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Digestive system

CH 20

QuestionAnswer
Intrinsc Factor is produced by? The stomach and its essential for the for the absorption of vitamin B12 in the ilium.
The liver is improtant bc? It has hepatocytes and it does production of plasma proteins and clotting factors
What enzymes and electrocytes does the pancreas secrete? Trypsin Chymotrypsin Carobodxypeptidase Ribonuclease Pancreatic amylase Bicarbonate ions
The PNS role in the digestive system Increased motility Increased secretions
The CNS role in the digestive system Stimulated by fear, anger etc Inhibits gastrointestinal activity Causes vasoconstriction Reduced secretions and regeneration of epithelial cells
What is Gastrin? Secreted by mucosal cells (stomach) in response to distention of stomach or partially digested substances Increases gastric motility, relax pyloric and ileocecal sphincters – promotes stomach emptying
What does histamine do? Increased secretion of hydrochloric acid
What does secretin do? Decreases gastric secretions
What does Cholecystokinin do? Inhibits gastric emptying; stimulates contraction of gallbladder
Anorexia,vomiting,and nausea are caused by? Systemic infection Uremia Emotional responses Motion sickness Pressure in the brain Overindulgence of food, drugs Pain
Anorexia and vomiting can cause? Dehydration, acidosis, malnutrition
Nausea is happens when? distention, irritation, inflammation of digestive tract
Vomiting is controlled where? Medulla where it;Coordinates activities involved in vomiting Protects airway during vomiting
What makes up vomit? Chyme from stomach and sometimes bile from the intestines.
What activates vomiting? Distention or irritation in digestive tract, Stimuli from brain(unpleasant sights or smells),ischemia,Pain or stress, inner ear motion, Increased intracranial pressure,Sudden projectile vomiting w/o previous nausea,drugs,toxins,chemicals
hematemesis Blood in vomit
"Brown coffee ground" looking blood means? indicates action of HCl on hemoglobin
Red blood vomit indicates? Hemorrhage
Yellow green vomit Bile from the duodenum
Deeper brown color vomit May indicate content from lower intestine
Recurrent vomiting from food means? Problem with gastric emptying or infection
Diarrhea May be acute or chronic Frequently with nausea and vomiting when infection or inflammation develops
Large-volume diarrhea (secretory or osmotic) Watery stool resulting from increased secretions into intestine from the plasma Often related to infection Limited reabsorption due to reversal of normal carriers for sodium and or glucose
small volume diarrhea Often due to inflammatory bowel disease Stool may contain blood, mucus, pus May be accompanied by abdominal cramps and tenesmus
Steatorrhea – “fatty diarrhea” Frequent bulky, greasy, loose stools Foul odor Characteristic of malabsorption syndromes i.e., celiac disease or cystic fibrosis Fat usually the first dietary component affected Presence interferes with digestion of other nutrients
Frank blood in stool Red blood – usually from lesions in rectum or anal canal
occult blood in stool Small hidden amounts, detectable with stool test May be caused by small bleeding ulcers
Melena stool Dark-colored, tarry stool May result from significant bleeding in upper digestive tract
You get gas from? From swallowed air, e.g., drinking from a straw Bacterial action on food Foods or alterations in motility
Excessive gas causes? Eructation Borborygmus Abdominal distention and pain Flatus
Constipation Acute or chronic problem May be due to decreased peristalsis Increased time for reabsorption of fluid
Chronic constipation causes? hemorrhoids, anal fissures, or diverticulitis.
Causes of constipation Weakened smooth muscle from age or illness, Inadequate dietary fiber,Inadequate fluid intake,Failed response to defecation reflex, Neurologic disorders,Drugs,antacids,iron medications Obstructions by tumors or strictres
Common digestive disorders Dehydration and Hypovolemia
Metabolic alkalosis Results from loss of hydrochloric acid with vomiting
Metabolic acidosis Severe vomiting causes a change to metabolic acidosis due to the loss of bicarbonate of duodenal secretions. Diarrhea causes loss of bicarbonate
Visceral pain (burning sensation) Inflammation and ulceration in upper digestive tract
Visceral pain (dull,aching) stretching of liver capsule
Visceral pain (cramping or diffuse pain) Inflammation, distention, stretching of intestines
Visceral pain (colicky, often severe) Response to severe inflammation or obstruction
Somatic pain Somatic pain receptors directly linked to spinal nervesMay cause,Steady,intense, often well-localized abdominal pain,Involvement or inflammation of parietal peritoneum, “Rebound tenderness”identified over area of inflammation when pressure is released
Referred pain Common phenomenon Pain is perceived at a site different from origin. Results when visceral and somatic nerves converge at one spinal cord level,May assist or delay diagnosis depending on problem
Specific problems of malnutrition Vitamin B12 deficiency Iron deficiency
General problems of malnutrition Chronic inflammatory bowel disorders Cancer treatments “Wasting syndrome” Lack of nutrients available Chronic anorexia, vomiting, diarrhea
Diagnostic tests Radiographs,ultrasounds,ct's,radioactive tracers through ct's and mri's, fiberoptic endoscopy,sigmoidoscopy,colonoscopy,analysis of stool, and blood tests
Dietary modification therapies gluten-free diet (celiac disease) Reduced intake of alcohol and coffee Increased fiber and fluid intake
Antacids relieve pyrosis
Antiemetics relieve vomiting
Laxatives or enemas reduce constipation
antidiahrreals reduce peristalsis and cramps
Sulfasalazine Anti-inflammatory and antibacterial For acute episodes of inflammatory bowel disease
Clarithromycin or azithromycin Effective against Heliobacter pylori infection
Sucralfate Coating agent Enhance gastric mucosal barrier against irritants such as NSAIDs
Anticholinergic drugs Reduce PNS activity Reduce secretions and motility
Histamine2 antagonists useful in gastric reflux
Proton pump inhibitors reduce gastric secretion
Congenital abnormalities of the oral cavity Cleft lip and cleft palate Arise in sixth to seventh week of gestation, Most likely of multifactorial origin, Feeding problems of the infant, High risk of aspirating fluid into respiratory passages,Speech development impaired,Surgical repair
Inflammatory lesions: aphthous ulcers Streptococcus sanguies may be involved Part of the oral resident flora Small, painful lesions on Movable mucosa Buccal mucosa Floor of the mouth Soft palate Lateral borders of the tongue Usually heal spontaneously
Candidiasis May appear as red, swollen areas May be irregular patches of a white curdlike material
Oral candidiasis (thrush) People receiving bread-spectrum antibiotics During and after cancer therapy Immunocompromised individuals or persons with diabetes
Candida albicans causative agent Often part of the resident flora Opportunistic organism
Herpes simplex virus type 1 (HSV-1) kissing or close,contact,remains dormant in sensory ganglion,Activated by stress,trauma,other infection,forms blister,ulcers,clear fluid,spread,heals in 7-10 days.Acute stage reduced by antivirals.spreads to eyes(Conjunctivitis and keratitis)
Syphilis Treponema pallidum May cause oral lesions Highly contagious during first and second stages
First stage of syphilis Chancre, a painless ulcer on tongue, lip, palate Heals spontaneously (1 or 2 weeks)
Seconds stage of syphilis Red macules or papules on palate – highly infectious Heals spontaneously
Caries Streptococcus mutans,Lactobacillus follows, break down sugars and produce large quantities of lactic acid Lactic acid, dissolves mineral in tooth enamel,Tooth erosion and caries formation, from frequent intake of sugars and acids Fluorideant treatment
Peridontitis organisms enter the gingival blood vessels and travel to the connective tissues,bone of the dental arch.Resorption of bone,loss of ligament fibers,weak attachment of teeth. result in loss of tooth,Treat by antimicrobials, surgery of gingiva,good hygiene
Hyperkeratosis Leukoplakia (example) Whitish plaque or epidermal thickening of mucosa Occurs on buccal mucosa, palate, lower lip May be related to smoking or chronic irritation. Epithelial dysplasia beneath plaque may develop into squamous cell carcinoma
Squamous cell carcinoma Most common oral cancer, Smokers, preexisting leukoplakia, alcohol abuse Floor of the mouth, lateral borders of the tongue Multiple lesions possible
Kaposi sarcoma in patients with aids
Sialadenitis Inflammation of the salivary glands May be infectious or noninfectious Most commonly affected – parotid gland
Mumps – infectious parotitis Viral infection Vaccine available
Noninfectious parotitis Often in older adults who lack adequate fluid intake and mouth care
Dysphagia difficulty swallowing from Neurologic deficit, Muscular disorder,Mechanical obstruction
Neurolic problems with dyphagia Infection Stroke Brain damage Achalasia Failure of the lower esophageal sphincter to relax due to lack of innervation
Muscular disorder from dyphagia muscular dystrophy
Congenital atresia Dyshagia obstrucion ;Developmental anomaly Upper and lower esophageal segments are separated
stenosis Dysphagia causing obstruction;Narrowing of the esophagus,developmental or acquired,secondary to fibrosis,chronic inflammation,ulceration,radiation therapy, Stenosis or stricture result from scar tissue.treatment with repeated mechanical dilation
Esophageal diverticula Dysphagia obstruction;Outpouchings of the esophageal wall Congenital or acquired following inflammation Causes irritation, inflammation, scar tissue Signs include dysphagia, foul breath, chronic cough, hoarseness
Esophogeal cancer Primarily squamous cell carcinoma,commonly in distal esophagus,dysphagia in later stages,Poor prognosis due to late manifestations, Associated with chronic irritation due to Chronic esophagitis, Achalasia Hiatal hernia, Alcohol abususe, smoking
haiatal hernia Part of the stomach protrudes into the thoracic cavity;Food may lodge in pouch of the hernia Causes inflammation of the mucosa Reflux of food up the esophagus May cause chronic esophagitis
Sliding hernia More common type Portion and part of stomach and gastroesophageal junction slide up above the diaphragm
Rolling or paraesophageal hernia Part of the fundus of the stomach moves up through an enlarged or weak hiatus in the diaphragm and may become trapped
Signs of hiatal hernia Heartburn or pyrosis Frequent belching Increased discomfort when laying down Substernal pain that may radiate to shoulder and jaw
Gastroesophageal Reflux Disease Periodic reflux of gastric contents into distal esophagus causing erosion and inflammation,seen w/ hiatal hernia, Delayed gastric emptying is a factor.Avoid of Caffeine,fatty/spicy foods,alcohol,smoking,certain drugs.meds reduce reflux and inflammation.
Gastritis – Acute Gastritis Gastric mucosa is inflamed.May be ulcerated and bleeding,May result from,Infection by microorganisms,Allergies to foods,Spicy or irritating foods,Excessive alcohol intake, Ingesting aspirin,other NSAIDs,corrosive toxic substances,Radiation,chemotherapy
Basic signs of gastrointestinal irritation Anorexia, nausea, vomiting,Hematemesis Epigastric pain, cramps or general discomfort With infection, diarrhea may develop.
Acute gastritis is usually self-limiting. Complete regeneration of gastric mucosa Supportive treatment with prolonged vomiting May require treatment with antimicrobial drugs
Gastritis – Chronic Gastritis atrophy of stomach mucosa,Loss of secretory glands,Reduced production of intrinsic factor H. pylori infection,Signs may be vague. Mild epigastric discomfort, anorexia, intolerance for certain foods Increased risk of peptic ulcers and gastric carcinoma
Peptic Ulcer – Gastric and Duodenal Ulcers Most are due to H. pylori infection.Occur most commonly in the proximal duodenum,found in the antrum of the stomach,begins with breakdown of mucosal barrier. Decreased mucosal defense,Increased acid secretion predominant factor in duodenal ulcers
Damage to mucosal barrier predisposes to development of ulcers and is associated with Inadequate blood supply by vasoconstriction,Interferes with rapid regeneration of epithelium,extra glucocorticoid secretion or medication, Ulcerogenic substances break down mucus layer.Aspirin,NSAIDs,alcohol,Atrophy of gastric mucosa,Chronic gastritis
Increased acid-pepsin secretions w/ Peptic Ulcer – Gastric and Duodenal Ulcers Increased gastrin secretion,vagal stimulation,sensitivity to vagal stimuli,number of acid-pepsin secretory cells in the stomach,stimulation of acid-pepsin secretion,Alcohol,caffeine,certain foods,Interference with normal feedback,Rapid gastric emptying
Complications with peptic ulcer Hemorrhage from erosion of blood vessels,perforation of walls,and obstruction causing scar tissue
s/s Peptic Ulcer – Gastric and Duodenal Ulcers Epigastric burning or localized pain usually following stomach emptying
Diagnostic tests of Peptic Ulcer – Gastric and Duodenal Ulcers Fiberoptic endoscopy Barium x-ray Endoscopic biopsy
Treatment of Peptic Ulcer – Gastric and Duodenal Ulcers Combination of antimicrobial and proton pump inhibitor to eliminate H. pylori Reduction of exacerbating factors
Stress ulcers Associated with severe trauma or systemic problems Burns, head injury Hemorrhage or sepsis Rapid onset
Gastric Cancer Arises primarily in mucous glands,Early carcinoma Confined to mucosa and submucosa Later stages Involves muscularis,Eventually invades serosa and spreads to lymph nodes Asymptomatic in the early stages,Often the prognosis is poor on diagnosis
Gastric cancer factors and s/s Diet seems to be a key factor particularly smoked foods, nitrites, and nitrates. Genetic influences play a role. Symptoms vague until cancer is advanced.
Dumping Syndrome Control of gastric emptying is lost and gastric contents get dumped in the duodenum W/O complete digestion.after gastric resection,chyme draws fluid from vascular compartment into intestine.Intestinal distention,Increased intestinal motility,Decreased BP
Dumoing syndrome causing factors Occurs during or shortly after meals,Hypoglycemia 2 to 3 hours after meal
Pyloric Stenosis Narrowing and obstruction of pyloric sphincter,develops anomaly,Signs appear w/in several weeks after birth.vomiting after feeding,mass can be palpated at pylorus.Infant fails to gain weight,dehydration,hunger,Surgery required.feeling full,vomiting
Cholelithiasis Formation of gallstones Solid material (calculi) that form in bile
Cholecystitis Inflammation of gallbladder and cystic duct
Cholangitis Inflammation usually related to infection of bile ducts
Choledocholithiasis Obstruction of the biliary tract by gallstones
Gallstones are made of? Cholesterol or bile pigment Mixed content with calcium salts
Risk factors for gallstones Women twice as likely to develop stones High cholesterol in bile High cholesterol intake Obesity Multiparity Use of oral contraceptives or estrogen supplements Hemolytic anemia Alcoholic cirrhosis Biliary tract infection
Obstruction of a duct by a large calculi severe pain,nausea and vomiting,jaundice,
Prehepatic jaundice Result of excessive destruction of red blood cells Characteristic of hemolytic anemias or transfusion reactions. Unconjugated bilirubin elevated
Intrahepatic jaundice Occurs with disease or damage to hepatocytes Hepatitis or cirrhosis Both unconjugated and conjugated bilirubin may be elevated
Posthepatic jaundice Caused by obstruction of bile flow into gallbladder or duodenum Tumor, cholelithiasis Increased conjugated bilirubin Light-colored stool due to absence of bile
Viral hepititis Cell injury results in inflammation and necrosis in the live. Liver is edematous and tender. Causative viruses Hepatitis A virus (HAV) Hepatitis B virus (HBV) Hepatitis C virus (HCV) Hepatitis D virus (HDV) Hepatitis E virus (HEV)
Hepititis A Small RNA virus,Infectious hepatitis,Transmitted by fecal-oral route in areas of inadequate sanitation or hygiene,contaminated H20 or shellfish,anal sex,Acute self-limiting,No carrier or chronic state Fecal shedding before signs,Vaccine available
Hepititis B Partially double-stranded DNA virus, Over 50% of HIV-positive, 50% of cases are asymptomatic but contagious due to carrier state.Chronic inflammation, Transmission by infected blood,Sexual transmission,Tattooing and body piercing, Vaccine
Hepititis C Single-stranded RNA virus Most common type transmitted by blood transfusion May exist in a carrier state About half the cases enter the chronic state. Increases risk of hepatocellular carcinoma Treated with interferon injections
Hepititis D Also called delta virus Incomplete RNA virus Requires HBV to replicate and produce active infection HDV infection increases severity of HBV infection Transmitted by blood
Hepititis E Single-stranded RNA virus Transmitted by oral-fecal route No chronic or carrier state
Preicteric stage of hepititis Fatigue and malaise Anorexia and nausea General muscle aching
Icteric stage of hepititis Onset of jaundice Stools light in color, urine becomes darker Liver tender and enlarged, mild aching pain
Posticteric stage of hepititis Reductions in signs Weakness persists for weeks
Treatment of heptititis Only body defense is formation of antibodies via vaccination,Chronic hepatitis can be treated with interferon
Toxic or Nonviral Hepatitis hepatotoxins can cause inflammation and necrosis of the liver.Drugs include Acetaminophen,halothane,phenothiazines, tetracycline,Chemicals include Carbon tetrachloride,toluene,ethanol,Direct effect of toxins
Cirrhosis Progressive destruction of the liver caused by Alcoholic liver disease.Extensive diffuse fibrosis,Interferes with blood supply,Bile backup. Loss of lobular organization,Degenerative changes asymptomatic until advanced.Liver biopsy and serologic test
Biliary cirrhosis Associated with immune disorders
Postnecrotic cirrhosis Linked with chronic hepatitis or long-term exposure to toxic materials
Metabolic cirrhosis Usually caused by genetic metabolic storage disorders
Initial stage of cirrhosis – fatty liver Enlargement of the liver Asymptomatic and reversible with reduced alcohol intake
Second stage of cirrhosis – alcoholic hepatitis Inflammation and cell necrosis Fibrous tissue formation – irreversible change
Third stage – end-stage cirrhosis Fibrotic tissue replaces normal tissue. Little normal function remains.
Functional Losses with Cirrhosis Decreased removal and conjugation of bilirubin,production of bile,Impaired digestion/absorption of nutrients, Decreased blood-clotting factors,Impaired glucose/glycogen metabolism,conversion of ammonia to urea ,inactivation of hormones/drugs and toxins
Manifestations of cirrhosis Initial often mild;Fatigue, anorexia,weight loss,anemia,diarrhea,Dull aching pain in upper right quad, Advanced cirrhosis;Ascites/peripheral edema Increased bruising,Esophageal varices May rupture,hemorrhage,circulatory shock Jaundice,encephalopathy
Cirrhosis – Treatment Avoidance of alcohol or specific cause Supportive or symptomatic treatment Dietary restrictions Balancing serum electrolytes Paracentesis Antibiotics to reduce intestinal flora Emergency treatment if esophageal varices rupture Liver transplant
Hepatocellular carcinoma Most common primary tumor of liver More common in cirrhotic livers
Secondary or metastatic cancer Arises from areas served by the hepatic vein or spread along the peritoneal membranes
Acute Pancreatitis Inflammation of the pancreas Results in autodigestion of the tissue May be acute or chronic,Pancreas lacks a fibrous capsule
Etiology of Acute Pancreatitis Gallstones Alcohol abuse Sudden onset may follow intake of a large meal or a large amount of alcohol
S/S acute pancreatitis Severe epigastric or abdominal pain radiating to the back,Signs of shock, Low-grade fever until infection develops, Abdominal distention and decreased bowel sounds,Decreased peristalsis and paralytic ileus
Diagnostic tests for acute pancreatitis Serum amylase: first rise, then fall after 48 hours Serum lipid levels are elevated Hypocalcemia Leukocytosis
treatment for pancreatitis Oral intake is stopped. Treatment of shock and electrolyte imbalances Analgesics for pain relief
Pancreatic Cancer Risk factors Smoking Pancreatitis and dietary factors,Weight loss and jaundice early manifestations Frequently asymptomatic until well advanced Metastases occur early. Mortality is close to 95%.
Adenocarcinoma most common form of pancreatic cancer Arises from the epithelial cells in the ducts
Celiac Disease Malabsorption syndrome,Primarily a childhood disorder,occurs in adults,genetic link Defect in intestinal enzyme,Prevents further digestion of gliadin, Toxic effect on intestinal villi, Malabsorption and malnutrition result
Chronic Inflammatory Bowel Disease Crohn disease and ulcerative colitis are chronic inflammatory bowel diseases (IBDs). Causes unknown Genetic factor appears to be involved. Crohn disease – often during adolescence Ulcerative colitis – second or third decade
Crohn Disease Affects digestive tract usually small intestine,Inflammation occurs,Skip lesions-affected areas,Progressive inflammation and fibrosis cause obstructed areas.Damaged walls impair processing and absorption of food.Inflammation stimulates intestinal motility
Ulcerative Colitis Inflammation in rectum,then through colon,inflamed Mucosa and submucosa.Tissue destruction interferes with absorption of fluid and electrolytes.acute episodes,toxic megacolon,Diarrhea.Contains blood and mucus Accompanied by cramping pain
Treatment of IBD Team approach Anti-inflammatory medications Sulfasalazine or glucocorticoids Antimotility agents Nutritional supplements Antimicrobials Immunotherapeutic agents Surgical resection Usually ileostomy or colostomy
Appendicitis – Development Obstruction of the appendiceal lumen,Fluid inside the appendix,wall becomes inflamed,Ischemia and necrosis of the wall,Bacteria and toxins escape,Abscess develop when inflamed area is walled off,Localized infection/ peritonitis.necrosi/gangrene,ruptures
Appendicitis s/s After rupture Pain subsides temporarily. Pain recurs severe generalized abdominal pain and guarding,fever and leukocytosis,inflammation “Boardlike” abdomen,tachycardia,hypotension, abdominal wall muscles spasm. Toxins lead to reduced blood pressure
Diverticulum Outpouching (herniation) of the mucosa through the muscular layer of the colon
Diverticulosis Asymptomatic diverticular disease
Diverticulitis Inflammation of the diverticula
Diverticular Disease Form at gaps between muscle layers Congenital weakness of wall may be a factor. Weaker areas bulge when pressure increases. Many cases are asymptomatic. Diverticulitis stasis of material in diverticula leads to inflammation and infection.
Colorectal Cancer Most malignancies develop from adenomatous polyps.Early diagnosis is essential. Cancer occurs primarily in persons over 50. Risk factors;Familial multiple polyposis Long-term ulcerative colitis;Genetic factors Environmental factors Diet low in fiber
Intestinal Obstruction Gases and fluids accumulate proximal to blockage,distending the intestine. Increasingly strong contractions of proximal intestine,Pressure increases in lumen.secretions enter the intestine. Compression of veins in wall,edematous.Prevention of absorption
Functional obstructions or paralytic ileus from? After abdominal surgery Spinal shock following spinal cord injuries Inflammation related to severe ischemia Pancreatitis, peritonitis, infection in the abdominal cavity Hypokalemia Mesenteric thrombosis Toxemia
Mechanical obstruction from? Adhesions that twist or constrict intestine Hernias Strictures caused by scar tissue Masses – tumors or foreign bodies Intussusception Volvulus Hirschsprung disease Gradual obstruction from chronic inflammatory conditions
Peritonitis Inflammation of the peritoneal membranes
Chemical peritonitis may result from? Enzymes released with pancreatitis Urine leaking form a ruptured bladder Chyme spilled from a perforated ulcer Bile escaping form the ruptured gallbladder Blood Any other foreign material in the cavity
Bacterial peritonitis By direct trauma affecting the intestine Ruptured appendix Intestinal obstruction and gangrene
S/S PERITONITIS Sudden,severe,generalized abdominal pain Localized tenderness at site of underlying problem Vomiting is common; abdominal disention Dehydration, hypovolemia, low blood pressure Decreased blood pressure, tachycardia, fever, and leukocytosis Treatment
Created by: cdanella