Gastrointestinal System Explained

Gastrointestinal System
By Toto subiakto

Gastrointestinal Tract
Upper 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


Mouth
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 glands
2.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 digestion
Major 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

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 pharynx
2.) the food moves into the upper esophagus
3.) 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
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Stomach
 made up of 5 layers of smooth muscle
2 types of contractions:
1.) tonus contractions – continuous contractions
2.) rhythmic contractions – may be slow ( q2-3 mins.) or fast –
responsible for the mixing of food and peristaltic movement
Vagus 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 motion
chyme – food in the stomach
- is pumped through the pyloric sphincter into the duodenum

Digestive Function of the Stomach:

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

Intestines
Small 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 intestines
b.) colon – 4 parts (ascending, transverse, descending, sigmoid colon)
c.) rectum – 17-20 cm. (7-8 inches) long,  anal canal

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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)


Secretion 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 acids
c.) Fat digestion
- fats require emulsification into small droplets before it can be broken
down into glycerol and fatty acids
Bile – from liver; emulsify fats so that it could be broken down
pancreatic lipase  breakdown fats into glycerol and fatty acids

Absorption
the intestinal wall has many folds which are covered by
fingerlike projections called (villi)  increase the absorptive area
of the small intestines
in the center of the villi are capillaries, veins, small arteries for
absorption of nutrients into the blood vessel system
90% of absorption occurs within the small intestines by active
transport or diffusion
amino acids, monosaccharides, Na+, Ca++ are transported by
active transport w/ the expenditure or use of energy
other nutrients, fatty acids and H2O – diffuse passively across
the cell membrane
reabsorption of H2O, electrolytes and bile occurs mainly in the
ascending colon


GIT 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 GIT
Nursing History : Subjective Data
1. General Data
a. presence of dental prosthesis, comfort of usage
b. difficulty eating or digesting food
c. nausea or vomiting
d. weight loss
e. 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 present
a. situations or events that effect symptoms
b. onset, possible cause, location, duration, character of
symptoms
c. relationship of specific foods, smoking or alcohol to severity
of symptoms
d. how the symptoms was managed before seeking medical help

3. Normal pattern of bowel elimination
a. frequency and character of stool
b. use of laxatives, enemas
4. Recent changes in normal patterns
a. 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 taken
d. measures taken to relieve symptoms

B. Physical Examination : Objective Data
a.) Mouth and Pharynx
1. lips – color, moisture, swelling, cracks or lesions
2. teeth – completeness (20 in children, 32 in adults), caries, loose
teeth, absence of teeth  impair adequate chewing
3. 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
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signs of inflammation (redness, edema, ulceration, thick
yellowish secretions), assess also for symmetry of uvula and
palate

b.) 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 Organs
RUQ – liver, gallbladder, duodenum, right kidney, hepatic flexure of colon
RLQ - cecum, appendix, right ovary and fallopian tube
LUQ – stomach, spleen, left kidney, pancreas, splenic flexure of colon
LLQ – sigmoid colon, left ovary and tube

1. 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

3. 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
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perineal skin and perianal skin
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assess for presence of pruritus, fissures, external
hemorrhoids, rectal prolapse

Diagnostic Tests
A. Laboratory tests
1. Stool examination (fecalysis)
 Stool for occult blood
o GI bleeding
o 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 intake
o Laxative
o Stool – white for 24-72 hrs.
o Observe for: impaction, distended abdomen,
constipation

Radiologic Tests
2. Barium Enema/LGIS
Purpose : 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
 Post
o Laxative or enema
o Same as UGIS

Other Tests
a.) 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 Tests
b.) 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

Endoscopy

1. 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 procedure
o Anticholinergics(atropine), sedatives are given
o Remove dentures
o Lidocaine spray – depress gag reflex
o 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

Endoscopy
2. 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

Endoscopy
3. 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 Disorders
Dysphagia

 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
gravis
2) esophageal disorders
 obstruction caused by enlarged thyroid, tumors, strictures  narrowed
opening
 absence of peristalsis of the esophagus
Pathophysiology
Weak 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 Disorders
Assessment
 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. Management
Pts. 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 acidity
Medications 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 hernia
Ex. Posterior gastropexy – returning the stomach to the abdomen and
suturing it in place
Nissen fundoplication – wrapping the fundus of the stomach around the
lower part of the esophagus to restore sphincter competence and prevent
reflux

Nsg. Intervention
Patient 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 pressure
3.small, frequent meals ( to prevent gastric distention with resulting
gastric acid secretion)
4.avoidance of :
a. smoking – it  LES pressure
b. supine position for 2-3 hrs after eating
c. 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
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S/Sx:
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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
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

Achalasia
Medical Mgt:
Medications – Nitrates, Nifedipine – to decrease LES pressure
Forceful 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 food
advise soft diet
elevate head during sleeping to prevent regurgitation
after 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 dysphagia
food may collect and partially or totally obstruct the esophagus
fluids are easier to swallow than solids
Interventions :
gradual dilation by mechanical dilators or balloons
rubber or metal mechanical dilators of increasing sizes are passed through
the area of strictures, producing mild discomfort
the balloon is inflated to create pressure
dilation procedure is done every 3-4 wks for 4-6 months
monitor 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 4070 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, vertebrae
Diagnosis: barium swallow, biopsy through endoscopy, CT scan

Medical Mgt.
Surgery :
o Esophagogastrostomy (removal of the lower part of the
esophagus and part of the stomach)
o Esophagectomy
o Radical neck dissection
Radiation and chemotherapy – done 3-4 wks before surgery,
reduces tumor size and facilitates surgery and length of
survival

Nursing 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

Structural Layers of the GIT
1. Mucosa – mucous membrane composed of three layers
a. Epithelium
b. 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
a. 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 digestion
4. Serosa or adventitia – a serous membrane covered with an outer layer of
squamous epithelial cells

Stomach
Gastric 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 Secretion

1. 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 secretion
2. 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 Gastritis
Clinical 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 days
Discontinuing injurious drugs, using antacids (ex. Maalox),
decreasing acid secretion using Histamine receptor blockers (ex.
Ranitidine, Cimetidine) facilitates healing
Provide bed rest
Eat 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 ulcer

is 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 layers
such breaks may expose the submucosal layers to gastric
acid secretions and pepsin and cause Autodigestion
True ulcers extend through the muscularis mucosa and
damage blood vessels, causing bleeding or may lead to
perforation of the GIT wall

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

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

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 Ulcers
1. 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 skin
1.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 environment
2. 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 Ulcers
Diet

 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 loss
A. 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 jejunum
C. Vagotomy – resection of the vagus nerve thus decreasing motility
and gastric secretions

Surgical Interventions (cont.)
Post-op Care:

 bloody drainage from NGT normal during 1 st 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

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, nausea
weakness, diaphoresis
tachycardia,
orthostatic hypotension
cold clammy skin
Abdominal cramping and pain
occurs 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 gastritis
S/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

Acute Abdominal Inflammations
Appendicitis

 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 peritonitis
Antibiotics
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
a.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

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 lavage
Post-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 abscesses
Nsg. 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 lips
maintain F/E replacement
encourage deep breathing exercises
use measures to reduce the pts anxiety

•Cholelythiasis
simptoms and signs
- sharp pain
- low fever
- nausea andfeeling bloated
- jaundice if gallstones are in the
common bile duct

Diagnostic test
*history and physical
*AbdominalUltra sound-fasting 8hrs
*Blood test :cbc,lft,coagulation time
*HIDA scan,choleschintygraphy
*endoscopic retrograde chlangiogram
*MRI
*cholangiopancreatography

Management treatment
Surgical: Cholecystectomy
*laparoscopic Cholecystectomy
*open Cholecystectomy
non surgical : *stones retrieval
*watchful waiting
*increased exercise
*diet changes

Pain control
*narcotics or opioids
*NSAIDs

*Non medicine PC: distraction
guided imaginary

Gastrointestinal System Explained

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