3.3.

GASTROINTESTINAL SYSTEM DISORDERS

33.1. Gastro-esophageal Reflux Disease (GERD)

Definition
Gastro-esophageal reflux disease is a condition in which stomach acid frequently
flows back into the oesophagus and irritates the oesophageal lining.
Pharmacouclapy

(Chaptes 3)
87
Etiology
Loe Eosephogtal Sphi nu
gtio condition, the LES
In nor.
closes
nes
becon relaxesiittremains tightly after food enters the stomach. If it
weak or relaxes
nes weak
agus, causing GERD. open and the stomach contents rise back up
the oesophag
into
mcessive
1) Excessive abdominal
pressure.
Following are the contributing factors:
heartburn daily due to this During pregnancy, some women
women experience
increased pressure. experience
Some specific food (eg, dairy, spicy or fried
Medications that include foods) and eating habits.
medicines for asthma, high blood pressure
allergies; aS well as
painkillers, sedatives and and
AHiatal hernia (i.e., the upper part of stomach anti-depressants.
obstruct the way of passage of food). bulges into the diaphragm, and

Pathogenesis
The onset of GERD is caused by an imbalance between harmful or
eliciting elements (reflux episodes, refluxate acidity, and symptom
hypersensitivity) and protective factors (oesophageal acid clearanceoesophageal
and
mucosal integrity). The frequency of reflux
episodes, length
acidification, and caustic potency of refluxed fluid
of mucosal
influence the amount of
mucosal damage. Although the same may be stated for
symptom intensity,
oesophageal hypersensitivity adds a complicating factor.
Oesophagitis is caused by cytokine-induced inflammation, instead of a direct
chemical reaction between the oesophagus epithelium and acid, pepsin, or bile.
This is supported by the fact that histopathological events in the
development
of oesophagitis (lymphocytic inflammation and dilated intercellular
spaces)
oCCur deep within the epithelium, and that restorative changes (basal cell
hyperplasia and papillary elongation) occur before the progression of surface
necrosis, which was previously thought to be the stimulus for those changes. In
the absence of oesophagitis, cytokine-induced inflammation can produce
changes in oesophageal sensitivity.
Clinical Manifestations
Heartburn (buming sensation in the chest) after eating, which may worsen at night
2) Chest pain
3) Difficulty in swallowing
Regurgitation offood or sour liquid
3) Sensation of a lump in the throat
patient experiencing night time acid reflux may also experience:
1) Chronic cough
2) Laryngitis
) New or worsening asthma
4) Disturbed sleep

Non-pharmacological Management
etary and lifestyle changes are generaly the first step in medical therapy for
GERD. Foods that increase gastric acidity (caffeinated beverages and
RD. toods,
ecaffeinated coffee), reduce lower oesophageal sphincter pressure (fatty
 D Pharm. 8Second Year (Pharmasaherapeste

Ocolale, peppermint, and spearmint), affect the oewophageal peristalsis futte

alcohol, and acidic liquids), or slow gastric emptying (fatty 1ods) enhance t
reflux. It also gets bad after heavy meals, which raise stonach presure. Hea
of the desire to vent the bloated stomach, smoking impairs oesophageal mt
function and promotes air swallowing, resulting in frequent belching
Gravity is vital in retaining gastric contents in the stomach and restrriny
recycled material to the stomach when reflux occurs, since the anti-reflux harrie
is frequently poor in people with GERD. As a result, reflux therapy
include
preventing lying down after dining and raising the head of bed. Reflux sympt
can
rise with weight gain and diminish with weight loss for unclear causes. As
result, people who are overweight are frequently advised to lose
weight
Common tips for reducing oesophageal reflux symptoms include:
1) Limiting the intake of food items that enhance stomach acidity.
2) Avoiding meals that lower the pressure in lower oesophageal sphincter.
3) Preventing meals that cause peristalsis problems.
4) Limiting the food items that take a long time to digest.
5) Staying away from heavy mcals.
6) Quitting of smoking.
7) Not lying down after eating.
8) Raising the head of bed.
9) Shedding weight (if overweight).

Pharmacological Management AleHy,"303,1 1Mgo ,

1) Antacids: These drugs, e-g, Tums, Rolaids,
neutralise the stomach acids and provide quickMylanta,
relief.
Riopan, and Maalox.
2) H Receptor Blockers: These
and Zantac, decrease acid
drugs, e.g., Tagamet, Pepcid AC, Axid AR,
production. Rani
3) Proton Pump Inhibitors: These hd
drugs,
Nexium, Protonix, AcipHex, and Dexilant,e.g.,are Prevacid, Prilosec, Zegerid.
also
heal the damaged stronger acid blockers that
4) Baclofen: It is a
oesophageal tissues. Prayo o
prescription drug that reduces the relaxation of LES and
prevents acid reflux.
5) Prokinetics: These drugs
help in emptying the stomach
6) Erythromycin: It is an antibiotic that faster.Csoigg, den poe
helps in emptying the stomach faster.
3.3.2. Peptic Ulcer Disease
Definition
Peptic ulcer is a condition in which wounds
duodenum (beginning part of the small appear in the lining of stomacho
pain. In this case, a low pH peptic juice intestine), along with a burning stoma
duodenum starts (or acid) secreted by the walls of
eroding the mucosa. stomacn
use of NSAIDs are the Bacterium Helicobacter
main causes of
peptic ulcer. pylori and
long-i
Types
1) Gastrie Ulcers: This ulcer
or chronic. type affects the stomach ite
Gastric ulcer is lining and may be acu
stomach and arises within a characterised by pain while the food is still in
short period of time
after food
u
consumption.
 cotherapy of Diseases-11 (Chapner 3)
Pharmacother

Quodenal Ukers: This ulcer type affects the upper part of small intestine
Dvod

andmay be ACute or chronic. Duodenal ulcer is characterised by pain when

mach is ermpty, or may resut after several hours of food
the stomaci sumption.
However, the pain improves after fooxd consumption.
Friology
Lining of the stomach, oesophagus, and smaill intestine generate due to the
factors ike
Helicobacter pylori infecting stomach and causing infiammafion.
NSAIDs like aspirin, ibuprofen, etc. used frequently. This increases the risk
2 in women and people in their 60s,
3) Smoking. 4) Alcoholism.
5) Radiotherapy, and 6) Cancer of stomach
Pathogenesis

Acidic secretions of stomach digest the ingested food, whereas intrinsic defences
protect the gastric mucosal membrane from injury. A thick. tenacious layer of
gastric mucus protects the stomach from auto-digestion. chemical and
mechanical trauma. An additional line of defense is provided by the
prostaglandins. Gastric ulcers result due to destruction of mucosal barrier

Brunner's glands present in the duodenum wall provide protection to it from

ulceration. These glands produce a mucoid, viscid. alkaline secretion that
neutralises the acidic chyme. Duodenal ulcers result due to excessi
production.
Bacieria H. pylori releases a toxin that destructs or damages the gastric and duodenal
mucosa, reducing the epithelium's resistance to acid digestion, and causing gastritis
and ulcer disease.

NSAIDs inhibit the secretion of prostaglandins actively involved in blocking

ulceration. In case of some diseased conditions like Crohn's disease, hepatic disease.
pre-existing gastritis, Zollinger-Ellison syndrome, ulceration may also occur.
Clinical Manifestations
Some people with ulcers have no symptoms at all. However following are the
indications of an ulcer
Between meals or at night, biting or burning discomfort in the middle or
upper stomach.
is taken.
A pain that goes away when something is ingested or an antacid
3) Bloating
4) Heartburn
5) Nausea or vomiting
neverecases, symptoms can include:
Dark or black stool (due to bleeding)
2) Vomiting
3) Weight loss
4) Severe pain in the mid-to-upper abdomen
 90 D. Pharm. Second Year (Pharmacotherapeutics) PCI
Non-pharmacologlcal Management
By changing lifestyle, symptoms of peptic ulcer can be relieved, such as:
1) Dietary Modification and Nutritional Supplements: A diet modification i
required for peptic ulcer patients. Food that
aggravates dyspeptic symptoms
should be avoided. Nutritional supplements are
loss resulting from diarrhoea,
required to counteract weight
vomiting, and anorexia. Also, blood loss
loss
resulted from haematemesis needs to be controlled.
2) Cessation of NSAIDs: Consumption of NSAIDs should be
stopped as they
reduce PGE synthesis, thus
acting as an aggravating factor for peptic ulcers.
3) Cessation of Smoking: Peptic ulcer
it is linked with an increased patients are advised to quit smoking as
risk of peptic ulcer development,
healing, and recurrence. delayed
4) Removal of Other Underlying Causes: Other
causes leading to
formation, eg, Zollinger-Ellison syndrome, peptic ulcer
gastric cell hyperplasia, increased
secretory states, etc., should be removed to cure the disease
completely.
Pharmacological Management
1) Proton Pump Inhibitors (PPIs): These medications
aciphex, protonix, and nexium) help the ulcer to heal (e-g., prilosec, prevacid,
2) Histamine Receptor Blockers by lowering acid levels.
Axid are examples of (H-Blockers): Tagamet, Pepcid, Zantac, and
Hz-blockers, which also loweracid production.
3) Antibiotics: This class of medicines
treat H.
pylori infections. destroys bacteria and should be used to
4) Protective Drugs: These
in drugs(eg, Carafate or Pepto-Bismol) cover
protective covering to prevent
a
additional damage from the ulcer
enzymes. digestive acids and
5) Antacids: These drugs
relieve the symptoms. swiftly deteriorate or neutralise stomach acid to
6) Anti-Secretory Agents: These agents are
(impaired digestion). administered to manage
7) Acid dyspepsia
Suppressors:
included in this H2-receptor antagonists and proton
group. H2-receptor
histamine for bindingg pump inhibitors are
cells. While the
to
H2-receptors antagonists
on the reversibly compete with
basolateral
inhibiting the proton pump inhibitors decrease gastric membrane of parietal
hydrogen-potassium
system, which catalyses the adenosine acid secretion by
final stage of acid triphosphatase gastric enzyme
8)
Cytoprotective Agents: These agents
and small intestine. production.
protect the tissues lining the stomacn