Gastro-Intestinal Diseases


Thedigestive system is a complex integration of organs that havedifferent functions to aid in the breakdown and absorption ofconsumed food in the body. Consumed food pass through a lot ofprocesses sand stages before its wastes gets out of the body throughthe responsible orifices (NDIC, 2012). The stomach is an importantorgan since it is here where food goes through intensive breakdownbefore being passé to the duodenum and the small intestines. Thestomach produces juices to help in breaking down the food. Theproduction of the juice takes place after the stimulation of thecells by the presence of food in the stomach. The condition of thestomach is highly acid, and it is only the enzymes that can survivein the acidic conditions that find an optimum condition in thestomach (Huether &amp McCance, 2012).

Thegastric parietal cells handle acid production in the stomach. Thecells have a region known as secretory canaliculus that has an acidicenvironment of more than eight. The production of the gastric acidinto the lumen occurs to respond to the messages delivered throughvarious hormones and merocrine inputs. Gastrin is the primaryhormone that leads to the production of gastric juice. Paracrenineand neurocrine messgers that lead to the production of gastric acidas a responsive message include histamine and acetylcholine (LaureateEducation, 2012). The contents of the gastric acid can digest thewalls of our stomachs. However, the stomach has a protective layerthat prevents the acid from corroding the internal parts of the wallof the stomach. Some conditions, however, may lead to gastricinflammation. The enzymes present in the gastric acid can havedegenerative corrosion that leads to ulcerations (McPhee &ampHammer, 2012).

Someconditions may interfere with the way the gastric acid gets releasedthrough stimulation. One such condition is like GastroesophagealReflux Disease (GERD). It is a disease condition that result from theintense reflux of the gastric material taking place through the loweresophageal sphincter. It extends to the esophagus, and it may causeinjuries to the esophageal tissue. The production of gastric acid,therefore, increases the intensity of the Gastroesophageal refluxdisease. The condition manifests due to the increase in the volume ofthe acid due to the defect of the lower esophageal. The gastric acidrefluxes back into the esophagus (McPhee &amp Hammer, 2012).

Gastritisis another condition that interferes with the proper release andfunctioning of the gastric acid. The disease manifests as aninflammation on the walls f the stomach due to a gradual erosion ofthe secretory glands. When these glands reduce in number, thesecretion of the acid becomes adversely affected. Peptic UlcerDisorder (PUD) is a condition characterized by a break in the wallsof the stomach. The wall breaks away leaving the internal parts ofthe stomach exposed. The disease also reduces the number of secretoryglands responsible for the production of gastric juice. Theconsequence is the reduction in the volume of the produced acid, andthis interferes with digestion.

Thechanges that occur in the stimulation of gastric acid affect thepathophysiology of these three conditions. The volume of the gastricacid tends to rise in the case if GERD. It affects the balancetowards pathologic reflux changing the normal capacity of the wallsof the esophagus to tolerate the acid. As the disease worsens, theprotective esophageal mechanisms such as resistance and acidclearance become adversely affected. Gastritis and PUD reduce thenumber of glands secreting the acid as since their characteristicsinclude breaking away of the skin. The unprotected parts of thestomach wall experience corrosions. Gastric acid production providesan optimum condition for Helicobacter pylori that cause gastritis.Therefore, it leads to the scaling up of the disease on the walls ofthe stomach.

Inchildren, the problem is likely to become less intense when theirdigestive system adapts to formulas. Parents may perform simpleexercises like holding the baby upright for about 30 minutes afterfeeding and thickening their feedings with cereal. They can alsochange the feeding schedules or try solid foods with the approval ofa physician.

Jamie’scase represents a condition may be due to behavioral factors. Various behaviors may have detrimental effects on the body and thuschange the pathophysiology of the gastro intestinal complications.Feeding n formula with high levels of fat reduces the LES pressureand this increases the chances of reflux. Feeding behavior that hasconcentrates that have corrosive characteristics may corrode thewalls of the stomach. The corroded walls affect the pathophysiologyof gastritis and PUD in that they reduce the protective layer andthis exposes the internal parts of the stomach to gastric acidcorrosions. Physicians can diagnosis of the diseases through meanslike using a pH probe, Upper GI endoscopy, Gastric emptying study orusing a barium swallow. Parents may often overlook this possibilityand take the disease to be an allergic reaction to differentformulas. However, the problem will persist even with theintroduction of hypo-allergic formulas. Parents should, therefore,adhere to some procedures as they assist their children out of theproblem like feeding them on the right diet and observing any changein behavior to spot any occurrence of regurgitation or discomfort(Gasiorowska et al., 2009).

Inconclusion, the disease may manifest themselves in similar ways and adetailed diagnosis of each is necessary to give the patients theright recommendations and treatments.


Inflammation of gastric mucosa

astritis mind map

Erosion of epithelium




Behavioral modifications

Diagnosis and treatment

Acute or Chronic


1.8 t 2.1 million visits to the doctor annually

Gnawing and biting pain


Epigastric Pain

Clinical manifestations

Very common with people above 60 years




Gasiorowska,A., Poh, C. H., &amp Fass, R. (2009). Gastroesophageal refluxdisease (GERD) and irritable bowel syndrome (IBS)—Is it one diseaseor an overlap of two disorders? Digestive Diseases and Sciences,54(9), 1829–1834.

Huether,S. E., &amp McCance, K. L. (2012). Understandingpathophysiology.Mosby: St. Louis.

McPhee,S. J., &amp Hammer, G. D. (2012). Pathophysiology of disease: Anintroduction to clinical medicine. McGraw-Hill Medical: New York.

LaureateEducation, Inc. (2012c). The Gastrointestinal System. Author MD:Baltimore.

NationalDigestive Diseases Information Clearinghouse (NDIC). (2012).Retrieved from