• Applied aspects of GIT: Physiological aspects

of Peptic ulcer, GERD, Diarrhoea,

Constipation, Vomitting, Adynamic ileus,
Hirschprung’s disease

• Dr. Pramita Dubey

Competency
• Discuss the physiological aspects of peptic ulcer, GERD, vomiting,
diarrhoea, constipation, adynamic ileus, Hirschprung’s disease
Learning objectives
• Pathophysiology of:
• Peptic ulcer
• GERD
• Vomiting
• Diarrhoea
• Constipation
• Adynamic ileus
• Hirschprung’s disease
Gastroesophageal reflux disease
• GERD is caused by frequent acid reflux or reflux of nonacidic content from
the stomach.

• When you swallow, a circular band of muscle around the bottom of your
esophagus (lower esophageal sphincter) relaxes to allow food and liquid to
flow into your stomach. Then the sphincter closes again.

• If the sphincter does not relax as it should or it weakens, stomach acid can
flow back into your esophagus. This constant backwash of acid irritates the
lining of your esophagus, often causing it to become inflamed.
Peptic ulcer
• Term referred to breakdown of mucosal epithelium of the stomach or duodenum
• Etiology and pathogenesis:
• 1. The mucosal bicarbonate barrier disruption : This barrier normally prevents
irritation and autodigestion of the mucosa by the gastric secretion. The substances
which disrupt the barrier include:
• A) Infection with Helicobacter pylori
• Ethanol
• Vinegar
• Bile salts
• NSAIDS
• B) Hypersecretion of gastric acid: due to :
• i) Pepsinogen I: Human gastric mucosa contains two
immunohistochemically distinct pepsinogen groups; pepsinogen I and
pepsinogen II. Pepsinogen I is found only in acid secreting region
whereas pepsinogen II is found in pyloric region. Maximal acid
secretion correlates with pepsinogen I levels and patients with
congenitally elevated pepsinogen I have a five fold greater incidence of
peptic ulcer than individuals with normal levels.
• ii) Role of Gastrin:
• In most patients parietal cells are hyperresponsive to gastrin
• Zollinger Ellison syndrome: In patients with gastrinomas (tumours secreting
gastrin)
Vomiting
• Vomiting or emesis is the forceful expulsion of the food from the stomach
and/or intestine through the mouth.
• Sequence of events:
• Nausea; increased salivary secretion; deep, rapid and irregular breathing
• Retching
• Glottis closes and remains shut till the expulsion of vomiting material is
ejected . This increases intra pulmonary pressure which also prevents
aspiration of vomitus into the trachea
• Pyloric part contracts firmly and at the same time, antiperistalsis may take
place in the stomach
• Flaccid stomach is compressed by the raised intraabdominal pressure
resulting from descent of diaphragm and contraction of abdominal wall
• The cardiac sphincter and oesophagus relaxes and gasrtic contents are,
therefore, driven into the oesophagus.
• Oesophagus contracts by active contraction through out its length. As a
result, esophageal contents are emptied into the mouth.
• Soft palate is raised and shuts off the nasal cavity from the throat.
• Towards the end of act of vomiting:
• 1) Diaphragm relaxes
• Expiratory muscles and abdominal wall contracts
Initiation of vomiting
• Vomiting centre: dorsla portion of lateral reticular formation in
medulla
• Afferents arise from:
1. Irritation of mucosa in the stomach and other parts of GIT
2. The limbic cortex, which may originate, in response to “emotions” such as
“nauseating smells” and “sickening sights”
3. Vestibular apparatus eg in motion sickness
4. Heart and other organs
• Impulses are relayed from the vomiting centre over visceral afferent
pathways in the sympathetic nerves and vagi
True vomiting centre
• Chemoreceptor trigger zone(CTZ) located in or near “area postrema”
on medullary surface. The CTZ contains “chemoreceptor” cells which
initiate vomiting when they are stimulated. Drugs like apomorphine,
digitalis, are called central emetics since they act by stimulating “CTZ”
Adynamic ileus/ paralytic ileus
i. Painless condition produced by: 1) Hnadling of intestine during
abdominal operations or trauma to intestine. This causes direct inhibition
of smooth muscles
ii. Irritation of peritoneum causes reflex inhibition of smooth muscles due
to increased discharge of noradrenergic fibres in splanchnic nerves
• i) and ii) decrease the intestinal motility to cause adynamic ileus. Therefor,
intestinal contents are not propelled into the colon causing retention of
contents it the small intestine. This produces irregular distension of the
small intestine by pockets of gas and fluid. The condition usually get
relieved by rest to the bowels, intestinal peristalsis returns in 6-8 hrs
Hirschsprung’s disease/ Aganglionic
megacolon
• Children commonly
• Congenital absence of ganglionic cells in both the plexus
• Mutation in endothelin b receptor necessary for cranial to caudal migration of
neural crest cell during development
• Site of involvement is distal colon and pelvic-rectal junction and anastomosing
the cut ends
• In some the disease is associated with dilated urinary bladder and ureters,
indicating some deficiency in parasympathetic supply to the urinary tract in
these individuals. In addition there are no ‘VIP’ containing cells or fibres and
the involved colon is hyperresponsive to exogeneous ‘VIP’. The substance P is
also low.
Constipation
• Result of neglected calls to defecate
• Due to adaptation of sensory mechanism and its reflex effects.
• Anorexia, abdominal discomfort, distension, furred tongue and foul
breath, etc
Diarrhoea
• Increase in frequency of passage of stools
• Due to infection, typhoid gastroenteritis (food poisoning), ulcerative
colitis, etc
• Severe diarhoea is debilitating and can be fatal specially in infants.
Loss of large amount of electrolytes (Na+ and K+) and water in the
diarhoeal stools causes dehydration, hypovolemia, electrolyte
imbalance, shock, cardiovascular collapse and finally death.
References
• Guyton, A K Jain
Thank you