Digestive System Disorders - 2 Flashcards
Antiemetic
E.g. dramamine - reduces vomiting resulting from drugs, motion sickness, radiation
Antidiarrheal
E.g. imodium - reduces intestinal motility
Anti-inflammatory
Prednisone - Reduces inflammation. Prednisone blocks immune response
Acid-reduction
Zantac, PPIs - Reduces secretion of HCl in stomach
Antimicrobial
Biaxin - combination therapy for H. Pylori infection
Coating agent
Carafate - covers ulcer to allow healing
Antacid
Maalox - reduces hyperacidity
Laxative
Psyllium - With water, increases fecal bulk
Anticholinergics
Pirenzepine - reduces PNS activity - reduces secretion and mobility
Histamine-2 blockers
Zantac - inhibits acid production in stomach
PPI
Reduces gastric secretions
Aphthous ulcers - canker sores
Strep Sanguis - resident flora of oral cavity, often accompany fevers, stress, ingestion of certain foods. Small, shallow, painful lesions. Punched out, whitish appearance
Candidiasis
Often part of the normal resident flora of the mouth, opportunist under certain conditions. Oral candidiasis (thrush) - fungal infection that occurs in individuals who have received broad-spectrum antibiotics, cancer chemo, or glucocorticoids, or diabetes or immunosuppressed.. Whitish patches that can be wiped off to reveal erythema.
Syphilis
Oral lesions, contain microorganisms that are highly contagious during the first and second stages. Primary stage characterized by a chancre, a painless ulcer usually found on the tongue, lips, or palate. The lesion healths spontaneously in a week or two. Second stage - red macules or papules on the palate, or by mucous patches, multiple irregular, loose, white necrotic material on the mucosa which is highly infectious, red rash. Usually treated with penicillin because the organism can exist in general ciruclation.
Dental caries
Tooth decay, cavities. Invection involving Streptococcus mutans as the initiator, followed by increased numbers of Lactobacillus and other acid-producing resident flora in the oral cavity. The bacteria act on sugars and create large quantities of lactic acid that dissolve minerals in tooth enamel. Fluoride - decreases solubility of minerals in enamel and enhances remineralization.
Periodontal disease
Peridonteum consists of the gingivae (gums) and the anchoring structure for the teeth - the alveolar bone around the teeth, the cementum (outer covering of the root of the tooth) and the periodontal ligament joining the cementum to the bone. Periodontitis is the infection and damage to the periodontal ligament and bone by microorganisms, and the loosening of teeth.
Gingivitis
Inflammation of the gingiva, tissue becomes red, soft and swollen and bleeds easily. Can be caused by accumulated plaque (mass of bacteria and debris adhering to the tooth)
Tartar
Calcified plaque
Necrotizing periodontal disease (trench mouth)
Common infection caused by anaerobic opportunistic bacteria in individuals in whom tissue resistance is decreased by stress, smoking, disease, or nutritional deficits.
Periodontitis
More serious forms of periodontal disease - increase in activity of gram-negative anaerobic bacteria as they enter the plaque. These microbes secrete toxins and enzymes destructive to the tissues and white blood cells.
Hyperkeratosis
Leukoplakia - whitish plaque or epidermal thickening of the mucosa that occurs on the buccal mucosa, palate, lower lip or tongue. Can lead to squamous cell carcinoma.
Oral squamous cell carcinoma
Smokers, leukoplakia, alcohol abuse. Malignant tumors can be hidden and painless. Can spread to lymph nodes. Appears initially as whitish thickening
Sialadentitis
Salivary gland disorder. Inflammation of the salivary glands, Can be infectious or non infectious.
Infectious parotitis
Mumps, viral infection, bilateral swelling of the gland.
Dysphagia
Difficulty swallowing
Neurological deficit - infection, stroke, brain damage, achalasia - failure of lower esophageal sphincter to relax due to loss of innervation, loss of peristalsis in lower esophagus.
Muscular disorder
Mechanical obstruction
Stenosis
Narrowing of the esophagus, developmental or acquired. Can also result from scar tissue - formed after ingestion of corrosive chemicals.
Esophageal diverticula
Outpouchings of the esophageal wall resulting either from congenital defects or inflammation. Obstructs the flow of food down the esophagus, causes irritation, inflammation and scar tissue. Dysphagia, bad breath, chronic cough, hoarseness.
Hiatal Hernia
Part of stomach protrudes through hiatus in diaphragm into the thoracic cavity. Sliding - the hernia moves back to normal when standing. Paraesophageal - part of the fundus moves up through hiatus and blood vessels in the wall may be compressed leading to ulceration. Food can lodge causing inflammation, reflux, and dysphagia. Caused by shortened esophagus, weak diaphragm, increased abdominal pressure. Signs include heartburn, sour taste in mouth from reflux
Gastroesophageal Reflux Disease
Periodic flow of gastric contents into the esophagus, often seen in conjunction with hiatal hernia. Severity depends on competence of the lower esophageal sphincter or relative pressures on either side. Inflammation and ulceration of mucosa, can cause fibrosis and stricture in the esophagus. Eliminating factors - caffeine, fatty foods, alcohol, smoking, drugs, spicy foods.
Gastritis
Inflammation of the stomach, acute or chronic. Acute - Gastric mucosa is inflamed and appears red and edematous, may be ulcerated and bleeding. Caused by:
Infection by bacteria or virus, allergies, ingestion of spciy or irritating foods, excessive alcohol intake, ingestion of aspirin on an empty stomach, ingestion of corrosive or toxic substances, radiation or chemo.
Signs: anorexia, nausea, vomiting, hematemesis, epigastric pain, cramps, fever, headache, possible diarrhea.
Usually self-limiting and gastric mucosa regenerates.
Gastroenteritis
Involvement of the stomach and intestines in an inflammatory process, from infection or allergic reaction. Inflammation of gastric mucosa stimulates vomiting, diarrhea results when the inflammation of the intestines causes increased motility. Nausea and abdominal cramps, fever and malaise.
Usually self-limiting.
Escherichia coli
E. Coli - usually harmless microbe, normally resident in the intestine.
Some infective types can adhere to the mucosa and secrete an enterotoxin, causing gastroenteritis - travellers diarrhea.
Some strains are invasive and cause five forms of intestinal disease.
Onset is acute with severe, watery diarrhea and cramps, progressing to bloody diarrhea and lasting up to a week. In some people the toxin is absorbed and circulates to cause hemolysis of blood cells, can cause anemia and renal failure.
Chronic gastritis
Atrophy of the mucosa of the stomach, with loss of secretory glands. Lack of parietal cells causes achlorhydria and lack of secretion of intrinsic factor, required for absorption of B12. H. pylori often present.
Signs: anorexia, food intolerance, epigastric discomfort, , increased risk of peptic ulcers and gastric carcinoma.
Peptic Ulcer.
Found in duodenum and stomach and lower esophagus
Round cavities, penetrate submucosa. Acid penetrates muscle wall. May erode muscularis and penetrate the wall. Can hit a blood vessel and cause bleeding. Iron deficiency and occult blood
Many factors contribute to decreased resistance of mucosa -
H pylori
Inadequate blood supply (vasoconstriction caused by stress, smoking or shock, severe anemia)
Glucocorticoid secretion or medication - prednisone with catabolic effects
Substances that break down the mucus layer like aspirin, nonsteroidal anti-inflammatory drugs or alcohol
Atrophy of gastric mucosa (chronic gastritis)
Increased acid-pepsin secretions associated with:
Increased gastrin secretion
Increased vagal stimulation or hyper sensitivity to stimuli
Increased number of acid-pepsin secretory cells in stomach
Increased stimulation of acid-pepsin secretion by alcohol, caffeine, or certain foods
Interference with the normal feedback mechanism that reduces acid-pepsin secretion when the stomach is empty
Rapid gastric emptying
What happens when an ulcer erodes completely through the wall?
Chyme enters the peritoneal cavity, resulting in chemical peritonitis, inflammation of the peritoneal membranes and other structures of the abdominal cavity. Inflammation can cause increased permeability of the intestinal wall, passage of bacteria and their toxins into the peritoneal cavity and bacterial peritonitis.
What can recurrent ulceration cause?
Obstruction of digestive tract can result from stricture from scar tissue.
Symptoms of ulcer
Epigastric burning or aching, usually 2 to 3 hours after meals and at night. Heartburn, nausea, vomiting, weight loss. Food intake can relieve discomfort between meals.
Anemia, and occult blood.
Treatment for ulcer
Two or three antimicrobial drugs and medication to reduce acid secretion. Coating agents, antacids. Reducing exacerbating factors. Surgery.
Stress ulcer
Result from severe trauma, such as burns or head injury, occur with serious systemic problems such as hemorrhage or sepsis. Form within hours of precipitating event as the blood flow to the mucosa is greatly reduced, leading to reduced secretion of mucus and epithelia regeneration. Mucosal barrier is lost, acid diffused into the mucosa.
Gastric Cancer
Arises primarily in the mucous glands, most occur in the antrum or pyloric area. Early involves mucosa and submucosa, advanced involves the muscularis layer. Can extend to serosa and to lymph nodes.
Signs are usually milk until advanced. Anorexia, indigestion, epigastric discomfort, weight loss, fatigue, feeling of fullness. Occult blood, anemia.
Dumping Syndrome
Control of gastric emptying is lost, may occur after gastric resection (partial gastrectomy) - large quantities of of food are rapidly dumped into the intestine
Storage stage, dilution of chyme by gastric secretions is missed. Osmotic chyme draws more fluid into intestine, increases distention and motility. During or shortly after meals, cramps, nausea, diarrhea, hypovolemia can cause dizziness, weakness, rapid pulse, sweating.
Hypoglycemia - rapid gastric emptying and absorption leads to high blood glucose levelsand increased insulin secretion, which results in rapid drop in blood glucose with no reserve nutrients from the stomach - tremors, sweating, weakness.
Pyloric stenosis
Narrowing / obstruction of the pyloric sphincter, presence of fibrous scar tissue. In infants, vomiting, small infrequent stool, failure to thrive, dehydration, persistent hunger.
Adults - interference with gastric emptying - persistent feeling of fullness and increased vomiting.
Cholelithiasis
Refers to formation of gallstones, which are masses of solid material that form in the bile
Cholecystitis
Inflammation of gallbladder and cystic duct
Cholangitis
Inflammation usually related to infection of bile ducts
Choledocholithiasis
Obstruction by gallstones of biliary tract
Composition of gallstone
Cholesterol, bile pigment (bilirubin), calcium salts
How do gallstones form?
When bile contains a high concentration of a component such as cholesterol or there is a deficit of bile salts, inflammation of biliary structures.
Gallstones can cause irritation and inflammation in the gallbladder wall (cholecystitis) and the susceptible tissue may then be infected.
Biliary colic
Severe spasms of pain resulting from strong muscle contractions attempting to move gallstone along. Upper right quadrant of the abdomen, often radiates to back and right shoulder. Nausea and vomiting.
High risk for gallstones
Obesity
High cholesterol
Multiparity
Oral contraceptives
Jaundice
Hyperbilirubinemia. Yellowish color of skin and other tissues resulting from high levels of bilirubin in blood. Usually first apparent in the sclera. Product of breakdown of hemoglobin. Not a disease by a sign of many different types of disorders.
Prehepatic jaundice - results from excessive destruction of red blood cells, characteristic of hemoytic anemias or transfusion reactions.
Physiologic jaundice of the newborn - increased hemolysis of red blood cells combine with immature infant liver
Intrahepatic jaundice - occurs in people with liver disease, such as hepatitis or cirrhosis. Impaired uptake of bilirubin from the blood and decreased conjugation of bilirubin by the hepatocytes.
Posthepatic jaundice - obstruction of bile flow into gallbladder or duodenum and backup of bile into blood.
Hepatitis
Inflammation of liver. Can be idiopathic (fatty liver) or from a local infection (viral hepatitis) or from infection elsewhere in the body (mononuceosis) or from chemical or drug toxicity.
Mild inflammation -impairs hepatocyte function
Severe inflammation and necrosis - obstruction of blood and bile flow in the liver and impaired liver function and
Hepatitis
Infection from a group of viruses that specifically target the hepatocytes. Hep A, Hep B, Hep C, Hep D and Hep E.
Liver cells are damaged by direct action of virus (Hep C) or cell-mediated immune responses (Hep B)
Cell injury results in inflammation and necrosis in the liver. Necrosis may be present. Biliary stasis and backup of bile into blood may happen.
Hepatic cells may regenerate, or fibrous scar tissue may form that obstructs the channels used for blood and bile, further damage from ischemia.
How is Hepatitis spread?
Hep B, C, and D may exist in a carrier state, asymptomatic people can carry the virus in their hepatocytes and transmit infection via blood or body fluids. Hep A - Oral-fecal Hep B - blood and body fluids Hep C - blood and body fluids Hep D - blood and body fluids Hep E - oral-fecal Toxic hep - Direct exposure
Hep A
Infectious hepatitis - small RNA virus called Hep A Oral-fecal Contaminated water / shellfish 2-6 weeks incubation Acute but self-limiting infection Detectable by antibodies in the blood
Hep B
Many cases asymptomatic
More than 1 million carriers in the US
5000 deaths annually from associated cirrhosis and cancer.
More than 50% of those who test HIV positive are also Hep B positive
Because so many cases are asymptomatic it spreads easily.
Infected blood and body secretions
Can be passed to fetus
2 months incubation period
Hep C
Most common type transmitted by blood transfusions
Single-stranded RNA
Approx half cases enter a chronic disease state
Increases risk of hepatocellular carcinoma
May exist in carrier state
Hep D
Delta virus
Incomplete RNA, requires presence of Hep B to replicate and produce active infection
Increases severity of Hep B infections
Transmitted by blood
Hep E
Caused by HEV, a single stranded RNA virus, spread by the oral-fecal route.
Lacks a chronic or farrier state.
More common in Asia and Africa, causes fulminant hep with high mortality for pregnant women.
Acute hepatitis
Vary from milk or asymptomatic to severe, often rapidly fatal.
3 stages:
Preicteric or prodromal - incidious, fatigue, malaise, anorexia and nausea, muscle aches, fever, headache, mild upper right quadrant discomfort.
Iceteric or jaundice - Onset of jaundice as serum bilirubin levels rise. As biliary obstruction increases, stools become light in color, urine becomes darker, skin become preuritic. Liver tender and enlarged, milk aching. Blood clotting may be prolonged.
Posticteric or recovery - reduction in signs.
Treatment for hepatitis
No method of destroying hep virus in body. Supportive measures like rest and nutrition.
Hep B and C - treated with interferon and antiviral drug have some good outcomes.
Otherwise gradual destruction of liver occurs - cirrhosis or hepatocellular cancer.
Toxic / Nonviral hepatitis
Hepatotoxins - chemicals or drugs may cause inflammation and necrosis.
Caused by direct effects or an immune response (hypersensitivity) to certain materials.
Hepatotoxic drugs - acetaminophen, tetracycline.
Solvents - ethanol
Hepatocellular damage - results from two processes - inflammation with necrosis or cholestasis (obstructed flow of bile)
Cirrhosis
Progressive destruction of liver tissue leading to liver failure after 80-90% is destroyed
Cirrhosis is the structural changes that take place
May be linked to specific underlying disorders congenital problems or inherited metabolic disorders.
Extensive diffuse fibrosis, loss of lobular organization
Vascular network or biliary ducts destroyed
Fibrosis interferes with blood supply, bile may back up, leading to ongoing inflammation and damage.
Liver can swell, then shrink with fibrosis.
Four general categories of cirrhosis
Alcoholic liver disease
Biliary cirrhosis - immune disorders, obstruction of bile flow, stones, or cystic fibrosis
Postnecrotic cirrhosis - chronic hepatitis, exposure to toxic materials
Metabolic - storage disorders
Alcoholic liver disease stages:
Accumulation of fat in liver cells causing fatty liver
Alcoholic hepatitis - inflammation and cell necrosis occur, fibrous tissue forms, acute inflammation, mild symptoms like anorexia, nausea, liver tenderness
End-stage cirrhosis - fibrotic tissue replaces normal tissue, alters basic liver structure, little function remains.
Major functional losses in people with cirrhosis:
Decreased removal and conjugation of bilirubin
Decreased production of bile
Impaired digestion and absorption of nutrients (fats and fat soluble vitamins)
Decreased production of blood clotting factors and plasma proteins
Impaired glucose / glycogen metabolism
Inadequate storage of iron and vit b12
Decreased inactivation of hormones like aldosterone and estrogen
Decreased removal of toxic substances
Hepatic encephalopathy
Altered blood chemistry, including abnormal levels of electrolytes or amino acids and excessive ammonia (end product of protein metabolism in the liver or intestine, converted by liver cells into urea for excretion by kidneys) affect central nervous system.
Effects related to obstruction of bile ducts and blood flow by fibrous tissue:
Reduction of the amount of bile entering intestine, impairing digestion / absorption
Backup of bile in liver, leads to obstructive jaundice with elevated conjugated and unconjugated bilirubin levels in blood
Blockage of blood flow through liver, leading to hgih pressure in portal veins
Congestion in the spleen increasing hemolysis
Congestion in intestinal walls and stomach
Development of esophageal varices
Development of ascites - fluid in peritoneal cavity causing abdominal distention and pressure
Common manifestations of liver disease
Fatigue, anorexia, indigestion, weight loss - decreased gluconeogenesis, decreased bile for digestions and absorption, portal hyertension leading to edema
Ascites - portal hypertension, elevated aldosterone and ADH levels, decreased serum albumin, lymphatic obstruction in liver
Edema - elevated aldosterone and ADH levels, decreased serum albumin
Esophageal varices - portal hypertension and collateral circulation
Splenomegaly - portal hypertension
Anemia - decreased absorption and storage of iron and Vit B12, malabsorption, splenomegaly, bleeding
Leukopenia, thrombocytopenia - splenomegaly, possible bone marrow depression by ammonia and other toxins
Increased bleeding - Decreased absorption of Vit K, decreased production of clotting factors by liver
Hepatic encephalopathy, tremors, confusion, coma - metabolic dysfunction with inability to remove ammonia from protein metabolism and other toxic substances
Gynecomastia, Impotence, irregular menses - Impaired inactivation of sex hormones
Jaundice - Impaired extraction and conjugation of bilirubin, decreased production of bile, obstruction of bile flow
Pruritus - bile salts in the tissues resulting from biliary obstruction
Splenomegaly
Backup of blood into spleen
Progression of liver disease
Fatigue, anorexia, weight loss, anemia, diarrhea
Dull aching pain in upper right quadrant
Ascites (abnormal fluid buildup in abdominal cavity) and peripheral edema, increased bruising
Esophageal varices
Jaundice
Encephalopathy - brain disease, damage, malfunction
Spider nevi on skin, testicular atrophy, impotence, gynecomastia (enlargement of male breast tissue, too much estrogen), irregular menses
Ruptured esophageal varices - hemorrhage, circulatory shock, acute hepatic encephalopathy.
Frequent infections - respiratory or skin - excess fluid interrupts diffusion of nutrients, delayed tissue regeneration.
Acute encephalopathy manifestation
Asterixis - “handflapping” tremor, confusion, disorientation, convulsions, and coma.
Personality changes, memory lapses, irritability, disinterest in personal care
Pancreatitis
Inflammation of the pancreas resulting from autodigestion of the tissues. Triggers appears to be activation of proenzyme trypsinogen into trypsin, which then converts other proenzymes and chemicals into active forms. The activated enzymes, trypsin, proteases amylase and lipases digest the pancreatic tissue leading to massive inflammation, bleeding and necrosis. Destruction by trypsin and other enzymes progresses into tissues surrounding pancreas - can lead to hemorrhage.
Cytokines and prostaglandins, released by tissue necrosis lead to widespread inflammation of the peritoneal membranes.
Inflammatory response, vasodilation and capillary permeability leads to hypovolemia and circulatory collapse.
Severe pain caused by autodigestion of nerves contributes to shock
Chemical peritonitis - bacterial peritonitis as intestinal bacteria escape through the more permeable membranes.
Septicemia = may result from escape of bacteria and toxins from intestines into general circulation.
Causes of pancreatitis
Gallstones - obstruct flow of bile and pancreatic secretions into the duodenum or cause reflux of bile into pancreatic duct
Alcohol abuse - stimulates an increased secretion of pancreatic enzymes and to contract the sphincter of Oddi, blocking flow
Signs and symptoms of pancreatitis
Intake of large meal or large amount of alcohol
Severe epigastric or abdominal pain radiating to the back, increases in supine position
Signs of shock - low blood pressure, pallor, sweating, rapid but weak pulse = inflammation and hemorrhage cause hypovolemia
Low-grade fever - common until infection develops
Abdominal distention - decreased bowel sounds
Pancreatic cancer
Risk factor - smoking, pancreatitis, dietary factors
Mortality of 95%
Liver failure from hepatobiliary obstruction is often cause
Celiac disease
Also called celiac sprue or gluten enteropathy
Malabsorption syndrome
Linked to genetic factors
Defect in the intestinal enzyme that prevents further digestion of gliadin, a breakdown product of gluten
Combo of digestive block and immunologic response results in toxic effect on intestinal villi, which atrophy, resulting in decreased enzyme production and less surface area available for absorption of nutrients.
Chronic Inflammatory Bowel Disease - Chrohn’s
Crohn’s and ulcerative colitis, causes unknown
High familial incidence
Could be immune related
May be overlap in clinical presentation between the two diseases
Remissions and exacerbations
Crohn’s - any area of GI tract, most frequently small intestine. Inflammation in characteristic distribution - skip lesions - affected segments clearly separated by areas of normal tissue.
Starts with lesions in mucosal layer, ulcers coalesce to form fissures, inflammation and fibrosis can affect all layers of wall, leads to thick, rigid, narrow lumen, can become totally obstructed. Impaired ability to process and absorb food. Inflammation stimulates intestinal motility, decreasing time for digestion and absorption.
Can lead to hypoproteinemia - lack of protein in blood, avitaminosis, malnutrition, steatorrhea -excretion of abnormal amounts of fat in feces
Adhesions between two loops of intestine when subserosa is inflammed, abscesses, fistulas
Signs and symptoms of Crohn’s
Diarrhea with cramping, abdominal pain, melena, right lower quadrant pain, anorexia, weight loss, anemia, fatigue.
Ulcerative Colitis
Inflammation commences in the rectum and progresses in a continuous fashion proximally through the colon, small intestine rarely involved. Mucosa and submucosa inflammed.
Tissue - edematous and friable, ulcerations
Granulation tissue form - fragile and bleeds easily
Ulcers coalesce, large areas of mucosa become denuded, interferes with absorption of fluid and electrolytes in colon
Toxic megacolon
Inflammation impairs peristalsis, leading to obstruction and dilation of the colon.
Signs of ulcerative colitis
Diarrhea, blood, mucus, cramping pain.
Tenesmus - spasms of rectum associated with need to defecate
Anemia
Fever, weight losss
Treatments for Irritable Bowel Disease
Reducing stress Anti-inflammatories Antimotility drugs Nutritional supplements Antimicrobials for secondary infection Ummunotherapeutic agents Surgical resection.
Irritable bowel syndrome
Gastointestinal disorder
Abdominal pain / discomfort
Changes in normal bowel habits
Diarrhea / Constipation / Pain
Different types of IBS
Abnormal gastrointestinal motility and secretion
Visceral hypersensitivity
Postinfectious IBS = low grade inflammation and abnormal immune response in gut - associated with bacterial enteritis
Overgrowth of flora - constipation, bloating
Food allergy or intolerance
Psychosocial factors - stress which affects autonomic nervous system
Signs and symptoms of IBS
Lower abdominal pain, diarrhea, constipation, gas, bloating, nausea
Appendicitis
Inflammation and infection of the vermiform appendix
Obstruction of the appendiceal lumen by a fecalith - stone made of feces, gallstone, or foreign material, twisting or spasm
Fluid builds up inside the appendix and microorganisms proliferate
Appendiceal wall becomes inflamed and purulent exudate forms, appendix is swollen, blood vessels in the wall are compressed
Increased congestion and pressure within the appendix leads to ischemia and necrosis of the wall, increased permeability
Bacteria and toxins escape through the wall, abscess formation, localized bacterial peritonitis
Infection may spread to peritoneal membranes
Increased pressure inside the appendix, increased necrosis and gangrene in the wall
Appendix ruptures or perforates, releases contents into peritoneal cavity, leads to generalized peritonitis, may be life threatening
Signs and symptoms of appendicitis
General periumbilical pain
Nausea and vomiting
Pain becomes more severe and localized in the right lower quadrant
Lower right quadrant tenderness develops
Severe abdominal pain as peritonitis develops
Fever and leukocytosis
“boardlike” abdomen, tachycardia, hypotension
Diverticular Disease
Congenital or acquired
Diverticulum - herniation or outpouching of the mucosa through the muscle layer of the colon wall, frequently in the sigmoid colon
Diverticulosis - multiple diverticula present, asymptomatic
Diverticulitis - inflammation of the diverticula.
Complications - intestinal obstruction, perforation with peritonitis, abscess formation
Signs and symptoms of diverticular disease
Mild discomfort, diarrhea, constipation, flatulence.
Inflammation related to stasis of feces. Lower left quadrant cramping or steady pain and tenderness with nausea and vomiting.
Elevated white blood cell count, slight fever
Treatment for diverticulitis
Food intake reduce, antimicrobial drugs, increased bulk, encouraging regular bowel movements
Colorectal Cancer
Second leading cause of cancer-related deaths
Many deaths could be prevented by early treatment of precancerous lesions such as polyps and early detection of malignancy.
Most malignant neoplasms develop from adenomatous (benign tumors in glandular tissue) polyps
As polyps increase in size they carry an increased risk of dysplasia and malignant changes.
All types of carcinomas invade the wall, mesentery and the lymph nodes and metastasize to the liver.
Diets high in fat, sugar and red meat are thought to produce carcinogenic substances. Low-fiber diets increase risk because they prolong contact of mucosa and carcinogens.
Signs and Symptoms of Colon cancer
Depend on location and characteristics of feces at that location
Rectosigmoid - feces more solid - partial obstruction, cramping, flat pellets or ribbon stool, feeling of incomplete emptying
Right colon - fecal material liquid - general signs like fatigue, weight loss, anemia
Intestinal Obstruction
Lack of movement of the intestinal contents through the intestine, most occur in small intestine because of smaller lumen. Twisting can cause a total obstruction, tumor can lead to progressive obstruction
Mechanical obstruction - tumor, adhesions, hernias etc
Functional - obstructions from neurologic impairment like spinal cord injury or lack of propulsion - often referred to as paralytic ileus.
Signs of mechanical obstruction
Gases and fluids accumulate proximal to blockage, distending the intestine
Strong contractions of the proximal intestine in an effort to move contents onward
Increasing pressure in he lumen, leads to more secretions entering the intestine, compresses veins in the wall preventing absorption, intestinal wall edematous
Intestinal distention leads to persistent vomiting with additional loss of fluid and electrolytes
Small intestinal obstructions - no opportunity to reabsorb fluid and electrolytes so hypovolemia occurs
Intestinal wall becomes ischemic and necrotic as blood supply to tissue is reduced, intestinal wall can become necrotic and gangrenous
Decreased innervation, cessation of peristalsis (decrease in bowel sounds)
Rapid reproduction of intestinal bacteria - some produce endotoxins. Affected intestinal wall becomes necrotic and more permeable, bacteria can leak into the peritoneal cavity (peritonitis) or the blood supply (bacteremia and septicemia)
Functional obstruction
Usually from neurologic impairment - peristalsis ceases and distention of intestine occurs as fluids and electrolytes accumulate. Reflex spasms of intestinal muscle do not occur.
When is functional obstruction or paralytic ileus common?
After abdominal surgery, effects of anesthetic combine with inflammation or ischemia in the operative area interfere with conduction of nerve impulses
Initital stage of spinal cord injuries
Inflammation related to severe ischemia
In pancreatitis, peritonitis, or infection of abdominal cavity
Hypokalemia, mesenteric thrombosis - blood clot forms in one or more major veins draining blood from intestines, toxemia
When can a mechanical obstruction result?
Adhesions from pervious surgery, infection, radiation that twist or constrict intestine
Hernias
Strictures from scar tissue
Masses such as tumors or foreign bodies
Intussusception (telescoping of a section of bowel inside an adjacent section), may also occur secondary to polyps or tumors that pull a section of bowel forward
Volvulus (twisting) ma be linked to adhesions
Congenital megacolon - parasympathtic innervation missing, impairing motility
Gradual obstruction from Crohn’s or diverticulitis
Signs and symptoms of mechanical obstruction
Severe colicky abdominal pain as peristalsis increases, audible rumbling caused by movement of gas and intestinal rushes as intestinal muscle forcefully contracts in attempt to propel contents forward
Vomiting
Abdominal distention
No stool or gas
Restlessness, diaphoresis, tachycardia, hypovolemia and electrolyte imbalance, dehydration, weakness, confusion, shock
Peritonitis
Inflammation of the peritoneal membranes
Chemical irritation or bacterial invasion
Chemical irritation - bile, chyme, foreign objects, increases permeability of intestinal wall, permits enteric bacteria to enter peritoneal cavity.
Peritoneum and omentum can stick to temporarily seal the area and localize it.
Because the peritoneum is highly vascular it provides a means of rapid dissemination of irritants or bacteria throughout the abdominal cavity
Abdominal distention, rigid abdomen as a reflex
Membrane inflammes leading to vasodilation and increased permeability, membrane edematous and red, can leak fluid into peritoneal cavity, hypovolemic shock
Nausea and vomiting add to fluid loss
Nerve conduction impaired, peristalsis decreases, obstruction (paralytic ileus)
Septicemia.
Chemical peritonitis
Enzymes released form pancreatitis, urine leaking from ruptured bladder, chyme, bile, flood
Bacterial Periotonitis
Direct trauma to intestines, ruptured appendix, intestinal obstruction
Abdominal surgery - if foreign material remains in the abdomen or infection develops
Pelvic inflammatory disease
Infection ascends through the uterus and into the fallopian tubes, which procede direct access to peritoneal cavity
Signs and symptoms of peritonitis
Sudden, severe, generalized abdominal pain, localized tenderness, vomiting, dehydration, hypovolemia, decreased skin turgor, pallor, low blood pressure, agitation, tachycardia
Fever
Leukocytosis
Abdominal distention
Rigid abdomen - involvement of parietal peritoneum
What exocrine products does the pancreas produce?
Amylase, lipase, trypsin, bicarbonate (neutralizes chyme)
What does histamine do in the stomach
Increases secretion of HCl
What does secretin do?
Released from mast cells, decreases gastric secretions, increases bicarbonate and bile release if chyme is acidic
What does cholecystokinin do?
Released by mucosal cells when chyme enters duodenum
Inhibits gastric emptying
Stimulates contraction of gallbladder
Where does digestion of carbs happen?
Oral cavity - salivary amylase
Duodenum - brush border enzymes
Where does protein digestion happen?
Starts in stomach, digestion of peptides happens in the small intestine
Where does lipid absorption happen?
Emulsification by bile, formation of chylomicrons due to enzymes in small intestine, absorption into lacteals
Where does vitamin absorption happen?
A, D, E and K are absorbed with fats
Water soluble B and C absorb into blood
Myenteric plexus
Lies between two layer of muscle in intestine, causes them to contract
How long does it take chyme to pass through small intestine?
5 hours
After surgery and a regimen of antibiotics, an individual often experiences diarrhea and sometimes vitamin K deficiency. What is a probable explanation for these conditions?
Irritation of the colon due to drugs or imbalance of intestinal flora may affect fluid absorption, resulting in diarrhea. The imbalance in the normal bacterial flora due to the antibiotics may affect the synthesis of vitamin K and vitamin B, which takes place in the colon.
Why might a patient with a malfunctioning liver also experience a bloody nose and excessive bleeding from minor cuts?
The liver is responsible for the synthesis of fibrinogen and other clotting factors.
Why might a patient with a damaged pancreas also experience irritation and reduction of nutrient absorption in the small intestine?
The pancreas secretes bicarbonate into the duodenum, neutralizing acidic chyme from the stomach.
Why might a patient with a head and neck injury also experience constipation or infrequent bowel movements?
Intestinal motility is controlled by the parasympathetic branch of the autonomic nervous system. Damage or trauma to the vagus nerve could affect intestinal motility and defecation.
What is the importance of the release of cholecystokinin in digestion?
Cholecystokinin is released when chyme from the stomach enters the duodenum. It in turn stimulates the release of bile by the contraction of the gallbladder, which is essential for the continuation of digestion in the small intestine. It also inhibits gastric emptying to allow the bile and bicarbonate to neutralize the chyme in the intestine before more chyme is emptied into the duodenum.
Why might the same liver damage also affect certain vitamin levels?
The liver stores lipid-soluble vitamins A, D, E, and K.
Referred pain
Occurs when visceral and somatic nerves join at one spinal cord level
Source of the visceral pain is perceived as the same as that of the somatic nerve, a situation that may delay an accurate diagnosis
Why do poorly absorbed solutes from the lumen of the GI tract cause diarrhea?
A significant amount of solutes will cause water and sodium to move into the lumen from the tissue, resulting in diarrhea.
How could repeated failures to respond to the defecation reflex (“holding back”) make the constipation worse?
Delaying passage of the feces may allow excessive water reabsorption by the colon, resulting in a compacted, hard, dry fecal plug.
Why do people who have lactose intolerance often experience excessive belching and/or flatus when they eat ice cream?
The lactose is inadequately digested by the body; however, the bacteria in the lower GI tract will break down the lactose, producing gas as a byproduct.
When fluids are lost from vomiting, how can two different and opposite imbalances be possible (alkalosis or acidosis)?
It depends where the fluid lost by vomiting comes from. If it comes from the stomach, the acid loss may cause alkalosis. If it comes from the duodenum (severe vomiting) and is high in bicarbonates, the result can be acidosis.
How can pain caused by trauma at one spot of the GI tract be felt on the opposite side?
Referred pain is where visceral nerves affect the somatic nerves in the same region of the spinal cord, so the pain is perceived at a point other than the origin.
Symptoms of GERD
Heartburn or burning sensation in the chest Increased by bending, lying down, or eating Worse at night Relieved by antacids Feeling that food is left in the esophagus Nausea after eating Less common symptoms: Cough or wheezing Difficulty swallowing Hoarseness or change in voice Regurgitation of food and hiccups Sore throat
Explain how a hiatal hernia may contribute to gastroesophageal reflux disease.
A hiatal hernia can put pressure on the proximal end of the stomach where the esophagus connects to the stomach. If the diaphragm puts pressure on that part of the stomach above the herniation, it could force stomach contents back up and into the esophagus.
How might chronic gastritis eventually lead to a more severe condition such as a peptic ulcer?
The chronic irritation of the mucosa can lead to an atrophy of the stomach lining, exposing deep tissue to the destructive effects of stomach acid and possible bacterial infection.
Explain how a urea breath test might work for detection of a peptic ulcer.
H. pylori is a major cause of peptic ulcers. This organism is known to secrete urease, which breaks down urea. The breakdown of urea produces ammonia, which can be detected in exhalation.
When patients suffer from dumping syndrome, why are diarrhea and hypoglycemia typical symptoms?
The large quantities of chyme from the stomach that enter the small intestine are hyperosmotic and fluid is drawn into the intestine, resulting in diarrhea. The large quantity of chyme dumping into the intestine also causes a large increase of insulin secretion, resulting in hypoglycemia within 2 to 3 hours after a meal.
3 stages of hepatitis
Preicteric - prodromal - Fatigue and malaise
Anorexia and nausea
General muscle aching
Fever, headache, distaste for cigarettes, and mild upper right quadrant discomfort may be present
Icteric - jaundice - Serum bilirubin levels increase (onset of jaundice).
Stools become light in color, urine becomes darker, and skin becomes pruritic; all are due to increased biliary obstruction.
Liver becomes enlarged and tender.
In severe cases, blood clotting may be impaired because the synthesis of blood clotting factors is decreased.
Serum bilirubin levels increase (onset of jaundice).
Posticteric - recovery
Causes of cirrhosis
Alcoholic liver disease (figure A)
Chronic hepatitis C (figure B)
Biliary cirrhosis, associated with immune disorder, those causing obstruction of bile flow such as stones or cystic fibrosis
Postnecrotic cirrhosis, linked with chronic hepatitis or long-term exposure to toxic materials
Metabolic problems, generally caused by storage disorders such as hemochromatosis
Loss of liver function
Decreased removal and conjugation of bilirubin
Decreased production of bile
Impaired digestion and absorption of nutrients
Decreased production of blood-clotting factors
Impaired metabolism of nutrients
Inadequate storage of iron and vitamin B12
Decreased inactivation of hormones
Decreased removal of toxic substances
Reduction of bile entering the intestine, which impairs digestion and absorption
Blockage of blood flow through the liver, leading to obstructive jaundice and increasing hemolysis
Backup of bile in the liver, leading to portal hypertension
Blockage of blood flow through the liver
Congestion in the spleen
Congestion in intestinal walls and stomach, impairing ingestion and absorption
Development of esophageal varices
Development of ascites, causing abdominal distention and pressure
Why is alcoholic cirrhosis a risk factor for the development of gallstones?
When the liver is damaged by cirrhosis, the cholesterol is not efficiently broken down and too much cholesterol is in the bile, which is stored in the gallbladder. The cholesterol gallstones form from this bile while stored in the gallbladder.
Why would a patient displaying jaundice also suffer from hemolytic anemia?
Jaundice is a result of high levels of bilirubin in the blood. The bilirubin is a product of the breakdown of red blood cells.
