Pharm Flashcards
ADHD stimulants
Amphetamine salts- increase release of dopamine and norepinephrine from synaptic terminal, shorter acting
Methylphenidate- less potent, less side effects, increase dopamine release from presynaptic terminal, shorter onset, longer acting
Stimulant side effects
Decreased appetite, psychosis (dose related risk), abuse/dependence, tremor, nausea, arrhythmia and sudden cardiac death, exacerbation of tics, hypertension, insomnia
ADHD non-stimulants
Lesser extent of blocking than stimulants
Requires time to have effect- like anti-depressants
Atomoxetine- increases NE only by blocking reuptake
Buproprion- blocks reuptake of DA and NE. Lowers seizure threshold, contraindicated in eating disorder patients, tremor, insomnia, side effects related to formulation (extended release has less SE)
Guanfacine/clonidine- alpha 2 agonist acts at autoreceptors to decrease calcium influx and subsequent decrease in NE/DA globally to act on the hyperactive/hyperkinetic symptoms. Increase NTs in prefrontal cortex with other meds.
Tic disorder treatments
Alpha 2 agonists
If this doesn’t work, try a D2 antagonist (antipsychotic)
But usually non pharmacological approaches
Glaucoma agent categories and MOA
Beta-adrenergic antagonists- decreased production
Cholinergic agonist (miotics)- increased outflow
Adrenergic agonist- alpha 2- decreased production at first and then later increased outflow
Carbonic anhydrase inhibitors- decreased production
Prostaglandins- increased outflow
Hyperosmotics
Cholinergic Agents for glaucoma
MOA
Pilocarpine- directly acting agonist
Indirect acting agonist- echothiophate binds AChE
Increases aqueous outflow through the trabecular meshwork by longitudinal ciliary muscle contraction (pupillary constriction and accommodation)
Beta-adrenergic blockers
-olol
These receptors usually cause pupillary dilation and make more aqueous humor
Reduced aqueous humor production by interrupting binding beta adrenergic receptors
SEs: fatigue, bradycardia, asthma
Alpha 2 Adrenergic agonists
Brimonidine, apraclonidine
Decreased aqueous production and increase uveoscleral outflow
Non-specific alpha agonists
Rarely used- epinephrine, pro-drug epi (dipivefrin)
Carbonic anhydrase inhibitors
-zolamide
Oral or topical
Aqueous suppression by inhibiting CA enzyme at the nonpigmented epithelium
Prostaglandin analogues
-prost
Increased uveoscleral aqueous outflow
Side effects are minimal
Most commonly used first line agent
Balanced anesthesia
A specific drug for each goal, limiting the side effects of each
Unconsciousness- propofol
Amnesia- benzodiazepine
Analgesia- fentanyl
Inhibition of reflexes- glycopyrrolate (anti-cholinergic)
Skeletal muscle relaxation- vecuronium (anti-cholinergic)
Premedication anesthesia
Allay fear and anxiety, create amnesia, reduce pain, reduce dose of subsequent anesthetics
Common choices: midazolam (benzo), morphine or fentanyl
Benzodiazepines- short acting and long acting
Oxazepam
Lorazepam
Midazolam- has an active metabolite (alpha-hydroxymidazolam)
Diazepam (Valium)- active metabolites: oxazepam, N-desmeyhyldiazepam, N-methyloxazepam
Elimination of benzosdiazepines and SEs
Redistribution is most important, conjugated to glucuronides, eliminated by the kidney
Elimination is slowed in elderly and critically ill (sepsis)
Long half life, but their effect doesn’t last the duration of their half life because they are redistributed out of the NS
Dissociative effect- can cause problems in those with baseline dementia and confusion
Opioids for anesthesia- examples and adv/disadv
Morphine- active metabolite 6-glucuronide excreted in urine. During academia, half life of morphine in brain is prolonged by over 50%
Fentanyl- short duration of action after a single dose due to high lipid solubility and redistribution. Elimination half life is longer than that of morphine
Adv: analgesia, sedation, respiratory depression, antitussive
Dis: decreased GI motility, sedation, respiratory depression, chest wall rigidity, no amnesia, tolerance
IV anesthetics for induction of anesthesia
Propofol
Ketamine
Etomidate
Dexmedetomidine
Secondary- methohexital, thiopental
After about half a minute, the blood concentration has already dropped and is high in the brain and viscera, but this drops after 4 minutes, so need a way to keep patients asleep after induction
Propofol
Adv: Rapid induction and emergence, pleasant, minimal hangover
DisAdv: Danger of contamination, hypotension, pain on injection, respiratory depression, expensive
Ketamine
Dissociative state, side effects may be useful (increases HR/BP/bronchodilators, in patients where propofol hypotensive SE’s are a worry)
Sympathomimetic, vagolytic
Slow arousal
Hallucinations
Will still breathe spontaneously but sedated- doesn’t cause respiratory depression
Etomidate
Also doesn’t cause hypotension (worried about inducing coronary ischemia with a drop in BP) so used a lot in cardio OR
Inhibits the enzyme that converts to cortisol- can cause adrenal insufficiency. Rely on cortisol production to respond to the stress state of surgery- can go into an adrenal crisis
Dexmedetomidine
Alpha 2 adrenergic agonist
Approved for sedation of intubated and ventilated patients in an ICU setting- via locus ceoruleus
Administered by continuous infusion for up to 24 hours
Sedative, anxiolytic, and analgesic
Not a controlled substance
No respiratory depression
Hypotension,bradycardia, nausea
Maintenance anesthetics
Inhalational anesthetics (volatile agents)- NO, isoflurane, desflurane, sevoflurane
MOA of general anesthetics
Unknown
Interfere with synaptic transmission- cerebral cortex, reticular activating system, and thalamus (consciousness centers)
Actions on gated ion channels- inhibition of excitatory transmission and potentiation of inhibitory transmission
Anesthetic uptake depends on:
Alveolar concentration- the speed at which you obtain general anesthesia depends on the equilibrium between the alveolar concentration and the inspired concentration (Fa/Fi). The faster this equilibrium happens, the faster achieved anesthesia
Variables that control alveolar concentration/anesthetic uptake
Inspired concentration- high=faster (overpressure)
Alveolar ventilation- increased=faster (resp rate/tidal volume increase)
Solubility (blood:gas partition coeff)- lower=faster (highly soluble gases means slower induction, because they redistribute to other organs besides CNS so the concentration in alveoli is not as high)
Cardiac output- lower= faster (allows build up in alveoli) a high CO will have high circulation, taking gas from alveoli at a quicker rate and decreases its conc.
Alveolar-venous difference- smaller= faster. If a high conc difference of gas, then the alveolar conc will fall. If the difference between the two are low, then slow movement and alveolar conc will remain high
Minute ventilation (8 vs 2) increases the speed of induction significantly only for very lipid soluble agents
MAC
Minimum alveolar concentration- alveolar partial pressure of an inhaled anesthetic that prevents movement of half the subjects in response to a noxious stimulus
Lower the MAC, the more potent the drug
MACs of individual drugs are additive*
Amnesia occurs at 0.2-0.4MAC
Factors affecting MAC
Decreases- extremes of age, hypothermia, hypotension, other CNS depressants (opioids, alcohol)
Increases- youth/vigor, hyperthermia, drug tolerance
Main mechanism of elimination for anesthetics
Exception
Exhalation
*halothane is metabolized
Stages of anesthetics
Stage 2- excitatory phase: increase in sympathetic tone, lid reflexes present, swallowing, increase muscle tone
Stage 3 (has 4 planes)- general anesthesia: decrease in sympathetic tone, controlled breathing, still have corneal/light reflexes
Stage 4- deep anesthesia, complete medullary depression of reflexes, silence on EEG, respiratory depression, etc. too dangerous
BIS for anesthesia
Bispectral index- 60 and less is a general anesthetic
Provides a EEG-derived number correlating with degree of sedation/anesthesia
Anesthetic elimination= emergence factors
Same as uptake apply Recovery from GA depends on rate of elimination of agent from brain: Solubility- lower=faster cardiac output- greater= faster alveolar ventilation- greater=faster
Nitrous Oxide
Bone marrow depression and peripheral neuropathies with long-term exposure
Diffusion into and expansion of closed gaseous spaces (bowel, pneumothorax)
Halothane
Hepatic metabolism
Rarely caused immune-mediated hepatitis
Isoflurane
Weak coronary vasodilator
Desflurane
Low solubility- rapid induction and emergence
Rapid increases in concentration can produce tachycardia and hypertension
Sevoflurane
Least pungent volatile anesthetic- pediatrics
Bronchodilator
Anesthetics effect on organ systems
BP- decrease HR- none or increase (ISO, des) SVR- decrease Tidal volume- decrease Respiratory rate- increase PaCO2 (Aeneid threshold)- increases Cerebral metabolic rate- decreases Portal, renal blood flow- decreases
