Pharm of Alch

Question 1

how does alcohol work as an NT?

Answer 1

GABA A agonist–>increases effect

NMDA/glutamate antagonist–>inhibits release of glutamate

Question 2

HABA major action

Answer 2

inhibitory

–relaxation, loss of coordination, motor slowing

Question 3

net effects of glutamate antagonism

Answer 3

sedation
impaired memory
impaired cognition

Question 4

how do opioids work?

Answer 4

indirect stimulation of b endorphins

–>pleasurable, euphoric effects via mu receptors

Question 5

two ways that alcohol inhibits glutamate system

Answer 5

Presyn action on meGluR and presyn voltage-sens Ca channels–>inhibit glutamate release

inhibit post-synp ionotrpic glutamate receptors (NMDA)

Question 6

chronic exposure to alcohol

Answer 6

compensatory increase in NMDA activity and R density leads to tolerance

Question 7

rate limiting step of alcohol metabolism

Answer 7

oxidation of each ethanol molecule requires 2 NAD+

–limited supply of NAD+ in the liver

Question 8

where does alcohol go?

Answer 8

2-10% excreted in urine

~90% removed by oxidation

Question 9

what causes a hang over?

Answer 9

acetaldehyde

Question 10

cystolic increase in NADH/NAD+ drives 4 biochemical pathways:

Answer 10

• inc. production of lactic acid–>hyperuricemia & gout
• inc ketone bodies–>ketosis
• inc triglyceride synthesis–>fatty liver
• inc gluconeogenesis and liver glycogen–>hypoglycemia

Question 11

microsomal liver enzyme

Answer 11

as the concentration of ethanol increases above 100 mg/dl, there is an increased contribution of MEOS, therefore increased NADPH (via cytochrome p450)

Question 12

acetyladehyde metabolism

Answer 12

acetyladehyde–aldehyde dehydrogenase–> acetate–>CO2 and H20–>acetyl-CoA

Question 13

Disulfiram/Antabuse

Answer 13

inhibitor of ALDH–> acetaldehyde accumulates

-causes extreme discomfort in patients who drink alcoholic beverages

Question 14

metabolism in GI tract

Answer 14

ADH in stomach and small intestine

Question 15

proof

Answer 15

% alcohol by volume x 2

Question 16

BAC

Answer 16

weight of alcohol per volume of blood, measured in mg of alcohol per 100cc of blood

Question 17

worsening, decrease in temp, decrease in bp, excessive sleepiness, amnesia

Answer 17

0.30-0.40 300-400%

Question 18

mood, behavioral changes
reduced coordination
impaired driving, machinery operation

Answer 18

20-100mg% (0.02-0.1)

Question 19

unresponsiveness
serious decrease in pulse, temp, bp, resp
urinary and bowel incontinence

Answer 19

400-800%

0.40-0.80

Question 20

markedly impaired thinking, memory, coordination
marked reduction in level of alertness
memory black outs
nausea and vomiting

Answer 20

200-300 mg%

0.20-0.30

Question 21

nervous system adverse alcohol effect

Answer 21

generalized symmetric peripheral nerve injury

Question 22

Wernicke-Korasakoff encephalopathy is because of

Answer 22

a thiamine deficiency

Question 23

Werncke’s enceph

Answer 23

Opthalmoplegia
nystagmus
ataxia
confusion

Question 24

Korsakoff’s psychosis

Answer 24

anterograde and retrograde amnesia
confabulation
lack of insight
apathy

Question 25

liver disease track

Answer 25

alcoholic fatty liver-->alcoholic hepatitis-->cirrhosis-->liver failure

Question 26

how does tolerance develop

Answer 26

- induction of hepatic enzymes with increased metabolism | - neuroadaptation-->induction dec GABA inc glutamate, inc dopamine

Question 27

alcohol withdrawal is problematic because

Answer 27

increased glut decreased GABA decreased DA

Question 28

primary goals of treatment of alcohol withdrawl syndrome

Answer 28

prevent serizures delirium werickes

Question 29

days of withdrawal for seizures

Answer 29

1-2

Question 30

days of withdarwal for remors

Answer 30

peak at 3-4

Question 31

purpose of thiamine

Answer 31

helps correct nerve problems due to ack of thiamine in WKS

Question 32

how is thiamine absorbed and metablolized

Answer 32

abosrbed- GI | metab- liver

Question 33

lorazapam class-

Answer 33

benzo | GABA modulator

Question 34

lorazapa/librium mechanism

Answer 34

binds to central benzo receptors-->interact allosterically to potetiate effect of inhibitory GABA

Question 35

librium/chloradiazepoxide issues

Answer 35

build up of active metabolites makes it less appropriate for eldely, hepatic metabolism bad for liver disease, cog effects persist for days-weeks

Question 36

chloradiazepoxide benefit

Answer 36

logner acting

Question 37

Gabapentin class

Answer 37

GABA analogue, anticonvulsant

Question 38

gabapentin action

Answer 38

interacts with voltage gated Ca channels

Question 39

Gabapentin benifits vs. disadvantages

Answer 39

benefits- non addictive | disadvantages- not FDA approved for this- not or high risk pts

Question 40

Naltrexone class

Answer 40

opiod antgonist

Question 41

most common adverse effect of naltrexone

Answer 41

nausea

Question 42

disadvantage of naltrexone

Answer 42

cant use with patients on opiates | non-compliance

Question 43

topiramate class

Answer 43

anti epileptic

Question 44

topiramate mechanism

Answer 44

blocking of voltage-gated Na+ channels, augmentation of GABA at GABAR antag of AMPA

Question 45

topiramax avantages

Answer 45

more robust than naltrexone

Question 46

topiramax disadvantages

Answer 46

not fda approved

Question 47

acamprosate class

Answer 47

analogue of GABA

Question 48

acamprosate action

Answer 48

NMDA antaonist + GABA R activator | may restore neuronal excitation and inhibit balance

Question 49

acamprosate adverse effects

Answer 49

caution in depressed patients or renal impairment patients

Question 50

gabapentin alcohol mech

Answer 50

not active at gabaR | modulates synthesis of GABA and glutamate release resulting in net + GABA effect