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Pharm Flashcards

1
Q

ADHD stimulants

A

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

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2
Q

Stimulant side effects

A

Decreased appetite, psychosis (dose related risk), abuse/dependence, tremor, nausea, arrhythmia and sudden cardiac death, exacerbation of tics, hypertension, insomnia

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3
Q

ADHD non-stimulants

A

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.

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4
Q

Tic disorder treatments

A

Alpha 2 agonists
If this doesn’t work, try a D2 antagonist (antipsychotic)
But usually non pharmacological approaches

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5
Q

Glaucoma agent categories and MOA

A

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

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6
Q

Cholinergic Agents for glaucoma

MOA

A

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)

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7
Q

Beta-adrenergic blockers

A

-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

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8
Q

Alpha 2 Adrenergic agonists

A

Brimonidine, apraclonidine

Decreased aqueous production and increase uveoscleral outflow

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9
Q

Non-specific alpha agonists

A

Rarely used- epinephrine, pro-drug epi (dipivefrin)

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10
Q

Carbonic anhydrase inhibitors

A

-zolamide
Oral or topical
Aqueous suppression by inhibiting CA enzyme at the nonpigmented epithelium

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11
Q

Prostaglandin analogues

A

-prost
Increased uveoscleral aqueous outflow
Side effects are minimal
Most commonly used first line agent

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12
Q

Balanced anesthesia

A

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)

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13
Q

Premedication anesthesia

A

Allay fear and anxiety, create amnesia, reduce pain, reduce dose of subsequent anesthetics
Common choices: midazolam (benzo), morphine or fentanyl

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14
Q

Benzodiazepines- short acting and long acting

A

Oxazepam
Lorazepam
Midazolam- has an active metabolite (alpha-hydroxymidazolam)

Diazepam (Valium)- active metabolites: oxazepam, N-desmeyhyldiazepam, N-methyloxazepam

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15
Q

Elimination of benzosdiazepines and SEs

A

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

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16
Q

Opioids for anesthesia- examples and adv/disadv

A

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

17
Q

IV anesthetics for induction of anesthesia

A

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

18
Q

Propofol

A

Adv: Rapid induction and emergence, pleasant, minimal hangover
DisAdv: Danger of contamination, hypotension, pain on injection, respiratory depression, expensive

19
Q

Ketamine

A

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

20
Q

Etomidate

A

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

21
Q

Dexmedetomidine

A

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

22
Q

Maintenance anesthetics

A

Inhalational anesthetics (volatile agents)- NO, isoflurane, desflurane, sevoflurane

23
Q

MOA of general anesthetics

A

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

24
Q

Anesthetic uptake depends on:

A

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

25
Q

Variables that control alveolar concentration/anesthetic uptake

A

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

26
Q

MAC

A

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

27
Q

Factors affecting MAC

A

Decreases- extremes of age, hypothermia, hypotension, other CNS depressants (opioids, alcohol)
Increases- youth/vigor, hyperthermia, drug tolerance

28
Q

Main mechanism of elimination for anesthetics

Exception

A

Exhalation

*halothane is metabolized

29
Q

Stages of anesthetics

A

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

30
Q

BIS for anesthesia

A

Bispectral index- 60 and less is a general anesthetic

Provides a EEG-derived number correlating with degree of sedation/anesthesia

31
Q

Anesthetic elimination= emergence factors

A 
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
32
Q

Nitrous Oxide

A

Bone marrow depression and peripheral neuropathies with long-term exposure
Diffusion into and expansion of closed gaseous spaces (bowel, pneumothorax)

33
Q

Halothane

A

Hepatic metabolism

Rarely caused immune-mediated hepatitis

34
Q

Isoflurane

A

Weak coronary vasodilator

35
Q

Desflurane

A

Low solubility- rapid induction and emergence

Rapid increases in concentration can produce tachycardia and hypertension

36
Q

Sevoflurane

A

Least pungent volatile anesthetic- pediatrics

Bronchodilator

37
Q

Anesthetics effect on organ systems

A 
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

BMB (10 decks)

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