Peptic Ulcer Disease and GI Drugs Lecture

What is the major defensive factor that protects the stomach and duodenum from self-digestion?

Where is ulceration most common in cases of peptic ulcer disease?

What bacterium is primarily responsible for causing most cases of peptic ulcer disease?

Which condition can severe ulcers from peptic ulcer disease be complicated by?

What serves the physiologic role of neutralizing any hydrogen ions that penetrate the mucus in the stomach and duodenum?

What promotes healing and greatly reduces the chance of recurrence in peptic ulcer disease when eradicated?

Which of the following is NOT considered a major aggressive factor in peptic ulcer disease?

What is the role of prostaglandins in the gastrointestinal mucosa?

Why is acid necessary for peptic ulcer formation?

What is the primary cause of Zollinger-Ellison syndrome?

What effect does smoking have on ulcer healing and recurrence?

What is the primary goal of drug therapy for peptic ulcers?

Why are antibiotics essential in the treatment of peptic ulcers with H.pylori infection?

What role do PPIs play in the treatment of PUD?

How do NSAIDs contribute to ulcer formation?

Why is eradication of H.pylori important for ulcer healing?

How do drugs promote ulcer healing?

What is the recommended treatment for NSAID-induced ulcers?

Which medication is preferred for treating NSAID-induced ulcers when the offending NSAID cannot be discontinued?

What is a method to evaluate ulcer healing according to the text?

What is a non-optimal measure for antiulcer therapy based on the text?

Which statement is true regarding alcohol consumption and peptic ulcers according to the text?

Which antibiotic is mentioned as highly sensitive to H.pylori in the text?

What is a potential side effect of bismuth therapy mentioned in the text?

What is the primary cause of changes in the esophageal mucosa in gastroesophageal reflux disease (GERD)?

Which factor is NOT mentioned as contributing to transient lower esophageal sphincter (LES) relaxation in severe GERD?

What effect does a hiatal hernia have on the occurrence of transient lower esophageal sphincter (LES) relaxations?

Which symptom is often associated with severe gastroesophageal reflux disease (GERD)?

Why is referral considered for patients with esophageal reflux who do not respond to medications?

Which aspect is NOT considered when determining the severity of reflux in gastroesophageal reflux disease (GERD)?

What is the principal function of the colon?

What is one symptom that helps define constipation?

What is a common cause of constipation according to the text?

How do laxatives help patients with cardiovascular diseases?

What is a contraindication for using laxatives according to the text?

How can laxatives be beneficial as an adjunct to anthelmintic therapy?

What is the first-line intervention in the management of GERD according to the text?

Why was ranitidine taken off the market in April 2020 as mentioned in the text?

What is the next step in pharmacologic management for GERD patients after lifestyle and diet modifications with antacids?

What is the main concern with prolonged use of PPIs for treating GERD as mentioned in the text?

In pediatric patients with GERD, which medication types are available for treatment according to the text?

What distinguishes a cathartic effect from a laxative effect as mentioned in the text?

Which group of laxatives is especially useful when the bowel is being prepared for diagnostic procedures or surgery?

Which laxative group consists of agents that produce a soft but formed stool within 1 to 3 days?

Which laxative group widely used in patients with diverticulosis and irritable bowel syndrome consists of natural or semisynthetic polysaccharides and celluloses derived from grains and plant materials?

Which category of laxatives is associated with the potential side effect of esophageal obstruction if swallowed without sufficient fluid?

Laxative salts like sodium phosphate and magnesium hydroxide belong to which group of laxatives that draw water into the intestinal lumen to soften the fecal mass and stimulate peristalsis?

Which laxative group, acting on the colon to produce a semifluid stool within 6 to 12 hours, is widely used yet has few legitimate applications?

What is the primary mechanism of action of lubiprostone in promoting bowel movement?

Why are magnesium salts contraindicated in patients with kidney disease?

How does sodium phosphate contribute to acute renal failure in some patients?

What is the primary function of plecanatide in regulating intestinal fluid secretion?

How do PEG-ELS bowel-cleansing solutions differ from sodium phosphate-based ones?

Why are sodium phosphate cleansers contraindicated in patients with cardiovascular disease?

What is the mechanism of action of sodium phosphate as an osmotic laxative?

How do sodium phosphate laxatives differ from PEG-ELS products in terms of adverse effects?

What is the purpose of drinking a large volume of clear fluid before, during, and after dosing with sodium phosphate products?

What is a potential severe adverse effect associated with sodium phosphate products?

How does Prepopik differ from PEG-ELS products in preparing for colonoscopy?

What caution should be taken with people using Prepopik or sodium phosphate products?

What misconception about bowel movements is highlighted in the text?

Why do people sometimes habitually self-prescribe laxatives according to the text?

What can strong laxatives potentially do to the entire bowel?

What is one of the potential serious pathologic changes that can result from laxative abuse?

Why might a laxative user think that constipation has returned after taking strong laxatives?

What is the recommended initial step to break the laxative habit?

What effect can chronic exposure to laxatives have on defecatory reflexes?

What should patients be informed about regarding bowel movements after abrupt cessation of laxative use?

How does strong laxative use set the stage for a repeating cycle of purging according to the text?

What is a consequence of chronic exposure to laxatives in terms of reliance on them?

What is the primary function of the vomiting center located in the medulla oblongata?

Which neurotransmitter receptor type is NOT mentioned as a target for antiemetic drugs in the text?

Which drug is specifically noted as the first serotonin receptor antagonist approved for Chemotherapy-Induced Nausea and Vomiting (CINV)?

What is the primary effect of serotonin antagonists like ondansetron on the body?

What is the mechanism of action of aprepitant in preventing CINV?

Why are serotonin receptor antagonists considered effective against nausea and vomiting induced by radiation therapy?

Why should ondansetron not be given to patients with long QT syndrome?

Which group of drugs is mentioned as effective for treating both inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS)?

How do glucocorticoids like dexamethasone suppress CINV?

What is the primary application of lorazepam in CINV suppression?

What is the main concern when using promethazine as an antiemetic in young children?

How does metoclopramide suppress emesis?

Which drug, related to marijuana, is a synthetic derivative of dronabinol?

What is the primary psychoactive agent in cannabinoids used for medical purposes?

For treating highly emetogenic drugs, what is the recommended antiemetic regimen?

What is the most effective drug for preventing and treating motion sickness?

What is the severe form of nausea and vomiting during pregnancy characterized by dehydration and weight loss?

Why may methylprednisolone be considered a last resort for managing nausea and vomiting during pregnancy?

What is the potential consequence of using loperamide to manage mild infectious diarrhea?

In the management of traveler's diarrhea caused by E.coli, when is treatment typically considered unnecessary?

Which drug is preferred for the prophylaxis of traveler's diarrhea due to E.coli and Vibrio cholerae?

What is the primary symptom that characterizes irritable bowel syndrome (IBS) according to the Rome IV criteria?

Which drug class has been employed for years to provide symptomatic relief in patients with IBS?

What is a common nondrug measure employed in the management of IBS?

What is the primary purpose of atropine in the combination with diphenoxylate (Lomotil)?

Which symptom results from activation of opioid receptors in the GI tract by opioids?

What is the primary role of diphenoxylate (Lomotil) when used as an antidiarrheal agent?

Why are antihistamines like dimenhydrinate and meclizine less effective than scopolamine for treating motion sickness?

What distinguishes nonspecific antidiarrheals from specific agents in terms of treating diarrhea?

Why are transdermal anticholinergic side effects generally less intense than with oral or subcutaneous dosing?

What is the main concern when prescribing alosetron for IBS-D in women?

What qualifies an IBS case as severe according to the text?

Which enzyme is involved in the metabolism of alosetron?

Why is alosetron approved only for women with severe IBS-D?

What is a notable risk associated with the use of alosetron?

Which drugs are specifically approved for IBS according to the text?

In what circumstance should prescribers consider a strict risk management program for patients using alosetron?

Why is bacterial colonization reduced when patients with concomitant IBS and SIBO are treated with antibiotics?

"Less than 5% of IBS cases qualify as severe" implies that most cases of IBS are:

Why are safety and efficacy of alosetron not demonstrated in men according to the text?

Which part of the GI tract is usually affected by Crohn disease?

What is the main difference in the location of inflammation between Crohn disease and ulcerative colitis?

Which of the following drugs is NOT employed in the treatment of inflammatory bowel disease (IBD)?

What is the main approved indication for using sulfasalazine?

Which of the following symptoms is common in patients with ulcerative colitis but not in Crohn disease?

Which type of ulcers is sulfasalazine most effective against?

What is a potential consequence of long-term high-dose therapy with intravenous metoclopramide?

How does nitroglycerin ointment relieve pain caused by chronic anal fissures?

What is the main purpose of pancreatic enzymes secreted into the duodenum?

Which trade name does NOT refer to a preparation of pancreatic enzymes?

What is the primary purpose of emollients in anorectal preparations?

Which compound is NOT a common ingredient in anorectal preparations?

How does bicarbonate secretion by the pancreas help protect digestive enzymes?

What symptom is characteristic of deficiency in pancreatic enzymes?

What is a severe adverse effect associated with prolonged use of glucocorticoids in the treatment of ulcerative colitis and Crohn disease?

'Rectiv' is primarily used for relief from which condition?

'Preparation H', 'Rectagene', and 'Anusol' are commonly associated with the treatment of which condition?

Which immunosuppressant acts faster and is stronger than azathioprine or mercaptopurine in inducing remission for acute, severe ulcerative colitis or Crohn disease?

Which drug, a monoclonal antibody designed to neutralize TNF-α, is indicated for moderate to severe Crohn disease and ulcerative colitis but has potential serious adverse effects like infections and infusion reactions?

Thiopurines, such as azathioprine and mercaptopurine, are generally reserved for patients with ulcerative colitis and Crohn disease who...

Which oral glucocorticoid is specifically approved for mild to moderate Crohn disease that involves the ileum and ascending colon?

What are the major adverse effects associated with thiopurines, such as azathioprine and mercaptopurine?

Which medication can promote short-term remission in patients with Crohn disease, reducing the need for glucocorticoids?

What is the primary purpose of sulfasalazine during pregnancy and lactation?

What is the indicated use of oral metoclopramide for diabetic gastroparesis?

Which protein is used to store iron within mucosal cells of the small intestine?

What is the primary impact of iron deficiency on red blood cells?

Where does most transferrin-bound iron go for incorporation into hemoglobin?

What is the main regulator of body iron content through control of intestinal absorption?

In what condition do adults have relatively low daily iron needs compared to infants and children?

What is the daily dietary iron requirement for adult women to replace iron lost through menstruation?

What is the primary role of erythropoietin in the development of red blood cells?

Which iron-containing molecule stores oxygen in muscle?

What is the primary function of reticulocytes in the process of red blood cell development?

Which factors are essential for the synthesis of hemoglobin in red blood cells?

In what stage do circulating red blood cells reach full maturity?

Which component of red blood cells constitutes a smaller amount compared to hemoglobin but is essential for various iron-containing enzymes?

Which iron salt is recommended as the treatment of choice for iron deficiency anemia?

What is the primary adverse effect associated with all four types of ferrous iron salts mentioned in the text?

Which additional laboratory data can help confirm a diagnosis of iron deficiency anemia?

What is the primary reason for using oral iron over parenteral iron according to the text?

Which iron supplement is mentioned in the text as having a reduced risk of toxicity in case of accidental ingestion by children?

What is the objective of iron deficiency anemia therapy according to the text?

Which therapy is indicated for patients with severe neurologic deficits caused by B12 deficiency?

What is the primary manifestation of moderate B12 deficiency?

Why is folic acid alone not recommended for the treatment of B12 deficiency?

What is the primary function of intrinsic factor in the absorption of vitamin B12?

What can happen if folic acid intake ceases suddenly?

What is the main consequence of vitamin B12 deficiency on DNA synthesis?

What is the enterohepatic recirculation responsible for in relation to folate?

What is one potential cause of impaired absorption of vitamin B12?

How does folic acid differ from vitamin B12 in terms of DNA synthesis?

Which specific characteristic distinguishes pernicious anemia from other types of anemia?

What is the main role of transcobalamin II in the process of vitamin B12 absorption?

How does vitamin B12 deficiency impact the cells that form the epithelial lining of the mouth, stomach, and intestine?

Why is it recommended that all women of reproductive age consume 400 to 800 µg of supplemental folic acid daily?

What is the most common cause of folate deficiency according to the text?

What is the effect of poor diet on correcting folate deficiency according to the text?

What is the consequence of indiscriminate use of folic acid according to the text?

Why is oral administration preferred for most patients when treating folic acid deficiency?

What is the primary difference between correcting folate deficiency due to poor diet and malabsorption?

What is a potential consequence of folic acid deficiency other than megaloblastic anemia?

Why should prophylactic folate be taken only when clearly appropriate according to the text?

'The modality for treating folic acid deficiency should be matched with the cause.' What does this mean when addressing poor diet as a cause?

What is the recommended initial therapy for folic acid deficiency?

How is therapy for folic acid deficiency evaluated according to the text?

What can be expected within 48 hours if treatment for folic acid deficiency has been effective?

What is the maintenance dose of folic acid recommended after the initial therapy?

When should reticulocyte count measurably increase if treatment for folic acid deficiency has been effective?