Nausea And Vomiting Flashcards
Name 6 risk factors for post op nausea and vomiting
Duration of GA
Female
Younger
Previous motion sickness
Non smoker
Previous PONV
Is it easier to treat N and V before it starts?
Yes
What is the mechanism of action of ondansetron?
blocks serotonin transmission at the 5-HT3 receptors located peripherally on vagal afferents in the gastrointestinal system and centrally in the chemoreceptor trigger zone and the vomiting center.
MOA of metoclopramide?
promotes gut motility by inhibiting presynaptic and postsynaptic D2 (dopamine) receptors as well as presynaptic 5-HT4 receptors. (B). Also inhibitions D2 and 5-HT3 receptors in the CTZ.
Metoclopramide antagonises central and peripheral dopamine-two receptors (D2) in the chemoreceptor trigger zone. It achieves this by decreasing the sensitivity of visceral afferent nerves that transmit from the gastrointestinal system to the vomiting center in the area postrema in the chemoreceptor trigger zone.[13]is its also an antagonist at 5HT3 and 5ht4 (type 3 serotonin receptors) and an agonist at 5HT4 receptors. Metoclopramide also blocks the antiperistaltic effects of apomorphine, allowing metoclopramide to slow apomorphine’s inhibition of gastric emptying, thereby accelerating gastric emptying by increasing the amplitude and duration of esophageal contractions.
MOA of haloperidol
competitively blocks post-synaptic dopamine (D2) receptors in the brain, eliminating dopamine neurotransmission
acts as a potent antiemetic, owing to its peripheral antidopaminergic effects on the chemoreceptor trigger zone (CTZ) in the brain.
MOA of cyclizine
Anti muscarinic and anti histamine
Which antiemetics are seratonin (5ht3) agonists?
Ondansetron / Metoclopramide
Which opioids are dopamine antagonists
Haloperidol
Metoclopramide
Domperidone - not commonly used now
What antagonist is aprepitant?
NK1
What is the MOA of Metoclopramide
5HT3 antagonist
D2 receptor antagonist
moa of hyocine hydrobromide
Anti Muscarinic -m1 antagonist
What is the MOA of dexamethasone
Corticosteroids produce their effect through multiple pathways. In general, they produce anti-inflammatory and immunosuppressive effects, protein and carbohydrate metabolic effects, water and electrolyte effects, central nervous system effects, and blood cell effects.[1][2][7] They have both genomic and nongenomic mechanisms of action. The genomic mechanism of action is mediated through the glucocorticoid receptor, leading to most anti-inflammatory and immunosuppressive effects.[2][5][8]
The glucocorticoid receptor is located intracellularly within the cytoplasm and, upon binding, trans-locates rapidly into the nucleus, where it affects gene transcription and causes inhibition of gene expression and translation for inflammatory leukocytes and structural cells such as epithelium.[1][2][7] This action leads to a reduction in proinflammatory cytokines, chemokines, cell adhesion molecules, and other enzymes involved in the inflammatory response.[2] The non-genomic mechanism occurs more rapidly and is mediated through interactions between the intracellular glucocorticoid receptor or a membrane-bound glucocorticoid receptor.[1] Within seconds to minutes of receptor activation, a cascade of effects is set off, including inhibition of phospholipase A2, which is critical for producing inflammatory cytokines, impairing release of arachidonic acid, and regulation of apoptosis in thymocytes.[1][7] Corticosteroids at high concentrations will also inhibit the production of B cells and T cells.[1][2]
Nearly all the antiemetics are antagonists. What do antagonists do in this case
Block the signals going from the body to the areas of the brain and telling them to vomit.
What are the side effects of anti Muscarinics
Can’t spit
Can’t shit
Can’t see
Can’t pee
Drowsy
Give examples of anti muscarinics
