front 1 ________ is the most powerful predictor of developing type 2 diabetes mellitus. | back 1 Obesity |
front 2 Congenital adrenal hyperplasia (adrenogenital syndrome) results from | back 2 blocked cortisol production. |
front 3 In type I diabetes, respiratory compensation may occur through a process of | back 3 respiratory alkalosis. |
front 4 Proton pump inhibitors may be used in the management of peptic ulcer disease to | back 4 decrease hydrochloric acid (HCl) secretion. |
front 5 Antidiuretic hormone (ADH) increases | back 5 water reabsorption in the collecting tubule of the kidney. |
front 6 A patient who should be routinely evaluated for peptic ulcer disease is one who is | back 6 being treated with high-dose oral glucocorticoids. |
front 7 An infusion of mannitol would be prescribed to treat | back 7 cerebral edema. |
front 8 A clinical finding that is consistent with a diagnosis of adrenocortical insufficiency is | back 8 hypoglycemia. |
front 9 A clinical finding consistent with a hypoglycemic reaction is | back 9 tremors. |
front 10 Diabetes mellitus is the ________ leading cause of death and a major cause of disability in the United States. | back 10 seventh |
front 11 The formation of active vitamin D | back 11 is impaired in renal failure. |
front 12 Epigastric pain that is relieved by food is suggestive of | back 12 gastric ulcer. |
front 13 Celiac sprue is a malabsorptive disorder associated with | back 13 inflammatory reaction to gluten-containing foods. |
front 14 What clinical finding would suggest an esophageal cause of a client’s report of dysphagia? | back 14 Chest pain during meals |
front 15 Myxedema coma is a severe condition associated with | back 15 hypothyroidism. |
front 16 A clinical finding consistent with a diagnosis of syndrome of inappropriate ADH secretion (SIADH) is | back 16 hyponatremia. |
front 17 Surgical removal of a gland may result in | back 17 hyposecretion. |
front 18 A thyroid gland that grows larger than normal is known as | back 18 goiter. |
front 19 A laboratory finding that would help confirm the diagnosis of hyperaldosteronism is | back 19 hypokalemia. |
front 20 Which response to an injection of ACTH indicates a primary adrenal insufficiency? | back 20 Which response to an injection of ACTH indicates a primary adrenal insufficiency? |
front 21 Narcotic administration should be administered carefully in patients with acute pancreatitis related to potential for | back 21 sphincter of Oddi dysfunction. |
front 22 Fecal leukocyte screening would be indicated in a patient with suspected | back 22 enterocolitis. |
front 23 Elevated serum lipase and amylase levels are indicative of | back 23 pancreatitis. |
front 24 Pathophysiologically, esophageal varices can be attributed to | back 24 portal hypertension. |
front 25 An urgent surgical consult is indicated for the patient with acute abdominal pain and | back 25 absent bowel sounds. |
front 26 A viral hepatitis screen with positive hepatitis B surface antigen (HBsAg) should be interpreted as ________ hepatitis B. | back 26 acute |
front 27 A patient with a history of alcoholism presents with hematemesis and profound anemia. The expected diagnosis is | back 27 gastroesophageal varices. |
front 28 A patient being treated for hepatic encephalopathy could be expected to receive a(n) ________ diet. | back 28 low-protein and high-fiber |
front 29 Chronic pancreatitis may lead to | back 29 diabetes mellitus. |
front 30 The definitive treatment for cholecystitis is | back 30 cholecystectomy. |
front 31 More than half of the initial cases of pancreatitis are associated with | back 31 alcoholism. |
front 32 A patient admitted with bleeding related to esophageal varices could be expected to receive a continuous intravenous infusion of | back 32 octreotide acetate. |
front 33 Liver transaminase elevations in which aspartate aminotransferase (AST) is markedly greater than alanine aminotransferase (ALT) is characteristic of | back 33 alcohol-induced injury. |
front 34 Hepatitis B is usually transmitted by exposure to | back 34 blood or semen. |
front 35 A patient with chronic gastritis would likely be tested for | back 35 Helicobacter pylori. |
front 36 Premature infants are at greater risk for developing | back 36 necrotizing enterocolitis. |
front 37 Normal bile is composed of | back 37 water, electrolytes, and organic solutes. |
front 38 A biliary cause of acute pancreatitis is suggested by an elevation in which serum laboratory results? | back 38 Alkaline phosphatase |
front 39 The finding of hypotension, rigid abdomen, and absent bowel sounds in a patient with pancreatitis | back 39 Indicates peritonitis with substantial risk for sepsis and shock. |
front 40 Common manifestations of gastrointestinal tract disorders: What is the manifestations of esophageal pain? | back 40 Heart burn (pyrosis) and Chest pain (esophageal distention or obstruction) |
front 41 Common manifestations of gastrointestinal tract disorders: What is the manifestation of abdominal pain? | back 41 Visceral pain, somatic pain, and referred pain. |
front 42 Common manifestations of gastrointestinal tract disorders: When is acute abdominal pain felt? | back 42 When you have perforated ulcer or ruptured organ |
front 43 Common manifestations of gastrointestinal tract disorders: When is chronic abdominal pain felt? | back 43 Diverticulitis or Ulcerative colitis |
front 44 TRUE/FALSE Vomiting is a common manifestation of gastrointestinal tract disorders. | back 44 True |
front 45 Common manifestations of gastrointestinal tract disorders: What are the 3 manifestations of intestinal gas? | back 45 Belching, abdominal gas and flatus |
front 46 Common manifestations of gastrointestinal tract disorders: What are bowel pattern alterations that can happen in gastrointestinal tract disorders? | back 46 Constipation and diarrhea. |
front 47 What is dysphagia? | back 47 Difficulty swallowing |
front 48 What sensation is felt with dysphagia? | back 48 Sensation that swallowed solids/liquids "stick" in esophagus |
front 49 TRUE/FALSE Patients with dysphagia have pain with swallowing? | back 49 True, and it is referred to as odynophagia. |
front 50 In dysphagia the patient has the __________ to initiate swallowing | back 50 inability |
front 51 What type of dysphagia? - Problems in delivery of fluid/food into esophagus -May be caused by R/T neuromuscular incoordination disorders -May be caused when the normal sequence is altered or absent | back 51 Type 1 |
front 52 What are the clinical manifestations of type 1 dysphagia? May _________ & ____________ the __________ ___________ & _____________. - _____________ when attempting to swallow -___________ with liquids than solids | back 52 May cough & expel the ingested food & liquids. - Aspirate when attempting to swallow -Worse with liquids than solids |
front 53 What type of dysphagia? -Problems in transport of bolus down esophagus. Causes: -Outpuching of one or more layer (diverticula) -Disorder of smooth muscle function (achalasia) -Structural interference of esophageal peristaltic activity (neoplasms, strictures) -Abnormal peristaltic activity | back 53 Type II |
front 54 What are the clinical manifestations of type II dysphagia? -Sensation that ______ is "________" behind __________ -Initially with ______ _______ may progress to __________. | back 54 Sensation that food is "stuck" behind sternum Initially with solid food, may progress to liquids. |
front 55 What type of dysphagia? - Problems in bolus entry into stomach Causes: Lower esophageal dysfunction or lesion obstruction | back 55 Type III |
front 56 What are the clinical manifestations of type II dysphagia? ______ or _______ in substernal area during ________ process. | back 56 Tightness or pain in substernal area during swallowing process. |
front 57 What is the esophageal disorder that causes backflow of gastric contents into esophagus through LES | back 57 GERD (gastroesophageal reflux disease) |
front 58 What are the causes of GERD *There are 7 :( | back 58 fatty foods, caffeine, large amounts of alcohol, cigarette smoking, pregnancy, anatomic features, hiatal hernia |
front 59 What are the clinical manifestations of GERD | back 59 Heartburn, regurgitation, chest pain, dysphagia |
front 60 What are treatments used for GERDS? There are 3 important ones | back 60 Over the counter antacids and histamine (H2)- blocking medications Proton pump inhibitors (PPI) are the mainstays for chronic GERD |
front 61 What is an important complication in GERD that can become esophageal cancer? | back 61 Barrett esophagus |
front 62 Complication of GERD in which columnar tissue replaces normal squamous epithelium of the distal esophagus? | back 62 Barrett esophagus |
front 63 What are pulmonary symptoms of Barrett esophagus? | back 63 cough, asthma, and laryngitis (from reflux in breathing passages) |
front 64 What can progression of Barrett esophagus cause? | back 64 ulceration and fibrotic scarring |
front 65 What is gastritis? | back 65 Inflammation of the stomach lining |
front 66 Acute gastritis is precipitated by _________ or ___________ ___________. | back 66 Acute gastritis is precipitated by ingestion of irritating substances. |
front 67 What are examples that will cause acute gastritis? | back 67 Alcohol and asprin, NSAIDs, viral, bacteria and autoimmune |
front 68 Chronic gastritis will become...... | back 68 peptic ulcer and gastric adenocarcinoma |
front 69 What is always nearly a factor of chronic gastritis? | back 69 Helicobacter pylori (transmission: person to person, fecal-oral route, reservoir in water sources) |
front 70 What are complications of chronic gastritis? * 4 of them - not so bad :) | back 70 Peptic ulcer disease, gastric adenocarcinoma, decreased acid and intrinsic factor. |
front 71 TRUE or FALSE Gastric adenocarcinoma is deadly and can cause MALT | back 71 TRUE |
front 72 What will not be absorbed if you have decreased intrinsic factor? | back 72 B-12 |
front 73 What are causes of peptic ulcer disease? * 4 of them :) | back 73 NSAIDs, stress (glucocorticoids), smoking, genetics |
front 74 What is a key role in promoting both gastric and duodenal ulcer formation? | back 74 H.pylori |
front 75 In what situations does H.pylori thrive and what does it cause? | back 75 in acidic conditions. It causes slow rate of ulcer healing, and high rates of recurrence |
front 76 What promotes ulcer healing? | back 76 Clearance of H.pylori |
front 77 Pain of ________ ________ typically occurs on an empty stomach but may present soon after a meal. | back 77 Pain of gastric ulcer typically occurs on an empty stomach but may present soon after a meal. |
front 78 Pain of _________ _________ classically occurs 2-3 hours after a meal and is relieved by further food ingestion. | back 78 Pain of duodenal ulcer classically occurs 2-3 hours after a meal and is relieved by further food ingestion. |
front 79 If you have pain at night is it most likely gastric or duodenal ulcer? | back 79 duodenal |
front 80 Gatric ulcers should be visualized with ____________ and _______________ to rule out _____________. | back 80 Gastric ulcers should be visualized with endoscopy and biopsied to ruled our malignancy. |
front 81 Treatment for peptic ulcer disease: Encourage _______ of the ___________ _________ by __________ gastric ________. Prevent ___________. __. _______ antibiotics _____ antagonits __________ ________ inhibitors ____________ (forms protective coating over injured mucosa) | back 81 Encourage healing of the injured mucosa by reducing gastric acidity. Prevent recurrence H. pylori antibiotics H2 antagonist Proton pump inhibitors Sucralfate (from protective coating over injured mucosa) |
front 82 Life style changes used as treatment for peptic ulcer disease: ___________ cessation Avoidance of _____ and ________ _________ reduction Avoid ______ ________ that exacerbate symptoms such as __________ ________ (sadness) and __________ (double sadness) | back 82 Smoking cessation Avoidance of ASA and NSAIDs Stress reduction Avoid irritating foods that exacerbate symptoms such as caffeinated beverages (sadness) and alcohol (double sadness) |
front 83 What is the inflammatory bowel disease that causes chronic inflammatory disease of the mucosa of the rectum and colon (Lower end)? | back 83 Ulcerative colitis |
front 84 What are the hallmark manifestations for ulcerative colitis? | back 84 Ulceration and remission. Bloody diarrhea and lower abdominal pain |
front 85 TRUE/FASLE Patients with ulcerative colitis don't have increased cancer risk. | back 85 False. They do, colon cancer, usually 7-10 yrs after 1st manifestation |
front 86 What are the main two treatments for ulcerative colitis? | back 86 Corticosteroids and broad-spectrum antibiotics. *Just for fun, a new medication is MAB. |
front 87 What type of inflammatory bowel disease affects all layers of intestinal wall of proximal portion of the colon or terminal ileum? | back 87 Crohn Disease aka regional enteritis or granulomatous colitis. |
front 88 Clinical manifestations for Crohn disease? | back 88 diarrhea, if blood not as severe as ulcerative colitis, constant chronic right lower quadrant pain, may have RLQ mass and tenderness |
front 89 What is antibiotic-associated colitis? | back 89 Enterocolitis |
front 90 What causes acute inflammation and necrosis of large intestine? | back 90 Enterocolitis |
front 91 What is enterocolitis caused by? | back 91 Our BFF: C-DIFF (exposure to antibiotics) |
front 92 Clinical manifestations of enterocolitis | back 92 Bloody diarrhea, abdominal pain, fever, leukocytosis, sepsis |
front 93 Fun fact: HISTORY IS CRITICAL for patients with enterocolitis | back 93 you need to know if they've been taking previous antibiotics and which type. |
front 94 Treatment for enterocolitis: STOP ______ _______. ________ _______ such as metronidazole or vancomycin | back 94 Stop current antibiotics Oral antibiotics such as metronidazole or vancomycin |
front 95 Gina's favorite entercolitis is..... | back 95 APPENDICITIS hahaha :) FYI its pretty rare in adults mostly common in kids |
front 96 Inflammation of the vermiform appendix causes.... | back 96 appendicitis |
front 97 Clinical manifestations of appendicitis | back 97 RLQ pain (McBurney point) rebound tenderness, nausea, vomiting, fever, diarrhea |
front 98 Treatment for appendicitis | back 98 immediate surgical removal Antibiotics with fluid/electrolyte replacement |
front 99 Type of enterocolitis where presence of diverticula in the colon | back 99 Diverticular disease |
front 100 Diverticular disease results from low intake of ...... | back 100 dietary fibers |
front 101 What motility disorder causes alternating diarrhea and constipation accompanied by abdominal cramping pain? *most common | back 101 IBS- Irritable bowel syndrome |
front 102 IBS is also called _______ ______ and ______ _______ syndrome | back 102 IBS is also called spastic colitis and irritable colon syndrome |
front 103 Clinical manifestations of IBS? | back 103 Diarrhea or constipation, abdominal cramping, and mucus in stool. |
front 104 What motility disorder causes twisting of bowel on itself causing intestinal obstruction and blood vessel compression (ischemia) *seen in elderly | back 104 Volvulus |
front 105 Motility disorder where telescoping/invagination of a portion of bowel into adjacent (usually distal) bowel, causing intestinal obstruction. *most often in infants- males more than females | back 105 Intussusception |
front 106 Malabsorption disorder that is familial intolerance of gluten-containing foods leading to inflammation and atrophy of intestinal villi. | back 106 Celiac disease |
front 107 Treatment for celiac disease | back 107 Gluten-free diet, supplemental iron folate, B12 fat-soluble vitamins (A.D,EK), and oral corticosteroids. |
front 108 What are warning signs of neoplasms of GI tract? | back 108 Black tarry, bloody, or pencil-shaped stool, and a change in bowel habit |
front 109 Who are more likely to get esophageal cancer, men or women? | back 109 Men by (3x) |
front 110 What are 3 main risk factors for esophageal cancer? | back 110 nitrosamine, Barrett esophagus, and smoking |
front 111 What is the most likely prognosis for a patient with esophageal cancer? | back 111 Poor, very high degree of metastasis |
front 112 What are the two types of esophageal cancer | back 112 squamous cell carcinoma adenocarcinoma |
front 113 Who are more likely to get gastric carcinoma, men or women? | back 113 Men who are older than 30yrs old |
front 114 What is the 1 main risk factor for gastric carcinoma? | back 114 H. pylori infection |
front 115 Who are most likely to get small intestinal neoplasms? | back 115 ha not men, people 50 years or older |
front 116 What neoplasm of the GI tract has a major precursor lesion in the development of colon cancer? | back 116 Colonic polyps |
front 117 Can Epstein barr virus case gastric carcinoma? | back 117 yes |
front 118 What are the risk factors for colon cancer -Don't say smoking. It's not there. For once. | back 118 Increases after age 40 high-fat, low fiber diet polyps chronic irritation or inflammation hereditary |
front 119 What are the majority of gallstones made of? | back 119 Cholesterol (75%) *pigment (25%) |
front 120 What are the three factors that contribute to the formation of gallstones: 1. ____________ of bile with ________ causing _________ of cholesterol. 2. ____________ of crystals 3.___________ (stasis of bile) allowing stone _________. | back 120 1. Supersaturation of bile with cholesterol, causing precipitation of cholesterol. 2. Nucleation of crystals 3. Hypomotility (stasis of bile) allowing stone growth. |
front 121 What determine the likelihood of cholesterol gallstone formation? | back 121 Concentration of cholesterol, lecithin, and bile acids. |
front 122 Risk factors for gallstones? 6 of them :( | back 122 -Prolonged fasting or rapid weight loss -Pregnancy -Oral contraceptives -Obesity -Women over 40 -Variety of medical factors. |
front 123 What percentage of Gallstones are pigment stones? | back 123 25% |
front 124 Contains a mixture of pigment polymers and calcium salts. | back 124 Pigment stones |
front 125 Pigment stones that are the most common and may be idiopathic or associated with cirrhosis or hemolysis. | back 125 Black pigment stones |
front 126 Differ in composition, much more common in developing countries, associated with biliary parasitosis, bacterial colonization, and infection. | back 126 Brown pigment stones |
front 127 Do adults who have cholelithiasis need treatment? | back 127 No and they may be asymptomatic. |
front 128 What disorder of the gallbladder associated with inflammation of the gallbladder wall and causes fibrosis and thickening? | back 128 Cholecystitis |
front 129 What is the most common cholecystitis? | back 129 Calculus cholecystitis caused by gallstones. |
front 130 Acute or chronic cholecystitis? -Cholelithiasis present in 90% of patients -Obstruction of cystic duct present in almost all patients: related to stasis of bile -Bacterial infection may be present. | back 130 Acute cholecystitis |
front 131 What is used to make a diagnosis of acute cholecystitis? | back 131 Abdominal Ultrasound |
front 132 Clinical manifestations of acute cholecystitis: -Severe ______ _______ abdominal pain: radiates to ______. -__________ tenderness -___________ -___________ -mild elevations of _________ and serum _______________. | back 132 -Severe right upper abdominal pain: radiates to back. -abdominal tenderness -Fever -leukocytosis -mild elevations of bilirubin and serum transaminases. *It is important to note fever and leukocytosis are not seen in patients with gallstones-that's the difference |
front 133 What are the two main treatments for cholecystitis? | back 133 Cholecystectomy and antibiotics |
front 134 TRUE or FALSE Acalculous cholecystitis is caused because of gallstones? | back 134 False |
front 135 -Occurs in patients without preexisting gallstones. -Males 50 years or older ( >50) -Tends to occur in the setting of major surgery, critical illness, trauma, burn-related injury or TPN | back 135 Acalculous cholecystitis |
front 136 Inflammation of the pancreas, autodigestion of the pancreas from enzyme activation. | back 136 Acute pancreatitis |
front 137 What are predisposing factors associated with acute pancreatitis? * 3 of them :) | back 137 Biliary tract disease, hypertriglyceridemia, alcohol (66%) |
front 138 99% of pancreas is _________. | back 138 Exocrine. (It produces enzymes) *Just 1% of the pancreas creates insulin- endocrine |
front 139 The 3 pathways for acute pancreatitis: ___________ of the pancreatic _________ by a ______ or other cause (usually unknown) - __________ cell injury -____________ intracellular transport | back 139 Obstruction of the pancreatic duct by a stone or other cause (usually unknown) -Acinar cell injury -Defective intracellular transport *all 3 will lead to activated enzymes (protease, protein breakdown, fat necrosis, damage of basal membrane, hemorrhage, and cause inflammation and edema) |
front 140 Clinical manifestations of acute pancreatitis: Steady, boring pain in _______ or _____. - __________ in intensity -___________ tenderness on palpitation -______ or _________ to back -________ and __________. | back 140 Steady boring pain in epigastrium or LUQ - Increases in intensity -Severe tenderness on palpation -Radiates or penetrates to back -Nausea and vomiting |
front 141 What are the general manifestations in hepatocellular failure | back 141 Jaundice, decreased clotting factors, hypoalbuminemia, decreased vitamins D and K. |
front 142 What are the general manifestations in portal hypertesnsion | back 142 GI congestion, development of esophageal or gastric varices, hemorrhoids, splenomegaly, ascites |
front 143 Hemolysis, ineffectve erythropeiesis, resorption of large hemattomas is a sign of what | back 143 Prehepatic causes - red blood cell or spleen |
front 144 Dysfunction of liver cells: increased levels of either unconjugated or conjugated bilirubin; imatrue UDPGT are signs of what? | back 144 Hepatic causes - Liver |
front 145 At level of canalicular bilirubin transport, cinjugated hyperbilirubinemia, mechanical obstruction to bile ducts is a sign of what | back 145 Post hepatic causes- bile and bile bladder |
front 146 What is the preferred test to diagnosis acute pancreatitis? | back 146 Lipase and amylase blood test. |
front 147 in acute pancreatitis, when will there be an increase in amylase and lipase? | back 147 during the first 12 hrs. |
front 148 In what diagnostic testing will ileus pattern, "sentinel loop." show a distended loop of small bowel in the area of the pancreas in a patient who has acute pancreatitis? | back 148 Abdominal x-ray |
front 149 TRUE or FALSE it is difficult to see acute pancreatitis in an abdominal ultrasound | back 149 True |
front 150 What is the best diagnostic tool "gold standard" for diagnosing acute pancreatitis? *not preferred, the best | back 150 CT of abdomen |
front 151 What is the treatment used for mild to moderate acute pancreatitis? | back 151 Reduce pancreatic secretions, conservation management, and withholding oral feeding |
front 152 What type of acute pancreatitis complication is the following: Collection of fluid within or adjacent to the pancreas. A patient will experience fever, tachycardia, abdominal mass, and tenderness. | back 152 Pseudocyst |
front 153 What management is done for pseudocyst? | back 153 endoscopic or surgical drainage |
front 154 What type of pancreatitis: -Chronic inflammatory lesions in pancreas. -Associated with alcohol intake -Can progress even if alcohol consumption is stoped | back 154 Chronic pancreatitis |
front 155 What type of acute pancreatitis complication is the following: Persistent leak in pancreatic duct into pleural space and mediastinum. | back 155 Pancreatic ascites |
front 156 Pathogenesis of Chronic Pancreatitis: -Presence of chronic __________ lesions in ____________. -Key element: necrosis of ______ _______ followed by __________. -Leads to ___________ which cause __________ flow of ___________ juices. | back 156 -Presence of chronic inflammatory lesions in pancreas. -Key element: necrosis of exocrine parenchyma followed by fibrosis. -Leads to calcification which cause obstructed flow of pancreatic juices. |
front 157 Clinical manifestations of chronic pancreatitis: Bouts of acute pancreatitis with progressive ______ and ________ pancreatic dysfunction. -___________: progressive loss of pancreatic islets -___________: fat and vitamin A, D, E. and K -___________: poor intake related to pain | back 157 Bouts of acute pancreatitis with progressive endocrine and exocrine pancreatic dysfunction. -Diabetes: progressive loss of pancreatic islets -Malabsorbtion: fat and vitamin A, D, E. and K -Weightloss: poor intake related to pain |
front 158 What are the two important complications of chronic pancreatitis? | back 158 Pseudocysts and pancreatic ascites. |
front 159 Treatment for chronic pancreatitis: - ________ control - Absolute abstention from __________. -_________ intervention -_______ _______ block. | back 159 - Pain control - Absolute abstention from alcohol. -Surgical intervention -Celiac plexus block. |
front 160 What type of cancer? -About 2% of all cancers -Ranks 4th among deaths from malignancies | back 160 Pancreatic cancer |
front 161 Two risk factors for pancreatic cancer? | back 161 Cigarette smoking and obesity |
front 162 Clinical Manifestations for pancreatic cancer: _______ _______ ________: jaundice, malabsorption,and weight loss __________ ______: abdominal pain and nausea | back 162 k |
front 163 Diabetes Insipidus/ DI is caused by | back 163 ADH Deficiency |
front 164 What are the three P's for Diabetes Insipidus | back 164 - Polyuria - Polydipsia - Polyphagia |
front 165 Insulin is synthesized in the pancreas by the _____ ______ of the islets of ____________. ______ ______ produce glucagon | back 165 Insulin is synthesized in the pancreas by the Beta cells of the islets of Langerhans. Alpha cells produce glucagon |