| Term 
 | Definition 
 
        | hollow muscular tube that begins at the mouth and ends at the anus; encompasses the pharynx, esophagus, stomach, small/large intestineprimary functios are to digest & absorb foods & fluids & excrete metabolic waste
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | affect the mouth or  esophagus, compromising a pt's ability to ingest food usually occur secondary to a primary disease (e.g. cancer, acquired immunodeficiency syndrome (AIDS), diabetes) or result from poor dentitionstomatitis, esophagitis, achalasia (slow transit of food from mouth to stomach), esophageal hiatal hernia & oral & esophageal cancers are disorders of food intakerisk factors: presence of primary disease, malnutrition, use of tobaccosome disorders, such as hiatal hernia & achalasia, have no specific risk factors
 |  | 
        |  | 
        
        | Term 
 
        | disorders of digestion & absorption |  | Definition 
 
        | disorders of digestion & absorption affect the stomach and small intestine, hindering the body's ability to break down food & absorb essential nutrientsgastritis, peptic ulcer disease, gastroenteritis  (stomach flu), malabsorption syndrome, stomach cancer & cancer of the small intestine are disordersulcerative colitis and regional enteritis (Crohn's disease) are considered disorders of digestion/absorption as well as eliminationrisk factors: genetic predisposition, stress, administration of certain drugs, use of tobacco
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | disorders of elimination affect the large intestine, rendering a person unable  to maintain a normal elimination patternthese may occur alone, as a sequal to another disease, or as a result of admin certain drugsdisorders in elimination result in abnormal amts or constituents of stoolulcerative colitis, regional enteritis (Crohn's), irritable bowel syndrome (exculsion diagnosis), diverticulitis, & cancer of the large intestinerisk factors: presence of cancer, genetic predisposition, stress, ingestion of foods that do not agree w/ the individual, admin of certain drugs, use of tobacco 
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | always made worse by the use of tobacco & ETOH; avoiding these substances is part of the treatment for any GI disorder |  | 
        |  | 
        
        | Term 
 
        | physiological responses to gastrointestinal dysfunction: |  | Definition 
 
        | Halitosis: foul smelling breath; may indicate periodontal or oral infectious processdysphagia: difficulty swallowing; may result from mechanical problem (e.g. neoplasm, surgery) or occur secondary to neurologic damage or dysfunction (e.g. CVA)Odynophagia: painful swallowing; important marker for infection or diseasePyrosis (heartburn): burning sensation usually in midsternal area caused by reflux of gastric contents into esophagusdyspepsia (ingestion): feeling of discomfort during digestive process, or inability to digest food secondary to GI disorderanorexia: loss of appetite, common complaint associated w/ GI disease; causes can include: neoplastic process ,anxiety, pain, depression, infection, or constipationsatiety: feeling of fullness, at times beyond the point of satisfactionmalabsorption: inability to absorb nutrients secondary to GI disorder or surgeryaltered bowel sounds: indicate passage of air/fluid in GI tract; diminished or absent after abdominal surgery or hyperactive/high pitched as a result of hypermotility of GI tractmelena: black or tarry stools indicating presence of blood
 |  | 
        |  | 
        
        | Term 
 
        | peptic ulcer disease (PUD) |  | Definition 
 
        | chronic condition characterized by ulceration of the gastric mucosa, duodenum; less frequently of the lower esophagus & jejunumduodenal ulcers are 3x more prevalent than gastric ulcers & usually occur between 20-50yrs of age
 |  | 
        |  | 
        
        | Term 
 
        | pathophysiology of peptic ulcer disease |  | Definition 
 
        | not fully understoodpossible contributing factors:mucosal breakdown secondary to infection w/ gram-neg Helicobacter pylorigenetic predispositiontobacco useingestion of food/drugs that injure or alter gastric mucosa or increase HCL production (e.g. ASA, corticosteroids, caffeine, spicy foods)stresspresence of disease that alter gastric secretion (e.g. pancreatitis, Crohn's)
increased Cl secretioninagdequate mucosal defense against gastric acid
 |  | 
        |  | 
        
        | Term 
 
        | protecting factors of PUD |  | Definition 
 
        | mucus   bicarbonate   prosteglandins  |  | 
        |  | 
        
        | Term 
 
        | treatment approaches for PUD |  | Definition 
 
        | eradicating H.pylori infectionreducing secretion of gastric acid or neutralizing the acid after it is released providing agents that protect the gastric mucosa from damage
 |  | 
        |  | 
        
        | Term 
 
        | regulation of gastric acid secretion |  | Definition 
 
        | gastric acid secretion by parietal cells of the gastric mucosa is controlled by acetylcholine, histamine, prostoglandins E2 & I2 & gastrinreceptor-mediated binding of Ach, histamine, or gastrin results in activation of a H/K-APTase proton pump that secretes HCl into the lumen of the stomachin contrast, receptor binding of prostaglandins E2 & I2, diminishes HCl production
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | H.pylori is a gram-neg, curved or spiral bacterium found primarily in the mucous layers of the gastric antrum of humansproduces significant amts of urease, which catalyzes the hydrolysis of urea into ammonia & CO2; ammonia neutralizes gastric acid & is toxic to gastric epithelial cells; also, stimulates gastric epithelial cells to release proinflammatory substances that participate in the initiation of inflammation & tissue injurymost common chronic bacterial infection in humans & is a well-established primary causative factor of PUD; has been linked to other types of gastritis, gastric adenocarcinoma, & low grade gastric lymphoma arising from mucosa-associated lymphoid tissue (MALT)H.pylori associated PUD afflicts about 10% of US popl'nmode of transmission is not known; thought to be person to person through fecal-oral or oral-oral contact, gastric routes, or hands (so, not blood)
 |  | 
        |  | 
        
        | Term 
 
        | clinical syndrome:   helicobacter pylori  |  | Definition 
 
        | factors that determine disease outcome - not fully understood; estimated that only 1 in 6-7 infected people will develop PUD; risks of gastric adenocarcinoma & gastric lymphoma are even lower 
 |  | 
        |  | 
        
        | Term 
 
        | treatment for helicobacter pylori |  | Definition 
 
        | a combo drug regimen; no regimen is ideal, and no regimen can eradicate the infection in 100% of treated ptstriple regimens comprising a PPI, clarithromycin & amoxicillin are regarded as first-line; should be used for 10-14 days (4 tablets BID)7-day & 3-day regimens are awaiting FDA approvalpts allergic to PCN-combo of PPI, clarithromycin & metronidazole;  this is associated w/ higher incidence of side effects; moreover, if this tx fails, H.pylori may be resistant to both clarithromycin & metronidazole after tx; therefore, not recommended for routine use
 |  | 
        |  | 
        
        | Term 
 
        | gastroesophageal reflux disease |  | Definition 
 
        | constellation of sx caused by the reflux of acidic gastric content into the esophaguscontributing pathophysiologic mechs: (H.pylori +)decreased esophageal clearanceincompetence of the lower esophageal sphincter (LES)impaired resistance of esophageal mucosadelayed gastric emptyingpresence of hiatal hernia
small amt of physiologic reflux (<5.5% of the time) - normal.  in majority of GERD pts, pathology's cause is not acid overproduction but length & frequency of esophageal acid exposure 
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | GER: passage of gastric contents into the esophagusregurgitation: passage of gastric contents into the oropharynxemesis: expulsion of gastric contents from the mouth
 |  | 
        |  | 
        
        | Term 
 
        | physiologic reflux      vs.     pathologic reflux  |  | Definition 
 
        | physiologic reflux: reflux that does not compromise health or well-being (the usual cause in infancy) - if baby is not gaining weight, the it could be a problempathologic refulx: reflux associated w/ esophagitis, growth failure, respiratory disease, apnea, or psychosocial dysfunction 
 |  | 
        |  | 
        
        | Term 
 
        | clinical presentation of gastroesophageal reflux disease |  | Definition 
 
        | heartburn, acid regurgitation, epigastric pain = most commonothers: belching, dysphagia, odynophagia, cough, hoarseness, nausea, noncardiac chest pain, respiratory complaints: asthma, chronic sinusitisalarm symptoms: serious damage may have already occurred if the followin are present:dysphagia: difficulty w/ swallowingbleeding: vomiting blood or having tarry, black BMschoking: sensation of acid refluxed into the windpipe causing SOB, coughing, or hoarsenessweight loss
 |  | 
        |  | 
        
        | Term 
 
        | management of gastroesophageal reflux disease |  | Definition 
 
        | individualized depending upon severity of symptoms; goals are to:relieve symptomsheal esophagitis if presentprevent complicationsmaintain remissiontreat complications
 |  | 
        |  | 
        
        | Term 
 
        | gastroesophageal reflux disease:   tx in infants  |  | Definition 
 
        | physiologic GER (infancy):smaller, more freqeunt feedingsmore frequent burpingpositioning (up at 30 degrees)thickening of feedings (some advise adding rice cereal to formula); will eat less volume elemental formula (simple amino acids to baby doesn't need gastrin to break down anything into amino acids); very expensive and not sure if it's necessary
only 10% of babies won't correct this by 18yrs old
 |  | 
        |  | 
        
        | Term 
 
        | lifestyle modifications for GER |  | Definition 
 
        | diet modificationsavoid food that aggrevate symptoms (peppermint, chocolate, citrus juice, tomatoes, coffee, smoking, ETOH, fatty foods, spicy foods, onions) - activate gastrin pathwayavoid eating 2-3hrs before bedavoid large meals & quantities of liquid
avoid medications that lower lES tone or decrease motilityelevate head of bedcurtain smoking & ETOH intakeavoid stooping & bendingdo not exercise immediately after eatingavoid tight-fitting clothingreduce weight, if overweight
 |  | 
        |  | 
        
        | Term 
 
        | pharmacodynamics of antacids |  | Definition 
 
        | gastric antacids are weak bases that react w/ gastric HCl to form salt & water: net result = increased gastric pHgoal of antacid tx: pH between 3-3.5 (from original 1.8)can effectively reduce the recurrance rate of peptic ulcers when used regularly in doses that significantly raise the stomach pHacid-neutralizing ability of an antacid depends on its capacity to neutralize gastric HCl & on whether the stomach is full or empty (food delays stomach emptying allowing more time for the antacid to react)since Ca salts stimulate gastrin release, use of Ca-containing antacids may be counterproductive
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | magnesium hydroxide (Milk of Magnesia)   aluminum hydroxide (AlternaGEL, Amphogel)   aluminum/magnesium cpds (Maalox, Riopan)   aluminum hydroxide & magnesium hydroxide (Maalox II, Mylanta II)   calcium carbonate (TUMS)   sodium bicarbonate  |  | 
        |  | 
        
        | Term 
 
        | pharmacokinetics of antacids |  | Definition 
 
        | duration of action is only 2hrs; need to be taken frequentlydiffer mainly in their absorption & effects on stool consistencyMg & Al compounds are not as absorbed from the bowelMg hydroxide has strong laxative effectsAluminum hydroxide has constipating actions; reacts w/ HCl to form an insoluble cpdboth calcium carbonate & sodium carbonate are absorbed from the gut; b/c of their systemic effects are less popular as antacids that Mg & Al saltssodium bicarb is used to treat metabolic acidosis; not recommended for tx of PUDcalcium carb's side effects: nephrolithiasis & constipation
 |  | 
        |  | 
        
        | Term 
 
        | contraindications of antacids |  | Definition 
 
        | pts w/ any known allergy to any antacid componentcaution in pts w/ any conditions that electrolyte or acid-base imbalances, GI obstruction, or renal dysfunction may exacerbate (esp Al)
 |  | 
        |  | 
        
        | Term 
 
        | drug interactions with antacids |  | Definition 
 
        | presence of antacids in the stomach may impair absorption of many other drugs; advisable to avoid concurrent admin of antacids & other drugs; by binding to drugs (e.g. tetracycline) Al cpds can form insoluble complexes that are not absorbed; on the other hand, antacids can increase the rate of absorption of some drugs e.g. levodopawhen antacids are taken w/ enteric-coated meds, coating is disintegrated & drug is released prematurely in the stomachCa & Mg preps exacerbate the action of digitalis (secondary to effect of K) - b/c Mg & K always go the same way (Ca goes opposite)
 |  | 
        |  | 
        
        | Term 
 
        | adverse effects of antacids |  | Definition 
 
        | Al cpds: constipation, delayed gastric emptying & hypophosphatemiaCa cpds: costipation, hypercalcemia & renal calcuriMg cpds: diarrhea, w/ resultant hypokalemia, iron deficiency & hypermagnesemia
 |  | 
        |  | 
        
        | Term 
 
        | nursing considerations of antacids |  | Definition 
 
        | onset of drug action is within 5-15min & duration is 2 hrs (short 1/2 life, so usually for short-term issues)admin at least 1 hr before or 2 hrs after any other PO drug to ensure adequate absorptionmonitor electrolytes of the pt who is taking antacids for early detection of an electrolyte imbalanceinstruct pt to chew antacids thoroghly and follow w/ one glass of water to ensure it reaches stomach f or direct action and to avoid development of intestinal concretions calculiinstruct pt to shake liquid preps before pouringacid rebound may be present & repeated use for 1-2wks might cause a rebound acid stim action, quickly leading to development of chronic antacid usepts who receive large quantities of antacids over prolonged period or those who are on a diet that is low in phosphorus (while taking antacids continuously) may develop hypophosphatemia within 2 wks
 |  | 
        |  | 
        
        | Term 
 
        | histamine2-receptor antagonists |  | Definition 
 
        | famotidine (Pepcid)   block histamine2-receptor sites in the gastric mucosa, thus reducing secretion of HClcapable of reducing more than 90% of basal secretions of gastric acid after a single dose (96-99%) - comparable to more expensive proton pump inhibitorPO absorption is good; routes of admin: PO/IV 
 |  | 
        |  | 
        
        | Term 
 
        | contraindications & drug interactions with histamine2-receptor antagonists |  | Definition 
 
        | cimetidine: contraindicated in preg/lactation & liver impairmentcaution in pts w/ renal insufficiency & elderly (dose adjustment recommended)cimetidine: potent inhibitor of enzymes of the P-450 system & can slow metabolism (and thus potentiate action) of several drugs (e.g warfarin, phenytoin, diazepam)famotidine: few drug interactions; do not exhibit inhibitory function on the P-450 system 
 |  | 
        |  | 
        
        | Term 
 
        | adverse effects of histamine2-receptor antagonists |  | Definition 
 
        | inform pt to seek help if symptoms do not subside within 1-2mo of therapyprolonged therapy w/ cimetidine associated with: confusional state, psychotic symptoms, nausea, headahce, reversible gynecomastiacan increase stomach pH sufficiently to allow for outgrowth of microorganisms (bacteria, candida) - not signif. unless has secondary conditions
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | omeprazole (Prilosec), lansoprazole (Prevacid), rabeprazole (Aciphex), pantoprazole (Protonix) IV, esomeprazole (Nexium)   act directly on the secretory surface of the gastric parietal cellsbecome active in an acidic environment & irreversibly inhibit the hydrogen-potassium ATPase gastric enzyme system, which catalyzes the final step of the acid production in the stomachmost effective agents: can essentially inhibit 100% of gastric acid secretion with a single daily dose; their antisecretory effect lasts up to 72hrs (so, better for noncompliant pts) most rapid acting (but very expensive)
 |  | 
        |  | 
        
        | Term 
 
        | pharmacotherapeutics for proton pump inhibitors |  | Definition 
 
        | PUDGERerosive esophagitisZollinger-Ellison syndrome & other hypersecretory syndromessuccessfully used w/ antimicrobials regimens to eradicate H.pylori
 |  | 
        |  | 
        
        | Term 
 
        | contraindications/drug interactions for proton pump inhibitors |  | Definition 
 
        | hypersensitivitypreg cat Ccaution in hepatic impairment (dose adjustment)absorption of concurrent drugs may be decreased b/c of alteration of gastric pH (e.g. Fe, digoxin, ampicillin) 
 |  | 
        |  | 
        
        | Term 
 
        | side effects of proton pump inhibitors |  | Definition 
 
        | as a group well toleratedHA, diarrhea, nausea, emesis (rare w/ short term use)can increase stomach pH sufficiently to allow for outgrowth of microorganisms (bacteria, candida)avoid opening, chewing, or crushing capsules; they should be swallowed whole for therapeutic effect; lansoprazole capsules can be opened and sprinkled on soft foodadvise pt to take PPIs before meals on empty stomach to ensure drug efficacy
 |  | 
        |  | 
        
        | Term 
 
        | safety of long term PPI treatment |  | Definition 
 
        | incidence & spectrum of adverse events similar to H2RAsno evidence that long term PPI tx promotes development of: gastric carcinoids, atrophic gastritis, gastric adenocarcinomarisk ofenteric infection does not seem to be a clinical problemabsorption of fats & minerals unimpairedprob no need to monitor B12 levels in routine practice 
 |  | 
        |  | 
        
        | Term 
 
        | mucosal protectant/citoprotective agent:   sucralfate (Carafate)  |  | Definition 
 
        | complex of Al(OH)3 & sulfated sucrose, a small, poorly soluble molecule that polymerizes in the acid environment of the stomach; this polymer binds to injured tissue & forms a protective coating over ulcer beds; creates a physical barrier that protects the ulcer form gastric acid, pepsin & bileits action is local rather than systemic; too insoluble to have significant systemic effects
 |  | 
        |  | 
        
        | Term 
 
        | pharmacokinetics of sucralfate |  | Definition 
 
        | contains an aluminum complexonly minimal amt is absorbed through GI tract90% of the paste is excreted in f ecesdo not admin w/ antacids; gastric acid is needed to activate sucralfate
 |  | 
        |  | 
        
        | Term 
 
        | pharmacotherapeutics of sucralfate |  | Definition 
 
        | used to protect the wall of the GI tract from ulceration or injury from excess acid (hyperacidity)to prevent or treat ulcer disease & used for short-term tx (up to 8wks) of duodenal & gastric ulcerscontraindicated in kidney impairment b/c Al is not removed via the impaired kidneys or dialysis
 |  | 
        |  | 
        
        | Term 
 
        | drug interactions/adverse effects of sucralfate |  | Definition 
 
        | may decrease absorption of other drugs; should be given 2hrs apart from other drugsvery well toleratedconstipation & dry mouth = most common
 |  | 
        |  | 
        
        | Term 
 
        | nursing considerations for sucralfate |  | Definition 
 
        | give PO in either tablet or suspension formadmin on an empty stomach (1 hr before meals and at bedtime) - or it won't form polymergive other PO meds 2 hrs before sucralfatecontinue therapy even when symptoms of ulcer disappear unless healing canbe confirmed by endoscopyadvise pt to avoid smoking & spicy foods that might aggravate ulcermonitor pt w/ chornic renal failure for increasing signs and symptoms of Al toxicity: acute dementia, osteomalacia, bone pain with or without fracturesadmin antacids 30 min before or after sucralfate
 |  | 
        |  | 
        
        | Term 
 
        | prostoglandin   misoprostol (Cytotec)  |  | Definition 
 
        | synthetic protaglandin E1 that decreases gastric acid secretion & helps protect the GI mucosamay be used in pts on NSAIDs & those who are at risk  or NSAID-induced gastric ulcers; usually used concurrently as long as the pt is on NSAIDsNSAIDsinhibit prostaglandin production, which leads to a decrease in bicarbonate & mucus production, which increases the risk of gastric mucosal injury from NSAIDsalso produces uterine contractions
 |  | 
        |  | 
        
        | Term 
 
        | contraindications of prostoglandins (misoprostol) |  | Definition 
 
        | hypersensitivityrenal dysfunctioncontraindicated in pregnancy b/c partial or complete abortion & uterine bleeding may resultcontraindicated in lactation & kidsantacids may reduce the action of misoprostol
 |  | 
        |  | 
        
        | Term 
 
        | adverse effects of prostoglandin (misoprostol) |  | Definition 
 
        | well toleratedmost common: diarrhea & abdominal pain; diarrhea usually dose-related, mild & self-limiting (resolving in about 8 days) 
 |  | 
        |  | 
        
        | Term 
 
        | nursing considerations for prostoglandin (misoprostol) |  | Definition 
 
        | no dose reduction is suggested for pts w/ renal impairment or older pts, unless dose is not toleratedadmin ac & ghs w/ food to prevent GI discomfort &diarrheaavoid admin w/ Mg-containing antacids, which may increase incidence & severity of diarrheaadvise pt w/ childbearing potential to avoid pregnancy & use effective contraception
 |  | 
        |  | 
        
        | Term 
 
        | prokinetic drugs/GI stimulants   metoclopramide (Reglan)  |  | Definition 
 
        | increase motion & movement through the GI tract & aceleration of GI emptying; no effect on peristaltic movement in the coloncholinergic drug that stimulates motility of the upper GI w/o increasing gastric, biliary &pancreatic secretionsalso has an antiemetic effect
 |  | 
        |  | 
        
        | Term 
 
        | pharmacotherapeutics of prokinetic drugs/GI stimulants (metoclopramide) |  | Definition 
 
        | GERDgastroparesis (slow motility)postoperative GI hypomobilitypostoperative & chemotherapy nausea & emesis
 |  | 
        |  | 
        
        | Term 
 
        | contraindications of prokinetic drugs/GI stimulants (metoclopramide) |  | Definition 
 
        | GI obstruction, hemorrhange, perfusionhypersenstivityepilepsythose receiving other drugs that are likely to cause EPS 
 |  | 
        |  | 
        
        | Term 
 
        | drug interactions & adverse effects of prokinetic drugs (metoclopramide) |  | Definition 
 
        | ETOH & other CNS depressants: increased sedationphenothiazins: increased risk of EPSanticholinergics & opiate analgesics: antagonize the therapeutic effect & decrease GI motilitymost common adverse effects: drowsiness, restlessness, fatigue, diarrhea & EPS, particularly acute dystonic rxnsEPS usually subsides 2-3mo after d/c
other adverse effects: dizziness, visual disturbances, confusion, depression (b/c blocking dopamine receptors), insomnia, suicidal ideation, galactorrhea, gynocomastia
 |  | 
        |  | 
        
        | Term 
 
        | nursing considerations for prokinetic drugs (metoclopramide) |  | Definition 
 
        | PO 30 min before meals & at bedtimedilute IV doses above 10mg or more in 50ml of parenteral sol'n & give slowly over 15 min or longer; 10mg or less may be given over 1-2minprotect IV metoclopramide from light w/ aluminum foil or other protective coveringmonitor fo EPS, which are most likely to occur early in tx, at high doses, in pts who are dehydrated, or in pediatric and young ptsbenadryl may be given IM to reverse EPSmonitor for tardive dyskinesia symptoms, including involuntary movements of the tongue, mouth, or jaw, face or extremities; potentially irreversible so withhold and notify PCPhave adequate fluid intakeavoid ETOH & other depressantsmonitor blood sugar & s/s of hypoglycemia
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | symptom rather than diseasehistorically defined as pasage of less than 3BMs/week (medical diagnosis - not pt's word)ROME II diagnostic criteria: two or more of the following for at least 12 wks in the last 12mo - strainin, lumpy or hard stools, sensation of incomplete evacuation, sensation of obstruction, manual maneuvers (all in more than 25% of defecations), loose stools not presentfor infants/young kids, at least 2 wks of pepple-like, hard stools for the majority of stools or firm stools two or fewer times/wk
most pts are found to have no discernible cause for constipation & are labeled as having a chronic functional or idiopathic constipation
 |  | 
        |  | 
        
        | Term 
 
        | treatment for constipation:   laxatives  |  | Definition 
 
        | promote bowel evacuation; generally glassified by simplified mechanism of action: stimulant laxativesbulk-forming laxativeslubricant laxativeshyperosmotic laxativessaline laxatives/saline catharticsstool softener/surfactant laxatives(cathartics = stronger agent, producing semi-liquid or liquid stools) 
 |  | 
        |  | 
        
        | Term 
 
        | stimulant/irritant laxatives |  | Definition 
 
        | senna (Senokot)   cathartic effect: stimulate peristalsis by irritating the lining of the small & large intestinal wallstrongest & most abused; results in 6-12hrs after PO admin; 15-60min after PR (rectal) admin (dose dependent)certain foods- prunes, raisins, rhubarb, pears-contain organic acids that cause irritation of the intestinal mucosa & stimulation of peristalsis 
 |  | 
        |  | 
        
        | Term 
 
        | contraindications/precautions with stimulant/irritant laxatives |  | Definition 
 
        | pts w/ hypersensitivity, undiagnosed abdominal pain, ulcerated hemorrhoids, Crohn's, ulcerative colitis, and other chornic inflammatory bowel diseasesb/c cascara sagrada contains ETOH, it should be avoided in pts w/ a known intolerance to ETOHenteric coating of ex-lax is prematurely removed when taken concurrently within 1hr of antacids or dairy products
 |  | 
        |  | 
        
        | Term 
 
        | adverse effects of stimulant/irritant laxatives |  | Definition 
 
        | most common: abdominal cramping from increased paristalsisexcessive & prolonged use may lead to dependence; if drug is stopped, pt is likely to experience constipation (so, discontinue after 3-5 days)Senokot may color uring and feces a reddish or yellow-browncastor oil is used less frequently b/c of high incidence of numerous adverse effects such as severe abdominal pain 
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | psyllium (Metamucil)   stimulate peristalsis by adding bulk to stools; results usually occur in 24hrs & may take up to 2-3days to establish regularitycombine w/ water in intestine to form a gelatinous or viscous stool; the stool expansion causes the colon to distend & stimulate peristalsisbulk laxatives are indigestible, mild & less apt to habit-forming than other laxativesno interference w/ absorption of nutrientsconsidered the safest laxative, produce the same natural action as do 6-10g of fiber/dayshould be taken w/ 8oz of fluid; the mixture should be taken immediately b/c it will congeal in a few mincan be used for diarrhea or constipation 
 |  | 
        |  | 
        
        | Term 
 
        | lubricant laxatives:   mineral oil (elderly pts still often use)  |  | Definition 
 
        | coats fecal material w/ a film, which prevents the reabsorption of water through the colon; softens the stool & lubricates the intestinal wall, w hich facilitates the smooth passage of fecesabsorption of food & fat-soluble vits (A,D,E,K) may be reduced if taken longer than 2 wksmost dangerous adverse effect = lipid pneumonia, when mineral oil droplets are aspiratedprolonged use may lead to bowel-elimination dependenceshould be taken after the evening meal & qhs to avoid loss of fat-soluble vits; should be taken at least 2hrs after meals to avoid interference w/ digestion of foodb/c aspiration of mineral oil appears to be greatest during sleep, it should be given well before bedtime to prevent aspiration & resultant lipid pneumonia 
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | polyethylene glycol-electrolyte soln (GoLYTELY)  hypertonic drugs that draw water from surrounding tissue into the intestine, thereby creating an increased osmotic pressure in the bowel; the fluid moves from extracellular compartments through intestinal mucosa into the bowel; additional fluid changes the stool consistency to liquid, distends the bowel, stimulates stretch receptors & peristalsisoral hyperosmotic laxatives should not be given within 1hr of other oral meds b/c the increased transit time of the laxatives will interfere w/ the absorption of other drugs
 |  | 
        |  | 
        
        | Term 
 
        | hyperosmotic laxatives are often used to ____ |  | Definition 
 
        | cleanse the entire digestive tract for diagnostic purposes (e.g. colonoscopy), flush poisons from the system, or remove parasites; inappropriate for long-term use |  | 
        |  | 
        
        | Term 
 
        | _______ gives the best & most complete evaculation of the GI tract of all of the available laxatives |  | Definition 
 
        | polyethylene glycol-electrolyte soln (GoLYTELY)   admin PO over 3-hr period and may be admin in 240cc (8oz) q10min; this should begin about 4-5hrs before exam or procedure; when the pt is unable to take PO, it may b e admin through a NG tube at a rate of 20-30cc/min; admin at home: 8oz every 10min until all 4L are taken; onset of action is 30min-3hrs for PO  |  | 
        |  | 
        
        | Term 
 
        | stool softeners:   docusate sodium, docusate calcium, docusate potassium  |  | Definition 
 
        | not considered to be laxatives in the truest sensesurface-active agents that emulsify & wet the stool by permitting water to penetrate & soften the stool for easier passageused to prevent constipation or two soften stool for a wide range of conditions in which straining of stool is contraindicated (e.g. cardiac disease or after rectal surgery)can be safely used for long-term management of chronic constipation, esp when the cause is a low-fiber diet; they are the least harmful of laxatives b/c they are less habit-forming & do not inhibit absorption of certain nutrientsfull effect may take up to 3 days at start of tx; on daily basis, work overnightcaps and tabs must be swallowed whole & not chewed or crushed; instruct pt to take PO dose w/ full glass of water
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | acute diarrhea: more frequent, looser than normal stools for less than 2 weeks; objectively: 200mg+ of stool output/day; often other GI s/spersistent diarrhea: >14dayschornic diarrhea: duration of at least 1mopathogens not detected in over 50% f cases; most cases resove in 48hrspersistent diarrhea should be tx secondary to danger of dehydration & electrolyte imbalancespeds patients & elderly are at risk for most complications
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | locally acting or systemically absorbed drugs used to decrease the vol or fluidity of bowel contents or to decrease peristalsis for both acute & chronic diarrheatypes of antidiarrheals: 
 opioids: most effective agentsabsorbantsintestinal flora modifiersbulk-forming agents
antibiotics used in tx of infectious diarrheacorticosteroids in tx of diarrhea in inflammatory conditionsoverdose of antidiarrheals = constipation
 |  | 
        |  | 
        
        | Term 
 
        | antidiarreal agents:   1. opioids  |  | Definition 
 
        | lopermadine (Imodium, Kaopectate) diphenoxylate Hydrocholride w/ atropine sulfate (Lomotil)  slow intestinal motility or propulsionboth are analogues of meperidine & have opioid-like actions on the gut, activating presynaptic opioid receptors in the enteric NS to inhibit ACh release & decrease paristalsisno or minimal potential for abuse b/c they do not cross the BBBside effects: drowsiness, abdominal cramps, dizziness, constipationsince these can cause toxic megacolon, they should not  be used inkids or pts w/ severe colitiscaution in increased ICP, h/o drug abuse, and severe pulmonary diseaseETOH & CNS depressants should be avoided during tx w/ opioid antidiarrhealsresponse to tx should be noticeable 48hrs after tx begins; these are not innocuous drugs & not intended for prolonged use
 |  | 
        |  | 
        
        | Term 
 
        | antidiarrheal drugs:   2. absorbents  |  | Definition 
 
        | bismuth subsalicylate (Pepto-Bismol) decreases fluid content in stoolhas demulcent, astrigent & anti-inflammatory properties; action may have direct antimicrobial & antiviral effectscontains salicylates-contraindicated in kids (below 13) recovering from flu-type illnesses or chicken pox in which ASA is contraindicated (questionable assocation w/ Reye's syndome), in concomitant anticoagulant therapy, and in pts hypersensitive to ASAadverse effects: gray-black tongue or stools & constipation 
 |  | 
        |  | 
        
        | Term 
 
        | antidiarrheal drugs:   3. intestinal flora modifiers  |  | Definition 
 
        | lactobacillus acidophilus (Lactinex, Bacid) promotes growth of E.coli-normal bacterium present in the bowelrestores gut flora depleted by abx therapyadmin w/ milk, 2 hrs before or after intake of other medsknow that adjunct of  dietary regimen high in lactose & dexrose is also effective in providing recolonization of colon (ex: yogurt, milk, buttermilk)in pts w/ milk product allergies or intolerance, admin of Lactobacillus acidophilus may cause similar s/s of bloating, cramps, diarrhea, flatulence 
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | n/v may occur in variety of conditions (e.g motion sickness, pregnancy, hepatitis, and as side effects of chemo)nearly 70-80% of all pts given chemo experience n/vemesis can produce dehydration, profound metabolic  imbalances & nutrient depletionmech that trigger vomiting = vomiting reflex pathway
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | chemoreceptor trigger zone (CTZ)located in the area postrema (structure at caudal end of fourth ventricle)outside BBB - so it can respond directly to stimuli in blood re cerebrospinal fluid
vomiting centerlocated in lateral reticular formation of mediullacoordinates motor mech of vomiting
vestibular systemlocated in middle earfunctions mainly in motion sickness
 |  | 
        |  | 
        
        | Term 
 
        | considering the complexity of the mechs involved in emesis, the antiemetics represent a variety of classes: |  | Definition 
 
        | some act by inhibiting the chemoreceptor trigger zone in the medulla by blocking the action of dopamine (e.g. phenothiazines)other act by decreasing the sensitivity of the vestibular apparatus in the middle ear (e.g. antihistamines, anticholinergics)other agentsdo not act in either of these waysantiemetics should be admin before emetogenic tx; it is easier to prevent nausea than to treat it!
 |  | 
        |  | 
        
        | Term 
 
        | antiemetic drugs:   phenothiazines/dopamine receptor antagonists    agents  |  | Definition 
 
        | prochlorperazine (Compazine) - tx of severe n/vpromethazine (Phenergan) - tx of motion sickness & drug of choice for n/v of gastroenteritistrimethobenzamide (Tigan) - tx n/v of radiation therapy, in postoperative nausea, and gastroenteritis 
 |  | 
        |  | 
        
        | Term 
 
        | antiemetic drugs:  phenothiazines/dopamine receptor antagonists |  | Definition 
 
        | block dopamine receptors in the CTZ; dopamine is required for the conduction of impulses from excited afferent nerves to stimulate the medullar-vomiting centerblocking dopamine receptors inhibits the stimulation of hte vomiting center & an antiemetic effect resultsused to manage nausea & emesis due to either ratdiation therapy or chemo, or do to the effects of toxinscontraindicated in depression, severe liver & CV disease, pregnancy, and kids < 2y.o.may drug interactions: check before admin; additive hypotensive effects w/ ETOH, antihypertensives, CNS depressants
 |  | 
        |  | 
        
        | Term 
 
        | adverse effects of phenothiazines/dopamine receptor antagonists |  | Definition 
 
        | major: EPS esp. w/ prolonged therapy; dehydrated pts are more likely to experience thisdystoniaakathisiapsuedoparkinsonismtardive dyskinesia
anticholinergic effects: dry mouth, flushing, blurred vision, tachycardia, photosensitivity, constipationagranulocytosis: rare
 |  | 
        |  | 
        
        | Term 
 
        | antiemetic drugs:   serotonin receptor antagonists  |  | Definition 
 
        | ondansetron (Zofran)  selectively block central & peripheral serotonin receptors, producing an antiemetic effectmost effective antiemetics for highly emetogenic chemo drugscan be used for postoperative n/v onset of action: 30min PO; IV route:1-3min; duration of action for PO drugs is 4-24hrs; peak is 30-90minHA-common side efect; may require analgesic for relief
 |  | 
        |  | 
        
        | Term 
 
        | miscellaneous antiemetics:   scopolamine (Transderm Scop)  |  | Definition 
 
        | works well for prevention/tx of motion sicknessavail as .33mg patchadults: apply one patch in hairless area behind ear 4hrs prior to when antiemetic effect is neededreplace after 3 dayskids: not recommendedside effects: anticholinergic
 |  | 
        |  | 
        
        | Term 
 
        | emetic agents (induce vomiting):   ipecac (Ipecac Syrup)  |  | Definition 
 
        | tx of oral poisoning or overdose; goal is to expel toxic substance from the body before material is absorbed from the GI tractstimulates the CTZ & acts directly on the gastric mucosa to stimulate vomiting emesis should not be induced when caustic substance (e.g. ammonia, bleach, drain opener, dye, battery acid, gasoline, kerosene, lighter fluid) have been ingested b/c will burn again on the way upOTC drug
 |  | 
        |  | 
        
        | Term 
 
        | contraindications of emetic agents: |  | Definition 
 
        | cardiac dysfunctionhypersensitivitydepressed gag reflexdeep sedationthose in shock & comadrug interactions:milk & activated charcoal may inactive ipecacvegetable oil may delay absorption of ipecacwhen given w/ carbonated bevs, abdominal distention may occur
 |  | 
        |  | 
        
        | Term 
 
        | adverse effects of emetic agents: |  | Definition 
 
        | diarrhea, drowsiness, mild GI upsetadverse effects that may occur when ipecac is not vomited and is absorbed or when it is overdosed include: persistent vomiting, severe myopathy, tremors, cardiotoxicity, arrhythmias, chest pain, bradycardia, tachycardia, hypotension, fatal myocarditis, depression, coma
 |  | 
        |  | 
        
        | Term 
 
        | nursing considerations for emetic agents |  | Definition 
 
        | follow w/ 8-16oz of water, dose may be releated in 20 min as needed (kids 1yr+, follow dose w/ 6-8oz of water, kids under 1yr, follow dose w/ 4-8oz of water)ipecac fluid extract is 14x stronger compared to the syrup and has caused death when mistakenly given as syrupwhen dose is not vomited and allowed to absorb, cardiotoxicity may occur (activated charcoal may inactive it)call poinson control before usuing ipecacgive ipecac before activating charcoalwhen vomiting does not occur within 15-20min, the ER should be contacted immediately and dose of ipecac given should be recovered using gastric lavage and activated charcoal 
 |  | 
        |  | 
        
        | Term 
 
        | antiflatulents   simethicone (Mylicon)  |  | Definition 
 
        | drug given to tx the discomfot of excessive gas in the GI tractgas is introduced to the body by:swalling air (primary reason)bacterial action leading to gas as byproductdiffusion of gas from blood stream into the GI tractavg of 7-10L of gas passes through GI tract, motof which is reabsorbed 
 |  | 
        |  | 
        
        | Term 
 
        | pharmacodynamics of antiflatulents |  | Definition 
 
        | changes the surface tension of gas bubbles in the stomach & intestinechanged surface tension allows gas bubbles to stick together to form larger bubbleslarger bubbles are easier than smaller ones to pass via peristaltic movement & motility in the GI tract through the mouth by belching or through the anus as flatusused in tx of flatulenceand of postoperative pts w/ gaseous distention
 |  | 
        |  | 
        
        | Term 
 
        | nursing considerations of antiflatulents |  | Definition 
 
        | (no contraindications, drug interactions, or adverse effects) give PO and may include an antacid or antidiarrheal medmix w/ water, infant formula, or other liquidskae suspensions thoroughlytablets must be chewed before swallowing (not gelatin caps)assess bowel sounsd for presence of peristaltic activity before adminacitvity will increase peristalsiseating in an upright position and avoiding gas-producing foods or carbonated bevs may help decrease swallowing of air and encourage gas movement 
 |  | 
        |  |