ATOC 2009

DIGESTIVE SYSTEM
NCM 102
DIGESTIVE SYSTEM
Review of anatomy and physiology

Oral Cavity Structures

1. deciduous teeth (20)
2. permanent teeth (32)
3. tongue
a. skeletal muscles
b. moves food mass “bolus”
c. appropriate use of “lingual” terminology
4. salivary glands (3 pair)
a. parotid
b. submandibular
c. sublingual
d. parasympathetic innervation (activation)
5. saliva
a. amylase - begins starch digestion (not very significant amount)
b. lysozyme - protective, digests bacterial cell walls
c. lingual lipase - begins lipid digestion (not very significant amount)
6. appropriate use of “buccal” terminology

MOUTH- speech, nutritional ingestion, initiation of chemical and mechanical digestion of

swallowing
a. teeth: mech. Breakdown of food, facilitates swallowing, articulation of words, tear
out of food into smaller pieces
b. tongue: speech, chewing/ mastication, swallowing
c. palate: facilitates mastication, forms roof of mouth, s it aspiration is possible
d. salivary gland: production of saliva
o saliva> lubricates the mouth and keeps mouth clean since it contains IgA
and it also lubricates food which aids in swallowing
• parotid: produces ptyalin for breakdown of starch
• submandibular: mixture of mucus and serous
• sublingual: produces lubricating fluid, mucus
PHYSIOLOGY OF MASTICATION
Food in mouth
↓
causes chewing reflex, inhibitors of muscles of mastication allowing lower mandible to drop
↓
drop initiates stretch reflex leads to rebound contraction raise jaw (closure of teeth) which
compresses bolus against palate
↓
mandible / jaw drops
↓
series of rebound contraction is repeated until chewing process is complete
↓
bolus broken down into smaller pieces with aid of salva and teeth
↓
deglutition/ swallowing

Pharynx
1. oropharynx
2. esophagus - connects pharynx to stomach
3. peristalsis - rhythmic smooth muscle contractions propel material inside

ESOPHAGUS
o transports food from mouth and oropharynx into the stomach
o secretes mucus but not enzymes
o sphincter normally are closed but opens in response to peristalsis but
remains

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o LES relaxes in response to peristalsis but remain tonically contracted at all
times, protecting the esophageal mucosa from gastric contents (avoid
reflux)

Upper & Lower Esophageal Sphincter

o prevents reflux from the esophagus into the oropharynx (UES) and from
the stomach to the esophagus (LES)
PHYSIOLOGY OF SWALLLOWING/ DEGLUTITION
I. Oropharyngeal/ Voluntary Phase
 food segmented into bolus by tongue and forced posteriously towards
pharynx
 epiglottis slides downward to prevent bolus from entering larynx and
trachea
 >respiration is inhibited
• (UES) movement of tongue & pharyngeal constrictions propel food into
proximal end of esophagus

II. Esophageal Phase

 food enters esophagus & transported by peristalsis
[aided by electrolytes: Na+, K+, Ca2+, Mg2+ since peristalsis are mainly contraction
of muscles]
 LES relaxes just before another peristaltic wave
 food enters stomach
 sphincter muscles return to its resting tone after the bolus passes
which is facilitated by nerve impulses (CNS & PNS)
Four Major Layers of GI Tract
1. mucosa - innermost lining of GI organs
a. epithelium
b. lamina propria – areolar CT, MALT, blood vessels, lymph vessels
c. thin muscularis layer
2. submucosa
a. areolar CT
b. blood vessels
c. autonomic nerves
3. muscularis
a. smooth & skeletal muscles
4 serosa - outermost lining of GI organs
a. CT + simple squamous epithelium (mesothelium)
b. peritoneum
i. visceral – mesothelium on organ surface
ii. parietal – mesothelium on abdominal wall
iii. major periotoneal folds – extensions of peritoneum layers
aa. mesentary – attaches SI to posterior wall
bb. mesocolon – attaches LI to posterior wall
cc. falciform ligament – attaches liver to anterior wall
dd. lesser omentum – attaches stomach & duodenum to liver
ee. greater omentum – attaches transv. colon & SI to stomach & duodenum

STOMACH- stores ingested food, digestive juices & propels partially digested food or chyme
into the duodenum; pH 0.5- 1.9
Three parts
 Fundus- has the highest concentration of chief cells
 Body- secretes gastric juices
 Antrum- responsible for parietal cells
• Pyloric Sphincter- located below the antrum, w/c prevents reflux duodenal
contents back to the stomach

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• Cardiac/ Esophageal Sphincter- located above fundus, w/c prevents reflux of
gastric contents back to esophagus
• Rugae- allows increase in size of stomach, w/o changing pressure
o folding muscles or folds w/c allows stomach to stretch w/c facilitates 4- 4.5
L of bolus
Four layers of stomach
 Serosa- outermost layer of stomach
 Muscularis (tunica muscularis)- produces peristaltic act of the stomach
during digestion
 Submucosa- connects the muscular and mucous layers of the stomach
walls & contain blood, lymph channels & nerve plexus
 Mucosa- innermost layer of stomach, exposed to gastric content
NOTE
: overdistention of stomach can cause nausea and vomiting
: it takes an average of 2 hours for gastric emptying to occur
Five types of cells in the stomach
1. mucous neck cells
2. surface mucous cell
3. parietal/ oxyntic cell
4. chief/ zygomonic cell
5. endocrine cell/ G cell

1. general anatomic regions

a. cardia
b. fundus
c. body
d. pyloric region
2. stomach is important in the process of physical digestion
3. rugae are undulations in stomach wall to help grind
4. gastric pits contain four major secretory cells:
a. chief cells
i. pepsinogen
aa. activation of pepsinogen by low pH to form pepsin
bb. pepsin is a protease for protein digestion
b. parietal cells
i. HCl
aa. secretion enhanced by histamine via H2 receptors
bb. Tagamet blocks H2 histamine receptors to inhibit HCl secretion
ii. intrinsic factor
aa. binds to and allows B12 absorption in intestines
c. G-cell
i. secretes gastrin hormone
aa. gastrin activates gastric juice secretion & gastric smooth muscle “churning”
bb. gastrin activates gastroileal reflex which moves chyme from ileum to colon
d. mucus cell
i. protective role of mucus against acids and digestive enzymes
5. pyloric sphincter regulates entry into the duodenum
6. chyme is liquified digested material
Gastric secretions happen when there is:
o presence of food in the mouth , when chewing & swallowing
o gastric distention
o taste and smell of food (stimulation)
o moderate amount of caffeine and alcohol(it explains why caffeinated and
alcoholic beverages increase appetite, bec. It stimulates gastric
secretions )
o emotions such as anger and hostility (decrease gastric during fear &
depression)
Functions of cells in the stomach (gastric secretion)
1. mucous neck cells and surface mucous cells

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o responsible for secreting viscous and alkaline mucous
o serves as barrier w/c aids in diffusion of hydrogen ions from gastric lumen
into mucosal cell
o if barrier is damaged ulcer is formed
o coats surface epithelial cells of stomach
2. parietal cells
o highly concentrated in antrum
o produces HCl and Intrinsic factor(mucoprotein that binds with vit. B12
“cyanocobalamine” w/c aids in maturation of RBCs – dec. Hgb & dec. Hct=
dec. O2 = easy fatigability and paleness )
3. Chief cells
o highly concentrated in fundus
o secretes water and pepsinogen w/c is stimulated by gastrin, calcium,
histamine, secretin
4. Endocrine cells
o secretes gastrin w/c stimulates parietal cells to increase secretion of HCl

Gastrin production is increased by:

a. gastric distention
b. vagal stimulation
c. calcium ions
d. presence of protein breakdown products
 Gastrin production is initiated by gastric pH lower than 1.5
How digestion occurs:
1. Ingestion nutrition remain in stomach until they have been thoroughly mixed
2. With gastric contents & converted to semi-fluid material called CHYME
3. mixing waves- primarily activity to combined ingested nutrient w/ gastric secretions
4. peristalsis aids in mechanical breakdown, stronger peristaltic wave actively sweeps the
liquid chyme towards pylorus
5. gastric juices converts food into simpler compound
• antrum- has normal peristaltic wave
• pylorus- has increase peristaltic wave
Phases of Gastric Secretions
1. Cephalic Phase- dependent on stimulation of gastric secretions by receptors in the
brain that are mediated by the vagus nerve
i. initiated by parasympathetic activation (vagal innervation)
ii. cortical (smell, thoughts, etc.) activation of medulla
iii. medulla activates gastric juice secretion
iv. medulla activates gastrin secretion
v. medulla activates smooth muscle “churning”
2. Gastric Phase- secretion occurs when the bolus of food reaches the antrum
i. food mass and chemicals trigger parasympathetic reflex
ii. enhance parasympathetic activation of stomach
iii. activate & enhance emptying of chyme into duodenum
The phase consists of three mechanisms:
 When food enters the stomach
 Secretion of gastric juices
 Continuity phase until acidity of gastric contents reaches 1.5
How does Gastric emptying takes place
Swallowing causes fundus to relax to receive a bolus of food from the esophagus
↓
mixing occurs as food is propelled towards antrum
↓
food approaches pylorus
↓
velocity of peristaltic wave increases
↓
passage of contractile wave over the gastric content forces the chyme back towards body of
stomach--- Retropulsion

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↓
food effectively mixes w/ digestive juices in oscillating motion, breaking down large particles
↓
due to peristaltic wave, small portion of food passes through pylorus and duodenum

NOTE: any alterations in sphincters will lead to regurgitation

3. Intestinal Phase- stimulated by passage of food into duodenum resulting to secretion

of small amount of gastrin by intestine

SMALL INTESTINE
a. duodenum (20-30 cm long)
o immobile w/ c- shaped segment
o common bile duct and pancreatic duct both empty at the duodenum then
at the ampulla of vater then through the pyloric sphincter
o CCK was secreted through the duodenal wall w/c signals the brain to
contract the gallbladder for it to release bile w/c emulsify fats
o 10 inches
b. Jejunum
o it is the major organ for absorption of nutrients
o has a very prominent villi
o consistent w/ its role in nutrient absorption
o 8 ft
c. Ileum
o provides absorption of nutrients not absorbed in duodenum
o villi are less prominent
o contains only one receptor site for absorption of intrinsic factor
o B12 and bile salts – It is found in terminal ileum
o 12 ft

- histology
a. mucosa has intestinal glands (cavities) for secretion of intestinal juice
b. mucosa also has circular folds, villi & microvilli for increased surface area
c. “brush border” has many enzymes embedded in plasma membranes
i. several carbohydrate-digesting enzymes
ii. peptidases
iii. nucleosidases
iv. enterokinase is released by epithelial cell “shedding”
aa. important enzyme activator – see later
Villi
 Basic unit of absorption
 Has microvilli and additional extensions
 Tiny finger- like structure protrudes from the wall of intestine & have additional
extensions called microvilli protrudes from epithelial cell wall lining villi
 Increase intestinal absorptive surface (30 folds- 600 folds, providing efficient
absorption)
Intestinal Phase of Regulating Digestion
1. chyme enters duodenum
2. three hormones secreted from SI mucosa
a. gastric inhibitory peptide (GIP)
i. fatty acids in chyme induce GIP secretion
ii. GIP inhibits gastric secretion
iii. GIP inhibits gastric “churning”
iv. GIP activates insulin secretion
b. secretin
i. secretin inhibits gastric secretion
c. cholecystokinin (CCK)
i. CCK fatty acids in chyme induce CCK secretion
ii. CCK slows gastric emptying

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3. receptors in SI mucosa sense food/chemical presence in duodenum
4. neuronal activation of sympathetic NS/ inhibiton of parasympathetic NS
LARGE INTESTINE / COLON
o expulsion of waste products, reabsorption of water and electrolytes,
storage of undigested particles
- Ileocecal Valve
• connection between ileum and large intestine
• appendix fxn: according to theory., w/o it puts a pd @ high risk of acquiring
infection but not proven
- Cecum
• connects ileum to colon, w/c contain the “ileocecal valve” w/c is a one-way
valve that prevents reflux of large intestine content into small intestine

- Colon
• Ascending—hepatic flexure—Transverse—splenic flexure—Descending—
sigmoid colon & rectum
• Organ responsible for storing & eliminating waste products produced by
nutrient digestion and absorption
• Absorption of water and electrolytes

Nutrient Absorption
1. carbohydrates
a. enzymatically digested to form monosaccharides (glucose, fructose, galactose)
b. absorbed in SI by active transport or facilitated diffusion
c. enter blood capillary in villi, then directed to hepatic portal vein
2. proteins
a. enzymatically digested to amino acids or di- and tri-peptides
b. absorbed in SI by active transport or facilitated diffusion
c. enter blood capillary in villi, then directed to hepatic portal vein
3. lipids
a. enzymatically digested to short or long chain fatty acids
b. suspended in SI in form of micelles with bile salts
c. micelle formation aids lipid diffusion into SI epithelial lining
d. inside epithelial cells, lipids bound into chylomicrons for transport
e. chylomicrons transported to lacteal villi; then into lymphatics and then to venous blood
NOTE
Application of suppositories
1. breath through nose and exhale through mouth
2. let px relax/ perform deep breathing before inserting suppository (during exhalation)
3. pinch gluteal muscles after inserting meds for 2-3 minutes

Colonic motility
- propulsive movement of colon occurs as mass movement w/c is a series
peristaltic wave that sweep stool rapidly
- these peristaltic movement occurs @ interval of 10-15 mins, 2-3 x a day
common in the first hours after breakfast
RECTUM
- if it is full, there is an increases intra=rectal pressure forces walls of anal
canal apart allowing fecal matter to enter the canal
- rectum shortens as material is forced into anal canal
- peristaltic waves launches feces out of rectum
- internal and external anal sphincters allow the feces out of rectum internal
and external anal sphincter allow the feces to be passed by muscles pulling
anus up over the exiting feces
- components : 75% water ; 25 % bacteria, fat CHON, inorganic matter,
undigested roughage, epithelial cells, components of digestive juices
Stool: normally brown due to derivatives of bilirubin
Flatus: action of colonic bacteria on undigested flatus; produces flatus or air which is CO2 (as a
product of bacterial metabolism)
ASSESSMENT OF DIGESTIVE SYSTEM

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NCM 102
1. complete history
2. demographic data
3. psychosocial status
4. family history
5. medication, diet & nutrition
6. socio-economic status
NOTE: NABS= Normoactive Bowel Sounds
HISTORY OF PRESENT ILLNESS
a. change in bowel habits
b. color and consistency of stool
c. occurrence of diarrhea
d. wt. gain or wt. loss planned or unplanned
e. blood in stool or vomitus
f. abdominal pain
OBJECTIVE CUES: PHYSICAL EXAMINATION
A. Inspection = mouth, tongue, buccal cavity, mucosa, teeth and gums, dentures should
be removed
Abdomen: Contour, symmetry of abdomen, skin changes and scars from previous
operation, bulging, distention, and visible peristaltic wave
Anal & perineal area areas of excoriation (deep scratch) or rash, fissures (crack or
cleft), fistula, external hemorrhoid
B. Auscultation= character and location/ frequency of bowel sounds
 bowel sounds : 4 quadrants
 Normoactive- every 5-20 seconds
 Hypoactive: 1-2 in 2 minutes
 hyperactive: 5-6 in less than 30 seconds
 absent 0 in 3-5 minutes
C. Percussion
- has limited value on PE
- it may be difficult to perform percussion to obese patients
- findings may vary in large portions
- appreciation of rebound tenderness (deep palpation)
- appendicitis (generalized pain, localized in R lower quadrant)
- inflammation in abdominal cavity
- pain in the abrupt release of palpation = 3-4 cm
- stone: appendicitis s/sx but pain rans down in inguinal area
- tympany: hollow organs eg: dyspepsia
- dullness: solid organs eg: liver, suspected masses
D. Palpation
- light palpation: used to identify area of tenderness/ swelling
- deep palpation: masses (4 quadrants)
- all quadrants: light > deep
- start away from painful point
- light palpation ; note palpable mass
- deep palpation, detail exam of mass found in light (liver, spleen)
Nursing responsibility
- instruct patient to void or empty bladder before PE

DIAGNOSTIC PROCEDURES
P: provide information about procedure
A: alleviate anxiety, help patient cope with discomfort
P: provide instructions about post procedure care & activities
E: encourage family members (emotional support)
R: reassess: assess patient for adequate hydration before, during and after procedure
GI STUDY
1. X-ray
- upper GI series/ barium swallow
- lower GI series/ Barium enema

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- swallow: 700-1000ml iodine based solution; enables to detect anatomic
functional deraignment of GI sphincter (cardiac); aids tumors, malabsorption
syndromes , ulcers etc.
- total procedure 6 hours
- Intervention
 Decrease residue diet before test
 NPO after midnight before test
 Withheld meds: follow – up to eliminate barium solution; increase fluids-
evacuation of stools; monitor stools to normal color brown to yellowish
stool
 Lower: detect presence of tumor, polyps, lesions; anatomy & malfunction
of colon; 10-15 minutes only
NOTE: barium enema first before barium swallow
Barium enema
Nursing intervention:
 ask patient to defecate
 decrease residue 1-2 days before test
 clear liquid diet & laxative the evening before test
 NPO after midnight
 Cleansing enema the next day
Contraindications
 Perforation/ obstruction of GI tract
 Use laxative after barium enema
 Increase fluid intake
 Monitor elimination of barium
 Active inflammation: contraindicated in cleansing enema
 Active bleeding: (-) laxative and enemas
2. Scopes- direct visualization
a. laparoscopy
- requires small incision in abdomen
- allows biopsy sample, excise structure & masses
- see peritoneal dse, abdominal masses, gallbladder and liver dse
b. fibercoscopy (EGO)- direct visualization of esophageal gastric and duodenal
mucosa through the lightest endoscope (esophagoduodenal gastroscopy)
c. Anuscopy; sigmoidscopy- through anus
- tx: limited bowel prep, do fleet enema
- no dieatary restrictions
- (-) sedation after procedure
- monitor s/ sx for rectal bleeding: fever, rectal drainage, abdominal
destention> pain; no s/sx provide sitz bath
d. endoscopy- enter through mouth
3. Radiographic studies / tests
a. CT scan (computed tomography)
- focused on the anatomical oart
- used to detect tumors, cysts, abscess, dilated bile ducts, pancreatic
inflammation and some bile stones
- Nsg responsibilities:
 Instruct patient of 4 hours fasting before the procedure
 administer enema
 ask if patient is pregnant; if so > do not proceed and notify the physician
 ask for allergies in iodine > since the contrast medium used is iodine
 instruct patient to notify the health care providers if symptoms of itching,
shortness of breath may manifest upon receiving the contrast media, then
observe
b. MRI (magnetic resonance imaging)- provides a clearer 3d image
c. Ultrasonography- most preferred for detection of suspected gallstones
- nursing responsibility:

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 prepare with special diet incorporated with laxative to decrease gas
and decrease roughage
 put patient in NPO for 6 hours> for abdominal ultrasound

4. Laboratory Studies
a. fecalysis- for detection of presence of ova, parasites, infection, fats
and blood feces
b. stool culture- to identify pathogenic agent present
c.
gastric analysis- test pH (N: 0.5-4.5)of gastric content; lower than
normal indicates presence of tumor > Zollinger Ellison Syndrome/
ulcer formation; insert NGT> lavage/ gastric decompression
COMMON SIGNS & SYMPTOMS PRESENT IN ALTERATION OF GIT
1. Anorexia
- lacks desire to eat despite of physiologic stimuli that would normally produce
hunger
- this is a non-specific symptom of associated with: a. nausea, b. abdominal
pain, c. diarrhea
- disorders of other systems accompanied by anorexia: a. cancer, b. heart
disease, c. renal disease
- treatment:
• icechips
• tea/ crackers
• small frequent feedings
• arrange / make food palatable
• modify environment
• food preference
• aromatic & palatable food
• enough condiments
• position desired by patient
- use more on cephalic phase to increase appetite
2. vomiting
- forceful emptying of stomach & intestinal content (chyme) through mouth
- stimuli that induce/ initiate vomiting reflex :
a. presence of ipepac (increase secretion to stimulate vomiting) and
copper salt (both components of poison ) in the duodenum
b. severe pain
c. distention of stonmach and duodenum > if fluid intake goes beyond
1.5 L
d. tension or trauma affecting ovaries / testes, uterus , bladder or
kidneys (stimulation of vagus nerve)> same intervention with
stiomach
e. activation of chemoreceptor trigger zone in the medulla
PATHOPHYSIOLOGY OF VOMITING
- retching begins with deep inspiration
- closure of glottis
decrease intrathoracic pressure
↓ ↓ ↓
distetion of esophagus ↓ abdominal muscles contract creating pressure greatest from
↓ abdomen and thorax
relaxation of LES and body of stomach →duodenum and antrum of stomach go into spasm
↓
reverse peristalsis & pressure gradient, forces chyme from the stomach, duodenum up to the esophagus
→ as the abdominal muscles relax the contents of esophagus, drop back into the stomach → the process repeated
several times → VOMITING → diffusion of sympathetic discharge: tachycardia, tachypnea
↓
parasympathetic discharge: copious saliva, increase gastric motility
3. Nausea

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- subjective, associated with different conditions. A complain that can be
similar to “I feel like vomiting” feeling
- retching> attempting to induce vomiting
- nausea & retching usually preceeds vomiting
- accompanied w/ manifestation such as : a. hypersalivation, b. tachycardia, c.
tachypnea
Projectile vomiting
- nausea and retching is absent
- no stimulant needed but stimulation is directly
4. Constipation
- difficult/ infrequent defecation
- s/sx
a. less frequent defecation
b. difficult evacuation of rectum
c. feeling of bowel fullness and discomfort
d. small stool volume
- cause:
a. Neuro: Hirschprung’s disease (pediatric case)> decrease peristaltic
movement due to absence of enteric plexus
b. Abdominal muscle weakness
c. Painful anal lesions: impacted feces
d. Low residue diet: decrease roughage
e. Depression: decrease gastric secretion and motility
f. Sedentary lifestyle: weakened muscles
g. Use of opiates, anticholinergics, anatacids
h. Systemic disorders – hypothyroidism, diabetic neuropathy (thyroid
dictates metabolism rate)
i. Megacolon (enlarged or dilated colon)
- Assessment:
 Due to different personal bowel habits, it must be individually
defined
 N: 2-3 evacuation / day to 1 per week
A. History and PE
 frequency- discover whether evacuation was stimulated by enema/
laxatives
 stool consistency/ presence of blood- result of bleeding hemorrhoids or
neoplastic lesions of colon
 cramping abdominal pain- symptom of bowel obstruction
 auscultate bowel sounds- usually hypoactive/ absent
 palpation- discloses colonic distention, masses, tenderness
Two types of constipation
1. functional: resulting from lifestyle or bowel habits, usually has
long history
2. dysfunctional: likely to be sudden; accompany development of
organic lesion that requires careful evaluation (eg: gastric
cancer)
B. Diagnostic Evaluation
⇒ proctosigmoidscopy- visualize lumen (rectum)
⇒ barium enema: required if no lesion is directly visualized
C. Treatment
⇒ If dysfunctional: manage the underlying cause
⇒ If functional: bowel draining (a bowel routine: 1 hour before
breakfast); engage in moderate exercise (increase fiber and fluids);
stool softeners and laxatives (eg: dulcolax); enema; avoidance of
high caloric irrigation with large volume of fluid – to avoid rupture
of the bowel
D. Complications
⇒ (Aneurysm) Valsalva maneuver: possible rupture of major artery in
brain or elsewhere

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⇒ fecal impaction, megacolon and atonic colon
→ caused by fecal mass that obstruct the passage of colon
⇒ Cathartic colon: mucosal atrophy of colon with muscle thickening
seubsequent to chronic use of laxatives

5. Diarrhea: increase in frequency of defecation & fluidity & volume of feces

- large volume diarrhea: caused by excessive amounts of water or secretions
in intestines
- small volume diarrhea: is not increased but is usually a result of excessive
intestinal motility
Three mechanisms of diarrhea
a. Osmotic: presence of unabsorbable substance in intestine causes to
be drawn into lumen by osmosis
⇒ Excess water (retained) in intestine together with unabsorbable
substance> increase ht and volume of stool > causing large
volume diarrhea
⇒ Example: LACTASE DEFICIENCY (non-absorbable subs: milk,
sugar, lactose)> intestine does not produce enough lactase>
lactose remain in intestinal lumen (since it is not digested and
absorbed) > causes large volume diarrhea (since lactose attracts
water)
b. Secretory : caused by excessive mucosal secretion of fluid and
electrolytes due to secretion of bacterial endotoxins
⇒ Eg. Cholera and strains of E. coli
⇒
Neoplasm> gastrinoma, thyroid carcinoma; both can produce
hormones that stimulates intestinal sec.
- Large Volume> diabetic neuropathy has lesion/ blockage of the nerve & it
impairs autonomic control of motility
- > excessive motility →decrease transit time → decrease mucosal surface
contract→ decrease fluid absorption→ large volume of stool reaches rectum→
produce urgency and frequency of elimination
- Small Volume: causes ulcerative colitis, chron’s disease inflammation of
intestine / colon, cramping pain, urgency & frequency
- * fecal impaction → secretion produce by colon → moving towards anal canal
flowing around → small volume secretory
c. Motility: caused by resection of small intestine; surgical bypass of
an area of intestine, fistula formation between loops of intestine
⇒ Food not mixed properly→ impaired digestion→ increase motility
→ diarrhea
 Systemic effects (prolonged diarrhea): dehydration, electrolyte
imbalance, weight loss
 Assessment & evaluation
o History
o PE (identify underlying systemic disease )
o Fecalysis / stool culture
o Abdominal x-ray
o Intestinal biopsy
 Treatment:
o Restore fluid and electrolyte balance
o Manage distress symptoms
o Correction nutrition deficiencies
o Administer substance that solidify stool (metamucil)
o Opium alkaloids like Lomotil which suppresses motility
relieves cramping & reduce stool volume & frequency
6. Abdominal Pain: a presenting symptom of # of GIT disease
- Causes:

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 Mechanical: organs sensitive to stretching and distention (eg.
Obstruction)
 Inflammatory: due to inflammatory response
 Ischemic: O2 supply in a certain part of GIT; necrosis / cell death
- Two kinds of abdominal pain
 Parietal pain: localized & tense; travels from peripheral nerves to spinal
cord
 Visceral pain: from stimulus or and abdominal organ felt near midline/
epigastrum
♦ Referred pain: (eg pancreatitis> scapular pain) pain felt aside from
original source due to same innervations
 s/sx: upper gi bleeding (dark red) → due to hemolysis / ulcer
[esophagus, stomach, duodenum]
 : lower GI bleeding (bright red) → blood not yet hemolyzed [polyps,
inflammatory disease, CA, hemorrhoids]
ACUTE BLOOD LOSS
a. hematemesis: presence of blood in vomitus
b. hematochecia: frank bleeding from rectum (upper GI digital exam)
c. melena: dark tarry stools (upper GI digital exam)
d.
occult bleeding: usually caused by slow, chronic blood loss that
results in iron deficiency anemia as iron stores in the bone marrow
are slowly depleted due to eroded mucosa etc.
- Treatment: treat underlying cause, stop meds if ti cause ulceration
 terms:
 hiatus: space in diaphragm
 LBM: water, decrease frequency
 Diarrhes: watery, increase frequency
 IBS: irritable bowel movement syndrome; common to young adult ;
immediate defecation after meal

Upper GI
> Acute massive bleeding Gi bleeding→ accumulation of blood in GIT,
increase peristalsis
Lower GI (loss of 20-25% BV w/in few hours) , diarrhea, digestion of blood CHON,
BUN
↓
blood volume depletion, decrease CO, decrease systolic BP;
increase HR
Pathophysiology of GI bleeding
↓
compensatory: constriction of peripheral arteries → decrease
blood flow to skin (pallor)
metabolic acidosis ↔ decrease blood flow to
C
kidneys= decrease urine output
O
↓ ↓
M
lactic acidosis tubular
P
necrosis
E
↓ N ↓
anoxia S renal failure=
anuria/ oliguria T
↓ O → decrease blood flow to GI
death R ↓
Y mesenteric
insufficiency> abdominal pain
Failur ↓ 12
e bowel infarction/
liver necrosis
→ decrease blood flow to brain
confusion, stupor
→ decrease coronary blood flow
----- angina, MI, heart failure
ATOC 2009
DIGESTIVE SYSTEM
NCM 102

ALTERATIONS IN ESOPHAGUS
 protrusion of a portion of stomach through hiatus & into thoracic cavity
 two types
- sliding hernia: stomach & gastro esophageal junction slip up into the chest
- paraesophageal/ rolling hernia: part of greater curvature of stomach rolls
through diaphragmatic defect
 s/sx: heartburn, dysphagia, chest pain, maybe asymptomatic
 etiology & precipitating factors: obesity, poor seating posture (slouching), frequent
cough, straining with constipation, frequent bending over or heavy lifting,
hereditary, smoking (contributory factors to peptic ulcer)
 pathophysiology
Possible cause (refer to etiology) ---- muscle weakening in aging ---- trauma
---- Esophageal carcinoma ---- surgery

weakening of diaphragm 

protrusion of upper part of stomach
 
clinical manifestations (refer to s/sx) complications: incarceration of
the portion of stomach in chest

constricts blood supply and
lung supply
esophagitis
GERD
 diagnostic evaluation:
- barium study of esophagus outlining hernia;
- endoscopic &
- visualized effect
 management:
- elevation of head (6-18 inches)
- ; antacid therapy;
- H2 receptor antagonist surgical repair of hernia (if sx severed);
- “angelschik”
 interventions & patient education
- instruct patient: prevent reflux of gastric contents
- eat smaller meals
- avoid caffeine; alcohol; smoking
- avoid fatty foods (promotes reflux & delays gastric emptying)
- avoid lying down directly after meal at least 1 hour
- lose weight (if obese)
- avoid bending from waist, or wearing tight fitting clothes
ALERT: advise to report immediately for onset of acute chest pain which may indicate
incarceration of large paraesophageal hernia
III. Achalasia: excessive resting tone of LES, incomplete relaxation of LES with
swallowing and failure of N peristalsis in the lower thirds of esophagus
- cause:

13
 ATOC 2009
DIGESTIVE SYSTEM
NCM 102
o defective innervation of myenteric plexus innervating involuntary
muscles of esophagus
- s/sx
o gradual onset of dysphagia w/ solids & liquids
o substernal discomfort/ feeling of fullness
o regurgitation of undigested food during a meal or w/in several hours
after meal ; wt. loss
- pathophysiology
Defective innervation myenteric plexus neurodisorders (causes paralysis or
abnormal sending of impulse )
 
incomplete relaxation of LES with swallowing & failure of normal
peristalsis in lower third of esophagus

- diagnostic evaluation: s/sx
o chest x-ray
o Ba 2+ esophagography
o Endoscopic ultrasound
o Chest CT
- Management
o Drug therapy using Ca2+ channel blockers such as nifidipine to decrease
LES pressure
o Esophageal dilatation using balloon typical catheter (preferred tx)
- FUNDIPLICATION: surgical therapy for patient who do not respond to balloon
dilatation
- Complication:
o Malnutrition
o Lung abscess, pneumonia, bronchioectasis from nocturnal regurgitation
o Esophagitis, esophageal diverticulation (patient is high risk of aspiration)
o Perforation from dilation procedure
o Peptic stricture from severe erosive esophagitis
- Nursing Assessment
o Asses difficulty in swallowing
o Vomiting
o Weight loss
o Such as position changes
o Eating
o Inquire as to what facilitates passage of food, such as position changes
- Possible Nursing Diagnosis
o Altered nutrition: < body requirement related to dysphagia
o Alteration in comfort: pain r/t surgical procedure / heart burn secondary
to regurgitation
- Nursing intervention
A. Improving nutritional status
1. direct patient to eat sitting in upright position; eat slowly & chew
food thoroughly can cause spasm → stimulates excessive
2. avoid spicy, very hot & very cold food to minimize symptoms
3. suggest patient to sleep with head elevated (to avoid reflux and
aspiration)
4. provide bland diet & avoid alcohol, ketchup, tomato products,
chocolate, mint and caffeine (increase gastric secretion→ induce
vomiting )
B. Promoting Care
1. assess for discomfort, chest pain, regurgitation, cough &
incisional pain (post op)
2. provide appropriate post-op care (hand washing)
3. administer analgesics as ordered

14
 ATOC 2009
DIGESTIVE SYSTEM
NCM 102
4. assess for effectiveness of pain medications
C. Patient education
1. encourage lifestyle change
2. advise patient to eat slowly, chew very well, drink plenty of water
after meal & avoid eating near bed time
3. advise to avoid meals with anticholinergics properties
(antihistamines) w/c increase LES pressure and dysphagia
4. provide info on all diagnostic procedures / surgeries
III. Gastroesophageal reflux disease (GERD)
- backflow of gastric contents in the esophagus ; chronic state of backflow;
chronic symptom of mucosal damage produced by abnormal reflux of gastric
contents into the esophagus w/c may result to esophagitis
- causes :
o incompetent LES
o impaired gastric emptying/ partial gastric outlet obstruction
o achalasia and impaired expulsion of gastric reflux , hiatal hernia
- NOTE: chest pain should be ruled out for possible cardiac causes dysphagia/
dynosphagia or wt. loss (rule out CA or esophageal stricture
- s/sx
o heartburn characteristic by burning sensation behind the sternum , 30-
60 minutes after meals with reclined position
o dysphagia (least common)
o chest pain , horseness, cough
o odynosphagia: sharp substernal pain on swallowing
- pathophysiology
cause of GERD
↓
mucosal damage produced by abnormal reflux of gastric contents into
esophagus
↓
s/sx of GERD
- Diagnostic evaluation
o Endoscopy
o Esophageal manometry: measure LES pressure & determines if
esophageal peristalsis is adequate
o pH monitoring
o Ba esophagography
- Management
o Lifestyle changes
 Head elevation 6-18 inches
 Do not lie down
 Bland diet / avoid over eating
 Avoid caffeine, alcohol, mint, chocolate
 Wt. control & smoking cessation
o Drug therapy
 Antacids PRN→ 1st line
 H2 blockers →1st line
 High dose of H2 blockers →2nd line
 Metochlopromide (anti-emetic) →2nd line
 CHON pump inhibitor (Lansoprazole) →2nd line
 Maintain CHON pump inhibitor or H2 blockers → 3rd line
 FUNDIPLICATION- surgery→ 4th line
 ANGELCHICK- anti- reflux prosthesis → 4th line (ring like around
gastroesophageal junction; makes LES competent, serves as weight

15
 ATOC 2009
DIGESTIVE SYSTEM
NCM 102
- Complications: esophageal stricture, ulceration of esophagus, aspiration,
presence of columnar epithelium associated with adenocarcinoma of
esophagus
- Nursing interventions and patient education
o Teach patient about prescribed meds and w/c meds to avoid
o Emphasize to the patient and family the food / activities to avoid (fatty
foods, onions, alcohol, smoking, straining, bending over, tight fitting
clothe, wt. lifting
o Sleep head elevated encourage wt. reduction if patient is overweight to
decrease intraabdominal pressure
NOTE: prostaglandin stimulates chief cells to secrete bicarbonate; take mefenamic on
a full stomach
BAYGON intoxication: administration activated charcoal (usually 2g, 100 mL saline);
has C to bind with acid, administered NGT
IV. Esophagitis: acute or chronic inflammation of esophagus
- causes
o GERD (most common) → if caused by GERD the disease aka reflux
esophagitis
o Infections (most commonly) candida, herpes simplex, cyclomegalovirus
(typically seen in immunocompromised people such as those with aids)
o Chemical injury by alkaline or acid solutions → usually seen in children or
in adults who attempt suicide
o Physical injury resulting from radiation txy or by nasogastric tubes may
also cause
- s/sx, management, NI → similar with GERD
ALTERATIONS IN STOMACH
PEPTIC ULCER DISEASE: refers to ulceration in mucosa or lower esophagus, stomach
/ duodenum
- causes
o helicobacter pyloric infection ( present in most PUD patients)
o ulcerogenic drugs like NSAIDS
o Zollinger- Ellison syndrome & other hypersecretory syndromes
(abnormal growth of tumor in GIT – secretes acid)
- Risk Factors
o Prolonged use of NSAIDS(steroids damages mucosal wall of stomach) /
corticosteroids/ smoking
o Stress, low socio economic status, alcohol, caffeine & family history
- s/sx
o gnawing, or burning epigastric pain, 1-3 hours after meal (can be
nocturnal)
o early satiety, anorexia, wt. loss, heart burn, belching (indicates reflux
o dizziness, syncope, hematemesis/ melena, anemia

Alert: sudden intense midepigastric pain radiating to right shoulder may

Indicate ulcer perforation
Gastric ulcer: (stomach): exacerbated by food
Duodenal ulcer: (duodenum): relieved by food
NOTE: gastric ulcer would give epigastric pain during meal as gastric acid
secreted / after meal as the alkaline duodenal contents reflux into the
stomach
NOTE: Sx of duodenal ulcer would manifest mostly before meal- when
Acid production, as stimulated by hunger is passed to duodenum
- Clinical manifestations
o gastric ulcer: wt. loss, burning sensation at left epigastric area food
aggravates pain, no pain HS, n/v
o duodenal ulcer: pain at HS, burning and cramping midepigastric pain,
pain of 2-4 hours pc, eating decrease pain, wt. gain, n/v
o stress/ drug induced: asymptomatic

16
 ATOC 2009
Helicobacter pylori- - - - DIGESTIVE
- - - - - - - - - - -SYSTEM
- -- - - - - - - - - - - - ulcerogenic drugs- - - - - - - - -- - - - - - -- - -
- - -- - - -- - - --related risk factors NCM 102
 (NSAIDS, Corticosteroid)
(socioeconomic, smoking, alcohol, family hx , stress)
colonization in the anthral mucosa 
 since these drugs inhibits prostaglandin  decrease prostaglandin
synthesis
failure of the immune system to clear infection despite of appearance 
of antibodies decrease secretion of
HCO3 w/c act as buffering mechanisms
 
defect in regulation of gastrin production in the stomach failure of buffer leads
to low pH gastric secretions; highly
 acidic gastric juice
increase gastric secretion   
because regardless of the gastrin in turn stimulates the production acid erodes mucosa
and causes ulcer
chyme reached pH of less of gastric acid to parietal cells 
than 1.5 gastric sec. will irritation of nerve
Diagnostics
- endings of GI wall
o Upper GI endoscopy with possible biopsy & cystology (most accurate)
continue 
o Upper GI radiographic exam (uses barium) appearance of s/sx
o Serial stool exam to detect occult blood
o Gastric secretion test and serology to test if (+) H. pylori antibodies
- Management
o Eliminate use of ulcerogenic drugs and cigarette smoking
o Well balanced diet → with meals at regular interval
- Medication
o Proton- pump inhibitor
o Metronidazole (antibiotc)
o Ranitidine
- Surgical management
o Vagotomy → removal of vagus nerve → to remove vagal stimulation
a. truncal/ total abdominal vagotomy → for recurrent ulcer and acid
reduction → completely severe vagal innervation to stomach at distal
part of the esophagus
b. selective vagotomy → recurrent ulcer and acid reduction → severe
vagus nerve and vagal innervation stomach (but retains abdominal
innervation); reduces acid production and impairs gastric motility
c. highly selective (parietal cells) → recurrent ulcer and acid reduction
→ severe only parietal cells branch of vagus and denervates acid
producing cells but preserves vagal nerves to gastric anthrum &
pylorus; no dumping syndrome
o Pyloroplasty → pyloric stricture / obstruction→ enlarges pylorus ,
eliminates obstruction; neutralizes w/o inhibiting gastric secretion;
increase gastric emptying
o Gastrectomy → removal of some parts of stomach
a. Billroth I (gastroduodenostomy) → gastric ulcers & pyloric
obstruction with Hge → resects anthrum, connects gastric remnants
to proximal duodenum destroys anthral and pyloric sphincter
functions, decrease gastric secretions, increase gastric emptying,
may result to bile reflux, steatorrhea, dumping syndrome , weight
loss, n/v, anemia
b. Billroth II (gastrojejunostomy )→ duodenal ulcer, prloric obstruction
& Hge → resects anthrum, attacks gastric remnant to proximal
jejunum
c. total gastrectomy (esophagojejunostomy) → ulcer disease,
perforation and gastric CA → resects stomach from LES to duodenal
bulb
d. Gastric resection antrectomy
- Complications

17
 ATOC 2009
DIGESTIVE SYSTEM
NCM 102
o GI bleeding (most common)
o Ulcer perforation (leads to perotinitis as gastric secretions goes to
peritoneum)
o Gastric outlet obstruction (since a lot of healed ulcers forms scars and so
serves as obstruction)
- Nursing intervention
o PQRST of pain
o Asses eating pattern and types of food / current meals
o Hx of illness
o Psychosocial hx
o PE (esp. abd)
o v/s (sp BP) → since bleeding may manifest orthostatic hypotension
- possible nursing diagnosis
o pain related to epigastric distress secondary to hypersecretion of acid /
mucosal erosion or perforation
o altered nutrition less than body requirement related to mucosal erosion
o knowledge deficit related to physical/ dietary / pharmacologic tx
o fluid volume deficit related to hemorrhage
- FVD prevention
o Monitor I/o, stool and vomitus
o Monitor Hgb / Hct? Electrolytes
o Administer IV fluids / blood as ordered
o Observe for increase pulse and decrease BP (signs of shock)
o Prepare for diagnostic procedure or surgery to determine or stop source
of bleeding
o Inset NGT as ordered & to monitor drainage for sign of bleeding
o Administer meds via NGT > to neutralize acid
o Preparation for lavage > cold/ ice lavage to constrict blood vessels &
thus, prevent further bleeding
- Pain relief
o Administer prescribed medicine (no OTC)
o Provide small frequent meal to precvent gastric distention if not on NPO
o Advise about the irritating effects of some food/ medications
- Client Education about treatment regimen
o Explain test and procedures to increase knowledge & cooperation to
decrease anxiety
o Allow to ask questions and clarify misunderstandings, review diet,
activity and medication, treatment
o Give listing of medications, dosage, time of administration & desired
effect to promote compliance
o Teach s/sx of bleeding & when to notify health care personnel provider
- Post gastric surgery education (sp. To prevent dumping syndrome ff. billroth
surgery)
o Advise to chew and eat slowly
o Instruct to drink ample amount of fluid after meals, not during meals
o Instruct to eat several small meals a day
o Follow a low CHO diet . since CHO are much difficult to digest
DUMPING SYNDROME: rapid gastric emptying where at lower end of intestine the
jejunum fills too quickly with
undigested food from stomach
a. early dumping: begins during/ right after meal; sx: n/v, feeling of bloatedness,
cramping, diarrhea, dizziness, fatigue
b. late dumping: happens 1- 3 hours after eating; sx: weakness, sweating, dizziness
- causes
o gastrectomty/ gastric bypass surgery/ billroth I & II
o esophagectomy from esophageal cancer (as diagnosis)
- clinical manifestation
o occurs 15 minutes after meals

18
 ATOC 2009
DIGESTIVE SYSTEM
NCM 102
o dizziness
o weakness
o diaphoresis
o epigastric fullness
o tachycardia (vagal stimulation)
o abdominal cramping
o self limiting
- management
o  CHO
o  fluids
o no fluids with meals only pc
o  salt > since it attracts water
o  high CHO food intake
GASTRITIS: diffused/ localized inflammation of gastric mucosa, it is the
common pathologic condition of the stomach
Two types of gastritis
a. acute gastritis: short term, inflammatory process: < 6 months :
b. chronic gastritis: long term, occurs for at least 6 months :
TYPE A > auto immune
TYPE B > H. Pylori
ACUTE GASTRITIS: ingestion of chemical agents & food products that irritates and
erode gastric mucosa; ingestion of
foods with food seasoning/ spices, alcohol, drugs (NSAIDS, ASA),
corrosive agents (kerosene,
insecticides, pesticides) or foods contaminated by bacteria such
as salmonella, staphylococci,
clostridium botulinum
---------------------------------------------------Presence of bacteria -----------------------------------
NOTE: do not lavage: if ingestion is more than 2 hours of corrosive agents
ingestion of irritating substance
PATHOPHYSIOLOGY:
l ↓
l
l surface contact with the gastric mucosa
l
salmonella, staphylococci, clostridium ↓
NSAIDS, ASA, spicy food, kerosene,
damage in mucosal layer
corrosive agents
------------------------------------------------------------------ ↓
↓ irritation/ exposure of nerve endings to gastric
acid
inflammatory response fever, diarrhea ↓
abdominal pain (epigastric)
CHRONIC GASTRITIS TYPE A: auto-immune in nature w/c involves all acid secreting
↓
gastric tissue particularly in the
n/v
fundus; circulating antibodies are produced w/c
attacks the parietal cells & eventually
causes pernicious anemia from loss of intrinsic
factor

Pathophysiology

19
 ATOC 2009
Antibodies attacks
DIGESTIVE SYSTEM parietal cells
NCM 102 
impairement of HCl and intrinsic factor
secretion → pernicious anemia


gastric irritants → atrophy of gastric glands and thinning of
mucosa low Hgb


damage of mucosa (inflammation)
fatigue
CHRONIC GASTRITIS TYPE B: associated with infection by H. Pylori w/c is currently believed to
be the direct cause of gastritis; it 
general manifestations
involves of inflammation
fundus and anthrum
: in functional damages mucosal protective mechanism and
leaves the mucosa vulnerable to side
effects of alcohol, smoking, gastric acid and alkaline reflux of
duodenum
Pathophysiology:
Infection (H. Pylori)

impairs normal mucosal layer

damage of mucosal layer
 --------------------------------------
gastric irritants
damage mucosa (inflammation)

- Nursing interventions
o Provides information to reduce anxiety especially in “E” cases--- suicide
o Promote nutrition if it will be on NPO, give ice chips then clear liquid the
solid ASAP or as sx have subside
o Maintain fluid balance – hydration either orally or IV
o Lifestyle modification – discourage alcohol, caffeine and smoking
o Administer sympathetic meds as ordered (analgesics, antacids,
antibiotics) to relieve pain and to decrease gastric acidity and treat
infection
o Teach effects of meds that irritates gastric mucosa
ALTERATION IN INTESTINES
APPENDICITIS: inflammation of the vermiform appendix; can affect many age group
but is most common in males 10-30
years old
- causes
o obstruction of intestinal lumen from infunctional
o stricture
o fecal mass
o foreign body
o tumor
- s/sx:
o generalized/ localized abdominal pain in the epigastric and pre-umbilical
areas & upper right abdomen w/in 2-12 hours then the pain localizes in
the right lower quadrant and of increase intensity
o anorexia, moderate malaise, mild fever, n/v
o usually constipation occurs, occasionally diarrhea
o (+) BRUMBERG’s sign: rebound tenderness, involuntary guarding and
generalized abdominal rigidity
- Diagnostics:
o CBC: increase WBC (leukocytosis)
o Urinalysis; to rule out urinary disorder
o Abdominal x-ray may visualize shadow consistent with fecalith
o Abdominal UTI and CT scan

20
 ATOC 2009
DIGESTIVE SYSTEM
NCM 102

Obstruction (infunctional)

Inflammatory response (fever,malaise, leukocytosis) stricture, fecal mass,
foreign body or tumor
 
edema and ischemia of appendix

development of intraluminal tension -----generalized/
localized abd. Pain & rebound tenderness

necrosis & perforation ----- peritonitis

pain localized in RLQ of increasing intensity

sudden relief of pain may indicate rupture of appendix thus, results to peritonitis

PERITONITIS: aka hot belly; inflammation of peritoneum usually due to rupture of a

gastric secreting/ containing organ of
GIT
- s/sx:
o pain over area
o presence of a disease condition
o rebound tenderness
o abdominal distention
o abdominal rigidity (board like abdomen d/t gas perforation)
o fever
o anorexia
o n/v
o increase pulse & BP
o decrease bowel sound
o dehydration (d/t bypassed colon)
- risk factors:
o perforation
o trauma
o ulcer
o appendix
o diverticulum or out pouching
- diagnostics
o CBC
o X-ray
o Paracenthesis or extraction of peritoneal fluid
o Hx taking
- Treatment
o identify & treat the underlying cause
o antibiotics
o admin. IV fluids
o decrease abdominal distention (by introducing continuous negative
pressure)
- nursing care
o maintain fluid and electrolyte balance and decrease GI distention: NG
suction, administer PNSS or LR , give K+ supplement for care for it may

21
 ATOC 2009
DIGESTIVE SYSTEM
NCM 102
induce heart attack, assess peristalsis / bowel sounds, monitor I/O and
look for s/sx of dehydration
o decreases infection process: antibiotics, monitor v/s, semifowlers
o prevent complications of immobility such as muscle wasting & bed sore
- management: surgical > appendectomy
o simple appendectomy or laparascopic appendectomy → in (-) of
rupture / peritonitis
o an incisional drain may be placed in an abscess or rupture occurs
 preoperatively : maintain bed rest , NPO status, IV hydration,
possible antibiotic, prophylaxis, analgesia
- complications
o perforation (most common)
o abscess formation
o peritonitis
- nursing assessment
o obtain history for location & extent of pain
o auscultate bowel sounds : absent/ hypoactive
o palpate “Mcburney’s point” → between umbilicus& right iliac crest, if
rebound tenderness
o assess Psoas sign : lie flat on bed, apply pressure on knee resist the
pressure and raise right , if there is pain and (+) for rebound tenderness
→ + Psoas
o assess Obturator sign: supine position with lateral hips, lower hip flex,
flex knee then rotate internally; if (+) pain = (+) obturator; if (-) = can
rotate internally
- possible nursing diagnosis
o alteration in comfort: pain related to inflamed appendix
o risk for infection related to perforation of intestinal lumen
- intervention with patient education
o monitor pain level: PQRST
o assist in comfortable position, such as semifowler’s and knees up
o restrict activities that may aggravate pain such as cough and ambulation
o apply ice bag to abdomen for discomfort
o give analgesics only as ordered after dx is determined
o avoid indiscriminate palpation of abdomen to avoid discomfort
o instruct to avoid heavy lifting for 4-6 weeks post-surgery → risk for
evisceration
o instruct to report sx of anorexia, n/v, fever, abdominal pain , incisional
redness and post-op drainage

INTESTINAL OBSTRUCTION: interruption of normal flow of intestinal contents along

intestinal tract; may occur is small/
large intestine, maybe complete/ incomplete, mechanical/
paralytic, may/ may not
compromise blood supply
- types and causes
o mechanical obstruction: physical blocks passage intestinal content w/o
disturbing blood supply
A. extrinsic: adhesion from surgery, hernia, masse, volvulus
B. intrinsic: fecal impaction, tumor, intussusception, stricture, stenosis,
congenital atresia (imperforate anus), inflammatory disease (Chron’s
disease)
C. intraluminal: foreign body(usually seen in children orally), fecal or Ba
2+
impaction, gallstones
o non- mechanical
A. paralytic ileus: (adynamic/ neurogenic) peristalsis is ineffective or
diminished motor activity perhaps because toxic/ traumatic

22
 ATOC 2009
DIGESTIVE SYSTEM
NCM 102
disturbances of ANS; (-) physical obstruction and (-) interrupted blood
supply; disappearance after 2-3 days→ causes: major trauma of spinal
cord/ vertebra, post-op abdominal/ GI surgery peritonitis/ sepsis,
electrolyte imbalance particularly hypokalemia
B. Mesenteric vascular infarction (compromised blood flow, resulting from
extensive athenosclerotic mesenteric arteries/ mesenteric thrombosis
creating ischemia to bowel) and strangulation ( prolonged mechanical
obstruction)
- Volvulus → twisting of bowel upon itself, usually at least 2 full 180 degrees,
obstructing the intestinal lumen both proximal / distal, maybe partial /
complete commonly occurs in sigmoid colon, common in very young/ very
old→ pathogomonic sign: Bird’s beak or edematous intestine; increase
concentration of solutes : attracts water (counter- clockwise twist)
- invagination/ intussusception → bowel segment containing mass propelled by
peristalsis onto the adjacent bowel segment (if preceeding segment has a
weak muscle)
- PATHOPHYSIOLOGY OF COMMON INTESTINAL OBSTRUCTION
A. Hernia: protrusion of intestine through a weak abdominal muscle or
through inguinal ring
B. Intussusception: telescoping of part of intestine into another, usually
case strangulation of blood supply , more common in infants than in
adults (10-15 months)
C. Volvulus: twisting of intestine with occlusion of blood supply, must
frequent in middle age and elderly men
D. Diverticulosis: inflamed saccular herniation (diverticuli) of mucosa. Most
common in individual older than 60 years old
E. Tumor: tumor growth into intestinal lumen adenocarcinoma of colon;
rectum is the most common tumoral obstruction , common in individual
60 years old and above
F. Paralytic ileus: loss of peristaltic motor active in the intestine , associated
with abdominal surgery, peritonitis, hypokalemia, ischemic bowel, spinal
trauma
> s/sx: abdominal pain (colicky), minimal diffuse tenderness, abdominal
distention, n/v (maybe persistent), tachycardia, decrease BP, body weakness,
increase WBC, fever, dOB (tachypnea, dilated intestine compressing thorax)
- Dx exams
A. abdominal and chest x-rays (PFA> plain film of the abdomen): may show
presence & location of small / large intestinal obstruction, “bird beak”
lesion in colonic volvulus, foreign body visualization
B. contrats studies (using barium): barium enema may diagnose colon
obstruction or intussusception, ileus be identified by oral barium
C. laboratory test: may show decrease Na, potassium, chloride level due to
vomiting, increase WBC count with necrosis, strangulation, peritonitis
D. endoscopic studies or protoscopy: direct visualization on a narrowed
intestinal lumen
- management: Non-surgical
o correction of fluid and electrolyte imbalances with NS/ LR w/ KCl (as
required)
o NG suction to decompress bowel
o Treatment of shock and peritonitis
o TPN (maybe necessary for CHON deficiency from chronic obstruction >
eg: paralytic ileus)
o Analgesics and sedatives, avoiding opiates d/t GI motility
o Antibiotics
- B. Surgical
o Consist of relieving obstruction
o Closed bowel procedure : lysis of adhesion, reduction of volvulus,
intussusception & incarcerated hernia
o Enterotany: for removal of foreign bodies

23
 ATOC 2009
DIGESTIVE SYSTEM
NCM 102
o Resection of bowel obstructing lesions/ strangulated lesions/
strangulated bowel with end to end anastomisis
o Temporary ostomy
- Complication???
o Dehydration due to loss of water , sodium and chloride
o Peritonitis
o Shock
o Death d/t shock
- Nursing intervention???
A. achieving relief of pain
o administer prescribed analgesics
o provide diversional activities
o provide supportive care during NG insertion to assist with discomfort
B. maintaining fluid and electrolyte balance
o monitor input and output, vital signs → a drop in BP may indicate
blood loss
o monitor serum electrolyte levels , blood cell count, and refer
abnormal results
o administer IV fluids and parenteral nutrition as ordered
C. maintaining normal bowel elimination
o collect stool samples to test for occult blood as ordered
o maintain adequate fluid balance
o record amount and consistency of stool
o maintain NGT to decompress as ordered
D. maintain proper lung ventilation
o keep in fowler’s position to promote ventilation and lung expansion
o monitor ABG for oxygenation level as ordered
o administer oxygen as ordered
- Complication
a. obstruction: typically occurs with strictures / adhesions which narrows
the lumen , blocking passage of intestinal contents
b. fistulae can develop between 2 loops of bowel, between bowel and
bladder , between vagina and bowel between bowel and skin
c. malnutrition and cancer
d. abscess are walled off collections of infunctional and can occur in the
abdomen or in perianal area in chron’s disease
- treatment
a. treat acute disease and maintain remission → involves use of medicines
to treat any infunctional and to reduce inflammation, usually involves
use of amino salycylate anti-inflammatory drugs and coticosteroids ; may
include antibiotics
b. surgery → resection and anastomosis → may require for complications
such as obstruction , abscess or if the dose does not responds to drugs
w/in a reasonable time
c. diet and lifestyle change → stress management techniques (eg: decrease
residue diet which may reduce volume of stool / day ; lactose intolerance
patient must avoid lactose containing foods)
- interventions:
o assess frequency and characteristics of stools to evaluate volume losses
and effectiveness of therapy
o have the patient describe location, severity and onset of abdominal
cramping / pain
o ask about wt. loss and anorexia ( weigh patient daily to monitor wt
changes)
o have patient describe the food eaten to elicit dietary exacerbation
o determine if patient smokes, including the duration and amount

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NCM 102
o ask about family history of gastrointestinal disease
- nursing diagnosis
o altered nutrition less than body requirement related to pain and nausea
o FVD related to diarrhea or vomiting
o Pain related inflammatory disease of small intestine

HIRSCHPRUNG’S DISEASE
- a congenital disorder of nervous and gastro intestinal system
- a condition wherein the autonomic ganglia in the smooth muscle wall of the
colon is not present
- takes place between the 5th and 12th week of pregnancy
- s/sx:
o poor or absent peristalsis→ hypoactive or absent bowel sounds
o constipation/ accumulation of feces→ abdominal distention
o dilatation of colon, intermittent vomiting and diarrhea
o small and increase frequency of stools → ribbon like stools (because of
accumulation of feces)
- it occurs in 1 out 5000 live births and it is males than in females
- children with down syndrome have a higher risk to acquire the disorder
- diagnostics
o abdominal x-ray → shows lack of stool in large intestine or near the anus
o lower GI series (barium enema) → shows areas of dilatation or
obstructions
o biopsy of rectum → (or large intestines) take a sample of the cells from
anus or large intestine
- management or treatment
o bowel resection → done within the first few months of life
o colostomy → can be temporary or permanent (opening of the colon)
o enemas are given until lumen is clear
o stool softeners are prescribed for life
- patient education and health maintenance

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o explain the rational of NG suction, NPO status and IV fluids ; advise to
progress of diet slowly as tolerated once home
o advise plenty of rest and slow progression of activities as directed by the
physician and other health care provider
o teach wound care if indicated
o encourage to ff up as directed and to notify surgeon for increasing
abdominal pain, vomiting or fever
CHRON’S DISEASE (aka regional enteritis)

- chronic, episodic inflammatory condition of GI tract

- characterized by transmural infunctional (affecting entire walll of involved
bowel) and skin lesions (areas of inflammation with areas of normal lining in
between)
- etiology: idiopathic
A. genetic and environmental factors have been invoked in the
pathogenesis of the disease
B. environmental factors
1. diet increase in sweet, fatty and refined foods
2. smoking
3. oral contraceptives
4. bacteria found in colon such as mycobacterium avium subspecies
paratuberculosis
- s/sx
o GI symptoms
 abdominal pain: crampy and may be relieved by defection; often
accompanied by diarrhea which may be bloody; often in the lower right
area,
 frequent BM – more than 20 bowel movement / day in severe cases
 bloody bowel movement: typically intermittent and may be bright /
dark in color
 (+) flatus and bloating
 n/v
 Rectal bleeding,
 weight loss,
o arthritis,
o skin problems,
o fever
- diagnostic procedures
o Blood tests may be done to check for anemia, which could indicate
bleeding in the intestines. Blood tests may also uncover a high white
blood cell count, which is a sign of inflammation somewhere in the body.
By testing a stool sample, the doctor can tell if there is bleeding or
infection in the intestines.

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o upper GI series to look at the small intestine. For this test, the person
drinks barium, a chalky solution that coats the lining of the small
intestine, before x rays are taken. The barium shows up white on x-ray
film, revealing inflammation or other abnormalities in the intestine.
o x rays of both the upper and lower digestive tract may be necessary to
see how much of the GI tract is affected by the disease.
o sigmoidoscopy or a colonoscopy. For both of these tests, the doctor
inserts a long, flexible, lighted tube linked to a computer and TV monitor
into the anus. A sigmoidoscopy allows the doctor to examine the lining of
the lower part of the large intestine, while a colonoscopy allows the
doctor to examine the lining of the entire large intestine. The doctor will
be able to see any inflammation or bleeding during either of these
exams, although a colonoscopy is usually a better test because the
doctor can see the entire large intestine.
o biopsy, which involves taking a sample of tissue from the lining of the
intestine to view with a microscope
- complication
o fistula
o malabsorption
o arthritis,
o skin problems,
o inflammation in the eyes or mouth, kidney stones, gallstones, or other
diseases of the liver and biliary system
- treatment
o drugs,
o nutrition supplements,
o surgery,
o or a combination of these options
Drug Therapy
o Anti-Inflammation Drugs. Most people are first treated with drugs
containing mesalamine, a substance that helps control inflammation.
Sulfasalazine is the most commonly used of these drugs. Patients who do
not benefit from it or who cannot tolerate it may be put on other
mesalamine-containing drugs, generally known as 5-ASA agents, such as
Asacol, Dipentum, or Pentasa. Possible side effects of mesalamine-
containing drugs include nausea, vomiting, heartburn, diarrhea, and
headache.
o Cortisone or Steroids. Cortisone drugs and steroids—called
corticosteriods—provide very effective results. Prednisone is a common
generic name of one of the drugs in this group of medications. In the
beginning, when the disease it at its worst, prednisone is usually
prescribed in a large dose. The dosage is then lowered once symptoms
have been controlled. These drugs can cause serious side effects,
including greater susceptibility to infection.
o Immune System Suppressors. Drugs that suppress the immune
system are also used to treat Crohn’s disease. Most commonly
prescribed are 6-mercaptopurine or a related drug, azathioprine.
Immunosuppressive agents work by blocking the immune reaction that
contributes to inflammation. These drugs may cause side effects like
nausea, vomiting, and diarrhea and may lower a person’s resistance to
infection. When patients are treated with a combination of
corticosteroids and immunosuppressive drugs, the dose of
corticosteroids may eventually be lowered. Some studies suggest that
immunosuppressive drugs may enhance the effectiveness of
corticosteroids.
o Infliximab (Remicade). This drug is the first of a group of medications
that blocks the body’s inflammation response. The U.S. Food and Drug
Administration approved the drug for the treatment of moderate to
severe Crohn’s disease that does not respond to standard therapies

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(mesalamine substances, corticosteroids, immunosuppressive agents)
and for the treatment of open, draining fistulas. Infliximab, the first
treatment approved specifically for Crohn’s disease is a TNF substance.
Additional research will need to be done in order to fully understand the
range of treatments Remicade may offer to help people with Crohn’s
disease.
o Antibiotics. Antibiotics are used to treat bacterial overgrowth in the
small intestine caused by stricture, fistulas, or prior surgery. For this
common problem, the doctor may prescribe one or more of the following
antibiotics: ampicillin, sulfonamide, cephalosporin, tetracycline, or
metronidazole.
o Anti-Diarrheal and Fluid Replacements. Diarrhea and crampy
abdominal pain are often relieved when the inflammation subsides, but
additional medication may also be necessary. Several antidiarrheal
agents could be used, including diphenoxylate, loperamide, and codeine.
Patients who are dehydrated because of diarrhea will be treated with
fluids and electrolytes.

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