E. et al. ;(2012): Textbook of Clinical Gastroenterology and Hepatology (2nd Ed.) Blackwell Publishing Ltd, USA. 3-132.

Chew R.;(2012): Crash Course Gastroenterology (3rd Ed.) Elsevier Saunders, USA. Pg. 151-158.

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