Gastrointestinal

Gastrointestinal System
Anatomy and Physiology

The Mouth
Important for the mechanical digestion of food
The saliva contains SALIVARY AMYLASE or PTYALIN that starts the INITIAL digestion of carbohydrates

The Esophagus
A hollow collapsible tube
Length- 10 inches
The upper third contains skeletal muscles
The middle third contains mixed skeletal and smooth muscles
The lower third contains smooth muscles and the esophago-gastric/ cardiac sphincter is found here
Functions to carry or propel foods from the oropharynx to the stomach

The stomach
J-shaped organ in the epigastrium
Contains four parts- the fundus, the cardia, the body and the pylorus
The esophageal sphincter prevents the reflux of the contents into the esophagus
The pyloric sphincter regulates the rate of gastric emptying into the duodenum
Capacity is 1,500 ml!

The functions of the stomach are generally to digest the food and to propel the digested materials into the SI for final digestion

The Glands and cells in the stomach secrete digestive enzymes:
1. Parietal cells- HCl acid and Intrinsic factor
2. Chief cells- pepsin digestion of PROTEINS!
3. Antral G-cells- gastrin
4. Argentaffin cells- serotonin
5. Mucous neck cells- mucus

The Small intestine
Grossly divided into the Duodenum, Jejunum and Ileum
The duodenum contains the two openings for the bile and pancreatic ducts
The ileum is the longest part (about 12 feet)

The intestinal glands secrete digestive enzymes that finalize the digestion of all foodstuff
Enzymes for carbohydrates
- disaccharidases
Enzymes for proteins
-dipeptidases and aminopeptidases
Enzyme for lipids
- intestinal lipase

The Large intestine
Approximately 5 feet long, with parts:
1. The cecum - widest diameter, prone to rupture
2. The appendix
3. The ascending colon
4. The transverse colon
5. The descending colon
6. The sigmoid - most mobile, prone to twisting
7. The rectum

Absorbs water
Eliminates wastes
Bacteria in the colon synthesize Vitamin K
Appendix participates in the immune system

Accessory Organs

The Liver
The largest internal organ
Located in the right upper quadrant
Contains two lobes- the right and the left

The hepatic ducts (right and left) join together with the cystic duct to become the common bile duct

Functions to store excess glucose, fats and amino acids
Also stores the fat soluble vitamins- A, D and the water soluble- Vitamin B12
Produces the BILE for normal fat digestion
The Von Kupffer cells remove bacteria in the portal blood
Detoxifies ammonia into urea

The gallbladder
Located below the liver
The cystic duct joins the hepatic duct to become the bile duct
The common bile duct joins the pancreatic duct in the sphincter of Oddi in the first part of the duodenum

Stores and concentrates bile
Contracts during the digestion of fats to deliver the bile
Cholecystokinin is released by the duodenal cells, causing the contraction of the gallbladder and relaxation of the sphincter of Oddi

The pancreas
A retroperitoneal gland
Functions as an endocrine and exocrine gland
The pancreatic duct (major) joins the common bile duct in the sphincter of Oddi

The exocrine function of the pancreas is the secretion of digestive enzymes for carbohydrates, fats and proteins Pancreatic amylase - carbohydrates Pancreatic lipase (steapsin) - fats Trypsin, Chymotrypsin and Peptidases - proteins Bicarbonate - to neutralize the acidic chyme.

Diagnostics

Guaiac Test - detects the presence of fecal occult blood . Positive guaiac test shown on right, as would be seen for this patient. Negative result (on left) included for comparison.

Fecal Occult Blood Testing-FOBT (Guaiac Test)
Instruct the patient to adhere to a 3-day meatless diet (avoid any blood-containing food, cantaloupe, uncooked broccoli, turnip, radish, or horseradish)
No intake of NSAIDS, aspirin and anti-coagulant
Avoid citrus fruits and vitamin C supplements
Screening test for colonic cancer

Barium swallow :
A series of x-rays of the esophagus and stomach. The patient drinks a liquid that contains barium (a silver-white metallic compound). The liquid coats the esophagus and x-rays are taken. This procedure is also called an upper GI series

Upper GIT study: barium swallow
Pre-test : NPO post-midnight; 6-8 hours before procedure
Post-test : Laxative is ordered, increase pt fluid intake, instruct that stools will turn white, monitor for obstruction

Barium enema procedure. The patient lies on an x-ray table. Barium liquid is put into the rectum and flows through the colon. X-rays are taken to look for abnormal areas.

Lower GIT study: barium enema
Examines the lower GI tract
Pre-test : Clear liquid diet and laxatives, NPO post-midnight, cleansing enema prior to the test
Lower GIT study: barium enema
Post-test: Laxative is ordered, increase patient fluid intake, instruct that stools will turn white, monitor for obstruction

EGD
(esophagogastroduodenoscopy)
Visualization of the upper GIT by endoscope

Pre-test : ensure consent, NPO 8 hours, pre-medications like atropine and anxiolytics
Intra-test: position : LEFT lateral to facilitate salivary drainage and easy access
Post-test : NPO until gag reflex returns, place patient in SIMS position until he awakens , monitor for complications, saline gargles for mild oral discomfort

ULTRASONOGRAPHY
1. A noninvasive test focuses high-frequency sound waves over an abdominal organ to obtain an image of the structure.
2. Ultrasound can detect small abdominal masses, fluid-filled cysts, gallstones, dilated bile ducts, ascites, and vascular abnormalities.
3. Ultrasound with Doppler may be ordered for vascular assessment.

COMPUTED TOMOGRAPHY (CT) SCAN
1. This is an x-ray technique that provides excellent anatomic definition and is used to detect tumors, cysts, and abscesses.
2. The CT can also detect dilated bile ducts, pancreatic inflammation, and some gallstones.

ENDOSCOPIC PROCEDURES
Endoscopy is the use of a flexible tube (the fiberoptic endoscope) to visualize the GI tract and to perform certain diagnostic and therapeutic procedures. Images are produced through a video screen or telescopic eyepiece. The tip of the endoscope moves in four directions, allowing for wide-angle visualization.

Customizable to meet specific surgical needs, endoscopes can be fitted with scissors, knives, lasers, or cameras. Here, the endoscope is fitted with a small grasping tool to remove a toy lodged in the esophagus of an infant

PROCTOSIGMOIDOSCOPY AND COLONOSCOPY
1. Proctosigmoidoscopy (rectosigmoidoscopy) is the visualization of the anal canal, rectum, and sigmoid colon through a fiberoptic sigmoidoscope.
2. Colonoscopy is the visualization of the entire large intestine, sigmoid colon, rectum, and anal canal.
3. Sigmoidoscopy or colonoscopy can be used to diagnose malignancy, polyps, inflammation, or strictures.

34 yr old female. She also had an endoscopy first. (bleeding and/or pain was the reason she came in.) That pinkish/white mass is cancer. It's right by/on the valve between the ileum (small intestine) and cecum (large intestine.)

TREATMENTS
gastrointestinal
ENEMA NASOGASTRIC INTUBATION TOTAL PARENTERAL NUTRITION

PURPOSES OF ENEMA ADMINISTRATION
1. Bowel preparation for diagnostic tests or surgery to empty the bowel of fecal content.
2. Delivery of medication into the colon ( such as enemas containing neomycin to decrease the bowel’s bacteria count or a kayexalate enema to decrease the serum potassium level)

PURPOSES OF ENEMA ADMINISTRATION
3. To soften the stool ( oil-retention enemas)
4. To relieve gas( tidal,milk and molasses,or fleet enemas)
5. Promote defecation and evacuate feces from the colon for patients with constipation or an impaction

PURPOSES OF NASOGASTRIC INTUBATION
Remove fluid and gas from the stomach (decompression).
Prevent or relieve nausea and vomiting after surgery or traumatic events by decompressing the stomach.
Irrigate the stomach (lavage) for active bleeding or poisoning.

PURPOSES OF NASOGASTRIC INTUBATION
Administer medications and feeding (gavage) directly into the GI tract.
Obtain a specimen of gastric contents for laboratory studies when pyloric or intestinal obstruction is suspected.

Nasogastric intubation

Ensuring proper NG tube placement:
examine the patient’s mouth and throat for signs of a coiled section of tubing.
watch for respiratory distress signs
try to aspirate stomach contents
auscultate for air sounds with your stethoscope (should hear a whooshing sound in the epigastric region)
Secure the NG tube to the patient’s nose with hypoallergenic tape

TOTAL PARENTERAL NUTRITION
TPN is administered to meet a client’s total nutritional needs when oral feedings, tube feedings, and standard IV feedings are contraindicated.
It’s used for client’s with various GI problems or other conditions that necessitate nutritional support such as some oncology clients.

IMPORTANT POINTS:
In most cases, administer TPN through a central vein such as subclavian. The fluid is highly concentrated to provide rapid dilution and thus decrease the risks of peripheral inflammation and thrombosis

GASTROINTESTINAL DISORDERS

HIATAL HERNIA
A. ETIOLOGY
1. Portion of the stomach protruding through a hiatus (opening) in the diaphragm into the thoracic cavity.
2. May result from a congenital weakness of the diaphragm or from injury, pregnancy, or obesity.
3. Function of the cardiac sphincter is lost, gastric juices enter the esophagus causing inflammation.

B. CLINICAL FINDINGS:
1. Subjective: substernal burning pain or fullness after eating; dyspepsia in the recumbent position; nocturnal dyspnea .
2. Objective: GI series and endoscopy show protrusion of the stomach through the diaphragm; regurgitation
C. THERAPEUTIC INTERVENTIONS:
1. Small, frequent, bland feedings.
2. Pharmacologic management: antacids, antisecretory agents, antiemetics, especially those that promote gastric emptying
3. Surgical repair (done infrequently)
Fundoplication

Nissen fundoplication. The fundus of the stomach is wrapped around the lower esophagus and the edges are sutured together.

NURSING CARE:
1. Teach the client and family about the dietary regimen.
2. Encourage attempts at weight loss.
3. Avoid constricting clothing and heavy lifting.
4. Encourage the client to sit up for at least 1 hour after eating.
5. Encourage the client to eat slowly and avoid drinking fluids with meals to limit the volume in the stomach.

Gastroesophageal reflux disease
Backflow of gastric contents, doudenal contents, or both past the lower esophageal sphincter (LES) into the esophagus without associated belching or vomiting.
Usually occur after a meal
Occurs when LES is deficient or pressure in stomach exceeds LES pressure.

Causes:
Food, alcohol, or cigarette that lower LES pressure
Increased abdominal pressure
Hiatal hernia
Weakened esophageal sphincter
Assessment:
Burning pain in epigastric area/ heartburn
Pain after meals or when lying down

Decrease LES pressure
LES relaxes
Gastrc contents regurgitates into the esophagus
Irritation of LES
Inflammation and injury
Reflux esophagitis

Nursing care:
Frequent, small meals
Avoidance of eating before going to sleep
Sitting upright during and after meals
Sleeping with head elevated
Antacid to neutralize acidic content of the stomach and minimize irritation.

H2 blocker to inhibit gastric acid secretion
Proton pump inhibitor to reduce gastric acidity
Smoking cessation to improve LES pressure ( nicotine lowers LES pressure)
Surgery (if hiatal hernia is the source.)

GASTRITIS
GASTRITIS is an inflammation of the gastric mucosa (the stomach lining).
It may be acute or chronic. Acute gastritis produces mucosal reddening, edema, hemorrhage, and erosion. Chronic gastritis is common among elderly people and people with pernicious anemia. In chronic atrophic gastritis, all stomach mucosal layers are inflamed.

POSSIBLE CAUSES:
Acute gastritis
Chronic ingestion of irritating foods, spicy foods or alcohol
Drugs, such as aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs)(in large doses), cytotoxic agents, caffeine, corticosteroids, antimetabolites, phenylbutazone, and indomethacin

Ingestion of poisons, especially dichlorodiphenyltrichloroethane (DDT), ammonia, mercury, carbon tetrachloride, and corrosive substances
Endotoxins released from infecting bacteria, such as staphylococci, Escherichia coli, and salmonella, viruses (gastroenteritis)

GASTRITIS
Break in the protective barrier of stomach lining(prostaglandin)
Autodigestion
HCL diffuses back to mucosa & injure small vessels
The walls & lining of stomach atrophy
Destruction of the gastric glands
Hemorrhage & forms ulcer

DIAGNOSTIC EVALUATION:
Fecal occult blood test can detect occult blood in stools if the client has gastric bleeding.
Blood studies show low Hgb level and Hct when significant bleeding has occurred.
Upper GI endoscopy with biopsy confirms the diagnosis when performed within 24hrs of bleeding.
Upper GI series may be performed to exclude serious lesions.

TREATMENT:
Blood transfusion
I.V. fluid therapy
NG lavage to control bleeding
Oxygen therapy, if necessary
Partial or total gastrectomy (rare)

IMPLEMENTATION :
If the client is vomiting, give antiemetics and I.V. fluids to prevent dehydration and electrolyte imbalance.
2. Monitor fluid intake and output and electrolyte levels.
3. Offer smaller, more frequent meals to reduce irritating gastric secretions. Eliminate foods that cause gastric upset.

4. If surgery is necessary, prepare the client preoperatively and provide appropriate postoperative care to decrease preoperative anxiety and prevent intraoperative and postoperative complications.
5. Administer antacids and other prescribed medications

PEPTIC ULCER DISEASE (PUD)
A. ETIOLOGY:
1. Ulcerations of the gastrointestinal mucus and underlying tissues caused by gastric secretions that have a low pH (acid)
2. Causes include conditions that increase the secretion of hydrochloric acid by the gastric mucosa or that decrease the tissue’s resistance to the acid.

PUD
h.pylori, acid & pepsin damages the barrier
Autodigestion of acids
Inc.production of of acid
Dysfunction of the pyloric sphincter
Large acid bolus into the doudenum
Mucosal inflammation & injury
Insufficient bile & p. enzymes to control the acid
ulceration

THERAPEUTIC INTERVENTIONS:
1 . Bland foods, and restriction of irritating substances.
2. Antibiotic therapy if microorganism is identified; tetracycline, metronidazole, and bismuth

3. Histamine H2 receptor antagonists or proton pump inhibitors, antacids
4. Sedatives, tranquilizers, anticholinergics, and analgesics
5. Antiemetics

. Surgical intervention:
Billroth I: removal of the lower portion of the stomach and attachment of the remaining portion to the duodenum.

. Billroth II: removal of the antrum and distal portion of the stomach and subsequent anastomosis of remaining section to the jejunum.

Vagotomy – surgical cuttting of any of the branches of the vagus nerve.
Antrectomy: removal of the antral portion of the stomach.
Gastrectomy: removal of 60%-80% of the
stomach.
Esophagojejunostomy (total gastrectomy): removal of the entire stomach with a loop of jejunum anastomosed to the esophagus

Total gastrectomy

dumping syndrome

The pathogenesis and manifestations of dumping syndrome

APPENDICITIS

MEDICAL DIAGNOSIS AND TREATMENT
Surgical removal of the appendix
Management of peritonitis, shock, dehydration, and infection
Chest x-ray to differentiate appendicitis from pneumonia(pneumonia may cause referred pain in the right lower quadrant and thus may be misdiagnosed as appendicitis)
Barium GI series and ultra-sonography to differentiate appendicitis from other abdominal problems

DIVERTICULAR DISEASE

Diverticular disease has 2 clinical forms: DIVERTICULOSIS and DIVERTICULITIS.
Diverticulosis occurs when the intestinal mucosa protrudes through the muscular wall. The common sites for diverticula are in the descending and sigmoid colon, but they may develop anywhere from the proximal end of the pharynx to the anus.
Diverticulitis is an inflammation of the diverticula that may lead to infection, hemorrhage, or obstruction.

POSSIBLE CAUSES:
Age (most common in people over age 40)
Chronic constipation, more common in obese individuals
Congenital weakening of the intestinal wall
Low intake of roughage and fiber
Straining during defecation
Stress
Men affected more than women

Low fiber diet, constipation
Musculature of the colon hyper trophies
Herniation of the mucosa & submucosa
Muscle weakness
Diverticula (diverticulosis)
Trapped undigested food, fecal materials
Bacteria builds up & impede blood flow
Inflammation (diverticulitis)

ASSESSMENT FINDINGS:
- Anorexia
- Stool with blood and mucus
- Change in bowel habits
- Constipation and diarrhea
- Fever
- Flatulence
- Nausea
- Rectal bleeding

TREATMENT:
- Generally no treatment for asymptomatic diverticulosis
- Colon resection (for diverticulitis refractory to medical treatment)
- High residue diet with no seeds for diverticulosis
- Low residue diet with diverticulitis
- high fiber diet

- Temporary colostomy possible for perforation, peritonitis, obstruction, or fistula that accompanies diverticulitis.
.

CROHN’s DISEASE ( Regional Enteritis)

CROHN’s DISEASE ( Regional Enteritis)
CROHN’s DISEASE is a chronic inflammatory disease of the small intestine, usually affecting the terminal ileum. It also sometimes affects the large intestine, usually in the ascending colon. It’s slowly progressive with exacerbations and remissions.

POSSIBLE CAUSES:
Emotional upsets
Fried foods
Milk and milk products
Unknown

CROHN’s DISEASE
Acute inflammation of entire intestines
Deep fissures & ulceration develops
Loss of healthy intestinal surface area & bacterial growth
Chronic changes include thickening of the bowel wall
Narrowing and strictures of bowel lumen
Formation of fistula, perforation, hemorrhage, obstruction, & abscess

TREATMENT:
DRUG THERAPY OPTIONS:
Analgesic: meperidine (Demerol), morphine
Antianemic: ferrous sulfate (Feosol), ferrous gluconate (Fergon)
Antibiotic: sulfasalazine (Azulfidine), metronidazole (Flagyl)
Anticholinergic: propantheline (Pro-Banthine), dicyclomine (Bentyl)

Antidiarrheal: diphenoxylate (Lomotil)
Antiemetic: prochlorperazine (Compazine)
Anti-inflammatory: olsalazine (Dipentum)
Corticosteroid: prednisone (Deltasone)
Immunosupressant: mercaptopurine (Purinethol), azathioprine (Imuran)
Potassium supplement: potassium chloride (K-Lor) administered with food, potassium gluconate (Kaon)

IMPLEMENTATION:
Bedrest, weigh daily
NPO in acute stage, TPN as ordered.
High CHON, calorie, bland, low residue diet.
Avoid gas-producers, irritating food, and milk products.

Offer small frequent feedings.
Vitamin replacement ADEK.
IVF, I/O, tepid fluids up to 3L/day.
Perianal care with lubricants and ointments.
Hot sitz baths, monitor stools.
Emotional support esp. family members.

ULCERATIVE COLITIS
ULCERATIVE COLITIS is a major health problem and a potentially debilitating disease. It’s a type of inflammatory bowel disease that produces lesions primarily confined to the large bowel, with ulcerations of the large bowel’s mucosa and submucosa .

POSSIBLE CAUSES:
Genetics
Idiopathic
Allergies
Autoimmune disease
Emotional stress
Viral and bacterial infections

ULCERATIVE COLITIS
Inflammation of the intestinal mucosa (rectum sigmoid entire colon)
Inflammation
Loss epithelium with erosion
Ulceration
Exudate edema with henorrhage
Abscess & mucupurulent exudate
Necrosis and scarring
Tissue replacement will narrow the colon
Loss characteristics of epithelium

Abdominal cramping, distention, and tenderness
Anorexia
Bloody, purulent, mucoid, watery stools (15 to 20 per day)
Dehydration
Fever
Hyperactive bowel sounds
Nausea and vomiting
Weakness
Weight loss

DIAGNOSTIC EVALUATION:
Barium enema shows ulcerations.
Blood chemistry shows decreased potassium level and increased osmolality.
Hematology shows decreased Hgb level and Hct.
Intestinal biopsy helps to differentiate between ulcerative colitis and regional enteritis.
Stool specimen is positive for blood and mucus.
Urine chemistry displays increased urine specific gravity.
TREATMENT:
Colectomy or ileostomy

IMPLEMENTATION:
Assess GI status and fluid balance to determine deficient fluid volume.
Monitor and record vital signs, intake and output, laboratory studies, daily weight, urine specific gravity, calorie count, and fecal occult blood to determine deficient fluid volume.

Monitor the number, amount, and character of stools to determine status of nutrient absorption.
Maintain the client’s diet; withhold food and fluid as necessary to prevent nausea and vomiting.
Administer I.V. fluids and TPN to maintain hydration and improve nutritional status

Types of Ostomy
Ostomy = opening made to allow passage of urine or stool
Piece of intestine is brought out onto the client’s abdomen.
Lacks nerve endings
Doesn’t hurt to touch but has other implications
Stoma = mouth like opening in the abdominal wall to drain urine or stool
Effluent – drainage from stoma

Ileostomy
End of small intestine
By passes large intestine = frequent liquid stools

Colostomy
Large intestine
More solid stool

OSTOMY CARE
Referral to enterostomal therapist.
Encourage verbalization of fears/concerns.
Teach character of drainage: ileostomy – liquid 4-6x/day, transverse colostomy – mushy OD, descending/sigmoid – soft formed q 2-3 days
Skin care – nystatin, karaya powder, soap/H2O pat dry
Odor control – deodorant drops, bismuth tabs, mouthwash solutions, spinach, parsley added to ostomy bag.
Odor – avoid gas-formers (cabbage, beans, broccoli, cauliflower, corn, onions, eggs, fish, condiments.

Differential features of colitis & crohn’s disease
Location : (UC)
Rectum-sigmoid-cecum
Etiology :
Unknown
Peak incidence:
15-25 or 55-65 y.o.
Stool :
10-20 liquid bloody stools per day
Location : ( crohn’s)
Terminal ileum
Etiology :
Unknown
Peak incidence:
15-40 y.o.
Stool :
5-6 soft loose rarely bloody stools per day
Common complications: Hemorrhage, perforation, fistula, nutritional deficiency

INTESTINAL OBSTRUCTIONS

Strangulated hernia adhesions tumor intussusceptions Volvulus or twisting

Complications:
Infection/septicemia
Gangrene of the bowel
Perforation of the bowel
Fluid imbalances

Treatment:
Mechanical and vascular intestinal obstructions are generally treated surgically; ileostomy or colostomy may be necessary.
Intestinal intubation and decompression
Maintain fluid and electrolyte balances and adequate nutrition.

CHOLELITHIASIS / CHOLECYSTITIS
A. ETIOLOGY AND PATHOPHYSIOLOGY:
cholecystitis is the Inflammation of the gallbladder; usually caused by the presence of stones (cholelithiasis), which are composed of cholesterol, bile pigments, and calcium.

Common locations of gallstones Abnormal metabolism of cholesterol & bile salts Gallstone fromation Gallstones may obstruct gall bladder Stasis of bile Autodigestion Migration of gallstones to ducts Inflammatory response Iiritation & impaired blood flow Ischemia of the gallbladder wall Necrosis & gangrene Perforation Abscess & peritonitis

Medical management
- Nasogastric suctioning to reduce nausea and eliminate vomiting
- Narcotics to decrease pain
- Antispasmodics and anticholinergics to reduce spasms and contractions of the gallbladder
- Antibiotic therapy if infection is suspected
- cholecystectomy- removal of the gallbladder

T-tube placement in the common bile duct. Bile fluid flows with gravity into a drainage collection device below the level of the common bile duct.

T tube care:
Semi fowlers position
Ensure that t-tube is connected to close gravity drain
Avoid kinks, clamping & pulling
MIO q shift
Expect 300-500ml bile colored drainage (1 st 24H) 200ml/ 24H (3-4 days)
Light colored stool
Skin care around the tube

TREATMENT OF STONES:
CHOLESTEROL DISSOLVENT:
Moctanin is administered through a nasal biliary catheter to dissolve stones left in the bile duct after cholecystectomy. Dissolution may take 1 to 3 weeks. Observe the client for anorexia, nausea, vomiting, and abdominal pain.

ORAL BILE ACIDS:
Chenodiol ( chenix ) and ursodiol ( actigall ) are administered to dissolve small stones. Side effects include diarrhea ( especially with chenodiol ), elevation of hepatic enzymes,gastritis, and gastric ulcers. Dissolution takes between 6 months and 2 years, and the success rate is only about 30 %

Percutaneous transhepatic dissolution

Endoscopic sphincterotomy/retrograde cholangio-pancreatography

ESWL
Lithotripsy is the use of high-energy shock waves to fragment and disintegrate biliary stones. ESWL
(Extracorporeal Shock-wave Lithotripsy) – uses soundwaves to pulverize gallstones (30-40mins)
- suitable only for radiolucent stones

PANCREATITIS
PANCREATITIS is the inflammation of the pancreas. In acute pancreatitis, pancreatic enzymes are activated in the pancreas rather than the duodenum, resulting in tissue damage and autodigestion of the pancreas.
In chronic pancreatitis, chronic inflammation resu lts in fibrosis and calcification of the pancreas, obstruction of the d ucts, and destruction of the secreting acinar cells.

POSSIBLE CAUSES:
1. Alcoholism - chronic
2. Bacterial or viral infection
3. Biliary tract disease - acute
4. Blunt trauma to the pancreas or abdomen
5. Drugs: steroids, thiazide diuretics, oral contraceptives

Inflammation caused premature acvtivation of enzymes Causes tissue damage Enzymes back up and spill out into pancreatic tissue Auto digestion Acute pancreatitis: Hemorrhagic necrotising pancreatitis Cell death & tissue damage Hemorrhage Multi organ failure Shock Chronic pancreatitis: Repeated attacks Cell replacement of fibrous tissue Inc.pressure & obstruction Inflammation & destruction Necrosis attack

Abrupt onset of pain in the epigastric / LUQ area that radiates to the shoulder , substernal area, back, and flank
Abdominal tenderness and distention
Aching, burning, stabbing, pressing pain
Knee-chest position, fetal position , or leaning forward for comfort d/t abdominal pain
Mental confusion, hypocalcemia – irritability
Nausea and vomiting

TESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCY

g. Tachycardia, shock, hypotension
h. Dyspnea
i. Low grade fever
j. Elevated serum amylase / lipase / glucose
k. Grey Turner’s, Cullens’s sign
l. Chronic steatorrhea
m. Jaundice
o. Hyperglycemia

TREATMENT: PANCREATITIS
NPO, TPN, Bland, low-fat, high-protein diet of small, frequent meals with restricted intake of caffeine, alcohol, and gas-forming foods
Bed rest
3. I.V. fluids (vigorous replacement of fluids and electrolytes) BT: packed RBC, FWB

Surgical intervention to treat the underlying cause, if appropriate
Maintain position, patency, and low suction of NG tube to prevent nausea and vomiting.
Monitor I/O, wt OD, abd girth, electrolytes.
Monitor blood glucose levels.
Meds: meperidine, H2 blockers, anticholinergics, antacids, Ca gluconate, pancreatic enzyme replacements (Viokase, Pancreatin, Pancrease)

24–7 Pancreatoduodenectomy (Whipple’s procedure). A , areas of resection; B , appearance following resection.

Cirrhosis of the liver

Lets go back to the function of the liver…
a. Carbohydrate metabolism by liver cells
-glycogenesis- glucose converted into glycogen
-glycogenolysis- glycogen is broken down into glucose
-gluconeogenesis- glucose into energy
b. Fat metabolism by liver cells
c. Storing reserves of nutrients (ADEK & B12)

d. Filtering poisons and wastes from blood
e. Production and synthesize variety of proteins.
Ex. Albumin (helps regulate the movement of water from the bloodstream)
globin- components of Hg (02 carrying substance in RBC)
globulin- group of protein that includes antibodies
fibrinogen & prothrombin- blood coagulation that helps heal wound

f. Regulating many chemicals found in the blood stream
g. Can regenarate or grow back
h. Bile production
Damaged repeatedly can cause irreversible changes that interfere function.
j. Conversion of ammonia to urea

HEPATIC CIRRHOSIS
A. ETIOLOGY AND PATHOPHYSIOLOGY
1. Irreversible fibrosis and degeneration of the liver
2. Several types of cirrhosis; La ënnec’s (alcoholic cirrhosis, nutritional cirrhosis) most common, biliary cirrhosis, & post necrotic cirrhosis
3. Incidence higher in alcoholics, who are often malnourished, and in those who have had hepatitis

Chronic alcoholism
Toxic effect on hepatocytes
Liver inflammation (alcoholic hepatitis)
Destructive phase
Fibrosis or scar formation
Necrosis
Hardened and lumpy liver
Liver Shrinks
Liver failure

Hepatic circulation

inc. hydrostatic pressure in portal circulation Dec.plasma osmotic pressure Inc.serum aldosterone & ADH Upward pressure on diaphragm impairs respiration inc. risk for peritonitis Impaired digestion & absorption

Rest
Restriction of alcohol, hepatotoxic drugs.
Vitamin therapy: especially the fat soluble vitamins A, D, E and K and vitamin B (thiamine chloride and nicotinic acid); zinc and calcium supplements
Diuretics to control ascites and edema
5. Neomycin and lactulose may be prescribed for elevated blood ammonia levels (2-4 soft stools)
6. Paracentesis if respiratory distress occurs as a result of ascites

Paracentesis is a procedure to take out fluid that has collected in the belly ( peritoneal fluid ). This fluid buildup is called ascites

Paracentesis Sites

Sites and position for paracentesis. A , Potential sites of needle or trocar insertion to avoid abdominal organ damage. B , The client sits comfortably; in this position, the intestines float back and away from the insertion site.

7. Surgical intervention to decrease portal hypertension: a portacaval shunt or TIPS

8. Esophageal varices management
Sengstaken-Blakemore tube:

9. Dietary modification:
a. Cirrhosis:
1. Protein as tolerated (80-100g); with increasing liver damage, protein metabolism is hindered
2. High carbohydrate , moderate fat; provides for energy ; vitamin, mineral , and electrolyte supplements
3 . Low sodium (500-1000mg daily); helps control increasing ascites
4. Soft foods if esophageal varices are present; prevents danger of rupture and bleeding
5. Alcohol contraindicated to avoid irritation and malnutrition

b. Hepatic coma
1. Protein : reduced according to tolerance; 15-30g
2. High calorie (1500-2000g) to prevent catabolism and liberation of nitrogen
3 . Fluid carefully controlled according to output

Peritonitis
Peritonitis is the generalized inflammation of the peritoneal cavity. Leading intraabdominal infection.

Intestinal motility is decreased, and fluid accumulates as a result of the inability of the intestine to reabsorb fluid.
Fluid will leak into the peritoneal cavity, precipitating fluid, electrolyte, and protein losses, as well as fluid depletion.

Inc. permeability Intestinal bacteria leak out into peritoneal cavity Bacterial peritonitis Constant severe pain Reflex contrxn of abdominal muscle Hypovolemicshock Dec. peristalsis adhesion

PYLORIC STENOSIS
Pyloric stenosis is the obstruction of the pyloric sphincter by hypertrophy and hyperplasia of the circular muscle of the pylorus.

Assessment
Risk factors/etiology
1. Occurs most often in firstborn, term infants (infantile hypertrophic stenosis)
2. More common in male infants.
3. Seen more frequently in white infants.

Clinical manifestations
1. Onset of vomiting may be gradual, occurring in first few weeks; or forceful, projectile vomiting may develop at 4 to 6 weeks of age.
2. Emesis is not bile stained but may be curdled from length of time in stomach.
3. Vomiting occurs shortly after feeding.
4. Infant is hungry and nurses well.

5. Infant does not appear to be in pain or acute distress.
6. Weight loss occurs, if untreated.
7. Stools decrease in number and in size.
8. Dehydration occurs as condition progresses; hypochloremia and hypokalemia as vomiting continues.
9. Upper abdomen is distended, and an “olive-shaped mass may be palpated in the right epigastric area.

Diagnostics
1. Palpation of abdominal mass.
2. Prolonged vomiting.
3. X-ray film and ultrasound examination of abdomen.
Treatment; surgical release of the pyloric muscle (pyloromyotomy)

Celiac disease is also known as sprue, gluten enteropathy , and malabsorption syndrome. This disease is an inborn error metabolism of rye, wheat, barley, and oat products.
Celiac disease

Symptoms generally begin between the ages of 1 year and 5 years, but they may also occur in those 50 to 60 years.
Severe malnutrition results from a loss of nutrients via the stool.
Atrophy of villi of intestines
Decrease absorptive surface
Decrease absorption of fats
Malabsorption of fat soluble vitamins
Severe malnutrition
Intolerance of gluten (BROW) steatorrhea

Assessment
Cause: congenital defect in metabolism.
1. Symptoms begin when child has increased intake of gluten-type foods: cereals, breads, pastas, etc.
2. Watery, pale diarrhea; steatorrhea.
3. Vomiting, anorexia.
4. Poor weight gain, failure to thrive.
5. Constipation, vomiting, and abdominal pain may be the initial presenting signs/symptoms.
6. Abdominal distention

Diagnostics
1. Stool analysis
2. Jejunal biopsy.
Treatment
Primarily dietary management; gluten-free diet

HIRSCHSPRUNGS'S DISEASE
- Hirschsprungs's disease (congenital aganglionic megacolon) absence of innervations in a segment of colon wall. Absent of ganglion cells needed for peristalsis.

Assessment
Risk factors/etiology; congenital, may be associated with Down syndrome.
1. varies according to age and amount of colon involved.
2. Inadequate or absent peristalsis.
3. Newborn.
a. Failure to pass meconium within 24 to 48 hours after birth.
b. Vomiting
c. Abdominal distention.
d. Reluctance to take fluids.

4. Older infant.
a. Passage of watery stools and diarrhea, ribbon like stools
b. failure to thrive.
c. Lack of appetite.
d. Persistent constipation, impactions.
Diagnostics
1. Rectal biopsy.
2. Barium enema.

Treatment
Surgical correction usually involves creation of a temporary colostomy, then a pull-through of the colon to a point near the rectum. After the reanastomosis has healed, the temporary colostomy is closed.

CLEFT LIP AND PALATE
Cleft lip- failure of maxillary and median nasal processes to fuse.
- 7-8 weeks lip closes at age of gestation.
Cleft palate- midline fissure of the palate
- 7-12 weeks palate closes at AOG

Types of cleft lip & cleft palate

Manifestation:
Difficulty swallowing
Distended abdomen
Feeding difficulty
Complication:
Malnutrition
Speech impediment
Possible aspiration
Impaired self-esteem

Mgt/ Interventio n:
Surgery:
Cheiloplasty (6-12 weeks old)
Uranoplasty- (4-6 weeks) to save speech
Palatoplasty (12-18 months old)
Feeding should be done in an upright position

Special nipples on feeding devices:
Lamb’s nipple, flanged nipple, rubber-tipped medicine dropper, asepto syringe
Bubble and burp frequently

Post-op care (cleft lip)
Metal appliance/ adhesive strips are taped to cheeks “logans bar”
Elbow restraints
Clear liquids initially, then formula feeding as tolerated
Oral hygiene
Meticulous care on suture line
Suctioning PRN
Maintain upright position

Post-op care ( cleft palate)
Lie on abdomen
Fluids best taken from the cups
Avoid use of suction or other objects in the mouth
Elbow restraints
Soft diet
Analgesic PRN- prevent crying of the patient

TRACHEOESOPHAGEAL FISTULA (TEF) with ESOPHAGEAL ATRESIA
TEF- An abnormal opening in esophagus and trachea
EA- blind pouch or no continuous passage of esophagus and stomach
Causes: unknown cause, malformation idiopathic
Diagnostic: x-ray of abdomen

Assessment:
Excessive salivation and drooling
3 C’s of TEF
Coughing
Choking
Cyanosis
Apnea
Respiratory distress
Abdominal distension

Surgical intervention:
Division and ligation of TEF
Anastomosis of esophagus
Age of surgery- 16-24 months
Temp. esophagostomy
Temp. gastostomy
Post-op care: gastrostomy feeding
No oral intake 10-14 days post-op

Gastrostomy . A , Gastrostomy tube placement. B , The tube is fixed against both the abdomen and stomach walls by cross bars.

Nursing care:
On NPO upon diagnosis, IV fluids
Frequent suctioning
02 administration
Supine position with head elevated at least 30 degrees
Pacifier periodically
Complication after surgery: leak of anastomosis, strictures, esophageal motility disorder

GOOD LUCK AND GOD BLESS!!!!
Post test after 10 minutes…

Gastrointestinal

by shenell delfin on Jun 25, 2010

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Gastrointestinal — Presentation Transcript