Neurologic and Psychiatric Drugs Flashcards

1
Q

What are the drugs used for headaches?

A

NSAIDS
Ergots
5-HT Agonists

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2
Q

NSAIDS

A

MOA: Inhibits cyclooxygenase, reduces prostaglandin and thromboxane synthesis
Result: decrease pain
Drugs: ibuprofen, naproxen, diclofenac

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3
Q

ERGOTS

A

Indications: abortive (you have it and need to get rid) migraine (ergot in name)
MOA: stimulates vascular 5HT1D receptors, may also affect dopamine and alpha-adrenergic receptors
Result: Constricts cranial and peripheral blood vessels, may decrease neurogenic inflammation
Drugs: ergotamine, dihyroergotamine

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4
Q

5-HT agonists

A

(…triptan)
Indications: migraine abortive, cluster headache abortive
MOA: Activates vascular serotonin 5HT1 receptors (selective serotonin agonist)
Result: Produces vasoconstriction, reduces inflammatory process along trigeminal nerve pathway
Drugs: sumatriptan, rizatriptan, zomitrapitan, frovatriptan, eletriptan

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5
Q

Drugs used for seizures (anti-epileptics) work by either

A
  1. Stopping seizure spread and/or
  2. Raising seizure threshold
    -Affecting excitatory neurotransmitters
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6
Q

T/F Not all drugs are used in all types of seizures because some can help seizures while worsening others and oftem times have drug-drug interactions

A

True

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7
Q

Benzos

A

(…zepam)
Indications: seizure disorder, status epilepticus (seizures you can’t break – continuous), GAD (generalized anxiety disorder)/panic disorders, sedation, muscle spasms, acute alcohol withdrawal (titrate it so pt wont have seizures) , sleep terrors, sleep walking, RLS – abortive treatment
MOA: binds to benzodiazepine receptors, enhances GABA effects, poorly understood
Drugs: diazepam, lorazepam, clonazepam
Addictive

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8
Q

Sulfamate-substituted monosaccharide

A

Indications: seizure prevention, migraine prophylaxis, sleep-related eating disorders, PTSD nightmares, alcohol dependence
MOA: Not totally clear, blocks sodium channels, augments GABA activity, antagonizes glutamate receptors
Drugs: Topiramate

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9
Q

Carboxylic acid derivatives

A

Indications: seizure prevention, bipolar disorder (acute manic), migraine prophylaxis
MOA: Exact mechanism unknown, increases GABA effects, questionable inhibition of glutamate/NMDA receptor-mediated neuronal excitement and membrane stabilization
Drug: Valproic acid, valproate, divaloproex

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10
Q

Iminostilbenes

A

Indications: seizure disorder (tonic-clonic, partial), bipolar disorder, trigeminal neuralgia***
MOA: thought to allow enhancement of sodium channel inactivation by reducing high-frequency repetitive firing of action potentials and has action on synaptic transmission, other MOA unclear
Result: reduces seizure spread or neuromuscular transmission
Drug: carbamazepine

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11
Q

Phenyltriazine

A

Indications: seizure prevention, bipolar I maintenance, migraine with aura prophylaxis
MOA: exact mechanism unknown, inhibits voltage-dependent sodium channels, decreases presynaptic glutamate and aspartate release
Result: may result in inhibition of excitatory neurotransmitters
Drug: Lamotrigine

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12
Q

1-(aminomethyl) cyclohexane acetic acids

A

Indications: partial seizure prevention, neuropathic pain, fibromyalgia, post-herpetic neuralgia, alcohol dependence
MOA: exact mechanism unknown, may bind to carrier protein and act on unknown receptor to elevate GABA (does not act at GABA receptor, affect GABA uptake, or interfere with GABA transaminase) , blocks voltage-dependent calcium channels,
Result: modulates excitatory neurotransmitter release
Drug: gabapentin

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13
Q

Hydatoins

A

Indications: Seizure disorder
MOA: modulates neuronal voltage-dependent sodium and calcium channels during generation of nerve impulses
Result: Stabilizes nerve cells preventing overexcitation, stops spread of seizure activity by working in motor cortex of brain (prop. + abortive treatment)
Drug: Phenytoin, Fosphenytoin

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14
Q

Other anticonvulsants

A

Indications: partial seizure prevention, primary generalized tonic-clonic seizure prevention
MOA: exact mechanism unknown, selectively prevents hypersynchronization (for seizures to spread) of epileptiform burst firing
Drug: levetiracetam

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15
Q

Drugs used for parkinsons

A

Anticholinergic drugs
Aka parasympatholytics
Indications: Early stages Parkinsons as monotherapy, later disease as adjunct to levodopa

Dopaminergic drugs
Many drugs in this class
Chemically unrelated
Mainstay is levodopa
Result in increase of dopamine concentration and/or enhancing neurotransmission of dopamine

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16
Q

Anticholinergic drugs

A

Aka parasympatholytics
Indications: Early stages Parkinsons as monotherapy, later disease as adjunct to levodopa (something other than tremor: skip this part)
MOA: inhibit Ach at receptors in parasympathetic nervous system
Result: Decreases tremors
Drugs/types: tertiary amines i.e. benztropine

17
Q

Dopaminergic drugs

A

Indications: Parkinsons, RLS, sleep-related eating disorder
MOA: Crosses blood-brain barrier and acts as dopamine precursor, inhibits peripheral dopamine decarboxylation

-Levodopa is converted to dopamine in brain thereby increasing dopamine concentrations in basal ganglia
-Carbidopa enhances levodopa’s effectiveness by blocking peripheral conversion of levodopa allowing more to get to the brain

Result: Counteracts the depletion of striatal dopamine in extrapyramidal centers and decreases rigidity, akinesia (slow to get up), rest tremor, and improves posture/balance (improves the walking in block)

Drugs: levodopa***/carbidopa (not active – giving only this = not treatment. Give with levodopa)

18
Q

Non-ergot Dopamine agonists

A

Indications: Parkinsons, RLS, sleep-related eating disorder, REM sleep behavior disorder
MOA: Dopamine agonists, stimulates dopamine receptors
Result: Improves rest tremor, rigidity, and voluntary muscle control
Drug: ropinirole, pramiprexole

19
Q

COMT inhibitors

A

Catechol-o-methyl transferase inhibitors (…-capone)
Indications: adjunct to levodopa in Parkinsons
MOA: Prevents catechol-O-methyl transferase (COMT) from deactivates levodopa in the body before it is absorbed into the bloodstream
Result: Prevents levodopa from wearing off too quickly
Drugs: Tolcapone, entacapone

20
Q

Drugs used for CVA/TIA

A

Antiplatelets
Indication: thrombotic stroke prevention with prior TIA or CVA
MOA: Dipyridamole inhibits adenosine uptake by platelets and increases cGMP production + ASA
Result: Reduces platelet aggregation and dilates coronary arteries
Drug: Aspirin/dipyridamole

21
Q

SSRI’s

A

Selective serotonin reuptake inhibitors
Indications: first line treatment Depression, anxiety and panic disorders
MOA: Inhibit the neuronal reuptake of serotonin
Drugs: citalopram (Celexa), escitalopram (Lexapro), fluoxetine (Prozac), paroxetine (Paxil), sertraline (Zoloft)

22
Q

SNRI’s

A

Selective serotonin-norepinephrine reuptake inhibitor
Indications: depression, anxiety, chronic pain syndromes (fibromyagia)
MOA: potentiates neurotransmitter activity by inhibiting the neural reuptake of serotonin and norepinephrine
Drugs: venlafaxine (Effexor), duloxetine (Cymbalta)

23
Q

Buproprion

A

Indications: treats depression, and aids in smoking cessation
MOA: Dopamine and norepinephrine reuptake-blocker
Decreases cravings for nicotine and symptoms of nicotine withdraw
Drugs: buproprion (Wellbutrin, Zyban)

24
Q

TCA’s

A

Tricyclic Antidepressants
Indications: Depression, bipolar disorder, panic disorders, OCD, (lots of side affects for psych) chronic pain**
MOA: Prevent the reuptake into the storage granules in the presynaptic nerves which increases the amount of norepinephrine and serotonin in the synapses
Drugs: doxepin, amitriptyline hydrochloride (Elavil), imipramine (Tofranil), nortriptyline (Pamelor)

25
Q

Trazadone

A

Indications: depression, first line treatment: insomnia
MOA: serotonin reuptake inhibitor, also blocks histamine release
Drugs: trazadone

26
Q

Remeron

A

Indications: depression, insomnia, PTSD, OCD, anxiety, appetite stimulant (cancer population)
MOA: It is not a reuptake inhibitor. It encourages the pre-synaptic release of norepinephrine and serotonin by inhibiting the presynaptic alpha-2-adrenergic receptors (which typically prevent the release of the neurotransmitters)
Drugs: Remeron

27
Q

MAO inhibitors

A

Monoamine oxidase inhibitors (lots of side affect, change diet, life threatening drug to drug interaction)
Indications: Depression, anxiety and panic disorders, phobia, PTSD
MOA: inhibit MAO which is an enzyme that normally metabolizes many neurotransmitters (norepinephrine, serotonin, dopamine), which then makes them stay present in between neurons and available to the receptors
Drugs: tranylcypromine (Promate), Phenelzine (Nardil)

28
Q

Lithium

A

Mood stabilizer
Indications: bipolar disorder primarily used to treat (acute) mania
Have to closely monitor levels for toxicity (confusion, lethargy, slurred speech)
MOA: thought to decrease swings in excessive catecholamine vs decreased catecholamine stimulation (epinephrine, norepinephrine, dopamine)
Stabilizes the amount of neurotransmitter in the synapses – as opposed to SSRI’s, it is thought to increase reuptake thus decrease neurotransmitters in the synapse (reducing mania)
Drugs: lithium

29
Q

Typical Antipsychotics

A

Much older antipsychotic drugs with lots of extrapyramidal side effects
-Now typically only used in more acute situations
-Used in schizophrenia

Indications: psychosis
MOA: largely not understood
-blocks postsynaptic dopaminergic receptors in the brain

Drugs:
Haloperidol (Haldol) – stabilizes patients, acute psychosis
chlorpromazine (Thorazine) – after all other treatments fail

30
Q

Atypical Antipsychotics

A

Drugs used to treat psychoses
Indications: eliminate signs and symptoms of psychosis, used in low doses for delirium
Tranquilize
Can give to people with depression so make them sleepy
MOA: block dopamine receptors (to a lesser extent than typical antipsychotics causing fewer extrapyramidal side effects), also block serotonin receptor activity
Drugs: olanzapine (Zyprexa), risperidone (Risperdal), quetiapine (Seroquel)