Pharmacology Flashcards
Butorphenol
What kind of receptor ant/agonist is it and where is it useful?
Mixed mu-opioid receptor agonist-antagonist, kappa-opioid receptor partial-agonist.
Mu effects make is a good for treating pain and neuraxial opioid-induced central pruritis
Kappa effects make it good for treating post-op shivering
Popular in OB, gives pain relief but helps with spinal pruritus, also seems to work better in females than males
Opioid receptors
What are they and what are they responsible for?
Mu: miosis, dependence, resp depression, sedation, nausea, and euphoria
Delta: respiratory depression, inhibits dopamine release, and modulates mu-receptor
Kappa: miosis, diuresis, dysphoria
ALL RECEPTOR PROVIDE ANALGESIA
Mixed opioid receptor agnonist-antagonists
What are their names and what receptors do they act on?
Butorphenol: Mixed mu-opioid receptor agonist-antagonist, kappa-opioid receptor partial-agonist
Buprenorphine: mu-opioid receptor partial agonist and kappa-receptor antagonist
Nalbuphine: primarily kappa-opioid receptor agonist and partial mu-receptor antagonist
Methadone: mu-opioid receptor agonist and NMDA receptor antagonist
Patients that need ppx abs
and
what procedures need ppx??
Prosthetic cardiac valve
Hx of IE
UNrepaired cyanotic CHD
CHD who have been repaired with prosthesis 6 mo or less prior to aggressive dental procedure
Heart transplant with valvulopathy
________________________________
Aggressive dental procedures
invasive resp tract procedures (incision or bx)
infected skin, skin structure, or MSK tissue
2G ampicillin 30-60 min before procedure
What kinds of drugs (relevant to us) are metabolized by plasma esterases?
Sux mivacurium ester LA ASA bambuterol heroin
Ester local anesthetics
chloroprocaine
procaine
cocaine
tetracaine
Morphine: CV and respiratory effects
reduces preload and afterload
can produce rigid chest
How do beta-agonists produce bronchodilation?
via increased cAMP
G-protein signaling pathway –> increases adenylyl–> increased levels of cAMP(from ATP) –> activates protein kinase A –> smooth muscle relaxation
for bronchodilation, stimulating beta-2-receptors; found in smooth muscles of blood vessels, muscles, mesentery, and bronchi
Cytochrome P450
cimetidine
carbamazepine
How are barbs metabolized/eliminated?
Hepatic metabolism, biliary conjugation,
Local anesthetics
What determines speed of onset?
What determines duration?
What determines potency?
Speed of onset: pKa (needs to be non-ionized to pass lipid bilayer)
(Long) duration of action: (high) tissue- protein binding esters don’t last long d/t metabolism mech
Potency: Lipid solubility
What LA has longest duration of action?
Bupivicaine
High protein binding.
Also makes it most dangerous for LAST because really binds!
PABA is a derivative of…
Ester LAs
Ester LA metabolism
Esterases
Makes them not last very long…(decreased duration)
Drugs that can cause histamine release
Thiopental
In which situations would you NOT want to use methylene blue?
Pt with G6PD (use ascorbic acid)
Pt taking serotonergic medications (meth blue is a potent MAOI, may interact with other meds leading to serotonin syndrome)
Ascorbic acid does not have the hemolytic effect that methylene blue has in a G6PD deficient patient.
Medications that can cause methemoglobinemia
Prilocaine Benzocaine Nitroglycerin Sodium nitroprusside Phenytoin Sulfonamides Metoclopramide
Benzodiazepines and muscle relaxation
Act centrally to cause HYPERpolarization —> muscle relaxation
Also used perioperatively for sedative, anxiolytic, and amnestic properties
GABA inhibitory neurotransmitter. (Selective for CNS)
Controls state of Cl ion channels
Activation —> neuronal hyperpolarization—> drives membrane potential AWAY from threshold potential
IE: DECREASES ability for membrane potential to occur
Some degree of muscle relaxation likely d/t potentiation of GABA effects on inter neurons of spinal cord (use for muscle spasms or spasticity d/o)
Aspirin overdose
Initial symptoms: non specific, tinnitus, N/V eventually AMS and death may occur if not treated.
Hyperpnea often occurs early as a result of salicylates causing stimulation of the medullary respiratory center. Hyperventilation—> respiratory alkalosis
Eventually aspirin overdose —> metabolic acidosis + respiratory alkalosis
HD may be indicated in acute overdose
PRIS
Rare complication of
*high-dose (> 4-5 mg/kg/hr or > 65-80 mcg/kg/min)
*long-term (> 24 hours)
Propofol infusion
More common in Peds pop
Additional risk factors: concurrent catecholamine or corticosteroid admin, concurrent acute neurologic or inflammatory dz, severe infection or sepsis
Lipid metabolism d/o may also increase risk (esp in Peds)
Treatment: stop propofol; supportive
Pathophys: propofol impairs cellular free fatty acid utilization and mitochondrial activity —> inadequate aerobic metabolism and increased reliance on anaerobic metabolism
Cardiac and skeletal muscle are particularly susceptible —> muscle damage or necrosis —> cardiac failure & rhabdo
Additional downstream effects: LA, hyperK, renal failure
Hypertrigly, hepatomegaly, & hyperlipidemic pancreatitis occur d/t impaired fatty acid utilization
Why does pee turn green with propofol infusion?
Phenol excretion during PRIS
