Gastrointestinal System Alterations

Gastrointestinal System Alterations

Comprehensive Essay on Gastrointestinal System Alterations

The purpose of this paper is to elaborate various illnesses pathology and pathogenesis, essential to nurse practitioners that enable them to accurately identify changes in the gastrointestinal system, Crohn’s disease, Pancreatic Cancer, Diabetes epidemic, Hepatitis, and Celiac disease for proper diagnosis of the patients and reference of patients to specialized treatment and care where necessary.

Comprehensive Essay on Gastrointestinal System Alterations

Obesity Epidemic

Obesity is an intricate illness resulting from high consumption of energy and reduced expenditure of energy. The gastrointestinal system performs a vital function in obesity illness’ pathogenesis and helps in the imbalance of calories. The inhibition of mechanisms and changes in the gastrointestinal hormones that limit caloric consumption, lead to weight increase. It is unclear if the digestive function in obesity is an effect or a root of obesity (Acosta, & Camilleri, 2014). Obesity is mostly related to cardiovascular disease, CVD, and type 2 diabetes mellitus, T2DM. It is also linked with gastrointestinal disorders, which are more common and pre-existing before CVD and T2DM. Illnesses such as non- alcoholic steatohepatitis, cholelithiasis, or gastroesophageal reflux disease are directly associated with abdominal adiposity and body weight (Pozza, & Isidori, 2018). Regular disposal of bowel wastes is beneficial to body functioning. Thus, alterations of bowel elimination are often premature signs or symptoms of problems associated with the gastrointestinal system as normal bowel functions depend on the balance of various factors and elimination habits and patterns among multiple individuals.(Comprehensive Essay on Gastrointestinal System Alterations)

The regulation and control of food consumption is a beneficial aspect of the development and maintenance of obesity. Digestive roles are, thus, significant to obesity, since the stomach is the storage that determines any caloric entry to the body (Pozza, & Isidori, 2018). It also facilitates to the sensation of satiation or postprandial fullness and indicates the urge to halt the caloric intake. Variations in gastrointestinal roles such as higher gastric accommodation or more rapid gastric emptying may result in the absorption of more calories, causing increased weight hence obesity (Acosta & Camilleri, 2014). Gastrointestinal hormones perform an essential role in satiety and the regulating appetite, along with simultaneous synchronization with the brain-gut bloc. The microbiome within the digestive system can impact obesity. The understanding of normal bowel activities, functioning, and elimination and factors that impede, promote, and cause alterations in elimination are helpful in the management of individuals’ elimination problems (Pozza, & Isidori, 2018).(Comprehensive Essay on Gastrointestinal System Alterations)

Celiac Disease

Celiac disease is an autoimmune illness caused by gluten ingestion. Characteristically, it shows through diarrhea and a not thriving during the first years of life. Diagnosis of the Celiac disease is founded on anomalies of the ileum biopsy. The clinical presentation of the Celiac disease acknowledged is varied and extensive and always associated with the gastrointestinal system (Therrien, Kelly, & Silvester, 2020). The illness has associations with most autoimmune conditions such as autoimmune thyroid and type 1 diabetes. The clinical manifestation of the sickness is considerably varied and age-dependent. The typical sign is diarrhea, abdominal pain, malnutrition, failure in thriving, and distension during the early years of life signifies the tip of a phenomenon regularly known as the “celiac disease iceberg.” (Therrien, Kelly, & Silvester, 2020).(Comprehensive Essay on Gastrointestinal System Alterations)

Contrary to the remarkable manifestation observed classically in young children, most individuals with the celiac disease manifest during late years of development through subtle symptoms and the diagnosis of the illnesses can delay. Gastrointestinal symptoms are constipation or diarrhea, excessive gas, bloating, and abdominal pain (Therrien, Kelly, & Silvester, 2020). Avoidance of gluten-rich foods can also take place, and cautious diet past information is essential for the identification of this symptom. Also, vitamin deficiencies as a result of fat malabsorption may transpire. With longer-standing illness, individuals may show reflective vitamin D deficiency leading to hypocalcemia or rickets (Comprehensive Essay on Gastrointestinal System Alterations)and coagulopathy or tetany tributary to the lack of vitamin K. Anemia secondary to folate or iron deficit is also observed.(Comprehensive Essay on Gastrointestinal System Alterations)

Adolescents and children mostly present constitutional delayed puberty and short stature. 2-8% of these individuals presenting for assessment of small size indicate Celiac disease (Therrien, Kelly & Silvester, 2020). Access to preceding growth points is essential in differentiating between the underlying pathological basis of short stature and constitutional delayed puberty, such as celiac disease. Children manifesting with this illness usually undergo a decrease in weight and height growth rate leading to a reduced growth percentile. In the situation of decreasing development percentiles, the diagnosis of this illness should get considered and a test of autoantibodies carried out. Adults present diarrhea as the main sign of the disease in almost 50% of cases (Therrien, Kelly & Silvester, 2020). They also may be diagnosed in osteoporosis or anaemia setting. Adults can be symptomatic for prior years or possess short physique signifying established celiac disease. Most individuals are misdiagnosed initially with irritable bowel syndrome, have several procedures performed or hospital admissions that may eventually get drawn to the undiagnosed celiac disease. Individuals discovered through screening due to genetic reasons are typically mildly symptomatic or asymptomatic for the disease, thus forming a growing populace of people with celiac disease due to increased screening efforts.(Comprehensive Essay on Gastrointestinal System Alterations)

Crohn’s Disease

Crohn’s disease, CD, is a long-lasting inflammatory illness of the digestive system affecting most American and European populations. CD is among the multiple primary forms of inflammatory bowel disease (IBD). The particular causal factors of CD are not established, although it has a likelihood to comprise a disordered immunological reaction to gastric microbiota in genetically vulnerable individuals (Fatahi, Al Asmari, & Bukhari, 2018). While the etiology of the illness is not known, it is explicit from initial epidemiological researches that a blend of environmental and genetic risk factors facilitates a person’s disease predisposition. The most common symptoms of this illness include weight loss, diarrhea, fatigue, and abdominal pain. Signs and symptoms mirror the behavior and site of the disease and the absence or presence of fistulae and strictures. Extraintestinal presentations may show and classically distress joints, eyes, liver, or skin. There is presently no established medicine, and the illness is manageable through a mixture of immune-suppressing drugs, surgery, dietary variations, anti-tumor necrosis factor therapy, or smoking cessation (Fatahi, Al Asmari, & Bukhari, 2018).(Comprehensive Essay on Gastrointestinal System Alterations)

The major established risk factor for CD is genetics as the incidence of the illness is higher among first-degree relatives. Although there is an absence of a clear-cut pattern of inheritance, individuals with the disease and their relatives, manifest a similar disease course. First-degree relatives with CD increase one’s risk of getting the disease. Familial aggregation is an indicator of a genetic component in CD. For instance, the significance phenotypic, which includes behavior, age, and the location at diagnosis concordance, occurs in monozygotic twins (Khanna, Levesque, McDonald, & Feagan, 2019). The Nucleotide-binding Oligomerization Domain consisting of protein 2, NOD2, on chromosome 16q12 (8,10) was the first CD gene identified (Fatahi, Al Asmari & Bukhari, 2018). NOD2 translates a cytoplasmic pathogen-associated molecular pattern that links to muramyl dipeptide, an element of both gram-negative and -positive cell walls. Genetic factors are the most apparent factors that influence CD. Approximately 10-15% of individuals suffering from CD have an ancestral connection with the illness (Khanna, Levesque, McDonald, & Feagan, 2019). Also, identical twins present not less than 53% similarity while fraternal twins manifest likeness for CD as individuals with familial history. Current genome-wide screening surveys indicate a susceptibility locus on chromosomes 1, 3, 4, 6, 12, 14, and 16 in CD.(Comprehensive Essay on Gastrointestinal System Alterations)

Hepatitis A, B, C, and Viral Hepatitis

Hepatitis A

It is primarily caused by poor personal hygiene and sanitation. Hepatitis A is spread by fecal-oral transmission or via the ingestion of hepatitis A virus-contaminated fluids (such as water) and food (Jain et al., 2013). Poor health and hygiene are mainly due to the lack of essential infrastructures such as clean water or waste management systems. Hepatitis A is an acute infection, and the virus usually lives for a short period; thus, recovery can take several weeks. It is, however, preventable through vaccination. It usually does not require treatment, although bed rest, proper nutrition, and hydration are recommended (Jain et al., 2013).(Comprehensive Essay on Gastrointestinal System Alterations)

Hepatitis B

Hepatitis B is a bloodborne virus whose primary mode of transmission is by blood-to-blood exposure with people infected with the pathogen (Jain et al., 2013). The illness starts as a short-term infection, although in some cases, it may progress into a life-long or chronic disease. Chronic Hepatitis B is the most common origin of liver cancer and other severe liver illnesses. Infected adults develop an acute infection and make a full recovery after around half a year. However, approximately 90% of infected newborns and 50% of young children contract a life-long disease as it may be spread from infected mother to baby after exposure to her blood (Jain et al., 2013). Also, it can be spread through infectious body fluids like semen and vaginal secretions that are infected with the hepatitis B virus. Antiviral medications treat the illness.(Comprehensive Essay on Gastrointestinal System Alterations)

Hepatitis C

Hepatitis C results from the Hepatitis C virus (HCV) that gets contacted via direct contact with infected body fluids; that is, sexual contact and injection substance use. HCV is the most prevalent viral infection in America transmitted through blood, as over 2 million individuals are currently living with the chronic form of the disease (Jain et al., 2013). It sometimes results in cirrhosis (liver scarring). There is no known vaccine for the prevention of Hepatitis C, although antiviral medications are used in the treatment of hepatitis C.(Comprehensive Essay on Gastrointestinal System Alterations)

Pancreatic Cancer

Pancreatic cancer is a terminal malignancy predominantly witnessed in men at a later age of 40-85 years and has an aggressive progression. Pancreatic cancer records 5% of cancer-related mortalities and 2% of all types of cancer. It is first among asymptomatic diseases, as around 90% of incidences are adenocarcinomas (Goral, 2015). The tumor is hard to detect since it shows no early signs and rapidly spreads to the neighboring organs. Additionally, it may lead to somatically acquired mutations or hereditary germline in cancer-associated mutations and genes, causing cancer progression and metastasis.(Comprehensive Essay on Gastrointestinal System Alterations)

Typically, this form of cancer initially metastasizes to liver, nearby lymph nodes, and lungs. Pancreatic cancer can directly attack its adjacent parts like the duodenum, colon, and stomach, or may metastasize to a surface in the abdominal area through peritoneal spread leading to ascites which has a threatening projection. It can also develop on the skin surface as painful nodular metastases, but bone metast(Comprehensive Essay on Gastrointestinal System Alterations)asis is not shared. It hardly establishes to the brain, although it can lead to the production of meningeal carcinomatosis.(Comprehensive Essay on Gastrointestinal System Alterations)

Case #26 (Nausea and vomiting)

Comprehensive Essay on Gastrointestinal System Alterations

Question 1

According to the provided data of the case study, the patient had several vomiting episodes, constant abdominal pain, and bloating. Thus, if graded regarding the degree of severity, the patient would receive IV fluids, required in the following 24 hours for his dehydration treatment.(Comprehensive Essay on Gastrointestinal System Alterations)

Question 2

According to Wilson and Shannon (2015), the mechanism of Amlodipine action is “a calcium channel blocker that selectively blocks calcium influx across cell membranes of cardiac and vascular smooth muscles without changing serum calcium concentrations. It reduces coronary vascular resistance and increases coronary blood flow. It reduces peripheral vascular resistance, and increases oxygen delivery to the myocardial tissue, and increases cardiac output.” Implying that the medication reduces vasodilation and vascular resistance; thus, lowering a patient’s hypertension.(Comprehensive Essay on Gastrointestinal System Alterations)

Question 3

According to Wilson and Shannon (2015), Glyburide’s action mechanism is “lower blood sugar concentration in both diabetic and nondiabetic individuals by sensitizing pancreatic beta cells to release insulin in the presence of elevated serum glucose levels.” This implies that a patient with T2DM still produces insulin; thus, the drug triggers the pancreatic release of insulin.(Comprehensive Essay on Gastrointestinal System Alterations)

Question 4

Anesthesia: Among anesthesia-associated risks is the Post-operative Nausea and Vomiting since he went through a surgical procedure.(Comprehensive Essay on Gastrointestinal System Alterations)

Medication: After the surgery, Morphine sulphate was administered to relieve pain and methyldopa for hypertension; these drugs have the main adverse effects of causing nausea and vomiting.(Comprehensive Essay on Gastrointestinal System Alterations)

Question 5

  • Dry mucous membranes.
  • Tachycardia: HR of 105.
  • Weak Pulses: hypoactive pulses at 1+ all through.
  • Altered Levels of Consciousness- The patient shows slight lethargic.
  • Sunken eyes.
  • Dry skin.
  • Tachypnea: On the fourth day post-operative, the patient’s respiratory rate was 28 per minute.
  • Cool skin
  • Augmented Creatinine
  • Decreased skin turgor.
  • Increased BUN.
  • Gray and cold extremities.
  • Tachycardia: HR of 105.

Question 6

Yes, he augmented hypokalemia, as confirmed by a K=3.2.

Question 7

Acute pancreatitis’ diagnosis is founded on various issues such as clinical manifestation (physical signs or symptoms), medical history (substantial tobacco and alcohol consumption, or a gallstones history), laboratory test information (increased lipase/amylase), and radiology information (X-rays or various scans that indicate a pancreatic inflammation). Wilson and Shannon (2015) suggest that “In a healthy individual, a normal blood amylase level is 23-85 units per liter (U/L), although some lab results for amylase go up to 140 U/L.” The patient’s amylase value is 31 IU/L; normal WBC at 3.5; an absence of tobacco history or EtOH for 15 years; thus, acute pancreatitis diagnosis may be ruled out. (Comprehensive Essay on Gastrointestinal System Alterations)

Question 8

While several clinical presentations in the patient may result in cecal perforation diagnosis, he fails to present with leukocytosis and fever. Cecal perforation arises when dilation is 13 cm or over that value.(Comprehensive Essay on Gastrointestinal System Alterations)

Question 9

Acute pseudo-obstruction is “severe colonic distension in the absence of mechanical obstruction” (Chudzinski, Thompson, & Ayscue, 2015). This suggests that the causal pathophysiological agent of acute colonic pseudo-obstruction includes “unopposed parasympathetic activity” and “the various neurotransmitters that mediate enteric nervous system control.” The parasympathetic nervous system gets stimulated by Neurokinin A, Substance P, and Acetylcholine neurotransmitters. At the same time, vasoactive intestinal peptide and nitric oxide act as repressive neurotransmitters. The high production of neurotransmitters that overstimulate the parasympathetic nervous system act as the causal agent that leads to “decreased contractility and dilation of the proximal colon.” Unobstructed parasympathetic stimulation of the digestive system seems to be the pathophysiologic agent contributing to the gut motility disorder.(Comprehensive Essay on Gastrointestinal System Alterations)

Question 10

Respiratory signs and symptoms are uneven with metabolic alkalosis. It involves the body attempting to recompense the disparity by sustaining the CO2 level to increase the blood acidity. For an individual’s body to maintain or preserve the CO2 during metabolic alkalosis, hypoventilation is a predictable and healthy response. The patient is tachypneic, with the rate of respiration as 25. While he manifests tachycardia (cardiac arrhythmias), the automatic body responses are not consistent with metabolic alkalosis, and his energy is unaffected. (Comprehensive Essay on Gastrointestinal System Alterations)


Various illnesses present similar symptoms in different patients. It is significant to make an accurate diagnosis through proper testing of patients considering their factors since it leads to correct treatments and avoidance of further complications in patients due to the severity of the disease. Proper diagnoses are established through the comparison between diagnostic statements and patient data, thus reflecting nursing interpretations to patient outcomes. Accurate diagnosis plays a significant role in the proper treatment of a disease. It also acts as the foundation of making the right choice of nursing interventions that result in positive patient outcomes.(Comprehensive Essay on Gastrointestinal System Alterations)


Acosta, A., & Camilleri, M. (2014). Gastrointestinal morbidity in obesity. Annals of The New York Academy of Sciences1311(1), 42-56. DOI: 10.1111/nyas.12385(Comprehensive Essay on Gastrointestinal System Alterations)

Fatahi, D., Al Asmari, A., & Bukhari, G. (2018). Crohn’s Disease: Pathophysiology and Management. The Egyptian Journal of Hospital Medicine70(11), 2004-2007. DOI: 10.12816/0044858(Comprehensive Essay on Gastrointestinal System Alterations)

Goral, V. (2015). Pancreatic Cancer: Pathogenesis and Diagnosis. Asian Pacific Journal of Cancer Prevention16(14), 5619-5624. DOI: 10.7314/apjcp.2015.16.14.5619

Jain, A., Jain, P., Prakash, S., Gupta, S., Singh, K., & Shrivastava, S. et al. (2013). Prevalence of hepatitis A virus, hepatitis B virus, hepatitis C virus, hepatitis D virus and hepatitis E virus as causes of acute viral hepatitis in North India: A hospital-based study. Indian Journal of Medical Microbiology31(3), 261. DOI: 10.4103/0255-0857.115631(Comprehensive Essay on Gastrointestinal System Alterations)

Khanna, R., Levesque, B. G., McDonald, J. W., & Feagan, B. G. (2019). Therapy for Crohn’s disease. Evidence-based Gastroenterology and Hepatology, 150.(Comprehensive Essay on Gastrointestinal System Alterations)

McCance, K. A. & Huether, S.E. (2010). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis: Mosby. (Chapters 40-42)

Pozza, C., & Isidori, A. M. (2018). What’s behind the obesity epidemic? In Imaging in bariatric surgery (pp. 1-8). Springer, Cham.

Therrien, A., Kelly, C., & Silvester, J. (2020). Celiac Disease. Journal of Clinical Gastroenterology54(1), 8-21. DOI: 10.1097/mcg.0000000000001267(Comprehensive Essay on Gastrointestinal System Alterations)

Wilson, B., & Shannon, M. (2015). Pearson nurse’s drug guide 2015. New York, NY: Pearson

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