Alterations in Nutrition - PowerPoint PPT Presentation

Alterations in Nutrition

Gastroesophageal Reflux Disease

Peptic Ulcer Disease

Cholecystitis/Gastric Surgery

• Occurs when contents of the stomach including stomach juices (flow back) into the esophagus

• Incompetent lower esophageal sphincter
• Transient LES relaxation
• Increased intragastric pressure

• Smoking
• Caffeine
• ETOH
• Fatty meals
• Obesity
• Increased gastric acid and pepsin production

Chest pain

Regurgitation

Pain after eating

Dysphagia

Belching

Sore throat

Hoarseness

Pain is worsened when the patient bends over at the waist or reclines.

• Esophageal strictures
• Ulcers
• Erosions

• Pre- malignant condition from irritation of gastric content on the normal cell epithelium of the esophagus. It may progress to adenocarcinoma.

• Barium swallow
• Endoscopy (EGD)
• Esophageal motility studies
• Ambulatory pH monitoring
• Esophageal manometry

• Practical changes in daily living
• Pharmacology
• Surgery

• Diet changes
• loose weight and eat smaller meals
• Refrain eating 3 hrs. after bed time and say upright 2 hours after a meal.
• Limit the amount of citrus juices, coffee, chocolate, spicy foods alcohol and peppermint.

• Stop smoking
• Avoid tight clothing
• Avoid bending

• H2 receptor antagonist (Cimetidine, Ranitidine, famotidine,nizatidine)
• Proton Pump inhibitors (Prilosec, Prevacid)
• Promotility agents (Cisapride=Propulsive)

• Antacids-to neutralize acidity, increased LES pressure.
• It is usually take 1-3hrs after a meal and at bed time.

• It is reserve for patients who can develop serious complication.
• The must common surgery done is called
• Nissen Fundoplication-This surgery involve wrapping the fundus of the stomach around the lower esophagus and suture the fundus to itself.

• What is it?
• Partial Stomach protrusion through the diaphragm.

Trauma

Intra-abdominal pressure

Chest pain

Occult bleeding

Regurgitation

Dysphasia

Belching

• Incarcerated necrotic hernia
• Hemorrhage

• EGD
• Barium swallow

• Pharmacological (same as GERD)
• Changes in life style
• Surgery (Nissen fundoplication)

• Pt. Experiences spastic contractions of the esophagus .
• Symptoms: angina-like chest pains and dysphasia.
• Treatment: Calcium channels blockers, nitrates and anticholinergics

• What is it ? Dilation and loss of tone in the esophagus with high gastroesophageal sphincter pressure.
• Why does it happen? Cause unknown.

• Nocturnal cough
• Chest pains
• Dysphagia
• Regurgitation
• Weight loss

• Small frequent feedings of soft warm food and fluids.
• Avoids hot spice food and ETOH
• LES dilatation with a balloon dilator
• Calcium channel blockers and nitrates
• Surgical myotomy(opening LES )

• Is the second most common cancer in the world.
• Every year 25,000 Americans develop gastric cancer.
• 13,000 Americans died every year
• Highest in Hispanic, African Americans, Asian Americans.
• Men affected twice as much as women.

• Common location for the stomach cancer: distal portion of the stomach. A mayor factor for the development of gastric cancer is H. Pylori

• Genetic predisposition
• Carcinogenic dietary
• Pernicious anemia
• Gastric polyps
• Chronic H. Pyloric gastritis
• Achlorhydria -lack of hydrochloric acid in the stomach.

• Adenocarcinoma which involves the mucous producing cells is the most common form of gastric cancer.
• These carcinomas may arise anywhere on the mucosa surface of the stomach but are more frequently found in the distal portions.

• When the disease is limited to submucosa and mucosa; it is early gastric carcinoma.
• Metastasis occur early due to rich blood supply of the area.
• Symptoms are vague and usually the discovery is done when the disease is advance.

Bloating or indigestion soon after eating.

Vague pain in the upper abdomen.

Heartburn

Nausea/vomiting

Poor appetite

Blood in vomits or blood in the stool

• Blood test will show presence iron deficient anemia or pernicious anemia.
• Gastric analyses-may reveal deficiency of hydrochloric acid.
• An upper GI X-ray study with barium swallow could identify lesions.
• (the special x-rays of the esophagus and the stomach in which the pt. Drinks a solution containing barium. It shows up in x-rays and may outline a tumor or abnormality).

• The stool may be tested for occult (hidden) blood.
• Computerized Topography (CT) Scan of the abdomen may show tumor particularly when combined with a barium swallow.
• Gastroscopy examination in which along thin tube is inserted down esophagus into stomach a small video camera at the other end pick up the image and displayed on monitor screen.

• If the gastric cancer is identified prior to the development of metastasis. Surgical intervention with total gastrectomy is the treatment of choice.
• Radiation and chemotherapy may be used to eliminated any suspected metastasis.
• If the disease is advanced, tx is palliative and includes surgery and chemotherapy.

• Billroth I (gastroduodenostomy): removal of the distal half of the stomach and anastomosis to the duodenum. Vagotomy usually is done.
• Billroth II (gastrojejunostomy): removal of the distal portion of the stomach with anastomosis to the proximal jejunum. Duodenal stump left intact so that bile can enter the intestines.

removal of the distal 1/2 to 2/3 of the stomach.

Antrectomy:

Removal of the gastrin producing cells area of the stomach.

Pyloroplasty:

Surgical enlargement of an opening between stomach and duodenum to improve gastrin emptying.

Vagotomy severing all or part of the vagus nerve to significantly reduce the parietal cell acid secretion.

• Anemia (both iron deficiency and pernicious)
• Dumping syndrome
• Folic acid defiency
• Decreased absorption of Vitamin D and calcium

• Decreased size of the stomach reservoir causing absorption and emptying problems.

• Dumping syndrome is define as the rapid passage of food bolus into the duodenum or jejunum.
• It usually occurs after gastric surgery when the pylorus has been resected or by passed.

• A hypertonic, undigested food bolus may rapidly enter the duodenum or jejunum….
• Then water is pulled into intestinal lumen...
• Peristalsis is stimulated…..
• Intestinal motility increased….

• It occurs 5-30 minutes after eating
• Hyperosmolar chyme enter the jejunum: why?
• Rapid rise in blood glucose: why?
• Excessive amount of insulin are secreted and released: Why?
• Hypoglycemia occurs 2-3 hours after a meal
• why?

Vomiting

Epigastric pain with cramping.

Diarrhea

Loud, hyperactive bowel sounds (borborygmi)

Symptoms of hypovolemia and reflex sympathetic stimulation: dizziness flushing, Diaphoresis

tachycardia

• Delay gastric emptying and allow smaller boluses of undigested food to enter the smaller intestine.
• Give smaller and more frequent meals
• Give liquids at a separate time from solids

• Increased protein and fats in the diet.
• Reduce carbohydrates, especially simple sugars
• After eating rest in a recumbent or a semirecumbent position for 30-60 minutes.
• May give antispasmodics, anticholinergics, and sedatives.

• A break in the mucous lining of the GI tract where it comes in contact with gastric juice.
• Can occur in the esophagus, stomach or duodenum.
• Ulcers of the duodenum are 5 times more frequent.

• About 20, 000 millions Americans develop at least one ulcer during their life time.
• Each year 4,000,000 millions are affected by ulcers.
• About 6,000 people die of ulcer related complications.

• People who smoke
• People who use NSAIDS
• People with chronic H. Pylori
• People with hypersecretory states.

• The gastric mucosa protects itself by creating a mucosal barrier make of mucosa gel and bicarbonate.
• An ulcer or break down of the mucosa develops when the mucosal barrier is unable to protect the mucosa from damage by hydrochloric acid and pepsin.

• Mucosal barrier is maintained by:
• Bicarbonate produced by the epithelial cells.
• Mucous gel production stimulated by prostaglandins.
• Adequate blood supply to the mucosa.

• An imbalance between digestive juices (hydrochloric acid and pepsin) and the stomach’s ability to defend itself against these powerful substances result in ulcers
• See the Table 14-1 on p.489 for the clinical features of ulcers of the stomach and duodenum.(could be test questions)

• **Non-steroidal anti-inflammatory drug use (NSAIDS).**Aspirin is the most ulcerogenic of the NSAIDS.
• Chronic Helicobacter Pylori(H. Pylori) infection.(90 of ulcers cause by this)
• Acid hypersecretory states with gastrin secreating tumor(Zollinger-Ellison syndrome)

Pain:gnawing,burning,aching or hunger like in the epigastric region

Pain occurs when the stomach is empty,2-3 hours after a meal or during the night.

May have heartburn, regurgitation or vomiting.

• Vague, poorly localized discomfort
• May have chest pain or dysphagia
• May have weight loss or anemia
• May present with GI hemorrhage or perforation of the stomach or duodenum.

H. Pylori

Stool for occult blood

Upper GI series less costly than gastroscopy and able to see 80% to 90% of ulcers (misses small and superficial ulcers)

Gastroscopy is definitive tool for diagnosis of PUD.

• Symptoms relief
• Healing of existing ulcers
• Preventing complications
• Preventing/reducing recurrences

• Behavior modification
• Pharmacologic therapy
• Surgical interventions

• Usually aims to eradicating H. Pylori and promoting healing.
• Medications to treat PUD are :
• agents that decreased gastric acid content.
• agents that protect the mucosa
• agents that eradicate H. Pylori

Proton pump binds the acid secreting enzyme (H+ K+ ATPase) that function as proton pump disabling it for 24hrs

H2- receptor antagonists which inhibits histamine binding to the receptors on the gastric parietal cell to reduce acid secretion.

Zantac, Pepcid, Tagamet and Axid

Bismuth compounds stimulate mucosal bicarbonate and prostaglandin production.

Prostaglandin analogs promote healing by stimulating mucous and bicarbonate secretions and by inhibiting acid secretion (Misoprostol)

Antacid stimulate gastric mucosal defenses.

Tetracycline or (Amoxicillin)

Metronidazole

Bismuth subsalicylate

The regimen to treat H. Pylori is usually taking for 14 days.

NU 230 students are responsible for understanding the actions, nursing implications, adverse effects and drug interaction of the drug classes to treat PUD.

• Why would a patient with hemorrhage have orthostatic hypotension?
• Why would a patient with perforation have rigid, boardlike abdomen, fever, and absence of bowel sounds.

• Hemorrhage
• Obstruction
• Perforation
• *See LeMone text p.491 for signs and symptoms of complications.

• 10% -20% ulcer can cause ulceration and erosion into the blood vessel or gastric mucosa.
• It occurs more commonly in older adults

• Maintain adequate circulatory status.
• By administering NS or Lactated Ringer’s to restore intravascular volume.
• Blood transfusion with whole blood or RBC’s to restore hgb or hct.
• NGT insertion and gastric lavage may be necessary.

• Additional measures to control bleeding.
• Vasopressin (ADH) IV a potent vasoconstrictor agent.
• Gastroscopy with direct injection of clotting or sclerosing agent into bleeding vessel.
• Laser photocoagulation using light energy or electrocoagulation which use an electrical current to generate heat.

• Pt. Needs to be kept NPO
• Antacids can be administer hourly via the NGT to protect the ulcer from gastric acid reflux.

• Inflammation may cause obstruction.
• Edema and poor ability to heal.
• Scarring
• Muscle spasm.

• Gastric or duodenal perforation result in contamination of the peritoneum with gastrointestinal contents require immediacy attention.
• Prepare pt. for surgical intervention.
• Give IV fluids and replace electrolytes.
• NG to LIS
• Pt. in Fowler’s and semi Fowler position.
• Give antibiotics

• Goals :
• Decreased gastric secretions
• Remove damage tissue
• Promote gastric emptying

• The area to be removed depends were ulcer is located

• Acute onset as a result of a major physiologic stressor.
• Examples of events which are followed by stress ulcer:
• trauma
• surgery involving the central nervous system or a head trauma(Cushing’s ulcer).
• burns (Curling’s ulcers).

• Respiratory failure
• Renal failure
• Shock.

Superficial

Usually fundus

Not usually painful

Gastric bleeding 2 or more days after the stressor.

Bleeding typically minimal but may be massive.

High mortality rate.

• Cause: ischemia of the gastric mucosa resulting from sympathetic vasoconstriction, and tissue injury from the gastric acid.
• Maintaining the gastric pH greater than 3.5 and decreasing gastric acid secretions decreased possibility of having stress ulcers being form.

• Unlike other ulcers, stress ulcer are not typically associated with pain.
• The first symptom is painless gastric bleeding occurring 2 or more days after the initial stress. The bleeding can be massive coming from multiple lesions.

• Peptic ulcer disease caused by a gastrinoma or gastrin-secreating tumor of the pancreas, stomach or intestine.
• 50% to 70% of the tumors are malignant.
• Gastrin is a hormone that stimulate the secretion of pepsin and hydrochloric acid.
• The increase gastrin levels cause ulcers.

• Characteristic ulcer like pain
• Diarrhea
• Steatorrhea(fat in the stool)
• Electrolytes imbalance.

• Associated with gastric gland atrophy and decrease protection of gastric mucosa by the mucosal barrier rather than with increased secretion of hydrochloric acid.
• Occur more commonly in older adults 60-70 years old.

• Gastric ulcers are consider to be pre-malignant lesions because of the incident of gastric cancer.
• Occur more common in the older adult above 60 years.

• Dull aching abdominal pains after eating.
• Pain is exacerbated by food intake.
• Vomiting is common as well.

• Pain
• Alteration in Nutrition: less than body requirements
• Fluid Volume deficit

Administer antiacids, H2-receptor antagonists, proton pump inhibitors or mucosal protective agents.

Provide adjunctive relief therapy such as distraction,relaxation (back rub, change position) and breathing exercises.

Teach life style management techniques.

Arrange a nutritional consult.

Monitor for symptoms of fullness, anorexia, nausea or vomiting.

Monitor lab values related to nutritional deficit.

Albumin

Iron studies

B12 levels

Orthostatic blood pressure at the beginning of shift

Maintain Accurate I &O (foley may be needed)

Weigh QD

Monitor stool and gastric drainage for occult and overt blood.

Maintain IV therapy with fluid volume and electrolytes replacement.

Insert NGT and lavage if needed.

Replace decreased HCT with whole blood or RBCS

Assess abdomen for distention, BS, and tenderness q4hrs and record.

• Cholelithiasis: stones or calculi
• Cholecystitis: inflamed gallbladder with or without stones.
• What are gallstones made of ? Cholesterol and bile pigments

• Gallstones are made of bile pigments or hardened cholesterol
• Stone formation occur when the bile crystallizes.
• Factors that contribute to stone formation
• stasis of bile in the gallbladder
• bile concentration

Native American, Caucasian, Mexican American

Females(oral contraceptive use and pregnancy)

Patients on TPN

Certain disease (see text, p.512)

causes gallbladder to distend, result in in severe cramping , colicky pain.

Secondary infection combined with severe inflammation and edema result in duct blockage and abdominal pain.

Obstruction of the common bile duct.

May result in bile reflux into the liver producing jaundice, pain hepatic damage, pancretitis or sepsis

Heartburn

Right upper abdominal pain.

Jaundice

Intolerance to fat containing foods

Female gender

pregnancy

use of oral contraception

Hyperalimentation

Aging

Diseases or conditions

Native Americans

Caucasians

Mexican Americans

• It is an inflammation of the gallbladder.
• It is commonly associate with stones in the cystic and common bile duct.
• It is classified as acute or chronic.

• Severe spasmodic pains ( it usually happens after a high fat meal)
• RUQ pain radiating to the mid line and posterior to the scapula region.
• Frequent nausea and vomiting.

• Symptoms are not as severe and are more vague.
• Long term intolerance to fatty food, increase flatulence.

Increase WBCs

Abdominal muscle guarding with rebound tenderness and rigidity

Elevated bilirubin

Elevated Alkaline phosphatase

Elevated amylase

• CBC for elevated WBC
• Serum amylase and lipase to see if pancretitis is present.
• Serum bilirubin to see if there is an obstruction in the biliary system.

• Cholangiograms to check for stones
• Ultrasound of the gallbladder(for non-obese clients)
• HIDA scan done done in nuclear medicine to assess acute cholecystitis.

Serum amylase and lipase to check for pancretitis.

Serum bilirubin

Gallbladder scans

oral cholecystogram

oral dye is use to assess the gallbladder’s ability to concentrate and excrete bile.

Diet therapy with low fat diet and weight loss.

Surgery: it depend on the stone location and severity of the complications

.

Urodeoxycholic (UDCA)

is for cholesterol stones less than 20mm in diameter.

Pt. Need to have hepatic enzymes monitor closely

watch for diarrhea

Other pharmacologic agents are use for palliative relief such as

Antibiotics -to decrease bacteria count and associate inflammation and edema.

Pain medications

Patients need to be put on a low fat diet.

If bile flow is reduced because of obstruction fat soluble vitamins A, D, E, and K and bile salts needs to be replaced.

Examples of high fat food to avoid : deep fried foods, whole milk etc..

If the stones are located only in the Gallbladder a simple Cholecystectomy is performed.

Conventional surgical methods.

Laparascopic laser surgery

• For a poor surgical risk clients, a cholecystostomy (for drainage) or a choleduchostomy ( removal stones and T-tube placement) may be performed as opposed to surgical removal of the gallbladder.

Percutaneous stone dissolution is a treatment option for patients who are a high risk for post surgical problems using a fluoroscopy the MD ,may position a catheter via the biliary system. Dissolution agents are then instill.

• Care of the patient with T-tube (Lemone p.517)
• Possible complications of a patient with T-tube(Lemone p.517)
• All readings and syllabus applications regarding the pharmacology and nutrition of GERD, PUD, cholecystitis, and gastric surgery.

• Ensure that the tube is connected to sterile container; keep the tube below the surgical wound.
• Monitor drainage for consistence, color, amount.
• Place patient in semi-Fowler’s position
• Assess skin around for bile leakage during dressing changes.

• Teach patient how to manage the tube when turning ambulating or doing activities.
• When drainage subsides and stool returns to normal brown color clamp the tube for 1 to 2 hours after a meal.

• Frequent problems with these conditions:
• Pains
• Altered nutrition due to nausea, vomiting, and impaired fat metabolism.
• Risk for impaired gas exchange/ risk for infection.

fat stimulate gallbladder contractions and is a stimulus for pain .

Administer prescribed medications such as Dicyclomine (Bentyl) used to decrease spasm and relax muscle.

If pain is not relieved by these methods administer prescribed narcotics

Check for elevation of temperature q4hrs.

Assist the patient to semi Fowler’s position.

Institute a regiment of turning, deep breathing and coughing at least every 2 hrs.

Use incentive spirometer every hour while awake.

OOB ambulating as soon as possible.

Asses for signs of systemic and localized infections during the post period.

Temperature q4hrs

Asses wound q4hrs

Performed abdominal assessment q4hrs.

Monitor labs QD

Administer prescribe antibiotics as order.

Use aseptic technique when doing invasive procedures,