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Pharm 2 > Neuropsych Meds- AEDs > Flashcards

Neuropsych Meds- AEDs Flashcards

1
Q

What should be done in the first five minutes of a seizure?

A
  1. ABC Stabilization
  2. Check BG
  3. Get labs and check for abnormalities
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2
Q

In the first five minutes of a seizure, a blood sugar should be treated at or below ___mg/gl?

A

If <60mg/dl

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3
Q

What is treatment for blood sugar <60mg/dl for a seizing patient?

A

Adult: Thiamine 100mg with 50ml D5W
Child>2yo: 2ml/kg D25 IV
Child<2yo: 4ml/kg D12.5 IV

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4
Q

What is the first phase of status epilepticus?

A

5-20 mins long seizure

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5
Q

What is second phase of status epilepticus?

A

20-40 mins long seizure

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6
Q

What is third phase of status epilepticus?

A

40-60 mins long seizure

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7
Q

What is first phase treatment for Status epilepticus?

A
  1. x1 Midazolam IM (>40kg=10mg, 13-40kg=5mg)
  2. Lorazepam IV (can repeat once) 0.1mg/kg (max 4mg)
  3. Diazepam IV (can repeat once) 0.15-0.2mg/kg (max 10mg)
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8
Q

If midaz, loraz, or diazepam are not available, what can also be given for first phase?

A
  1. Phenobarb IV 15mg/kg x1
  2. Diazepam PR 0.2-0.5mg/kg (max 20mg)
  3. Nasal or buccal midazolam
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9
Q

If status epilepticus has progressed to second phase, what can be used to treat?

A
  1. Fosphenytoin IV 20mg/kg (max 1500mg)
  2. Valproic Acid IV 40mg/kg (max 3000mg)
  3. Keppra IV 60mg/kg (max 4500mg)
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10
Q

If fosphen, VPA, or keppra not available in phase 2, what can also be used?

A

Phenobarb IV 15mg/kg (if not previouslt used)

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11
Q

T/F: In second phase status epilepticus, fosphenytoin is the drug of choice based on research evidence?

A

False; no evidence based first choice. Can use any of the choices available (keppra, VPA, fosphenytoin)

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12
Q

If status epilepticus has progressed to third phase, what can be used to treat?

A

No clear evidence, but choices include:

  1. Repeat any second line therapy
  2. Anesthetic doses of thiopental, midazolam, pentobarbital, or propofol
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13
Q

T/F: If anticonvulsant medication is held or stopped, there is only a risk of seizures if patient has or has previously had epilepsy?

A

False; even if patient has not had a seizure and that medication is not specifically prescribed for seizure. there is still a risk

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14
Q

What are the 7 different MOA for anticonvulsant therapy?

A
  1. Sodium channel blockade
  2. Calcium channel blockade
  3. GABA enhancers
  4. Glutamate blockers
  5. Carbonic anhydrase inhibitors
  6. Sex hormones
  7. Synaptic vesicle protein 2A (SV2A)
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15
Q

What are examples of Sodium channel blockers?

A
  1. Carbamazapine (Tegretol,Carbatrol)
  2. Oxcarbazepine (Trileptal)
  3. Eslicarbazepine (Aptiom)
  4. Phenytoin/fosphen (Dilantin)
  5. Lamotrigine (Lamictal)
  6. Zonisamide (Zonegran)
  7. Lacosamide (Vimpat)
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16
Q

What are the four uses for Carbamazepine?

A
  1. Partial and generalized seizures (less often for seizures)
  2. Mood stabilizer
  3. Neuropathic pain
  4. Trigeminal neuralgia (1st line therapy)
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17
Q

T/F: Carbamazepine is most frequently prescribed for seizures compared to its other uses?

A

False

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18
Q

What is unique about the pharmacokinetics of Carbamazepine?

A
  1. Induces its own metabolism
  2. CYP3A4 inducer and substrate
  3. 75-85% protein bound
  4. Has active metabolite
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19
Q

If carbamazepine induces its own metabolism, how does that affect its administration?

A

Will have increasingly higher dosage requirement with time

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20
Q

Side effects of carbamazapine?

A
  1. Dizzness, ataxia, diplopia, nausea.
  2. Aplastic anemia, agranulocytosis, thrombocytopenia
  3. Stevens Johnson
  4. Increased LFTs
  5. Hyponatremia
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21
Q

Which side effect is seen in nearly all patients taking carbamazapine?

A

Hyponatremia

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22
Q

How is oxcarbazepine (Trileptal) different than carbamazapine?

A
  1. Not self inducing
  2. Better tolerated
  3. Fewer drug interactions
  4. Slightly less side effect risk
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23
Q

How is eslicarbazepine (Aptiom) different than carbamazapine?

A
  1. Its a prodrug broken down to S-licarbazepine
  2. Needs renal dose adjustment
  3. Even less side effects when compared to oxcarbazepine/carbamazapine
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24
Q

What anticonvulsant has non-linear pharmacokinetics?

A

Phenytoin/fosphenytoin (Dilantin)

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25
Q

What does non-linear pharmacokinetics mean?

A

When you increase the dose of the medication, the serum levels do not go up in a normal linear line. They can go up exponentially and are different for each patient. Its zero order, so the eliminates a certain amount every hr, independent of drug concentration in the body

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26
Q

The non-linear pharmacokinetics of Dilantin can pose a specific problem when?

A

When changing from IV to PO or PO to IV

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27
Q

What are two adverse side effects that can be seen with long term dilantin use?

A
  1. Gingival hyperplasia

2. Osteoporosis/Bone marrow hypoplasia

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28
Q

What are side effects of dilantin?

A
  1. Arrythmias, CV depression, HoTN
  2. Ataxia, nystagmus, N/V
  3. Blood dyscrasias
  4. Vit K and folate deficiency
  5. Osteoporosis, rash
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29
Q

T/F: Dilantin is one of the few drugs that is recommended in pregnant women?

A

False; can cause cleft palate, cleft lip, CHD, slowed growth rate, mental deficiency

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30
Q

How is lamotrigine (Lamictal) similar to carbamazapine pharmacokinetically?

A

It can autoinduce, but only at high doses

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31
Q

If not tapered correctly, lamotrigine (Lamictal) has a high risk of causing ________ when used in combo with VPA

A

Stevens Johnson reaction

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32
Q

Does lamotrigine (Lamictal) have active metabolites?

A

No

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33
Q

What are the two most common CNS related symptoms seen with lamotrigine (Lamictal)?

A

Psychosis and insomnia

so risk of post-op delirium, agitation with Lamictal

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34
Q

What drug does lamotrigine (Lamictal) have a an interaction with?

A

Valproic Acid. Causes steven-johnson syndrome

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35
Q

What drug does zonisamide have an interaction with?

A

None. No drug interactions

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36
Q

What side effect does zonisamide cause specifically in children?

A

Oligohidrosis

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37
Q

What two medications is it common to see “psycho-motor disconnect” (slowed down thought process)?

A

Zonisamide and Topiramate

aka “mental slowing”

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38
Q

Side effects of zonisamide (zonegran)?

A
  1. Dizziness, ataxia, HA, confusion, speech abnormalities, mental slowing,
  2. Anorexia or weight gain
  3. Irritability, tremor
  4. Renal stones in 1.5% pts
  5. Rash, skin reactions
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39
Q

Half lives of Phenytoin, lamotrigine, zonisamide, lacosimide?

A

Phenytoin= variable 7-42hrs
Lamotrigine=24-41hrs
Zonisamide=60hrs
Lacosamide=13hrs

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40
Q

Pros/Cons Lacosamide (Vimpat)?

A

Pros:
Minimal protein binding
No induction/inhibition CYP
Nice side effect profile

Cons:
Expensive
Pregnancy Category C

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41
Q

What are the four categories of GABA Agents?

A
  1. GABA Agonists
  2. GABA Reuptake Inhibitors
  3. GABA Transaminase Inhibitors
  4. GABA “Other” (Not agonists, but enhance the GABA activity
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42
Q

Of all the benzos, what has the most significant withdrawal risk?

A

Clobazam (Onfi)

its only use is actually for seizures, not anxiety like the other benzo’s

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43
Q

What drug is metabolized to phenobarbital and what is it used for?

A

Primidone is a prodrug that is metabolized to phenobarbital and it is seen with patients with musculo-skeletal disorders.

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44
Q

What drug classes/drugs fall under GABA Agonists?

A
  1. Benzos
  2. Phenobarbital
  3. Primidone (Mysoline)
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45
Q

What drug classes/drugs fall under GABA Reuptake Inhibitors

A

Tiagabine (Gabitril)

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46
Q

What drug classes/drugs fall under GABA Transaminase Inhibitors?

A

Vigabatrin (Sabril)

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47
Q

What drug classes/drugs fall under GABA “Others”?

A
  1. Gabapentin (Neurontin)
  2. Pregabalin (Lyrica)
  3. Valproate (Depakote)
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48
Q

What is REMS?

A

Medication Monitoring system. Special pharmacies are the only distributors and the patient needs to be monitored very closely

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49
Q

What is gabapentin mostly used for?

A

More often used for neuropathy than seizure control

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50
Q

Pharmacokinetics of Gabapentin?

A
  1. Not protein bound
  2. Not metabolized
  3. No induction
  4. Excreted completely unchanged in kidneys
  5. No PK Drug interactions
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51
Q

Pre-operative Gabapentin does what two things?

A
  1. Reduces opiate requirements

2. Increased post op sedation

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52
Q

Side effects of Gabapentin?

A

Overall very, very mild side effects- rash, neutropenia, somnolence, dizziness, ataxia, fatigue, nystagmus, diplopia, HA, tremor, N/V (all only really seen at high doses)

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53
Q

What is pregabalin (Lyrica)’s most common use?

A

Diabetic neuropathy

considered to be “Neurontin like”, but has more sedation and ataxia compared to gabapentin

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54
Q

What are two other (less common) uses for Pregabalin (Lyrica)?

A

Seizures and anxiety

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55
Q

MOA of Pregabalin(Lyrica)?

A

GABA Analogue, binds alpha-2 and delta receptor sites which reduces release of excitatory neurotransmittors via Ca++ currents

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56
Q

Pharmacokinetic considerations for pregabalin(Lyrica)?

A
  1. Half life 6 hours
  2. Food reduces absorption
  3. No plasma protein binding
    4, 90% unchanged in urine
  4. No notable PK drug interactions
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57
Q

Pregabaline (Lyrica) ADRs?

A
  1. Dizziness, drowsiness, blurred vision, difficulty concentrating
  2. Dry mouth
  3. Edema, rare angioedema
  4. Weight gain
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58
Q

Post-operative considerations for Pregabalin (Lyrica)?

A

Post-op delirium and confusion risk

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59
Q

T/F: There are several different forms of Valproic Acid (VPA), and they all have different effects and side effects to remember?

A

False; many different forms, but all have same SE/effects

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60
Q

How would a low albumin effect VPA?

A

It is 85-90% protein bound and low protein could have higher risk of toxicity

This can occur in trauma, burn, liver dz, malnutrition, hypoalbuminemia

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61
Q

Where is VPA metabolized?

A

Liver

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62
Q

If VPA at toxic levels d/t overdose, what should be done?

A

Stop the medication and within 2.5 days, levels will fall to safe levels

b/c half life is about 16hrs

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63
Q

Three main SEs to watch for with VPA?

A
  1. Hepatoxicity (highest risk in children, accompanied with rare but fatal pancreatitis)
  2. Thrombocytopenia (risk of bleeding)
  3. Hyperammonemia (may present as liver failure/very confused patient)

Emily harped on all 3 of these

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64
Q

T/F: Though VPA is associated with drug interactions, it is safe for pregnant women?

A

False; it is associated with drug interactions through inhibition of oxidation and glucoronidation pathways, but it is NOT recommended for parturients (cat D-X)

VPA can cause lower IQ kids

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65
Q

Why is felbamate rarely used in the US?

A

High risk of aplastic anemia and fatal hepatic failure

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66
Q

Three main uses of topiramate (Topamax)?

A
  1. Alcohol withdrawal
  2. Migraine Prophylaxis
  3. Seizures
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67
Q

MOA of Topiramate (Topamax)?

A
  1. Sodium Channel blocker
  2. GABA enhancement of unknown mechanism
  3. AMPA Inhibition (part of NMDA, so inhibits glutamate)
  4. Weak carbonic anhydrase inhibitor

(Basically, global potential suppression. It “kind of hits all the different sites”, per Emily”

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68
Q

T/F: Topiramate (Topamax) has many drug interactions, but compared to many other drugs, it has a good side effect profile?

A

False; It has not drug interactions

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69
Q

What is the side effect profile of Perampanel?

A
  1. BB Warning for life threatening psych/behavioral effects
  2. Dizziness (43%-Most common)

high risk of SE, so it’s not used a lot. If on it, risk of post-op agitation and delirium

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70
Q

MOA of levetiracetam (Keppra)?

A
  1. Possibly related to synaptic vesicle protein 2A (SV2A)= important for the Ca++ dependent neurotransmitter vesicles ready to release their content
  2. Reduces bicuculline induced hyperexcitability
  3. Inhibits Ca++ release from IP3-sensitive stores
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71
Q

Does keppra play nicely with other drugs?

A

Yes, yes it does

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72
Q

Levetiracetam ADRs?

A
  1. Somnolence, asthenia, dizziness, HA, convulsion, cognitive impairment, pain
  2. Accidental injury
  3. Infection (URI, pharyngitis, flu-like symptoms)
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73
Q

Which GABA Analog has significant withdrawal risk?

A

Baclofen

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74
Q

MOA Baclofen?

A
  1. Presynaptic Hyperpolarization
    A. Reduced Ca++ influx
    B. Reduced glutamate release
    C. Decreased alpha-motor neuron activity
  2. Post-synaptic activation
    A. Increased K+
    B. Hyperpolarization
  3. Substance P Inhibition in spinal cord to reduce pain (Emily mentioned this one as the big one)
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75
Q

What are withdrawal symptoms of baclofen?

A
  1. Hallucinations
  2. Fever
  3. Agitation
  4. Tremor - significant
  5. Tachycardia
  6. Seizures
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76
Q

MOA of Tizanidine?

A

Centrally acting Alpha 2 Agonist (may potentiate glycine)

77
Q

Tizanidine ADRs?

A
  1. Dry Mouth
  2. Sedation
    (mostly look like anticholinergic effects)
78
Q

MOA of Dantrolene?

A

Blocks ryanodine channel—-reduces Ca++ release from sarcoplasmic reticulum

It’s similar to phenytoin

79
Q

What is BB warning for dantrolene?

A

Dose dependent diarrhea and hepatotoxicity

80
Q

At what dose does Dantrolene have black box warning symptoms?

A

> 800mg/day with long term use

81
Q

Primary three ADRs of skeletal muscle relaxants?

A
  1. Significant sedation
  2. Confusion
  3. Lethargy
  4. Dizziness

Worry about oversedation when they come in for surgery

82
Q

What are signs of sedative hypnotics withdrawal?

A
  1. Confusion

2. Insomnia

83
Q

Examples of sedative hypnotics:

A
  1. “Z-Drugs and like benzo-lites”: zolpidem (Ambien), zaleplon (Sonata), eszopiclone (Lunesta)
  2. Ramelteon (Rozerem)
  3. Suvorexant (Belsomra)
  4. Melatonin and Velerian root
84
Q

What does Nuedexta treat?

A

Falls under antidepressant, but is used for pseudo-bulbar affect

85
Q

What class of antidepressants is the oldest group?

A

Tricyclic

86
Q

MOA of tricyclic antidepressants?

A

Serotonin and NE reuptake inhibition, anticholinergic, and 1A antiarrhythmic properties

Dosed at bedtime

87
Q

What are the two major ADRs of tricyclic antidepressants?

A
  1. Anticholinergic side effects

2. Cardiovascular- QT prolongation and arrhythmias

88
Q

Overdose treatment of tricyclic overdose consists of what?

A
  1. Admin NaHCO3 d/t metabolic acidosis

2. Supportive therapy

89
Q

What drug class does Emily consider the primary medication for depression?

A

SSRIs

90
Q

Examples of SSRIs?

A
  1. citalopram (Celexa)
  2. fluoxetine (Prozac)
  3. paroxetine (Paxil)
  4. sertraline (Zoloft)
  5. escitalopram (Lexapro)
  6. fluvoxamine (Luvox)
91
Q

T/F: All SSRIs work the same way, but have slightly different affinity for specific serotonin receptors

A

True

92
Q

What are the G-Couple 5-HT receptors?

A

1, 2, 4, 5, 6, 7

93
Q

What are Na/K Ion channel 5-HT receptors?

A

3

94
Q

What are Excitatory 5-HT receptors?

A

2, 3, 4, 6, 7
(4,6,7 Increase cAMP)
(2- Increase IP3 and DAG2)
(3-Depolarizes Plasma membrane)

95
Q

What are Inhibitory 5-HT receptors?

A

1, 5

96
Q

What do inhibitory 5HT receptors do?

A

Decrease cAMP

97
Q

What does 5HT-3 receptor do?

A

CNS, GI Tract, PNS
(GI Motility, emesis, nausea)

ex. zofran

98
Q

What does 5HT-1 receptor do?

A

Blood vessels and CNS
(addiction, aggression, anxiety, appetite, heart rate, vasoconstriction, emesis, memory, mood, nausea, pain, sexual function, thermoregulation)

99
Q

What does 5HT-2 receptor do?

A

Blood vessels, CNS, GI tract, Platelets, PNS, Smooth Muscles
(Addiction, anxiety, appetite, cognition, learning memory, mood, perception, sexual function, platelet aggregation, perception)

100
Q

Side effects of SSRIs?

A
  1. Hyponatremia - very high rates
  2. Thrombocytopenia
  3. Suicidality (gives people a higher level of energy, so now they have the energy to carry out suicide plan
  4. Arrhythmias
  5. Serotonin Syndrome - like MH, but no rigidity. hyper reflexes instead
  6. N/V/D and weight fluctuations
101
Q

MOA of SNRIs?

A

Serotonin and NE reuptake inhibition

102
Q

Examples of SNRIs?

A
  1. duloxetine (Cymbalta)
  2. venlafaxine (Effexor)
  3. desvenlafaxine (Pristiq)
  4. levomilnacipran (Fetzima)
103
Q

How does thiamine help with low blood glucose during seizures?

A

Helps to utilize carbohydrates, esp in the nerves

104
Q

What class of meds are 1st line treatment for status epileptics?

A

Benzodiazepines

2nd is phenobarbitals

105
Q

2 off-label uses of Topamax

A

Migraines and alcohol dependence

106
Q

Seizure meds whose MOA is calcium channel blockade work or _ - type channels in the thalamus

A

T-type

107
Q

What electrolyte is mediated by GABA enhancers?

A

Cl-

108
Q

What three seizure meds are highly protein bound?

A

Carbamazepine (75-85%)
phenytoin (70-95%)
VPA (Depakote) (85-95%)

109
Q

Why is it important to adjust phenytoin in small baby doses?

A

Has a narrow TI (10-20), so easy to become toxic

doubling a dose can quadruple drug levels d/t non-linear, zero-order PK’s

110
Q

T/F Dilantin has no active metabolite

A

True

111
Q

Dilantin is a ___ anti arrhythmic

A

1b

112
Q

T/F There is a risk of hyponatremia with Lamictal

A

FALSE. no hyponatremia risk

113
Q

Is there a high or low fetal risk with Lamictal?

A

Low. Not completely gone, but a lot less compared to dilantin

114
Q

What is the safest sodium channel blocking seizure med available?

A

lacosamide (Vimpat)

115
Q

What is important to know about vigabatrin?

A

needs REMS dispensing bc of risk of permanent vision loss

116
Q

T/F

Gabapentin is not protein bound, not metabolized, and excreted completely unchanged by kidneys

A

True

117
Q

What med has more sedation and ataxia complications, lyrica or neurontin?

A

Lyrica

118
Q

VPA is associated with drug interactions through inhibition of _____ and _____ pathways

A

Oxidation
glucoronidation

HAS NO CYP INTERACTIONS

119
Q

What electrolyte plays a role in Keppra’s MOA?

A

Ca+

120
Q

T/F

Muscle relaxants have no withdrawal risk

A

FALSE
some are very severe like Flexeril and Tizanidine (Zanaflex)

Most Significant is Baclofen

121
Q

Can you go into withdrawal from sleep meds?

A

Yes, especially the z-ones (zolpidem (Ambien), zaleplon (Sonata), eszopiclone (Lunesta)

122
Q

Examples of TCA’s

A 
Amitriptyline (Elavil) – used for HA’s, neuropathic pain
Clomipramine (Anafranil)
Desipramine (Norpramin)
Doxepin (Sinequan)
Imipramine (Tofranil)
Nortriptyline (Pamelor)
123
Q

What is a major adverse reaction from SNRI’s? Why does it occur?

A

HTN. b/c you block NE reuptake, so there is more readily available.

124
Q

What are other adverse effects of SNRI’s?

A 
Serotonin syndrome
Hepatotoxicity
Hyponatremia
Insomnia, abnormal dreams, somnolence
N/V/D
Weight loss
Tremor, agitation
125
Q

What med is an example of a DNRI? What is it’s MOA?

A

Bupropion (Wellbutrin)

Dopamine and NE reuptake inhibitor, hence it is a
Excitatory-type antidepressant

126
Q

2 approved uses Bupropion (Wellbutrin)

A

smoking cessation and antidepressant

can also be used to supplement ADHD meds, and approved for PTSD

127
Q

ADR’s of Bupropion (Wellbutrin)

A

Causes a fight/flight scenarios, so…

Insomnia
Agitation, Anxiety
Tachycardia, HTN
Weight loss
promotes seizures
128
Q

Who would not be a good candidate for wellbutrin?

A

someone who already has anxiety b/c it is very stimulating

129
Q

Per Emily, What is a the big difference b/w SSRI’s and SNRI’s?

A

SNRI’s have a greater risk of HTN

SSRI’s - have to worry about sodium and PLT’s

130
Q

Examples of 5HT2A Antagonists?

A

Mirtazepine (Remeron)
Nefazodone (Serzone)
Trazodone (Desryl)
Vilazodone (Viibryd)

131
Q

ADR’s of 5HT2A Antagonists?

A

HIGHLY SEDATING (only dosed at bedtime)
Increased appetite
Hepatotoxicity

Think of fall risk in the elderly

132
Q

What two drugs make up Nuedexta? Who would be on Nuedexta?

A

Dextromethorphan/Quinidine

Dx: Pseudobulbar affect from strokes or TBI’s

133
Q

MOA of Nuedexta

A

Quinidine increases DM levels through enzyme inhibition. DM may inhibit NMDA receptors, sigma 1 agonist.

Quinidine levels are so low that it doesn’t really affect HR

134
Q

Why don’t you get cough suppressant effects form Nuedexta?

A

DM has to be metabolized to get cough suppression

135
Q

What is the main concern if a patient is on Nuedexta?

A

Drug interactions because quinidine is a POTENT 2D6 inhibitor

136
Q

ADR’s of Nuedexta

A 
QT prolongation
lupus
GI (Most common)
edema
anemia
thrombocytopenia
137
Q

What class of medication is lithium?

A

Mood stabilizer

it is NOT a antidepressant, antipsychotic

138
Q

MOA of lithium

A

Alters neuronal sodium transport (Tricks the body into believing it is sodium)

Both have 1+ charge, so replaces sodium in neuronal firing. But because it is not sodium, it does not complete first part of action potential, hence slows down action potential

139
Q

ADR’s of lithium

A 
Diabetes insipidus, polyuria, polydipsia
Coma, Seizures, Tremors (at toxic levels)
Arrhythmias, syncope
Hypothyroidism
weight gain
N/V/D
Cognitive impairment, fatigue
Skin damage, acne, alopecia
140
Q

What are common complications of long term lithium?

A

Kidney damage, lot of CNS issues

141
Q

Doe lithium have a narrow or wide therapeutic window?

A

Narrow, very prone to being affected by fluid shifts and electrolyte abnormalities (b/c since its similar to Na+, it follows water).

Even more so if they have kidney damage

142
Q

What happens if you give NSAIDS to someone on lithium?

A

pain levels will go up

143
Q

T/F

The more dopamine you have, the more agitated you are

A

True

The less you have, you get more parkinson-like movements

144
Q

Which 2nd gen antipsychotic has anticholinergic effects?

A

Seroquel (Highly sedating)

145
Q

Which 2nd gen antipsychotic has alpha2 blockade?

A

Geodon

This one can cause orthostatic hypotension

146
Q

What is important to know about 1st gen antipsychotics?

A

More sedating, higher risk of EPS/tardative dyskinesia, possible more CV effects

147
Q

EPS, parkinson-like movement and tardative dyskinesia from antipsychotics come from the blockade of _____

A

dopamine

can be permanent

148
Q

what are the metabolic side effects fo antipsychotics

A

hyperglycemia
weight gain
HLD

149
Q

What antipsychotic has the highest risk of QT prolongation?

A

Haldol

geodon and zyprexa (2nd gen’s) have it as well to some degree

150
Q

What is the blackbox warning for all antipsychotics?

A

Dementia-related death

151
Q

T/F

patients who are started on antipsychotics have a higher risk of death

A

True

usually from CVA’s, sometimes from MI’s

152
Q

What are two important things to consider when starting someone on antipsychotics

A

Only start if pt is at risk of harming self or others

Use lowest dose for shortest amount of time

153
Q

Which antipsychotic has risk of agranulocytosis?

A

Clozapine (Clozaril)

dispensed through REMS because of this.

Want to check ANC (Absolute Neutrophil Count) with CBC to monitor for agranulocytosis

154
Q

How many dopaminergic pathways are there in the body?

What are they?

A

4

Mesolimbic
Mesocentric
Nigrostriatal
Tuberohypophyseal

155
Q

Which dopaminergic pathway is associated with hyperprolactinemia?

A

Tuberohypophyseal

will see gynocomastia

156
Q

Which dopaminergic pathway is assoc. with EPD, TD, and parkinson movement when blocked?

A

Nigostriatal

157
Q

Which dopaminergic pathway is assoc. with positive symptoms of schizophrenia and psychosis?

A

Mesolimbic

158
Q

Which dopaminergic pathway is assoc. with negative symptoms?

A

Mesocentric

159
Q

Who should you never administer antipsychotics to?

A

Delirium-associated dementia

only as an absolute last resort

160
Q

What the big difference between antipsychotics and parkinson meds

A

Trying to block dopamine with antipsychotics

Trying to increase dopamine with parkinson meds

161
Q

4 classes of parkinson meds

A

Dopamine analogs
Dopamine agonists
Anticholinergics
MAOB inhibitors

162
Q

What two meds are dopamine analogs?

A

Carbidopa/Levodopa (Sinemet)
Carbidopa/Levodopa/Entacapone (Stalevo)

Levodopa = dopamine precursor
Carbidopa = false dopamine, “suicide inhibitor”
Entacapone (Comtan) = COMT inhibitor

all increase the amount of dopamine

163
Q

ADR and SE’s of dopamine analogs?

A

CNS: Hallucinations, psychosis, MDD, +SI
CV: Hypotension, syncope
Heme: Blood dyscrasias, GIB
GI: N/V, constipation

we get side effects of too much dopamine, so agitation, psychosis, drops in BP

so will see post-op agitation with low BP

164
Q

What meds are dopamine agonists?

A 
Pramipexole (Mirapex)
Ropinirole (Requip) - can get nightmares, insomnia
Rotigotine (Neupro Patch)
Bromocriptine (Parlodel)
Apomorphine (Apokyn)
165
Q

MOA of dopamine agonists

A

simply activate dopamine receptors. Don’t look like dopamine, so can’t be broken by MAO and COMT

used for restless leg syndromes

166
Q

SE’s of dopamine agonists

A

same as dopamine analogs

167
Q

What meds are anticholinergic parkinson meds?

A

Benztropine (Cogentin)

Trihexyphenidyl (Artane)

168
Q

What meds are MAOB inhibitors?

A

Rasaligine (Azilect)

Selegiline (Eldepryl)

169
Q

MOA of MAOB inhibitors?

A

Increase DA availability via enzyme inhibition

170
Q

What med has no dopamine activity and is given specifically for a diagnosis of parkinson’s with psychosis?

A

Nuplazid (Pimavanserin)

171
Q

MOA of Nuplazid (Pimavanserin)

A

Inverse agonist and antagonist at 5HT2A and 5HT2C receptors

172
Q

ADR’s of Nuplazid (Pimavanserin)

A

QT prolongation - risk of torsades

173
Q

What are two non-specific class meds for parkinson’s?

A

Amantadine (Symmetrel)

Nuplazid (Pimavanserin)

174
Q

T/F

There is no risk of withdrawal with alzheimer meds

A

True

175
Q

Type of alzheimer meds

A

Acetylcholinesterase Inhibitors:
Donepezil (Aricept)
Galantamine (Razadyne)
Rivastigmine (Exelon)

NMDA receptor antagonists:
Memantine (Namenda)

176
Q

Side effects acetylcholinesterase inhibitors

A

“rest and digest” SE’s bc there is more ACh floating around to activate the PNS, so…
Bradycardia
Loose stools
Overactive bladder

usually taken at night

177
Q

2 major drug interactions with acetylcholinesterase inhibitors

A

can potentiate succinylcholine and reduce the blockade of NDNMB’s

178
Q

What is the only side effect with Namenda?

A

Dizziness

179
Q

Post-op delirium may be fatal, preventable in up to __% of cases and __% of cases are not reported

A

40%

50% (because they are hypoactive)

180
Q

T/F

Post op delirium may be hypo or hyperactive or mixed presentation

A

True

181
Q

Difference between delirium and dementia

A

Delirium – rapid, acute

Dementia – long term, slow

182
Q

Preferred treatment for prevention/treatment of post-op delirium

A

non-pharmacological

also make sure they aren’t having increased pain bc that can increase neurotransmitters

183
Q

T/F

changes in the depth of anesthesia reduce the risk of post-op delirium

A

FALSE

does not reduce the risk

184
Q

What class of meds absolutely increase the chance of post-op delirium?

A

BZD’s

185
Q

What is the only time BZD’s may be appropriate to treat post-op delirium?

A

If its related to ETOH withdrawal

186
Q

What is important to know about the STRIDE trial?

A

limiting the level of sedation provided no significant benefit in reducing incident delirium.

187
Q

Should antipsychotics be used to treat post-op delirium

A

Only if at risk to harm self or others. Use lowest dose for shortest duration possible

188
Q

Two important things to know about prophylactic haldol from studies

A

Px low dose po haloperidol did not reduce delirium incidence in acutely hospitalized older patients.

Px Haldol does not reduce mortality in critically ill adults at high risk of delirium

189
Q

Which two 2nd gen antipsychotics have a higher risk of QT prolongation?

A

Geodon and Zyprexa

Pharm 2 (19 decks)

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