Gastrointestinal Disorders

PN 4

Changes through the lifespan

• Relatively immature at birth

• Teeth at 6-7 months

• Peristalsis slows to allow formed stool at 8 months

• Stomach acidity increases at 1-5 yrs

• Bowel control

• Stomach capacity increases; weight issues at 6-12 years

Lifespan

• Stomach capacity, increased acidity and peristalsis adult like at 13-19 years

• Stomach capacity 2000 to 3000 age 20-45• Obesity common• Caloric needs decrease age 46-64• Stress = ulcers or reflux• Increase gallbladder problems• Taste buds begin atrophy = loss of sweet• Liver begins to decrease size

Lifespan

• Age 65+ mucosa atrophies and secretions decrease

• Gag reflex weakens• Dental disease• Decrease hydrochloric acid and other

enzymes• Decrease of absorption of vitamins and

nutrients• Decreased motility, and nerve impulses

Alimentary Canal

Begins at Pharynx; Ends at Anus

GI Track

Continuous structure beginning with the oral cavity terminating with the anal sphincter

Carries out activities of:• ingestion, • movement or passage of food, • digestion, • absorption and • removal of waste (defecation)

Assessment

• Family

Meds

• Travel

Diet

• Smoking

• Pain “1- 10”Other

It begins with the mouth

• Lips, tongue, cheeks, teeth, taste buds and salivary glands prepare food for eventual absorption.

• Saliva contains mostly H2O; enzymes and electrolytes = 1000 to 1500 mL/day

What can go wrong?

• Stomatitis (primary and secondary)

• Leukoplakia and Erythroplakia

• Cancer

• Acute and Post irradiation Sialadenitis;

• Dental problems

• Facial fractures

• Lack of taste or smell

Pharynx

• Better known as the throat

• Beginning of the esophagus

• Tongue and saliva make ball of food called a bolus

• When you swallow the bolus bounces off the epiglottis and is diverted from the larynx and falls into the esophagus

Esophagus

• Two sphincters UES and LES

• 24 cm long

• Peristalsis moves bolus into

stomach

Esophagus

– Essential role in the ingestions of food and liquids

– Disorders can be inflammatory, mechanical or cancerous

– Esophageal disorders may mimic those of a variety of other illnesses because of its proximity to neighboring organs

What can go wrong?

• GERD

• Hiatal Hernia (sliding and rolling)

• Achalasia

• Cancer

• Diverticula

• Varicies

Gastric Reflux Disease (GERD)

Backward flow of GI contents = exposure of esophagus to gastric/duodenal contents = inflammatory changes of esophageal mucosa

Reflux esophagitis Pathophysiology

Incompetent lower esophageal sphincter (LES) Irritation due to refluxate Abnormal esophageal clearance Delayed gastric emptying

Gastric Reflux Disease-Clinical Manifestations

Dyspepsia (heartburn) Regurgitation Hypersalivation Dysphagia/odynophagia Other

Diagnostic Tests

• Barium swallow

• Upper endoscopy

• 24-hour ambulatory pH monitoring

• Esophageal manometry

Gastric Reflux Disease-Interventions

Nonsurgical (conservative) management Diet therapy Client education Lifestyle changes Drug therapy

1. Antacids

2. Histamine receptor antagonists

3. Other drugs

• Surgical management

Hiatus Hernia

Hiatal Hernia (Diaphragmatic Hernias)

Protrusion of stomach through esophageal hiatus into the thorax Asymptomatic or S/S similar to GERD Sliding hernia

Most common Esophageal reflux and complications

Rolling hernia Slow bleeding resulting from venous obstruction Iron deficiency anemia

Hiatal Hernia-Interventions

Nonsurgical management Similar to GERD Client education

1. HOB 8 to 12 inches

2. Remain several hours after eating

3. Avoid straining or excessive vigorous exercise

4. Refrain from wearing tight constrictive clothing

Surgical management

Stomach

• Few diseases affect stomach

• Those that do can be serious

• Pear-shaped; hollow; can distend

• Parts include: cardiac, fundus, body, antrum and pylorus

• Interior composed of rugae; glands that secrete gastric juice

• Food and gastric juice = chyme

What can go wrong?

• Most common include: gastritis; peptic ulcer; Zollenger-Ellison syndrome and Cancer

Gastritis

• Inflammation of the gastric mucosa

• Erosive or non erosive

• Acute or chronic

• Auto digestion of the stomach

• Chronic associated with risk of gastric cancer

Prevention

• Avoid increased amts of alcohol and smoking

• Caution when taking ASA, NSAID’s, corticosteroids

• Avoid excess caffeine • Avoid contaminated foods• Workplace hazards such as lead and

nickel• Seek medical help for Sx

Stress Ulcers

• Result from a “stress” situation

• Multiple and superficial

• May be asymptomatic until massive, painless gastric bleeding occurs

• What would you see in your client?

Peptic Ulcer Disease

• Common; caused by acid-protective barrier imbalance

• Associated with NSAID drugs and Helicobacter pylori (H pylori) infection

• Gastric and duodenal

Gastric Ulcers

• Usually solitary and small

• Caused by ingested substances; H pylori and chronic bile reflux

• Bleeding may occur

• Pre-malignant so follow up needed

• Diagnosed with ba swallow; endoscopy; bx

• Sx include epigastric pain

Peptic Ulcer Disease

Gastric Deep and penetrating Occur on lesser curvature of stomach

Duodenal 95% occur in first portion of duodenum Deep, sharply demarcated lesions Penetrate through mucosa and submucosa into

muscle layer 95% to 100% due to H. pylori infection

Stress ulcers

Duodenal Ulcer• Usually in the pyloric region

• Type O blood type (genetic)?

• H pylori; alcoholic; hyperparathyroid; COPD; renal failure; chronic pancreatitis

• “pain-food-relief” pattern

Signs and Syptoms

Epigastric tenderness With perforation

Rigid, board-like abdomen Rebound tenderness Hyperactive bowel sounds, that may diminish

Dyspepsia (indigestion) Melena Gastric ulcer pain/vomiting S/S fluid volume deficit

Associated Nsg Diagnosis

Acute pain Risk for deficient fluid volume Ineffective therapeutic regimen management Ineffective coping Imbalanced nutrition Disturbed sleep pattern Risk for injury

Complications

Hemorrhage Most serious complication Most common in older adults with gastric ulcers

Perforation Pyloric obstruction Intractable disease

Pharmacological treatment

Hyposecretory drugs Antisecretory agents H2-receptor antagonists

Prostaglandin analogs Antacids Mucosal barrier fortifiers

Gastric Cancer

• Survival rate poor; greater if diagnosed early

• Etiology factors: ulcers, nitrates in food, type A blood,

• Early metastasis to lymph nodes in region• Dx with biopsy• S & S: loss of apetite; wt loss; abd pain;

vomiting; change in bowel habits; anemia; blood in stool; massive hemorrhage.

Dumping Syndrome

Constellation of vasomotor symptoms after eating caused by: Rapid emptying of gastric contents into small intestines Fluid shift into gut Abdominal distension

Early symptoms occur within 30 minutes of eating Late dumping syndrome 90 minutes to 3 hours

after eating Managed by dietary measures

Moving to the Small BowelConditions of the small bowel

Small & Large Bowel

• Cancer• Polyps• Diverticulitis• Colitis• Irritable Bowel• Hemorrhoids• Obstruction• Hernia

Parasites

Malabsorption & Maldigestion

• Most nutrient absorption occurs in small intestine

• Malabsorption refers to inadequate mucosal absorption of ingested water and nutrients;

• Maldigestion refers to inability to absorb foodstuff because it has not been broken down properly

Celiac or Gluten Intolerance

• Gluten proteins have antigenic properties• Frequent foul smelling stools with a fatty or

greasy appearance• Wt loss; malabsorption of vitamins • Muscle wasting• Diet that removes barley; wheat; rye and

oats = less malabsorption• Usually diagnosed in children who fail to

thrive

Inflammatory: Enteritis

• Caused by bacteria; virus; parasites or allergic reaction

• Usually returns to normal when precipitator is removed

• Vomiting and/or diarrhea

Inflammatory Bowel (Crohn’s)

• Idiopathic, chronic, inflammatory disease

• Affects any segment of the GI tract; most common terminal ileum or colon;

• S & S vary; Diarrhea dominant; fever and RLQ pain

• Stress and personality factors

• Wt loss, occult blood, N & V, fistulas and peritonitis

Moving to the Large BowelProblems with the Colon

Paralytic ileus

• Functional obstruction of bowel (S or L)

• Lack of proulsive peristalsis; absence of bowel sounds and distention

• Causes: anesthesia; peritonitis; appendicitis; interruption of nerve supply; abd injury or surgical manipulation; intestinal ischemia and electrolyte imbalance (which one?)

Colorectal Cancer

Colorectal Cancer

Most prevalent in patients over the age of 50 70% occur in the right side of the proximal colon Liver is the most frequent site of metastasis Complications

Obstruction/perforation Peritonitis Abscess formation Fistula formation to bladder/vagina

Etiology

Genetic predisposition Personal factors

Age Polyps

Dietary factors Decreased bowel transit time High-fat diet Chemical mutagens Refined carbohydrates

Inflammatory bowel disease

Signs and Symptoms

Rectal bleeding Anemia Changes in stool Symptoms of obstruction Gas pains, cramping, incomplete evacuation Hematochezia Straining to pass stools/narrowing of stools Mass lower right quadrant Changes in bowel sounds

Nursing Diagnosis

Pain Disturbed body image Compromised family coping Imbalanced nutrition Fear Powerlessness Alteration in bowel elimination

Colostomy sites

Bowel Obstruction

Signs and Syptoms

Midabdominal pain or cramping Vomiting: bile/mucus Obstipation/diarrhea Colicky abdominal pain Alternations in bowel patterns Abdominal distention/peristaltic waves Borborygmi Decreased to absent bowel sounds Abdominal tenderness

Intestinal Obstruction

• When blockage occurs, gas and air cause distention proximal to obstruction

• Secretions begin to pool = more distention

• Bowel wall edema = 3rd spacing

• Decrease blood supply = infarction, ischemia, necrosis, perforation, peritinitis.

• Hypovolemic shock, septic shock, very ill

Other Conditions

• Hernia’s

• Megacolon

• Diverticular Disease

• Ulcerative Colitis (different to crohn’s)

• Hemorrhoids

• Polyps

Irritable Bowel

Liver, Pancreas and Gallbladder

Liver: Cirrhosis

Chronic, progressive Irreversible reaction to hepatic

inflammation/necrosis Alteration in vascular system/lymphatic bile duct

channels Types:

Laënnec's or alcoholic Postnecrotic Biliary Cardiac

Complications of cirrhosis

Portal hypertension Ascites Bleeding esophageal varices Coagulation defects Jaundice Portal-systemic encephalopathy (PSE) with hepatic

coma Hepatorenal syndrome

Signs and Symptoms

Early signs Generalized weakness Weight loss GI symptoms Abdominal pain/liver tenderness

Late signs GI bleeding Jaundice Ascites Spontaneous bruising

Hepatitis

Widespread inflammation of liver cells Most common viral hepatitis Five major categories of viruses

Enteral forms1. Hepatitis A and E

2. Transmitted by fecal-oral route

Parenteral forms1. Hepatitis B, C, D

2. Transmitted through venous blood/sexual contact

Acute or chronic

Etiology

Hepatitis viruses Drugs, chemicals, toxins Blood transfusion reactions Hyperthyroidism Ingestion of ethyl alcohol (ETOH) Wilson's disease Other viruses: Epstein-Barr, cytomegalovirus,

yellow fever

Disorders of the GB

Cholecystitis Acute

1. Inflammation of gallbladder

2. Gallstones/bacterial invasion via lymphatic or vascular routes

Chronic1. Repeated bouts of acute cholecystitis

2. Gallstones usually present

3. Pancreatitis/cholangitis

Cholelithiasis Cancer of gallbladder

Gall Stones

Biliary Lithotripsy

Disorders of the Pancreas

Acute Inflammatory process of the pancreas Premature activation of pancreatic enzymes Destruction of ductal tissue/pancreatic cells Autodigestion/fibrosis of pancreas Pathophysiologic processes

1. Lipolysis2. Proteolysis3. Necrosis of blood vessels4. Inflammation

Theories of enzyme activation Chronic

Acute Pancreatitis

Abdominal pain Midepigastric/left upper quadrant Radiates/intense, continuous Affected by position

Generalized jaundice Gray-blue discoloration of abdomen/periumbilical area

(Cullen's sign) Gray-blue discoloration of flanks (Turner's sign) Decreased bowel sounds/paralytic ileus Tenderness, rigidity/guarding Palpable mass Elevated temperature/tachycardia/ B/P

Chronic Pancreatitis

Progressive, destructive Remissions/exacerbations Inflammation/fibrosis Repeated episodes of alcohol-induced acute

pancreatitis Types of chronic:

Calcifying pancreatitis (CCP) (alcohol-induced) Obstructive pancreatitis