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pancreatitis
pn 141 test 3 book burke pg 489
| Question | Answer |
|---|---|
| what is it | inflammation of the pancrease |
| it can be either _______ or _________ | acute or chrinic |
| acute: when does it usually develop | in middle life |
| acute: what is the primary risk factors of it | gallstones and alcoholism |
| chronic: what is the primary risk factor of it | alcoholism |
| chronic: what does it eventually lead to | pancreatic insufficiency |
| acute: when does it occur | when the pancreas is damaged or the duct is blocked |
| acute: when the pancreas is damaged or the duct is blocked what happens to the pancreatic enzymes | they begin to accululate w/in the pancreas itself |
| acute: what can obstruct the pancreatic duct | a gallstone, or spasm of the sphintyer of oddi |
| acute: a spasm of the sphintyer of oddi is associated with what | alcoholism |
| acute:when ostruction happens what occurs | a self-destructive process known as autodigection |
| acute: what is interstitial edematous panctreatitis | it occurs in the milder form of acute pancreatitis, the pancreas becomes inflamed and edematous. it is self limiting and pt fully recovers |
| acute: nectrotizing panctreatitis- is it a more severe for m | yes |
| acute: nectrotizing panctreatitis- what is it | an acute inflamm. process, pancreatic tissue bleeds and becomes nectrotic and secondary bacteria infection can lead to absess formation |
| acute: nectrotizing panctreatitis- prognosis | they may recover completely, have recurrent attacks or develop chronic panctreatitis |
| acute: what is the onset | usually sudden |
| acute: what pain do they experience | severe epigastric and abdominal pain, it radiates to the back and is releived somewhat |
| acute: how is the pain relived | is releived somewhat by sitting up and leaning forward |
| acute: when does the onset of pain usually occur | after a fatty meal or excessive alcohol consumption |
| acute: s/s | acute, severe epigastic pain, may radiate to back, N/V, abdominal distention, decreased bowel sounds, low grade fever, tachycardia, hypotension, cool clammy skin, elevated WBC, serum amylase, lipase, low calcium and mag |
| acute: what serious thing can they develop | hypovolemic shock |
| acute: why do they develop hypovolemic shock | due to vasodilation and fluid shift into the small bowel |
| acute: where can bleeding occur; s/s of it | into the retroperitoneal space; evidenced by bruising in the flanks or around the umbilicus |
| acute: what is bruising in the flanks the called | tuner's sign |
| acute: what is bruising around the umbilicus the called | cullen's sign |
| acute: what is pancreatic pseudocyst | a collection of blood fluid and pancreatic secretions in the abdominal cavity |
| acute: if the pseudocyst ruptures what can occur | peritonitis |
| acute: pancreatic absess def; is it serious | a collection of secretions and necrotic products w/ in the pancreus; fatal |
| acute: when so s/s occur | w/ in 2-3 weeks after the onset of acute |
| chronic: what does it lead to | the gradual destruction of the pancreus |
| chronic: cause | may follow acute, or may have no identifiable cause |
| chronic: risk factors | alcoholism, and malnutrition (high triglycerides and cholesterol diet) |
| chronic: what happens to the small ducts of the pancreus | they are blocked by calcified proteins |
| chronic: what blocked ducts cause what | an inflammatory process in which normal pancreatic tissue is destroyed and replaced by fibrous scar tissue |
| chronic: is it reversable | no |
| chronic: what does it lead to | pancreatic insuficciency |
| chronic: the pancreatic insuficciency lead to what | malabsorbtion and DM |
| chronic: when does DM develop | if the endocrine function of the pancreas is effected |
| chronic: what are the primary complications | malabsorption, malnutrition, peptic ulcer disease |
| chronic: what does it increase the risk for | pancreatic cancer and narcotic addiction |
| chronic: why does narcotic addiction occur | due to frequent episodes of severe pain |
| chronic: s/s | persisteny episodes of U abd. pian, anorexia, N/V, wt loss, flatulence, constipation, steatorrhea, elevated serum amylase and lipase, elevated BG |
| chronic: what is steatorrhea | fatty, frothy, foul smelling stool |
| diagnostic tests: serum amylase and lipase- what is it in disease | elevated in acute and chronic may be elevated in cancer |
| diagnostic tests: serum amylase - when is it critical | when >500 IU/L |
| diagnostic tests: serum lipase - when is it critical | when >600 IU/L |
| diagnostic tests: urine amylase- what is it in disease | elevated in acute |
| diagnostic tests: serum calcium and mag- what is it in disease | decreased in acute |
| diagnostic tests: serum calcium - when is it critical | <6 mg/dL |
| diagnostic tests: serum magnesium - when is it critical | <1 mg /dL |
| diagnostic tests: WBcs- what is it in disease | elevated in acute |
| diagnostic tests: carcinoembryonic angtigen (CEA)- what is it in disease | elevated in pancreatic cancer |
| diagnostic tests: carcinoembryonic angtigen (CEA)- what is norm | <5 ng/ML |
| diagnostic tests: why is a abd. xray or ultrasound done | may show inflammatory changes or the presence of gallstones in acute |
| diagnostic tests: why is a CT scan done | helps differentiate acute and chronic |
| diagnostic tests: why is a ERCP done | is used to diagnose chronic scope goes down esophagus and it can be thread thru ducts etc |
| acute: tx- what is the focus | on eliminating its cause (gallstones, alcohol abuse. minimizing additional damage by reducing pancreatic secretions, relive pain, and prevent complcations |
| tx: diet; what may be inserted | NPO; NG tube |
| tx: NG does what | it decreases panctreatic enzyme production while maintaining hydration and nutrition |
| tx: diet- when are orla food and fluids resumed | when serum amylase levels return to normal, BS are present, and pain has disapeared |
| tx: new diet given | clear liquids and progresses to low fat diet |
| meds: what is gievn for pain | parental narcotic analgesics |
| meds: why are antiboitics given | to treat and prevent infection |
| tx: when acute episodes are resolved, what is doen; why | a laparoscopic cholecystectomy; to reduce future episodes |
| Tx: focus of chronic | pain management, nutritional support, replacement of deficient enzymes and hormones |
| tx: chronic- why are narcotic analgesics avaoided | b/c the risk for adiction is high |
| meds: octreotide (sandostatin) what does it do | a synthetic hormone that suppresses pancreatic enzyme secretion |
| meds: octreotide (sandostatin)- use | to relieve pain of chronic |
| why is alcohol forbidden | it may parcipitate an attack |
| meds: why are pancreatic enzyme suppliments given | to manage steatorrhea |
| meds: why are ameprazole (prilosec), and ranitidine (zantac) given | to reduce gastric acidity |
| gastric acidity stimulates what | pancreatic enzyme production |
| surgery: what is doen | to drain persistent pseudocysts or dilate an obstructed duct |
| what are Nursing Dx | acute pain,risk for imbalanced nutrition, risk for injury |
| nx dx: acute pain- hy is NPO ordered | gastric secretions stimulate panctreatic secretions which agravate pain |
| what may steatorrhea indicate | an increase in the severity of pancreatitis |
| what is fluid loss associated with | vomiting, diaphoresis, third space shifts, and NG suction |
| acute: what are the gallbladder problems | if the ducts are bloacked |
| acute: if acute problems are not cleared up what could that lead to | chronic |
| acute: what is the goal of tx | remove the underlying cause |
| acute: what is the #1 s/s | pain in the center that radiates to the left side and the back |
| acute: why is pain worse after fatty foods | b/c the acid in the stomachincreases and it triggers production of the digestive enzymes |
| tx: what will NPO do | it will decrease pancreatic enzymes release |
| labs: what are the two to keep an eye on; why, when are they high, when are they low | amylase and lipase; those are the digestive enzymes; when first admitted; when pt is recovering |
| acute: s/s pt is imporving | no pain with food and amylase and lipase are low |
| functions of the pancreus: endocrine; exocrine | insulin and glucagon regulation; digestive enzymes that are released to the small intestines |
| chronic: what is the cause | ongoing inflammation |
| chronic: what does the ongoing inflammation eventually cause | scarring and pancreus is being destroyed |
| chronic: complications | no insulin relase, malabsorbtion, |
| chronic: complications- no insulin release causes what | body can't regulate BG |
| chronic: complications- why is there malabsorbtion | b/c enzymes aren't being developed and the food can't be digested enough |
| chronic: tx | give enzyme meds to digest foods better, pain meds |
| acute: what is the onset | sudden, after eating |
| acute: how long does it last | a few days, will go away |
| chronic: onset | slow onset, pt recognizes s/s |
| chronic: duration | forever, progressive |
| acute : what is the pain liek | sudden, left abd side |
| chronic: what is the pain like | dull |
| amylase and lipase: what are they in acute | super high |
| amylase and lipase: what are they in chronic; why | not as high as acute bc pancreas is being destroyed |
| chronic: what is a | a cypt that collects those enzymes, it increases in size on the outside of pancreus it is hard to get rid of |
| chronic: pseudocyst tx | NPO surgery place drain |
| nursing care: what should we know about pt health hx | meds, last meal, ETOH |
| any inflammation in the body increases what | BG |
| labs: why is albumin, prealbumin and protein looked at | for nutriion |
| why is pain assessed | to see if tx is working |
| meds for pain: | pain meds, |
| meds: why are proton pump inhibitors and H2 blockers used | they reduce the secretions of gastric acid |
| meds: proton pump inhibitors and H2 blockers- names | protonix (pantroprazole), prilosec (omeprazole); prevacid (lansoprazole)- these are all pp inhibitors |
| meds: action of H2 blockers | they inhibit the action of histamine at H2 receptor cells of the stomach, which reduces the secretions of gastric acid |
| meds: H2 blockers- adverse reactions | rare, dizziness, somnolnce, HA, |
| meds: proton pump inhibitors: action | they suprpess gastric acid secretion by inhibiting the hydrogen potassium adensine triphosphate (ATPase) enzyme system of the gastric parietal cells, they block the final step in gastric acid production |
| if there is fluid volume deficit what will pulse be like | thready and fast |
| diet: what should be limited | fats |
Created by:
jmkettel
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