Kaplan-4 (Histamine&Antihistamines) Flashcards
What are the non-sedating H-1 antagoinists?
Loratadine and Fexofenadine
What can we use for Zollinger-Ellison syndrome?
H2-antagonists
Cimetidine
Ranitidine
Famotidine
Other uses include GERD and PUD (peptic ulcer)
What is a protective mucosal drug that acts by polymerizing on grastrointestinal luminal surface to from a protective gel-like coating of ulcer beds?
Sucralfate, promotes healing and decreases ulcer recurrence.
What is the MOA of Misoprostol?
It is a PG analog and it increases mucous secretion and protects stomach from acid and secretes bicarb.
What are the D2 receptor inhibitors that act as antiemetics?
Prochlorperazine and Metoclopramide
What is the MOA of Dronabinol?
It is a THC agonist and used for nausea induced chemotherapy. It disconnects the chemoreceptor trigger zone (CTZ) from vomiting center.
What drugs inhibits 5-HT3 receptor in chemoreceptor trigger zone (CTZ) in the area postrema?
Ondansetron
What do we use for the treatment for the onset of the active headache?
Sumatriptan, agonist at 5HT-1D receptors in cerebral vessels used for migraine, contracting vessels. Decreases migraine pain.
What do we use prophalaxis for migraine?
Propranolo, verapamil, amitriptyline, valproic acid / topiramate
What is the MOA of Zileuton?
How about the Lukast drug such as Zafirlukast?
It inhibits lipoxygenase , decreasing leukotrienes metabolism.
Lukast drugs blocks leukotrienes receptors.
How does aspirin help post-MI?
Aspirin. Thromboxane A2 (TxA2) is a platelet aggregator (inhibition of synthesis underlies protective role of ASA).
Low doseIt is also an anti-platelet, used for TIA prophylaxis.
What drug do we use along with oxytocin to induce labor?
Dinoprostone, it dilates the cervix (cervical ripening) while oxytocin contracts the uterus.
What’s the only NSAIDs that irreversibly COX1/COX-2?
Aspirin
What drug is an antiemetic and prokinetic in GERD?
Which other drug uses the same MOA and its not a prokinetic of GERD?
Metoclopramide
Prochlorperazine (It’s only a D2 blocker, not a prokinetic of GERD)
What are the acid-base balances of ASA at toxic doses?
Toxic doses can produces inhibition of respiratory centers —-decreased respiration—-increased pCO2——respiratory acidosis.
Plus inhibition of Krebs cycle and severe uncoupling of oxidative phosphorylation (decreased ATP)—metabolic acidosis, hyperthermia, and hypokalemia (decreased K).
