ms gastro intestinal %28hepa%29

Medical Surgical Nursing

NORMAL ANATOMY AND PHYSIOLOGY

Mouth-Buccal/Oral Cavity

1. Lips and Cheeks made up of skeletal muscles covered by a skin keep food in mouth while chewing

2. Palatea. Hard

Covers bone and provides hard surface against which the tongue forces foodb. Soft

Ends at uvula When food is swallowed, soft palate rises as a reflex to close oropharynx

3. Tongue Contains mucus and serous glands, taste buds Mixes food and saliva during chewing, forms the food into a mass (bolus) Initiates swallowing

Saliva Produced by the salivary gland Moistens food to form bolus Dissolves food substances that begin chemical breakdown of starches

4. Teeth Used to chew (masticate) 32 permanent embedded at the gingiva

Pharynx Nasopharynx and oropharynx Provide passageway for food, fluids and air Its skeletal muscles move food to the esophagus (peristalsis) It has mucus producing glands that provide fluid for easy swallowing

Esophagus A muscular tube about 10 inches (25 cm) Serves as passageway of food Descends through the thorax and diaphragm

1. Epiglottis A flap of cartilage over the top of larynx Keeps food out of larynx during swallowing

2. Gastroesophageal sphincter- between esophagus and stomach

Stomach Located high on the left side of the abdominal cavity A distensible organ – can hold up to 4 liters Regions:

a. cardiac regionb. fundusc. bodyd. pylorus

Pyloric sphincter- controls emptying of the stomach into the duodenum

Functions:1. Storage reservoir for food2. Mechanical digestion3. Gastric glands has 4 cells:

a. Mucous Alkaline mucus Serves as protection against gastric juice

b. Zymogemic cells Pepsinogen (inactive pepsin-protein digesting enzyme)

c. ParietalHCI Increases the activity of protein digesting cellsIntrinsic factor Absorption of vitamin B12

d. Enteroendocrine Gastrin, histamine, endorphirs, serotonin and sonatoslatin Gastrin- regulates secretion and motility of the stomach

Small Intestine Starts at pyloric sphincter and ends at ileocecal junction About 20 feet, one inch by diameter Divisions:

a. Duodenum Begins at the pyloric sphincter up to around the head of the pancreas Pancreatic enzymes and bile from the liver enter the small intestine

b. Jejunum - middle partc. Ileum - terminal end of small intestine

Site of chemical digestion and absorption througha. microvillib. villic. circular folds

Gastro-intestinal System of 12


Breaks carbohydrates and proteins Enzymes

a. Pancreatic amylase acts on starchy

b. Pancreatic enzymes breaks protein peptides

c. Pancreatic lipase breaks lipids

d. Triglycirides Enters as fat globules Coated by bile salts and emulsified

Large Intestine (Colon) Divisions

a. Cerum - first partb. Colon

o Ascendingo Transverseo Descendingo Sigmoid

Functions:1. Eliminates indigestible food residue

a. Goblet cells produce mucus- facilitates lubricationb. Defecation reflex

stretching of the rectal wall can be suppressed voluntarily expulsion can be attained by Valsalva maneuver

2. Absorbs water, salts and vitamins formed by the bacteria

Liver Largest gland Approximately 3 pounds (1.4 kg) Located at the right side Made up of lobules (composed of plates of hepatocytes) Sinusoids

- blood filled spaces- lined with Kaupffer cells (phagocytic cells)

Functions:1. Secretes bile2. Stores fat-soluble vitamins3. Conjugates bilirubin4. Stores blood and releases during hemorrhage5. Synthesizes protein albumin6. Synthesizes Prothrombin, Fibrinogen and factors I, II, VII, IX and X7. Synthesizes fats from carbohydrates and protein energy or adipose tissue8. Synthesizes cholesterol production of bile salts, steroid hormones and plasma membranes9. Deamination (Amino acid carbohydrates)10. Releases during hypoglycemia11. Takes up glucose during hyperglycemia12. Detoxification13. Stores iron as ferritin (necessary for RBC production)

Pancreas Triangular gland extending across the abdomen

Functions1. Produces 1-1.5 L of pancreatic juice everyday2. Pancreatic juice

- clear with high bicarbonate content- can digest all categories of food

ALTERATIONS IN GASTROINTESTINAL SYSTEM

INGESTION PROBLEMS

ORAL INFLAMMATORY LESIONS

Etiology:1. Mechanical = trauma2. Chemical = irritants, drugs, toxins3. Biological = infections

HS virus I & II Spirochete Bacteria - Staphylococcus, Streptococcus

1. Stomatitis = Mouth inflammation & erosions Etiology: trauma, irritants as tobacco and alcohol, chemotherapy, renal, liver and blood dis. S/S: halitosis, soreness of mouth, excessive salivation

2. Glossitis = Tongue inflammation & ulcers Etiology: trauma, irritants

3. Gingivitis = Gum inflammation & ulcers Etiology: poor dental care, malocclusion, irregular teeth, low fiber diet



S/S: Bleeding esp. with brushing, pain, swelling, redness; Periodontitis (pus, abscess, loose teeth)

4. Herpes Simplex: Etiology: HS virus I & II Also called “cold sore or Fever blisters” Classified as STD S/S: Vesicles on an erythematous base; lesions @ junction of lips & face Activated by: sunlight, heat, fever, menses, digestive disturbances, food allergies.

5. Vincent’s Angina Known as “ Trench Mouth” / Acute necrotizing ulcerative gingivitis Etiol: Fusiform bacteria, Spirochetes (Borrelia vincentii) Purple-red gums with pseudomembrane S/S: fever, anorexia, foul breath, cervical lymphadenopathy Maybe acute, sub-acute or chronic

6. Aphthous Ulcer Very painful, (1cm) shallow erosions of called “canker sores” circumscribe with white or yellow center, encircle by a red ring

7. Parotitis = inflammation of parotid glands Etiology: Staphylococcus (usual)/ Streptococcus S/S: Pain at ear and area of gland; No salivation Pus exudates

8. Oral Candidiasis Moniliasis or thrush Etiol: prolonged high-dose antibiotic tx or steroids S/S: Pearly, bluish-white milk curd membranous lesion at oral mucosa/larynx; sore mouth yeasty halitosis

NCP: Oral Inflammations

NDx1 = Pain: Topical Xylocaine Analgesics Bland, Soft/liquid diet Mild antiseptic mouthwash

NDx2: Nutrition, < BR At least 1,500 cal/d Fluid intake at least 2l/d

NDx3: Imp. Oral M. M. Oral care q 4h Gingival massage (gingivitis) Antibiotics for infections; Acyclovir; Steroids Mild oral antiseptics Prof’l dental care Fibrous rather than soft diet Adequate fluid intake Conscientious brushings habits with flossing

ESOPHAGITIS

A. Description: inflammation of the esophagus; may be acute or chronic.B. Etiology:

Commonly caused by gastroesophageal reflux disease (GERD) - a syndrome caused by a reflux of gastric contents into the esophagus:a. Lower esophageal sphincter (LES) tone is decreased or relaxed.b. Hiatal herniac. Emesis d. Delayed gastric emptying time (eg, gastroparesis), common in diabetics.e. Ingestion of hot or corrosive substancesf. infectious process (eg, herpes or monilial invasion)

A. Pathophysiology and manifestations

Backflow of HCl / intake of corrosive agents

Damage of the epithelial cells of esophagus

Frequent exposure to chemicals

Pain

Signs and Symptoms:1. N/V2. Pyrosis (hallmark symptom); may radiate to the back, neck, or jaw.3. Pain after eating and at night when in a supine position.4. Pain aggravated by an increase in intraabdominal pressure (eg, straining, lifting).5. Bleeding 6. Strictures may also occur

B. Overview of nursing interventions:1. Medications

AntacidsGastro-intestinal System

of 12


H2-receptor antagonists – Tagamet (Cimetidine)2. Diet

Low-fat Small frequent feedings no alcohol, no caffeine, no spices high-Fowler’s during and 1 hour eating

3. Weight reduction4. Avoid activities that increase intraabdominal pressure.5. Encourage the patient to:

stop smoking, if applicable. avoid wearing tight, restrictive clothing

ESOPHAGEAL HIATAL HERNIA

Refers to herniation or displacement of a portion of the lower esophagus or the stomach into the thoracic cavity.

Types:

1. Sliding esophageal hernia (90% of occurrences): herniated portion of the stomach slides back and forth upward through the hiatus secondary to positional changes.

weakening of the muscles of the esophageal hiatus due to the aging process (more than 60%) Trauma Hereditary factors Symptoms are associated with gastro-esophageal reflux:

1. Dysphagia2. Pyrosis3. Regurgitation4. Bloating

2. Rolling / paraesophageal esophageal hernia: fundus and possibly the greater curvature of the stomach herniated alongside the esophagus into the thorax

Occurs less commonly Complications are high and include gastric volvulus, strangulations, or obstruction. Symptoms are related to increased intrathoracic pressure:

1. Chest pain2. Shortness of breath3. Tachycardia with subsequent impaired gas exchange.

Chest pain is characteristic because it mimics anginal pain and usually is not relieved when the patient is recumbent.

Nursing Interventions:1. Medications

Antacids H2-receptor antagonists – Tagamet (Cimetidine) Analgesics

2. Diet Low-fat Small frequent feedings no alcohol, no caffeine, no spices high-Fowler’s during and 1 hour eating

3. Advise patient to: Reduce weight, if indicated



Avoid wearing tight-fitting or restricted clothing. Alcohol and cigarette use.

4. Prepare for herniorrhapy / hernioplasty

Nissen Fuldoplicaion

GASTRITIS

A. Description: Inflammation of the stomach mucosa. B. Etiology1. Acute (transient intermittent inflammation)

Caused by:a. Local irritants (eg, drugs, alcohol, corrosive substances),b. Allergy and bacterial endotoxin invasion (eg, Salmonella, Escherichia coli).

Associated with mucosal hemorrhages and erosions. 2. Chronic gastritis

Secondary to bile acid reflux or to peptic ulcer disease. Related to chronic use of local irritants (eg, alcohol, drugs)

C. Pathophysiology processes and manifestations

Prolonged exposure to irritants / HCl

Irritation of gastric mucosa

Erosion

S/Sx

S/Sx may include:a. Mild to severe abdominal discomfort or pain (may or may not be accompanied by N/V and diarrhea.)b. Intolerance to spicy or high-fat food.c. Diarrhea FVD if unabatedd. May lead to PUD if not relievede. Hemorrhage (as hematemesis or melena) anemia

D. Nursing Interventions1. Correct fluid and electrolyte disorders.2. Diet therapy.3. Avoid oral feeding until emesis subsides.4. Avoid foods contributing to gastric distress.5. Parenteral therapy6. Teach the patient about diet and lifestyle changes to prevent exacerbation.7. Avoid cigarette smoking and alcohol consumption.8. Medications:

a. Antacidsb. H2-receptor antagonist

PEPTIC ULCER DISEASE

A. Description1. A chronic condition characterized by an ulceration of the gastric mucosa, duodenum, or less frequently, of the lower esophagus and

jejunum.2. It is an acute response to medical or surgical stress.



B. Etiology and incidence

1. Unknown Infection (H. pylori) mucosal breakdown Genetic predisposition Tobacco use Ingestion of food or drugs that:

a. injure or alter gastric mucosa b. increase hydrochloric acid production Stress

Diseases that alter gastric secretion (eg, pancreatitis, Crohn’s disease)

2. Duodenal ulcers are thought to occur more prevalent than gastric ulcers and usually occur between the 2nd and 5th decades of life.

C. Pathophysiology and manifestations1. Gastric ulcers

Injury

Histamine release

Production of HCl by the parietal cells

More injury

Erosion of gastric mucosa Stricture

Hematemesis and Melena Pyloric obstruction and perforationGastric ulcers are slow to heal, in part because of poor circulation to the ulcerative site.

2. Duodenal ulcers.1. Increased rate of gastric acid secretion (increased number of parietal cells or secondary to vagal stimulation, affects gastric

release.)2. Dumping syndrome reduces the buffering effects of food.3. Complications include hemorrhage, obstruction, or perforation.

3. Stress ulcers1. Coffee ground aspirate - hallmark sign2. Multiple ulcerations felt to be erosions develop secondary to gastric ischemia.

4. S/Sx common to all PUDs:1. Bloating 2. Belching3. Nausea 4. Vomiting5. Pain (usually described as burning or aching)

a. Gastric – relieved by eatingb. Duodenal – aggravated by eating

6. Pain may be associated with:a. ingestion of specific foods (spicy or fried)b. Alcoholc. medications

D. Medical Management1. Medications

a. Antacids Neutralizes HCl Taken 1-2 hours pc Examples: Amphogel (AL-OH), Basaljel (AL-Carbonate), Milk of Magnesia (Mg-PH), Maalox (AL-MG-OH) Magnesium-based diarrhea Aluminum-based constipation

b. H2 receptor antagonists Reduces HCl secretion Taken with meals Examples: Tagamet (Cimetidine), Zantac (Ranitidine) Side effects:



Diarrhea Abdominal cramps Confusion Dizziness Weakness

c. Cytoprotective drugs Coats ulcer Taken on an empty stomach (30-60 mins ac) Example: Carafate (Sucralfate)

d. H. Pylori Drug Treatment Pepto-Bismul Amoxicillin/Tetracycline Flagyl

2. Surgeriesb. Vagotomy

Resection of the vagus nerve Decreases cholinergic stimulation decreases HCL secretion

c. Pyroplasty – surgical dilatation of the pyloric sphincterd. Antrectomy

Billroth I Billroth II Subtotal Gastrectomy

o Removal of 75% of the distal stomach

E. Nursing Interventions1. Relieve pain: Take prescribed medications as ordered2. Promote a healthy lifestyle

a. Diet 1. Liberal bland diet during exacerbation2. Eat slowly and chew food properly3. Small, frequent feedings during exacerbation4. Avoid the following:

a. Fatty foodsb. Coffee, tea, cola drinks, chocolatec. Spices, red /black pepperd. Alcohole. Bedtime snacksf. Binge eatingg. Large quantities of milk (400 mls/day is allowed)

b. Quit smokingc. Coping

Stress Therapy(a) Recreation and hobbies(b) Regular pattern of exercise(c) Stress reduction at home and at work

GASTROENTERITIS

A. Description1. Is an inflammation of the GI; it most commonly affects the small intestine.2. A.K.A Traveler’s diarrhea, dysentery.3. History – will differentiate from other conditions

B. Etiology and Incidence1. Bacterial

E. Coli – Traveler’s Diarrhea Shigellosis – Bacillary Dysentery By way of fecal-oral Affects all ages Affects in warm climates

2. Viral gastroenteretits rotavirus and parvovirus-type by way of the respiratory system. Affects primarily infants and the aged Crowded living conditions

C. Pathophysiology and manifestations.1. Symptoms common to all types of gastroenteritis include:

Nausea Vomiting Diarrhea

2. Bacterial – stool specimens with high WBC, possibly high RBC3. Viral - high WBC and the presence of pus 4. Fever depends on microorganism, bacterial usually causes higher temp.5. S/Sx of viral gastroenteritis include

Headache Weakness muscle aches and pains abdominal distention and tenderness (but no rebound tenderness)

6. Infection can last anywhere from 2 to 7 days.7. In diarrhea and vomiting become severe FVD

D. Nursing Intervention



1. Drugs – anti-infective agents, analgesics, and electrolyte replacement medications (eg, potassium). No drugs to suppress gastric motility.

2. Monitor I & O3. Watch out for F & E imbalances4. Dietary changes

intake of clear liquids initially lactose-free foods for 1 to 2 weeks (after symptoms subside)

5. Parenteral therapy for severe cases.6. Collect stool specimen.7. Provide meticulous perianal skin care.8. Provide patient teaching covering:

Adherence to medication regimen Appropriate sanitary methods for cooking and personal hygiene

ULCERATIVE COLITISA. Description: Is an inflammatory process affecting the mucosa of the colon and rectum.

B. Etiology and Incidence:1. Exact cause unknown but closely associated with:

a. Infection b. Autoimmune dysfunctionc. Genetic predispositiond. Psychological stressor

2. Incidence is higher in young adults (15 to 20 years old)

C. Pathophysiologic Processes and Manifestations1. Diffuse inflammation of intestinal mucosa swelling of epithelial cells necrosis crypt formation site of abscess ulceration2. Chronic narrowing of lumen3. Symptoms include:

a. Bloody diarrhea (15-20 times daily) – with or without pusb. Abdominal tendernessc. N/Vd. Fevere. Anorexia f. Weight loss

D. Overview of Nursing Interventions1. Administer medications, as ordered.

a. Antimicrobial c. Antidiarrhealb. Antispasmodics

2. Institute dietary management:a. Low-residue c. Elemental type (fast GI absorption)b. Lactose-free d. TPN if needed

3. Monitor I & O4. Collect stool specimen5. Monitor weight6. Prepare for surgery and institute postoperative care.

REGIONAL ENTERITIS (CROHN’S DISEASE)

A. Description1. Chronic inflammatory bowel disease affecting segmental areas along the entire wall of the GI tract.

B. Etiology1. Exact cause unknown; usually associated with:

a. Infectious processb. Allergy or autoimmune disordersc. Genetic predispositions

C. Pathophysiologic Processes and Manifestations 1. Thickening and inflammation is present (Telescoping)2. Healing lesions result in scar tissue formation obstruction of GI tract3. Diarrhea , 3-5 / day without blood.4. Other symptoms:

a. Weakness d. Malaiseb. Nutritional deficits e. Weight lossc. Fever with leukocytosis

D. Overview of Nursing Interventions1. Administer medications, as ordered.

a. Antimicrobial c. Antidiarrhealb. Antispasmodics

2. Institute dietary management:a. Low-residue, lactose-freeb. Elemental typec. TPN if necessary

3. Observe for fluid and nutritional status4. Monitor bowel movement consistency, frequency and volume.

DIVERTICULITIS

A. Description: An inflammation of the diverticula or herniations within the wall of the intestinal tract.

B. Etiology and Incidence:1. Chronic constipation 2. Increased incidence associated with ulcerative colitis and Crohn’s disease.



3. Diverticula occurs more in adult.

C. Pathophysiology and Manifestations1. Commonly affects the sigmoid colon.2. Increased luminal pressure (chronic constipation) formation of diverticula / herniation through a weak structure bacteria

formation through a weak muscular structure local abscess intraabdominal perforation and peritonitis.3. Symptoms include:

a. Pain on LUQb. Intermittent rectal bleedingc. Constipationd. Fever (with leukocytosis)

D. Overview of Nursing Interventions

During an acute phase:1. Bed rest2. NPO, later on clear liquids3. Low fiber4. Analgesics, antibiotics, anticholinergics

Everyday life:1. Administer antimicrobial agents as ordered.2. Bulk-forming laxatives3. Dietary regimen:

a. Low fiber dietb. Eliminate foods with seeds and nuts.

4. Encourage fluid intake5. Observe fluid status and bowel movement.6. Prepare for colostomy; institute postoperative care.

APPENDICITISA. Description: Is the inflammation of the vermiform appendix.

B. Etiology:1. Exact cause is unknown. Factors may include:

a. Fecal impactionb. Kinking of the appendixc. Parasitesd. Infections

C. Pathophysiologic processes and manifestations

1. Psoas sign (lateral position with right hip flexion)2. Severe abdominal pain with rebound tenderness at Mcburney’s point (RLQ) – Blumberg Sign3. Other symptoms:

Rigid abdomen, guarding Anorexia N/V Fever (38-38.5 oC) Leukocytosis (more than 10,000 / cu mm

D. Overview of Nursing Interventions1. Bed rest2. NPO3. Avoid enemas, heat application and laxatives - prevent rupture.4. IVF therapy5. Antibiotic therapy6. Appendectomy to avoid peritonitis.

Done under spinal anesthesia Flat on bed (6-8 hours) NPO until peristalsis returns Institute postoperative care. Activities can be resumed within 2-4 weeks.

7. If the diagnosis is not definitive, prepare for exploratory laparotomy.

PANCREATITIS

A. Description: Is acute / chronic inflammation of the pancreas.

B. Etiology: Results from alterations in the structure or function of the pancreas, commonly caused by chronic alcohol abuse.

C. Pathophysiology and manifestations

Disruptions of pancreatic ducts

Pancreatic enzymes spill out the pancreatic tissues

Autodigestion (hallmark sign)



Incapacitating pain

Neurogenic shock

Hemorrhage

Necrosis

Spill out to the peritoneum

Peritonitis

D. Overview of Nursing Interventions1. Avoid excessive food intake to prevent autodigestion.2. Demerol for pain. Avoid morphine as it stimulates release of pancreatic juice3. Monitor for signs of shock.

HEMORRHOIDS

• Dilated blood vessels beneath the lining of the skin in the anal canal• Two Types of Hemorrhoids

– External hemorrhoids – occur below the anal sphincter– Internal hemorrhoids – occur above the anal sphincter

• Causes – Chronic constipation– Pregnancy– Obesity – Prolonged sitting or standing– Wearing constricting clothings– Disease conditions like liver cirrhosis, RSCHF

Signs and Symptoms:1. Constipation ( in an effort to prevent pain or bleeding associated with defecation.)2. Anal pain3. Rectal bleeding4. Anal itchiness5. Mucous secretion from the anus6. Sensation of incomplete evacuation of the rectum

Collaborative Management:1. High fiber diet, liberal fluid intake2. Bulk laxatives3. Hot Sitz bath, warm compress4. Local anesthetic application – Nupercaine5. Surgery

Hemorrhoidectomy Sclerotherapy (5% phenol in oil) Cryosurgery Rubber – band ligation

6. Preop Care Low residue diet to reduce the bulk of stool Stool softeners

7. Postop Carea. Promotion of comfort

Analgesics as prescribed Side – lying position Hot Sitz bath 12 to 24 hrs. postop

b. Promotion of elimination Stool softener as prescribed Encourage the client to defecate as soon as the urge occurs Analgesic before initial defecation Enema as prescribed, using a small – bore rectal tube

c. Patient Teaching Clean rectal area thoroughly after each defecation Sitz bath at home especially after defecation Avoid constipation:

o High – fiber dieto High fluid intakeo Regular exercise o Regular time for defecation

Use stool softener until healing is complete Notify physician for the following:

o Rectal bleedingo Continued pain on defecationo Continued constipation

LIVER CIRRHOSIS

Irreversible chronic inflammatory disease characterized by massive degeneration and destruction of hepatopcytes.

Types: 1. Laennec’s cirrhosis – the most common

1. Caused by the liver’s toxic to alcohol2. Occurs primarily in middle-aged men

2. Postnecrotic cirrhosis1. Results from severe liver disease 2. Post - acute viral or chemical hepatitis

3. Primary biliary cirrhosis: inflammation and intrahepatic bile duct destruction.4. Secondary biliary cirrhosis: chronic partial or complete common bile duct obstruction due to gall stones, pancreatitis or tumor.5. Cardiac cirrhosis results from right-sided CHF.

Pathohysiology and Manifestations1. Laennec’s Cirrhosis



Alcohol causes changes fatty infiltration of the hepatocytes liver cell necrosis and scarring as it progresses, inflammation decreases but fibrosis increases liver distortion structural (biliary channel) and vascular changes.

Scar tissue formation and irregular hepatocyte regeneration compression of portal vein obstruction portal hypertension Decreased Vitamin ADEK absorption

1. bleeding tendencies2. poor calcium transport3. poor skin turgor4. visual disturbances

Depletion of glycogen hypoglycemia Decreased albumin decreased COP anasarca Increased HP ascites Decreased bilirubin metabolism hyperbilirubinemia jaundice

2. Manifestations postnecrotic - same as Laennec’s cirrhosis.3. Biliary cirrhosis

Chronic obstruction increased pressure in the hepatic bile duct accumulation of bile areas of necrosis edema, fibrosis and hepatocellular destruction scar tissue destruction hepatomegaly

1. Hyperbilirubenemia2. Jaundice3. Pruritus4. clay-colored stools5. RUQ pain.

4. Cardiac cirrhosis Enlarged liver congested venous blood flow failure of the heart to pump blood to different areas of the body. Congestion causes anoxia to the liver necrosis and fibrosis

Hepatorenal syndrome A major complication of cirrhosis characterized by renal failure in an anatomically normal kidneys progressive oliguria and azotemia.

Nursing Interventions:1. Assess for signs of bleeding2. Monitor V/S and laboratory results (platelets, creatininine)3. Monitor I/O.4. Monitor daily weight and abdominal girth to detect ascites.5. Administer the following as ordered to combat symptoms:

1. Vitamin K2. Stool softeners3. Diuretics

6. Assess for changes in cardiac output, decreased renal function and electrolyte imbalances.7. Assess for impaired skin integrity related to edema, ascites and pruritus.8. Use preventive measures to keep skin intact.9. Assess the patient for signs of impaired breathing related to congestion or infection.10. Relieve breathing difficulty.11. Observe for signs of encephalopathy (lethargy, confusion, personality changes, motor changes, depression, irritability).12. Teach ways to decrease bleeding tendencies.14. Patient teaching:

a. Nutritional needs b. Avoidance of alcoholc. Drug interactions related to decreased liver function.d. Enough reste. Signs and symptoms needing medical intervention.

15. Provide counseling for the patient and family.

CHOLELITHIASIS/CHOLECYSTITIS

• Cholelithiasis is stone formation in the GB• Cholecystitis is inflammation of the GB• Cause: unknown• Predisposing factors

female fatforty fair complexionfertile

• Theories• Metabolic factors• Biliary stasis• Inflammation

• Composition of Gall stonecholesterol bile saltsCa bilirubinprotein

Signs and Symptoms:1. Decreased fat emulsification

• fat intolerance• anorexia, N/V• flatulence• steatorrhea

2. Inflammation• pain (RUQ)• fever• leukocytosis

3. Decreased bile flow in colon• acholic stool• poor absorption of fat soluble vitamins

4. Increased serum bilirubin• Jaundice• Pruritus



• Tea-colored urine5. Infection

• Cholecystitis• Pancreatitis

Management:1. Relief of pain

• Meperidine HCL, not MorphineSO42. Diet: low fat diet3. Bile salts: chenodeoxycholic acid, ursodioxycholic acid given after meals4. Surgery: cholecystectomy

Preop care:1. IVF to replace loss in vomiting2. DBCT3. Vit K injection

Postop Care1. Low or semi-fowler’s position2. NGT for decompression3. Diet: low fat for 2-3 months4. Ambulation after 24 hrs post op5. T tube if with CBD exploration

Purpose is to drain bile Drainage:

o Brownish red for 1st 24 hrso 300-500 ml of bile drainage for 1st 24 hrso Drainage bottle should be placed in bed at level of incision to drain excess but not all of the bile


ms gastro intestinal %28hepa%29

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