PYLORIC STENOSIS

A congenital hypetrophy of muscular tissue of the pyloric sphincter, usually asymptomatic until 2-4 weeks after birth 5 times more common in male than female

CLASIIFICATION 1. Grossly enlarged circular muscle of pylorus 2. Narrowed opening between the stomach and duodenum 3. Inflammation and edema can result in total obstruction CLINICAL FINDINGS 1. 2. 3. 4. 5. Vomiting, progressively projectile None-bile stained vomitus Constipation Dehydration and weight loss Distention of the epigastrium, visible peristalsis and palpable olive-shaped mass in the right upper quadrant

THERAPEUTIC INTERVENTION Pyloromyotomy or Fredet Ramstedt Procedure longitudinal splitting of the hypertrophied muscle

NURSING CARE 1. 2. 3. 4. 5. 6. Feeding history and vomiting Failure to gain weight Presence of projectile vomiting No evidence of pain or discomfort Upper abdominal distention Palpable olive-shaped mass in the epigastrium just to the right of umbilicus

NURSING DIAGNOSIS 1. Risk for disorganized infant behavior r/t pain and discomfort and need to restrict oral intake 2. Altered family processes r/t having a child with life-threatening illness 3. Altered nutrition: less than body requirement r/t vomiting 4. Fluid volume deficit r/t vomiting IMPLEMENTATION 1. Preoperative Nursing Care a. Keep NPO b. Monitor I and O c. Monitor signs of dehydration 2. Postoperative Nursing Care a. Same as for any abdominal surgery b. Teach parents on specific feeding methods - Give small, frequent, diluted feedings and feed slowly - Hold infant in high-fowlers position during feeding and place on the right side after feeding with head of bed slightly elevated. EVALUATION 1. Infant does not become dehydrated 2. Infant consumes adequate calories for growth and development 3. Family demonstrates ability to care for infant

TRACHEOESOPHAGIAL FISTULA & ESOPHAGEAL ATRASIA, CHOANALA ATRASIA

Congenital atresia of the esophagus and tracheoesophageal fistula are a rare malformation that represents a failure of the esophagus to develop as a continuous passage. They may occur as separate entities or in combination, without early diagnosis and treatment are rapidly fatal.

Choanal Atresia a nasopharyngeal anomaly that exhibits as a lack of an opening on one or both of the nasal passages and the nasopharynx.

Chalasia incompetent cardiac sphincter ETIOLOGY Not known Low birth weight, premature

CLINICAL FINDINGS 1. Excessive drooling 2. Excessive mucus in nasopharynx causing cyanosis, who is easily reversed by suctioning 3. Choking, sneezing and coughing during feeding, with regurgitation of formula 4. Inability to pass a catheter into the stomach

THERAPEUTIC INTERVENTIONS

Thoracotomy with division and ligation of TEF

End to end anastomosis of the esophagus

Bougienage - a blunt metal instrumentis used to dilate a fistula or lengthen membranous tissue.

NURSING CARE Assessment 1. Three Cs of tracheoesophageal fistula: Coughing, Choking, Cyanosis 2. Monitor for signs of respiratory distress 3. Observe parent/infant interaction NURSING DIAGNOSIS 1. Ineffective airway clearance r/t physical defect 2. Anxiety r/t inability to swallow r/t surgical pain 3. Risk for disorganized behavior r/t pain and discomfort and need to restrict oral intake 4. Risk for injury r/t surgical procedure 5. Altered family processes r/t having an infant with disability 6. Impaired swallowing r/t physical defect IMPLEMENTATION 1. Preoperative Nursing Care a. Keep NPO b. Maintain in upright position c. Suction oropharynx to remove accumulated secretions d. Observe for signs of respiratory distress e. Change position to prevent pneumonia f. Monitor I and O 2. Postoperative Nursing Care a. Frequently suction mouth and pharynx b. Provide high humidity to liquify thick secretions c. Stimulate crying and change position of position to prevent pneumonia d. Perform proper care of chest tubes if used e. Maintain nutrition by oral, parenteral or Gastrostomy method f. Provide a pacifier if oral feedings are contraindicated or before a tube feeding g. Provide comfort and physical contact because hospital stay is usually long EVALUATION 1. 2. 3. 4. 5. 6. 7. Airway is maintained and infant does not aspirate secretions Infant receives adequate calories for growth and development The surgical site is not injured Infant rest calmly Family demonstrated ability to care for infant Infant alert when awake Family able to list potential complications

II. ADULT
DIVERTICULUM
Outpouching of mucosa and submucosa that protrudes through a weak portion of the musculature.

Diverticula may occur in the three areas of the esophagus: 1. Pharyngoesophageal upper area of the esophagus,most common 2. Midesphageal area middle, uncommn 3. Epiphrenic lower area of the esophagus Pharyngoesophageal found 3 times more frequently in men than in women CLINICAL MANIFESTATION A. PHARYNGOESOPHAGEAL difficulty swallowing, fullness in the neck, belching, regurgitation of undigested food and gurgling noises after eating (bec. the pouch become filled with food or liquid) coughing (due to irritation of the trachea halitosis (due to decomposition of the food retained in the diverticula) sour taste in the mouth (due to decomposition of the food retained in the diverticula)

B. MIDESOPHAGEAL less accurate C. EPIPHRENIC asymptomatic, dysphagia, chest pain ASSESSMENT AND DIAGNOSTIC FINDINGS 1. Barium swallow determines the exact nature and location 2. Blind insertion of NGT should be avoided 3. Esophagoscopy contraindicated, danger of perforation of the diverticulum

MANAGEMENT 1. 2. 3. 4. Diverticulectomy removal of diverticulum Myotomy of the cricopharyngeal muscle to relieve spacticity of the musculature NGT post-operatively Foods and fluids are withheld until x-rays shows no leakage at the surgical site

PEPTIC ULCER DISEASE

Is an excavation forms in the mucosal wall of the stomach, pylorus (opening between stomach and duodenum) in the duodenum or in the esophagus PREDISPOSING FACTOR 1. Hereditary 2. Emotional 3. Smoking vasoconstriction GIT ischemia 4. Alcoholism stimulates release of histamine = Parietal cell release Hcl acid = ulceration 5. Caffeine tea, soda, chocolate 6. Irregular diet 7. Rapid eating 8. Ulcerogenic drugs NSAIDS, aspirin, steroids, indomethacin, ibuprofen Indomethacin - S/E corneal cloudiness. Needs annual eye check up. 9. Gastrin producing tumor or gastrinoma Zollinger Ellisons 10. Microbial invasion helicobacter pylori. Metromidazole (Flagyl) TYPES OF ULCER ASCENDING TO SEVERITY 1. Acute affects submucosal lining 2. Chronic affects underlying tissue heals & forms a scar ACCORDING TO LOCATION 1. 2. 3. Stress ulcer Gastric ulcer Duodenal ulcer most common

sign

Stress ulcers common among eritically ill clients

2 TYPES 1. CURINGS ULCER cause: trauma & birth hypovolemia GIT schemia Decrease resistance of mucosal barriers to Hcl acid Ulcerations 2. CUSHINGS ULCER cause stroke/CVA/ head injury Increase vagal stimulation Hyperacidity Ulcerations PATHOPHYSIOLOGY 1. It occurs when the gastroduodenal mucosa cannot withstand with the digestive action of HCl and pepsin 2. The erosion is caused by increased concentration or activity of acid-pepsin, or by decreased resistance of the mucosa 3. Patients with duodenal ulcers secreted more acids than normal 4. Patients with gastric ulcers tends to secrete normal or decrease level of acid DIFFERENCES Location Pain Pain location Pain character GASTRIC Antrm 30 mins-1 hr after meal Epigastrium Gaseous, regular, nocturnal, burning, gnawing pain accompanied by epigastric tenderness, not relieved by foods and antacids Loss Normal Hematemesis Hemorrhage, stomach cancer 60 y/o and above DUODENAL Duodenal bulb 2-3 hrs after meal, 12mn3am, pain is severe Mid-epigastrium (right) Cramping and burning accompanied by belching, nausea and vomiting, relieved by food and antacids Gain Increased Melena Perforation 20 y/o and above

Weight Gastric acid secretion Hemorrhage Complications High risk

NURSING MANAGEMENT: 1. Diet bland, non irritating, non spicy 2. Avoid caffeine & milk/ milk products Increase gastric acid secretion

3. Administer meds

a.) Antacids
AAC Aluminum containing antacids Ex. aluminum OH gel (Ampho-gel) S/E constipation Maalox (fever S/E) Magnesium containing antacids ex. milk of magnesia S/E diarrhea

b.) H2 receptor antagonist

1. 2. 3. Ex: Ranitidine (Zantac) Cimetidine (Tagamet) Tamotidine (Pepcid) Avoid smoking decrease effectiveness of drug

NURSING MANAGEMENT: 1. Administer antacid & H2 receptor antagonist 1hr apart -Cemetidine decrease antacid absorption & vise versa

c.) Cytoprotective agents

Ex 1. Sucralfate (Carafate) - Provides a paste like subs that coats mucosal lining of stomach 2. Cytotec

d.) Sedatives/ Tranquilizers - Valium, lithium e.)Anticholinergics

1. Atropine SO4 2. Prophantheline Bromide (Profanthene) (Pt has history of hpn crisis with peptic ulcer disease. Rn should not administer alka seltzer- has large amount of Na). 4. Surgery: subtotal gastrectomy - Partial removal of stomach

Billroth I

Billroth II

(Gastroduodenostomy) (Gastrojejunostomy) -Removal of of stomach & anastomoses - Removal of -3/4 of stomach & of gastric stump to the duodenum. duodenal bulb & anastomostoses of gastric stump to jejunum. Before surgery for BI or BII - Do vagotomy (severing of vagus nerve) & pyloroplasty (drainage) first

NURSING MANAGEMENT 1. Monitor NGT output a.) Immediately post op should be bright red b.) Within 36- 42h output is yellow green c.) After 42h output is dark red 2. Administer meds: a.) Analgesic b.) Antibiotic c.) Antiemetics 3. Maintain patent IV line 4. VS, I&O & bowel sounds 5. Complications: a.) Hemorrhage hypovolemic shock Late signs anuria b.) Peritonitis c.) Paralytic ileus most feared d.) Hypokalemia e.) Thromobphlebitis f.) Pernicious anemia

DUMPING SYNDROME
Dumping syndrome common complication rapid gastric emptying of hypertonic food solutions CHYME leading to hypovolemia. Sx of Dumping syndrome: 1. Dizziness 2. Diaphoresis cold and clammy skin 3. Diarrhea hypovolemic shock 4. Palpitations reflex tachycardia, decrease urine output NURSING MANAGEMENT 1. Avoid fluids in chilled solutions avoid drinking after meals (It should be in between meals) half of water and then later drink the half 2. Small frequent feeding s-6 equally divided feedings 3. Diet decrease CHO, moderate fats & CHON 4. Flat on bed 15 -30 minutes after q feeding after meals MEDICAL MANAGEMENT Antibiotic to eradicate H. Pylori Management of gastric acidity Lifestyle changes

- Surgical interventions a. Pharmacology Theraphy 1. Antacid: Mg and Aluminum Hydroxide (Maalox) to inactivate acid pepsin and to neutralize acid secretion 2. Anti-cholinergic: Atropine SO4, Propanthiline Bromide supresses gastric secretion and delays gastric emptying time 3. Histamine H2 receptor Antagonist: Cimetidine, Ranitidine blocks/inhibits gastric acid secretion 4. Ctytoprotective agents: Sucralfate, Cytotec coats the mucosal lining 5. Proton pump inhibitor: Omeprazole supresses gastric acid secretion b. Stress reduction and rest decrease HCl secretion c. Dietary modifications 1. Avoid black pepper and food that causes distresshighly seasoned, gas-forming foods 2. Avoid prolonged use of milk and cream - stimulates acid secretion 3. Avoid tea, coffee, alcohol 4. Avoid snacks at bedtime stimulates acid secretion 5. Give iron and ascorbic acid to promote healing d. Surgical management

PYLOROPLASTY

PARTIAL CELL VAGOTOMY

TOTAL GASTRECTOMY

NURSING MANAGEMENT 1. Relieve pain 2. Reducing anxiety 3. Maintaining optimal nutritional status 4. Monitoring and managing potential complications a. Hemorrhage hematemesis, melena - Promote bedrest - Monitor V/S and I/O - D5LR and BT - NGT to empty stomach of blood clots, to watch rate of bleeding - Gavage with ice water to increase vasoconstriction - If bleeding persist for 24 hrs prepare and assist pt. for gastric surgery. b. Perforation erosion of the ulcer through the gastric serosa into the peritoneal cavity without warning - sudden severe epigastric pain, board-like rigidity. If accompanied by circulatory failure peritonitis develop - D5LR - NGT - Gastric surgery c. Penetration erosion of the ulcer through the gsatric mucosa into adjacent structures such as pancreas, biliary tract or gastrohepatic omentum d. Pyloric obstruction projectile vomiting e. Intractability to pain failure of medical management to treat PUD, continuous pain despite of medical management - gastric surgery. POST OP COMPLICATIONS 1. 2. 3. 4. 5. Hemorrhage Hypovolemic shock Respiratory complication pneumonia Steatorrhea due to rapid gastric emptying Vit. B 12 deficiency due to lack of intrinsic factor in the gastric juice 24 hrs. Urine test 5-10ng/dl for absorption of B12 < 5 ng/dl not candidate for oral / inject B12 month (For lifetime)

SCHILLINGS TEST

6. Reflulx gastritis with removal of the pylorus which acts as a barrier to the reflux of duodenal contents - Aluminum Hydroxide Gel (Amphogel)

CHOLECYSTITIS / CHOLELITHIASIS
Inflammation of gallbladder with gallstone formation. PREDISPOSING FACTOR 1. High risk women 40 years old 2. Post menopausal women undergoing estrogen therapy 3. Obesity 4. Sedentary lifestyle 5. Hyperlipidemia 6. Neoplasm

CLINICAL MANIFESTATION Symptoms occur due to the following: a. The disease of the gall bladder itself b. Obstruction of the bile passages by a gallstones

1. Pain and Biliary Colic o Pain a gallstone obstructs the cystic duct, the gall bladder become distended, inflamed and eventually infected o Biliary Colic caused by contraction of the gall bladder, which cannot release bile because of obstruction 2. Jaundice occurs due to obstruction of the common bile duct. The bile, which is no longer carried to the duodenum, is absorbed by the blood and gives the skin and mucous membrane a yellow color. 3. Changes in urine and stool color Urine becomes very dark in color. Stools are grayish like putty, clay-colored because of absence of bile pigments. 4. Vitamin deficiency obstruction of the bile flow interferes the absorption of fat soluble vitamin (ADEK) ASSESSMENT AND DIAGNOSTIC FINDINGS 1. Abdominal x-ray 15%-20% calcified are visible 2. Ultrasonography rapid and accurate, used in patients with liver dysfunction and jaundice 3. Radionucleide imaging or chloscintigraphy radioactive agent is administerzed IV 4. Cholecystography 5. Endoscopic Retrograde Cholangiography - Hydration 6. Percutaneous Transhepatic Cholangiography 7. Serum lipase elevated 8. Indirect bilirubin elevated NURSING MANAGEMENT 1.Meds a.) Narcotic analgesic - Meperdipine Hcl Demerol b.) Anti cholinergic - Atropine SO4 c.) Anti emetic Phenergan Phenothiazide with anti emetic properties 2.Diet increase CHO, moderate CHON, decrease fats 3.Meticulous skin care

4.Surgery:

Cholecystectomy

Nursing Mgt post cholecystectomy -Maintain patency of T-tube intact & prevent infection MEDICAL MANAGEMENT 1. Cholecystectomy 2. Laparoscopic cholesyctectomy 3. Choledocystectomy NON SURGICAL REMOVAL OF GALLSTONES 1. Dissolving Gallstones by infusion a solvent Mono octanon or methyl tertiary butyl ether into the gallbladder. 2. Lithotripsy repeated shock waves directed at the gallstone in the gall bladder or common bile duct fragment the stones.

PANCREATITIS

Short acting insulin Regular (via IV) CLASSIFICATIONS

A. ACUTE PANCREATITIS - Ranges from a mild, self-limiting disorder to a severe, rapidly fatal disease that does not respond to any treatment. - Etiology: unknown - Obstruction of the pancreatic duct accompanied by Hypersecretion of the exocrine enzymes of the pancreas. The enzymes enter the bile duct where they are activated and together with bile, back up (reflux into the pancreatic duct) causing pancreatitis. Cant wake up dead hallmark sign PATHOPHYSIOLOGY Self-digestion of the pancreas by its own proteolytic enzymes principally the trypsin 80% of patients have biliary tract disease 5% with gallstones develop the disease

Gallstones enter the common bile duct and lodge at the ampulla of water, obstructing the flow of pancreatic juice or causing a reflux of bile from the common bile duct into the pancreatic duct. Thus, activating the powerful enzymes with the pancreas. These enzymes will be activated when it reached the duodenum causing vasodilation, increase vascular permeability, necrosis, erosion and hemorrhage Long term use of alcohol Bacterial or viral infection

CLINICAL MANIFESTATIONS 1. Severe Lt epigastric pain radiates from back &flank area Aggravated by eating, with DOB 2. N/V 3. Tachycardia 4. Palpitation due to pain 5. Dyspepsia indigestion 6. Decrease bowel sounds 7. (+) Cullens sign - ecchymosis of umbilicus hemorrhage 8. (+) Grey Turners spots ecchymosis of flank area 9. Hypocalcemia ASSESSMENT AND DIAGNOSTIC FINDINGS 1. 2. 3. 4. 5. 6. History of abdominal pain and presence of risk factors Serum amylase and lipase l;evel 3 times higher than normal WBC increased Hypocalcemia Glycemia, glucosuria, increase serum bilirubin level Stools bulky, pale and foul smelling

NURSING MANAGEMENT 1. Meds a.) Narcotic analgesic - Meperidine Hcl (Demerol) Dont give Morphine SO4 will cause spasm of sphincter. b.) Smooth muscle relaxant/ anti cholinergic - Ex. Papavarine Hcl Prophantheline Bromide (Profanthene) c.) Vasodilator NTG d.) Antacid Maalox e.) H2 receptor antagonist - Ranitidin (Zantac) to decrease pancreatic stimulation f.) Ca gluconate 2. Withold food & fluid aggravates pain 3. Assist in Total Parenteral Nutrition (TPN) or hyperalimentation Complications of TPN 1. Infection 2. Embolism 3. Hyperglycemia 4. Institute stress mgt tech a.) DBE b.) Biofeedback 5. Comfy position - Knee chest or fetal like position 6. If pt can tolerate food, give increase CHO, decrease fats, and increase CHON 7. Complications: Chronic hemorrhagic pancreatitis

B. CHRONIC PANCREATITIS - Inflammatory disorder characterized by progressive and anatomic functional destruction of the pancreas. - There is mechanical obstruction of the pancreatic and common bile ducts and the duodenum because of fibrous tissues on the site due to repeated attacks of pancreatitis causing pressure within the pancreas CLINICAL MANIFESTATIONS 1. 2. 3. 4. Severe abdominal pain (upper) and back pain accompanied by vomiting Severe pain cant be relieved by opiods Weight loss decrease dietary intake secondary to anorexia Stoosl become frequent, fatty, frothy and foul smelling (F4) due to poor digestion of fats and proteins 5. Steatorrhea stools with high fat content ASSESSMENT AND DIAGNOSTIC FINDINGS 1. MRI, CT Scan and ultasound to rule out pancreatic cyst 2. Glucose tolerance test MEDICAL MANAGEMENT Directed toward preventing and managing acute attacks, relieving pain and discomforts, and managing exocrine and endocrine insufficiency of pancreatitis. SURGICAL MANAGEMENT

PANCREATICOJEJUNOSTOMY (ROUX-EN-Y) PANCRATICODUODENECTOMY NON SURGICAL MANAGEMENT Indicated to patients who refuses surgery Endoscopy remove pancreatic duct stones and obstruction Avoiding alcohol Diet with insulin or oral antidiabetic agent

HEPATIC DYSFUNCTION / LIVER CIRRHOSIS

Results from damage to the livers parenchymal cells, either directly from primary liver diseases or indirectly from obstruction of bile flow or derangement of hepatic circulation Can be acute or chronic Cirrhosis chronic liver disease

ETIOLOGY Infectious agent: viruses, bacteria Anoxia, metabolic disorders, toxins and medications, nutritional deficiencies and hypersensitivity states

CLINICAL MANIFESTATIONS Early signs: a.)Weakness, fatigue b.)Anorexia, n/v c.)Stomatitis d.)Urine tea color Stool clay color e.)Amenorrhea f.)Decrease sexual urge g.)Loss of pubic, axilla hair h.)Hepatomegaly i.)Jaundice j.)Pruritus or urticaria Late signs a.) Hematological changes all blood cells decrease Leukopenia- decrease Thrombocytopenia- decrease Anemia- decrease b.) Endocrine changes Spider angiomas, Gynecomastia, Caput medusate, Palmar errythema c.) GIT changes Ascitis, bleeding esophageal varices due to portal HPN d.) Neurological changes: TYPES OF JAUNDICE 1. Hemolytic jaundice result of increased destruction of the RBC 2. Hepatocellular jaundice caused by inability of the damaged liver cells to clear normal amount of bilirubin from the blood 3. Obstructive jaundice caused by occlusion of the bile duct by a gallstone, an inflammatory process, a tumor, or pressure from enlarged organ 4. Hereditary hyperbilirubinemia resulting from several inherited disorders (causes: inborn errors or biliary metabolism) ASSESSMENT AND DIAGNOSTIC EVALUATION 1. The presence and extent of ascites are assessed by percussion of the abdomen 2. When fluid accumulated in the peritoneal cavity, the flanks bulge when the patient assumes a supine position 3. Daily measurements MEDICAL MANAGEMENT 1. Dietary modifications - Negative sodium balance to reduce fluid retention - Table salts, salty foods, salted butter and margarine and all ordinary canned foods should be avoided 2. Diuretics Spironolactone, Lasix 3. Bed rest 4. Paracentesis

NURSING MANAGEMENT 1. Assessment and documentation of I & O, abdominal girth and daily weight taking to assess fluid status. 2. Monitor serum ammonia and electrolyte levels to assess electrolyte balance, response to therapy and indicators of encephalopathy. HEPATIC ENCEPHALOPATHY Hepatic encephalopathy - ammonia (cerebral toxin) Late signs: Early signs: asterexis Headache (flapping hand tremors) Fetor hepaticus Confusion Restlessness Decrease LOC Hepatic coma Diagnosis: 1. Liver enzymes- increase SGPT (ALT) SGOT (AST) 2. Serum cholesterol & ammonia increase 3. Indirect bilirubin increase 4. CBC pancytopenia Blood component 5. PTT prolonged 6. Hepatic ultrasonogram fat necrosis of liver lobules NURSING MANAGEMENT 1. CBR 2. Restrict Na! 3. Monitor VS, I&O 4. With pt daily & assess pitting edema 5. Measure abdominal girth daily notify MD 6. Meticulous skin care 7. Diet increase CHO, vit & minerals. Moderate fats. Decrease CHON Well balanced diet 8. Complications: a.) Ascites fluid in peritoneal cavity Nursing Mgt: 1. Meds: Loop diuretics 10 15 min effect 2. Assist in abdominal paracentesis - aspiration of fluid - Void before paracentesis to prevent accidental puncture of bladder as trochar is inserted b.) Bleeding esophageal varices - Dilation of esophageal veins

III. ACROSS THE LIFE SPAN

STOMATITIS (MUCOSITIS)
Inflammation and breakdown of the oral mucosa - Often a side effect of chemotherapy or radiation therapy. ASSESSMENT Bruising and flossing routines Frequency of dental visits Awareness of any lesions or irritated areas in the mouth, tongue or throat History of sore throat or bloody sputum Discomforts caused by certain foods Daily food intake Use of alcohol and tobacco Chewing of smokeless tobacco

GASTRITIS
Inflammation of the gastric or stomach mucosa may be acute or chronic.

CLASSIFICATIONS A. ACUTE GASTRITIS - Often caused by dietary indiscretion, the person eats foods that is contaminated with disease-carrying microorganisms or that is irritation or too highly seasoned - Overuse of aspirin and other NSAID, excessive alcohol intake, bile reflux and radiation therapy - Ingestion of strong acid or alkali can cause the mucosa to become gangrenous or to perforate result to scarring pyloric obstruction B. CHRONIC GASTRITIS - Caused by either benign or malignant ulcers of the stomach or by bacteria Helicobacter pylori

- Sometimes associated with autoimmune disease such as pernicious anemia, use of caffeine, medications, alcohol, smoking, and reflux of intestinal contents into the stomach PATHOPHYSIOLOGY Gastric mucosa membrane becomes edematous and hyperemic (congested with fluid and blood) and undergoes superficial erosion. It secretes a scanty amount of gastric juice, containing a very little acid but much mucus. Superficial ulceration may occur and can lead to hemorrhage. CLINICAL MANIFESTATIONS A. Acute Gastritis - abdominal discomforts - headache, lassitude - nausea B. Chronic Gastritis - anorexia - heartburn after eating - belching - vomiting - hiccuping - anorexia - nausea and vomiting - malabsorption of B12 - sour taste inthe mouth

ASSESSMENT AND DIAGNOSTIC FINDINGS Achlorhydia absence of HCl Hypochlorhydia low level of HCl Hyperchlorhydia high level of HCl Diagnosis can be determined by endscopy, upper GI radiographic studies, histologic examination of a tissue obtained by biopsy Serologic examination to detect H .pylori

MEDICAL MANAGEMENT Instruct patient to refrain from alcohol and foods until symptoms subside Non-irritating diet after the patient take food by mouth Fluid may need to administer parenterally if symptoms persist Aluminum hydroxide use to neutralize acids Neutralize an alkali diluted lemon juice or diluted vinegar is used Corrosion emetics and lavage are avoided because of the danger of perforation and damage to the esophagus NGT, analgesics, sedatives, antacids and IVF Gastrojejunostomy to treat pyloric obstruction Antibiotics (tetracycline, amoxicillin) H. pylori PLANNING AND GOALS Reduce anxiety Avoidance of irritating foods Adequate intake of nutrients Maintenance of fluid balance Increased awareness of dietary management Relief of pain

INTRA-ABDOMINAL INJURIES

CATEGORIES 1. Penetrating Abdominal Injuries results in high incidence of injury to hallow organs, particularly the small bowels and liver (most frequently injured) a. Gunshot wounds b. Stab wounds 2. Blunt Trauma may result from motor vehicle crashes, falls, blows or explosions - Commonly associated with extra-abdominal injuries to the chest, hear or extremities - Injuries maybe hidden or difficult to detect - Complications are greater than in penetrating

ASSESSMENT AND DIAGNOSTIC FINDINGS 1. The abdomen is inspected for obvious signs of injury, including penetrating, bruises and abrasions 2. Absence of bowel signs may be early S/S of peritoneal involvement 3. Peritoneal irritations - abdominal distention, involuntary guarding, muscular rigidity, rebound tenderness, pain 4. Hypotension and S/S of shosk 5. Urinalysis to detect hematuria urinary tract injury 6. Serial hematocrit levels to evaluate trends reflecting the presence or absence of bleeding 7. WBC count to detect elevation 8. Serum amylase analysis to detect rising levels, suggests pancreatic injury or perforation of the GIT MANAGEMENT Resuscitation procedures (ABC) are initiated Pressure to control external bleeding IV fluid replacement Monitor for signs of shock Tetanus prophylaxis LOWER GASTROINTESTINAL SYSTEM ASSESSMENT 1. Nursing history 2. Physical assessment 3. Diagnostic assessment COMMON NURSING DIAGNOSIS

1. 2. 3. 4.

Alteration in bowel elimination: diarrhea, constipation or incontinence Fluid volume deficit Altered sexuality pattern Disturbances in self-concept

PLANNING FOR HEALTH RESTORATION AND MAINTENANCE Constipation and Impaction may result from multiple causes such as: diminished or absent sphincter control. Cognitive or perceptual impairment neurologic factor Diet Immobility DIAGNOSTIC Impaired bowel elimination NURSING INTERVENTIONS 1. Promoting bowel continence - bowel training program - regular, complete emptying of the lower bowel results in bowel continence - regular time for defecation, Rectal suppository - Mechanical stimulation digital, gloved hand, lubricated - normal squatting position (knee higher than hips) - Instruct patient to bear down and to contract the abdominal muscles - The nurse records defecation time, character of stool, nutritional intake, cognitive abilities and functional self care abilities for 5-7 days 2. Preventing constipation - Assess bowel elimination, character of stool, food and fluid intake, level of activity, bowel sounds, medications, etc. - Well balanced diet, adequate intake of high fiber diet - Fluid intake should be between 2 and 3 L/day unless contraindicated - Prune juice - Physical activity and exercise - Stool softeners, bulk forming agents, mild stimulants and suppositories - Encourage patient to respond to the natural urge to defecate ALTERED MODES OF ELIMINATION 1. Intestinal Decompression removal of intestinal contents to prevent gas and liquid from distending the coils of the intestines 2. Ileostomy surgical creation of an opening into the ileum or small intestines 3. Colostomy surgical creation of an opening into the colon

COMMON HEALTH PROBLEMS I. NEONATE AND INFANT

IMPERFORATE ANUS

Failure of the membrane separating the rectum from the anus to absorb during the 8th week of fetal life. Incidence: 1:2000-5000 live births CLASSIFICATIONS OF ANORECTAL MALFORMATIONS LEVEL High MALE Anorectal agenesis with rectoprostatic-urethral fistula - Rectal atresia - With fistula FEMALE - Anorectal agenesis with rectovaginal fistula rectal atresia without fistula

Intermediate -

Recto-bulbar urethral fistula Agenesis without fistula

Rectovestibular fistula - Rectovaginal fistula - Agenesis without fistula Anovestibular fistula Anocutaneous fistula Anal stenosis cloaca Rare malformations

Low

Anocutaneous fistula - Anal stenosis - Rare malformations

CHOANAL EXTROPHY Rare, severe defect in which there is externalization of the bladder and bowel through the abdominal wall.

DIAGNOSTIC EVALUATION 1. Checking for patency of the anus and rectum 2. Passage of meconium does not always indicate anal patency (particularly in girls) 3. Rectourinary fistulas should be suspected if there is meconium in the urine 4. Anal stenosis may not be identified until the shild is older and presents with a history of difficult defecation, abdominal distention, ribbon-like stools 5. Abdominal ultrasound THERAPEUTIC MANAGEMENT 1. Manual dilations for anal stenosis 2. Colostomy temporary, for infants with high anomalies 3. Anorectoplasty final procedure

NURSING CONSIDERATIONS 1. Identify undetected anorectal malformations 2. Assess passage of meconium 3. Healing the post anorectoplasty toprevent infection and complications (perineal care, dressings) 4. Side-lying prone position to prevent pressure on the perineal area

5. For patients with colostomy frequent changes of dressings, meticulous skin care and correct application of a collection dvice

CONGENITAL MEGACOLON

Mechanical obstruction caused by inadequate motility of part of the intstine of all cases of neonatal obstruction More common in children with Down syndrome Rectosigmoid is commonly affected

PATHOPHYSIOLOGY Absence of parasympathetic ganglion cells in one or more segments of the colon Aganglionic segment almost always includes the rectum and a proximal portion of the large intestines Skin segment rare Total aganglionosis Absence of peristalsis Accumulation of intestinal contents Distention of bowel proximal to the defect

DIAGNOSTIC EVALUATION Neonate, based on clinical signs of intestinal obstruction and failure to pass meconium Radiographs, barium enema and anorectal manometric exams confirmed by histologic examination of a full thickness rectal biopsy demonstrating absence of ganglion cells

THERAPEUTRIC MANAGEMENT 1. Ostomy temporary, created proximal to the aganglionic segments to relieve obstruction and allow the normally enervated and dilated bowel to return to its normal size 2. Removal of aganglionic portion of the bowel 3. Complete corrective surgery followed when the child weights approximately 9 kgs. PULL THROUGH PROCEDURE

NURSING CONSIDERATIONS A. Main Objectives - To help the parents adjust to a congenital defect of their child - To foster infant-parent bonding - To prepare them for the medical / surgical intervention - Assist them in colostomy care after discharge

MECONIUM ILEUS

- Initial manifestation of cystic fibrosis - Luminal obstruction of the distal small intestine by abnormal meconium

CELIAC DISEASE
Also known as GLUTEN-INDUCED ENTEROPATHY, GLUTEN SENSITIVE ENTEROPATHY A disease of the proximal small intestines characterized by abnormal mucosa and permanent intolerance to gluten Cause is not known, inherited, influence by environmental factors

PATOPHYSIOLOGY Characterized by an intolerance to the protein gluten Unable to digest the gliaden component of gluten Resulting in an accumulation of a toxic substances that is damaging to the mucosal cells DIAGNOSTIC EVALUATION Symptoms are noted several months after the introduction of gluten-containing grains into the diet Evidence by failure to thrive and diarrhea Biopsy Diarrhea and steatorrhea Serologic testing

THERAPEUTIC MANAGEMENT Dietary management gluten-free diet Vitamins, iron and caloric supplements AVOID GLUTEN RICH FOODS

B arley R ye O atmeal W - heat

Explosive Diarrhea NURSING CONSIDERATIONS Explain the disease process to the child and parents Inform them of the foods to be avoided Low fat diet

IRRITABLE BOWEL SYNDROME

Occurs more commonly in women than in men Syndrome: heredity, psychological conditions or stress such as depression and anxiety, a diet high in fat and stimulating or irritating foods, alcohol consumption or smoking.

PATHOPHYSIOLOGY Results from a functional disorder of intestinal motility

The change in motility maybe related to the neurologic regulatory system, infection or irritation, or a vascular or metabolic disturbance The peristaltic waves are affected at specific segments of the intestines and in the intensity with which they propel the fecal matter forward

CLINICAL MANIFESTATIONS Primary Symptoms: Alteration in Bowel Patterns - Constipation, diarrhea or combination of both - Pain, bloating and abdominal distention - Abdominal pain is sometimes precipitated by eating and is frequently relieved by defecation. ASSESSMENT AND DIAGNOSTIC FINDINGS 1. 2. 3. 4. Stool studies, contrast x-ray studies and proctoscopy Barium enema and colonoscopy may relieve apsm Distention, or mucus accumulation in the intestine Electromyelography to study intraluminal pressure changes generated by spasticity

MEDICAL MANAGEMENT Control of abdominal pain, diarrhea or constipation Reduce stress Determining irritating foods Heatlhy high-fiber diet to relieve diarrhea or constipation Exercise to increase motility of the intestines Anti-diarrheal drugs to control fecal urgency Anti-cholinergics to relieve spasm, cramping and constipation

NURSING MANAGEMENT Provide health education (good dietary habits) Eat at regular time, chew foods thoroughly and slowly Fluids are necessary, but fluid should not be taken with medicines because this results in abdominal distention Discourage alcohol use and cigarette smoking

III. ADOLESCENT AND YOUNG ADULT INFLAMMATORY BOWEL DISEASE

ULCERATIVE COLITIS
Recurrent ulcerative and inflammatory disease of the mucosal and submucosal layers of the colon and rectum. Peak incidence: between 30 and 50 y/0

PATHOPHYSIOLOGY Affects the superficial mucosa of the colon and is characterized by multiple ulcerations, diffuse inflammation and desquamations or shedding of the colonic epithelium. Bleeding occurs as a result of ulcerations The mucosa becomes edematous and inflammed Lesions are continuous, occurring one after the other Abscess form and infiltrate is seen in the mucosa and submucosa Disease progress, usually begins in the rectum and spread approximately to involve the entire colon Eventually, the bowel narrows, shortens and thickens because of muscular hypertrophy CLINICAL MANIFESTATIONS Diarrhea Passage of 10-20 liquid stools/day Left lower quadrant abdl pain Weight loss anorexia fever vomiting cramping

Rectal bleeding Urgent need to defecate intermittent tenesmus

dehydration Pallor

ASSESSMENT AND DIAGNOSTIC FINDINGS Assess for tachycardia, hypotension, tachypnea, fever and pallor, level of hydration and nutritional status Assess bowel sounds, distention and tenderness Positive blood in the stool, low hematocrit and hgb concentration, elevated WBC, low albumin levels and electrolyte imbalance Abdominal x-ray Sigmoidoscopy and colonoscopy CT Scan, MRI Barium enema Stool exam- to rule out entamoeba histolitica and clostridium difficile COMPLICATIONS Toxic megacolon, perforation and bleeding result of ulceration and vascular engorgement

MEDICAL MANAGEMENT 1. Nutritional Therapy - Oral fluids and a low-residue, high protein, high calorie diet with supplemental vitamins therapy and iron replacement are prescribed to meet nutritional needs and control pain and diarrhea 2. Pharmacologic Therapy - Sadatives, Anti-peristaltic, Immunomodulators(Azathioprene, Methotrexate, Cyclosporin), Anti-diarheal, Corticosteroids 3. Surgical Management - Total colectomy and ileostomy, Proctocollectomy with ileostomy, ileoanal anastomosis. NURSING MANAGEMENT 1. Maintain normal elimination pattern 2. Relieving pain 3. Maintaining fluid intake 4. Maintaining optimal nutrition parenteral nutrition 5. Promoting rest 6. Reducing anxiety 7. Enhancing coping measures 8. Preventing skin breakdown 9. Monitoring and managing potential complications 10. Teaching patients self care

CROHN'S DISEASE

A sub-acute and chronic inflammation that extends through all layers of the bowel wall from the intestinal mucosa characterized by periods of remissions and exacerbations. PATHOPHYSIOLOGY Disease process begins with edema and thickening of mucosa Ulcers begin to appear on the inflammed mucosa Lesions are not in continuous contact with one another and are separated by normal tissue Fistulas, fissures and abscesses form as the inflammation extends into the peritoneum CLINICAL MANIFESTATIONS Usually insidious RLQ abdominal pain Abdl tenderness & spams Emaciated Abscesses, fistulas, fissures intestinal perforation - diarrhea - crampy abdominal pains - Scarring and granuloma formation - anorexia, weight loss

COMPLICATIONS Intestinal obstruction or stricture formation Perianal disease Fluid and electrolyte imbalance Malnutrition from malabsorption Fistula and abscess formation

ASSESSMENT AND DIAGNOSTIC FINDINGS 1. 2. 3. 4. Proctosigmoidoscopy to determine inflammation Stool exams occult blood, steatorrhea Barium study the most conclusive diagnostic procedure CT scanning, CBC

NURSING AND MEDICAL MANAGEMENT Same with ulcerative colitis

IV. ADULT
DIVERTICULITIS & DIVERTICULOSIS

DIVERTICULUM A sac-like outpouching of the lining of the bowel that extends through a defect in the muscle layer, may occur anywhere along the GIT DIVERTICULOSIS Exist when multiple diverticula are present without inflammation or symptoms. DIVERTICULITIS Results when food and bacteria retained in the diverticulum, produce infection and inflamamiton, 95% in the sigmoid colon.

PATHOPHYSIOLOGY High intraluminal pressure, low volume in the colon, a decreased muscle strength in the colon wall Mucosa and submocusal layers of the colon herniated Diverticulum Bowel contents accumulate and decompose causing inflammation and infection Inflammation spread to surrounding bowel wall giving rise to irritability and spacticity of the colon Abscess develop, perforate Peritonitis and erosion of the blood vessels with bleeding CLINICAL MANIFESTATIONS Bowel irregularities - narrow stool

Diarrhea Crampy pain the LLQ Low grade fever Nausea Bloating & abdl distention

increased constipation weakness fatigue septicemia Anorexia

COMPLICATIONS Peritonitis Abscess formation Bleeding

MEDICAL MANAGEMENT 1. Dietary and Medical Management - Diet: clear liquid initially until inflammation subsides, then high fiber, low fat diet 2. Drugs - Anti-spasmodic: Probanthine, Oxyphencycline - Stool softeners: Metamucil. Colace, Dulcolax - Analgesics: including opiods - Antibiotics 3. Surgical management - PRIMARY BOWEL RESECTION -

BOWEL RESECTION WITH COLOSTOMY

NURSING INTERVENTIONS 1. Maintaining elimination patterns - increase fluid intake - soft food and high fiber

- encourage use of laxative, stool softeners 2. Relieving pain - Analgesics - Anti-spasmodics to relieve intestinal spasm 3. Monitoring and managing potential complications - Watch out for signs of perforation (increase abdl pain and tenderness ccompanied by abdl rigidity, elevated WBC, increase body temp., elevated sedimentation rate, tachycardia, and hypotension.

HEMORRHOIDS
Dilated portion of veins in the anal canal By the age of 50, 50% of people have hemorrhoids

2 TYPES OF HEMORRHOIDS 1. Internal 2. External CLINICAL MANIFESTATIONS Bright red bleeding with defecation (caused by itching and pain Inflammation and edema (caused by thrombosis) Ischemia ( due to thrombosis leading to necrosis) Prolapse (when enlarged)

NURSING MANAGEMENT High residue diet Warm compress Bed rest increase fluid intake sitz bath

MEDICAL MANAGEMENT 1. non-surgical (to prevent prolapse) - infrared photocoagulation, bipolar diathermy, laser therapy) 2. Surgical treatment HEMORRHOIDECTOMY

VI. ACROSS THE LIFE SPAN

DIARRHEA
- Abnormal increase in the frequency and liquidity of the stool weight or volume PATHOPHYSIOLOGY Increased production and secretion of water and electrolytes by the intestinal mucosa into the intestinal lumen. (secretory diarrhea) Water is pulled into the intestines by osmotic pressure of unabsorbed particles, slowing the reabsorption of water (osmotic diarrhea) Increased peristalsis and a combination of increased secretion and decreased absorption in the bowel (mixed diarrhea)

CLINICAL MANIFESTATIONS Abdominal cramps tenesmus Distention watery stool Intestinal rumbling anorexia Thirst Other S/S depends on the degree and its cause ASSESSMENT AND DIAGNOSTIC FINDINGS CBC Chemical profile Urinalysis Routine stool exam Stool exam for infectious or parasitic organism Bacterial toxins, blood and electrolytes Endoscopy or barium enema COMPLICATIONS Cardiac dysrhythmias (due to fluid and electrolyte loss)

MEDICAL MANAGEMENT Primary management is directed towards controlling symptoms, preventing complications and eliminating or treating the underlying cause Antibiotic and anti-inflammatory

NURSING MANAGEMENT Assess and monitor characteristic and pattern of diarrhea Bed rest and intake of liquids and foods low in bulk until acute attacks subside Avoid caffeine, carbonated beverages very hot and very cold must be avoided Administer anti-diarrheal meds IV fro rapid rehydration Monitor serum electrolyte levels Perianal care

APPENDICITIS

PATOHPYSIOLOGY The appendix becomes inflamed and edematous as a result of either becoming kinked or occluded by a fecalith (hardened mass or stool), tumor or foreign body The inflammatory process increases intraluminal pressure, initiating a progressively severe, generalized upper abdominal pain that becomes localized in the right lower quadrant of the abdomen within few hours Eventually, the inflamed appendix fills with pus

CLINICAL MANIFESTATIONS Vague epigastric or pre-umbilical pain progress to RLQ accompanied by low grade fever, nausea and vomiting Loss of appetite Local tenderness is elicited when pressure at Mc Burneys point is applied Rebound tenderness when pressure is released Pain on defecation (tip of appendix rests against the rectum) Abdominal distention (results of paralytic ileum)

ASSESSMENT AND DIAGNOSTIC FINDINGS 1. CBC mild leukocytosis increase WBC 2. PE (+) rebound tenderness (flex Rt leg, palpate Rt iliac area rebound) 3. Urinalysis COMPLICATIONS - PERITONITIS Absence of bowel sounds TREATMENT Treatment: - appendectomy 24 45 NURSING MANAGEMENT 1. Consent 2. Routinary nursing measures: a.) Skin prep b.) NPO c.) Avoid enema lead to rupture of appendix 3. Meds: Antipyretic Antibiotics *Dont give analgesic will mask pain - Presence of pain means appendix has not ruptured. 4. Avoid heat application will rupture appendix. 5. Monitor VS, I&O bowel sound MEDICAL MANAGEMENT 1. Prevent fluid and electrolyte imbalances and dehydration, antibiotics and IV fluids are administered until surgery is performed 2. Analgesics administered after diagnosis 3. Appendectomy NURSING MANAGEMENT: POST OP 1. Position patient to semi-Fowlers after surgery (reduces tension on the incision

 If (+) to Pendrose drain indicates rupture of appendix Position- affected side to drain 2. Meds: analgesic due post op pain Antibiotics, Antipyretics PRN 3. Monitor VS, I&O, bowel sound 4. Maintain patent IV line 5. Complications- peritonitis, septicemia

PERITONITIS

ETIOLOGY 1. 2. 3. 4. 5. Bacterial infection Trauma Inflammation that extends from an organ outside the peritoneal area Perforated ulcers, diverticulitis and bowel resection Peritoneal dialysis

PATHOPHYSIOLOGY Caused by leakage of contents from abdominal organs as a result of inflammation, infection, ischemia, trauma or tumor perforation. CLINICAL MANIFESTATIONS Pain Paralytic ileus Increase body temp and pulse Rebound tenderness Nausea and vomiting Increased Leukocyte

ASSESSMENT AND DIAGNOSTIC FINDINGS Increase leukocyte count Decrease Hgb and Hct Serum electrolyte shows altered level of K, Na, Cl Abdominal x-ray shows air and fluid levels as well as distended bowel loops CT scan shows abscess formation Peritoneal aspiration COMPLICATIONS

Generalized sepsis Shock Intestinal obstruction Bowel adhesions Wound evisceration (post-op complication) Abscess formation (post-op complication) MEDICAL MANAGEMENT Analgesics for pain Anti-emetics for nausea and vomiting Intestinal intubation and suction to relieve abdominal distention Oxygen therapy by nasal canula Antibiotic therapy Surgery (if the causes are: appendicits, perforation, abscess, etc.)

NURSING MANAGEMENT Assess pain, V/S, GI function and fluid and electrolyte balance Report nature and location of pain Administer analgesics Comfortable position I&O Observe for character of drainage (post-op) Observe for signs of peritonitis: decrease temp and PR, softening of the abdomen, return of peristaltic sounds, passing of flatus, bowel movement

INTESTINAL OBSTRUCTION

2 TYPES 1. Mechanical Obstruction an intraluminal obstruction or a mural obstruction from pressure on the intestinal walls occurs - Intussusception, polypoid mucus and neoplasms, stenosis, strictures adhesions, hernias and abscesses 2. Functional Obstruction the intestinal musculature cannot propel the contents along the bowel - Amyloidosis, muscular dystrophy, endocrine disorders such as DM, or neurologic disorders such as Parkinsons A. SMALL BOWEL OBSTRUCTION

CAUSES:

Invagination or shortening of the colon caused by the movement of one segment of bowel into another.

TWISTING OF THE COLON, USUALLY COUNTERCLOCKWISE INGUINAL HERNIA

Abdominal contents pass through the hernial opening into the hernial sac CLINICAL MANIFESTATIONS Crampy pain that is wavelike and colicky initial symptoms May pass blood and mucus, but no fecal matter of no flatus\ Vomiting (if obstruction is complete, the peristaltic waves becomes vigorous and eventually assumes a reverse direction) Fecal vomiting (if obstruction is in the ileum) Dehydration (S/S: thirst, drowsiness, general malaise, aching, parched tongue and mucus membrane) Abdominal distention

ASSESSMENT AND DIAGNOSTIC FINDINGS Diagnosis is based on the symptoms described previously on x-ray findings abnormal quantities of gas, fluid or both in the bowel Laboratory studies: electrolyte studies CBC count

MEDICAL MANAGEMENT 1. Decompression 2. IV therapy to replace water, Na, Cl and K loss 3. Anastomosis NURSING MANAGEMENT 1. Non-surgical patient - Maintaining NGT function - Assessing and measuring NGT output - Assessing fluid and electrolyte imbalance - Assessing nutritional status and improvements 2. Surgical patient - Interventions are the same with other abdominal surgeries A. LARGE BOWEL OBSTRUCTION

PATHOPHYSIOLOGY Blood supply may be cut off Intestinal strangulation Necrosis CLINICAL MANIFESTATIONS Symptoms and progress relatively slow Obstructed sigmoid colon constipation may only be the symptom Marked distended abdomen Loops of large bowel become visible Crampy lower abdominal pain Fecal vomiting Obstruction results in accumulation of intestinal contents, fluids and gas proximal to the obstruction Obstruction of the bowel lead to distention and perforation unless some gas and fluid can flow back through the ileal valve

ASSESSMENT AND DIAGNOSTIC FINDINGS Based on x-ray studies Barium studies are contraindicated

MEDICAL MANAGEMENT Colonoscopy ( to untwist and decompress bowel)

Cecostomy (urgent relief of obstruction) Use of rectal tube (to decompress an area) Colostomy (permanent or temporary) Ileoanal anastomosis (entire large colon is removed)

NURSING MANAGEMENT Monitor signs that indicates intestinal obstruction Administer IVF and electrolyte as prescribed Prepare patient for surgery if they do not respond to non-surgical treatment