DIGESTIVE SYSTEM

GI Tract Anatomy:
- Includes the structures from the mouth to the anus
- Composed of mucous membranes
- Composed of connective tissues that cause peristalsis to move food throughout the system
- Upper part:
o Acts as an intake source and receptacle through which food passes and in which initial digestive
processes take place
o Mouth
 Lips, tongue, teeth involved in mastication
 Tonsils are lymphoid tissue
o Salivary Glands
 Sublingual & Submaxillary
 Secrete water, salt, mucin, amylase
 Job is to break down carbohydrates & proteins
 Parotid
 Secrete water, salt, amylase
 Mumps
o Esophagus
 10-12 in. long, 1 in. in diameter
 Lined with stratified squamous epithelium,
 Only time spincter will relax is when you’re passing food, otherwise it’s always closed
o Stomach
 Very little digestion happens in the stomach
 Job is to mix & grind food into smaller pieces and mix food with digestive juices (pepsin, HCl)
 Breaks food down into chyme
 Usually holds 1-1.5 L
 Cardiac (just below sphincter), Fundus, Body, Pyloric region
 Mucosa, submucosa, muscularis
- Middle portion:
o Most digestive and absorptive processes occur in the small intestine
o Small Intestine = duodenum, jejunum, and ileum
 Duodenum – first 25 cm, surrounds the head of the pancreas (gets biliary drainage from liver &
pancreatic secretions), hepatic arteries supplies duodenum
 Jejunum – next 40%, supplied by superior mesenteric artery (right off aorta)
 Ileum – remaining length, supplied by superior mesenteric artery
o Different layers of mucosa
o Contains villi – important role in movement of bolus
 Villi movement causes neuronal stimulus to stimulate peristalsis
 Contains artery, vein, and lymph duct
o Vitamin B12 and bile salts are absorbed here
o Modulate fluid balance
o Goblet cells produce mucus
o Brush border enzymes help with digestion of carbohydrates, proteins, fats
- Lower segment:
o Serves as a storage channel for the efficient elimination of waste
 Water, digestible fiber, bilirubin, bile salts, unabsorbed nutrients, dead mucosal cells, bacteria
o Cecum, Colon (5 ft. total in length), Rectum (5-6 in.)
- Fourth part:
o Produces digestive secretions that help dismantle foods and regulate the use and storage of nutrients
o Accessory organs: salivary gland, liver, pancreas
 o Liver
 3 lbs. big organ
 75% of blood flows through liver through the portal vein, the rest is hepatic artery
 Lobules (each lobule is around the central vein)
 Capillaries in liver are lined with Kupffer cells (macrophages)
 Functions:
1. Synthesis – produce serum proteins (albumin, fibrinogen, prothrombin), enzymes,
lipoproteins, gluconeogenesis
2. Secretion – bile
3. Detoxification – hormones, drugs, dietary/general pollutants
o P450 system – different genetics help with metabolism of drugs
4. Storage – hold glycogen, lipids, vitamins, minerals, cholesterol

Functions of the Digestive System:

1. Production of enzymes and hormones
2. Storage and synthesis of vitamins
3. Dismantling and reassembling of food
4. Entrance of nutrients, vitamins, minerals, electrolytes, and water through the GI tract
5. Collection and elimination of wastes

Swallowing
- 3 Phases:
o Oral Phase
 The bolus is collected at the back of the mouth
 The tongue lifts the food upward until it touches the posterior wall of the pharynx
 Manifestations: pocketing of food in mouth; greater risk of pneumonia & aspirations
o Pharyngeal Phase
 The soft palate is pulled upward
 The palatopharyngeal folds are pulled together so that food does not enter the nasopharynx
 The vocal cords are pulled together
 The epiglottis covers the larynx
 Respiration is inhibited
 The bolus is moved backward into the esophagus by constrictive movements of the pharynx
 Manifestations: food comes out of nose, coughing
o Esophageal stage
 As food enters the esophagus and stretches its walls, local and CNS reflexes that initiate
peristalsis are triggered.
 Manifestations: food stuck in esophagus
- Mechanism:
o Depends on the coordinated action of the tongue and pharynx
o These structures are innervated by cranial nerves V, IX, X, and XII

Process of Digestion and Absorption of Nutrients

- Requires an intact and healthy GI tract epithelial lining that can resist the effects of its own digestive secretions
o Protection of the gastric mucosa
 Gastric mucosal barrier
 Impermeable epithelial cell surface covering
 Mechanisms for the selective transport of hydrogen and bicarbonate ions
 Characteristics of gastric mucus
 Water-insoluble mucus
 Forms a thin, stable gel that adheres to the gastric mucosal surface
 Provides protection from the proteolytic (protein-digesting) actions of pepsin
  Forms an unstirred layer that traps bicarbonate, forming an alkaline interface between
the luminal contents of the stomach and its mucosal surface
o GI wall structure
 Inner mucosal layer – lining epithelial tissue
 Cells produce mucus that lubricates & protects the inner surface of the alimentary canal
 Millions of indentations, or gastric pits
o Secrete bicarbonate – protect epithelium from HCl
 Neck & ECK mucosal cells
o At the pyloric, cardiac, fundic glands
o Secrete neutral mucous to protect areas from damage
 Parietal cells
o Line fundus
o Secrete HCl and intrinsic factor
 Lamina propria – submucosal connective tissue
 Blood vessels
 Neural innervations – enteric nervous system (mind/body); all the NTs in the brain are
also in the gut
 Structures responsible for secreting digestive enzymes
 Muscularis mucosae – smooth muscle cells
 Contract & change shape and surface area of the mucosal layer
 Facilitate movement of the contents of the GI tract, peristalsis
 Circular & longitudinal muscles
 Neuronal innervations
 Problem in this area cause Irritable Bowel Syndrome
 Peritoneum – Loosely attached to the outer wall of the intestine
- Involves movement of materials through the GI tract at a rate that facilitates absorption
o Different movements based on different NTs and receptors
o Movement is one way; retrograde movement results in disease
o ANS Modulation – always overrides enteric NS if need be
 Sympathetic – stops activity
 Parasympathetic – normal day to day activity
o Enteric Nervous System
 Myenteric and submucosal plexuses
 Mechanoreceptors
 IBS – make sure patients don’t get stress
o Cells of Cajal - generation of slow waves, movement of bolus through system
o Tonic movements
 Continuous movements that last for minutes or even hours
 Contractions occur at sphincters
 No periods of relaxation
o Rhythmic movements
 Intermittent contractions responsible for mixing and moving food along the digestive tract
 Peristaltic movements are rhythmic, propulsive movements
 Defined rest periods – no rest periods would result in depletion of NTs
- Requires the presence of enzymes for the digestion and absorption of nutrients
o Control of secretory function
 Local
 Acts as stimuli for neural & humoral mechanisms
 pH, osmolality, chyme – all plays an important role in disease
 Humoral
 Cholecystokinin
o Stimulates contraction of the gallbladder
 o Stimulates secretion of pancreatic enzymes
o Slows gastric emptying
 Secretin
o Stimulates secretion of bicarbonate-containing solution by pancreas & liver
 Gastrin
o Stimulates the secretion of gastric acid & pepsinogen
o Increase gastric blood flow
o Stimulate gastric smooth muscle contraction
o Stimulates growth of gastric, small intestine, and colon mucosa
o Without gastrin, protective mechanism of gut is lost  GI bleeds
 Neural influences
 Mediated through the ANS (increased with PSNS, inhibited with SNS)
o Enzymes Used in Digestion of Carbohydrates
 Lactase
 Sucrase
 Amylase
 Maltase
 Alpha-dextrinase
o Pancreatic Enzymes that Break Down Proteins
 Trypsin
 Chymotrypsin
 Carboxypeptidase
 Elastase

Control of Defecation
- Internal Sphincter
o Several cm long
o Circular thickening of smooth muscle that lies inside the anus
o Under reflexive control of the enteric NS
- External Sphincter
o Composed of striated voluntary muscle
o Surrounds the internal sphincter
o Controlled by nerve fibers in the pudendal nerve

Bacterial Flora
- Functions:
o Salvage energy – recycling area
o Retain absorbable nutrients
o Trophic effects on intestinal epithelial cells
o Protection against invasion by pathogenic organisms
- HCl protects the body from ingestion of pathogens
- Lining of liver with macrophages also protect gut
 DISORDERS OF THE DIGESTIVE SYSTEM

Common Symptoms of the GI Patient

- Anorexia
o Loss of appetite or lack of desire for food
o Hunger, smell, fear, depression, frustration, anxiety
o Can include N/V, diarrhea (i.e. chemo patients)
o Hypothalamic regulation
o Not a symptom limited to the GI tract
o Physiological stimuli is functional
o Causes:
 Drug effects
 Can be a result of slow gastro transit  feeling of fullness
 High stress cortisol levels
- Nausea
o Sensation resulting from stimulation of the medullary vomiting center that often precedes or
accompanies vomiting
o Caused by distention or irritation anywhere in the GI tract or stimulated by higher brain centers
- Vomiting
o Stimulation of the dorsal portion of the reticular formation of the medulla oblongata near the sensory
nuclei of the vagal (X) nerve
o Afferent impulses travel to the vomiting center as both vagal and sympathetic afferents
o Causes: excessive distention or irritation, chemical stimulation by emetics, hypoxia, pain, drugs, increase
in intrathoracic pressure
o Dry vomiting – retching; spasmodic GI/respiratory; nothing comes out
o Fecal vomiting – Smells or contents that looks like feces
o Pernicious vomiting – uncontrolled nonstop vomiting
o Vomiting of pregnancy – normally in the first trimester
o Projectile vomiting – no nausea, it just flies out at great forces
o Psychogenic vomiting – anxiety or emotional event
o Retention vomiting – when someone has GI obstruction, happens every time the patient eats
- N/V differentials
o Medications – oral antibiotics, strong analgesics, beta blockers
o Viral infections o Increased intracranial pressure
o Motion sickness, inner ear infection o Bulimia, anorexia
o Migraine headaches o Alcohol, drug abuse
o Pregnancy o Meningitis, cephalitis
o Food poisoning, allergies o Anesthesia
o Chemotherapy, radiation o Heart attacks
- Gastrointestinal Bleeding
o Hematemesis
 Blood in the vomitus
 Bright red (esophageal/stomach) or have coffee-grounds appearance (small/large intestine)
o Melena
 Blood in the stool
 Ranges in color from bright red (lower GI) to tarry black (upper GI)
 May be occult (hidden) – 1st diagnosis: Fe deficiency anemia
Alterations in Swallowing
o Dysphagia: difficulty swallowing
 Mechanical – obstruction
 Intrinsic obstruction – tumors, strictures, herniations
 Extrinsic obstruction – tumors
 Impaired motility – nerve problems
o Odynophagia: painful swallowing
o Achalasia: failure of esophageal sphincter to relax

Esophageal Diverticulum
- Food stops before it reaches the stomach
- Symptoms:
o Gurgling
o Belching
o Coughing
o Foul-smelling breath – rotting of food in esophagus

Gastroesophageal Reflex (GERD)

- Definition: Heartburn
o Backflow of esophageal or gastric contents without belching or vomiting
o 30-60 min after meal
o Evening onset
- Risk Factors: obesity, pregnancy, males, smoking, alcohol intake
- Negative relationship between H. pylori and GERD
- Causes:
o Weakness in esophageal sphincter, it’s partially closed
 Normally, the sphincter smooth muscle relaxes when a peristaltic wave delivers a bolus of food
to allow food to enter the stomach.
 Weakened sphincter can be a congenital defect or a result of damage to esophagus
o Hiatal hernias (protrusion of a part of the stomach through the opening in the diaphragm)
o Increased abdominal/stomach pressure
o Medications
o Lying down after a meal
- Manifestations:
o Dyspepsia - Pain in epigastric area that radiates to throat, shoulder, or back
 30-60 min after eating, during sleep, or when lying down
o Bleching or sour taste
o Fluid accumulating in throat area
o In elderly, strictures are developed  damage of tissue  fibrosis  problem clearing esophagus
- Diagnosis: pH probe
- Complications: Barrett’s eophagitis  esophageal carcinoma, vomiting, dysphagia, chronic inflammation, spasm
of the muscles, scarring of the esophagus, stricture development
- Management:
o Avoid large meals; eat more frequent, o Avoid recumbent position several hours
small meals after a meal
o Avoid alcohol use and smoking o Avoid bending for long periods
o Drinking extra fluids o Sleep with the head elevated
o Eat meals sitting up o Lose weight if overweight
- Treatment: lots of OTC drugs (antacids, H2 blockers, PPIs); Tagamet is deadly in the elderly

Esophageal Cancer
- Squamous cell carcinoma – assoc. with alcohol & tobacco use
 - Adenocarcinoma – assoc. with Barrett esophagus
- Manifestations:
o Dysphagia o Fatigue
o Weight loss o Painful swallowing
o Anorexia o Not easily diagnosed

Gastric Irritation and Ulcer Formation

- Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs)
o Irritate the gastric mucosa and inhibit PGE synthesis
o Most common reason of loss of blood at slow pace  Fe deficiency anemia
- Infection with Helicobacter pylori
o Thrives in acid environment of the stomach
o Disrupts the mucosal barrier that protects the stomach from harmful effects of its digestive enzymes
o Increases chance for gastric cancer

Types of Gastritis
- Gastritis – inflammation of the lining of the stomach
- Manifestations: nausea, abdominal distension, passing gas
- Acute Gastritis
o Transient inflammation of the gastric mucosa
o Focal mucosa erosion and bleeding
o Most commonly assoc. with local irritants such as bacterial endotoxins, alcohol, and aspirin
o Can lead to a peptic ulcer
- Chronic Gastritis
o Cells have gone through adaptive process of metaplasia & dysplasia
 Increased risk of cancerous growth
o Charac. by the absence of grossly visible erosions and the presence of chronic inflammatory changes
o Leads eventually to atrophy of the glandular epithelium of the stomach
o Commonly seen in patients with RA or osteoarthritis who have higher risks
o Types:
 Helicobacter pylori gastritis
 Spreads from fecal to oral route – contaminated water a danger
 Develops a lot more in children
 Colonizes mucus-secreting epithelial cells of the stomach
 Produces enzymes and toxins that have the capacity to interfere with the local
protection of the gastric mucosa against acid; stops parietal cells
 Produces intense inflammation
 Elicits an immune response
 Burrows under the mucosa layer and may live there for years without you realizing
 Diagnostic tests:
o C urea breath test using a radioactive carbon isotope
o Stool antigen test
o Endoscopic biopsy for urease testing
o Blood tests to obtain serologic titers of H.pylori antibodies
 Autoimmune gastritis – autoimmune deficiency that seems mucosa as not self
 Multifocal atrophic gastritis – atrophy of mucosa layers
 Chemical gastropathy – ingestion of a substance that damages mucosa

Peptic Ulcer
- Ulcerative disorders that occur in areas of the upper GI tract that are exposed to acid-pepsin secretions
- Destroys the mucosal barrier
- Spontaneous remissions and exacerbations are common
 - Can develop at: lower esophagus, stomach, pylorus, duodenum, jejunum
o 70-80% in duodenum
- Do not extend below epithelium
- Acute or chronic (depending on process of inflammation)
- Most commonly in men 20-50 y/o
- 5-10% need surgery
- Ask patient: NSAIDs? Alcohol? Tobacco?
- Causes:
o Decreased mucus production – H. pylori, aspirin, NSAIDs, corticosteroids, alcohol, caffeine, nicotine
 Decreased blood flow to the gut (from shock)  hypoxia
 Inhibition of mucus production in the duodenum by sympathetic stimulation
o Excess acid production in the stomach
 Greater number of parital cells than normal
 Over-reactive parietal cell response
 Increased gastrin secretion
 Increased vagal stimulation to the parietal cells
o Excess acid delivered to the intestine
 Too rapid movement of stomach contents into the duodenum (i.e. dumping syndrome)
- Corresponding factors: age, warfarin, smoking
- Complications:
o Hemorrhage – caused by bleeding from granulation tissue or erosion of an ulcer into an artery or vein
o Obstruction – caused by edema, spasm, or contraction of scar tissue and interference with the free
passage of gastric contents through the pylorus or adjacent areas
o Perforation – occurs when an ulcer erodes through all layers of the stomach or duodenum wall
- Symptoms depend on type of ulcer
o Pain is worse after eating (gastric ulcers)  weight loss
o N/V, hunger (relieved by antacids)
o Weight gain w/ duodenal ulcers b/c eating relieves the discomfort
- Diagnosis: history, endoscopy, H. pylori
- Treatment: Eradicate the cause ad promote a permanent cure for the disease.
o Eradicate H.pylori - antimicrobials
o Relieve ulcer symptoms
o Heal the ulcer crater
 Acid-neutralizing, acid-inhibiting, and mucosal-protective drugs
 Antacids
 Proton pump inhibitors
o Dietary measures – avoidance of alcohol, caffeine, tobacco
o Discontinue or reduce NSAID ingestion
o Relieve psychological influences

Stress Ulcers
- Risk factors: Large surface area burns, trauma, sepsis, acute respiratory distress syndrome, severe liver failure,
major surgical procedures, Zollinger-Ellison syndrome
- Patients in a constant physiological stress hormone: high levels of cortisol
- Symptoms: anorexia, N/V

Gastric Cancer
- Most common: adenocarcinoma, H.pylori, nitrites/nitrates in food, alcohol/tobacco use
- Risk factors:
o Genetic predisposition
o Carcinogenic factors in the diet
o Autoimmune gastritis
 o Gastric adenomas or polyps
- Manifestations: bleeding, abdominal pain, black & tarry stool, N/V, heartburn, weakness, fatigue, ascites,
indigestion, unintentional weight loss
______________________________________________________________________________________

Conditions Causing Altered Intestinal Function

 Irritable bowel syndrome  Alterations in bowel motility
 Inflammatory bowel disease  Malabsorption syndrome
 Diverticulitis  Cancer of the colon and rectum
 Appendicitis

Irritable Bowel Syndrome

- Characteristics:
o Persistent or recurrent symptoms of o Nausea and anorexia
abdominal pain (significant pain) o Constipation or diarrhea
o Altered bowel function o Anxiety or depression
o Varying complaints of flatulence, o Chronic inflammation of colon
bloating o Leads to diverticulitis
- 3 Types:
o IBS C – constipation
o IBS D – diarrhea
o IBS M – mixed
- Mind/gut, stress makes it worse; “functional GI disorder”
- Effects through motor disturbances of the entire colon
- ANS is not working, myenteric plexus also not working

Inflammatory Bowel Disease – Crohn Disease

- A recurrent, granulomatous type of inflammatory response that can affect any area of the GI tract from the
mouth to the anus
- Extends through all layers of the intestinal wall
- Involves regional lymph nodes
- Most prevalent in adults age 20-40 y/o
- Contributing factors: allergies, immune disorder, problems with lymph node clearance
- Strong genetic influences and are exacerbated by stress
- Bowel becomes narrower & fibrotic due to the inflammatory process  bowel stiff and inflexible  shortening
of intestines
o Interferes with nutrient absorption if in the small intestine
o Disturbed water & electrolyte balance if in the colon
- Sharply outlined granulomatous lesions that appear in skip pattern scattered throughout the gut
- Manifestations:
o Steady pain o Anal fistulas
o Cramping o Nutrition problems, malabsorption
o Tenderness on palpation o Weight loss
o Bloody stools o Malaise
o Diarrhea o Low-grade fevers
o Steatorrhea o Fluid & electrolyte imbalance
- Diagnosis: colonoscopy reveals irregular, scarred bowel
- Complications: toxic megacolon, dilation of colon, obstruction, fistulas,
- Treatment: anti-inflammatory drugs, nutritional supplement, diet education, surgical resection, psychological
support, total parenteral nutrition, immunosuppression

Inflammatory Bowel Disease – Ulcerative Colitis

 - Strong genetic influences and are exacerbated by stress
- Autoimmune disease of unknown cause
- A nonspecific inflammatory condition of the colon
- Begins in the sigmoid colon of the rectum
- Spread continuously through the entire colon, rarely goes into the small intestine
- Begins with inflammation of mucosa  areas of erosions  deep ulcerations
- More prevalent in women
- Bimodal incidence: 15-20, 55-60 y/o
- Manifestations: periods of exacerbations & remissions
o Edema o Recurrent bloody diarrhea (pus & mucus) –
o Abscesses (pockets of pus) small volume
o Thicker fibrotic bowel o Anemia
o Rectal urgency o Fever
o Weight loss o Abdominal pain
- Diagnosis: sigmoidoscopy reveals hemorrhagic mucosa with ulceration, anemia, low K+
- Complications:
o Toxic megacolon
o Perforation of the gut  peritonitis
o Increased incidence of colon cancer
o Electrolyte imbalances
- Treatment: immunosuppression, nutrition supplementation, bulk-free diet to decrease stool frequency,
psychological support, surgical resection

Infections of the Intestine

- Types:
o Viral infection
 Rotavirus
o Bacterial infection  major cause of diarrhea
 Clostridium difficile colitis
 Escherichia coli O157:H7 infection
 Entero hemorrhagic E.coli  adheres & damages epithelial cells, no damage to mucosa
 Found in intestines of cows
 Spreads by uncooked ground beef, unpasteurized milk, contaminated water
 Enterotoxin E.coli  diarrhea, consider fluid & electrolytes, minimal damage to layers
 Entero pathogenic E.coli  adheres to mucosal cells, destroys microvilli
 Entero invasive E.coli  invading & enters mucosa
 General S/S E. coli bacterial infection: watery diarrhea that turns bloody, severe abdominal
cramps, N/V, onset 1-8 days of exposure, lasts 5-8 days
 Hemolytic uremic syndrome: hemolytic anemia, thrombocytopenia, acute renal failure
 Must keep patients hydrated
o Protozoal infection
- May result in hypovolemia  lose different electrolytes quickly
- Toxins bind to epithelial membrane  causes Cl, Na, K, H2O to quickly pass through

Diverticulitis
- Outpouching of the GI wall, pushing the mucosal layers out into the muscle
- Commonly found in the sigmoid colon, but it can develop anywhere
- Diverticulosis – no symptoms
- Causes:
o Seen a lot in the elderly who get constipated
o Low fiber diet
 o Weakness in colon wall
o Believed to occur when an individual frequently exerts high pressures inside the lumen of the colon
while straining to pass a low-bulk stool.
- Diminished colonic motility
- Increased intra-luminal pressure
- Manifestations:
o Change in bowel habits o Slight fever
o Excess gas o Confused in the elderly
o Pain in the LLQ when mild o Elevated white blood cell count
o N/V o Rigid abdomen & LQ pain when
o Tenderness in the lower left quadrant ruptured
- Chronic diverticulitis:
o Patient will complain of diarrhea or constipation, with ribbon-like stool
o ESR level will be elevated
- Complications: perforation  peritonitis
- Treatment: dietary modification to increase stool bulk, exercise to increase rate of stool passage, antibiotics

Types of Diarrhea
- Diarrhea is an increase in fluidity and frequency of stools
- Large volume: osmotic (presence of non-absorbable solute in stool), secretory
o Causes: psychological factors, E. coli, pathogen, Cholera
- Small volume: IBD, infectious disease, irritable colon
o Ex: ulcerative colitis, Crohn’s disease
- Severe diarrhea can lead to hypovolemic shock and electrolyte irregularities

Common Causes of Constipation:  Fecal Impaction:

Constipation is difficult or infrequent defecation (subjective)
Defecation can be difficult if the stool is hard and compact.

- Failure to respond to the urge to defecate - Painful anorectal disease

- Inadequate fiber in the diet - Tumors
- Inadequate fluid intake - Neurogenic disease
- Weakness of the abdominal muscles - Use of constipating antacids or bulk laxatives
- Inactivity and bed rest - Low-residue diet
- Pregnancy - Drug-induced colonic stasis
- Hemorrhoids - Prolonged best rest and debility
- Spinal cord trauma, MS, intestinal neoplasm,
hypothyroidism, Hirschsprung’s disease
- Stress  increased sympathetic activity
- Drugs (antacids, opioids)

Intestinal Obstruction
- Can be partial or complete
- Can happen in small (more common, more serious) or large bowel
- Normally seen after abdominal surgery
- In people with limited physiological reserves  death in 24 hrs
- Causes:
o Mechanical
o Adhesions
o Strangulated hernia
o Carcinomas
o External tumor obstructing bowel from external force
 - Fluid + air + gas all start to combine above the area of the obstruction
- Peristalsis will temporarily increase  injurying the mucosa  inflammatory response  distension of the
bowel  venous blood supply cut off  absorptive processes stop  bowel secrete H20, Na, K  fluid builds in
the lumen
- Diagnosis: blood ABG
o Metabolic alkalosis  small bowel
o Metabolic acidosis  lower bowel
- 3 Types:
o Simple – blockage prevents intestinal contents from passing
o Strangulated – blood supply to the obstructed section cut off, in addition to blockage of lumne
o Closed-loop – both ends of bowel section is occluded
- Paralytic ileus
o Physiologic form of intestinal obstruction that usually develops in the small bowel after abdominal
surgery
o Causes: trauma, toxemia, peritonitis; electrolyte deficiencies, vascular causes
o Treatment: intubation, intestinal tube, cholinergic agents
- Manifestations:
o N/V o Dehydration
o Abdominal distension o Hypovolemic shock
o Malaise o Sepsis
o Tenderness upon palpation o Hypokalemic

Peritoneal Cavity and Peritonitis

- Permit rapid absorption of bacterial toxins
- Favors the dissemination of contaminants
- Great inflammatory response – thick, fibrinous protective substance
- Causes:
o Perforated peptic ulcer
o Perforated diverticulum
o Gangrenous bowel
o Pelvic inflammatory disease
o Gangrenous gallbladder
o Abdominal trauma and wounds
o Ruptured appendix:
 Inflam. of wall of appendix  Epigrastric or periumbilical cramping pain 
 Obstruction of lumen of shifts to RLQ
appendix  ruptures  N/V, low grade fever
 Due to bacterial invasion  Leukocytosis
 Perforation  Surgical removal
 Septicemia  Can lead to death
- Manifestations:
o Pain / Rebound pain
o Increased HR as a result of hypovolemia
o N/V
o Rigid abdomen indicative of widespread inflammation
o Sepsis
- Treatment: surgery, antibiotics, fluid & electrolyte replacement

Intestinal Malabsorption
- Failure to transport dietary constituents from the lumen of the intestine to the extracellular fluid
- Causes:
o Sprue or celiac disease o Bacterial overgrowth
 o Bowel resection o Colorectal cancer
o Infection of intestines o Mesenteric atherosclerosis
o Ischemic small bowel disease o Drug induced w/ Neomycin
o Inflammatory reaction o Cystic Fibrosis
o Neoplasm o Total gastrectomy
- Symptoms:
o Diarrhea o Abdominal pain
o Steatorrhea o Cramps
o Flatulence o Weakness, muscle wasting
o Bloating o Edema due to loss of protein
o Weight loss
- Complications: Fe deficiency anemia, vitamin B12 anemia, osteoporosis, tetany

Celiac Disease
- Presents in infancy
- Manifestations: failure to thrive, diarrhea, abdominal distension, occasionally, severe malnutrition

Colorectal Cancers
- Usually begin in the secretory glands of the mucosal layer
- Risk factors: age, family history, Crohn disease, ulcerative colitis, familial adenomatous polyposis, diet (high fat,
low fiber, nitrates), withholding stools, long term use of aspirin and NSAIDs
- Manifestations: changes in bowel habits, fatigue, occult blood in stool
- Diagnosis: stool occult blood tests, anemia, digital rectal examination (palpable mass), X-ray studies using
barium, flexible sigmoidoscopy and colonoscopy, blood tests for specific antigens
- Treatment: preventive measures are important, surgery with or without chemotherapy
_______________________________________________________________________

The Pancreas
- Endocrine pancreas: supplies the insulin and glucagon needed in cell metabolism
- Exocrine pancreas:
o Small intestine  CCK hormone  secretion of pancreatic enzymes (trypsin, amylase, lipase)
o Small intestine  secretin  sodium bicarbonate  neutralizes acidic chyme

Acute Pancreatitis
- Inflammation of the pancreas characterized by autodigestion of the pancreas by pancreatic enzymes.
- Leads to cell necrosis and hemorrhage.
- Immune and inflammatory systems contribute to the swelling and edema of the organ.
- Causes:
o Blockage of the pancreatic duct, usually from gallstones in the common bile duct
o Hyperlipidemia
o Chronic alcoholism
- Manifestations: pain, N/V
- Diagnosis: elevated serum amylase and lipase, hyperglycemia, hyperlipidemia, increased WBC count
- Complications: decreased BP, CV shock, pancreatic abscess
- Treatment:
o Withholding of food & fluids to reduce pancreatic secretions
o IV fluids to maintain blood volume & pressure
o Narcotics to relieve pain
_______________________________________________________________________

The Liver
- The liver and pancreas produce digestive secretions.
- Over 20 different roles
o Synthesizes glucose, plasma proteins, and blood-clotting factors
o Responsible for metabolism of carbohydrates, proteins, and fat
o Responsible for the degradation and elimination of drugs and hormones (i.e. estrogen)
o Storage of minerals and vitamins
o Filtration of blood and removal of bacteria
o Production of bile salts
o Metabolism of steroid hormones
o Elimination of bilirubin
 Causes of jaundice
 Excessive destruction of RBCs
 Impaired uptake of bilirubin by the liver cells
 Decreased conjugation of bilirubin
 Obstruction of bile flow in the canaliculi of the hepatic lobules or in the intrahepatic or
extrahepatic bile ducts
 Categories:
 Prehepatic
o Related to RBCs rupturing fastering that the liver can conjugate bilirubins
o Seen in patients with transfusion reactions, sickle cell anemia
o Major cause is excessive hemolysis of RBCs
o Unconjugated bilirubin
 Intrahepatic
o Caused by disorders that directly affect the ability of the liver to remove biliubin
from the blood or conjugate it so it can be eliminated in the bile
o Seen in hepatitis, cirrhosis, metastatic cancer to the liver, or drugs that use liver
heavily for metabolism
o Conjugated bilirubin
 Posthepatic
o Bilirubin forms at a normal rate, but inflammatory process or gallstones block
the flow of bile into the intestines
o Conjugated bilirubin
- Assessment of liver function:
o Serum aminotransferase levels – assess injury to liver cells
o Serum bilirubin, GGT, and alkaline phosphatase – measure hepatic excretory function
o Ultrasonography, CT scans, and MRI – evaluate liver structures
o Angiography – visualizes the hepatic or portal circulation
o Liver biopsy – used to obtain tissue specimens for microscopic examination
- Pathologic conditions affecting the hepatobiliary system:
o Injury from drugs and toxins
o Infection, inflammation, and immune responses
o Metabolic disorders
o Neoplasms
- Types of reactions involved in hepatic detoxification and metabolism:
o Phase 1 reactions – chemical modification or inactivation of a substance
o Phase 2 reactions – conversion of lipid-soluble substances to water-soluble derivatives
o Biotransformations
- Host factors contributing to susceptibility to drug-induced liver disease
o Genetic predisposition
o Age – elderly, young
o Underlying chronic liver disease
o Diet and alcohol consumption
 o Use of multiple interacting drugs

Hepatitis
- Definition: Inflammation of the liver
- Nonviral
o Inflammation of the liver that usually results from exposure to certain chemicals or drugs.
o Most patients recover from this illness, although a few develop fulminating hepatitis or cirrhosis.
o Causes hepatic cellular necrosis.
o Kuffper cells and macrophages go into hyperplasia to try to control it
o History of alcohol, anorexia, and preexisting liver disease can exacerbate chances of getting disease
o Causes: hepatotoxic chemicals, hepatotoxic drugs, idiopathic
o S/S: anorexia, N/V, hepatomegaly, abdominal pain, jaundice, pruritus, dark urine, clay-colored stool
o Dx: elevated liver enzyme, bilirubin, alkaline phosphate levels, elevated WBC & eosinophil count
o Complications: cirrhosis, hepatic failure
- Viral
o Most common kind
o Infection of liver that causes hepatic cellular destruction and necrosis
o Mechanism of liver injury: direct cellular injury, induction of immune responses against viral antigens
 Varying factors of hepatotropic viruses
 Mode of transmission and incubation period
 Mechanisms, degree, and chronicity of liver damage
 Ability to evolve to a carrier state
o Hepatitis A (HAV) o Hepatitis C (HCV)
 Infectious  20% of all hepatitis patients
 Fecal-oral route  Post-transfusion cases
 Self-limiting  Bloodborne
o Hepatitis B (HBV) o Hepatitis D
 Bloodborne  Frequently exposed to blood products
 Mother to child, sexual  High mortality rate
transmission (seen in HIV+ or IV o Hepatitis E (HEV)
users)  People from endemic area or where
 Self-limiting hepatitis is high
 Serum  Contaminated water
o Hepatitis B-associated delta virus (HDV)  Oral or fecal route
- 3 Stages of symptoms:
o Prodromal – easily fatigued, malaise, anorexia, N/V, dark urine, clay-colored stool, RUQ tenderness
o Clinical – worsening of symptoms, jaundice, pruritus
o Recovery – symptoms subside, return of appetite
- Diagnosis: abnormal liver enzymes, elevated antibodies to virus, viral antigen in blood
- Complications: cirrhosis, hepatic failure, death
- Treatment: rest as needed, avoid consumption of alcohol, education towards modes of transmission, drug
therapy, inferferons & nucleotide analogues, gamma globulins, vaccines
- Causes:
o Autoimmune disorders
o Reactions to drugs and toxins
o Infectious disorders
 Malaria, infectious mononuceleosis, salmonellosis, and amoebiasis
o Hepatotropic viruses that primarily affect liver cells or hepatocytes
 Direct cellular injury and induction of immune responses against viral antigens

Alcohol-Induced Liver Disease

- Causes:
 o Alcohol abuse – end products of EtOH digestion include O2 free radicals which are toxic to hepatocytes
o Poor nutrition
- Metabolism:
o Directly absorbed in stomach
 MEOS – acetaldehyde, free radicals
 Cytochrome P450 enzyme required
 NAD system – without it, hypoglycemia & increased lactic acid results
 Alcohol dehydrogenase  acetaldehyde
- Stages:
o Fatty liver disease
 Relatively benign stage
 Reversible condition characterized by triglyceride accumulation in the hepatocytes
 EtOH causes triglycerides to accumulate in the liver by acting as fuel for energy
production such that cells use alcohol and fatty acids are no longer needed
 Alcohol end products also interfere with the oxidative phosphorylation of fatty acids by
the hepatocyte mitochondria  trapping of fatty acids inside the hepatocytes
 Occurs in up to 90% people of abuse alcohol chronically
 Can be reversed if alcohol ingestion stops
o Alcoholic hepatitis
 20-40% of individuals
 Damage to the hepatocytes occurs as a result of the cellular toxicity of the end products
 Liver cells undergo apoptosis  scarring, fibrosis
 Can be reversed if alcohol ingestion stops
o Cirrhosis
 Final, irreversible stage
 Dead liver cells are replaced by scar tissue
 Interstitial swelling and edema  small blood vessels collapse and cause increased resistance to
blood flow through the liver  portal hypertension & ascites
 Esophageal, rectal, abdominal varices common
 Jaundice apparent
 Deterioration of liver function
- Manifestations:
o Hepatomegaly
o Abdominal discomfort, anorexia, nausea, fatigue
o Edema, ascites, jaundice
- Diagnosis: liver function tests, elevated bilirubin levels, prolonged prothrombin time, liver biopsy
- Complications: liver failure
- Treatment:
o Diet with adequate nutrition
o Cessation of alcohol ingestion
o Corticosteroid administration to reduce inflammation
o Inhibition of TNF-alpha to slow apoptosis

Cirrhosis
- Chronic disease
- Destruction and fibrosis of hepatic tissue  liver scarring
- Loss of liver function
- Diverse etiology:
o Hepatic cellular disease – hepatitis, toxin exposure, infections, alcoholism, autoimmune diseases,
o Cholestatic disease – biliary tree change
o Metabolic disease – Wilson’s disease
o Other – cardiac cirrhosis, hepatic vein obstruction, bile duct obstruction
 o Angiotensin II stimulates hepatic inflammation and collagen synthesis.
- More often in males, after age 50, often in alcoholics
- High rate of mortality
- Manifestations:
o Anorexia (early) o Menstrual irregularities
o N/V (early) o Pruritus
o Diarrhea (early) o Jaundice
o Anemia o Ascites
o Hepatic encephalopathy o Hepatomegaly
o Bleeding tendencies
- Complications: respiratory compromise, esophageal varices, portal hypotension, renal failure

Liver Failure
- Ultimate outcome of any severe liver disease
- Hepatic Encephalopathy:
o Complex of CNS disorders
o Characterized by memory lapses, personality changes, tremor, jerking movements, poor balance
o Results from accumulation of toxins in the blood (i.e. ammonia)  increased osmotic pressure  brain
swelling & cerebral edema
- Hepatorenal Syndrome:
o Kidneys fail to function although the kidneys appear to be physically capable of functioning
o Blood volume expands, H+ accumulates, electrolyte imbalance
o Shock  decrease in renal blood flow
- Manifestations:
o Jaundice o Peripheral edema
o Abdominal pain or tenderness o Varices of esophagus, rectum, abdominal wall
o Nausea, anorexia o Bleeding tendencies, petechiae from
o Fatigue, weight loss thrombocytopenia
o Splenomegaly o Amenorrhea
o Ascites o Gynecomastia
- Diagnosis: altered liver function tests, blood analysis, hypoglycemia
- Treatment: specific for various manifestations