Introduction
Disorders of the gastrointestinal (GI) tract affect the organs and muscles due to a decrease in the absorption of needed nutrients or loss of nutrients. Disorders of the musculoskeletal system may affect the ability of the person to obtain and ingest food. In diagnosis and in treating a particular system, one must consider the interaction and effects on other systems.
The GI tract begins with the mouth and ends at the anus. The movement of food and fluids through the GI system, including defecation, is controlled by hormones, the sympathetic and parasympathetic nervous system, and local stimuli from the intestinal walls.
The amount of fluid produced by the GI system and then reabsorbed is an important fact when evaluating the intake and output of a client, especially if there is GI suctioning or diarrhea. The mouth produces approximately 1 liter of saliva per day and the production is controlled by the autonomic nervous system. Saliva has a pH of 7.4, which neutralizes bacterial acids and prevents tooth decay. Saliva also contains IgA and other antimicrobial substances that form the first line of defense against viruses and bacteria (McCance & Huether, 2006). Swallowing saliva and food is controlled by several cranial nerves. Strokes and other disorders affect the ability to swallow, as well as the motility of the esophagus, increasing the risk of aspiration.
The lower esophageal sphincter (LES) is usually contracted, preventing reflux of stomach contents into the esophagus. Gastroesophageal reflux disease (GERD) is usually related to a weak LES that allows stomach contents to splash back into the esophagus. The squamous cells that line the esophagus just above the sphincter are exposed to the acid contents and over time will be replaced by columnar epithelial cells. The change in cell type increases the risk for Barrett esophagus and esophageal cancer. The strength of the LES in repelling gastric contents can be adversely affected by fatty foods, caffeine, alcohol, cigarettes, and morphine (Copstead & Banasik, 2005; McCance & Huether, 2006). The following suggested treatments other than medications are not based on good evidence at this point. Treatment includes avoiding foods and substances that decrease LES pressure; the body should remain in an upright position for several hours after eating. If needed, the head should be elevated while sleeping. Antacids can be used to minimize the heartburn in mild cases. H2 blockers and proton pump inhibitors are the mainstay treatment to prevent further damage to the esophagus and allow healing.
The stomach is a reservoir capable of holding more than 1,000 mL of food and liquid. In a 24-hour period, the stomach produces approximately 2 liters of gastric secretions that aid in the breakdown of food and drugs. Porth (2007) lists the glands and their secretions. Disorders that affect the stomach include gastritis, peptic ulcer disease, and stress ulcers.
Bacterial endotoxins, alcohol, and aspirin can irritate the mucosa, causing a gastritis that may show as simple irritation and edema to hemorrhagic erosions. In chronic gastritis, H pylori, common bacteria, is the culprit and causes inflammation of the antrum of the stomach.
Peptic ulcer disease encompasses esophageal, gastric, and duodenal ulcers. The ulcers can penetrate only the mucosal surface or extent into the smooth muscle. Most peptic ulcers are caused by an H pylori infection. Aspirin and other NSAIDs have been implicated as the next most common cause of ulcers (Porth, 2007). In the duodenum, excess secretion of acid is a major factor in the development of ulcers. Cigarette smoking has been shown to be a serious risk factor. If not treated, the complications of peptic ulcers are hemorrhage, obstruction, and perforation. The treatment is to determine the cause and stop it, encourage healing of the injured mucosa, and prevent further occurrence. The medications commonly used are the H2 blockers such as famotidine (Pepcid) and proton pump inhibitors such as Protonix.
Stress ulcers occur most often in the fundus of the stomach and proximal duodenum, and seem to be the result of tissue ischemia and acidosis in critically ill or injured patients. Patients suffering from intracranial injury, operations, or tumors may also develop ulcers related to hypersecretion of gastric acid. Because of the risk, many patients in the intensive care units (ICU) receive H2-blockers or proton pump inhibitors prophylactically. Evidence-based research seems to indicate this practice may not be needed. Frequently, patients admitted to regular hospital units receive H2-blockers or proton pump inhibitors, but there is not supporting evidence for this practice. The duodenum and jejunum of the small intestine are responsible for digesting and absorbing the majority of nutrients. The small intestines secrete hormones that promote the digestion and absorption of nutrients. Cholecystokinin (I cells) production stimulates the release of pancreatic and biliary enzymes, and it seems to mediate the amount of food intake. GIP or glucose-dependent insulinotropic polypeptide (K cells in jejunum), and GLP-1 (L cells in distal small bowel) augment the release of insulin when a meal high in carbohydrates is eaten (Porth, 2007). GIP and GLP-1 are the latest enzymes being researched to treat diabetes.
The crypts of Lieberkühn secrete 2,000 mL/day of serous fluid that supports the absorption of nutrients by the small bowel. There is a small concentration of aerobic microorganisms proximal to the ileum, but generally no anaerobes. Distal to the ileocecal valve, anaerobes such as clostridia, anaerobic lactobacilli, and coliforms are the most common microorganisms. These bacteria are important to the metabolism of bile salts, estrogens, androgens, various nitrogenous substances and drugs (McCance & Huether, 2006).
Bacterial infections related to the bowel commonly seen in hospitalized patients are caused by two bacteria: clostridium difficile and Escherischia coli 0157:H7. C difficile is a gram-positive bacillus that is part of the normal flora of the bowel in 3% of humans. Antibiotic therapy reduces other bacteria in the bowel that keep C difficile in check, allowing for colonization and a release of toxins that cause mucosal damage and inflammation. Diarrhea is the result of the inflammation.
E coli 0157:H7 generally spreads through food-borne transmission. The symptoms are usually watery, nonbloody diarrhea and abdominal cramping lasting up to 7 days. The complications seen with E coli seem to affect the very old and very young. There is no real treatment for the infection other than treatment of the symptoms.
Crohn’s disease and ulcerative colitis are considered inflammatory bowel diseases. They have many similarities such as pattern of inheritance, systemic manifestations, and no real discernible cause. Crohn’s disease can most often affect the proximal portion of the colon and sometimes the terminal ileum, while ulcerative colitis has lesions in the crypts of Lieberkühn. The alterations of the mucosa and submucosa cause fluid and electrolyte losses, diarrhea, colicky pain, weight loss, and low-grade fever. The treatment for ulcerative colitis is similar to the treatment for Crohn’s disease. The inflammatory response in the bowel is blunted by medications and healing is promoted through an elemental diet that is high in nutrients but residue- and bulk-free.
Colorectal cancer is “associated with genetic alterations on chromosomes 5, 17, and 18” (McCance & Huether, 2006, p. 1430). High-fat, low−fiber, and low-calcium diets also promote the genetic alterations. The tumors often begin as polyps. As they enlarge, they penetrate the mucsularis mucosa and the blood stream, allowing for metastasis. In the ascending and transverse colon the tumors are large and ulcerated, bleed, and cause loose stools. Tumors in the descending colon grow circumferentially, causing obstruction. These tumors also ulcerate, causing blood in the stool. The risk of malignancy can be decreased by increasing fiber and calcium intake while decreasing fat. Sigmoidoscopy and colonoscopy are also used as screening tools to identify polyps. Treatment usually involves removing the cancerous colon followed by chemotherapy.
The liver is a diverse organ that degrades and clears the blood of endogenous and exogenous substances, but also metabolizes fats, proteins, glucose, bile salts, and clotting factors. It stores vitamins and minerals and conjugates bilirubin and urea.
Liver function tests provide information on the liver’s ability to function. Elevation of enzymes associated with the hepatocytes indicates injury to these cells. Altered levels of serum protein, albumin, and prothrombin may be related to liver damage.
Hepatitis is used most often when referring to inflammation of the parenchyma of the liver caused by the A, B, C, and D viruses. However, hepatitis may be due to chronic alcoholism, drug toxicities, and autoimmune disorders. The virus causes cell damage that initiates inflammation that then stimulates the immune system. The amount of damage is related to the amount of inflammation and immune response.
Cirrhosis is the irreversible end stage of many liver diseases in which the parenchyma of the liver has been replaced by fibrous tissue. The most common cause of cirrhosis is alcohol. The alcohol causes fat deposits within the hepatocytes, which eventually disrupts the functioning, causing an inflammatory response that leads to the fibrotic changes and ultimately liver failure.
Liver failure tends to occur secondary to hepatitis C and cirrhosis. The manifestations of liver failure range from skin disorders to hepatic encephalopathy. All of the symptoms relate to the liver’s synthesis and storage of substances and its ability to metabolize and excrete substances. In particular, the liver’s ability to convert ammonia (NH) to urea is diminished and elevated levels of ammonia affect the brain, leading to encephalopathy. Hypertension is a result of obstruction of blood flow through the liver. The increased pressure causes ascites, development of collateral channels primarily to the esophagus leading to varices and splenomegaly. Once the kidneys have become involved, the prognosis is poor.
Inflammation of the pancreas, or pancreatitis, is due to the activation of pancreatic enzymes within the pancreas secondary to acinar cell injury. Pancreatic enzymes are secreted in an inactive form so they do not destroy the pancreas itself. With acinar cell damage, the trypsin inhibitor is not secreted in the amounts necessary to maintain the inactivation of the enzymes and parenchymal inflammation occurs. Serum amylase and lipase levels are elevated in pancreatitis. The liver enzymes may also be elevated. Chronic pancreatitis can eventually cause diabetes.
Diabetes is an imbalance between insulin availability and insulin need, resulting in altered metabolism of carbohydrates, proteins, and fat. Diabetes type 1 is due to the autoimmune destruction of the insulin-secreting beta cells in the pancreas. In the absence of insulin that moves glucose into the cells for ATP production, fatty acids are used and ketones are the byproduct, causing ketoacidosis. Type 1 diabetics require exogenous administration of insulin.
Type 2 diabetes seems to be an acquired condition with obesity and decreased physical activity as primary risk factors. Obesity is linked with peripheral insulin resistance and an increased hepatic output of glucose, causing hyperglycemia. There is also an inadequate secretion of insulin by the beta cells. The increased amount of adipose tissue is related to an alteration in the amounts of FFA, adipokine, and peroxisome proliferators-activated nuclear receptors produced (Porth, 2007). All three substances are related in insulin resistance.
Type 2 diabetics often have other metabolic abnormalities such as elevated levels of plasma triglycerides and low levels of HDL. Blood pressure is elevated and there is a systemic inflammation identified by C-reactive protein levels. There is an abnormal function of the vascular endothelium leading to microvascular and macrovasular changes seen as neuropathies, retinopathies, and nephropathies. Macrovascular changes lead to coronary artery disease, CVAs, and peripheral vascular complications. Ulcers of the foot and leg are commonly seen in diabetes, leading to systemic infections if not treated promptly and properly.
Structure of Bone
Bones provide the major structural support to the human body, while ligaments, tendons, and cartilage provide the movement. Cancellous, or spongy bone, is found in the middle of most bones. Surrounding cancellous bone is compact bone that is laid down in concentric circles, providing density and strength. In the middle of the longer bones, there are cavities that contain fatty marrow, and these are lined with endosteum. Undifferentiated osteogenic cells are located in the endosteum (Copstead & Bansik, 2005). The bone is covered with periosteum that has an extensive blood supply and provides anchorage for blood vessels that enter into the bone. When bones are broken, the blood loss is due to disruption of this blood supply. “Just underneath the periosteum is a layer of osteoblasts that are responsible for bone growth” (Copstead & Bansik, 2005, p. 1232). Osteocytes are the mature bone cells and osteoclasts are the cells that break down osteocytes during remodeling.
Within the bone “a network of osteoblasts and osteocytes according to Wolff’s law, replace bone where needed and resorb bone where it is not needed” (Copstead & Banasik, 2005, p. 1233). Disuse of the skeletal structure through immobilization will cause an increase in resorption of the bone and a decrease in bone mass. Bone mass also decreases with age, possibly due to calcium and vitamin D deficiencies and decrease in estrogen production.
Osteoporosis is a disease associated with an imbalance between osteoblast and osteoclast activity. The lattice work structure of cancellous bone becomes more fragile. Vertebrae are primarily cancellous bone and extremely susceptible to compression fractures. The compact bone surrounding the cancellous bone becomes less dense and is unable to withstand even normal stress, leading to fractures. Primary risk factors are small bone structure, being postmenopausal, and advanced age. Lifestyle risk factors include minimal physical activity, caffeine intake, smoking, and alcohol. Corticosteroids have been implicated in causing osteoporosis. The treatment involves modifying those lifestyle factors that increase the risk along with improving intake of vitamins D and C and calcium. Medications used to treat osteoporosis either block the reabsorption of calcium or stimulate bone formation. Estrogens, selective estrogen receptor modulators, bisphosphonates, and calciton block the osteoclast activity. A drug approved by the FDA, teriparatide, increases osteoblast production and the function of already active osteoblasts (Porth, 2007).
The purpose of articular cartilage covering the ends of bones is to spread the mechanical stress of weight over a broader surface and transmit the weight to the bone. Cartilage has no direct blood supply, lymph channels, or nerve endings. Chondrocytes are the major cellular component of cartilage. Synovial fluid contains an enzyme called lubricin that lubricates the cartilage. Synoviocytes found in the synovial membrane secrete hyaluronic acid, which increases the viscosity of the synovial fluid and decreases friction.
Osteoarthritis (OA) is a progressive loss of articular cartilage, particularly the knees and hips. The development of OA has been related to factors that increase the wear and tear on the joint, such as obesity, age, and joint trauma. Diabetes, hormonal status, and genetic predisposition are also factors. Articular cartilage, as it is normally worn out, undergoes repair by the chondrocytes. Synthesis of new collagen is decreased and old collagen is broken down more rapidly. The cartilage loses some of its tensile strength and ability to disperse the weight. As the cartilage becomes more worn, chondrocytes release cytokines which stimulate proteases to cause further breakdown of the cartilage. Eventually the cancellous bone is reached and damaged. During the repair process, osteophytes or spurs are formed along the uncartilaged areas, causing more friction and stress in the joint. Eventually the synovial membrane becomes inflamed.
The first sign of OA is pain in the joint that worsens with activity along with crepitus that occurs as the two ends of the bone grind against one another. The joint becomes limited in movement and unstable. The treatment involves NSAIDs that reduce inflammation and provide pain relief. Heat and cold can be used to relieve pain and muscle spasm. Corticosteroid injections are also meant to decrease the local inflammatory response. Injections of sodium hyaluronate into the joint improve lubrication. Surgical replacement of the joint is the last treatment of choice.
Rheumatoid arthritis is due to an abnormal immune response in individuals who have a genetic predisposition. While rheumatoid arthritis is a systemic inflammation, it is the synovial joints that are most often affected. T-cells are activated by an unknown antigen trigger and cause the formation of immune complexes (Porth, 2007). Neutrophils and macrophages phagocytize the immune complexes, recruit other immune cells to the synovium, and release inflammatory enzymes. The synovial membranes become edematous, there is hyperplasia of the synovial cells, and angiogenesis of the synovium. This altered synovial membrane begins to invade other tissues such as the ligaments, cartilage, and tendons. Pannus, as it is called, erodes and destroys articular cartilage, resulting in bone cysts, bone destruction, and alteration of the total joint structure secondary to fibrosis (Porth, 2007).
The signs and symptoms of rheumatoid arthritis relate to the swelling of the synovium of the joints. Stiffness in the joints is one of the first signs. Pain usually accompanies the stiffness. There is swelling of the joints, usually three or more. The signs and symptoms must continue for over 6 weeks to establish the diagnosis of rheumatoid arthritis.
Drug treatment involves preventing further destruction of the joint, decreasing inflammation, and decreasing pain. NSAIDs reduce the pro-inflammatory enzymes and provide pain relief. Corticosteroid drugs also interrupt the inflammatory response, as well as slow the immune response. The disease-modifying anti-rheumatic drugs (DMARDs) hold the best hope for decreasing the damage to the joint, if given early enough in the disease process (Porth, 2007). Methotrexate, sulfasalazine, and azathioprine are potent anti-inflammatory agents. Newer anti-rheumatic drugs include leflunomide, etanercept, and adalimumab. Their mechanism of action is to block proliferation of T-cells or block TNF-α, which blocks the immune and inflammatory cascade before all the destructive enzymes are produced.
Conclusion
Disorders of the GI system are not very glamorous. Nausea, vomiting, diarrhea, and constipation are often associated with these disorders. With production of about 5 liters of fluid a day, monitoring intake and output is an important nursing role. Assessing whether the symptoms are a side effect or a sign of a more serious dysfunction along with collaborating with the physician to provide the most effective treatment are also vital roles. Medications that decrease nausea and acid production are some of the most frequent medications given by nurses.
The ability of one to ambulate, particularly to the bathroom, is dependent upon muscle strength, ease of joint movement, and strength of bone. Movement is vital to activities of daily living and continuing health. Nursing in conjunction with physical therapy assists patients in maintaining or achieving the maximum amount of mobility.
References
Copstead, L. C., & Banasik, J. L. (2005). Pathophysiology (3rd ed.). St. Louis, MO: Elsevier Saunders.
McCance, K. L., & Huether, S. E. (2006). Pathophysiology: The biological basis for disease in adults and children (5th ed.). St. Louis, MO: Elsevier Saunders.
Porth, C. M. (2007). Essentials of pathophysiology: Concepts of altered health states (2nd ed.). Philadelphia, PA: Lippincott Williams & Wilkins.
The case scenario provided will be used to answer the discussion questions that follow.
Mr. C., a 32-year-old single man, is seeking information at the outpatient center regarding possible bariatric surgery for his obesity. He reports that he has always been heavy, even as a small child, but he has gained about 100 pounds in the last 2–3 years. Previous medical evaluations have not indicated any metabolic diseases, but he says he has sleep apnea and high blood pressure, which he tries to control with sodium restriction. He current works at a catalog telephone center.
Objective Data
Height: 68 inches; Weight 134.5 kg
BP: 172/96, HR 88, RR 26
Fasting Blood Glucose: 146/mg/dL
Total Cholesterol: 250mg/dL
Triglycerides: 312 mg/dL
HDL: 30 mg/dL
Critical Thinking Questions
What health risks associated with obesity does Mr. C. have? Is bariatric surgery an appropriate intervention? Why or why not?
Mr. C. has been diagnosed with peptic ulcer disease and the following medications have been ordered:
Magnesium hydroxide/aluminum hydroxide (Mylanta) 15 mL PO 1 hour before bedtime and 3 hours after mealtime and at bedtime.
Ranitidine (Zantac) 300 mg PO at bedtime.
Sucralfate/Carafate 1 g or 10ml suspension (500mg / 5mL) 1 hour before meals and at bedtime.
The patient reports eating meals at 7 a.m., noon, and 6 p.m., and a bedtime snack at 10 p.m. Plan an administration schedule that will be most therapeutic and acceptable to the patient.
Assess each of Mr. C.’s functional health patterns using the information given. (Hint: Functional health patterns include health-perception – health management, nutritional – metabolic, elimination, activity-exercise, sleep-rest, cognitive-perceptual, self-perception – self-concept, role-relationship, sexuality – reproductive, coping – stress tolerance.)
What actual or potential problems can you identify? Describe at least five problems and provide the rationale for each.