More Block 2 Flashcards
BZD MOA?
Activates GABAa receptors
Increases Cl influx
No analgesic affect
Diazepam
Lorazepam
Midazolam
Which one has the shortest and longest t1/2?
Midazolam = shortest (2hrs)
Diazepam = longest (up to 55hrs)
BZD AE (especially w/ opioids)?
Respiratory depression
Propofol MOA?
Activates GABAa receptors
Increases Cl influx
No analgesic affect, but induces anesthesia + an antiemetic
Propofol formulation info?
Not an antimicrobial preserved product (must have strict aseptic technique when handling)
Reported to have injection site pain and hyperlipidemia
Stored at 4-25C, no freezing
Water INsoluble
Propofol PK info?
Zero oral bioavailability
Elimination is unchanged if you have liver/kidney damage
Propofol AE?
Respiratory depression (needs monitoring!)
Hypotension (dose-dependent vasodilation)
Bradycardia, reduction in heart contractility
Propofol Infusion Syndrome (PRIS) – rare but potentially fatal
Fospropofol metabolism?
Metabolized by alkaline phosphatase
Fospropofol formulation and AE?
Minimal injection site pain and hyperlipidemia
Water Soluble
Less frequent of respiratory depression or hypotension
Ketamine MOA?
NMDA antagonist
Ketamine use?
For analgesia (supposedly no respiratory depression)
Hallucinations + Date rape drug
Ketamine PK?
Typically given as IV, IM is too painful
Ketamine AE?
Emergence reactions
Transient increase in BP, HR, CO
Precedex MOA?
Alpha 2 agonist
Locus coeruleus – activates sleep pathways
Spinal cord – analgesia
Precedex AE?
Hypotension/hypertension
Bradycardia
Does NOT cause respiratory depression
How is skeletal muscle initiated?
Action potential causes depolarization of calcium channel
Calcium channel opens and influx of calcium releases ACh
ACh binds to ACh nicotinic receptor
Sodium enters the muscle cell and ACh is degraded by AChE
General paralytic MOA?
Blocks ACh from binding to ACh nicotinic receptor
What is the only depolarizing paralytic?
Succinylcholine
Everything else is competitive/non-depolarizing (roc, vec, nimbex)
Competitive/non-depolarizing paralytic MOA?
Blocks ACh from binding to receptor however the effect can be overcome by excessive ACh like AChE inhibitors unless there is a high dose of this paralytic, then excessive ACh cant overcome it
How does paralysis occur based on susceptibility?
First: face, eye
Then: fingers, limbs, neck, trunk
Last: Intercostal muscle, diaphragm
PK info on competitive/non-depolarizing paralytics?
Zero oral bioavailability + cant cross BBB
Roc
Vec
Pancuronium
Nimbex
Metabolism info?
Roc + Vec = deacetylated in liver, no excreted into bile unchanged
Pancuronium = excreted unchanged in urine
Nimbex = degraded by plasma and ester hydrolysis
Succinylcholine MOA?
Drug causes membrane depolarization but AChE cant hydrolyze it and causes fasciculations
After a prolonged time,
Phase I - Depolarizing = flaccid paralysis (can be augmented by AChE inhibitors
Phase II - slowly converts to this phase of non-depolarization
Succinylcholine AE?
Soreness, hyperthermia, hyperkalemia, apnea
What does the BPS pain scale look at? CPOT
Facial expression
Upper limbs
Ventilation compliance
Scores from 3-12, intervene when score is ≥6
CPOT adds vocalization, muscle tension instead of upper limbs, body movement
CPOT ≥2 is significant