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
Signs of onset of MH
Tachycardia, tachypnea, rapidly increasing CO2, skin mottling, arrhythmias, hyperthermia, unstable BP, Dark urine, musle rigidity, and masseter muscle rigidity
treatment for MH
Stop triggering agent
hyperventilate w/ 100% and high flow
administer dantrolene or ryanodex
correct metabolic acidosis
correct hyperkalemia
acitvely cool pt
check labs q 15 min until stable
maintain urine output > 2ml/kg/hr with hydration, mannitol or lasix
Dantrolene dose for MH
dilute each 20 mg of dantrolene vial in 60 ml of sterile water
2.5 mg/kg IV repeats q5-10 min until symptoms controlled
max 10mg/kg
in ICU continue 1 mg/kg every 4-6 hrs or 0.25 mg/kg/hr for 24 hrs
Dantrolene MOA
Blocks ca++ release channels/ the ryr compelx
Physiology of MH
Disordered opening of the Ryanodine calcium release channels on the sarcoplasmic reticulum in skm that are triggered to open by the dihydropyradine receptors in the T tubules = massive calcium in the cell and massive amount of myosin/ actin cross bridge cycling.
Ryanodex dose
2.5 mg/kg
dilute 250 mg vial in 5 ml of sterile water.
