1. Alterations of the GI Tract

2. Clinical Manifestations of GI Dysfunction
Anorexia
Vomiting
Constipation
Diarrhea
GI Bleeding
Anorexia – “Is the lack of a desire to eat despite physiologic stimuli that would normally produce hunger. Anorexia is a nonspecific symptom that is often associated with nausea, abdominal pain, diarrhea, and psychologic distress” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1482).
Vomiting – “Is the forcful emptying of the stomach and intestinal contents (chyme) through the mouth” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1452).
Constipation – “Is difficult or infrequent defecation [and]… must be defined individually because patterns of bowel evacuation differ greatly among individuals. Constipation usually means a decrease in the number of bowel movements per week, hard stools, and difficult evacuation” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1453). Disorders involving constipation include: Hirschsprung disease, acquired megacolon, hypothyroidism, pelvic hiatal hernia, multiple sclerosis, spinal cord trauma, cancer, cerebrovascular disease, and irritable bowel syndrome.
Diarrhea – “Is an increase in the frequency of defication and the fluidity, volume, and weight of feces and is often a protective response. Three or more stools per day are considered abnormal” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1454).
GI Bleeding – Is divided into two classifications. Upper GI bleeding occurs in the esophagus, stomach or the duodenum, and is frequently caused by a bleeding peptic ulcer. Lower GI bleeding occurs in the jejunum, ileum, colon, or rectum, and can be caused by many different GI disorders. Hematemesis is vomiting up bright red blood or dark red grainy blood that appears as coffee grounds. Melena is characterized by black, tarry, sticky, foul smelling stool, and is caused by the digestion of blood in the GI tract. Hematochezia is characterized by the passing of bright red blood from the rectum, and occult blood is the presence of trace ammounts of blood in the stool from a slow bleed. This is only detectable with a guiac test (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1456)

3. Disorders of Motility Dysphagia
Defined as difficulty swallowing, and can result from mechanical obstruction or a functional disorder that impairs esophageal motility.
Mechanical obstructions can be intrinsic (e.g. esophageal tumor) or extrinsic (e.g. a tumor pressing on the esophagus from a nearby part of the body).
“Functional dysphagia is caused by neural or muscular disorders that interfere with voluntary swallowing or peristalsis” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1456).
Clinical manifestations vary depending on the cause and location. Discomfort 2-4 seconds after swallowing is indicative of an upper esophageal obstruction. Discomfort seconds after swallowing is indicative of middle to lower esophageal obstruction. Other clinical manifestations include retrosternal pain, regurgitation of undigested food, unpleasant taste, vomiting, weight loss, and aspiration (which can lead to aspiration pneumonia) (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1458).

4. Disorders of Motility Gastroesophageal Reflux Disease (GERD)
GERD “is the reflux of chyme from the stomach to the esophagus” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1458).
GERD is caused when the lower esophageal sphincter spontaneously relaxes 1-2 hours after eating allowing stomach contents to regurgitate into the esophagus. It takes the esophagus 1-3 minutes for the esophagus to clear the acid and for the lower esophageal sphincter (LES) to regain its tone.
Contributing factors include decreased LES muscle tone, vomiting, coughing lifting bending, obesity, and delayed gastric emptying. Prolonged exposure to acidic chyme can lead to esophagitis and ulcerations of the esophageal mucosa. Long term exposure can increase the risk of esophageal cancer.
Clinical manifestations include heartburn, regurgitation of acidic chyme, and upper abdominal pain within one hour of eating. Symptoms increase with increased intra-abdominal pressure and ling down.
The most common treatments include proton-pump-inhibitors which block the receptors H2 receptors and decrease the acidity of the stomach’s contents.

5. Disorders of Motility Hiatal Hernia
A type of diaphragmatic hernia in which the upper portion of the stomach herniates up through the diaphragm into the thorax (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1459).
There are two types of hiatal hernias, sliding and paraesphageal. Sliding hiatal hernias comprise 90% of hiatal hernias. It occurs when the upper portion of the stomach slides up through the esophageal hiatus and into the thorax. Contributing factors include a congenitally short esophagus, trauma, or weakening of the diaphragm. In these cases, ling down causes the stomach to slide into the thorax, and standing causes the stomach to slide back into the abdomen. This contributes to GERD and esophagitis, because it lowers the pressure of the LES. Paraesophageal hiatal hernias are hernias where the greater curvature of the stomach through a secondary opening in the diaphragm (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1459).
Hiatal hernias are often asymptomatic, but clinical manifestations may include GERD, dysphagia, heartburn, vomiting, epigastric pain, regurgitation, and substernal discomfort (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1460).

6. Disorders of Motility Pyloric Obstruction
Defined as the narrowing or blocking of the opening between the stomach and the duodenum (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1460).
Pyloric obstructions may be congenital (pyloric stenosis) or acquired (Peptic ulcer disease).
Clinical manifestations include vague epigastric fullness, nausea, epigastric pain, anorexia, weight loss, gastric distention, atony, vomiting several hours after eating, dehydration, hypokalemia, hypochloremia, and metabolic alkalosis.

7. Disorders of Motility Intestinal Obstruction and Ileus
“Caused by any condition that prevents the normal flow of chyme through the intestinal lumen or failure of normal intestinal motility in the absence of an obstructing lesion” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1460).
There are a variety of types and causes of intestinal obstruction and Ileus which are summarized in tables 39-2 and The consequences of these obstructions depends on the size and location of the obstruction. Clinical manifestations also vary greatly depending on the location and size of the obstruction. See Table 39-4 and figure 39-4 for classifications and types of obstructions (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, pp ).

8. Gastritis Two Types Acute Chronic
Acute Gastritis – Erosion of “surface epithelium in a diffuse or localized pattern,” and it can be caused by drugs, chemicals of H. pylori infection. Non-steroidal anti-inflamatories (NSAID’s) inhibit prostaglandins which stimulate mucous production. “Alcohol, histamine, digitalis, and metabolic disorders such as uremia are risk factors” for developing acute gastritis (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1463). Clinical manifestations include vague abdominal discomfort, epigastric tenderness, and bleeding.
Chronic gastritis – “Tends to occur in older adults and causes chronic inflammation, mucosal atrophy, and epithelial metaplasia” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1463). Chronic gastritis is subdivided into two categories: type A (immune or fundal) and type B (nonimmune or antral).
Chronic fundal gastritis is the most rare and severe of these disorders, and it is characterized by extensively degenerated mucosa in the fundus and body of the stomach and atrophy of the stomach. “ Loss of chief cells and parietal cells diminishes secretion of pepsinogen, hydrochloric acid, and intrinsic factor” McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1464). This leads to increased plasma levels of gastrin and pernicious anemia because there is not enough intrensic factor to facilitate the absorption of vitamin B12. This disorder is an autoimmune disease in which the immune system attacks the parietal cells and other gastric cells.
Chronic antral gastritis only involves the antrum of the stomach and is four times more common that chronic fundal gastritis. This disease is associated with chronic alcohol, tobacco, and NSAID use; however, the most common cause is infection with H. pylori.

9. Peptic Ulcer Disease (PUD)
                                                                                                                                  
Peptic Ulcer Disease (PUD)
Three Types
Duodenal Ulcers
Gastric Ulcers
Stress-Related Mucosal Disease
Postgastrectomy
Syndrome
PUD “is a break or ulceration of the protective mucosal lining of the lower esophagus, stomach or duodenum. Risk factors include H. pylori infection and habitual use of NSAIDs” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1464). Peptic ulcers are classified as acute or chronic, and as superficial or deep.

10. Peptic Ulcer Disease (PUD)
Duodenal Ulcers
Greatest frequency of any PUD.
Possible association with type “O” blood.
Risk factors other than H. pylori and NSAID’s include:
Increased mass of gastric parietal cells
Serum gastrin levels remain higher than normal after eating and continue to stimulate acid and pepsin secretion.
Failure of the feedback mechanism whereby acid in the antrum inhibits gastrin release.
Rapid gastric emptying, which overwhelms the buffering capacity of the bicarbonate-rich pancreatic secretions.
Acid production stimulated by cigarette smoking.
Decreased duodenal mucosal bicarbonate secretion.
Clinical manifestations include chronic intermittent epigastric pain which begins 30 minutes to 2 hours after eating. Ingestion of antacids or food often relievs symptoms quickly. Some older adults have no clinical manifestations until they start hemorrhaging or their bowel perforates. Bleeding causes melena production.
Duodenal ulcers typically heal spontaneously and exacerbations occur in the spring and fall (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, pp ).
Duodenal Ulcer

11. Peptic Ulcer Disease (PUD)
Gastric Ulcers
Occur in populations between ages 55-65
One fourth as common as duodenal ulcers
Symptoms similar to duodenal ulcers.
Gastric ulcers typically occur “in the antral region, adjacent to the acid-secreting mucosa of the body, and are frequently caused by H. Pylori” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1467). This causes increased permeability of the gastric mucosa to H+ ions. Other contributing factors include inhibition of pyloric sphincter resting tone allowing bile reflux into the stomach. Damaged mucosa released histamines which increases acid and pepsinogen production. The damaged tissue becomes edematous and begins to lose plasma proteins. As blood vessels become damaged, hemorrhaging develops (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1467).
H. pylori

12. Peptic Ulcer Disease (PUD)
Stress Related Mucosal Disease
Acute peptic ulcer disease associated with physiologic stress.
Three Categories
Ischemic Ulcers
Curling Ulcer
Cushing Ulcer
Ischemic Ulcer – Occurs within hours of an injury that causes extensive intravascular fluid loss leading to a lack of O2 supply to the GI mucosa.
Curling Ulcer – Similar to an ischemic ulcer, but Develops as a result of a burn injury.
Cushing Ulcer – Associated with severe head trauma or brain surgery in which the vagal nuclei are over-stimulated leading to hypersecretion of gastric acid.
The primary clinical manifestation of these disorders is bleeding (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1467).

13. Peptic Ulcer Disease (PUD)
Postgastrectomy Syndromes
Dumping Syndrome
Alkaline Reflux Gastritis
Afferent Loop Obstruction
Diarrhea
Weight Loss
Anemia
Dumping Syndrome – “Is the rapid emptying of hypertonic chyme from the surgically created, residual stomach into the small intestine minutes after eating” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1468).
Alkaline Reflux Gastritis – “Is a stomach inflamation caused by reflux of bile and alkaline pancreatic secretions that contain proteolytic enzymes and disrupt the mucosal barrier” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1469).
Afferent Loop Obstruction – A rere disorder associated with Billroth II procedures “caused by recurring tumor growth, volvulus, hernia, adhesion, or stinosis of the duodenal stump on the proximal side of the gastrojejunostomy. Partial obstruction causes bile and pancreatic secretions to accumulate and distend the loop” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1470).
Diarrhea – One of the most common long term complications associated with gastric surgery.
Weight Loss – Occurs because individuals that have undergone gastric surgeries can no longer tolerate the same amounts of food, and the GI tract has a diminished ability to digest and absorb food.
Anemia – Gastric surgeries result in anemia because decreased acid secretion leads to impaired iron absorption, and decreased intrinsic factor results in decreased B12 absorption.

14. Malabsorption Syndromes
Pancreatic insufficiency
Lactase Deficiency
Bile Salt Deficiency
Pancreatic insufficiency – is a deficiency in pancreatic enzymes (lipase, amylase, trypsin, and chymotrypsin). These enzymes are essential for the digestion of proteins, carbohydrates, and fats. Causes include pancreatitis, pancreatic cancer, pancreatic resection, and cystic fibrosis. Decreases in pancreatic enzymes causes maldigestion of all nutrients (especially fats since the pancreas is the only organ to produce an enzyme to break down fats). In addition, if pancreatic bicarbonate is decreased as well, it will caused decreased intestinal pH which will deactivate the enzymes that the pancreas does produce. This all leads to severe malnutrition if untreated .
Lactase Deficiency – lactase deficiency inhibits the breakdown of lactase (milk sugar) which results in varying degrees of gastric discomfort depending on the extent of the deficiency and the amount of lactose ingested (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1470). The undigested lactose is fermented by intestinal bacteria which leads to gas production and flatulence. The fermentation also increases the osmotic gradient in the intestines, which causes irritation and diarrhea (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1471).
Bile Salt Deficiency – Bile salts are required for adequate digestion and absorption of fats, therefore deficient levels of bile salts inhibit fat digestion and absorption. This may be caused by advanced liver disease, billiary obstruction, intestinal stasis, and/or diseases of the ileum (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1471). Clinical manifestations are related to fat and fat soluble vitamin deficiencies.
Vitamin A Deficiency – Night Blindness
Vitamin D Deficiency – decreased calcium absorption, bone demenarilization (osteoperosis), bone pain, and fractures.
Vitamin K Deficiency – Prolongs prothrombin time leading to bleeding disorders.
Vitamin E Deficiency – May cause testicular atrophy and neurological defects in children.

15. Inflammatory Bowel Disease
Five Types
Ulcerative Colitis
Crohn’s Disease
Diverticular Disease of the Colon
Appendicitis
Irritable Bowel Syndrome

16. Inflammatory Bowel Disease
Ulcerative Colitis
“Chronic inflammatory disease that causes ulceration of the colonic mucosa and extends proximally from the rectum into the colon” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1471).
Risk factors for ulcerative colitis include being between the ages of 20 and 40, family history of disease or Jewish decent, or being or white northern European decent. Smoking seems to provide a form of resistance to ulcerative colitis.
Although the exact cause of ulcerative colitis is unknown, studies suggest that it is a genetically linked autoimmune disorder in which T-lymphocytes have cytotoxic effects on the epithelium of the colon. The lesions in ulcerative colitis do not extend below the mucosal layer of the colonic epithelium, however in severe inflammation, the tissue can become hemorrhagic. Inflammation is most severe in the rectum and sigmoid colon with milder inflammation proximally. As inflammation progressed, abscesses form in the crypts, and “necrosis and ragged ulceration of the mucosa ensue” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1471).
Clinical manifestations include intermittent phases of remittance and exacerbation, and the manifestations vary depending on the severity of the exacerbation. During an exacerbation, a patient may experience large volumes of watery diarrhea, bleeding, cramping pain, an urge to defecate, fever elevated pulse, dehydration, weight loss, and anemia. Common complications include toxic megacolon, anal fissures, hemorrhoids, and perirectal abscesses (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1472).

17. Inflammatory Bowel Disease
Crohn’s Disease
“An idiopathic inflammatory
disorder that affects any part
of the [GI] tract from the
mouth to the anus” (McCance,
K.L., Huether, S.E., Brashers,
V.L., & Rote, N.S., 2010, p 1473).
Risk factors for developing Crohn’s Disease (CD) include Jewish decent, tobacco use, family history of disease, urban residency, and CARD15/NOD2 genetic mutation. Genetic mutation it thought to cause an abnormally strong immune response normal GI flora in which the GI tract gets caught in the crossfire. This leads to an inflammatory response in the intestinal submucosa and spreads to the to the “mucosa and serosa in areas overlying lymphoid tissue” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1473). Eventually neutrophils infiltrate the crypts causing abscess formation and crypt destruction. “The ulcerations in CD produce longitudinal and transverse fissures that extend inflamation into lymphoid tissue… The lumen may narrow with inflammation, edema, and fibrotic strictures. Fistulae may form in the perineal area between loops of the intestine or extend into the bladder”
(McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1473).
Clinical manifestations may be nothing but an irritable bowel. Diarrhea, with blood and mucous, accompanied by abdominal pain are the most common symptoms. Other symptoms are
related to the location and extent of the inflammation. These include malabsorption of vitamins B12 and D leading to anemia and osteoporosis for chronic inflammation of the ileum. This
may also lead to malabsorption of proteins leading to hypoalbumenemia. Weight loss is another common manifestation. Anal manifestations include anal fissures, perineal abscesses, and
fistulas.

18. Inflammatory Bowel Disease
Diverticular Disease of the Colon
“Herniations or saclike outpouchings of the mucosa through the muscle layers of the colonic wall” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1474).
Two Types
Diverticulosis (Asymptomatic)
Diverticulitis (Symptomatic)
Diverticular disease is most common in individuals older than age 60 whose diets consist largely of refined foods. Diverticula typically occur at weakened points in the colonic muscle layers (e.g. where arteries penetrate the muscle layer to nourish the mucosa). Another risk factor is consuming a diet low in dietary fiber. Diverticula formation can leas to diverticulitis. Clinical findings in diverticulitis include abscess formation, fistula formation, peritonitis, or obstruction.
Clinical manifestations are typically vague or nonexistent, but may include diarrhea, constipation, distention, or flatulence. If the diverticua becomes inflamed or an abscess forms, fever, leukocytosis, and left lower abdominal pain are evident (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, pp ).

19. Inflammatory Bowel Disease
Appendicitis
“An inflammation of the vermiform appendix, which is a projection from the apex of the cecum” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1475).
Appendicitis is the most common surgical emergency, and it occurs most commonly between the ages of 20 and 30. The exact cause of apendicitis is unknown, but many believe that it is caused by some form of obstruction (e.g. stool entering the appendix) followed by inflammation and bacterial infection. With the appendix obstructed, mucosal secretions cannot drain which leads to increased pressure within the appendix. This restricts the blood flow resulting in ischemia and hypoxia. This cases ulceration in the mucosa within the appendix which promotes bacterial growth. Gangrene develops secondary to occlusion of blood flow which is followed by perforation.
Clinical manifestations include epigastric or periumbilical pain. At first the pain may be vague, but the intensity typically increases over the next 3-4 hours. The pain may subside temporarily but then relocate to the right lower abdominal quadrant. This indicates that the inflammation has extended to the tissues surrounding the appendix, and this pain is often associated with rebound tenderness. “Nausea, vomiting, and anorexia follow the onset of pain, and fever is common” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1476). The most common complications include perforation, peritonitis, , and abscess formation.

20. Inflammatory Bowel Disease
Irritable Bowel Syndrome (IBS)
Is a nonspecific disorder
describing an inflammation
of the GI tract related to
life circumstances
behaviors or dietary
intolerances.
There is no specific cause for the symptoms associated with IBS, but there are several contributing factors associated with IBS which include, abnormal GI motility and secretion, visceral hypersensitivity or hyperalgesia, post infection, overgrowth of intestinal flora, food allergy or intolerance, and psychosocial factors
(McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1476).
Clinical manifestations include lower abdominal pain, diarrhea, constipation, alternating diarrhea and constipation, gas, bloating, nausea, fecal urgency, and incomplete evacuation (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1476).

21. Disorders of Nutrition
Obesity
Anorexia Nervosa
Bulimia Nervosa
Starvation

22. Disorders of Nutrition
Obesity
Defined as having a body mass index greater than 30 (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1477).
Obesity is the most common nutritional disorder in the united states affecting approximately 35% of the population. It can be caused by genetic predisposition and behavioral factors, but it is ultimately caused by an energy imbalance in which energy input exceeds energy output. This causes the body to store the excess energy in the form of adipose tissue (fat). It contributed to high rates of morbidity and mortality, and it is implicated in high rates of many disorders including diabetes, cancer, and cardiovascular disease. Obesity is also a major expense for the health care industry (billions of dollars per year). Genetic abnormalities associated with obesity are rare, and most obesity is behaviorally related (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1477). People who over eat develop leptin resistance. Leptin is the hormone that induces satiety (feeling of fullness). This resistance allows obese people to take in progressively more food without feeling full, which perpetuates the cycle of excess energy, and increases the volume of adipose tissue.
Clinical manifestations include metabolic syndrome (increased triglycerides, decreased HDL’s, increased LDL’s, hypertension, and insulin resistance), increased respiratory effort, obstructive sleep apnea, osteoarthritis, and increased risk of cancer.

23. Disorders of Nutrition
Anorexia Nervosa
An obsessive compulsive psychiatric disorder revolving around weight and food intake (McCance, K.L., Huether,
S.E., Brashers, V.L., & Rote,
N.S., 2010, p 1480).
Anorexia nervosa “has the highest mortality rate of any psychiatric disease and has a familial tendency” (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1480). Characteristics of anorexia nervosa include:
A fear of becoming obese despite progressive weight loss.
A distorted body image: the perception that the body is fat when it is actually underweight.
Body weight 15% below normal for age and height because of refusal to eat.
In women and girls, absence of three consecutive menstrual periods (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1480).
This disorder affects multiple body systems. Once the body has depleted the energy stores in the adipose tissue, the body begins to use proteins from muscle tissue for fuel. The lack of body fat and the atrophy of muscle tissue gives the body a skeleton-like appearance. Demineralization of the bones places the individual at risk for osteopenia and osteoporosis. Low iron levels causes anemia and chronic fatigue. Most electrolytes will be below normal levels. Reproductive function ceases in women to conserve energy. Eventually death occurs related to starvation induced cardiac failure (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1481).

24. Disorders of Nutrition
Bulimia Nervosa
More common than anorexia
nervosa.
Affects the same population
Body weight remains near
normal with aspirations of
weight loss (McCance, K.L.,
Huether, S.E., Brashers,
V.L., & Rote, N.S., 2010, p
1481).
Bulimia nervosa tends to affect older less affluent women than anorexia nervosa, and it is characterized by:
Recurrent episodes of binge eating durring which the individual fears not being able to stop.
Self-induced vomiting, use of laxatives (purging type).
Two binge eating episodes per week for at least three months (purging type).
Fasting to oppose the affect of binge-eating or excessive exercise (nonpurging type) (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1481).
Clinical manifestations from vomiting include pitted teeth, pharyngeal and esophageal inflammation, and trachealesophageal fistula. Laxative abuse can lead to rectal bleeding. Bulemia nervosa is usually associated with some form of depressive disorder which perpetuated the cycle of binging and purging.

25. Disorders of Nutrition
Starvation
Short Term
Long Term
Short term starvation consists of total dietary deprivation over the course of a few days. Between 4 and 6 hours since its last meal the body begins to produce glucose via glycogenolysis and gluconeogenesis. During short term starvation the body does this through splitting glycogen into glucose, and through converting noncarbohydrate molecules such as lactate, pyruvate, amino acids, and the glycerol portion of fats. At this point, there is minimal use of proteins for nutrition (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1481).
Long term starvation causes decreased use of gluconeogenesis and increased use of ketone bodies (products of lipid and pyruvate metabolism). Long term starvation results in depressed insulin levels and increased glucagon, cortisone, epinephrine, and growth hormone levels resulting in lipolysis to liberate fatty acids for metabolism. Once adipose tissue is gone, the body begins metabolizing protein tissue from the muscles. This is the body’s last resort to sustain itself. If the body does not receive needed nutrition, death results from severe electrolyte imbalance and loss of renal pulmonary and cardiac function (McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S., 2010, p 1482).

26. The End