Gastrointestinal System Disorders

Gastrointestinal System

Gastrointestinal TractUpper GIT

• consists of structures that aid in the ingestion and digestion of food

• includes the mouth, esophagus, stomach, duodenum Hypothalamus – satiety center

is responsible for notifying the body that it is satisfied or has received sufficient food

Lower GIT• consists of the small and large intestines• digestion is completed in the small intestine , and

most nutrients are absorbed in this part of the GIT• the large intestine serves primarily to absorb water

and electrolytes and to eliminate the waste products of digestion through the feces

Gastrointestinal TractMouth 1.Salivation

the “thought” of food initiates saliva production a.) serous secretions contain ptyalin for starch digestion – produced by parotid and submaxillary glands b.) mucous secretions - for lubrication of food – produced by the buccal, sublingual and submaxillary glands1.Mastication

chewing of food teeth - for initial breakdown of food to small particles it helps prevent excoriation of the lining of the tract and

increase rate of digestionMajor Structures in the Mouth

• teeth – to grind the food• salivary glands – moisten food and mucous membranes and

begin carbohydrate digestion• tongue – to push the food to the pharynx to initiate

swallowing

Gastrointestinal Tract Esophagus

is a hollow tube, the upper 1/3 is composed of skeletal muscles, the rest is smooth muscle

lined with mucous membrane – secretes mucoid substance for protection

the bolus of food arrives at the cardiac sphincter of the stomach w/in 5-10 secs. after ingestion

the lower esophageal sphincter (LES) prevents reflux of food in the stomach back into the lower esophagus

Swallowing (deglutition)3 phases:1.) tongue forces the bolus of food into the pharynx2.) the food moves into the upper esophagus3.) the food moves down into the stomach* Food is prevented from passing into the trachea by closing of the trachea (epiglottis) and the opening of the esophagus

Gastrointestinal TractStomach

made up of 5 layers of smooth muscle2 types of contractions:1.) tonus contractions – continuous contractions2.) rhythmic contractions – may be slow ( q2-3 mins.) or fast – responsible for the mixing of food and peristaltic movementVagus nerve – supplies the nervous stimulation for the stomach - has both symphathetic and parasymphatetic fibers

movement of food through the stomach and intestines is by peristalsis the alternate contraction and relaxation of the muscle fibers that propels the food in a wave-like motionchyme – food in the stomach - is pumped through the pyloric sphincter into the duodenum

Gastrointestinal TractDigestive Function of the Stomach:

Pepsin – needed for protein digestionHCL acid – aids in pre-digestion of food

Gastrointestinal TractIntestinesSmall Intestine

2.5 cm. (1 inch) wide and 6 meters (20 feet) long – fills most of the abdomen

3 parts :a.) duodenum – which connects to the stomach (10 inches)b.) jejunum – middle portion (8 feet long)c.) ileum – with connects to the large intestine (12 feet long)Large Intestine

6 cm. (2 ½ in.) wide and 1.5 meters (5 feet long) 3 parts :a.) cecum – which connects to the small intestinesb.) colon – 4 parts (ascending, transverse, descending, sigmoid colon)c.) rectum – 17-20 cm. (7-8 inches) long, anal canal

Gastrointestinal Tract ileocecal valve – prevents backward flow of fecal contents

from the large intestine to the small intestine vermiform appendix – has no function , near the ileocecal

valve anus – anal opening, is controlled by a smooth muscle

internal sphincter and a striated muscle external sphincter chyme is propelled toward the anus by peristalsis, also

mixes the intestinal contents in the colon, the feces is pushed forward by mass

movements – stimulated by gastrocolic reflexes initiated when food enters the duodenum from the stomach

Defecation reflex when feces enter the rectum and cause distention of wall

of the rectum send impulses to the sacral segment of the spinal cord – then back to the colon, sigmoid and rectum initiate relaxation of the internal anal sphincter relaxation or contraction of external anal sphincter (voluntary control)

Gastrointestinal TractSecretion and Digestion

major portion of digestion occurs in the small intestines by the action of pancreatic and intestinal secretions (enzymes) and bile

a.) Carbohydrate digestion start in the mouth Ptyalin – breakdown polysaccharides to disaccharides intestinal enzymes (maltase, lactase, sucrase)

breakdown disaccharides to monosaccharides (glucose, galactose fructose) b.) Protein digestion - start in the stomach pepsin – breakdown of proteins to polypeptides - small intestines trypsin – breakdown of polypeptides into peptides and amino acidsc.) Fat digestion - fats require emulsification into small droplets before it can be broken down into glycerol and fatty acidsBile – from liver; emulsify fats so that it could be broken downpancreatic lipase breakdown fats into glycerol and fatty acids

Gastrointestinal TractAbsorptionthe intestinal wall has many folds which are covered by fingerlike projections called (villi) increase the absorptive area of the small intestinesin the center of the villi are capillaries, veins, small arteries for absorption of nutrients into the blood vessel system90% of absorption occurs within the small intestines by active transport or diffusionamino acids, monosaccharides, Na+, Ca++ are transported by active transport w/ the expenditure or use of energyother nutrients, fatty acids and H2O – diffuse passively across the cell membranereabsorption of H2O, electrolytes and bile occurs mainly in the ascending colon

Gastrointestinal TractGIT role in Fluid and Electrolytes Balance GIT secretions contain electrolytes severe fluid and electrolyte imbalance may occur with excessive

losses of gastrointestinal fluids Ex. 1.) Na+ and K+ deficits : vomiting, diarrhea, gastric suctioning, intestinal fistula

2.) Ca++ & Mg++ deficits: malnutrition, malabsorption, intestinal fistula

3.) Metabolic alkalosis : loss of gastric acid by suctioning or persistent

vomiting 4.) Metabolic acidosis : loss of bicarbonate-rich intestinal

secretions by severe diarrhea or fistula

Other functions of the GIT the GIT supports bacterial growth and has a role in antibody

formation intestinal bacteria synthesize Vit. K required for production of

clotting factors II (Prothrombin), VII, IX,X

Assessment of the GITNursing History : Subjective Data1. General Data

a. presence of dental prosthesis, comfort of usageb. difficulty eating or digesting foodc. nausea or vomitingd. weight losse. pain – may be caused by distention or sudden

contraction of any part of the GIT - specify the area, describe the pain

2. Specific data if symptoms are presenta. situations or events that effect symptomsb. onset, possible cause, location, duration, character of

symptomsc. relationship of specific foods, smoking or alcohol to

severity of symptomsd. how the symptoms was managed before seeking

medical help

Assessment of the GIT

3. Normal pattern of bowel eliminationa. frequency and character of stoolb. use of laxatives, enemas

4. Recent changes in normal patternsa. changes in character of stool (constipation, diarrhea, or

alternating constipation and diarrhea)b. changes in color of stool melena - black tarry stool (upper GI bleeding) hematochezia – fresh blood in the stool (lower GI bleeding)c. drugs /medications being takend. measures taken to relieve symptoms

Assessment of the GITB. Physical Examination : Objective Dataa.) Mouth and Pharynx

1. lips – color, moisture, swelling, cracks or lesions2. teeth – completeness (20 in children, 32 in adults), caries,

loose teeth, absence of teeth impair adequate chewing3. gums – color, redness, swelling, bleeding, pain (gingivitis)4. mucosa – color (light pink)

examine for moisture, white spots or patches, areas of bleeding, or ulcers

white patches – due to candidiasis (oral thrush) white plaques w/in red patches may be malignant lesions

5. tongue – color, mobility, symmetry, ulcerations / lesions or nodules

6. pharynx – observe the uvula, soft palate, tonsils, posterior pharynx signs of inflammation (redness, edema, ulceration, thick

yellowish secretions), assess also for symmetry of uvula and palate

Assessment of the GITb.) Abdomen - assess for the presence or absence of tenderness, organ enlargement, masses, spasm or rigidity of the abdominal muscles, fluid or air in the abdominal cavity

Anatomic Location of OrgansRUQ – liver, gallbladder, duodenum, right kidney, hepatic flexure of colonRLQ - cecum, appendix, right ovary and fallopian tubeLUQ – stomach, spleen, left kidney, pancreas, splenic flexure of colonLLQ – sigmoid colon, left ovary and tube

Assessment of the GIT1. Inspection

assess the skin for color, texture, scars, striae, engorged veins, visible peristalsis (intestinal obstruction), visible pulsations (abdominal aorta), visible masses (hernia)

assess contour (flat, protuberant, globular) abdominal distension, measure abdominal girth

or circumference at the level of umbilicus or 2-5 cm. below


2. Auscultation presence or absence of peristalsis or bowel sounds

Normoactive – every 5-20 secs.

Hypoactive – 1 or 2 sounds in 2 mins. Absent – no sounds in 3-5 mins.

peritonitis, paralytic ileus,

Hyperactive – 5-6 sounds in less than 30 sec. diarrhea, gastroenteritis, early intestinal

obstruction

Assessment of the GIT3. Percussion

done to confirm the size of various organs to determine presence of excessive amounts of air or

fluid Normal – tympany dullness or flatness – area of liver and spleen, solid

structure – tumor

4. Palpation to determine size of liver, spleen, uterus, kidneys – if

enlarged determine presence and chac. of abdominal masses determine degree of tenderness and muscle rigidity

(rebound or direct)c.) Rectum

perineal skin and perianal skin assess for presence of pruritus, fissures, external hemorrhoids, rectal prolapse

Diagnostic Tests

A. Laboratory tests1. Stool examination (fecalysis)

Stool for occult blood o GI bleedingo No red meat, turnips, horseradish, steroids,

NSAIDS, iron Stool for Ova and parasites proper collection of specimen should not be

mixed with water or urine, should be sent immediately to the laboratory

Diagnostic Tests

2. CEA (Carcinoembryonic antigen)

(+) colon cancer and other forms of cancer

it is useful as in indicator of the effects of

therapy

CEA - recurrence or spread of tumor

effectiveness of therapy

A blood sample is withdrawn or sent to

laboratory

Diagnostic Tests

3. Exfoliative Cytology

Detect malignant cells

Liquid diet

UGI: NGT insertion – saline lavage

LGI: laxative, enema, proctoscope

Radiologic Tests visualization of the GIT by barium swallow, upper

GI series or barium enema

Barium – is a radiopaque substance that when ingested or given by enema in solution, outlines the passage ways of the GIT for viewing by x-ray or fluoroscopy

Radiologic Tests

1. Barium swallow/UGIS for identification of disorders of esophagus, stomach,

duodenum – esophageal lesions, hiatal hernia, esophageal reflux, tumors, ulcers, inflammation

Pt. swallows a flavored barium solution and the radiologist observes the progress of the barium through the esophagus and take x-ray films

NPO for 6-8 hrs Post procedure:

o Increase fluid intakeo Laxativeo Stool – white for 24-72 hrs.o Observe for: impaction, distended abdomen,

constipation

Radiologic Tests

2. Barium Enema/LGISPurpose : to visualize the colon to detect tumors, polyps, inflammation, obstruction

Prep. o low residue diet (1-2 days), clear liquid diet

(evening meal)o Laxative, cleansing enema in AM

Posto Laxative or enemao Same as UGIS

Other Testsa.) Gastric analysis

to quantify gastric acidity Normal 1-5 mEq / L

gastric acid : gastric cancer, pernicious anemia gastric acid : duodenal ulcer Normal gastric acid : gastric ulcer

NPO for 12 hours an NGT is inserted and gastric contents are aspirated, connected to suction

Other Testsb.) Biopsy

Upper GI biopsy – biopsy of the oral cavity or tongue, or any lesion or ulcerated area

- local anesthesia assess site for bleeding , give oral

hygiene Biopsy of stomach - done during endoscopy Rectal biopsy – biopsy of lesions, polyps, tumors of the

lower sigmoid colon, rectum and anal canal during sigmoidoscopy- monitor for signs of bleeding

Endoscopy directly visualize the GIT by the use of a fiberscape fiberscope – has a thin, flexible shaft that can pass through and around bends in the GIT, transmit light and the image can be seen in the monitor

Endoscopy1. Upper GI endoscopy

Esophagoscopy, Gastroscopy and Duodenoscopy To identify upper GI bleeding, gastric cancer, gastric

ulcers, duodenal ulcers useful in detecting tumor, hernia, esophageal strictures

Preparation : o NPO 6-8 hrs prior to procedureo Anticholinergics(atropine), sedatives are giveno Remove dentureso Lidocaine spray – depress gag reflexo Place on left side lying position

Post-procedure :o NPO until gag reflex returns (2-4 hrs.)o monitor vital signs, assess for dyspnea, dysphagia,

abdominal pain, fever, bleeding

Endoscopy2. Colonoscopy

to visualize the colon useful to identify tumors, colonic cancer, colonic polyps not done when there is active bleeding or inflammatory

disease Preparation :

clear liquid diet 24 hrs. before fleet or cleansing enema dulcolax tabs NPO 8 hrs. prior to procedure Position: left side, knees flexed

Post-procedure : provide rest, monitor VS (vasovagal response-

HR,BP) assess for sudden abdominal pain (perforation), fever,

active bleeding Hot sitz bath

Endoscopy3. Sigmoidoscopy – examination of sigmoid colon, rectum and anus Proctoscopy – examination of rectum and anus

used as a screening test for persons 40 yrs old and above, with history of colonic cancer

used for pt with lower GI bleeding or inflammatory disease

Preparation : light dinner and light breakfast - dulcolax tab. Fleet enema or cleansing enema

Post-procedure : provide rest period assess for sudden abdominal pain, bleeding

Alternative Feeding:

1. Enteral hyperalimentation- delivery of nutrients directly to the GI tract.

a. Short- term- esophagostomy; nasogastric tube

b. Long- term- gastrostomy; jejunostomy

Indications of NGT:

a) Gavage- to deliver nutrients; for feeding purposes

b) Lavage- to irrigate the stomach

c) Decompression- to remove stomach contents or air

2. Hyperalimentation (total parenteral nutrition)- method of giving highly concentrated solutions intravenously to maintain a patient’s nutritional balance when oral or enteral nutrition is not possible

Nursing Managements:

• Filter is used in the IV tubing to trap bacteria

• Solution and administration equipment should be changed every 24 hours

• Dressing changes every 48-72 hrs with antibiotic ointment to catheter insertion

• Medication is never administered in a TPN line

• Observe for complications

• Infection

• Venous thrombosis

• Hyperglycemia

Esophageal DisordersDysphagia

problem in ingesting necessary nutrients because of difficulty in swallowing

Causes : 1) pharyngeal muscle weakness

disease or trauma of glossopharyngeal nerves neuromuscular disorders (poliomyelitis, multiple sclerosis,

myasthenia gravis2) esophageal disorders

obstruction caused by enlarged thyroid, tumors, strictures narrowed opening

absence of peristalsis of the esophagusPathophysiologyWeak pharyngeal/esophageal muscles difficulty moving the food from the oropharynx into the esophagus immediate regurgitation of fluids into the nasal passages aspiration of feedings may occur from failure of the glottis to close

Esophageal DisordersAssessment

history of difficulty in swallowing assess for gag reflex – touching the posterior tongue or pharynx

with a tongue depressor ask the pt to swallow and observe movement of the larynx

Nsg. ManagementPts. with pharyngeal weakness:

can tolerate solids more easily than liquids teach “double-swallow” technique – 1) inhale, 2) put food in

pharynx and swallow 3) exhale 4) swallow again helps minimize the possibility of aspiration closely supervise the pt during feeding, suction equip. shld. be

ready elevate head of bed during feeding or position on the unaffected

side - to ensure better control if the ability to swallow is absent NGT or gastrostomy feeding

Pts. With esophageal weakness: small-frequent feedings are advised to pts elevate head of bed

Gastroesophageal Reflux Disease (GERD)

refers to a group of conditions that cause reflux of gastric and duodenal contents back to the esophagus

Causes :- idiopathic incompetent lower esophageal sphincter (LES)- pregnancy - obesity - surgical removal lower esophagus due to cancer- ascites- hiatal hernia major cause

Hiatal hernia – refers to protrusion of part of the stomach, through the diaphragmatic hiatus into the thoracic cavity caused by obesity, trauma, weakening of muscles


Pathophysiology

Lower esophageal sphincter (LES) – muscle at the junction between esophagus and stomach

When food enters the pharynx and esophagus LES relaxes to permit or allow food to enter into the stomach LES is usually contracted to prevent reflux of gastric material back to the esophagus LES pressure reflux can occur

caused by anticholinergics, caffeine, alcohol, smoking, when the person is lying down


S/SX :

heartburn (pyrosis) – major symptom of GERD burning sensation below the sternum that may be referred or radiate to the back or neck if severe

frequently accompanied by a sour regurgitation of gastric contents into the mouth but is not accompanied by nausea

Hiatal hernia – may be diagnosed by x-ray, upper gastrointestinal series (UGIS)


Medical Mgt.Liquid antacids (ex. Maalox) – 30 ml taken 1 hr. and 3 hrs. after meals and at bedtime or whenever heartburn occurs to decrease gastric acidityMedications that increase LES contraction

Urecholine, Metoclopramide HCL (reglan, plasil) to be taken 30 mins. before meals and at bedtime

Cimetidine, Ranitidine, Famotidine (histamine H2 receptor blockers) – used for severe reflux, acts by reducing gastric secretions, thereby decreasing irritating effects

Surgery for hiatal herniaEx. Posterior gastropexy – returning the stomach to the abdomen and suturing it in placeNissen fundoplication – wrapping the fundus of the stomach around the lower part of the esophagus to restore sphincter competence and prevent reflux


Nsg. InterventionPatient teaching for GERD:1.high-protein, low-fat diet ( to stimulate release of gastrin and cholecystokinin LES pressure)2.avoidance of foods containing caffeine (coffee, tea, colas), theobromine (chocolate) and alcohol LES pressure3.small, frequent meals ( to prevent gastric distention with resulting gastric acid secretion)4.avoidance of :

a. smoking – it LES pressureb. supine position for 2-3 hrs after eatingc. bending over ( intraabdominal pressure)d. lifting heavy objects and wearing tight belts or girdles after

eating ( to prevent abdominal pressure)5.sleeping with the head slightly elevated to prevent regurgitation while pt is sleeping

Achalasia also called cardiospasm or aperistalsis there is absence of peristalsis in the esophagus and in

which the esophageal sphincter fails to relax after swallowing

cause is unknown little or no food enters the stomach

S/Sx: gradual onset of dysphagia for both fluids and solids loss of weight substernal chest pain regurgitation of esophageal contents onto pillow at

night

Diagnostic tests : Barium swallow, esophagoscopy

AchalasiaMedical Mgt:Medications – Nitrates, Nifedipine – to decrease LES pressureForceful dilation of the LES by pneumatic dilators a balloon is inserted and inflated for 1 min., 2-3 times

- opens the sphincter and relieves the dysphagia

Nsg. Interventions:encourage pt. to drink fluids with meals and use the valsalva maneuver (bearing down with a closed glottis) while swallowing to help push the foodadvise soft dietelevate head during sleeping to prevent regurgitationafter esophageal surgery, monitor for signs of esophageal perforation as evidenced by chest pain, shock, dyspnea and fever

Esophageal Strictures narrowing of the lumen of the esophagus

Causes : ingestion of corrosive substances (alkaline or acid)reflux esophagitis - prolonged NGT

irritation of the esophageal walls lead to formation of a stricture that the esophageal lumen and leads to dysphagiafood may collect and partially or totally obstruct the esophagusfluids are easier to swallow than solids

Interventions :gradual dilation by mechanical dilators or balloonsrubber or metal mechanical dilators of increasing sizes are passed through the area of strictures, producing mild discomfortthe balloon is inflated to create pressuredilation procedure is done every 3-4 wks for 4-6 monthsmonitor pt for signs of esophageal perforation

Esophageal Carcinoma most common cause of obstruction of the esophagus Risk factors – chronic GERD, achalasia, smokers,

alcoholics tumor occur commonly in the middle and lower third of

esophagus common type is squamous cell carcinoma, occur in

ages 40-70 y.o early diagnosis and treatment is important for

treatment to be successful report and consult to the doctor for any sign of dysphagia

S/Sx progressive dysphagia – 1st w/ solid food then w/

liquids regurgitation may occur, aspiration coughing and

pneumonitis foul breath and foul taste in the mouth metastasis rapidly occurs to the pulmonary system,

diaphragm, heart, vertebraeDiagnosis: barium swallow, biopsy through endoscopy, CT scan

Esophageal Carcinoma

Medical Mgt.Surgery :

o Esophagogastrostomy (removal of the lower part of the esophagus and part of the stomach)

o Esophagectomyo Radical neck dissection

Radiation and chemotherapy – done 3-4 wks before surgery, reduces tumor size and facilitates surgery and length of survival

Esophageal CarcinomaNursing Management: Post-op care

Fowler’s position – to prevent reflux

observe for regurgitation and dyspnea

prevent aspiration pneumonia – turn to sides

w/ NGT attached to low intermittent suction (for decompression);

do not manipulate bec. damage to the anastomosis may occur;

removed after 5-7 days

Feeding through tube jejunostomy

Start oral feeding w/ small sips of water soft diet (after 1-2

wks)

Remain upright for at least 2 hours after each meal

Antacids and metoclopramide - promote gastric motility

Gastric Disorders

Structural Layers of the GIT1. Mucosa – mucous membrane composed of three layers

a. Epitheliumb. Lamina propria – connective tissue containing blood vessels,

lymph nodes and glands: cardiac glands – secrete mucus chief (peptic) cells – secrete mucus and pepsinogen pepsin parietal cells – secrete hydrochloric acid (HCL) and water,

also produce intrinsie factor neck cells - secrete mucus pyloric glands – secrete gastrin and mucus

c. Muscularis mucosa – thin layer of smooth muscle between mucosa and submucosa

2. Submucosa – connective tissue containing blood vessels, lymph channels, nerves and glands

3. Tunica muscularis – layers of smooth muscle produce peristaltic activity of the stomach as it mixes food

during digestion4. Serosa or adventitia – a serous membrane covered with an outer

layer of squamous epithelial cells

StomachGastric Secretion

The stomach secretes 1500 to 3000 ml of gastric juice per day. Major secretions are HCL, pepsin and mucus

HCL and pepsin provide the corrosive power of gastric secretion Pepsin is the most active factor in the digestive processes of the

stomach, acting to break proteins into polypeptides Mucus has a neutralizing effect which protects the stomach

mucosa

3 Phases of Gastric Secretion1. Cephalic Phase

is stimulated by hunger, food odors, sight and smell, taste it begins before food enters the stomach is mediated by the vagus nerve, releasing acetylcholine which

stimulates the parietal cells and chief cells to secrete acid, pepsin and mucus

Gastric secretion2. Gastric Phase

begins with the arrival of food in the stomach distention of the stomach and presence of digested proteins

stimulate gastrin hormone secretion Gastrin stimulates the parietal cells of the stomach to secrete

HCL this phase continues for several hours, until the acidity of

gastric contents reaches pH of 1.5

3. Intestinal Phase is stimulated by food entering the duodenum a substance similar to gastrin is released from the intestines

it stimulates gastric secretion of pepsin and mucus when the pH in the duodenum decreases ( acidity) this

results to release of Secretin hormone – w/c inhibit gastric acid secretion and slows gastric motility and gastric emptying

Acute Gastritis transient inflammation of the gastric mucosa char. by erosion of the surface epithelium in a diffuse or

localized pattern, that are usually superficial

Causes / precipitating factors : injury of the protective mucosal barrier by drugs or

chemicals anti-inflammatory drugs ex. Aspirin, NSAIDs inhibit

prostaglandin which normally stimulate mucus secretion

steroids ex. Prednisone food or substance poisoning

bacterial infection (staphylococcus organism) alcohol abuse extreme physical stress or prolonged emotional tension excessive amounts of coffee, tea, pepper, spices

stimulate acid secretion severe trauma, injuries, infection (sepsis), renal and

respiratory failure

Acute GastritisClinical Manifestations:

epigastric pain or discomfort abdominal tenderness cramping severe nausea and vomiting eructation (belching / burping) anorexia sometimes gastrointestinal bleeding – hematemesis

Healing usually occurs spontaneously within a few daysDiscontinuing injurious drugs, using antacids (ex. Maalox), decreasing acid secretion using Histamine receptor blockers (ex. Ranitidine, Cimetidine) facilitates healingProvide bed restEat non-irritating bland diet ( avoid highly seasoned, greasy or spicy foods)Anti-emetics (Plasil)

Peptic Ulcer Disease Normally, the gastric and duodenal mucosa is protected

from acid and pepsin by mucus and bicarbonate (base) that are secreted by surface epithetical cells

Peptic ulceris a sharply defined break or ulceration in the protective mucosal lining of the lower esophagus, stomach or duodenum which may involve the submucosa and muscular layerssuch breaks may expose the submucosal layers to gastric acid secretions and pepsin and cause AutodigestionTrue ulcers extend through the muscularis mucosa and damage blood vessels, causing bleeding or may lead to perforation of the GIT wall

Peptic Ulcer Disease

Predisposing Factors excessive use of aspirin, non-steroidal anti-inflammatory

drugs (NSAID’s) (ex. Mefenamic, Ibuprofen), steroids (ex. Prednisone) cause mucosal injury, gastric acid secretion, and gastric mucus secretion

cigarette smoking genetic predisposition dietary indiscretion – not eating on time severe physiological / psychological stress – stimulation of

the vagus nerve alcohol abuse infection of the gastric and duodenal mucosa with

Helicobacter pylori caffeine – stimulate acid production chemotherapy drugs – damage normal cells in the GIT

mucosa

Predisposing factors (cont.)

prolonged stress from severe burns, injuries, severe trauma, infection, head injury may cause “stress ulcer” – due to sympathetic response vasoconstriction of blood vessels of the GIT perfusion of the mucosal lining and ischemia mucosal secretion, protective ability of the mucosa damage of mucosal barrier by acids & pepsin

Ulcer and bleeding

Peptic Ulcer Disease

Pathophysiology of Peptic Ulcers

Gastric acid is secreted in parietal cells of the fundus of the stomach

Gastric acid secretion is stimulated by:a.acetylcholine (from the vagus nerve)b.gastrin (secreted by cells in the pyloric area of stomach)c.histamine (found in cells throughout the gastric mucosa)

- H2 receptors found in the cells of the stomach mediate HCL acid secretion


Gastric Ulcers


Duodenal Ulcers

Gastric ulcer

Duodenal Ulcer

Clinical Manifestations

Clinical Manifestations nausea and vomiting – occurs more often in gastric ulcer anorexia eructation (belching) weight loss bleeding – when an ulcer erodes through a blood vessel

Hematemesis caffe-ground emesis melena (black, tarry stool)

Diagnostic tests:- Endoscopy (gastroscopy)- Barium swallow- UGIS- stool exam for occult blood

Complications of Ulcers1. Bleeding and Hemorrhage (more common in gastric ulcers)

due to perforation of a blood vessel Mild bleeding

less than 500ml - may result to weakness and diaphoresis seen as melena or coffee-ground emesis

Massive bleeding bright red blood vomitus (hematemesis) severe blood loss over 1 liter per 24 hrs hypovolemic shock

weak pulse, hypotension, tachycardia, cold clammy skin1.Perforation – when ulcer penetrates entire stomach or duodenum wall, releasing stomach contents into the peritoneal cavity peritonitis

more common in duodenal ulcers and in long-term disease states S/Sx: sudden onset of severe abdominal pain, diffuse abdominal tenderness

diminished or absent bowel sounds abdominal distention rigid or board-like abdomen may result to shock – rapid, weak pulse, hypotension, LOC,

diaphoresis

Complications of Ulcers (cont.)3. Obstruction of the GIT (Gastric Outlet Obstruction)

repeated cycles of ulceration and healing in the pyloric region may cause scar tissue build-up and cause an obstruction or narrowing of the lumen of the GIT

result to obstruction or blockage in the flow of GI contents

S/Sx : nausea abdominal distention feeling of fullness abdominal pain profuse vomiting of undigested food

Medical Management 1. Providing rest – physical and mental rest, sedative, mild tranquilizer,

ensure calm, peaceful environment2. Protecting the mucosa:

by neutralizing acid content eliminating sources of irritation by slowing down gastric motility

Medications:1. Antacids

pain by reducing gastric acid activity by physical absorption or by chemical neutralization of acid

given 1 hr after meals and at bedtime (severe pain, give every 30 mins)

ex. MgAlHydroxide (Maalox), Simethicone, Amphogel, Calcium carbonate

liquid antacids are more effective than solid antacids tablets must be chewed thoroughly S.E – constipation, flatulence, diarrhea (milk of magnesia)

Medical Management (cont.) 2. Anticholinergics

gastric motility and delay gastric emptying, gastric acid secretion

ex. Probanthine, Bentyl S.E. – dryness of the mouth, drowsiness, constipation

3. H2 Receptor Blockers reduce the onset of pain and hasten healing of duodenal ulcers inhibit acid secretion - blocks the effect of histamine given with meals and at bedtime ex. Cimetidine, Ranitidine, Famotidine

4. Sucralfate – mucosal protector, coats the ulcer, prevents action of acid and pepsin on ulcer

prevent further irritation and promote mucosal healing heals ulcer in 4-6 wks Ex. Iselpin should be given 1 hr before meals and at bedtime

5. Gastric acid pump inhibitor Ex. Omeprazole (Losec) given 30 mins. before breakfast

Management for Peptic UlcersDiet

Bland diet, small frequent feedings (5x or more per day) avoid foods that cause increase pain avoid stimulants of gastric acid secretion (coffee, alcohol, spicy

foods, caffeine, cola drinks) raw fruits, whole grain cereals, fried or greasy foods are also

avoided Milk is also avoided bec. it can also stimulate gastric acid

secretion

Health Teachings: Stop smoking Dietary modifications eliminate caffeine and alcohol intake teach about medications that irritate ulcer (aspirin, NSAIDs,

steroids) - shld. be taken w/ meals or antacids

Stress management, relaxation techniques Regular exercise program Balance work, play and rest Encourage follow-up care and medications

Management of Perforation and Bleeding

Monitor VS, I/O Control bleeding

insertion of NGT – irrigate stomach (gastric lavage) w/ cold saline solution until return flow is clear; connect to suction machine

give antacid or mucosal protector (sucralfate) after acute bleeding has stopped

Replace blood loss – blood transfusion Minimize consequences of perforation

give antibiotics as ordered keep pt. on Fowler’s position to localize gastric contents to

one area of the peritoneum Surgery

Surgical Interventions

A. Gastrectomy total removal of the stomach result to no gastric juice for digestion, malnutrition,

pernicious anemia, weight lossB. Subtotal Gastrectomy

removal of a part of the stomach and the remaining stomach is anastomosed to the intestine

Billroth I (Gastroduodenostomy) – removal of the distal ½ of the stomach w/ anastomosis to the

duodenum Billroth II (Gastrojejunostomy) – removal of the lower stomach

and antrium w/ anastomosis to the jejunumC. Vagotomy – resection of the vagus nerve thus decreasing

motility and gastric secretions

Surgical Interventions (cont.)

Post-op Care: bloody drainage from NGT normal during 1st 12 hrs. eventually

dark green color indicating presence of bile & intestinal secretion Turn, cough, deep breathe q 2-4 hrs. to prevent atelectasis and

hypostatic pneumonia Pain medications, splint the incision insertion of NGT for gastric decompression, connected to drainage

bottle or to intermittent suction tube may be irrigated w/ 30 ml. of NSS to keep the tube patent Keep pt. on Fowler’s position to promote lung expansion and

gastric drainage Pt. is kept on NPO for 5-7 days to allow incision to heal TPN while on NPO, provide oral care Monitor for return of peristalsis, progress to clear liquids then DAT

Post-op Care

Dumping Syndrome

may occur following subtotal or total gastrectomy food enters duodenum rapidly hyperosmolarity of intestinal contents

pulls H2O from the vascular bed

resulting to rapid fluid shift(intestines swell)

circulating blood volume

S/Sx:vertigo, dizziness, nauseaweakness, diaphoresistachycardia,orthostatic hypotensioncold clammy skinAbdominal cramping and painoccurs 5-30 mins. after eating

Dumping Syndrome (cont.)

Interventions:

Eat frequent small meals that are dry and contain moderate protein, fat and reduced carbohydrate Blood glucose levels can rise rapidly after a meal

containing simple sugars, triggering a reactive hypoglycemia several hours after the meal

Do not take fluids with meals to slow gastric emptying (take fluids in between meals)

Rest or lie down on the left side for 30 mins. after meals if possible to slow down gastric emptying

Gastric Cancer

May develop in any part of the stomach but is found commonly at the distal third

More common in men and in age 50-70 years old

Causes: heredity, chronic gastric ulcer, chronic gastritisS/Sx:

Gastric distress Flatulence Early satiety Loss of appetite, anorexia Loss of strength and weight loss

Dx: UGIS, absence of HCL – due to destruction of parietal cells by cancer cells

Tx: Gastrectomy, chemotherapy

Gastric Cancer

Acute Abdominal InflammationsAppendicitis an inflammatory lesion of the vermiform appendix, located near

the ileocecal valve can be caused by occlusion of the lumen of the appendix by

hardened feces (fecaliths), by foreign objects, or by kinking of the appendix may impair circulation and lower resistance to organisms such as bacilli or streptococci

a small part of the appendix may be edematous or necrotic or entire appendix may be involved abscess formation may lead to rupture and peritonitis

S/Sx: pain on the umbilical area and throughout the abdomen then

become localized at the RLQ specifically at the McBurney’s point nausea, vomiting direct tenderness and rebound tenderness in the RLQ abdominal muscle rigidity WBC, Neutrophil count above 75% fever, temp= 38-38.5, PR rigidity of the whole abdomen may indicate rupture and

peritonitis

Appendicitis (cont.)Med. Mgt.surgery – Appendectomy – as soon as possible to prevent rupture with subsequent peritonitisAntibiotics Nsg. Mgt.a.Preoperative Care

bed rest placed pt on NPO – in preparation for surgery intravenous fluids – to maintain F/E balance ice bag may help relieve pain, no heat is applied because

this may circulation and congestion to the appendix and lead to rupture

b.Post-operative care general post-op care food permitted when peristalsis returns

Peritonitis is an inflammation of the peritoneum caused by trauma or by

rupture of an organ containing bacteria, which are then introduced into the abdominal cavity

ex. of organisms – E-coli, streptococci, staphylococci, gonococci can also be caused by rupture of the fallopian tube in ectopic

pregnancy, perforation of a gastric ulcer, traumatic rupture of the spleen or liver

Pathophysiology: inflammation causes adhesions, abscess formation peritoneum there is redness, edema and production of large

amounts of fluid containing electrolytes and proteins hypovolemia, electrolyte imbalance, dehydration hypovolemic shock

cessation of peristalsis occurs due to severe peritoneal infection and lead to acute intestinal obstruction

CAUSES OF PERITONITIS

Peritonitis (cont.)S/Sx: abdominal pain and tenderness (local or diffuse, often rebound)

abdominal rigidity (board-like abdomen) nausea, vomiting high fever, high leukocytosis weakness, diaphoresis, pallor, tachycardia, shock later signs : paralytic ileus, abdominal distention

Medical Mgt.Surgery – depending on underlying cause , peritoneal lavagePost-operative medical mgt. 1) NGT insertion – to prevent GIT distention 2) IV fluids and electrolytes 3) antibiotics – to control infection 4) maintain drains – to remove abscessesNsg. Mgt.bed rest in semi-fowler’s position to help localize pus in lower abdomen give mouth care – prevent drying of mucous membranes and cracking of lipsmaintain F/E replacementencourage deep breathing exercisesuse measures to reduce the pts anxiety

PERITONITIS

Gastrointestinal System Disorders

Health & Medicine

Transcript of Gastrointestinal System Disorders