complications and treatment Flashcards
treatments for sphincter of Oddi spasm
Glucagon
Naloxone
Atropine
Nalbuphine
NTG
Glucagon dose for Oddi spasm
2 mg IV
Naloxone dose for Oddi spasm
40 mcg IV
Glucagon MOA
inhibits gastrointestinal and duodenal motility by relaxing smooth muscles, decreasing the frequency and amplitude of phasic activity of the sphincter of Oddi.
Atropine dose for Oddi spasm
0.2 mg IV
Atropine MOA on the heart
no machR activation -> K+ channels are not activated to hyperpolarize the cell since they are blocked = they are excitable = increase HR
Why do diabetics have decreased gastric mobility?
The vagus nerve, which controls how quickly the stomach empties. When it’s damaged by hyperglycemia the digestion slows down.
Atropine MOA on sphincter of oddi
Distention of the stomach causes Sphincter of Oddi contraction, producing a resistance to reflux of duodenal contents through the Sphincter of Oddi= pylori-sphincter reflex.
The reflex is abolished by atropine suggesting mediation by cholinergic nerves.
Nalbuphine dose for oddi spasm
10 mg IV
Nalbuphine MOA
opioid agonist- antagonist
µ receptors agonist: equally potent to Morphine
+ competitive Antagonist
NTG dose for Oddi spasm
50 mcg IV
NTG MOA
vasodilator by
Releasing NO that activates soluble guanylyl cyclase and increases CGMP that stimulates PKG to phophorilate ca channels = decrease constriction and then increase myosin light chain phosphatase activity by phosphorilation to increase the speed of removal of phosphate from the myosin head resulting in relaxation.
Laryngospasm treatment
positive pressure ventilation (close apl to 40cmh20)
- wait for them to breathe
Larsons maneuver (Apply for 3-5 seconds, then release for 5-10 seconds)
succ 10-20 mg IV
Drug most likely to cause sphincter of oddi spasm
fentanyl
MH triggers
Halothane, enflurane, isoflurane, sevoflurane, desflurane, and succinylcholine