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0.5 L
1L
2L
5L
10L
18 hours
24 hours
30 hours
40 hours
90 hours
Doubling the rate of infusion
Maintaining the rate of infusion but doubling the loading dose
Doubling the rate of infusion and doubling the concentration of the infused drug
Tripling the rate of infusion
Quadrupling the rate of infusion
25 mcg
50 mcg
75 mcg
100 mcg
Decreases its water solubility
Usually leads to inactivation of the drug
Is an example of a Phase I reaction
Occurs at the same rate in adults and newborns
Involve cytochrome P450
Agonist
Partial agonist
Competitive antagonist
Irreverisble antagonist
Inverse agonist
If 10 mg of Drug A produces the same response as 100 mg of Drug B, Drug A is more efficacious than Drug B.
The greater the efficacy, the greater the potency of a drug.
IN selecting a drug, potency is usually more important than efficacy.
A competitive antagonist increases the ED50.
Variation in response to a drug among different individuals is most likely to occur with a drug showing a large therapeutic index.
Efficacy
Potency
Therapeutic index
Graded dose-response curve
Quantal dose-response curve
The number of spare receptors determines the maximum effect.
Spare receptors are sequestered in the cytosol.
A single drug-receptor interaction results in many cellular response elements being activated
Spare receptors are active even in the absensce of agonist.
Agonist affinity for spare receptors is less than their affinity for nonspare receptors.
THe PNS uses norepinephrine as a neurotransmitter
The PNS often discharges as a single, functional system
The PNS division is involved in accomodation of near vision, movement of food and urination.
The postganglionic fibers of the PNS are long compared to those of the sympathetic nervous system
The PNS controls the secretion of the adrenal medulla.
Decrease in intestinal motility
Inhibition of bronchial secretion
Contraction of sphincter muscle in the iris of the eye (miosis)
Contraction of sphincter of urinary bladder
Increase in heart rate
Discrete response to activation
Actions mediated by muscarinic and nicotinic
Effects only mediated by norepi
Responses predominate during physical activity or when experiencing fright
Subjected to voluntary control
Nicotoinic receptors
Alpha receptors
Muscarinic receptors
Beta receptors
Action to terminate acetylcholinesterase
Selectivity for nicotinic receptors
Ability to inhibit secretions, such as tears, saliva and sweat
Ability to lower intraocular pressure
Inability to enter the brain
Do nothing until you confirm the nature of the nerve agent
Administer atropine, and attempt to confirm the nature of the nerve agent
Adminsiter atropine and 2-PAM (pralidoxime)
Administer pralidoxime
Donepezil
Edrophonium
Atropine
Ecthothipohate
Neostigmine
Physiostigmine
Scopolamine
Carbachol
Acetylcholine
Pilocarpine
Ipratropium bromide
Scopolamine patches
Mecamylamine
Oxygen
Nicotine
Physostigmine
Atropine
Pilocarpine
Echothiophate
Tropicamide
Urinary atony
Depressed levels of plasma cholinesterase
A mutation in acetylcholinesterase
A mutation in the nicotinic receptor at the NMJ
Weak histamine releasing action
Physostigmine
Norepi
Trimethaphan
Atropine
Edrophonium
Initial activation of AcH receptor and depolarization of the motor end plate
Effects are reversible by acetylcholinesterase inhibitors
Intermediate to long duration of action
Bind but do not activate AcH receptor
Most of these agents have minimal cardiovascular effects
Albuterol
Dobutamine
Epi
Norepi
Phenylephrine
Albuterol
Atropine
Epinephrine
Norepi
Phenylephrine
Epi
Isoproterenol
Norepi
Epi
Terbutaline