Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
39 Cards in this Set
- Front
- Back
|
Vomiting can be triggered by a variety of stimuli including...
|
--stimulation of the sensory nerve endings in the GI tract and pharynx
--disturbance of vestibular apparatus --stimuli to sensory nerves of the heart and viscera --endocrine factors --rise in intracranial pressure --drugs --endogenous emetic substances produced as a result of radiation damage or disease --nauseating smells --repulsive sights --disgusting experience |
|
|
The central neural regulation of vomiting is vested in 2 separate units in the medulla. Name these units.
On which unit do most drugs and toxins act? |
(1) chemoreceptor trigger zone (CTZ)
(2) vomiting center Drugs and toxins act on the CTZ. It is very sensitive to chemical stimuli and since the blood-brain barrier is poorly developed in the CTZ, it is readily accessible to emetic substances in the general circulation. |
|
|
This emetic drug is used to treat non-corrosive poisoning when the patient is conscious. It has an irritant action that act locally on the stomach.
a) apomorphine b) L-dopa c) ipecacuanha d) hyoscine |
This emetic drug is used to treat non-corrosive poisoning when the patient is conscious. It has an irritant action that act locally on the stomach.
c) ipecacuanha |
|
|
This morphine derivative activates DA receptors in the CTZ to induce vomiting.
a) apomorphine b) L-dopa c) ipecacuanha d) hyoscine |
This morphine derivative activates DA receptors in the CTZ to induce vomiting.
a) apomorphine |
|
|
Cinnarizine and cyclizine:
a) are muscarinic antagonists that act on the vestibular nucleus b) are dopaminergic antagonists that act on the CTZ c) are peripherally acting dopaminergic antagonists d) are H1-receptor antagonists that act on the vestibular nucleus in the medulla |
Cinnarizine and cyclizine:
d) are H1-receptor antagonists that act on the vestibular nucleus in the medulla |
|
|
What is the clinical use of cinnarizine and cyclizine?
What is the clinical use of promethazine? |
Cinnarizine and cyclizine are effective at preventing motion sickness and block substances acting locally in the stomach.
Promethazine is uesd to treat severe morning sickness. |
|
|
This anti-emetic agent is the most potent agent available for the prevention of motion sickness but is ineffective against agents that stimulate the CTZ.
|
HYOSCINE is the most potent anti-emetic agent available for the prevention of motion sickness but is ineffective against agents that stimulate the CTZ.
|
|
|
This anti-emetic agent blocks DA receptors in the CTZ and antagonizes 5-HT3 receptors in the GI tract.
|
METOCLOPRAMIDE is an anti-emetic agent that blocks DA receptors in the CTZ and antagonizes 5-HT3 receptors in the GI tract.
|
|
|
This anti-emetic agent is a peripheral DA receptor antagonist but does not cross the blood-brain barrier. It is the preferred treatment of L-dopa-induced vomiting.
|
DOMPERIDONE is a peripheral DA receptor antagonist but does not cross the blood-brain barrier. It is the preferred treatment of L-dopa-induced vomiting.
|
|
|
These 2 5-HT3 antagonist agents are of immense value in treating vomiting caused by cytotoxic drugs. Their anti-emetic action synergizes with the use of steroids like dexamethasone.
|
ONDANSETRON and GRANISETRON are 5-HT3 antagonist agents that are of immense value in treating vomiting caused by cytotoxic drugs. Their anti-emetic action synergizes with the use of steroids like dexamethasone.
|
|
|
Describe common ulcer symptoms as well as their onset and duration.
What often relieves these symptoms? |
The most common ulcer symptom is gnawing or burning pain in the epigastrium. The pain occurs when the stomach is empty, between meals and in the early morning hours. It lasts from minutes to hours and may be relieved by eating or by taking antacids.
|
|
|
These agents are the gold standard in treating ulcers:
a) cholinergic antagonists b) proton pump inhibitors c) antacids d) H2 receptor antagonists |
These agents are the gold standard in treating ulcers:
d) H2 receptor antagonists |
|
|
What is the general mechanism of action by which H2 blockers improve symptoms of heartburn and regurgitation?
|
H2 receptor antagonists decrease the flow of stomach acid. They promote healing of gastric and duodenal ulcers and are useful in hypersecretory states.
|
|
|
Identify the H2-receptor antagonist described by the following..
1) does not have anti-androgenic properties and does not alter drug metabolism; it is up to 10x mroe potent than cimetidine 2) does not alter drug metabolism and does not bind testosterone receptors and is 2x more potent than ranitidine 3) may cause gynecomastia in males and increased prolactin release in females 4) inhibits gastric acid production and does not have anti-cholinergic side effects but may prolong the half-life of many durgs and can cause GI upset and headache |
1) does not have anti-androgenic properties and does not alter drug metabolism; it is up to 10x mroe potent than cimetidine = ranitidine or nizatidine
2) does not alter drug metabolism and does not bind testosterone receptors and is 2x more potent than ranitidine = famotidine 3) may cause gynecomastia in males and increased prolactin release in females = cimetidine 4) inhibits gastric acid production and does not have anti-cholinergic side effects but may prolong the half-life of many durgs and can cause GI upset and headache = cimetidine |
|
|
Name the 4 H2-receptor antagonists used to treat ulcers.
|
1) cimetidine
2) ranitidine 3) nizatidine 4) famotidine |
|
|
These agents are useful to treat ulcers in patients resistant to H2 blockers. They decrease acid secretion and motility of the GI tract.
a) antacids b) proton pump inhibitors c) cholinergic antagonists |
These agents are useful to treat ulcers in patients resistant to H2 blockers. They decrease acid secretion and motility of the GI tract.
c) cholinergic antagonists |
|
|
Name the 3 cholinergic antagonists used to treat ulcers.
|
1) propantheline
2) isopropamide 3) scopolamine |
|
|
These agents neutralize gastric acid and reduce the pain associated with ulcers.
a) H2 blockers b) antacids c) proton pump inhibitors |
These agents neutralize gastric acid and reduce the pain associated with ulcers.
b) antacids |
|
|
For each of the following, identify if the statement is describing (a) calcium carbonate (b) magnesium hydroxide (c) aluminum hydroxide or (d) sodium bicarbonate.
1) binds bile acids and not absorbed from the GI tract 2) not absorbed from the GI tract and may cause hypotension and diarrhea 3) partially absorbed from the GI and may cause rebound acid production upon cessation of its use 4) stimulates mucus secretion 5) absorbed systemically and contraindicated in people with hypertension 6) contraindicated in patients with renal disease 7) stimulates gastrin release and its overuse may lead to hypercalcemia |
1) binds bile acids and not absorbed from the GI tract = ALUMINUM HYDROXIDE
2) not absorbed from the GI tract and may cause hypotension and diarrhea = MAGNESIUM HYDROXIDE 3) partially absorbed from the GI and may cause rebound acid production upon cessation of its use = CALCIUM CARBONATE 4) stimulates mucus secretion = ALUMINUM HYDROXIDE 5) absorbed systemically and contraindicated in people with hypertension = SODIUM BICARBONATE 6) contraindicated in patients with renal disease = CALCIUM CARBONATE 7) stimulates gastrin release and its overuse may lead to hypercalcemia = CALCIUM CARBONATE |
|
|
These ulcer therapy agents can heal erosive esophagitis within 8 weeks in 75% to 100% of cases.
a) proton pump inhibitors b) antacids c) H2 receptor antagonists |
These ulcer therapy agents can heal erosive esophagitis within 8 weeks in 75% to 100% of cases.
a) proton pump inhibitors |
|
|
Describe the mechanism of action of omeprazole.
What are its side effects? |
Omeprazole is a proton pump inhibitor that directly inhibits the parietal cell proton pump. It reduces both stimulated and basal acid secretion.
Side effects include gastrin producing cell hypertrophy, inhibition of microsomal enzymes and may cuse tumors in animals at high doses. |
|
|
These 2 classes are useful in treating Zollinger-Ellison Syndrome:
a) H2 blockers and antacids b) antacids and cholinergic antagonists c) H2 blockers and proton pump inhibitors d) proton pump inhibitors and sulcralfate |
These 2 classes are useful in treating Zollinger-Ellison Syndrome:
c) H2 blockers and proton pump inhibitors |
|
|
What is the mechanism of action of urogastrone and enterogastrone in their treatment of ulcers?
a) neutralize gastric acid b) form crosslinks in the presence of acidic gastric pH to repair ulcers c) decrease basal and stimulated acid secretion |
What is the mechanism of action of urogastrone and enterogastrone in their treatment of ulcers?
c) decrease basal and stimulated acid secretion |
|
|
Why is sulcralfate useful in treating ulcers?
|
Sulcralfate is a complex polysaccharide complexed with aluminum hydroxide that crosslinks as a result of acidic gastric pH. The polymer has affinity for exposed proteins in peptic ulcers and essentially fills in the ulcers to repair them.
|
|
|
In order for sulfalcrate to be efficacious, it requires:
a) alkaline gastric pH b) acidic gastric pH |
In order for sulfalcrate to be efficacious, it requires:
b) acidic gastric pH |
|
|
Describe the pathophysiology of H.pylori infections.
|
H.pylori is a spiral shaped bacterium that burrows through the gastric mucus layer to adhere to the epithelial lining of the stomach.
It produces urease which provides teh organism alkaline environment, allowing it to survive the harsh acidic environment of the stomach. Its continued survival results in further destruction fo the protective mucus layer and a chronic infection. |
|
|
What illnesses does H.pylori cause?
|
1) chronic active gastritis
2) atrophic gastritis 3) duodenal ulcers 4) gastric ulcers 5) gastric cancer 6) MALT lymphoma |
|
|
What are the clinical tests that can be done to determine if a patient has a H.pylori infection?
|
1) serological tests to measure H.pylori IgG
2) breath test 3) upper EGD endoscopy and biopsy |
|
|
Describe the H.pylori breath test?
|
A patient is given labeled urea to drink. If the patient has a H.pylori infection, the bacteria will metabolize the urea and the labeled carbon is absorbed. The labeled carbon can then be measured as CO2 in the patient's expired breath.
|
|
|
In general, what is the treatment regimen used for H.pylori eradication?
|
Therapy for H.pylori infection consists of 1-2 weeks of one or two antibiotics plus an agent to treat the painful symptoms.
Antibiotics that are used include amoxicillin, tetracycline, metronidazole or clarithromycin. Agents used to treat the pain include proton pump inhibitors, H2 blockers and antacids. |
|
|
What is the general mechanism of action of laxatives?
|
They increase the fluid in the bowel which stimulates peristaltic reflexes. This increases the transit RATE and decreases the transit TIME of contents.
|
|
|
How do psyllium and dietary fiber increase fecal bulk? Are they immediate?
|
Psyllium and dietary fiber are not well absorbed, are hydrophilic and retain water in the bowel. The increased mass results in peristalsis.
Laxation ocurrs after 2-4 days. |
|
|
How does polycarbophil increase fecal bulk?
|
Polycarbophil is not absorbed from the lumen and can retain 60-100x its weight in water. The increased luminal volume stimulates peristalsis.
|
|
|
How do irritant agents increase fecal bulk?
|
They decrease water absorption in the lumen and stimulate intestinal secretions. This stimulates peristalsis.
|
|
|
Identify the correct anti-diarrheal (either class or specific agent) described by the following...
1) agent that has antibacterial properties that reduces intestinal secretions and inhibits prostaglandins 2) class that absorbs toxic compounds from intestinal water 3) class that has little effect on diarrhea but can inhibit peristalsis 4) front-line agent that has little CNS activity and significant effects in the intestine by binding to GI opiod receptors 5) class that inhibits longitudinal contractions but stimulates segmental contractions 6) class that is useful in treating Crohn's and stimulates sodium absorption in intestine 7) class that binds to opiod mu receptors and can cause nausea and sedation |
1) agent that has antibacterial properties that reduces intestinal secretions and inhibits prostaglandins = BISMUTH
2) class that absorbs toxic compounds from intestinal water = ADSORBENTS 3) class that has little effect on diarrhea but can inhibit peristalsis = ANTI-CHOLINERGICS 4) front-line agent that has little CNS activity and significant effects in the intestine by binding to GI opiod receptors = LOPERAMIDE 5) class that inhibits longitudinal contractions but stimulates segmental contractions = OPIOD PREPS (diphenoxylate) 6) class that is useful in treating Crohn's and stimulates sodium absorption in intestine = GLUCOCORTICOIDS 7) class that binds to opiod mu receptors and can cause nausea and sedation = OPIOD PREPS (diphenoxylate) |
|
|
This class of drugs is most effective at preventing severe vomiting due to cancer chemotherapy.
a) corticosteroids b) anti-histamines c) 5-HT3 receptor antagonists d) muscarinic receptor antagonists |
This class of drugs is most effective at preventing severe vomiting due to cancer chemotherapy.
c) 5-HT3 receptor antagonists |
|
|
To what class of drugs do cimetidine and ranitidine belong?
a) muscarinic antagonists b) H2 receptor antagonists c) proton pump inhibitors What are the key differences between cimetidine and ranitidine? |
To what class of drugs do cimetidine and ranitidine belong?
b) H2 receptor antagonists Cimetidine inhibits microsomal enzymes and may prolong the half-life of many drugs. It also acts as an androgen receptor antagonist and can cause gynecomastia and it binds to testosterone receptors and may cause impotence. Ranitidine is 5-10x more potent than cimetidine and does NOT have the anti-androgenic properties of cimetidine nor does it bind to testosterone receptors. In addition, ranitidine does not alter drug metabolism. |
|
|
Which of the following antacids is/are absorbed systemically?
Which of the following is/are not absorbed from the GI tract? a) calcium carbonate b) magnesium hydroxide c) aluminum hydroxide d) sodium bicarbonate |
(1)Which of the following antacids is/are absorbed systemically?
d) sodium bicarbonate __________ (2)Which of the following is/are not absorbed from the GI tract? b) magnesium hydroxide c) aluminum hydroxide |
|
|
What are the 2 main drug interactions associated with antacids?
|
1) they alter the bioavailability of other durgs by altering gastric pH
2) they may chelate other durgs and prevent their absorption (ex: digoxin, tetracycline) |
