Alterations in Nutrition

Gastroesophageal Reflux Disease Peptic Ulcer Disease Cholecystitis/Gastric Surgery

Upper GI

Gastroesophageal Reflux Disease(GERD)

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

Causes for GERD

Incompetent lower esophageal sphincter Transient LES relaxation Increased intragastric pressure

Contributing Factors to GERD

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

Signs and Symptoms of GERD

Heartburn,indigestion Chest pain Regurgitation Pain after eating Dysphagia Belching Sore throat Hoarseness Pain is worsened when the patient bends over at the waist or reclines.

Complications of GERD
Esophageal strictures Ulcers Erosions

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

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

Treatment for GERD

Practical changes in daily living Pharmacology Surgery

Practical changes in life style

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.

Practical changes in life style

Stop smoking Avoid tight clothing Avoid bending

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

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

Surgery
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.

Hiatal (diaphragmatic) Hernia

What is it? Partial Stomach protrusion through the diaphragm.

Why does Hiatal Hernia happen?

Congenital problems Trauma Intra-abdominal pressure

What are the symptoms of Hiatal Hernia ?

Reflux Chest pain Occult bleeding Regurgitation Dysphasia Belching

Complications of Hiatal hernia

Incarcerated necrotic hernia Hemorrhage

How is hiatal hernia diagnosed

EGD Barium swallow

Treatment for Hiatal hernia

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

Hiatus hernia repair

Hiatus hernia repair

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

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

Achalasia symptoms
Nocturnal cough Chest pains Dysphagia Regurgitation Weight loss

Achalasia treatments
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 )

Cancer of the stomach

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.

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

Risk Factors for Stomach cancer

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

Cancer of 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.

Stomach cancer
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.

Symptoms of gastric carcinoma

A general feeling of being tired or weak. Heartburn Nausea/vomiting Bloating or indigestion soon after eating. Poor appetite Vague pain in the upper abdomen. Blood in vomits or blood in the stool

Stomach cancer diagnostic studies

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).

Stomach cancer diagnostic studies

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.

Endoscopy vie o gastric

Upper GI series

Stomach cancer treatments

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.

Gastric Surgeries
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.

Gastric surgery

Gastric surgery billroth I

Billroth 2

Total gastrectomy

Other gastric surgeries:

Partial-gastrectomy:
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.

Complications of gastric surgery.

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

Disadvantages of the Billroth I and Billroth II

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

Most common complication:dumping syndrome.

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.

Dumping syndrome (how does it happens?)

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.

Dumping syndrome with a closer look

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?

What might be the manifestation of Dumping syndrome

Nausea Vomiting Epigastric pain with cramping. Diarrhea Loud, hyperactive bowel sounds (borborygmi) Symptoms of hypovolemia and reflex sympathetic stimulation: dizziness flushing, Diaphoresis tachycardia

How to treat or prevent gastric syndrome

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

How can we treat or prevent Dumping Syndrome?

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.

Peptic Ulcer Disease

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.

Peptic Ulcer Disease

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.

Peptic ulcers and population at risk

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

Pathophysiology of Peptic ulcers

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.

Pathophysiology of Peptic ulcers

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

Pathophysiology of Peptic ulcers

Peptic Ulcers
An imbalance between digestive juices (hydrochloric acid and pepsin) and the stomachs 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)

Major causes of Peptic ulcer disease (PUD)

**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)

Manifestation of Peptic Ulcer Disease

May have heartburn, Classic: regurgitation or Pain:gnawing,burning, vomiting. 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.

Older adult manifestation might be different

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.

Lab and Diagnostic testing used for peptic ulcer disease

Gastric analyses H. Pylori Stool for occult blood Gastroscopy is definitive tool for diagnosis of PUD. Upper GI series less costly than gastroscopy and able to see 80% to 90% of ulcers (misses small and superficial ulcers)

Goals in the management of Peptic ulcer disease

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

Management strategies
Behavior modification Pharmacologic therapy Surgical interventions

Pharmacologic treatment
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

Medications that decreased the gastric acid content in PUD

Proton pump inhibitors such a Prevacid, Prilosec.
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

Agents that protect the mucosa in PUD

Sulcrafate-bids to protein in the ulcer base forming a protective barrier. 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.

Eradication of H. Pylori in PUD

Usually two antibiotics with either bismuth or proton pump.
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.

Questions regarding the complications of 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.

Complications of peptic ulcer disease

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

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

Hemorrhage in PUD
Maintain adequate circulatory status.
By administering NS or Lactated Ringers to restore intravascular volume. Blood transfusion with whole blood or RBCs to restore hgb or hct. NGT insertion and gastric lavage may be necessary.

Menu

Hemorrhage in PUD
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.

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

Obstruction as a complication for PUD

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

Perforation/Peritonitis
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 Fowlers and semi Fowler position. Give antibiotics

If efforts to control bleeding fail surgery is indicated

Goals :
Decreased gastric secretions Remove damage tissue Promote gastric emptying

Anatomy o the I

If efforts to control bleeding fail surgery is indicated

If efforts to control bleeding fail surgery is indicated

The area to be removed depends were ulcer is located

Stress ulcer
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(Cushings ulcer). burns (Curlings ulcers).

Events that follow stress ulcers

Respiratory failure Renal failure Shock.

Characteristics of stress ulcers:

Multiple lesions 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.

Why do stress ulcers occur?

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.

Signs and symptoms of stress ulcers

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.

Zolliger-Ellison Syndrome
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.

Zolliger-Ellison Syndrome
Characteristic ulcer like pain Diarrhea Steatorrhea(fat in the stool) Electrolytes imbalance.

Gastric ulcers
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 6070 years old.

Gastric ulcer

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

Gastric ulcer signs and symptoms

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

Nursing Diagnosis for GERD, PUD, Disease

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

Pain : nursing interventions

Assess location, quality, acuity,frequency and duration. 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.

Alteration in nutrition
Assess the patient current diet, including pattern of food intake, eating schedule, and food that precipitate pain. 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

Fluid volume deficit

Monitor vital signs closely.
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.

Fluid volume deficit

Monitor laboratory data for hemoglobin, hematocrit, and serum electrolytes. Replace decreased HCT with whole blood or RBCS Assess abdomen for distention, BS, and tenderness q4hrs and record.

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

Pathophysiology of cholelithiasis disease

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

Who is at risk for gallstones?

Family History Native American, Caucasian, Mexican American Females(oral contraceptive use and pregnancy) Patients on TPN Certain disease (see text, p.512)

Gallbladder stones

Cholethiasis
Stones in cystic duct
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

Clinical manifestation of cholelithiasis

Epigastric pain Heartburn Right upper abdominal pain. Jaundice Intolerance to fat containing foods

Factors that increase the risk for cholelithiasis

Family history of gallbladder stones Female gender
pregnancy use of oral contraception Native Americans Caucasians Mexican Americans

Aging Diseases or conditions

Hyperalimentation

Cholecystitis
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.

Acute cholecystitis signs and symptoms

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.

Chronic cholecystitis signs and symptoms

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

Signs and symptoms that might be present with cholecystitis

Fever Increase WBCs Abdominal muscle guarding with rebound tenderness and rigidity Elevated bilirubin Elevated Alkaline phosphatase Elevated amylase

Important lab test for cholecystitis

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.

Diagnosis studies in cholecystitis

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

Diagnosis studies in cholecystitis

Complete blood count Serum amylase and lipase to check for pancretitis. Serum bilirubin Gallbladder scans oral cholecystogram
oral dye is use to assess the gallbladders ability to concentrate and excrete bile.

Treatment of cholethiasis
Pharmacology with oral bile acids. Diet therapy with low fat diet and weight loss. Surgery: it depend on the stone location and severity of the complications .

Pharmacology
The major pharmacological interventions are aimed at curing gallstones involves a group of agents oral bile acid call dissolvers.
Urodeoxycholic (UDCA) is for cholesterol stones less than 20mm in diameter. Pt. Need to have hepatic enzymes monitor closely watch for diarrhea

Pharmacology
Chenodeoxycholic (Chenodiol) which work by decreasing cholesterol in the diet. Other pharmacologic agents are use for palliative relief such as Antibiotics -to decrease bacteria count and associate inflammation and edema. Pain medications

Diet therapy
If bile flow is reduced Dietary fats are a because of obstruction stimulus for fat soluble vitamins A, gallbladder contraction D, E, and K and bile salts needs to be Patients need to be put replaced. on a low fat diet. Examples of high fat food to avoid : deep fried foods, whole milk etc..

Surgery
The type of surgical procedure performed for the client with gallstones depends on were the stones are located and severity of complications. If the stones are located only in the Gallbladder a simple Cholecystectomy is performed.
Conventional surgical methods. Laparascopic laser surgery

Surgery

Surgery
When stones are lodged within the ducts, a Cholecystectomy with common bile duct exploration and Ttube insertion may be indicated.

Surgery
Inserted after common bile duct exploration a T-tube maintain patency of the duct and promotes bile passage while the edema decreases.

Surgical risk in cholecystitis.

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

Treatment alternatives
Lithotrypsy or Percutaneous stone dissolution. With extracorporal shock wave lithotrypsy (ESWL). The physician uses ultrasound to align the stones with the source of shock waves and computerized lithotripter. 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.

Students responsible for :

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

Nursing care of the client with a T-tube

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-Fowlers position Assess skin around for bile leakage during dressing changes.

Nursing care of the client with a T-tube

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.

Nursing care for patients with cholelithiasis and cholecystitis

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

Pain related to gallbladder problems

Teach clients to avoid fat in their diets
fat stimulate gallbladder contractions and is a stimulus for pain .

If pain is not relieved by these methods administer prescribed narcotics Check for elevation of temperature q4hrs. Assist the patient to semi Fowlers position.

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

Risk for impair gas exchange

Patients may have Use incentive problems with spirometer every hour effective breathing and while awake. gas exchange because of abdominal incision. OOB ambulating as Institute a regiment of soon as possible.
turning, deep breathing and coughing at least every 2 hrs.

Risk for infection

Infections may arrive from various sources.
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,

The end