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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.

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Alterations in nutrition l.jpg

Alterations in Nutrition

Gastroesophageal Reflux Disease

Peptic Ulcer Disease

Cholecystitis/Gastric Surgery



Gastroesophageal reflux disease gerd l.jpg
Gastroesophageal Reflux Disease(GERD)

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


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Causes for GERD

  • Incompetent lower esophageal sphincter

  • Transient LES relaxation

  • Increased intragastric pressure


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Contributing Factors to GERD

  • Smoking

  • Caffeine

  • ETOH

  • Fatty meals

  • Obesity

  • Increased gastric acid and pepsin production


Signs and symptoms of gerd l.jpg

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.

Signs and Symptoms of GERD


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Complications of GERD

  • Esophageal strictures

  • Ulcers

  • Erosions


Barrette s esophagus l.jpg
Barrette's Esophagus

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


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Diagnosing GERD

  • Barium swallow

  • Endoscopy (EGD)

  • Esophageal motility studies

  • Ambulatory pH monitoring

  • Esophageal manometry


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Treatment for GERD

  • Practical changes in daily living

  • Pharmacology

  • Surgery


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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.


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Practical changes in life style

  • Stop smoking

  • Avoid tight clothing

  • Avoid bending


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Pharmacological treatments

  • H2 receptor antagonist (Cimetidine, Ranitidine, famotidine,nizatidine)

  • Proton Pump inhibitors (Prilosec, Prevacid)

  • Promotility agents (Cisapride=Propulsive)


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Pharmacological treatments

  • Antacids-to neutralize acidity, increased LES pressure.

    • It is usually take 1-3hrs after a meal and at bed time.


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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.


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Hiatal (diaphragmatic) Hernia

  • What is it?

  • Partial Stomach protrusion through the diaphragm.


Why does hiatal hernia happen l.jpg

Congenital problems

Trauma

Intra-abdominal pressure

Why does Hiatal Hernia happen?


What are the symptoms of hiatal hernia l.jpg

Reflux

Chest pain

Occult bleeding

Regurgitation

Dysphasia

Belching

What are the symptoms of Hiatal Hernia ?


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Complications of Hiatal hernia

  • Incarcerated necrotic hernia

  • Hemorrhage


How is hiatal hernia diagnosed l.jpg
How is hiatal hernia diagnosed

  • EGD

  • Barium swallow


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Treatment for Hiatal hernia

  • Pharmacological (same as GERD)

  • Changes in life style

  • Surgery (Nissen fundoplication)




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Esophageal spasm

  • Pt. Experiences spastic contractions of the esophagus .

  • Symptoms: angina-like chest pains and dysphasia.

  • Treatment: Calcium channels blockers, nitrates and anticholinergics


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Achalasia

  • What is it ? Dilation and loss of tone in the esophagus with high gastroesophageal sphincter pressure.

  • Why does it happen? Cause unknown.


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Achalasia symptoms

  • Nocturnal cough

  • Chest pains

  • Dysphagia

  • Regurgitation

  • Weight loss


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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 )


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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.


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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


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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.


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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.


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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 l.jpg

A general feeling of being tired or weak.

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

Symptoms of gastric carcinoma


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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).


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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.


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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.


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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.





Other gastric surgeries l.jpg

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.

Other gastric surgeries:


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Complications of gastric surgery.

  • Anemia (both iron deficiency and pernicious)

  • Dumping syndrome

  • Folic acid defiency

  • Decreased absorption of Vitamin D and calcium


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Disadvantages of the Billroth I and Billroth II

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


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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.


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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….


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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 l.jpg

Nausea

Vomiting

Epigastric pain with cramping.

Diarrhea

Loud, hyperactive bowel sounds (borborygmi)

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

tachycardia

What might be the manifestation of Dumping syndrome


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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 l.jpg
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.


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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.


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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 l.jpg
Peptic ulcers and population at risk

  • People who smoke

  • People who use NSAIDS

  • People with chronic H. Pylori

  • People with hypersecretory states.


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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.


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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.



Peptic ulcers l.jpg
Peptic Ulcers

  • 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)


Major causes of peptic ulcer disease pud l.jpg
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 l.jpg

Classic:

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.

Manifestation of Peptic Ulcer Disease


Older adult manifestation might be different l.jpg
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 l.jpg

Gastric analyses

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.

Lab and Diagnostic testing used for peptic ulcer disease


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Goals in the management of Peptic ulcer disease

  • Symptoms relief

  • Healing of existing ulcers

  • Preventing complications

  • Preventing/reducing recurrences


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Management strategies

  • Behavior modification

  • Pharmacologic therapy

  • Surgical interventions


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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 l.jpg

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

Medications that decreased the gastric acid content in PUD


Agents that protect the mucosa in pud l.jpg

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.

Agents that protect the mucosa in PUD


Eradication of h pylori in pud l.jpg

Usually two antibiotics with either bismuth or proton pump. protective barrier.

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.

Eradication of H. Pylori in PUD


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Questions regarding the complications of PUD. protective barrier.

  • 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 l.jpg
Complications of peptic ulcer disease protective barrier.

  • Hemorrhage

  • Obstruction

  • Perforation

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


Hemorrhage l.jpg
Hemorrhage protective barrier.

  • 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 l.jpg
Hemorrhage in PUD protective barrier.

  • 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.


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Hemorrhage in PUD protective barrier.

  • 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.


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Hemorrhage in PUD protective barrier.

  • Pt. Needs to be kept NPO

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


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Obstruction as a complication for PUD protective barrier.

  • Inflammation may cause obstruction.

  • Edema and poor ability to heal.

  • Scarring

  • Muscle spasm.


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Perforation/Peritonitis protective barrier.

  • 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


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If efforts to control bleeding fail surgery is indicated protective barrier.

  • Goals :

    • Decreased gastric secretions

    • Remove damage tissue

    • Promote gastric emptying



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If efforts to control bleeding fail surgery is indicated protective barrier.

  • The area to be removed depends were ulcer is located


Stress ulcer l.jpg
Stress ulcer protective barrier.

  • 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).


Events that follow stress ulcers l.jpg
Events that follow stress ulcers protective barrier.

  • Respiratory failure

  • Renal failure

  • Shock.


Characteristics of stress ulcers l.jpg

Multiple lesions protective barrier.

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.

Characteristics of stress ulcers:


Why do stress ulcers occur l.jpg
Why do stress ulcers occur? protective barrier.

  • 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 l.jpg
Signs and symptoms of stress ulcers protective barrier.

  • 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 l.jpg
Zolliger-Ellison Syndrome protective barrier.

  • 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.


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Zolliger-Ellison Syndrome protective barrier.

  • Characteristic ulcer like pain

  • Diarrhea

  • Steatorrhea(fat in the stool)

  • Electrolytes imbalance.


Gastric ulcers l.jpg
Gastric ulcers protective barrier.

  • 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 ulcer l.jpg
Gastric ulcer protective barrier.


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Gastric ulcers protective barrier.

  • 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.


Gastric ulcer signs and symptoms l.jpg
Gastric ulcer signs and symptoms protective barrier.

  • Dull aching abdominal pains after eating.

  • Pain is exacerbated by food intake.

  • Vomiting is common as well.


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Nursing Diagnosis for GERD, PUD, Disease protective barrier.

  • Pain

  • Alteration in Nutrition: less than body requirements

  • Fluid Volume deficit


Pain nursing interventions l.jpg

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

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.

Pain : nursing interventions


Alteration in nutrition l.jpg

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

Alteration in nutrition


Fluid volume deficit l.jpg

Monitor vital signs closely. intake, eating schedule, and food that precipitate pain.

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


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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.

Fluid volume deficit


Gallbladder disorders l.jpg
Gallbladder disorders serum electrolytes.

  • Cholelithiasis: stones or calculi

  • Cholecystitis: inflamed gallbladder with or without stones.

  • What are gallstones made of ? Cholesterol and bile pigments


Pathophysiology of cholelithiasis disease l.jpg
Pathophysiology of cholelithiasis disease serum electrolytes.

  • 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 l.jpg

Family History serum electrolytes.

Native American, Caucasian, Mexican American

Females(oral contraceptive use and pregnancy)

Patients on TPN

Certain disease (see text, p.512)

Who is at risk for gallstones?


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Gallbladder stones serum electrolytes.


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Stones in cystic duct serum electrolytes.

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

Cholethiasis


Clinical manifestation of cholelithiasis l.jpg

Epigastric pain serum electrolytes.

Heartburn

Right upper abdominal pain.

Jaundice

Intolerance to fat containing foods

Clinical manifestation of cholelithiasis


Factors that increase the risk for cholelithiasis l.jpg

Family history of gallbladder stones serum electrolytes.

Female gender

pregnancy

use of oral contraception

Hyperalimentation

Aging

Diseases or conditions

Native Americans

Caucasians

Mexican Americans

Factors that increase the risk for cholelithiasis


Cholecystitis l.jpg
Cholecystitis serum electrolytes.

  • 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 l.jpg
Acute cholecystitis signs and symptoms serum electrolytes.

  • 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 l.jpg
Chronic cholecystitis signs and symptoms serum electrolytes.

  • 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 l.jpg

Fever serum electrolytes.

Increase WBCs

Abdominal muscle guarding with rebound tenderness and rigidity

Elevated bilirubin

Elevated Alkaline phosphatase

Elevated amylase

Signs and symptoms that might be present with cholecystitis


Important lab test for cholecystitis l.jpg
Important lab test for cholecystitis serum electrolytes.

  • 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 l.jpg
Diagnosis studies in cholecystitis serum electrolytes.

  • 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 cholecystitis139 l.jpg

Complete blood count serum electrolytes.

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.

Diagnosis studies in cholecystitis


Treatment of cholethiasis l.jpg

Pharmacology with oral bile acids. serum electrolytes.

Diet therapy with low fat diet and weight loss.

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

.

Treatment of cholethiasis


Pharmacology l.jpg

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


Pharmacology142 l.jpg

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

Pharmacology


Diet therapy l.jpg

Dietary fats are a stimulus for gallbladder contraction cholesterol in the diet.

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..

Diet therapy


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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


Surgery145 l.jpg
Surgery with gallstones depends on were the stones are located and severity of complications.


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

Surgery


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

Surgery


Surgical risk in cholecystitis l.jpg
Surgical risk in cholecystitis. maintain patency of the duct and promotes bile passage while the edema decreases.

  • 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.


Treatment alternatives l.jpg

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.

Treatment alternatives


Students responsible for l.jpg
Students responsible for : extracorporal shock wave lithotrypsy (ESWL). The physician uses ultrasound to align the stones with the source of shock waves and computerized lithotripter.

  • 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.


Nursing care of the client with a t tube l.jpg
Nursing care of the client with a T-tube extracorporal shock wave lithotrypsy (ESWL). The physician uses ultrasound to align the stones with the source of shock waves and computerized lithotripter.

  • 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.


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Nursing care of the client with a T-tube extracorporal shock wave lithotrypsy (ESWL). The physician uses ultrasound to align the stones with the source of shock waves and computerized lithotripter.

  • 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.


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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 l.jpg

Teach clients to avoid fat in their diets cholecystitis

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.

Pain related to gallbladder problems


Risk for impair gas exchange l.jpg

Patients may have problems with effective breathing and gas exchange because of abdominal incision.

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.

Risk for impair gas exchange


Risk for infection l.jpg

Infections may arrive from various sources. exchange because of abdominal incision.

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,

Risk for infection


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The end exchange because of abdominal incision.


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