complications and treatment Flashcards

1
Q

treatments for sphincter of Oddi spasm

A

Glucagon
Naloxone
Atropine
Nalbuphine
NTG

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2
Q

Glucagon dose for Oddi spasm

A

2 mg IV

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3
Q

Naloxone dose for Oddi spasm

A

40 mcg IV

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4
Q

Glucagon MOA

A

inhibits gastrointestinal and duodenal motility by relaxing smooth muscles, decreasing the frequency and amplitude of phasic activity of the sphincter of Oddi.

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5
Q

Atropine dose for Oddi spasm

A

0.2 mg IV

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6
Q

Atropine MOA on the heart

A

no machR activation -> K+ channels are not activated to hyperpolarize the cell since they are blocked = they are excitable = increase HR

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7
Q

Why do diabetics have decreased gastric mobility?

A

The vagus nerve, which controls how quickly the stomach empties. When it’s damaged by hyperglycemia the digestion slows down.

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8
Q

Atropine MOA on sphincter of oddi

A

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.

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9
Q

Nalbuphine dose for oddi spasm

A

10 mg IV

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10
Q

Nalbuphine MOA

A

opioid agonist- antagonist

µ receptors agonist: equally potent to Morphine
+ competitive Antagonist

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11
Q

NTG dose for Oddi spasm

A

50 mcg IV

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12
Q

NTG MOA

A

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.

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13
Q

Laryngospasm treatment

A

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

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14
Q

Drug most likely to cause sphincter of oddi spasm

A

fentanyl

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15
Q

MH triggers

A

Halothane, enflurane, isoflurane, sevoflurane, desflurane, and succinylcholine

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16
Q

Signs of onset of MH

A

Tachycardia, tachypnea, rapidly increasing CO2, skin mottling, arrhythmias, hyperthermia, unstable BP, Dark urine, musle rigidity, and masseter muscle rigidity

17
Q

treatment for MH

A

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

18
Q

Dantrolene dose for MH

A

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

19
Q

Dantrolene MOA

A

Blocks ca++ release channels/ the ryr compelx

20
Q

Physiology of MH

A

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.

21
Q

Ryanodex dose

A

2.5 mg/kg
dilute 250 mg vial in 5 ml of sterile water.