Flashcards in Ch. 13: Intro to CNS (Vickroy) Deck (49):
produces a calming effect at low doses and sedation at higher doses. Patient is relaxed, reluctant to move, awake, and unconcerned with surroundings (.e. ace, diazepam)
depresses most behaviors and diminishes excitability WITHOUT producing sleep. Patient can be aroused with sufficient stimuli (i.e. phenobarb, xylazine)
produces strong behavioral depression and promotes state of light sleep from which the animal can be aroused
produces a deeper state of sleep from which an animal CANNOT be easily aroused (i.e. morphine)
produces deep sleep with a loss of sensation. (ex. halothane, ketamine, propofol)
For nearly all classes of CNS depressants, the level of CNS depression is dose-dependent and synergistic with other CNS depressants**
Can you achieve anesthesia with benzodiazepines?
No (very difficult)
4 main excitatory CNS transmitters
Ach, DA, NE/EP
3 main inhibitory CNS transmitters
Adenosine (Ado), GABA, serotonin (5-HT)
Rank CNS stimulants in increasing order of CNS activity
analeptics < pscychomotor stimulants < convulsants
Rank CNS depressants in increasing order of CNS activity
anesthetics < narcotics < hypnotics < sedatives < tranquilizers
T/F: Benzos do not produce analgesia*
2 distinct pathways to depress CNS function**
1) antagonism of excitatory NT glutamate (via blockage of NMDA receptors)
2) agonism of inhibitory NT GABA (by enhancing GABA receptors)
What drug uses antagonism of excitatory NT glutamate via blockage of NMDA receptors as its pathway to depress CNS function?
Is ketamine a barbiturate-type agent?
Administered by some means other than oral or rectal intake, particularly intravenously or by injection.
How does diazepam work?*
enhances actions of the inhibitory NT GABA on GABA receptors, which opens Cl channels, makes cell less excitable, and thereby depresses CNS function
Why is ketamine commonly coupled with diazepam?
synergistic effect for more adequate CNS depression. Allows you to use drugs at lower doses to reach desired effect and avoid negative side effects
Elements of BBB that stop drugs from passing
-very tight junctions in cerebral blood vessels
-pinocytotic vessels to capture drugs that do manage to diffuse across endothelial cells
-astrocytic foot processes surround capillaries
Does phenylephrine normally cross BBB?
T/F: drugs w/n the same therapeutic group can exhibit marked differences in their abilities to cross the BBB
T/F: disease patterns or genetic dysfuction can affect BBB permeability
T (i.e. hypertonic solutions, ivermectins in collies, encephalitis)
ivermectins in collies
can cross BBB because they lack normal MDR-1 gene that codes for P-glycoprotein, which carries drugs back across BBB that leaked through
glutamate is pro-stimulatory or pro-inhibitory?
pro-stimulatory. Blocked by ketamine.
serotonergic agents primarily used for:
tx of behavioral disorders
6 CNS monoamines
-DA (only one that acts almost entirely within CNS)
4 rep. examples of amino acids & derivates
6 rep. ex. of neuropeptides
Do monoamines cross BBB?
What does DA control?
motor function, sleep/wake cycle. It is a catecholamine like NE,EP
Primary elim. of Ach
Primary elim. of DA, EP, NE
Catecholamine (CA) uptake, monoamine oxidases (MAO)
primary elim. of serotonin
serotonin (5-HT) transporters, MAO
biosynthetic precursor of DA, NE, EP
biosynthetic precursor of serotonin
How do synthesis, release, and elim. mechs. of monoamines in the CNS compare to in the periphery?
CNS catecholamines are excitatory/inhibitory for most brain functions
are dopamine receptors abundant or scarce?
drugs that inhibit CNS CA fx tend to stimulate/depress CNS fx
DA antagonist. Produces CNS depression (sedative/tranquilizer)
alpha-2 agonist. Sedative/analgesic
how do alpha-2 agonists depress CNS?*
alpha-2 receptors on presynaptic neurons sense when there is too much NE (which is stimulatory) and shut down NE release. Alpha-2 agonists encourage this process so that NE is released even less, resulting in net CNS depression
Name 6 alpha-2 agonists
regulations of mood, appetite, sleep/wake cycles, sensory perception.etc
T/F: there are a lot of different 5-HT receptors
why don't use serotonergic agents with MAO inhibitors?
may produce serotonin syndrome that can lead to coma and death
major inhibitory aa transmitter in the CNS*
What kind of drugs mimic or enhance GABA function?
barbiturates, benzos, propofol