The document covers the gastrointestinal (GI) system, detailing its structure, functions, and common disorders, including upper and lower GI problems, as well as liver and pancreatic disorders. It emphasizes assessment techniques such as health history, physical examination, diagnostic tests, and outlines conditions such as peptic ulcer disease and cirrhosis along with their causes, pathophysiology, and clinical manifestations. It concludes by discussing medical management and collaborative care for patients with GI disorders.

1. GASTROINTESTINAL DISORDERS
For Level one
Midwifery and MHN

2. Organ systems
• Includes:
– Mouth, pharynx & esophagus
– Stomach
– Small intestine
– Large intestine
• Accessory digestive organs:
teeth, tongue, gall bladder,
salivary glands, liver &
pancreas

3. FUNCTIONS OF THE DIGESTIVE
SYSTEM
Overall, the digestive system performs six basic
processes:
1. Ingestion. This process involves taking foods and
liquids into the mouth (eating).
2. Secretion. Release of water acids, buffers, enzymes &
salts by epithelium of GI tract and glandular organs
3. Mixing and propulsion. Alternating contractions and
relaxations of smooth muscle in the walls of the GI
tract mix food and secretions and propel them toward
the anus. This capability of the GI tract to mix and
move material along its length is called motility.

4. FUNCTIONS OF THE DIGESTIVE
SYSTEM
4. Digestion. Mechanical and chemical processes break
down ingested food into small molecules.
In mechanical digestion the teeth cut and grind food
before it is swallowed, and then smooth muscles of
the stomach and small intestine churn the food.
In chemical digestion: the large carbohydrate, lipid,
protein, and nucleic acid molecules in food are split
into smaller molecules by hydrolysis.
• A few substances in food can be absorbed without
chemical digestion. These include vitamins, ions,
cholesterol, and water.

5. FUNCTIONS OF THE DIGESTIVE
SYSTEM
5. Absorption. Is the entrance of ingested and secreted
fluids, ions, and the products of digestion into the
epithelial cells lining the lumen of the GI tract is called
absorption. The absorbed substances pass into blood
or lymph and circulate to cells throughout the body.
6. Defecation /Elimination. Here the wastes, indigestible
substances, bacteria, cells sloughed from the lining of
the GI tract, and digested materials that were not
absorbed in their journey through the digestive tract
leave the body through the anus. The eliminated
material is termed feces.

6. GASTROINTESTINAL DISORDERS
Nutritional problems: Malnutrition and Obesity
Eating disorders: Anorexia nervosa, Bulimia nervosa
Upper GI problems: nausea and vomiting, oral inflammations and
infections(gingivitis, oral candidiasis, herpes simplex, stomatitis,
parotitis,…), oral cancer, esophageal disorders (gastroesophageal
reflux disease(GERD), hital hernia, esophageal cancer, esophageal
diverticula, esophageal strictures, achalasia, esophageal varices),
upper gastrointestinal bleeding, disorders of the stomach and
upper small intestine (gastritis, peptic ulcer disease, stomach
cancer, foodborne illness)

7. GASTROINTESTINAL DISORDERS
Lower gastrointestinal problems: diarrhea,
fecal incontinence, constipation, acute and
chronic abdominal pain, irritable bowel
syndrome (IBS) abdominal trauma,
inflammatory disorders (appendicitis,
gastroenteritis, IBS, intestinal obstruction,
polyps of large intestine, colorectal cancer),
diverticulosis and diverticulitis, hernia, celiac
disease, lactase deficiency, short bowel
syndrome, gastrointestinal tromal tumors)

8. GASTROINTESTINAL DISORDERS
Anorectal problems: hemorrhoids, anal fissure,
anorectal abscess, anal fistula, pilonidal sinus
Disorders of the liver: hepatitis, cirrhosis, liver
cancer
Disorders of the pancreas : acute and chronic
pancreatitis, pancreatic cancer.
Disorders of biliary tract: cholelithiasis and
cholecystitis, gallbladder cancer.

9. Assessment of the GI System-
Subjective data
A. Health History
history or existence of :
 abdominal pain, nausea and vomiting
 diarrhea , constipation, Intestinal Gas
 abdominal distention, jaundice, anemia
 Heartburn, dyspepsia
 changes in appetite
 hematemesis, food intolerance
 allergies , indigestions
 excessive gas, bloating,
 melena, hemorrhoids, rectal bleeding

10. Assessment….
B. Medications:
past and current use of medications
 OTC drugs
prescription drugs
herbal products and nutritional supplements
Drug allergies
C. Surgeries and other treatments
 information about hospitalizations for any
problems related to GI system

11. Common sites of referred abdominal pain

12. Assessment…Objective Data
A. INSPECTION
Lips – symmetry, color and size
observe for abnormalities : pallor or cyanosis, cracking,
ulcers, or fissures.
Tongue : color, fissures, deviation and lesions
Buccal Mucosa : color and lesions and distinctive breath odors
Teeth and gums : caries, loose teeth, abnormal shape and
position of the teeth, presence of swelling , bleeding,
discoloration.

13. Assessment….
Abdomen
 Skin changes ( color, texture, scars, striae, dilated
veins, rashes, and lesions.)
 umbilicus – location and contour
 contour – flat, rounded, distended.
 observable masses, hernias and other
masses.
 movement – observable peristalsis and
pulsation.

14. Assessment: Inspection (Skin changes)

15. Abdominopelvic Regions
• Epigastric
• Umbilical
• Hypogastric
• Right and left
hypochondriac
• Right and left lumbar
• Right and left iliac or
inguinal
Figure 1.11a

16. Organs of the Abdominopelvic
Regions
Right hypochondriac
region:
liver gallbladder
right kidney
hepatic flexure of colon
Epigastric region:
liver (left lobe) pylorus
duodenum omentum
transverse colon
the head and body of
pancreas
Left hypochondriac
region:
spleen stomach
splenic flexure of colon
pancreas (tail part )
left kidney
right lumbar region:
ascending colon
jejunum
right kidney
umbilical region:
duodenum jejunum
ileum
mesentery abdominal
aorta
lymph node omentum
left lumbar region:
descending colon
jejunum ileum
right iliac region:
cecum appendix
right ovary and tube
hypogastric region:
bladder womb ureter
left iliac region:
sigmoid colon
left ovary and tube

17. Abdominopelvic Quadrants
• Right upper (RUQ)
• Left upper (LUQ)
• Right lower (RLQ)
• Left lower (LLQ)

18. Assessment….
B. AUSCULTATION
done before percussion and palpation
 listening for increased or decreased
bowel sounds.
 diaphragm of the stethoscope –
bowel sounds are high pitched, occur
5-35x per minute.
 warm up stethoscope in the hands to
prevent abdominal muscle
contraction.
 listen for BS for 2-5 minutes. Absent
BS means no sounds for 5
minutes on each quadrant.

19. C. PERCUSSION
Purpose: Determine the presence of fluid,
distention, and masses.
Presence of air : tymphany,
fluid or masses : dull sounds

20. Assessment….
D.PALPATION is used
to detect muscle
guarding,
tenderness, and
masses.

21. Diagnostic Studies
A. Upper GI Series or Barrium Swallow
 X-ray study with fluoroscopy with contrast medium
 used to diagnose structural abnormalities of the esophagus,
stomach, and duodenal bulb
 NPO for 8-12 hours
 pt. will drink contrast medium
 give pt. laxatives and fluid to prevent contrast medium
impaction.
 the stool may be white up to 72 hours after the test
B. Small Bowel Series – same as upper GI series

22. Diagnostic tests
C. Lower GI or Barium Enema
 Fluoroscopic examination of the colon using contrast
medium w/c is administered rectally.
 administer laxatives and enemas the night before the
procedure
 clear liquid diet the night before.
 NPO for 8 hours before the procedure.
 cramping and urge to defecate may occur.
 explain that pt will be assuming various position in tilt
table.
 give laxatives, fluids to assist in expelling barium.

23. Diagnostic tests
C. Ultrasound
 noninvasive procedure uses high frequency sound waves
to visualize the solid organs.
 NPO 8-12 hours
D. CT-Scan
 non invasive radiologic examination that combines x-ray
machine and computer.
E. MRI
 non invasive procedure using radiofrequency waves and
magnetic field
 NPO for 6 hours
 C/I in pt with metal implants or who is pregnant

24. Diagnostic tests

26. PEPTIC ULCER DISEASES(PUD)
• PUD is a condition characterized by erosion of
the GI mucosa resulting from the digestive
action of HCl and pepsin.
• Any portion of GIT that comes into contact with
gastric secretions is susceptible to ulcer dvpt
including:
• Lower esophagus, stomach, duodenum and
margin of gastrojejunal anastomosis after surical
procedures

27. TYPES
According to the degree and duration of mucosal involvement:
Acute ulcers: superficial erosion and minimal inflammation.
It is of short duration and resolves quickly when the cause is
indentified and removed.
Chronic ulcers: is one of long duration, eroding through the
muscular wall with formation of fibrous tissue. It is more
common than acute ulcer
According to the location:
Gastric ulcers
Duodenal ulcers

29. Comparing Duodenal and Gastric
Ulcers
DUODENAL ULCER
GASTRIC ULCER

30. Causes and predisposing factors
• PUDs develop only in the presence of an acid environment.
• stress and anxiety
• Infection with the gram-negative bacteria H. pylori
• The ingestion of milk and caffeinated beverages, smoking, and
alcohol also may increase HCl secretion.
• chronic use of NSAIDs, alcohol ingestion, and excessive
smoking.
• people with blood type O are more susceptible to peptic ulcers
than are those with blood type A, B, or AB.
• Zollinger-Ellison syndrome (ZES)
• Familial tendency may be a significant predisposing factor

31. Breakdown of gastric mucosal barrier
Histamine
Acids, Bile salts, NSAIDs, alcohol, ischemia, H.Pylori
Acid back-diffusion into mucosa
Destruction of mucosal cells
Increased acid and
pepsin release
Vasodilation
Capillary permeability
ulceration
•Loss of plasma
protein into gastric
lumen
•Mucosal edema
•Further mucosal erosion
•Destruction of blood vessels
•bleeding

32. Clinical manifestation
• Pain is classic symptom: burning, aching hunger like
in epigastric region possibly radiating to back;
• Duodenal ulcers: pain relieved by eating
• Gastric ulcers: pain exacerbated by food
• 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

33. Complications of PUDs
3 major complications of chronic PUD
Hemorrhage
Perforation
Gastric outlet obstruction
• All are emergency situations and may require
surgical intervention

34. Diagnostic studies
• History and physical examination
• Upper GI endoscopy with biopsy
• H.P testing of breath, urine, blood, tissue
• Barium contast study for ulcer detection
• Laboratory tests: CBC, urinalysis, liver
enzymes studies, serum amylase
determination, and stool examination

35. MEDICAL MANAGEMENT
Medications
Lifestyle changes
Surgical intervention

36. MEDICAL MANAGEMENT
• PHARMACOLOGIC THERAPY:
a combination of antibiotics, proton pump
inhibitors, and bismuth salts that suppresses
or eradicates H. pylori
histamine2 (H2) receptor antagonists
 proton pump inhibitors

41. MEDICAL MANAGEMENT
LIFESTYLE CHANGES:
stress reduction and rest
smoking cessation
dietary modification
SURGICAL INTERVENTION:
intractable ulcers (those that fail to heal
after 12 to 16 weeks of medical treatment)
life-threatening hemorrhage
Perforation
Obstruction
ZES not responding to medications

42. Collaborative care
Acute exacerbation without complication Acute exacerbation with
complication( hemorrhage,
perforation , obstruction)
•NPO
•NG suction
•Adequate rest
•IV fluid replacement
•Drug therapy:
•H2-receptor blockers ( cimetidine,
famotidine,nizatidine, ranitidine)
•Proton pump inhibitors (omeprazole, dexlansoprazole,
esomeprazole, lansoprazole, pantoprazole,rabeprazole)
•Antacids (aluminium hydroxide, aluminium carbonate,
calcium carbonate,…)
•Antibiotic for H.pylori
•Cytoprotective drugs
•Anticholinergics
•sedatives
•Stress management
•Dietary modifications
•NPO
•NG suction
•Bed rest
•IV fluid replacement (lacted
Ringer’s solution)
•Blood transfusions
•Stomach lavage
•Surgical therapy

43. Nursing care plan
• See on nursing care plan of patient with PUD

44. CIRRHOSIS
• Cirrhosis is a chronic progressive disease of the liver
• Characterized by extensive degeneration and
destruction of the liver parenchymal cells
• The liver cells attempt to regenerate but the
regenerative process is disorganized, resulting in
abnormal blood vessel and bile duct architecture.
• The overgrowth of new and fibrous connective tissue
distorts the liver’s normal lobular structure, resulting
in lobules of irregular size and shape with impeded
blood flow.

45. CIRRHOSIS
• Irregular, disorganized regeneration, poor
cellular nutrition and hypoxia caused by
inadequate blood flow and scar tissue result in
decreased functioning of the liver.
• Cirrhosis is twice as common in men as in
women

46. TYPES OF CIRRHOSIS
There are three types of cirrhosis or scarring of the liver:
 Alcoholic cirrhosis, in which the scar tissue characteristically
surrounds the portal areas.
• This is most frequently due to chronic alcoholism and is the most
common type of cirrhosis.
 Postnecrotic cirrhosis, in which there are broad bands of scar
tissue as a late result of a previous bout of acute viral hepatitis.
 Biliary cirrhosis, in which scarring occurs in the liver around the bile
ducts.
• This type usually is the result of chronic biliary obstruction and
infection (cholangitis); it is much less common than the other two
types.

47. Causes, & Risk Factors
• Cirrhosis is caused by chronic liver disease.
• Common causes of chronic liver disease include:
• Chronic Hepatitis C and chronic hepatitis B
• Long-term alcohol abuse
Other causes of cirrhosis include:
• Autoimmune inflammation of the liver
• Disorders of the drainage system of the liver (the biliary system), such as
primary biliary cirrhosis and primary sclerosing cholangitis
• Medications
• Metabolic disorders of iron and copper (hemochromatosis and Wilson’s
disease)
• Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis
(NASH)

48. Pathophysiology
• Primary event is injury to hepatocellular elements
• Initiates inflammatory response with cytokine release
• Destruction of hepatocytes, bile duct cells, vascular endothelial
cells
• Repair thru cellular proliferation and regeneration
• Formation of fibrous scar
• Prevents normal flow of nutrients to hepatocytes and
increases vascular resistance
• Initially, fibrosis may be reversible if inciting events are
removed
• With sustained injury, process of fibrosis becomes irreversible
and leads to cirrhosis

49. Pathophysiology
Major functional losses in person with cirrhosis
include:
Decreased removal and conjugation of bilirubin
Reduced production of bile
Impaired digestion and absorption of nutrients,
particularly fats and fat-soluble vitamins
Decreased production of blood clotting
factors(prothrombin, fibrinogen) and plasma protein
(albumin)

50. Pathophysiology
Impaired glucose/glycogen metabolism
Inadequate storage of iron and vitamin B12
Decreased inactivation of hormones, such as
aldosterone and estrogen
Decreased removal of toxic substances such
as ammonia and drugs

51. Pathophysiology
The second group of effects is related to obstruction of
the bile ducts and blood flow by fibrous tissue as
follows:
Reduction of the amount of bile entering the intestine,
impairing digestion and absorption
Back up of bile in the liver, leading to obstructive
jaundice with elevated conjugated and unconjugated
bilirubin levels in the blood
Blockage of the blood flow through the liver leading to
high pressure in the portal veins, or portal hypertension

52. Pathophysiology
Congestion in the spleen (splenomegaly),
increasing hemolysis
Congestion in intestinal walls and stomach,
impairing digestion and absorption
Development of esophageal varices
Development of ascites, an accumulation of
fluid in the peritoneal cavity that cause
abdominal distention and pressure

53. • Clinical manifestations include intermittent jaundice and
• fever. Initially the liver is enlarged, hard, and irregular,
but eventually it atrophies.
• Symptoms may develop gradually, or there may be no
symptoms.
• When symptoms do occur, they can include:
Gastrointestinal
• Nausea and vomiting
• Anorexia
• Pale or clay-colored stools
• Pyrosis, dyspepsia
Symptoms & Signs

54. • Gastrointestinal:
• Weight loss/malnutrition
• Constipation
• Flatulence
• Vomiting blood or blood in stools
• Gastritis, hemorrhoidal varices
• Abdominal indigestion or pain
• Esophageal and gastric varices
• Caput medusa (superficial abdominal veins)
Symptoms & Signs Cont’d

55. Integumentary (Skin)
• Small, red spider-like blood vessels on the skin
• Edema
• Ecchymosis
• Propensity for bleeding
• Yellow color in the skin, mucus membranes, or eyes
(jaundice)
• Palmar erythema
• Loss of body hair
Symptoms & SignsCont’d

56. Neurological:
• Fatigue
• Hepatic encephalopathy
• Asterixis
• Peripheral neuropathy
Symptoms & Signs Cont’d

57. • Reproductive:
• Testicular atrophy
• Erectile dysfunction
• Menstrual irregularities
• Gynecomastia
• Hematologic:
• Coagulation disorders: Nosebleeds or bleeding gums
• Anemia, splenomegaly
• Trombocytopenia, leukopenia
Symptoms & Signs Cont’d

58. Symptoms & Signs
Metabolic:
• Hypokalemia
• Hyponatremia
• Hypoalbuminemia
Cardiovascular :
• Fluid retention
• Peripheral edema
• ascites

59. Complications of cirrhosis
Portal hypertension and esophageal and
gastric varices
Peripheral edema and ascites
Hepatic encephalopathy
Hepatorenal syndrome

60. Collaborative management
Health promotion:
Common risk factors for cirrhosis include
alcohol, malnutrition, hepatitis, biliary
obstruction, obesity and right sided heart
failure
Prevention and early treatment of cirrhosis
must focus on reducing or eliminating these
risk factors.

61. Collaborative management
• Rest
• Administration of B-complex vitamins
• Avoid alcohol
• Minimize or avoid aspirin, acetaminophen and NSAIDS
• Vitamin K: correction of clotting abnormalities
• Ascites: low sodium diet, diuretics, paracentesis if
indicated, peritoneovenous shunt if indicated
• Esophageal and gastric varices: drugs (octreotide,
vasopressin,nitroglycerin, B-adrenergic blockers
(propranolol, …)) and surgery
• Hepatic encephalopathy: antibiotics, lactulose

62. PERITONITIS
 Peritonitis is inflammation of the peritoneum ,
the serous membrane lining the abdominal
cavity and covering the viscera.
 Causes:
1) Bacterial infection such as E.coli, Proteus,
Pseudomonas.
2) External sources such as injury or trauma .
3) Inflammation that extends from an organ
outside the peritoneal area such as the kidney.

63. PERITONITIS
Other common causes of peritonitis are
appendicitis ,perforated ulcer ,diverticulitis and
bowel perforation .
Peritonitis may also be associated with
abdominal surgical procedures and peritoneal
dialysis.

64. PATHOPHYSIOLOGY
• Primary peritonitis occurs when blood-borne
organisms enter the peritoneal cavity.
• Primary (blood-borne organisms, genital tract
organisms, cirrhosis with ascites)
• Secondary peritonitis is much more common.
• It occurs when abdominal organs perforate or
rupture and release their contents (bile,
enzymes, and bacteria) into the peritoneal cavity

65. PATHOPHYSIOLOGY
Peritonitis is caused by leakage of contents
from abdominal organs into the abdominal
cavity, usually as a result of inflammation,
infection, ischemia, trauma, or tumor
perforation.
Edema of the tissues results, and exudation
of fluid develops in a short time.

66. PATHOPHYSIOLOGY
Fluid in the peritoneal cavity becomes turbid
with increasing amounts of protein, white
blood cells, cellular debris, and blood.
The immediate response of the intestinal tract
is hypermotility, soon followed by paralytic
ileus with an accumulation of air and fluid in
the bowel.

67. Clinical Manifestations
Symptoms depend on the location and extent
of the inflammation.
The pain tends to become constant, localized,
and more intense near the site of the
inflammation. Movement usually aggravates it
The affected area of the abdomen becomes
extremely tender and distended, and the
muscles become rigid.

68. Clinical Manifestations
Rebound tenderness and paralytic ileus may
be present.
Nausea and vomiting
Peristalsis is diminished.
The temperature and pulse rate increase.
Elevation of the leukocyte count.
Tachypnea ( shallow respiration because deep
respiration and slight mvt cause pain

69. Assessment and Diagnostic Findings
The leukocyte count is elevated
The hemoglobin and hematocrit levels may be
low if blood loss has occurred
Serum electrolyte studies may reveal altered
levels of potassium, sodium, and chloride.
An abdominal x-ray is obtained, and findings
may show air and fluid levels as well as
distended bowel loops.

70. Assessment and Diagnostic Findings
A CT scan of the abdomen may show abscess
and ascites formation.
Peritoneal aspiration and culture and
sensitivity studies of the aspirated fluid may
reveal infection and identify the causative
organisms.

71. Complications
Hypovolemic shock.
Sepsis
Intraabdominal abscess formation
Paralytic ileus
Acute respiratory distress syndrome
Peritonitis can be fatal if treatment is delayed

72. Complications
Postoperative complications are wound
evisceration and abscess formation.
The sudden occurrence of serosanguineous
wound drainage strongly suggests wound
dehiscence.

73. Medical Management
NPO
Fluid, and electrolyte replacement.
Hypovolemia occurs because massive
amounts of fluid and electrolytes move from
the intestinal lumen into the peritoneal cavity
and deplete the fluid in the vascular space.
Analgesics, Antiemetics are prescribed
NG suction assist in relieving abdominal
distention and in promoting intestinal function.

74. Medical Management
Oxygen therapy by nasal cannula or mask can promote
adequate oxygenation.
Massive antibiotic therapy is usually initiated early in
the treatment of peritonitis.
Preparation for surgery
Surgery:
Post operative management: NPO, NGT, semi-Fowler’s
position, blood transfusion as needed, ATBs, parenteral
nutrition as needed and sedatives and opioids and Fluid,
and electrolyte replacement

75. Nursing Management
IV line is inserted to replace vascular fluids lost to the
peritoneal cavity and as an access for antibiotic therapy.
Monitor the pt for pain and response to analgesic
therapy.
Knees flexed position to increase comfort.
Sedatives may be given to allay anxiety
Accurate monitoring of fluid intake and out put and
electrolyte status is necessary to determine replacement
therapy.

76. Nursing Management
Antiemetic may be administered to decrease nausea and
vomiting and prevent further fluid and electrolyte losses.
Pt is placed on NPO status and may need an NG tube to
decrease gastric distension and further leakage of bowel
contents into peritoneum.
The nurse must prepare the patient for emergency surgery
Low-flow oxygen may be needed.
Post operative care if a surgical operation has been done.

77. COMPULSORY READINGS
• Liver function tests
• Esophageal Varices, Hernia, Esophageal CA,
• Gastro Esophageal Reflux Disease (GERD), Gastritis,
• Pyloric Stenosis
• Pancreatitis, Hepatobiliary Disorders,
• Conditions of Malabsorption, Intestinal
Obstruction, Ulcerative Colitis, Crohn’s Disease,
Appendicitis, Colon Cancer, Hemorrhoids

78. Exercise
• Mr. T.C, age 25 visited the emergency department
complaining a severe abdominal pain, anorexia,
nausea and vomiting since one day. On assessment
the BP:
90/55mmhg,HR:110bpm,RR:26bpm,To
:38.8o
C,GCS:1
5/15,weight:60 kg, height:165cm.on auscultation
the bowel sound is present, on palpation, the
physician reveals rebound tenderness in LRQ of the
abdomen at McBurney’s point, CBC: elevated WBC
count,

79. Exercise
• Make the differential medical diagnosis for Mr.
T.C.
• Among the proposed differential medical
diagnosis, which may be a working medical
diagnosis? what assessment findings do you
base on to confirm the working medical
diagnosis?
• According to the priority needs of Mr T.C, Make
a nursing care plan for him