Digestive System Disorders

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Presentation Transcript

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%