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Neurology > Neuro Pharm > Flashcards

Neuro Pharm Flashcards

1
Q

Immediate precursor to DA converted in periphery and brain to DA by L-AAD
Replenishes DA stores in the remaining DA terminals in the striatum

Readily absorbed from GI tract but is dependent on gastric emptying
Excreted in urine as HVA and DOPAC
* Single most effective treatment for PD  can completely ameliorate all the symptoms of PD particularly during initial treatment
Drug is only effective for 3-5 years  delay treatment until symptoms of PD yield functional impairment

Drug?

A

L-DOPA

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2
Q

Interactions & contraindications w/ L-DOPA

A

Drug-drug interactions: VitB6 increases L-Dopa metabolism (use decarboxylase inhibitor) and food can impair absorption (give before a meal)
Contraindications: DO NOT GIVE WITH MAO-A INHIBITOR  hypertensive crises

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3
Q

L-AAD inhibitor that cannot cross the BBB  prolongs L-Dopa t1/2, reduces the amount of L-Dopa needed to be administered by up to 75% and redues side effects due to reduced peripheral [DA

A

Carbidopa

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4
Q

DA - Receptor Agonist for Parkinsons

A

activates the D2 receptors to reduce activation of the indirect pathway
do not need to compete with other substances for G.I. absorption or across BBB. They may also be more selective, which reduces ADEs

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5
Q

D2 agonist and partial D1 agonist

A

Bromocriptine

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6
Q

D1/D2 agonist

A

Apomorphine

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7
Q

D2 selective agonist + free radical scavenger

A

Pramipexole

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8
Q

D2 selective agonist + metabolized by CYP1A2

A

Ropinirole

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9
Q

Antiviral agent that was found to alleviate parkinsonian symptoms by enhancing release and possibly DA synthesis, inhibiting DA uptake and possible interaction with NMDA receptors

Restlessness, depression, agitation, irritability, insomnia, excitement, hallucinations and confusion
Overdose may produce psychosis
Can also produce ADEs similar to those produced by L-Dopa and DA
Contraindication: patients with history of seizures or heart failure

A

Amantadine

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10
Q

Selective MAO-B inhibitor retards the breakdown of DA

Metabolites include amphetamine and methamphetamine increase DA release, may be neuroprotective and prevent the progression of PD by inhibiting MAO-B generation of free radicals

May potentiate the adverse effects of L-Dopa

Contraindications: DO NOT TAKE WITH meperidine, TCAs or SSRIs

Used primarily in patients whose responsiveness to L-Dopa has declined
Little effect when administered alone

A

Selegiline

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11
Q

More potent MAO-B inhibitor for combined therapy with L-Dopa in late-stage PD or alone in early PD

A

Rasagiline

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12
Q

Selective COMT inhibitor  prolongs action of L-Dopa, reduces the production of 3OMD, which may compete for transport carriers in GI and BBB & increases bioavailability of L-Dopa

  • peripheral effects only and no liver damage so it is the preferred agent

Rapidly absorbed and extensively protein bound

A

Etacapone

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13
Q

COMT inhibitor, prolongs action of DA / has peripheral and central side effects
Increased liver enzymes and hepatic failure (*Requires signed patient consent)

Rapidly absorbed and extensively protein bound

A

Tolcapone

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14
Q

locking cholinergic activity was a widely used form of therapy for PD prior to advent of L-Dopa therapy. Currently, these agents are used in early PD or as adjunct to L-Dopa.
ADEs: drowsiness, mental slowness inattention, confusion, delusions, hallucinations, mood changes, dry mouth, blurred vision, mydriasis, urinary retention, N/V, constipation, tachycardia, increased intraocular pressure, palpitations and arrhythmias
Contraindications: prostatic hyperplasia, OBD, glaucoma and avoid with concomitant use of drugs with anti-muscarinic effects (i.e. TCAs of antihistamines)

A

Benzotropine

Diphenhydramine

Trihexyphenidyl

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15
Q

Huntington’s disease (initially the loss of the indirect pathway, followed by loss of the direct pathway)
VMAT inhibitors - DA depleting agents

A

Reserpine

Tetrabenazine

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16
Q

Anti-depressants commonly used to tx Huntington’s:

A

Fluoxetine, carbamazepine

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17
Q

D2 receptor antagonists

A

Chlorpromazine, Haloperidol

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18
Q

4 endogenous opiates

A

POMC, B-endorphins, proenkalain, dynorphins

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19
Q

modulate initial signal transduction

A

NSAIDS

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20
Q

block the signal conduction in nociceptive fibers

A

Sodium Channel Blockers

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21
Q

block the signal conduction in nociceptive fibers

A

Allodynia

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22
Q

high intensity stimuli perceived as more painful

A

Hyperalgesia

23
Q

arises from transection of mechanical damage to the nerve axon  loss of C-fiber and “rewiring” with A fiber proliferation into these areas  changes in gene expression and altered sensitivity as well as changes in the Na-channel expression that leads to enhanced cellular excitability, which is the basis for treatment of neuralgia with carbamazepine (Na channel blocker)

A

Neuropathic pain

24
Q

Supraspinal/spinal analgesia, sedation,  respiration,  GI transit, modulation of hormone and neurotransmitter release
endorphins > enkephalins > dynorphins

A

Mu/ OP-3

25
Q

Supraspinal/spinal analgesia and modulation of hormone and neurotransmitter release
enkephalins > endorphins and dynorphins

A

Delta/ OP-1

26
Q

Supraspinal/spinal analgesia, psychotomimetic effect and  GI transit
dynorphins&raquo_space; endorphins and enkephalins

A

kappa/ OP-2

27
Q

occurs with continued opiate use  internalization and degradation of receptors  loss of potency regarding pain relief and disappearance of some ADEs

A

Tolerance

28
Q

mu partial agonist; Can be converted to morphine via CYP2D6 through glucuronidation

A

codeine

29
Q

mu agonist, low oral: IV potency, IV

A

Hydromorphone

30
Q

mu agonist, high oral potency, long elimination halflife allows use for tx of opiate withdrawal

A

methadone

31
Q

mu and kappa agonist
low oral potency
mostly given IV

A

morphine

32
Q

patches provide 48-72 hours of relatively stable drug delivery (application of too many patches has been associated with suicides)

A

Fentanyl

33
Q

can also interact with cholinergic receptors
Medium oral:IV potency
Can be metabolically converted into a metabolite that has increased CNS toxicity. The pathway that creates this toxin is usually a minor pathway, but can be more active in some people.

A

Merperidine

34
Q

Medium oral:IV potency
Not converted to morphine
Percocet

A

Oxycodone

35
Q

specifically: constipation, mild drowsiness, excess sweating, peripheral edema, QT prolongation/ arrhythmias, reduced testosterone  reduced libido and sexual performance and erectile dysfunction
High oral:IV potency
Used as opioid dependence treatment (DOC for opioid-dependent pregnant women)
* Physicians require a special state and federal license to administer this type of treatment

A

Methadone again

36
Q

mu partial, and kappa agonist

IV only

A

Butorphanol

37
Q

mu partial agonist, delta and kappa antagonist, used as opioid dependence treatment, low oral:IV, binds tightly to the opioid receptor, no bioaccumulation, has a ceiling effect (low risk of OC), poor oral absorption (can be formulated w/ naloxone to prevent pt was trying to inject drug)

A

Buprenorphine

38
Q

mu partial agonist, not converted to morphine, medium potency

A

Hydrocodone

Vicodin

39
Q

mu antagonist and kappa agonist, IV only

A

Nalbuphine

40
Q

medium oral, IV potency
mu partial agonist
Kappa agonist

A

pentazocine

41
Q

mu, kappa, delta antagonist given IV to treat opiate intoxication

A

Naloxone

42
Q

mu, kappa, delta antagonist given for long term effect
Used in maintenance programs for opioid addicts and to decrease alcohol craving by alcoholics by decreasing baseline –endorphin release

A

Naltrexone

43
Q

mu, kappa, delta antagonist w/ intermediate halflife

A

Nalmefene

44
Q

Block NMDA receptor in order to prevent surgery induced neural and central sensitization
Can cause hallucinations, amnesia, increased intracranial pressure

A

ketamine

45
Q

Block NMDA receptor in order to prevent surgery induced neural and central sensitization
can cause dizziness, confusion, fatigue, low affinity Rx

A

Dextrimetmorphan

46
Q 
Anticonvulsants - 2
Inhibition of voltage-gated Ca channels via the alpha 2 delta subunit, which prevents channel’s trafficking to the cell surface  inhibition of neuronal excitability
Sedation and dizziness 
Peripheral edema
GI issues
 Dose in renal insufficiency
A

Gabapentin

Pregabalin

47
Q

Na channel blocker  used in neuropathy, stroke, MS and phantom limb
Diplopia and blurred vision
can cause rash

A

Lamitrigene

48
Q

Na channel blocker
Pain relief associated with blockade of synaptic transmission in trigeminal nucleus (neuropathic pain)
Dizziness and drowsiness
Agranulocytosis (rare)

A

Carbamazepine

49
Q

TCA’s block reuptake of serotonin and NE in ascending corticospinal monoamines pathway

A

Amitriptyline
Nortiptyline
Imipramine
Desipramine

50
Q 
Inhibition of Na channel
ADEs: Hypo-TN
Motor block
Myotoxicity
Systemic toxicity in high doses: seizures, arrhythmias or cardiac arrest
A

Bupivacaine

Lidocaine

51
Q

alpha 2-agonist

sedation, HOTN, bradycardia

A

clonidine

Dexemedetomide

52
Q

treatment for PTSD, SSRIs: Paroxetine & Sertaline

A

Paroxetine and Sertraline

53
Q

Toxin screen for opitates?

A 
urine antibody enzymes, different ratios of morphine:codeine can indicate what the patient is taking 
M:D>2:1 (heroin) 
<2:1 (codeine)
Synthetic opiatesa re negative 
Fluoroquinolones can be false positives

Neurology (7 decks)

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