S2 Prep - Pharm Flashcards
Succinylcholine Dose + MOA
1.5mg/Kg
Depolarizing NMBA. As acetylcholine, it combines with cholinergic receptors of the motor end plate to produce depolarization.
Subsequent neuromuscular transmission is inhibited so long as adequate concentration of succs remains at the receptor site
Rocuronium Dose
0.6-1.2mg/kg
Rocuronium classification
non-depolarizing neuromuscular blocking agent
Rocuronium MOA
- Roc acts by competing for cholinergic receptors at the motor end plate. This action is antagonized by acetylcholinesterase inhibitor.
- The binding decreases the opportunity for Ach to bind to the nicotinic receptor at the post junctional membrane of the myoneural junction.
- as a result, depolarization is prevented, calcium ions are not released and muscle contraction does not occur
Propofol induction/bolus/maintenance and duration
induction - 1-2mg/kg
bolus - 10-20mg
Maintenance - 20-50mcg/kg/hr
duration: 3-10minutes
Propofol classification and MOA
class: general anesthetic
MOA: Works by increasing the GABA mediated inhibitor tone in the CNS. This results in increased Cl- into the neuronal cell causing them to becoming hyperpolarized, resulting in CNS depression
Midazolam Classification
Benzodiazepine
A short acting sedative-hypnotic drug with anxiolysis, muscle relaxant, anticonvulsant, hypnotic and amnesic properties
Midazolam MOA
Works by intensifying the activity of GABA-A receptors.
This causes Cl- channels to open allowing an influx of chloride into the cell, making the neuronal hyperpolarized.
When midaz binds to the benzodiazepine sites on the GABA-A receptors, which potentiates the effect of GABA by increasing the frequency of Cl- channels opening, enhancing the inhibitor actions of the neurotransmitter GABA
Ketamine class and characteristics
Ketamine is a non-competitive NMDA receptor antagonist of glutamate, cause neuro-inhibition and anesthesia; dissociative anesthetic
Rapid acting general anesthetic producing an anesthetic state.
Characterized by profound analgesia, slightly enhanced skeletal muscle tone, CVS, and respiratory stimulation and occasionally a transient/minimal respiratory depression
Ketamine
Ketamine is a non-competitive NMDA receptor antagonist of glutamate, causes neuro-inhibition and anesthesia
Fentanyl description and MOA
is a synthetic opioid that works on the mu, delta, kappa opioid receptor sites.
MOA: it inhibits ascending pain pathways in the CNS. Altering pain perception by binding to opioid receptors causing analgesia and euphoria.
Fentanyl Pharmacokinetics
Onset: 2 minutes
Duration: 30-60minutes
Fentanyl doses
Induction: 2-4mcg/kg
Maintenance: 50mcg/hr
Bolus: 25-50mcg/hr or .5-1mcg/kg
Drugs that effect metabolic coupling
Propofol and benzos and ketamine = effect metabolism, great!
Opiate = doesn’t effect matched metabolic coupling, unless you want to control pain or breathing
Ketamine doesn’t increase ICP does maintain flow maintained coupling
Morphine description and MOA
Opioid Analgesic, acts primarily on mu receptors but also on kappa receptors which results in analgesia, euphoria and sedation. Also causes vasodilation by release of histamine.
-Interacts with receptors at the spinal cord level, depressing pain impulse transmission
Morphine Pharmacokinetics and doses
Onset: rapidly Duration: 4-5hr Induction: 1-10mg Maintenance: 50-100mg/hr Bolus: 2.5-5mg
Midazolam dosages
Induction: .2mg/kg
Maintenance: 5-10mg/hr
Bolus: 2.5-5mg
Epi doses
ACLS = 1mg
Infusion = 1-10mcg/min
IM = .5mg of 1:1000
IV pre-arrest: 25-100mcg for asthma/anaphylaxis
Epinephrine classification
○ Epinephrine is a hormone and neurotransmitter and produced by the adrenal glands that can also be used as a drug due to its various functions
Sympathomimetic drug, it causes an adrenergic receptive mechanism on effector cells and mimic all actions of the sympathetic nervous system
sympathomimetic.
it works on a1 to vasoconstriction, works on B1 for inotropy/chronotropy/dromotropy.
b2 for bronchodilator effect
and prevents mast cell degranulation therefor inhibits release of histamine
Norepinephrine MOA
- Norepi acts on both alpha-1 and alpha 2 adrenergic receptors to cause vasoconstriction
- Increasing of blood pressure through antagonising alpha-1 and alpha-2 receptors and causing a resultant increasing in SVR
- It is also an inotropic stimulator of the heart and dilator of coronary arteries as a result of it’s activity at the beta-adrenergic receptors
Levophed Dosages and kinetics
Onset: immeditaly
duration: 1-2minutes
Dose: 5-12mcg/min
Vasopressin (ADH)
- G-protein coupled, smooth muscle contraction
- ADH binds to receptors in the distal/collecting tubules of the kidneys and promotes reabsorption of H20 back into the circulation
- Acts on V1 receptors causing vasoconstriction
Vasopressin Dose
0.2-0.4u/min
Dobutatmine dose
2-20mcg/kg/min
Dobutamine MOA
- Inodilator
- Synthetic catecholamine with primarily B1, adrenergic effects with mild B2 stimulation causing vasodilation.
- Dobutamine effectively increases myocardial contractility.
Dopamine doses and onset/duration
Onset: 2-5 minutes
Duration <10minutes
Doses:
2-5mcg/kg/min dopaminergic
5-10mcg/kg/min beta effect
10-20mcg/kg/min alpha effect
Labetalol class/MOA
Class: Selective A1 and nonselective B-blocker
MOA: Competeivley blocks adrenergic stimulation of B-receptors within the myocardium (B1) and within bronchial and vascular smooth muscles (b2) and A1 within vascular smooth muscle
Labetalol Dosages
5,10,20,40,80 mg up to a max of 300mg, then infusion as needed (.5-2mg/min)
Halperidol MOA and classification
- Is a high potency first generation antipsychotic
- It exerts its effect through its antagonism of the dopamine receptors particularly within the mesolimbic system.
Blocks postsynaptic mesolimbic dopaminergic δ1 (Delta 1) and δ2 (Delta 2) receptors in the brain; depresses the release of hypothalamic and hypophyseal hormones; believed to depress the reticular activating system thus affecting basal metabolism, body temperature, wakefulness, vasomotor tone, and emesis sites
Halperidol dosages
2-10mg q 15
Transexamic Acid MOA
- Hemostatic agent/anti-fibrinolytic agent.
- Works by preventing clot deflation by competing for TPA receptor sites
TXA dose
1G/10minutes bolus
1G/8hours maintenance
Ondansetran MOA and onset/duration
Anti-emetic, selective inhibitor of type 3 serotonergic receptors.
Onset= 15 minutes
Duration = 5 hours
