Anti-Kinetic Drugs (Quiz 4) Flashcards
what is gastroparesis
- failure of the stomach to empty properly
what does motilin do
- stimulate motility
what does dopamine do for motilityhow
- inhibits motility- inhibitory presynaptic dopamine receptor (D2)
what does acetylcholine do for motility
- stimulates motility
MOA of Metoclopramide
- inhibition of dopamine D2 receptor- increase contraction and motility
Toxicities of Metoclopramideshort or long term use
- acute dystonia - short term- tardive dyskinesia - long term- hyperprolactinemia- anxiety, restlessness, depression
what are acute dystonia and tardive dyskinesia known as
- extrapyramidal symptoms (EPS)
how EPS’s causedimportant brain parts involved
- inhibition of central dopamine pathway that regulates skeletal muscle movement- substantia nigra- dorsal striatum
how does Metoclopramide cause hyperprolactinemia
- inhibits central dopamine pathway that inhibits release of prolactin- therefore excessive prolactin secreted
Erythromycin MOA
- motilin receptor agonists
side effect of Erythromycin
- GI distress
pharmacokinetics issues with Erythromycin
- tachyphylaxis (desensitization) after 10-14 days
what drug do you use if metoclopramide fails
- erythromycin
MOA of Neostigmine
- indirect acting cholinergic agonist- inhibits acetylcholinesterase and increases amount of acetylcholine at synapse
toxicities of Neostigmine
- pro parasympathetic effects- excessive saliva production- decreased CO- bradycardia
what is the antidote to Neostigmine
- atropine
role of prostaglandin E2
- inhibits gastric acid secretion
MOA of Sucralfate
- polymerizes at low pH of stomach- negatively charged so binds positively charged proteins in stomach ulcer- forms a barrier
types of antacids
- NaHCO3- CaCO3- Al(OH)3- Mg(OH)2
MOA of antacids
- directly neutralize stomach acid
toxicity of NaHCO3
- metabolic alkalosis
toxicity of Mg(OH)2 and Al(OH)3how do we solve this
- diarrhea- constipation- combine the two to off-set each other’s toxicities
toxicity of antacidshow
- hypophosphatemia- molecules are insoluble and prevents PO4 absorption
which are the antihistamines
- Ranitidine- Famotidine- Cimetidine
MOA of Antihistamines
- competitive, reversible inhibitors of H2 receptor in parietal cells
can acid-peptic antihistamines significantly cross the blood brain barrier
- no
pharmacodynamics issue with Antihistamines
- other pathways may compensate for blockage and build up tolerance
important toxicity of Cimetidinewhich drugswhat’s the exception to the rule
- drug interactions due to inhibition of CYP enzymes- will reduce their clearance- warfarin- anti-epileptics- theophylline- clopidogrel - doesn’t get activated- oral contraceptives
importance of theophylline
- low therapeutic index
proton pump inhibitor drugs
- omeprazole- esomeprazole- lansoprazole- pantoprazole- rabeprazole
MOA of PPIs
- irreversible non competitive antagonist of H+/K+ pump
toxicities of PPIs
- C. diff infection- hypomagnesia- vitamin B12 malabsorption - AIN
pharmacokinetics issues with PPIs
- pH trapping drives them into secretory canaliculus
MOA of Misoprostol
- prostaglandins E2 analog- inhibits gastric H+ secretion
toxicities of Misoprostsal
- promotes abortion of fetus
what are some neurotransmitters associated with signals that affect vomiting
- dopamine- serotonin- acetylcholine- neurokinin
MOA of Ondansetronwhat’s it used for
- serotonin antagonist- anti-emetic
Toxicities of Odansetron
- prolonged QT interval
MOA of Prochlorperazine and promethazinewhat are they used for
- D2 receptor antagonists- anti-emetic
toxicities of Prochlorperazine and promethazine
- acute dystonia- tardive dyskinesia- prolonged QT
for what conditions do you use sucralfate
- GERD (pregnancy)
for what conditions to you use antacids
- GERD
for what conditions do you use antihistamines
- GERD- peptic ulcer disease
for what conditions do we use PPIs
- GERD- peptic ulcer disease- Zollinger-Ellison syndrome- NSAID associated ulcers- H. pylori eradication
for what conditions do we use misoprostol
- NSAID associated ulcers