GASTROINTESTINAL

SYSTEM

REVIEW OF ANATOMY AND

PHYSIOLOGY
STRUCTURES OF THE G.I. SYSTEM
1.
MOUTH (BUCCAL MUCOSA)
2.
ESOPHAGUS
3.
STOMACH
4.
SMALL INTESTINE
5.
LARGE INTESTINE
6.
VERMIFORM APPENDIX
7.
LIVER
8.
GALLBLADDER
9.
PANCREAS

REVIEW OF ANATOMY AND

PHYSIOLOGY
FUNCTION OF THE G.I. SYSTEM
1.
DIGESTION- break down
2.
ABSORPTION-transport
3.
METABOLISM
4.
ELIMINATION

Function of G I system
4

1.
2.
3.

1.
2.
3.
4.

Chewing & Swallowing

1.5 L of saliva are secreted daily
Ptyalin salivary amylase starch digestion
Saliva lubricate food as it chewed &
swallowed
Gastric function
Hydrochloric acid to destruct most ingest
bacteria ,& break down food
Pepsin for initiation of protein digestion
Intrinsic factors
The food mixed with gastric secretions is
called chyme
Husni Rousan

A & P of GI system

GI tract

Hollow muscular tube, lumen surrounded

by 4 tissue layers:

Mucosa- innermost, thin layer of smooth

muscle and exocrine cells
Submucosa- connective tissue
Muscularis- smooth muscle
Serosa- outermost, connective tissue

GI tract

Function:

Secretion- secretes HCL acid, digestive

enzymes
Digestion- mechanical and chemical, food is
broken down to chyme
Absorption- from GI tract to blood supply
Motility
Elimination

Division of Alimentary Canal

Upper : mouth, pharynx, esophagus,
stomach, duodenum(1st half)
2.
Middle(2nd half) duodenum, jejunum,
ileum, ascending colon (2nd half)
3.
Lower: (2nd half) ascending colon,
transverse colon, descending
colon,sigmoid colon and rectum: anal
sphincters
4.
Accessory organs: salivary glands, liver,
gall bladder, and pancreas
ABDOMINAL CAVITY: Peritoneum
1.

DIGESTION
2.

Types:
a. Mechanical digestion: all movements of
alimentary tract that:
a) Change physical state of foods
b) Propel food along the alimentary tract
1) Deglutination: swallowing
2) Peristalsis: wavelike movements that
squeeze food downward in the tract
3) Sequential contractions: movements that
mix intestinal contents with digestive juices
b. Chemical digestion: series of hydrolytic
processes dependent on specific enzymes; an
additional substance may be necessary to act as
a catalyst to facilitate the process

ABSORPTION
1.

2.

3.

Passage of substances through the

intestinal mucosa into the blood or lymph
Accomplished mainly through the movement
of molecules against a concentration
gradient because of energy (ATP)
expenditure (active transport) by the
intestinal cells; makes it possible for both
water and solutes to move through the
intestinal mucosa in a direction opposite
that expected in osmosis and diffusion
Majority occurs in the small intestine; most
water is absorbed form the large intestine

METABOLISM
A.

B.

C.

DEFINITION: sum of all the chemical

reactions in the body
ANABOLISM: metabolic process in
which complex substances are broken
down into simple compounds
CATABOLISM: metabolic process in
which complex substances are broken
down into simple compounds; energy
is liberated for use in work, energy
storage, and heat production

GI tract

Nerve Supply

Intrinsic stimulation by myenteric plexus in

smooth muscle and submucosa plexus in
inner layer
Autonomic system- Parasympathetic
stimulation by vagus nerve, connects with
intrinsic system
Vagus-stimulates

motor and secretory activity

and relaxes spinchters

Sympathetic system- thoracic and lumbar

splanchnic nerves slows movement, inhibits
secretions and contracts spinchters

Mouth

Function:

Mastication, taste, begin movement

Glands produce 1 L of saliva/day
Saliva contains mucin and salivary amylase with
begins to break down CHO
Oral preparatory phase- food is softened, made into
a bolus and tongue moves to the back of the mouth
Oral phase- tongue presses bolus against hard
palate, elevates the larynx and forces the food bolus
to the pharynx, triggering swallowing
Pharyngeal phase- soft palate elevates and seals
nasal cavity, inhibits respirations and allows
esophagus to open
Esophageal phase- is when bolus enter at
cricopharyngeal juncture, peristalsis now takes food to
the stomach
All this takes about 10 seconds !

MOUTH (BUCCAL MUCOSA)

A.
B.
C.
D.

Lips and cheeks

Hard palate; soft palate
Gums (gingivae); teeth- 32 pcs
Tongue
1.
2.

E.

F.

Papillae: rough elevations on surface

Taste buds: receptors of CN VII and CN IX; located in
papillae

Tonsils: lymphatic tissue that produces

lymphocytes; defense against infection
Parotid glands
1.
2.

Parotid, submandibular, and sublingual

Produce saliva, a mixture of water, mucin, salts, and
the enzyme, salivary amylase (parotid glands:
Ptyalin-starch)

ESOPHAGUS
A.

B.

C.

D.

Posterior to the trachea; anterior to

the vertebral column
Extends from the pharynx through
an opening in the diaphragm
(hiatus) to the stomach
Collapsible muscular tube; about 25
cm (10 inches) long
Secretes mucus; facilitates
movement of food

Esophagus

Canal about 10 in long, passes through the center of

the diaphragm
Upper end is the upper esophageal sphincter, at rest
it is closed to prevent air from entering the
esophagus
Lower end is the lower esophageal sphincter, it sits
at the gastroesophageal junction, at rest it is closed
to prevent reflux of gastric contents, this is where
GERD occurs
Function- to propel food and fluids and prevent reflux
Mucous is secreted to move the food along
Cardiac sphincter of the stomach opens to allow the
food to enter

Stomach widest section of alimentary canal

J shaped structures
1. Anthrum
2. Pylorus
3. Fundus
Valves
1. cardiac sphincter
2. Pyloric sphincter

Stomach

Digestive and endocrine organ, in midline and

LUQ
Four regions:

Cardia- narrow part that is distal to the

gastroesophageal junction
Fundus- left above the GE junction
Body or corpus- largest area
Antrum- pylorus, is the distal portion and is separated
from the duodenum by the pyloric sphincter, prevents
backflow from the duodenum
Surface is covered in rugae or folds and have smooth
muscle for motility
Has intrinsic and extrinsic nerves

STOMACH
A.

B.

C.

D.

E.

F.

Size varies in different persons and

according to degree of distension
Elongated pouch, with greater curve forming
the lower left border(J shape, below liver)
Highly muscular, widest section aliementary
canal
In epigastric and left hypochondriac portions
of the abdominal cavity
Functions: food storage and liquefaction
(CHYME)
2-3 hrs average storage time, fatty foods: 34

Stomach

Function:

Parietal cells secrete HCL acid and intrinsic factor,

which absorbs B 12, without it, what anemia can occur?
Chief cells secrete Pepsinogenpepsin
Cephalic phase- sight, smell and taste of food,
regulated by vagus, begin secretory and contractile
activity
Gastric phase- G cells in the antrum secrete gastrin,
which causes HCL and pepsinogen to be released. HCL
changes pepsinogen to pepsin, which digest proteins.
Mucous and Bicarb are secreted to protect the stomach
wall
Intestinal phase- chyme produced empties into the
duodenum and causes distention, this produces secretin,
which stops the acid production and gastric motility !

3 MAJOR DIVISION
CARDIA
FUNDUS
CORPUS OR BODY
PYLORUS

STOMACH
E.

Divisions
1.

2.
3.
F.

Fundus: the uppermost portion; the

bulge adjacent to and extending above
the esophageal opening
Body: central portion
Pylorus: constricted lower portion

Sphincters
1.
2.

Cardiac: at opening of the esophagus

into the stomach
Pyloric: at opening of the pylorus into
the duodenum

STOMACH
G.

Secretes gastric juice

1.

2.
3.

4.

Stomach wall cells secrete gastrin

that stimulates the flow of gastric
juices
Chief cells secrete pepsin
Parietal cells secrete hydrochloric
acid and intrinsic factor(Vit. B12)
Goblet cells secret mucin

Function of the stomach

1.Mechanical
2.Chem
3.Storage of food
-CHO, CHON- stored 1 -2 hrs. Fats stored 2 3
hrs

Cells
1. Chief/ Zymogenic cells secrets
a.) Gastric amylase - digest CHO
b.) Gastric lipase digest fats
c.) Pepsin CHON
d.) Rennin digests milk products
2. Parietal / Argentaffin / oxyntic cells
Function:

a.) Produces intrinsic factor promotes reabsorption of vi

B12 cyanocobalamin promotes maturation of RBC
b.) Secrets Hcl acid aids in digestion
3. Endocrine cells - Secrets gastrin increase Hcl acid

Small Intestine

Longest portion of the GI tract, 16-19 ft.

Made up of 3 sections:

Duodenum- first 12 and is attached to the pylorus.

The CVD and pancreatic duct join to form the
ampulla of Vater and empty into the duodenum at
the duodenal papilla. This surrounded by a muscle,
called the Sphincter of Oddi
Jejunum- middle 8 ft portion
Ileum- last 8-12 ft. The ileocecal valve separates
the ileum form the cecum of the large intestine
Inner lining is made up of intestinal villi and folds of
mucosa and submucosa for digestion.

Small Intestine

3 main functions:

Movement- mixing and peristalsis

Moves

chyme by segmental contractions and mixes

with enzymes

Digestion- enzymes produced by the intestinal

cells make:
Enterokinase,

peptidases, lactase, maltase and

sucrase
Help to digest, CHO, proteins and lipids

Absorption- absorbs most of the nutrients from

food, takes 3-10 hours for the contents to pass
through

Major organ for absorption

Small intestine

Large Intestine

Function:

Movement- segmental contractions, to allow

time for the water and electrolytes to be
absorbed
Absorption- absorbs most of water and
electrolytes, reduces fluid volume of chyme
and creates a more solid mass for elimination
Elimination- 3-4 strong peristaltic contraction
/day triggered by colonic distention in proximal
large intestine to propel contents to rectum,
until urge to defecate.

VERMIFORM APPENDIX
A.

B.

Blind-end tube off the cecum just

beyond the ileocecal valve
Function: part of the immune
system

GALLBLADDER
A.

B.

C.

Lies on the undersurface of the

liver
Sac made of smooth muscle, lined
with mucosa arranged in rugae
Functions: concentrates and stores
bile

Liver
largest gland - Occupies most of right
hypochondriac region
Color: scarlet red
-Covered by a fibrous capsule Glissons
capsule
- Functional unit liver lobules

Function:
1.Produces bile
Bile emulsifies fats - Composed of H2O & bile
salts -Gives color to urine urobilin . Stool
stircobilin
2. Detoxifies drugs
3. Promotes synthesis of vit A, D, E, K - fat soluble
vitamins
-Hypevitaminosis vit D & K
-Vit A retinol Def Vit A night blindness
-Vit D cholecalciferon - Helps calcium Rickets,osteoarthritis

LIVER
A.

B.
C.

Occupies most of the right

hypochondrium and part of the
epigastrium
Divided into thousands of lobules
Ducts:
1.
2.
3.

Hepatic duct: from liver

Cystic duct: from gallbladder
Common bile duct: formed by the union
of the hepatic and cystic ducts; drains
bile into the duodenum at the sphincter
of Oddi

PANCREAS
A.

Structure
1.

2.

Fish-shaped, with body, head, and tail;

extends form the duodenal curve to the
spleen
Both a duct and a ductless gland
a.

b.

Pancreatic cells: secrete pancreatic juice via

a duct to the duodenum; enzymes include
tyrpsin, lipase, and amylase; stimulated by
the duodenal hormones secretin and
pancreozymin and parasympathetic impulses
Islets of Langerhans: clusters of cells not
connected with pancreatic ducts; composed
of alpha and beta cells

PANCREAS
B.

Functions
1.

2.

Pancreatic juice composed of

enzymes that help digest
carbohydrates, proteins, and fats
Islet cells constitute the endocrine
gland
a.

Alpha cells secrete the hormone

glucagon, which accelerates liver
glycogenolysis and initiates
gluconogenesis; tends to increase
blood glucose level

PANCREAS
b.

Beta cells secrete insulin, which exerts a

profound influence on the metabolism of
carbohydrates, proteins, and fats
1)

2)

Accelerates the active transport of glucose,

along with potassium and phosphate ions,
through cell membranes; decreases blood
glucose and increases glucose utilization by
the cells for either catabolism or anabolism
Inhibits liver cell phosphatase and therefore
inhibits liver glycogenolysis

Nursing Assessment

Family history- GI disorders, cancer

Personal history- what kinds of things?
Diet history- anorexia, dyspepsia- what is that?
What should you question them on for diet
history?
Health history- diarrhea, constipation, # and
color of stools, change in wt. or appetite
Abdominal pain

P- precipitating
Q-quality- how intense, severe, type
R-region or radiation
S- severity scale- 0-10
T-timing- when did it first occur, duration and frequency

PANCREAS
b.

Beta cells
3)

4)

5)

Stimulates the production of liver cell

glucokinase; promotes liver glycogenesis
which lowers blood glucose
Accelerates the rate amino acid transfer
into cells promoting anabolism of
proteins within the cells
Accelerates the rate of fatty acid
transfer into cells, promotes fat
anabolism (lipogenesis); inhibits fat
catabolism

DIETS

HIGH K : ABC VEG/FRUITSA

ASPARGUS APPLE
B BROCCOLI
BANANA
C CAROT
CANTALOUPE
Raisins, nuts

Clear liquid
Full liquid diet
Low fat,chole
Na restricted
Inc roughage,fiber
Inc protien

Assessment Abdomen

Instruct pt: empty bladder, supine position,

use warm hand and stetoscope
SEQUENCE: Inspection, Auscultation,
Percussion & Palpation(IAPP)
INSPECT: skin, umbilicus, contour, symmetry,
masses, pulsation and peristalsis
Auscultate: Bowel sounds: 5-34 /min,
borborygmi loud prolonged gurgles or
bruits(HPN)
Percussion: ascites
Palpate

Phenylketonuria

Deficiency of phenylalanine hydroxylase result to

dec. metabolism of amino acid phenylalanine
which can possibly leads to mental retardation
Newborn manifestations: DALS (diarrhea-anorexialethargy-anemia-skin rashes)
LAB test: Guthrie test greater than 8 mg/dl(24-48
hrs needed high protein diet before test)
Nsg Dx: Impaired growth & development
Nsg Alert: genetic counseling, restrict food high in
protein.
LOFENALAC meds prescribed

MAJOR DISORDERS OF THE G.I.

SYSTEM
CANCER OF THE
ORAL CAVITY
2.
GASTROESPHAGE
AL REFLUX (GERD)
3.
CANCER OF THE
ESOPHAGUS
4.
HIATAL HERNIA
5.
GASTRITIS
DUMPING SYNDROME
1.

6.

7.

8.

9.

10.

PEPTIC ULCER
DISEASE (PUD)
CANCER OF THE
STOMACH
CHOLELITHIASIS/
CHOLECYSTITIS
ACUTE
PANCREATITIS
CANCER OF THE
PANCREAS

NURSING CARE OF
PATIENTS WITH
ALTERATIONS IN THE GI
TRACT

MAJOR DISORDERS OF THE G.I.

SYSTEM
1.
2.

3.

4.
5.

6.

HEPATITIS
HEPATIC
CIRRHOSIS
CANCER OF THE
LIVER
APPENDICITIS
IBD REGIONAL
ENTERITIS
(CROHNS DISEASE
IBD ULCERATIVE
COLITIS

7.

8.

9.

10.
11.
12.

INTESTINAL
OBSTRUCTION
DIVERTICULAR
DISEASE
CANCER OF THE
SMALL INTESTINE,
COLON, OR
RECTUM
PERITONITIS
HEMORRHOIDS
HERNIAS

Disorders of the Jaw

51

Abnormal conditions affecting the

mandible (Jaw)& the tempomandibular
joint include congenital malformation,
fractures , chronic dislocation , cancer ,
& syndrome ch.ch pain & limited motion
Tempomandibular Disorders
Are a group of conditions that cause pain
&\or dysfunction of the tempomandibular
joint &/or the muscle of mastication, as
well as contiguous tissue components

Husni Rousan

Disorders of the Jaw

52

1.
2.

3.
4.
5.

Clinical Manifestations
Pain (from dull to throbbing )
Debilitating pain radiated to the ears,
teeth, neck muscle & facial sinuses
Restricted jaw motion & clicking
Difficulty chewing & swallowing
Depression may accompany

Husni Rousan

Disorders of the Jaw

53

1.

2.
3.
4.

Management
Patient education in stress
Management
Range of motion exercises
Pain Management (NSAID)
Muscle relaxant &/or mild
antidepressant

Husni Rousan

Parotitis
54

1.
2.
3.
4.

Inflammation of the parotid gland is the

most common inflammatory condition of
the salivary gland
Mumps (epidemic Parotitis) viral seen in
children

Clinical Manifestations
Fever & red shiny skin
The gland swells ,tense ,&tender
Pain felt in ear
Swollen gland interfere with swallowing
Husni Rousan

Parotitis
55

1.

2.
3.
4.
5.

Medical Management
Preventive Measures (dental care, oral
hygiene, adequate fluid& nutrition ,&
D/C of medication that may diminished
salivary secretion)
Antibiotics for infection
Analgesic for pain
Drainage of gland
Parotidectomy
Husni Rousan

56

Impaired Esophageal Motility

Achalasia

1.
2.
3.

4.

Achalasia: characterized by impaired

peristalsis of smooth muscle of
esophagus and impaired relaxation of
lower esophageal sphincter
Manifestations:
Dysphagia
chest pain (pyrosis)
Sensation of food stick in lower
esophagus
Food regurgitation
Husni Rousan

Achalasia
57

Treatment
1.
2.
3.

4.

5.

Eat slowly &drink fluids with meals

Calcium channel blockers
Endoscopically guided injection of
botulinum toxin
Balloon dilation of lower
esophageal sphincter or pneumatic
dilation
Esophageal myotomy (abdominal
or thoracic approach
Husni Rousan

58

Conditions of the
Upper GI Tract

GastroEsophageal Reflux Disease (G.E.R.D.)

Gastritis
Peptic Ulcer Disease (PUD)
Gastric CA

59

Gastroesophageal Reflux
Disease (GERD)
1. Definition
1.
GERD common, affecting 15 20%
of adults
2.
Because of location near other
organs symptoms may mimic other
illnesses including heart problems
3.
Gastroesophageal reflux is the
backward flow of gastric content
into the esophagus.
Husni Rousan

60

Gastroesophageal Reflux
Disease (GERD)
2.
Pathophysiology
a.
Gastroesophageal reflux results from
transient relaxation or incompetence of lower
esophageal sphincter, sphincter, or increased
pressure within stomach
b. Factors contributing to Gastroesophageal
reflux
1.Increased gastric volume (post meals)
2.Position pushing gastric contents close to
Gastroesophageal juncture (such as bending or
lying down)
3.Increased gastric pressure (obesity or
tight clothing)
4.Hiatal hernia
Husni Rousan

61

Gastroesophageal Reflux
Disease (GERD)
1.
2.
3.

4.
5.

Manifestations
Heartburn after meals, while
bending over, or recumbent
Dyspepsia or indigestion
May have regurgitation of sour
materials in mouth, pain with
swallowing
Atypical chest pain
Sore throat with hoarseness

Husni Rousan

62

Gastroesophageal Reflux
Disease (GERD)
6. Diagnostic Tests
a. Barium swallow (evaluation of
esophagus, stomach, small
intestine)
b. Upper endoscopy: direct
visualization; biopsies may be done
c. 24-hour ambulatory pH
monitoring
Husni Rousan

Gastroesophageal Reflux
Disease (GERD)

63
7.
Medications
a. Antacids for mild to moderate symptoms,
e.g. Maalox, Mylanta, Gaviscon
b. H2-receptor blockers: decrease acid
production; given BID or more often, e.g.
cimetidine, ranitidine, famotidine, nizatidine
c. Proton-pump inhibitors: reduce gastric
secretions, promote healing of esophageal
erosion and relieve symptoms, e.g.
omeprazole (prilosec); lansoprazole
d. Promotility agent: enhances esophageal
clearance and gastric emptying
Husni Rousan

64

Gastroesophageal Reflux
Disease (GERD)
Dietary and Lifestyle Management

a. Elimination of acid foods (tomatoes, spicy,

citrus foods, coffee)
b. Avoiding food which relax esophageal
sphincter or delay gastric emptying (fatty foods,
chocolate, alcohol)
c. Maintain ideal body weight
d. Eat small meals and stay upright 2 hours post
eating; no eating 3 hours prior to going to bed
e. Elevate head of bed on 6 8 blocks to
decrease reflux
f. No smoking
g. Avoiding bending and wear loose fitting
clothing
Husni Rousan

65

Gastroesophageal Reflux
Disease (GERD)
9. Surgery indicated for persons not
improved by diet and life style changes
a. Laparoscopic procedures to tighten
lower esophageal sphincter
b. Open surgical procedure: fundoplication
10. Nursing Care
a. Pain usually controlled by treatment
b. Assist client to institute home plan

Husni Rousan

Hiatal Hernia

Protrusion of stomach through the esophagus

Sliding or Rolling hernias
Symptoms are similar to GERD patient
Nonsurgical management is like GERD
Surgical:

Lap Nissen Fundoplication- reinforces the LES, wraps

a portion of the stomach around the distal esophagus
to anchor it
Post op- risk for bleeding, infection and respiratory
complications

Have an NGT, begin PO once BS return

Watch for gas-bloat syndrome and air swallowing

Hiatal Hernia
67

1. Definition
Part of stomach protrudes through the
esophageal hiatus of the diaphragm
into thoracic cavity

Types
1.
Sliding hiatal herni
2.
Paraesophageal hiatal hernia:
( hernia can become strangulated; client
may develop gastritis with bleeding)

Husni Rousan

Hiatal Hernia
68

1.
2.

1.
2.

3.

Manifestations: Similar to GERD

Diagnostic Tests
a.Barium swallow
b.
Upper endoscopy

Treatment

Similar to GERD: diet and lifestyle

changes, medications
If medical treatment is not effective or
hernia becomes incarcerated, then
surgery; usually
Fundoplication by thoracic or abdominal
approach
Husni Rousan

HIATAL HERNIA(Diaphragmatic
Hernia)
A portion of stomach is herniated through esophageal hiatus of

the diaphragm
Heart burn/pyrosis common complain
ETIOLOGY AND PATHOPHYSIOLOGY
Portion of the stomach protruding through hiatus (opening) in
the diaphragm into the thoracic cavity
May result from a congenital weakness of diaphragm or from
injury, pregnancy, obesity
Function of the cardiac sphincter is lost, gastric juices enter the
esophagus causing inflammation
Lab: Endoscopy reveals herniation
Nsg Alert: UPRIGHT position aftermeals
Avoid bending
small frequent feeding
avoid anticholinergic drug and coughing

Nursing Diagnosis: GERD

Impaired Nutrition: less than body

requirements

Acute Pain r/t irritation of the esophagus

What things can be done to improve their intake and

decrease pain?
What would be the expected outcomes?
How would you monitor their progress?
What interventions can be performed?

Risk for aspiration r/t reflux of gastric

contents

How can you determine that this does not occur?

75

Husni Rousan

76

Husni Rousan

Diverticulum
77

1.
2.
3.
4.
5.
6.

It is an outpouching of mucosa&
submucosa that protrudes through a
weak portion of the musculature

Clinical Manifestations

Difficulty of swallowing & neck fullness

Belching
Regurgitation of undigested food
Gargling noise after eating
Halitosis & sour taste in the mouth
May dysphagia & chest pain
Husni Rousan

Diverticulum
78

1.

2.

3.

Management
Diverticulectomy &myoectomy for
muscle
NPO until x-ray show no leakage at
surgical site
During O.P. avoid trauma to carotid
artery and jugular vein

Husni Rousan

UGI Bleeding
Gastric Erosions

NSAIDs

Stress:

Serious trauma

Extensive burns

Major surgery

Major illness (ICU)

Major neurological disease (CVA, tumor, trauma)

Alcohol abuse

UGI Bleeding
Malignancy

Malignant:

Esophageal cancer

Gastric cancer or lymphoma

Small intestinal lymphoma or cancer

Benign:

Leiomyoma

UGI Malignancy

Lower GI Bleeds
Four most common causes of LGI bleeds

vascular ectasias

colonic diverticuli

neoplasm

internal hemorrhoids

LGI bleeds - Other Causes

solitary rectal ulcer

syndrome (SRUS)
colonic varicies
mesenteric vascular
insufficiency
ischemic colitis
Meckels diverticulum
small intestinal
ulceration
intussusception

radiation-induced
injury
diversion colitis
mesenteric venous
thrombosis
small bowel diverticuli
Dieulafoy lesion
vasculitis
long-distance running
endometriosis

Acute Lower GI Bleeding

Initial management similar to acute

upper GI bleeding

Presentation: wide range of

presentation:

Mostly self-limiting bleeding that does

not require hospitalization

Rarely massive with hemorrhagic shock

Acute Lower GI Bleeding

Diverticulosis of the Colon

Common cause (25%)

Acute, painless, bright red, maroon or melena

(depending on site)

May compromise hemodynamics (elderly)

Diagnosis: per exclusion

Significant recurrence

Treatment: most subside spontaneously,

some need angiographic embolization or
surgery

Perforation
86

1.
2.
3.

May result from stab or bullet wounds

of the neck & the chest as well as from
accidental puncture by surgical
instrument

Clinical Manifestations
Persistent pain followed by dysphagia
Infection ,fever ,& leukocytosis
May sign of Pnuemothorax
Husni Rousan

Perforation
87

1.
2.
3.

4.

Management
Broad spectrum antibiotics
Nasogastric tube & suctioning
NPO total parenteral nutrition
gastrostomy
Closed the wound &post op
management

Husni Rousan

Gastritis
88

1. Definition: Inflammation of stomach

lining from irritation of gastric mucosa
(normally protected from gastric acid and
enzymes by mucosal barrier)
2. Types
a. Acute Gastritis
1.Disruption of mucosal barrier allowing
hydrochloric acid and pepsin to have
contact with gastric tissue: leads to
irritation, inflammation, superficial erosions
2.Gastric mucosa rapidly regenerates; selflimiting disorder
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Gastritis
89

Causes of acute gastritis

a. Irritants include aspirin and other
NSAIDS, corticosteroids, alcohol, caffeine

b.Ingestion of corrosive substances: alkali or

acid

c.food contamination (microorganisms)

Manifestations
headache, mild epigastric discomfort,
abdominal pain, nausea anorexia, vomiting
Belching, heart burn , &sour taste in mouth
If perforation occurs, signs of peritonitis

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90

Treatment
As a rule the patient recover in a day
NPO status to rest GI tract for 6 12 hours,
reintroduce clear liquids gradually and
progress; intravenous fluid and electrolytes
if indicated
b. antacids If gastritis from corrosive
substance: immediate dilution and removal
of substance by gastric lavage (washing out
stomach contents via nasogastric tube),
If extreme condition Gastrojejunostomy or
gastric resection
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Gastritis
91

1.
2.
3.
4.

Nursing Management
Reducing anxiety
Promoting optimal nutrition
Promoting fluid balance
Relieving pain
Chronic Gastritis
Progressive disorder beginning with
superficial inflammation and leads to
atrophy of gastric tissues (prolong Gastritis)
Husni Rousan

PEPTIC ULCER DISEASE (PUD)

excoriation / erosion of submucosa & mucosal lining
due to:
a.) Hypercecretion of acid pepsin
b.) Decrease resistance to mucosal barrier
Incidence Rate:
1. Men 40 55 yrs old
2. Aggressive persons

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Peptic Ulcer Disease

(PUD)
Definition and Risk factors
Break in mucous lining of GI tract comes
into contact with gastric juice , referred
to as gastric ,duodenal , or esophageal
ulcer
Duodenal ulcers: most common; affect
mostly males ages 30 55 ulcers found
near pyloris
Gastric ulcers:affect older persons(ages
55 70)
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Peptic Ulcer Disease

(PUD)
2.
Pathophysiology
a.
Ulcers or breaks in mucosa of GI tract
occur with
1.H. pylori infection (spread by oral to oral,
fecal-oral routes) damages gastric epithelial
cells reducing effectiveness of gastric mucus
2.Use of NSAIDS: interrupts prostaglandin
synthesis which maintains mucous barrier of
gastric mucosa
b. Chronic with spontaneous remissions and
exacerbations associated with trauma,
infection, physical or psychological stress
Husni Rousan

Peptic Ulcer (Duodenal vs

DUODENAL-proximal
GASTRIC antrum of
Gastric)
Inc Hcl level in stomach
stomach

s/s: Right epigastric pain 23hrs after meal

Lab: gastric analysis
Nsg Action:
Avoid spicy, caffeine,
alcohol and smoking
Maintain high carbs,fat and
low protein diet
Relieved by food(wt gain)
and relieved by vomiting
Pain hrs of sleep
Middle age grp(male)

Weak gastric mucosa

s/s: Left epigastric pain
30mins-1hr after meal
relieved by vomiting
Lab: Endoscopy: lesser
curvature of stomach
Nsg Action:
Avoid spicy, caffeine,
alcohol and smoking
Maintain high carbs,fat
and low protein diet
Aggravated by eating(wt
loss)

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Predisposing factors:
1. Hereditary
2. Emotional
3. Smoking vasoconstriction GIT ischemia
4. Alcoholism stimulates release of histamine = Parietal cell
release Hcl acid = ulceration
5. Caffeine tea, soda, chocolate
6. Irregular diet
7. Rapid eating
8. Ulcerogenic drugs NSAIDS, aspirin, steroids, indomethacin,
ibuprofen Indomethacin - S/E corneal cloudiness. Needs annual
eye check up.
9. Gastrin producing tumor or gastrinoma Zollinger Ellisons sign
10. Microbial invasion helicobacter pylori. Metromidazole
(Flagyl)

Types of ulcers Ascending to severity

1. Acute affects submucosal lining
2. Chronic affects underlying tissue
heals & forms a scar
According to location
1. Stress ulcer
2. Gastric ulcer
3. Duodenal ulcer most common

Stress ulcers common among eritically ill clients

2 types
1.Curings ulcer cause: trauma & birth
hypovolemia
GIT schemia
Decrease resistance of mucosal barriers to Hcl acid
Ulcerations

2.Cushings ulcer cause stroke/CVA/ head injury

Increase vagal stimulation
Hyperacidity
Ulcerations

GASTRIC ULCER DUODENAL ULCER

SITE
PAIN

HYPERSECRETION
VOMITING
HEMORRHAGE
WT
COMPLICATIONS
HIGH RISK

Intrum or lesser
curvature
-30 min 1 hr after
eating
- epigastrium
- gaseous & burning
- not usually relieved
by food & antacid

Duodenal bulb

Normal gastric acid

secretion
common

Increased gastric acid

secretion
Not common

hematemeis

Melena

Wt loss

Wt gain

a. stomach cause
b. hemorrhage

a. perforation

60 years old

20 years old

-2-3 hrs after eating

- mid epigastrium
- cramping & burning
- usually relieved by
food & antacid
- 12 MN 3am pain

Diagnosis:
1. Endoscopic exam
2. Stool from occult blood
3. Gastric analysis N gastric
Increase duodenal
4. GI series confirms presence of
ulceration

Nursing Mgt:
1. Diet bland, non irritating, non spicy
2. Avoid caffeine & milk/ milk products
- Increase gastric acid secretion
3. Administer meds

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

B. H2 receptor antagonist
Ex :
1. Ranitidine (Zantac)]
2. Cimetidine (Tagamet)
3. Tamotidine (Pepcid)
- Avoid smoking decrease
effectiveness of drug
**Administer antacid & H2 receptor antagonist
1hr apart
-Cimetidine decrease antacid absorption &

c. Cytoprotective agents
Ex :
1. Sucralfate (Carafate)
- Provides a paste like subs that coats mucosal
lining of stomach
2. Cytotec
d.) Sedatives/ Tranquilizers - Valium, lithium
e.)Anticholinergics
1. Atropine SO4
2. Prophantheline Bromide (Profanthene)
*Pt has history of hpn crisis With peptic ulcer disease.
Rn should not administer alka seltzer- has large amount

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

Nursing Mgt:
1. Monitor NGT output
- Immediately post op should be bright red
- Within 36- 42h output is yellow green
- After 42h output is dark red
2. Administer meds:
- Analgesic
- Antibiotic
- Antiemetics
3. Maintain patent IV line
4. VS, I&O & bowel sounds

Complications:
a. Hemorrhage hypovolemic shock
- Late signs anuria
b. Peritonitis
c. Paralytic ileus most feared
d. Hypokalemia
e. Thrombophlebitis
f. Pernicious anemia

Nursing mgt:
1. Avoid fluids in chilled solutions

2. Small frequent feeding s-6 equally divided

feedings

3. Diet decrease CHO, moderate fats & CHO

4. Flat on bed 15 -30 minutes after q feeding

Dumping syndrome
common complication
rapid gastric emptying of hypertonic food solutions
CHYME leading to hypovolemia.

S/Sx of Dumping syndrome:

1. Dizziness
2. Diaphoresis
3. Diarrhea
4. Palpitations

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Peptic Ulcer Disease

(PUD)

Manifestations
Pain is classic symptom: burning, aching
hunger like in epigastric region possibly
radiating to back; occurs when stomach is
empty and relieved by food (pain: food:
relief pattern)
Vomiting , nausea , constipation &diarrhea
Symptoms less clear in older adult; may
have poorly localized discomfort, dysphagia,
weight loss; presenting symptom may be
complication: GI hemorrhage or perforation
of stomach or duodenum
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115

Peptic Ulcer Disease

(PUD)

Treatment

1.
2.
3.
4.

Pharmacologic therapy
H2 receptor antagonist
Proton pump inhibitors
Cytoprotective agents
Antacid
Stress Reduction & Rest
Smoking Cessation
Dietary Modification
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116

Peptic Ulcer Disease

(PUD)

1.
2.

1.
2.
3.

Surgical Management
Vagotomy
Truncal
Selective
Pyloroplasty
Antrectomy
Gastroduodenostomy
Gastrojejunostomy
Subtotal gastroectomy with
anastomosis
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Post-op Care
117

Post-op concerns:
Dumping syndrome
Post Prandial hypoglycemia
bile reflux gastritis