parkinsons

Question 1

_ disease

degeneration of dopaminergic neurons projecting from substantia nigra to the striatum

Answer 1

parkinson’s diease

Question 2

parkinson’s
normally, activativation of _Galphai receptors in the striatum affect ACh and GABA release. degeneration of this neurons projecting to the striatum attenuates dopamine release and leads to a loss of proper control of motor fxn

Answer 2

dopamine D2

L-DOPA - what is left of the projections, they provide more DA to the synapse -

L-DOPA crosses BBB

Dopamine does not cross BBB

Question 3

generally L-DOPA treatment good for _ years

sometimes need to diminish does over time because of side effects
patients become lesss responsive(more degenerative)

Answer 3

3-4years

Question 4

when given L-DOPA we give it with carbidopa a peripheral dopa decarboxylase inhibitor

why

Answer 4

get more drug into CNS because Da doesn’t cross BBB

without it 80% of patients experience nasusea and vomiting due to activate of Da receptors in gut

Question 5

some advantages of Da agonists over L-DOPA

Answer 5

not as toxic as L-DOPA

dont require neuron from substantia nigra for delivery

Question 6

parkinson’s also treated by metabolic enzyme inhibitors

_ and _

Answer 6

MAO and COMT inhibitors

Question 7

goal of anticonvulsants - epilepsy

phenytoin and other anti-seizure drugs block _

Answer 7

block high frequency firing APs
they look a lot like LA

sustains Na channel is refractory state

Question 8

some anti-convulsants potentiate the effects of _ to dampen synaptic nerve impulses

Answer 8

GABA

can inhib gaba transaminase - metabolism of GABA

inhib GABA reuptake

Question 9

_ are favored by dentists in ER treatment of seizure or epileptic episode

GABA potentiation

Answer 9

benzodiapines
anti-convulsants

barbs also safe way to treat epilepsy - sedative effects limit utility

Question 10

blockade of T-type calcium channels

drugs that block these in the thalamus are effective as _

Answer 10

anti-convulsants

Question 11

sedative hypnotic drugs, anti-anxiety drugs, central acting muscle relaxing drugs primarily are _ and _

Answer 11

barbiturates(more toxic) and benzodiapines

anxiolysis
sedation - without loss of consciousness
hypnosis - depressed sleepy state - impaired sensory responsive
anesthesia - unconsciousness without possibility of arousal
resp failur

Question 12

what do we give for muscle sparms barbs or benzodiapines

Answer 12

benzodiazepines - potentiate GABA

Question 13

which gaba receptor do barbs and benzos bind to

Answer 13

gaba A receptor - ligand gated ion channel - mediate Cl- conductance

gaba b - g protein coupled

Question 14

barbs and benzo are allosteric regulators of GABA A - CL

_ increase the duration of GABA mediated channel opening - increase duration of Cl-

_ increase the frequency of GABA mediated channel opening

Answer 14

barbiturates increase opening of channel more Cl- - knock out everything

benzodiazepines increase frequency (less toxic) - more anti-anxiety - better therapeutic index,less potential for abuse

both cause membrane hyperpolarization
CNS depression

Question 15

at higher dose barbs or benzos can act as GABA mimetic

Answer 15

barbiturates at high dose can mimetic GABA

Question 16

Valium is a long acting _

Answer 16

benzodiazepine

Question 17

Flumazenil is a barb or benzo antagonist

Answer 17

benzodiazepine

Question 18

structurally unrelated to benzodiazepines but bind to same site on GABA
sedation within 15min - used to tx insomina

Answer 18

ambein(zolpidem)

Question 19

barbs or benzo
although a general downer on the CNS, the reticular formation is especially sensitive - arousal,attention,sleep,awareness

Answer 19

barbiturates

Question 20

_ are first line of tx of Bipolar disorder

more effective in treating manina but does augment other anti-depressants

Answer 20

lithium salts
do they work - don’t really know
decrease adrenaline and increase serotonin

toxic at high dose