Pharm II Final Exam
Neurotransmitters related to Anxiety & Depression ANS: serotonin, norepinephrine, dopamine, GABA
In Anxiety & Depression which of the following neurotransmitters is increased? ANS: GABA
MOA of Levodopa ANS: increases synthesis of dopamine in striatum
_______ is the precursor of dopamine ANS: Levodopa
Can Levodopa cross the BBB ANS: Yes
Onset and effectiveness of Levodopa ANS: delayed onset and limited effectiveness
Levodopa binds to Dopamine receptors on _______ neurons ANS: GABA
Levodopa is metabolized in the _______ from _____________ enzymes & COMT ANS: periphery;
decarboxylase enzymes
What drug is used to enhance the effects of Levodopa ANS: Carbidopa
MOA of Carbidopa ANS: inhibits decarboxylation of levodopa in the periphery (intestine and peripheral
tissues)
Does carbidopa have any pharmacologic/adverse effects of its own ANS: no
Is carbidopa able to cross the BBB ANS: no
,Advantages of combining carbidopa with levodopa ANS: - allows the dosage of levodopa to be reduces
by 75%
- reduces CV response and nausea and vomiting by reducing the conversion of levodopa to dopamine in
the periphery
- the interaction of Vitamin B6 (pyridoxine) with levodopa is removed since decarboxylase is inhibited
The combination pill with carbidopa and levodopa can also contain ANS: Entacapone (COMT inhibitor)
Interactions with Dopamine replacement ANS: - first gen antipsychotic drugs
- nonselective MAO inhibitors
- high protein meals
- pyridoxine (vitamin B6) if levodopa given alone
- anticholinergics enhances levodopas therapeutic response
What interaction occurs only when Levodopa is given alone ANS: pyridoxine (vitamin B6)
What interaction enhances Levodopa's therapeutic response ANS: anticholinergics
Prototype for COMT inhibitors ANS: entacapone
MOA of entacapone ANS: - prevents destruction of levodopa in intestine & peripheral tissues (prolongs
plasma half-life)
- decreases production of levodopa metabolites
Entacapone can significantly reduce the "________ _____" time experienced during Levodopa Therapy
ANS: "wearing off"
,ADRs of Entacapone (COMT inhibitors) ANS: - dyskinesias
- postural hypotension
- hallucinations
- sleep disturbances
- impulse control disorders
Should you stop COMT inhibitors (entacapone) abruptly? ANS: No, may cause worsening of symptoms
MOA of phenytoin ANS: selective inhibition of sodium channels (slows recovery of Na channels from the
inactive state)
Phenytoin has a ______ margin of safety ANS: narrow
Why is phenytoin teratogenic ANS: it decreases the synthesis of vitamin K-dependent clotting factors in
neonates causing bleeding tendencies
IV route for phenytoin is administered slowly to avoid causing significant ANS: dysrhythmias and
hypotension
What drug is administered once the seizure(s) is/are controlled ANS: phenytoin or fosphenytoin is
administered for long-term suppression
ADRs of Phenytoin ANS: - stevens-johnsons syndrome/toxic epidermal necrolysis
- gingival hypertrophy
- interferes with metabolism of vitamin D
- hirsutism (excessive hair growth)
, Therapeutic level of phenytoin ANS: 10-20mcg/mL
MOA of carbamazepine ANS: selective inhibition of sodium channels
Therapeutic serum levels for carbamazepine ANS: 4-12 mcg/mL
Half life of carbamazepine _______ (increases/decreases) with continued use ANS: decreases
MOA of valproate (2 mechanisms) ANS: 1. Suppresses neuronal firing by blocking sodium channels
2. Potentiates the inhibitory influence of GABA
Drug interaction of vaproate with topiramate ANS: hyperammonemia
Ethosuximide is used for what type of seizures ANS: absence seizures
ADRs of Lamotrigine ANS: - life threatening rashes (SJS and TEN)
- aseptic meningitis (stiff neck, headache)
Approved therapeutic uses for Gabapentin (besides seizures) ANS: postherpetic neuralgia
Off label therapeutic uses for Gabapentin ANS: neuropathic pain, migraine prophylaxis, fibrimyalgia, and
postmenopausal hot flashes
MOA of topiramate (4 mechanisms) ANS: 1. potentiation of GABA-mediated inhibition
2. blockade of voltage-dependent sodium channels
Neurotransmitters related to Anxiety & Depression ANS: serotonin, norepinephrine, dopamine, GABA
In Anxiety & Depression which of the following neurotransmitters is increased? ANS: GABA
MOA of Levodopa ANS: increases synthesis of dopamine in striatum
_______ is the precursor of dopamine ANS: Levodopa
Can Levodopa cross the BBB ANS: Yes
Onset and effectiveness of Levodopa ANS: delayed onset and limited effectiveness
Levodopa binds to Dopamine receptors on _______ neurons ANS: GABA
Levodopa is metabolized in the _______ from _____________ enzymes & COMT ANS: periphery;
decarboxylase enzymes
What drug is used to enhance the effects of Levodopa ANS: Carbidopa
MOA of Carbidopa ANS: inhibits decarboxylation of levodopa in the periphery (intestine and peripheral
tissues)
Does carbidopa have any pharmacologic/adverse effects of its own ANS: no
Is carbidopa able to cross the BBB ANS: no
,Advantages of combining carbidopa with levodopa ANS: - allows the dosage of levodopa to be reduces
by 75%
- reduces CV response and nausea and vomiting by reducing the conversion of levodopa to dopamine in
the periphery
- the interaction of Vitamin B6 (pyridoxine) with levodopa is removed since decarboxylase is inhibited
The combination pill with carbidopa and levodopa can also contain ANS: Entacapone (COMT inhibitor)
Interactions with Dopamine replacement ANS: - first gen antipsychotic drugs
- nonselective MAO inhibitors
- high protein meals
- pyridoxine (vitamin B6) if levodopa given alone
- anticholinergics enhances levodopas therapeutic response
What interaction occurs only when Levodopa is given alone ANS: pyridoxine (vitamin B6)
What interaction enhances Levodopa's therapeutic response ANS: anticholinergics
Prototype for COMT inhibitors ANS: entacapone
MOA of entacapone ANS: - prevents destruction of levodopa in intestine & peripheral tissues (prolongs
plasma half-life)
- decreases production of levodopa metabolites
Entacapone can significantly reduce the "________ _____" time experienced during Levodopa Therapy
ANS: "wearing off"
,ADRs of Entacapone (COMT inhibitors) ANS: - dyskinesias
- postural hypotension
- hallucinations
- sleep disturbances
- impulse control disorders
Should you stop COMT inhibitors (entacapone) abruptly? ANS: No, may cause worsening of symptoms
MOA of phenytoin ANS: selective inhibition of sodium channels (slows recovery of Na channels from the
inactive state)
Phenytoin has a ______ margin of safety ANS: narrow
Why is phenytoin teratogenic ANS: it decreases the synthesis of vitamin K-dependent clotting factors in
neonates causing bleeding tendencies
IV route for phenytoin is administered slowly to avoid causing significant ANS: dysrhythmias and
hypotension
What drug is administered once the seizure(s) is/are controlled ANS: phenytoin or fosphenytoin is
administered for long-term suppression
ADRs of Phenytoin ANS: - stevens-johnsons syndrome/toxic epidermal necrolysis
- gingival hypertrophy
- interferes with metabolism of vitamin D
- hirsutism (excessive hair growth)
, Therapeutic level of phenytoin ANS: 10-20mcg/mL
MOA of carbamazepine ANS: selective inhibition of sodium channels
Therapeutic serum levels for carbamazepine ANS: 4-12 mcg/mL
Half life of carbamazepine _______ (increases/decreases) with continued use ANS: decreases
MOA of valproate (2 mechanisms) ANS: 1. Suppresses neuronal firing by blocking sodium channels
2. Potentiates the inhibitory influence of GABA
Drug interaction of vaproate with topiramate ANS: hyperammonemia
Ethosuximide is used for what type of seizures ANS: absence seizures
ADRs of Lamotrigine ANS: - life threatening rashes (SJS and TEN)
- aseptic meningitis (stiff neck, headache)
Approved therapeutic uses for Gabapentin (besides seizures) ANS: postherpetic neuralgia
Off label therapeutic uses for Gabapentin ANS: neuropathic pain, migraine prophylaxis, fibrimyalgia, and
postmenopausal hot flashes
MOA of topiramate (4 mechanisms) ANS: 1. potentiation of GABA-mediated inhibition
2. blockade of voltage-dependent sodium channels
