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Pharm 2 Nef > Neruopsychiatric Meds > Flashcards

Neruopsychiatric Meds Flashcards

1
Q

What do you do during 0-5 minutes of Status Epilepticus?

A
  1. ABC stabilization-VS, O2, ECG monitor
  2. Check BG-if < 60mg/dL
    Adult: Thiamine 100mg IV with. 50ml D5W
    Child>= 2 yo: 2ml/kg D25W IV
    Child < 2yo: 4 ml/kg D12.5W IV
  3. Get labs, check for abnormalities
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2
Q

What medications do you give in the First Phase %-20 minutes of Status Epilepticus?

A 
Benzodiazepine is the treatment of choice
Midazolam IMx1
        >40kg=10mg
        13-40kg=5mg
Lorazepam IV (may repeat X1)
        0.1 mg/kg/dose. Max 4mg/dose
Diazepam IV (may repeat x1)
        0.15-0.2 mg/kg/dose. Max 10mg/dose

If the above is unavailable may try
Phenobarbital IV 15mg/kg/dose x1
Diazepam rectal 0.2-0.5 mg/kg, max 20mg
Nasal or buccal Midazolam

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3
Q

What do you give in the second therapy phase 20-40 mins. Of Status Epilepticus?

A

No evidence based first choice. May use any of the following
Fosphenytoin IV: 20mg/kg max 1500 mg/dose
Valproic acid IV: 4o mg/kg max 3000 mg/dose
Keppra IV 60mg/kg max 4500 mg/dose

If above not available
Phenobarbital IV 15mg/kg x1 (if not previously used)

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4
Q

What medications do you give in the third phase 40-60 minutes of Status Epilepticus?

A

No clear evidence, but choice includes
Repeat any second line therapy
Anesthetic doses of thiopental, midazolam, pentobarbital, or propofol

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5
Q

What are the 5 approved and unapproved indication for anticonvulsants?

A
  1. Seizures
  2. Neuropathic pain
  3. Mood Stabilization
  4. Migraines
  5. Alcohol dependence
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6
Q

What the is MOA of a Sodium Channel Blockade?

A

Prevent the return of the sodium channel from the inactive state to the active state by stabilizing them in the inactive state.

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7
Q

What is the MOA of the calcium channel blockade?

A

Particularly the T-type channels located in the thalamus which act as “pacemakers” of the normal rhythmic brain function.

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8
Q

What is the MOA of GABA enhancers?

A

Increase chloride movement through the GABA receptor, blocking pre-synaptic GABA uptake, inhibiting GABA metabolism by GABA transaminase, increasing GABA synthesis (modulate glutamic acid decarboxylase)

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9
Q

What is the MOA of Glutamate Blockers?

A

NMDA, AMPA, Kainate receptors- reduces the NA in/K out

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10
Q

What is the MOA of carbonic anhydrase inhibitor?

A

Blocks the normal function of increasing H+ ions/reducing pH leading to K+ shifts to buffer acid base status and increasing seizure threshold.

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11
Q

What is the MOA of sex hormones?

A

Increases Chloride conductance at the GABA-A and attenuated glutamate activity (progesterone).

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12
Q

What is the MOA of synaptic vesicle protein 2A (SV2A)

A

Possible calcium dependent, function not clearly defined at this time. A lack of SV2A results in seizures.

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13
Q

List the Sodium Channel Blockers

A 
Carbamazepine (Tegretol, Carbatrol)
Oxcarbazepine (Trileptal)
Eslicarbazepine (Aptiom)
Phenytoin/ Fosphenytoin ( Dilantin)
Lamotrigine (Lamictal)
Zonisamide (Zonegran)
Lacosamide (Vimpat)
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14
Q

What are the uses of Carbamazepine?

A

Partial and generalized seizures
Mood stabilizer
Neuropathic pain
Trigeminal Neuralgia

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15
Q

What is the PK of Carbamazepine?

A 
Induces it’s own metabolism- reduces its own levels
  Active metabolite
-CYP3A4
-75-85% protein bound
-T 1/2 recanted 5-26 hours
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16
Q

What are the ADR’s of Carbamazepine?

A 
Dizziness, ataxia
Diploid, blurred vision 
Nausea
Aplastic anemia, agranulocytosis, thrombocytopenia
Stevens-Johnson syndrome
Increased LFT’s
Hyponatreamia
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17
Q

Why was Oxcarbazepine created?

A

To eliminate the auto-induction of carbamazepine.
-still induces 3A4/5 and 2C19

Active metabolite——-> 10-monohyrdoxy metabolite (MHD)

38% protein bound

Better tolerated with fewer drug interactions
-similar side effect profile

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18
Q

Eslicarbazepine

A

Prodrug——> S-licarbazepine (also a oxcarbazepine metabolite)

-adjust does in renal impairment

-similar ADR’s profile to CBZ/OXCBZ
     Most common (>10%): dizziness, somnolence, nausea, headache, diplopia
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19
Q

Phenytoin/Fosphenytoin

A

Non-linear Pharmacokinetics (zero -order)
CYP enzyme inducer an substrate
70-95% protein bound
No active metabolites
T1/2= 7-42 hours
Fosphenytoin= prodrug for parenteral administration
Safer, better tolerated, faster infusion rates

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20
Q

What are the ADR’s of Phenytoin/Fosphenytoin?

A 
Ginginval hyperplasia 
Arrhythmias, CV depression, hypotension
Ataxia
Nystagmus
Osteoporosis 
Blood dyscrasias
N/V
Rash
Vitamin K and folate deficiencies
Bone marrow hyperplasia
-If given during pregnancy: cleft palate, cleft lip, congenital heart disease, slowed growth rate, mental deficiency
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21
Q

Lamotrigine

A

Protein bound =55%
T1/2= 24-41 hours
At high doses may autoinduce, but has no active metabolites

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22
Q

What are the ADR’s of Lamotrigine?

A 
Drug interactions with VPA
Rash, hypersensitivity
Headache
Blood dyscrasias
Ataxia, Tremor
Diplopia
Gi upset
Psychosis, insomnia
Less CNS toxicity and congenital malformations
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23
Q

Zonisamide

A

T1/2= 60 hours
P450 metabolism
-no induction
-no active metabolite

24
Q

What are the ADR’s of Zonisamide?

A 
Oligohidrosis in children 
Dizziness, Ataxia, headache, confusion, speech abnormalities, mental slowing
Anorexia, weight gain
Irritability, tremor
Renal stones in 1.5% of pts
Rash, skin reactions
25
Q

Lacosamide

A 
T1/2= 13 hours 
Minimal protein binding
No induction/inhibition of CYP430
Low side effect profile
Pregnancy Category C with ongoing pregnancy register
26
Q

List the GABA Agonist?

A

Benzodiazepines
Phenobarbital
Primidone (Mysoline)

27
Q

List the GABA Reuptake Inhibitor

A

Tiagabin (Gabitril)

28
Q

List the GABA Transaminase Inhibitor

A

Vigabatrin (Sabrina)

29
Q

List the GABA Other drugs

A

Gabapentin (Neurontin)
Pregabalin (Lyrica)
Valproate (Depakote)

30
Q

List the Benzodiazepines

See Pharm 1 lecture: Induction agents

A 
Clobazam (Onfi)
Diazepam (Valium)
Clonazepam (Klonopin)
Lorazepam (Ativan)
Clorazepate (Tranxene)
Trina Zola morning (Halcion)
Oxazepam (Serax)
Alprazolam (Xanax)
Midazolam (Versed)
Temazepam (Restroril)
31
Q

Phenobarbital

See pharm 1 lecture on induction agents

A

Primidone is a prodrug-metabolized to PHB

32
Q

Tiagabine

A

CYP450 substrate, no induction, no active metabolites
Most significant side effects
-dizziness, asthenia, nervousness, tremor, depressed mood, emotional lability, diarrhea, rash

33
Q

True or False

Because of risk of permanent vision loss, Vigabatrin is only available through a very specific program with REMS monitoring.

A

True

34
Q

True or false

Gabapentin is more often used for seizure control?

A

False, gabapentin is more often used for neuropathy than seizure control.

35
Q

Gabapentin is not _________ ________, not ___________, no __________, excerpted completely __________ by the __________, no PK drug interactions.

A 
Protein bound
Metabolized
 Induction 
 Unchanged 
Kidneys
36
Q

True or False
New meta analysis of RCTs suggests: gabapentin 1x30 minutes pre-operatively in regional anesthesia for multiple procedures improve post-op pain and reduces opiate requirements with increases post-op sedation being the highest safety risk.

A

True

37
Q

What are the ADR’s of Gabapentin

A

Very well tolerated

At higher doses

  • rash
  • neutropenia
  • somnolence, dizziness, ataxia, fatigue
  • nystagmus, diplopia
  • headache
  • tremor
  • N/V
38
Q

What are the uses of Pregabalin and what is the MOA?

A

Main use in neuropathy, may be used for seizures and anxiety.

-GABA analogue, binds alpha 2 and delta receptor sites-reduces release of excitatory neurotransmitters via Calcium currents.

39
Q

What are the pharmacokinetics of Pregabalin?

A 
T1/2= 6 hours
Food reduces absorption 
No plasma protein binding
90% unchanged in urine
No notable PK drug interactions
40
Q

What are the ADR’s of Pregabalin?

A

Well tolerated

  • dizziness, drowsiness
  • dry mouth
  • edema
  • blurred vision
  • weight gain
  • difficulty concentrating
  • rare angioedema
41
Q

True or False

Different forms of Valproic Acid have different effects and side effects.

A

False

Different forms do not have different effects/ side effects.

42
Q

What is the MOA of Valproic Acid?

A

Uncertain MOA-enhances GABA fxn, may increase Gaba synthesis, selective modulation of sodium channels.

43
Q

What are the pharmacokinetics of VPA?

A
  • 85-95% protein bound
  • liver metabolism (CYP, UGT), less than 4% excreted in the urine unchanged
  • T1/2=16 hours
  • Drug interactions through inhibition of oxidation and glucuronidation pathways
44
Q

What re the ADR’s of VPA?

A
  • In utero exposure- lower IQ in children compared to other anti-epileptics (category D-X)
  • N/V
  • tremors
  • sedation, confusion, irritability
  • weight gain, insulin resistance
  • hepatotoxicity (highest risk in children), rare but fatal pancreatitis
  • thrombocytopenia
  • hyperammonemia
45
Q

List the Glutamate Blockers

A

Felbamate (Felbatol)
Topiramate (Topamax)be most familiar with
Perampanel (Fycompa)

46
Q

Felbamate has a high risk of _______ ________ and _______ _______ failure.

A

Aplastic anemia
Fatal hepatic

Very limited use in the US.

47
Q

What are the MOA’s of Topiramate?

A
  • inhibitory sodium efffects
  • GABA enhancement via unknown mechanism
  • AMPA inhibition
  • weak carbonic anhydrase inhibitor
48
Q

What are the pharmacokinetics of Topiramate?

A

15% plasma protein bound
85% excreted unchanged in the urine
-may be reduced by enzyme inducers despite small percentage metabolized
-T1/2= 18-23 hours

49
Q

What are the ADR’s of Topiramate?

A
  • ataxia, slowed speech
  • concentration impairment, confusion, memory disturbance
  • depression, agitation
  • dizziness, fatigue, somnolence
  • parenthesia
  • weight loss d/t appetite suppression
  • renal calculi
50
Q

What is the drug information on Perampanel?

A
  • noncompetitive antagonist of AMPA
  • CYP interactions
  • BB warning: serious or life threatening psychiatric and behavioral adverse effects
    • aggression , hostility, irritability, anger, homicidal ideation, threats
  • common ADR
  • dizziness (43%), somnolence, headache, fatigue, irritability
51
Q

List the drugs with “Other MOA.”

A

Levetiracetam (Keppra)
Brivaracetam (Briviact)
Ezogabine (Potiga)

52
Q

What are the MOA’s of Levetiracetam?

A

Is used for Seizures

  • MOA possible related to synaptic vesicle protein 2A (SV2A) which apprears to be important for the availability of Ca-dependent Neurotransmitter vesicles ready to release their content.
    • with SV2A-reduced action potential- dependent neurotransmissio, while action protential-independent neurotransmission remains normal
  • reduces bicuculline-induced hyperexcitability
  • inhibits Ca release from IP3-sensitive stores
53
Q

What is the pharmacokinetics of Levetiracetam?

A
  • no protein binding
  • minimal metabolism (27%) via non-CYP pathways- 66% unchanged in the urine
  • T1/2=6-8 hours
  • no significant drug interactions
54
Q

What are the ADR’s of Levetiracetam?

A
  • somnolence
  • asthenia
  • dizziness, headache
  • accidental injury
  • convulsion
  • infection (URI, pharyngitis, flu-like symptoms)
  • pain
  • cognitive impairment
55
Q

List the Sedative Hypnotics

A

Z-drugs

  • Zolpidem (Ambien)
  • Zaleplon (Sonata)
  • Eszopiclone (Lunesta)

Ramelteon (Rozerem)
Suvorexant (Belsomra)
Melatonin, Valerian Root

56
Q

What happens with Z drugs?

A
  • crazy side effects
  • look and smell like Benzos with less systemic absorption
  • shouldn’t be used in hospital
  • increase post-op confusion

Ramelteon -0 crazy side effects
Melatonin, Valerian Root are not effective

57
Q

List the Anti-Depressants

A

Tricyclics Antidepressants (TCA)
Selective Serotonin Reuptake Inhibitors (SSRI)s
Serotonin Norepinephrine Reuptake Inhibitors (SNRI)s
Dopamine Norepinephrine Reuptake Inhibitor (DNRI)
5HT2A Antagonists
Neudexta

Pharm 2 Nef (1 decks)

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