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Nutrition/ adult
test 4 level 3
| Question | Answer |
|---|---|
| 2 major disorders of stomach and UPPER small intestine? | Gastritis and Peptic ulcer disease |
| an inflamtion of the gastric mucosa is one of the most common problems affecting the stomach | Gastritis |
| gastritis may be clasified as ? | acute or chornic and diffuse or locaziled |
| occurs as a result of a breakdown in the normal gastric mucosal barrier. | Gastritis |
| protects the stomach tissue from the corrosive action of HCL acid and pepsin | Function of gastric mucosal barrier |
| In gastritis when the mucosal barrier is broken, HCL acidm and pepsin can diffuse back into the mucusa resulting in? | tissue edema, disruption of cappilary walls with loos of plasma into gastric lumen and possibly hemmorhage |
| Drugs that contribute to the development of acute/chronic gastritis? | NSAIDS, inlduign aspirin and corticosertiods, as they inhibit prostaglandin(which is protective to GI mucosal wall) and anticoagulants and digoxin |
| Injesting alchol, eating large quanitites of spicy, irriating foods and renal failure can cause? | Gastritis |
| an important cause of chronic gastritis? | Helicobacter pylori |
| Bacterial, viral and funfal infections have been associated with? | chronic gastrites |
| Intense emotional responses and CNS lesion may produce inflmation of mucosal lining as a result of hypersecretion of HCL acid | cause of gastritis |
| Anorexia, nausea, vommiting, epigastric tenderness and a feeling of fullness. Hemmorhage is associated with alchol abuse and at time is the ONLY symptom | S/S of acute gastrits |
| Prognosis of acute gastritis? | Self limiting, lasts a a couple hours or days, complete healing |
| When the parietal cells are lost as a result of atrohy the source of intrinsic factor is lost. | Chronic gastritis and results in cobalmin deficiency/ pernicious anemia |
| A CBC in gastritis may show? | anemia from blood lossor lack of intrinsic factor |
| If vommiting accompanies acute gastritis do what? | rest, NPO status and IV fluids, antimetics |
| treatmet of acute gastiris focuses on reducing irritation of the gastric mucosa and providing symptomatic relief through giving? | PPI's( azoles) or H2 receptor blockers (tidine) |
| Treatment of chronic gastrits? | Antibitotics for H. pylori, colabalmin therapy, non irritating diet w/ six small meals a day |
| drug and alchol abuse think? | gastritis |
| in gastritis check stool for? | occult blood |
| a severe case of acute gastritis may require? | NG tube for lavage |
| Neutralize acid in stomach and esophagus, rapid onset and short effect | Antacids |
| When give antacids? | before a meal |
| Reduce gastric HCL secretion, slower onset longer duration | H2 receptor blockers |
| Inhibits gastric acid secretion has a prolonged effect | Proton pump inhibitor |
| smoking is contraindicated in? | all forms of Gastritis |
| A condition charecterized by errosision of the GI mucosa resulting from digestive action of HCL acid a pepsin | Peptic ulcer disease |
| What part of GI tract is suspetible to ulcer development? | Any portion of the GI tract that comes into contact with gastric secretions |
| How are petic ulcers classified? | acute or chronic |
| accoiated with superficial erosion and minimal inlamation, resolves quickly when the cause is removed | The acute ulcer |
| eroding throguh the musclular wall with the formation of fibrous tissue | A chronic ulcer |
| peptic ulcers develop only in an? | acidic enviorment |
| histamine in released from the damaged mucosa, resulting in vasodilation and increased cappilary permeability in peptic ulcers results in? | further secretion of acid and pepsin |
| In adition to chronic gastritic H pylori is associated with? | peptic ulcers |
| alters gastric secretion and produces tissue damage leading to? | peptic ulcer disease |
| Aspirin and NSAIDS inhibit prostaglandis, increase gastric acid secretion and reduce the integrity of the mucosal barrietr | Ulcerogenic drufs |
| Coffe and alchol | Stimulate gatric acid production this Peptic ulcers |
| stress affects what in ulcers? | The healing of them |
| gastric ulcers are most commonly found in the? | Antrum |
| Gastric ulcers are more likely than duodenal ulcers to result in? | Obstruction |
| H.Pylori, meds, smoking and bile reflux are R/F for? | Gastic ulcers |
| Most common ulcer? | Duodenal |
| Most common cause of duodenal ulcer? | H. pylori |
| high epigastrum pain, occurs 1-2 hours after meals, pain is burning, if ulcer has eroded through mucosa food agravates this | Gastric ulcer |
| Occurs when gastric acid comes in contact with the ulcers/ With meal ingestion food is present to help buffer the acid, symptoms occur 2-5 hours after a meal, pain is burning and is midepigastrum and possible back pain antacids /h2 receptor block fix S/S | Duodenal ulcers |
| Tendencey to occur continously for a few weeks or months and then disaper for a time then recurs | Duodenal ulcers |
| Older adults and ulcers | usually siletn |
| Three major complications of PUD? | Hemorrhafe, perforation and gastric outlet obstruction, EMERGENCIES |
| Hemmorahfe is the more common in | Duodenal ulcers |
| Most lethal complication of PUD? | Perferation |
| the ulcer penetraties the serosal surface with spillage of either gastric or fuadenal contents into the periotenal cavity | Perferation |
| Sudden severe upper abdominal pain that quickly spreads throughout the abdomen. The pain radates to the back and is not relievedd byt food or antacids | Perforation |
| Bowel sounds usally absent, absomen appears rigid and boardlike tachy/ HISTORY of ulcer disease or recurrent symptoms of indigestion | [erforation |
| if perforaiton is untreaed bacterial periotnitis may occur within? | 6-12 hours |
| obstruction in the distal stomavh and duodenum is the result of what in regards to PUD? | edema, inflamation or pylorspasm and fibrous scar tissue formation |
| how can relief be obtained with gastric out obstruction due to PUD? | belching or self-induced vommiting |
| Vomit that contains food particles that were injested hours or days before the vommiting episode signals? | Gastic outlet obstrcution due to PUD |
| most accurate diagnostic procedure for PUD? | Endoscopy |
| Eoscopy with biopsy is used in PUD to rule out? | H. Pylori |
| no invasive tests for H. Pylori? | Stool or breath test. |
| A CBC in PUD? | may show anemia |
| A serum amlyasyse determination s done to determine _______________ when posterior duodenal ulcer penetration of the pancreas is suspected | Pacreatic |
| aim of treatment with PUD? | Decrease gastric acidity and enhnace mucosal defense mechanisms |
| Pain from ulcers disaper in? | 3-6 days but not heal till 3-9 weeks |
| important follow up for PUD? | follow up endoscoppy |
| Patietns with H. Pylori are treated with? (and PUD) | Antibiotics and PPI |
| with PUD it is important to stop? | smoking |
| Because ulcers frequently recur, interupption or discontinuation of therapy can have? | harmfull results so encourage continuing and follow up |
| H2 receptor blockers and PPIs may be stopped after? | the ulcer has healed or used as low dose maintance |
| This promotes ulcer healing, onset is one hour and lasts 12 hours | H2 receptor blockers |
| More effective than others in reducing gastric secretion and promoting ulcer healing | Proton pump inhibiros |
| These increase gastric Ph by neutralzaing the HCL acid. magnesium hydroxide or aluminum hydroxide | Antacids |
| Whent take antacids | after meals so they last a long time |
| If Ph is less than 5 with PUD consider? | NG suction |
| used for short term treatment of ulcers. It proovides cytoprotection for the esophagus, stomach and duodenum, should be given 30 minutes before an antacid. | Sucrafate |
| what antidepressants for PUD? | Tricylic |
| DIet for PUD? | No caffeine, no aclhol, do bland diet, (no broth tho) |
| PUD vleeding, increased pain and discomfort and N/V | Acute exacerbation |
| What to do in perferoation? | NG tube for decompression/stop aspiration, volume replacement, antibitoics, pain meds and surgery |
| What to do in gastric outlet obstruction? | Decompress stomach, fix fluid imbalance, clamp tube overnight and see if its still backing up. |
| symtpms related to gastric irritation during PUD? | Epigastric pain |
| Treatment of acute phase of PUD? | NP, NG tube/suction, IV fluid replacement |
| sudden severe abdominal pain, rigid boardlike abdomen, severe generalized abdominal and shoulder pain, fetal position and grunting respirations, bowel sounds ABSENT | perforation |
| direct result of surgical removal of a large portion of the stomach and the pyloric sphincter | Dumping syndrome |
| what is more common acute or chronic PUD? | chronic |
| Pathology of PUD? | Not neccesarly the amount of HCL secreted but the ability of it to penetrate the mucosal barrier |
| pain in high epigastrum | Gastric ulcer |
| pain is burning or gaseous pain is spnontaineous usually 1-2 hours after meals, food can agravate it? | Gastric ulcers |
| occurs 2-4 hours after eating, relieved by antacids or H2 receptor blockers, burning cramplike pain in mid epigastric and may radiate to back | Duodenal ulcers |
| Duodenum ulcers involves the duodenum and the? | pylorus |
| This ulcer pain is often relived by food? | duodenum ulcer |
| serum or whole blood antibody testing including IGg | Does not distinguish between current or past PUD but good still |
| Upper Barium GI contrast studies with gastric analysis may be helpful in diagnosing? | PUD |
| What diet in PUD? according to powerpoint? | 6 bland small meals a day, no spicy, alchol, carbonated beverage/caffeine stop smoking dont take NSAIDS/aspirin |
| Most common complication of PUD? | Hemmorhage |
| sudden sharp severe abdominal/shoulder pain, black or bloody stools bloody vomit that looks like coffee grounds rebound tenderness think? | Perforation |
| In pud, hemmorage, perforation and gastric outlet obstruction are all? | medical emergencies |
| acute ulcers that follow a major physiologic insult | Physiologic stress ulcer |
| dx: for physiologic stress ulcer? | endoscopy |
| prevention of physiologic stress ulcer? | prophylaxis with antisecretory agents |
| treatment of physiologic stress ulcer | reduction of gastric acid secretion with PPI or h2 receptor blockers |
| physiologic stress ulcers occurs most often in? | infants and children |
| Acute inflamtion of the pancreas. varies from mild edema to severe hemorrhagic necrosis | Acute pancreatitis |
| Acute pancreatis is more common in? | Middle aged men and women. |
| race for pancreatis? | more african americans |
| Most common cause of acute pancretitis? | Gallbladder, second is chronic alchol intake |
| Independent risk facto for | acute pancretitis |
| a mixture of cholesterol crystals and calcium salts found in patients with acute pancreatis? | Biliary sludge |
| Formation of bilary sludge is seen in patients with bile? | staiss |
| hypertriglyceridema is associated with | Acute pancretitis |
| most common pathogenic mechanism of acute oancreatis is? | autodigestion of the pancreas |
| Activated trypsin in the __________ can digest the ________ and produce bleeding | Pancreas |
| Edematous or interstial pacreatitis | Mild pancreaitis |
| Necrotizing pancreatitis | Severe pacreatitis |
| Predominant manifestation of acute pancreatitis | Abdominal pain |
| The pain is due to distention , peritoneal irritation and obstruction of the billary tract | Pain in pancreaitis |
| Where is the pain in pancreaittis? | Left upper quadrant, may be midepigastrium radiates to back commonly |
| The pain has a steady onset and is described as severe, deep, piercing and continous or steady, pain is agravated by eating and occurs when recumbnent | Pancreaitis |
| Patient may assume various positions involving flexion of the spine in an attempt to relieve severe pain, may see N/V fever, leukocytosis, hypotension, jaundice, muscle guarding | Pacereatis |
| Bowel sounds in pacreatis? | decreased or absent |
| Paralytic illeuls and crackles of lungs may be present in? | pancreatitis |
| cyanosis or greenish to yellow-brown discolaration of the abdominal wall. | Pancreatisis |
| in pancreatis echmyoses of the flanks | Grey turners, and the periumbical area is cullens |
| Result from seepage of blood stained exufate from the pacreas | Grey turner/cullens, discolorations of abdominal walls |
| Two significant local complications of acute pancreaitis? | Pseudocyst and abscess |
| An acummulation of fluid, pancreatic enzymes, tissue debrs, and inflamatory exudate surronded bt a wall | A pancreatic pseudocyt |
| Palpable epigastric pain is evident of? | pacreatic pseudocyts |
| Serum amlysase levls in pancreatits is? | high |
| Pacreatic pseudocysts can perferoate cuasing | perotonitis |
| A pancreatic absess is a? | collection of pus |
| upper abdominal pain, abdominal mass, high fever and leuko cytosis | pacreatic absess need to treat to prevent sepsis |
| Main systemic complications of acute pancreatis? | pulmonary (pneumonia, ARDS, pleural effusion) and cardiovasculare (hyptension) and tetant thanks to hypocalcemia |
| enzyme induced inflamtion of the diapragm occurs with the end result being? | atelectasis |
| Trypsin in pancreatis puts the patient at risk for? | DIC, thrombi |
| primary diangostic tests for acute pancreatits? | serum amylase and serum lipase |
| Why is serum lipase more important than serum amylase in DX pancreatitis | amylase is raised in other disoreders |
| increase i liver enzymes, increase in trigluycerides and decrease in calcium points to? | pancreatits |
| Goals of tx for acute pancreatits? | Prevent shock, reduce pancreatic secretions, corect FE imbalances, prevent/treat infections, remove cause |
| in aute pancreatis pain meds are given in addition to? | antispasmodics |
| To pevent shock in pacreatis | blood volume replacements are used, like lR |
| It is important to reduce or supress pancreatic enzymes to decrease stimulation of the pancreas and allow it to rest in acute pancreatits how is this accomplished? | NPO, NG suction to reduce vommiting/gastric distention and to prevenet gastric acidic contents from entering the duodenum, PPI'S/antacids |
| In patients with acute necrotizing pancreatitis, what is the leading cause of death? | Infection |
| drugs that cure pancreaitis? | none |
| When food is allowed, in aucte pancreatits what is the diet? | Frequent feedings, high in carbs that is least stimulatinf no alchol |
| is frequent vommiting seen in acute pancreatis? | yes |
| major focus of care in acute pancreatits is? | pain |
| Diet teaching for acute pancreatits includes? | reduction of fat as the stimulare onacreas, carbs are less stimulating |
| If a person with acute pancreatitis recognizes symptoms of infection diabetes or steatorrhea do what? | Call dr. |
| A continous, prolonged inflamatroy and fibrosing of the pancreas, the pancreas is progressivly destroyed as it is replaced by fibroitic tissue | Chronic pancreaitis |
| Strictures and calcifications may occur in the pancreas in what disease? | Chronic pnacreatis |
| Can be due to alchol, obstruction by gall stones, timor, pseudocyts or traumas, disease, autoimmune pancreatis and cystic fiboris, may have NO history of acute condiition | Chronic pancreatis |
| Most common cause of obstructive pancreaitis is? | inflamation of the sphincter of oddi ascociated with gall stones |
| in non obstructive pancreaitis there is inflamtion and sclerosis mainly in the head of the oancres and around the pancreatic duct this type of chronic pancreatiis is the? | most commobn |
| Chronic pancreatits can be caused by those who abuse? | alchol |
| abdominal pain that is heavy gnawing feeling or burning and cramplike, not relived with food, come and goes | Chronic pancreatis |
| Malabsotption with weight loss, consitpation, mild jaundice with dark urine, steatorrhea and diabetes melitys are signs of | Chronic pancreaitis |
| Frothey urine and stool, steatorhea can become severe with vommitius | Chronic pancreatis |
| The level of serum amylase and lipase may be elvated slightly, bilirubin is increased, incresred ESR and mild leukocytosis, alkaline phosphate | Chronic pancreatis |
| Used to visualize the pancreatic and common bile duct | ERCP |
| Deficiency of fat-soluble vitamins, cobalmin, glucose intelerance and dibetes may be found in | chronic pancreaitis |
| Ways to control pancreatic insufficency in chronic pancreatits? | Diet, pancreatic enzyme replacement and control of diabetes, small bland frequent meals, no alchol or caffeine prescribe bile salts to help with fat absorption |
| Pacreatic enzymes are taken with ? | a meal or snack |
| shock/vasodilation is seen in? | acute pancreatis |
| Cavity continous with or surronding outside of pancreas filled with necrotic produts and liquid secretions | pancreatic pseudocytst |
| Large fluid containing cavity within the pnacreas resulting from extensive necrosis in the pancreas | Pancreatic absess |
| urinart amylase may be seen in? | acute pancreatits |
| TPN in acute pancreatis may be needed if there is a ? | severe nutritional defict |
| if enteral feedings are needed in acute pancreatits it is via a ? | jejunal feeeding tube |
| Two major types of chronic pancreatis? | Chronic obstructive pancreaitis, and chronic calcifying pancreatisi |
| chronic pancreatis may be associated with acute? | billary diseae |
| Mild jaundice with dark urine is seen in? | Chronic pancreatits |
| Most common disorder of the bilairy sytem is? | Cholelithias (stones of gallbladdder |
| Where may the gallstones lodge ? | neck of the gallbladder or in the cystic duct. |
| Inflamation of the gall bladder, this is usually associated with choleithiasis (gall stones) | Cholecystis (usually occur with gall stones) |
| Many people with stones are | asymptomatic |
| Cholecystectomy is? | removal of the gall bladder |
| Who is at higher risk for cholilithiasis? | Women, multipara and over 40, oral contraceptives, sedetary lifestyle and obesity. asins |
| Cause of gallstones? | Unknown |
| Develops when the balance that keeps cholesterol, bile salts calcium in solution is altered so that these substances precipitate | Cholelithiasis |
| Conditions that upset the balance of cholesterol, bile salts and calcium in solution | Infection and disturbances in metabolism of cholesterol |
| when bile is supersaturated with cholesterol what occurs? | Gall stones |
| besides cholesterol what 4 things can cause gall stones? | Protein, calcium, bilirumbin and bile salts. |
| Most common gallstone? | mixed predominatly cholsterol |
| stasis of bile as well as changes in composition of bile (bilary sludge) can lead to? | gall stones |
| The gallstones may remain in the gallbladder or migrate to the? | cystic duct or the common bile duct |
| Gallstones cause pain as they? | pass through the ducts and produce an obstruction |
| What size gallstones are more liekly to produce an obstruction | Smalls |
| if blockage of gallstone is in cytic duct? | bile can still get though |
| Choleosytisi is most commonly associated with? | obstruction caused by gallstones or billary sludge |
| asccoiated with prolonged immobility, elderly, diabetes and prolonged PN? | Just choleocytis |
| The gallblader is edmeatous and hypermic and may be distended with bile or pus | During an acute attack of cholecystits |
| When a stone is lodged in the ducts or when stones are moving through the ducts, | spasms may result |
| bilarly colic, pain is often steady, pain can be excurtating and accomponied by tachy , diaphoresis, may last up to an hour | Cholelithiasis |
| When the pain of cholethiasis subsides resuldual tenderness is felt in the? | right upper quadrant |
| The attacks of pain from gallstones occurs 3-6 hours after? | a high fatty meal or patient lays down |
| dark amber urine, obsructive jaundice, clar colored stools, bleeding tendencies, steatorheaa | Total obstrutction by gall stones related to bilary obstruction |
| indgestionand pain / tendeness in right upper quadrant | Choliethesiais |
| History of fat intoleracne, dyspesia, heartburn and flatulence | Chronic Chlecytutus |
| Most common complications of choleysitis in older or diabetic | Gangrenous cholecytisi and bile peritonits |
| Commonly used to dx gallstones? grear id allergic to contrast! | ultrasound |
| Allows visualaztion of the gall bladder , the cystic duct, the common hepatic duct and the common bile duct, bile taken during this is sent for culture. | ERCP |
| Insertion of a needle directly into the gallbladder duct followed by injection of contrast | Percutaneous transhepatic cholangiography |
| WBC in choleothasis? | increased |
| Blood levels elevated in cholestais? | ALT, AST, and alkaline phosphate |
| Once gallstones become syptmotic do what? | Surgical intervention with cholecystectomy |
| during an acute episode of cholecystits, treatment focus on? | pain control, control of possible infection with antibiotics and maintece of FE NG insertion of N/V is severe |
| may be used to drain purluent material from the obstructed gallbladder | a cholecysstostomy |
| Treatment of choice for symptomatic cholethiasis | Laproscoprtic cholecystectomy |
| able to return to work how long after choleystecomy? | a week |
| Common complication in laproscopic cholestectomy? | Injury to common bile duct |
| most common drrugs used in the treatment of gallbladder disease? | Analgesics, anticholinergics(antispasmodics) , fat soluble vitamins and bile salts |
| fat soluble vitamis needed if? | bilary tract is obstructed |
| Nutrition during acute gallbladder disease? | Small frequent meals with some fat at end of meal to increase gallblader emptying |
| After laproscopic cholestrectomy nuttrition adive? | Eat nutrion foods avoid fat for 4-6 weeks |
| jaundice, clay colored sools, dark foamy urine, steatorhea, fever and increased WBC count | Bilary tract obstruction |
| bleeding may result in cholesthiasis from | decreased prothrombin time thus take care during injections |
| abdominal pain and fever may indicate? | Pancreaitis |
| A common complication postop from laparscopic chlecystectomy is? | shoulder pain |
| how help with shoulder pain after a lap choleystectomy? | SIMS position, nsaids/codeine |
| after surgery for gallstones as well as acute period? | avoid exess fat |
| inflamation to mucosa lining or entire wall of gallblader, edmea | CholthiatITIS |
| absess, pancreatis, cholingitis, billary cirhosis and fistula are common complications of? | Gallbladder disease |
| in gallbladder disease what is a major complication if not treated? | rupture of gallblader resulting in peritonitis |
| antimetics are often given in? | choliethithais |
| ESWL | can use a lithiotripter to break apart a gallstone |
Created by:
rebo14