Digestive System Disorders: Digestive System Disorders Chapter 20
Pgs 362-419
Overview: Overview Common Manifestations of Digestive System Disorders
Anorexia, nausea, vomiting
Diarrhea
Constipation
Pain
Malnutrition
Basic Diagnostic Tests
Common Therapies
Upper Gastrointestinal Tract Disorders
Hiatal hernia
Gastritis
Peptic ulcer
Disorders of the Liver and Pancreas
Gallbladder disorders
Hepatitis
Lower Gastrointestinal Tract Disorders
Colorectal cancer
Common Manifestations—Anorexia, Nausea, Vomiting: Common Manifestations—Anorexia, Nausea, Vomiting Digestive system disorders or sign of other problems
Nausea and vomiting common indicators of GI disorder
Anorexia precedes the above
Nausea
General unpleasant, subjective feeling
Vomiting
Forceful expulsion of irritant
Medulla coordinates reflex
Steps of Vomiting: Steps of Vomiting
Anorexia, Nausea, Vomiting: Anorexia, Nausea, Vomiting Retching before vomiting
Characteristics of vomitus
“coffee grounds”
Blood
Partial digestion in stomach of protein in blood
Yellowish-green
Contains bile (from duodenum)
Deeper brown
Content from lower intestine
Common Manifestations—Diarrhea : Common Manifestations—Diarrhea Excessive freq of stools
Usually loose and watery
Acute or chronic
Accomp by cramps and pain
Severe, prolonged may lead to
Dehydration, electrolyte imbalance, acidosis, malnutrition
Diarrhea—Classification : Diarrhea—Classification Lg. vol diarrhea
Secretory or osmotic
Leads to watery stool (increased secretion into intestine)
Often related to infection or short transit time
Sm vol diarrhea
Inflammatory bowel disease
Stool with blood, mucus, pus
Steatorrhea
“fatty diarrhea”
Freq, bulky, greasy, loose stools with foul odor
Characteristic of malabsorption disorder
Diarrhea—Classification : Diarrhea—Classification Blood
Frank blood
Red blood on surface of stool
Lesions in rectum/anal canal
Not been “digested”
Occult blood
Small hidden amounts
Not visible to eye
Caused by bleeding ulcers in stomach, sm intestine
Melena
Dark-colored
Significant bleeding higher in digestive tract
Hb acted on by bacteria = darker color
Gas
Develops normally in digestive tract
From swallowed air and digestion/bacterial action
Manifestations—Constipation : Manifestations—Constipation Less freq bowel movements and passage of small hard stools
Acute or chronic
Can alt with periods of diarrhea
Causes
Inadeq dietary fiber
Inadeq fluid intake
Failure to respond to defecation reflex
Muscle weakness and inactivity
Neurologic disorders
Drugs
Some antacids, iron meds, bulk laxatives
Obstruction by tumor
Chronic can lead to hemorrhoids
Severe can lead to impaction
Manifestations—Pain : Manifestations—Pain Visceral pain
Pallor, sweating, nausea, vomiting
Burning sensation
Inflammation and ulceration in higher digestive tract
Related to oral ulcerations and heartburn
Dull aching pain
Higher right quadrant
Typical of liver capsule stretching
Cramping diffuse pain
Characteristic of inflammation, distention, stretching of intestines
Colicky severe pain
Recurrent smooth muscle spasm
Response to severe inflammation/obstuction (ex: gallstones)
Pain: Pain Somatic pain
Steady, intense, well-localized
Indicates involvment/inflammation of parietal peritoneum
Ex: appendicitis
Referred pain
May delay diagnosis
Manifestations—Malnutrition : Manifestations—Malnutrition Limited or general
Specific
General malnutrition
Chronic anorexia, vomiting, diarrhea
Diets (“fad diets”)
May lack certain req elements of nutrition
Child
Growth/development delayed/impaired
Basic Diagnostic Tests : Basic Diagnostic Tests Radiographs
X-ray (common w/ barium)
Ultrasound
CT and MRI
Liver and pancreatic abnormalities
Fiberoptic endoscopy
Improved visualizations or biopsy
Lab analysis
Stool samples
Blood Tests
Check liver function
Eval serum protein levels, clotting times, serum liver enzymes, bilirubin levels
Pancreatic function
Serum enzyme levels
Stool analysis for enzyme, fat content
CEA (carcinoembryonic antigen)
Blood tumor marker
Colon cancer
Common Therapies: Common Therapies Dietary Modifications
Stress Reduction
Stress exacerbates peptic ulcers, chronic inflammatory bowel disorders
Severe, prolonged stress
stim SNS
Vasocontriction, ischemia of mucosa
Decrease peristalsis
Increase glucocorticoid secretion
Increase cortisol levels
Drugs
Common Therapies—Drugs : Common Therapies—Drugs Antacids (Maalox)
Antiemetics
Dramamine
Compazine
Laxatives, enemas
Bulk supplements (Metamucil)
Stool softeners (Colace)
Antidiarrheal (Imodium)
Antinflammatory and antibacterial agent
Salazopyrin Antibacterial (Biaxin, Zithromax)
Heliobacter pylori
Coating agent (Carafate)
Anticholinergic drugs
Histamine 2 antagonist drugs (Tagamet, Zantac)
Proton pump inhibitors (Prevacid, Prilosec)
Upper Gastrointestinal Tract Disorders—Hiatal Hernia: Upper Gastrointestinal Tract Disorders—Hiatal Hernia Part of stomach elevated, protrudes thru hiatus of diaphragm into thoracic cavity
2 types
Sliding hernia
More common
Portion of stomach and gastroesophageal junction move up diaphragm
Esp when supine
Standing herniated portion slides down into ab cavity
Rolling (paraesophageal) hernia
Fundus moves up thru enlarged or weak hiatus in diaphragm
Bv in wall of stomach may be compressed = ulcers
Hiatal Hernia: Hiatal Hernia Food lodges in pouch
Inflammation of mucosa, reflex of food up to esophagus, dysphagia (difficulty swallowing)
Often incompetent gastroesophageal sphincter
Contributing factors
Shortening of esophagus
Weakness of diaphragm
Increased abdominal pressure (pregnancy)
Hiatal Hernia: Hiatal Hernia Signs
Heartburn
Brief substernal burning sensation
Freq belching
Discomfort when lying supine
Dysphagia common
b/c inflammation of esophagus or mass of food in pouch compresses esophagus
Gastroesophageal Reflux Disease (GERD): Gastroesophageal Reflux Disease (GERD) In conjunction with hiatal hernia
Severity depends on lower esophageal sphincter (LES)
Freq episodes at night
Eliminate factors that decrease LES pressure
Avoid spicy foods, take anatcids
GERD: GERD
Gastritis—Gastroenteritis : Gastritis—Gastroenteritis Inflammation of stomach, intestine
Usually caused by an infection
Inflammation of gastric mucosa = vomiting
Inflammation of intestines causes increased motility, impaired absorption = diarrhea
Nausea and abdominal cramps
Microorganism transmitted by contaminated food, water, oral-fecal route
Most infections mild, self-limiting
Epidemics (common in day-cares)
Careful hand washing, food-handeling
Supportive treatment
Peptic Ulcers: Gastric and Duodenal Ulcers—Pathophysiology : Peptic Ulcers: Gastric and Duodenal Ulcers—Pathophysiology Proximal duodenum most common
Also found in antrum of stomach or lower esophagus
Usually appear as single, small, round cavities
Smooth margins; penetrate submucosa
Once acid or pepsin penetrate mucosal barrier tissues exposed to continuous damage
Acid diffuses into gastric wall
May erode deeply into musculature and eventually perforate wall
Inflammation surrounds crater
Gastric and Duodenal Ulcers—Pathophysiology : Gastric and Duodenal Ulcers—Pathophysiology Erosion invades bv wall, bleeding occurs
Persistent loss of small amt of blood
Or massive hemorrhage
Development begins w/ break down of mucosal barrier
Decreased resistance of mucosa or increase HCl or pepsin secretion
Impaired mucosal defenses (gastric ulcer)
Increased acid secretion (duodenal ulcer)
Most have H. pylori present
Ulcers—Pathophysiology : Ulcers—Pathophysiology Mucosal barrier damaged by:
Inadeq blood supply
Excessive glucocorticoid secretion or meds (Prednisone)
Ulcerogenic substances
Atrophy of gastric mucosa Increased acid/pepsin secretion assoc w/
Increased gastrin secretion
Increased vagal stim or increased sensitivity to stim
Increased # acid-pepsin secretory cells in stomach
Increased stim of acid-pepsin secretion
Interference with normal feedback mechanism
Rapid gastric emptying
Ulcers—Pathophysiology : Ulcers—Pathophysiology Stress affects
Healing is difficult
Granulation tissue forms deep in cavity
Breaks down (subject to damage by chyme)
Longer healing time = more fibrous tissue
Complications
Hemorrhage
Perforation
Obstruction
Ulcers—Etiology : Ulcers—Etiology Common, particularly in men
Western countries have higher incidence
Genetic factor
Duodenal
Gastric common in older people
Ulcers—Signs and Symptoms: Ulcers—Signs and Symptoms Epigastric burning/aching
2-3 hours after meals, at night
Cyclic pain relieved by eating
Heartburn, nausea, vomiting
Ulcers—Diagnostic Tests and Treatment: Ulcers—Diagnostic Tests and Treatment Tests
Fibroscopic endoscopy
Barium X-ray
Biopsy
Treatment
Combo of drugs
2-3 antimicrobial drugs and meds to decrease acid secretion
Disorders of the Liver and Pancreas—Gallbladder Disorders: Disorders of the Liver and Pancreas—Gallbladder Disorders Gallstones
Cholelithiasis
Formation
Masses of solid material (calculi) that form in bile
Gallstones—Pathophysiology : Gallstones—Pathophysiology Vary in shape, size
Small stones “silent”
Lg can obstruct flow of bile
Initially form in bile ducts, gallbladder, cystic ducts
May consist primarily of cholesterol (white), bilirubin (black), or both
Tend to form when bile contains high concentration of component or when bile salts low
Stone grows as more deposits
Gallstones—Pathophysiology : Gallstones—Pathophysiology Presence causes irritation and inflammation of gallbladder wall
Stone can obstruct bile flow in cystic or common bile duct
Severe spasms of pain
Can cause pancreatitis
Gallstones—Etiology : Gallstones—Etiology Cholesterol gallstones
Common in females
High cholesterol level in bile
Obesity, oral contraceptive, estrogen supplements
Bile pigment stones
Common in indiv w/ hemolytic anemia, alcoholic cirrhosis
Gallstones—Signs and Symptoms: Gallstones—Signs and Symptoms Freq asymptomatic
Lg stone obstruct duct
Sudden severe waves of pain
Upper R quad
Radiates to back and R shoulder
Pain increase and may decrease if stone moves on
Risk of ruptured gallbladder
Surgery to remove gallbladder and stone
Gallstone: Gallstone
Gallstones—Treatment : Gallstones—Treatment Remove surgically
Sometimes stones fragment
Drugs to break down stone
Hepatitis: Hepatitis Inflammation of the liver
May result from local infection (viral), infection elsewhere (mono) or from chem/drug toxicity
Mild inflammation and necrosis
Obstruction of blood and bile flow in liver
Decrease liver cell function
Damage to liver cells
b/c of function of liver
But good b/c functional reserve and excellent regeneration
Viral Hepatitis—Pathophysiology : Viral Hepatitis—Pathophysiology Infection from group of viruses that specifically target hepatocytes
HAV, HBV, HCV, HDV, HEV
Liver cells damaged in 2 ways:
Direct action of virus (HCV)
Cell-mediated immune responses (HBV)
Cell injury results in:
Inflammation and necrosis
Swollen hepatocytes and liver
w/ severe inflammation bilary stasis
Backup of bile into blood
Viral Hepatitis—Pathophysiology : Viral Hepatitis—Pathophysiology Degree of inflammation and damage varies
Many cases mild and not identified
Some show few manifestations but not jaundice
Others massive necrosis and liver failure
Depending on severity:
Hepatic cells may regenerate or fibrous tissue forms
Blocks channels for blood and bile = further damage
Viral Hepatitis—Pathophysiology : Viral Hepatitis—Pathophysiology Chronic inflammation
B, C, D
Persistent inflammation and necrosis of liver
Eventually causes permanent liver damage
Carrier state
B, C, D
Asymptomatic indiv carries virus in hepatocytes
Can transmit
Viral Hepatitis—Etiology: HAV (Infectious Hepatitis) : Viral Hepatitis—Etiology: HAV (Infectious Hepatitis) Small RNA virus
Transmitted by oral-fecal route
Contaminated water, shellfish
Outbreaks in day care
Sexually transmitted
Short incubation period (2-6 weeks)
Causes acute, self-limiting infection
No carrier, chronic state
HAV: HAV Contagious period (fecal shedding)
Begins several weeks before onset of symptoms
1st antibodies IgM-HAV appear
2nd IgG-HAV
Remain for years (further protection)
Vaccine for travel to endemic areas
Gamma globulin provides temp. protection
Viral Hepatitis—Etiology: HBV (Serum Hepatitis): Viral Hepatitis—Etiology: HBV (Serum Hepatitis) Double stranded DNA virus
3 antigens
2 core antigens
HBcAg, HBcAg
1 surface
HBsAg
e/ antigen stimulates antibody production in body
Antigens/bodies useful in diagnosing and monitoring
HBV: HBV Carrier state common
Relatively long incubation (2 mo)
More difficult to tract source of infection
Asymptomatic, can’t be detected, but can be transmitted
Transmission
Primarily by infected blood
Transfusions
IV drug users
Sexual transmission
Woman fetus
Vaccine for long-term protection
Health-care professionals
Now given to kids
Viral Hepatitis—Etiology: HCV (NANB Hepatitis): Viral Hepatitis—Etiology: HCV (NANB Hepatitis) Single strand RNA
Transmission
Most common thru blood transfusion
half cases enter chronic
Increased risk of hepatocellular carcinoma
Carrier state
Viral Hepatitis—Etiology: HDV (Delta Virus): Viral Hepatitis—Etiology: HDV (Delta Virus) Incomplete RNA virus
Requires presence of HBsAg to replicate and produce active infection
Increases severity of HBV
Transmission
Blood
Increased incidence in IV drug users
Viral Hepatitis—Etiology: HEV: Viral Hepatitis—Etiology: HEV Single stranded RNA virus
Spread by oral-fecal route
Similar to HAV
Lacks chronic/carrier state
Common in Asia and Africa
Viral Hepatitis—Signs and Symptoms: Viral Hepatitis—Signs and Symptoms Asymptomatic mild fatal
3 stages
Precicteric (prodomal)
Icteric (jaundice)
Postieteric (recovery)
Viral Hepatitis—Treatment : Viral Hepatitis—Treatment No method to destroy virus
Gamma globulin helpful when given early
Supportive measures
Rest, diet high in protein, carbos, vit
Chronic B and C treated w/
Interferon alpha
Lamivudine
Gradual destruction of liver
Cirrhosis, hepatocellular cancer
Lower Gastrointestinal Tract Disorders: Colorectal Cancer : Lower Gastrointestinal Tract Disorders: Colorectal Cancer In U.S. ranks high as lethal cancer in indiv 50+
Increased emphasis on routine rectal exams, colonoscopy, fecal tests for occult blood
Early detection and treatment
Colonoscopy: Colonoscopy
Colorectal Cancer—Pathophysiology : Colorectal Cancer—Pathophysiology Malignant neoplasms from adenomatous polyps
Polyp mass that protrudes into the lumen
As increases in size, increase risk of dysplasia and malignant changes
Adenocarcinomas distributed = in R colon, L colon, distal sigmoid colon and rectum
Manifest differently
Circumferential (“napkin ring”) growths
Common in L
Projecting polyp masses
R colon
All invade wall, mesentary, lymph nodes
Metastize to liver
Staging based on # lymph nodes involved, local invasion, distant metastases
Most release CEA into blood
Not great for screening but good to monitor recurrence
Polyps: Polyps
Colorectal Cancer—Etiology : Colorectal Cancer—Etiology Primarily in +55
Western hemisphere
Genetic factors
Environmental factors (diet)
High in fat, sugar, red meat produce carcinogenic substance
Decrease fiber and increase risk
Prolong contact of mucosa with carcinogen
Colorectal Cancer—Signs and Symptoms: Colorectal Cancer—Signs and Symptoms Initial depend on location and charac of feces at that location
Ex: Circumferential lesion in recto-sigmoid
Fecal mass solid
Causes partial obstruction w/dilation of proximal sigmoid
Vague cramping, small, flat pellets, feeling of incomplete emptying
Ex: Right colon
Feces liquid; no obstruction
General systemic signs
Unexplained change in bowel habits
Blood in feces
Colorectal Cancer—Treatment : Colorectal Cancer—Treatment Surgical removal of involved area
Colostomy (bag to collect feces)
Radiation, chemo
Early diagnosis essential
Localized lesion (Stage I)
Confined to mucosa
5 yr survival rate 85-100%
Lymph node involvement (Stage III)
5 yr survival rate 30-50%