CPP 301

DISORDERS OF THE GASTRINTESTINAL TRACT

(GIT)
 DISORDERS OF THE GASTRINTESTINAL TRACT (GIT)
•The GIT consists of the stomach and the intestine

•The stomach is continuous with the esophagus at the cardiac orifice and the duodenum
at the pyloric sphincter.

•The intestine extends from the duodenum to the rectum.

•The major diseases affecting the GIT are those of ulceration and inflammation all of
which affect the integrity of the walls or thickness of the stomach or intestine.

•Diseases of the stomach include:

•Gastritis Peptic ulcer, appendicitis, inflammatory bowel disease,

• Others are tumors, Diverticular disease, intussusception hernia

 GASTRITIS
This is a disease condition due to an imbalance between the corrosive action
of gastric juice and the protective effect of mucus on the gastric mucosa.

•Gastritis occurs when the amount of mucus in the stomach is insufficient to

protect the surface epithelium from the destructive effect of hydrochloric acid
(HCL). Gastritis is caused by:

a) Prolong regular use of aspirin

b) Excessive alcohol consumption
c) Food poisoning eg caused by Staph. Aureus, S. paratyphi and viruses
d) Heavy cigarrete smoking
 GASTRITIS

a) Treatment with cytotoxic drugs

b) Ingestion of corrosive poisons, acids and alkalis
c) Regurgitation of bile into the stomach

•Acute haemorhagic gastritis is the most severe form. Destruction of

surface epithelium of stomach ---> exposure to gastric juice (HCL) 
cells absorb hydrogen ions  increased internal acidity  disruption in
metabolic activity  inflammatory reactions
 PEPTIC ULCER DISEASE

•This is a group of disorders characterized by ulceration of the upper gastrointestinal

(GIT) mucosa

• Autodigestion by the acid-pepsin complex underlies the main pathogenesis of these

disorders

• The autodigestion is caused by disruption of the normal balance of the corrosive effect
of gastric juice and the protective effect of mucus on the gastric epithelial cells

•The most common sites are the stomach and the first few centimetres of the duodenum

•In some cases, the ulcer penetrates into blood vessels leading to hemorrhage or
completely through the gut wall into adjacent organs or as a free perforation into the
peritoneal cavity
 PEPTIC ULCER DISEASE

•Chronic use of corticosteroids, alcohol, coffee, NSAIDs predisposes to PUD

by virtue of their ability to alter the characteristics of gastric mucus, interfere
with epithelial cell replication or increase gastric secretion
•All peptic ulceration occurs at any level of the GIT due to imbalance between
the aggressive action of acid-pepsin secretion and the normal defense of the
gastroduodenal mucosa
•Another implicating factor is Helicobacter pylori (a G-ve commensal bacteria)
which attaches to the surface epithelium beneath the mucus and promotes
back-diffusion of proton (H+) to increase HCL production and secretion.
 PEPTIC ULCER DISEASE

Pathogenesis

•Gastric secretion occurs in phases and is mediated by +ve and -Ve feedback stimuli:

•Cephalic phase – sight, smell, thought and smell of food and is a vagal response mediated by
Ach.

•Gastric phase – presence of food or chemical substances in the food  gastrin release 
histamine release acid and pepsinogen secretion acid converts pepsinogen to pepsin  acid-
pepsinogen complex which is proteolytic on food and is responsible for the autodigestion.

•Intestinal phase – stimulated by presence of Chyme in the small intestine

•Major secretion here is enterogastrone which decreases acid-pepsinogen release by a -Ve

feedback mechanism when the PH in the small intestine is too low.
 PEPTIC ULCER DISEASE

Normal protective mechanism

•The proteolytic effect of acid-pepsin complex on the surface epithelial cells is

prevented by some protective mechanisms such as:

i. Secretion of mucus
ii. Enterogastrone
iii.Bicarbonate secretion to buffer and decrease acidity
iv.Rapid regeneration of mucosal cells to replace damaged ones
v. Rapid blood flow which quickly removes erosive substances
PEPTIC ULCER DISEASE

• When the protective mechanisms are defective, acid-pepsin complex

gains access to gastric epithelium causing the initial cell damage that
leads to ulceration
• When the defect is chronic and not treated immediately could cause
massive mucosal erosion ranging from hyperemia and hemorrhage to
deep ulceration and perforation from the fundus of the stomach to the
duodenum
 PEPTIC ULCER DISEASE

•Defective protective mechanism could arise due to:

- Reduced blood flow and ischaemia caused by: stress (physical and mental)
- Excessive cigarette smoking
- Altered composition and quantity of mucus production due to regular
prolonged administration of aspirin and NSAIDs
- Defective epithelial cell replacement due to: - a) increased steroids levels used
as drugs or as a response to stress b) chronic gastritis c) irradiation therapy and
use of cytotoxic drugs
 PEPTIC ULCER DISEASE

a) DUODENAL ULCER

•In duodenal ulcer, the major causal influence appears to be exposure of the duodenal
mucosa to excessive amount of acid-pepsin complex.

•Onset is usually associated with hypersecretion of acid due to:

- Increased parietal cell mass increased acid production

- Increased vagal and hormonal drive to secret acid
- Increased gastric emptying – not allowing sufficient buffering of the secreted acid in
the stomach b/4 it enters the duodenum  defective negative feedback mechanism
 PEPTIC ULCER DISEASE

•Pain begins 90-180min after food, relieved by food, milk, antacids

or vomit
•DU patients in general have - ↑capacity to secrete acid and pepsin
- Increased responsiveness to stimuli of acid secretion as a result of
increased parietal cell mass
• More rapid gastric emptying which does not allow for sufficient
buffering of the secreted acid in the stomach before getting to the
duodenum
 PEPTIC ULCER DISEASE

GASTRIC ULCER

•In gastric ulcer, the major causal influence appears to be some breakdown in the gastric mucosal
defense against acid and pepsin

•Onset is usually associated with pyloric sphincter dysfunction  reflux of bile salts into the stomach

•Pain begins in the first 30min of eating and is not relieved by eating

Symptoms/Clinical Manifestations

•Abdominal pain, nausea and vomiting, haematemesis, bleeding with black tarry stool.

•Diagnosis – X-ray after barium chloride meal could reveal visual ulcerations

- Endoscopy may reveal visual ulcers

- History of ulcerogenic medication use
 PEPTIC ULCER DISEASE

•Complications of PUD

a) - Haemorhage – multiple capillary bleeding points leading to hypovolemic

anaemia or iron deficiency anaemia due to malabsorption of iron
– Shock
– haematemesis
b) - Perforations – contents leak into the peritoneum  acute peritonitis
c) - Pyloric stenosis – due to fibrous tissues formed which heals and
narrows the pylorus causing persistent vomiting
 APPENDICITIS

•The lumen of the appendix is very small giving little room for swelling when inflamed

•Causes of inflammation may be microbial infections or other foreign bodies

•Inflammatory exudates often containing fibrin and phagocytes cause swelling and
ulceration of the mucus lining

•In more severe cases, progressive microbial growth cause suppuration, abscess and
congestion  increased pressure

•The major complication is peritonitis which occur when:

- Microbial spread and infect the peritoneum

- Appendix abscess ruptures and pus enters the peritoneal cavity
• Appendix becomes gangrenous and ruptures discharging its content into the peritoneal
cavity
 INFLAMMATORY BOWEL DISEASE (IBD)
•This is a generic classification for a group of non-specific inflammatory disorders of the GIT consisting of
Crohn’s Disease and Ulcerative Colitis. These differ in pathophysiology, anatomic distribution and clinical
course. They occur intermittently with periods of relapse and self-remission with or without scars.

a) Ulcerative Colitis

•This is a chronic inflammatory disease of the colon. It always affects the rectum and extends proximally to
involve a variable portion of the colon.

•The particular cause is not clear but it appears to be primarily immune response, infection and allergy to dietary
components and has a familial incidence.

•Immunopathogenesis

• The intense infiltration of the inflamed mucosa with plasma cells, B- and T- lymphocytes and macrophages
suggests immunological activity but whether this is a cause or response to a cause is not clear. The mucosa
becomes edematous, intensely hemorrhagic and perforated. Mucosal capillaries are congested and dilated
causing extravasation of RBCs.
INFLAMMATORY BOWEL DISEASE (IBD)

Symptoms
•Sudden onset of severe diarrhea, hemorrhage, dehydration,
electrolyte imbalance and hypovolemic shock death.
•Diagnosis
- Endoscopic appearance of the colon
- History of slow onset of symptoms of bloody and mucoid stool
- Sigmoid inflammation
 INFLAMMATORY BOWEL DISEASE (IBD)

a) Crohn’s Disease

•This is a chronic granulomatous inflammatory disease of the GIT which can affect any portion
from the mouth to the anus but mainly the ileum. It is frequently discontinuous and with tendency
to form fistulae (abnormal passage between two epithelial surfaces) and deep ulcerations
•The cause is not known but has some familial incidence (without clear mode of inheritance)
interplaying with environmental factors.
•The bowel is thickened and sometimes stenosed. The surface may be inflamed while the
mesenteric attachments are oedematose
•In areas of severe disease, deep ulcers occur and coupled with inflammation, the affected
intestinal part may become adherent to the adjacent loop of other parts of the intestine or other
organs like the bladder with subsequent formation of fistulae.
INFLAMMATORY BOWEL DISEASE (IBD)

•Clinical manifestations include:

- Low-grade fever, acute blood loss and abdominal pain

- Diarrhea, weight loss, fatigue and pain mainly due to anaemia
- Rectal bleeding with colonic involvement
- Massive hemorrhage is usually a late manifestation when deep ulceration cuts into
a major blood vessel
- Major intestinal complications are stricture and obstruction, growth retardation in
children

•Others GIT disorders include Tumors (benign and malignant), Diverticular disease,
Hernias, Intussusception and Intestinal obstruction (as complication of other diseases)
 PATHOLOGY OF RESPIRATORY DISORDERS
•The amount of energy needed to maintain the respiratory muscles during quiet breathing is small,

•Approx 2% of basal oxygen consumption. Increasing ventilation in normal humans consumes relatively
little oxygen until ventilation approaches 70L/min

• In patients with lung diseases, the energy requirements are greater at rest and increase
dramatically with exercise. Patients with emphysema may not be able to increase their ventilation by
more than a factor of 2 because the extra cost of breathing exceeds the additional O 2 made available to e
body.
• The lunges inflate and deflate passively in response to changes in plural pressure, the control over
respiration lies in control of e striated muscles, chiefly the diaphragm but also the intercostal
abdominal wall that changes plural pressure.
 PATHOLOGY OF RESPIRATORY DISORDERS

•The respiratory process can go wrong in many ways to include :

- Obstruction of gas flow in the airway
- Impaired alveoli diffusion
- Restricted thoracic capacity and expansivity
- Impaired ventilatory drive
 PATHOLOGY OF RESPIRATORY DISORDERS
•Obstructive defects are the commonest and usually affect the smaller airways

•They may be a consequence of bronchoconstriction, inflammatory or excessive mucus

secretion
•A foreign body may lodge in a large airway constituting a medical emergency, this may be
inhaled food or in children, any small toy or object.
•Chronic diffusion defect, where there is impaired gas transfer across alveolar membrane due
to thickening and fibrotic damage
•Restrictive defect as in inability to expand the lungs adequately due to poor lung compliance.

•Ventilatory failure is due to inadequate ventilatory drive to the respiratory muscles, this may
be caused by CNS depressants (anaesthetics, diseases, or trauma) or neuromuscular damage
(e.g poliomyelitis).
 PATHOLOGY OF RESPIRATORY DISORDERS
Clinical features of respiratory diseases

•The following signs and symptoms are characteristics of respiratory diseases

1. Dyspnea – a subjective, unpleasant sensation of shortness of breath resulting in labored breathing, rapid
breathing and hypercapnia
2. Wheezes – are sounds caused by gas flowing through the airway narrowed by spasm or excessive
secretions
3. Cough and sputum – are usually due to infection and cough could be dry (as in asthma and pneumonia)
or productive with mucoid sputum (as in tuberculosis, carcinoma and pulmonary embolism)
4. Hyperinflation – Because expiration is more difficult than inspiration, severe obstructive lung disease
could lead to progressive air trapping, not all of the air in the lung can be exhaled before the next
inspiration, the chest thus remain partially expanded at all times
5. Chest pain – Pain of respiratory origin may be due to pleurisy (inflammation or infection).
 RESPIRATORY DISEASES

•TUMORS

•Benign Tumors: - occur in the nasal septum and consist of abnormal proliferation of
blood vessels interspersed with collagen fibres of different sizes and arrangement. The
blood vessel may rupture leading to persistent bleeding (epistaxis).

•Bronchial Carcinoma: - The tumor develop in a main bronchus, form a friable mass that
projects into the lumen to cause obstruction. Collection of mucus predisposes to infection
leading to hemoptysis. Is mostly caused by cigarrete smoking.

•
 RESPIRATORY DISEASES

ASTHMA

•This is a hyperresponsiveness of the tracheobronchial tree to multiple variety of

stimuli resulting in the widespread inflammation and narrowing of the
tracheobronchial tree. Classical symptoms include:
- Wheezing
- Dyspnea
- Cough

•These classical symptoms of asthma occur within 15min of exposure to precipitants.

•Asthma could be intrinsic or extrinsic

 RESPIRATORY DISEASES

•Extrinsic asthma – common in children to adolescence

- Has genetic predisposition revealed by family history of asthma and hay
fever
- Attacks are more frequently seasonal with incidence associated with
increase pollen counts, cold weather, fog, wind
- Reactions are mediated by IgE
- Precipitated by allergens, exercise and viral infections. Allergens include
eggs, flour, house dust, feathers and fungal spores
RESPIRATORY DISEASES

•Intrinsic asthma – has no genetic or familial origin

- Depend on the level of irritability at which the bronchi react to various
stimuli
- Attack is triggered by non-specific irritants such as smoke, cold air and
dust, viral infections, exercise and emotional stress
- Drug-induced eg with aspirin (which inhibits PG synthesis) and
histamine occur in hypersensitive individuals
 RESPIRATORY DISEASES

•IgE is produced by antibody producing cells induced by antigens in sensitive individuals. IgE become
bound to mast cell surface in the bronchial mucosa.

•Upon subsequent exposure, antigen-antibody reaction takes place on the surface of the mast cells mast
cell degranulation accompanied by the release of cellular granules of humoral mediators (SRS-A, PGs,
Histamines, Kinins).

•These mediator substances acting in different ways combine to give the classical picture of asthma.

•Mucus production is normally a defense mechanism but in asthma, the mucus is thick and plugs the
airway which also becomes blocked with epithelial and inflammatory debris.

•Mucocilliary clearance is also decreased due to inflammation of epithelial cells. All these contribute to
airway resistance that is characteristics of asthma.
 RESPIRATORY DISEASES

•Clinical presentation include:

- Wheezing, dyspnea, hacking dry cough

- Tightness of the chest  labored breathing with prolong expiratory phase
- These paroxysms are associated with orthopnea, tachycardia and agitation
- Production of thick, viscous sputum
- Frequent expectoration of mucus plugs
- Chest deformity and growth retardation

- Diagnosis I revealed by a fall in FEV, measure by use of a spirometer. Positive

eosinophilia in WBCs differential count. Elevated IgE levels and sputum analysis reveals
the oesinophils
 RESPIRATORY DISEASES

COLD/COPD

•This is a collective term for a number of conditions which produce widespread persistent airway
obstruction causing dyspnea and abnormal blood gas level. The underlying condition is often chronic
bronchitis or emphysema.

a) Chronic Bronchitis – is defined by a progressive cough initially dry but later productive for about
3months in two consecutive years due to prolong irritation of the epithelial cells
Irritation is usually secondary to viral infection of the bronchus or most commonly due to cigarette
smoking
In this, the symptoms, work lost, hospital admissions and deaths are related to the extent of smoking.
• Symptoms of chronic bronchitis include – cough (Copious and tenacious), dyspnea, fever and
cyanosis
 RESPIRATORY DISEASES

a) Emphysema – is an irreversible distension of the bronchioles and the alveoli reducing the
surface area for gaseous exchange.
The lung becomes extended and increased in capacity, with normal breath constituting a
smaller proportion of the total volume of air in the distended alveoli
This leads to decreased partial pressure of oxygen.
• Emphysema is caused by reduced α1-antitrypsin activity.

• This enzyme protects the delicate alveolar tissue from autodigestion by the proteolytic
enzyme which it produces to clear accumulated debris. Increased amount of cell debris
and decreased antitrypsin levels are produced by smoking. Most emphysemics are
smokers.
RESPIRATORY DISEASES

RESTRICTIVE LUNG DISEASE (RLD)

•This is an inability to expand the lungs even though the airways are unobstructed.
The noncompliance of the lung may be caused by :
- Diffuse fibrosing alveolitis with destruction of lung tissues
- Thoracic cage deformity caused by tuberculosis
- Pleural disease leading to fibrosis which may be due to poisoning by asbestos

•There is often very little to be achieved by way of treatment because by the time
symptoms occur, the pathological changes may be irreversible.
DISEASES OF THE PULMONARY CIRCULATION
a) Pulmonary Embolism – This usually result from thrombi arising in the systemic
veins
These break away and travel through the veins which widens progressively and
eventually become trapped in the pulmonary circulation where the vessels narrow
progressively
Hyperlipidaemias are predisposing factors.
• Symptoms include – when embolism is massive  decreased C/Output making
the patient shocked, pale and cyanosed
• – medium size emboli usually present with chest pain, cough with bloody
sputum, fever and breathlessness.
 DISEASES OF THE PULMONARY CIRCULATION

a) Pulmonary Oedema – This is infiltration of pulmonary tissues with excess fluid

This usually result secondary to left heart failure with increased pulmonary capillary
pressure which causes accumulation of fluid in the normally minimal interstitial
space of the lungs.
• The increased vascular pressure restricts the bronchioles and reduces lung
compliance, ventilation and perfusion. When the condition persists, the fluid begins
to flow into the alveoli and the terminal bronchioles producing severe dyspnea
• Initial symptoms include – dyspnea on exertion, shortness of breath, cough,
orthopnea. Symptoms of advanced disease include cyanosis and coughing up of
foamy, bloody sputum.
 INFECTIOUS DISEASES OF THE LUNGS

a) Pneumonia – This infection occurs when protective mechanisms fail to prevent inhaled
or blood-borne microbes from reaching and colonizing the lungs which may be due to:
• – Impaired coughing
• – defective alveoli phagocytosis
• – pulmonary oedema and congestion
• – Decreased resistance to infection

•Two types of pneumonia are (1) Lobber pneumonia – infection of 1 or more lobes by
Streptococcus pneumoniae and (2) Bronchial pneumonia (Staph aureus, Strept.
Pneumoniae and Strept pyogens) – spread of infection to from bronchi to terminal
bronchioles and alveoli occurring mostly in infancy and old age

a) Tuberculosis -