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Nurs 711 Pharmacology > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

CNS neurotransmitters are?

A

Acetylcholine
Dopamine
Glutamate
GABA

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2
Q

What balance of neurotransmitters are out in Parkinson’s Disease?

A

Too little Dopamine
Too Much acetylcholine

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3
Q

What are the two types of medications for Parkinson’s?

A

Dopaminergic Agents
Anticholinergic agents

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4
Q

Dopaminergic agents are used to?

A

Directly or indirectly activate dopamine receptors

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5
Q

Anticholinergic Agents are used to?

A

Block receptors for acetylcholine

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6
Q

How long does Parkinson’s Disease take to develop?

A

5-7 years

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7
Q

What is Levodopa?

A

A drug used to treat Parkinson’s that is a dopamine replacement

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8
Q

What type of drug is Levodopa?

A

A prodrug that is converted into it’s active form after crossing the BBB

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9
Q

How much of Levodopa reaches the brain?

A

2%

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10
Q

Pharmacokinetics:
What is important about the administration of Levodopa?

A

It has a very short half life and food delays absorption especially meals high in protein

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11
Q

Which drug exhibits the “loss of effect” and what is it?

A

Levodopa, and the “loss of effect” is like a wearing off->As dose wears off symptoms appear

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12
Q

What are the adverse effects of Levodopa?

A

N/V (Significant)
Darkening of sweat and urine
Involuntary movement (Dyskinesis)
Orthostatic Hypotension/dysrythmias
Psychosis
Drug interations

I Never Did Open Dad’s Present.

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13
Q

What are the drug interactions of Levodopa?

A

Bad: Medications that block dopamine such as 1st gen Parkinson’s drugs
Good: Anticholinergics block acetylcholine

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14
Q

What should a patient taking Levodopa report to the nurse?

A

Report:
“loss of effect”
“New Tremors/twitching”
Palpitations/Racing heart
Hallucinations/paranoia

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15
Q

Which drug acts as an assistant to Levodopa, helping as much as possible reach the brain, and is only available in a combo pill?

A

carbidopa/levodopa (sinemet)

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16
Q

What is the MOA of carbidopa/levodopa?

A

Prevents decarboxylase action, allowing us to give a lower dose of levodopa

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17
Q

What is Entacapone?

A

A drug with no therapeutic effect on it’s own, but works like railroad crossing arm and extends the half life of levodopa

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18
Q

What is the MOA of Entacapone?

A

Inhibits COMT enzyme from breaking down levodopa (catechol-O-methyltransferase)

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19
Q

Which drug works directly to activate dopamine receptors in brain?

A

Pramipexole

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20
Q

Which drug for Parkinson’s is often used in as the first line in the early stages?

A

Pramipexole

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21
Q

What are the adverse effects of Pramipexole?

A

Sleep Attacks
Impulse control disorders/compulsive behaviors

*The adverse effets are produced by receptor activation

Pramipexole: nausea, dizziness, weakness, sleep changes (Sleepyness in daytime and insomnia at night)

Pramipexole + Levodopa/carbidopa: Orthostatic hypotension, dyskinesias, hallucinations

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22
Q

What is Pramipexole added to after first line treatment is tried?

A

Levodopa/carbidopa

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23
Q

What are the nursing considerations for Pramipexole?

A

It is ok to take with meals
Rise slowly from supine to sitting
Report sleep attacks
Report impulse control concerns

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24
Q

Which neurotransmitters have low levels in Alzheimer’s Disease?

A

Acetylcholine

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25
Q

What are the two major drug classes to treat Alzheimer’s Disease?

A

Cholinesterase inhibitors
NMDA antagonists

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26
Q

What is the MOA of Donepezil?

A

Prevents the breakdown of acetylcholine by the acetylcholinesterase enzyme in the CNS

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27
Q

What are the benefits of Donepezil?

A

Improved QOL
Memory
Reasoning

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28
Q

Donepezil ___________ __________ delay disease progression.

A

Donepezil does not delay disease progression.

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29
Q

What are the pharmacokinetics of Donepezil?

A

Available as ODT
96% protein bound
Long half life

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30
Q

What are the adverse effects of Donepezil?

A

The high acetylcholine causes cholinergic effects-> SLUDGE

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31
Q

What is the MOA of Rivastigmine?

A

Prevents the breakdown of acetylcholine by the acetylcholinesterase enzyme in the CNS

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32
Q

What are the benefits of Rivastigmine?

A

Improved QOL
Memory
Reasoning

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33
Q

What is the administration method for Rivastigmine?

A

Available as a transdermal patch

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34
Q

What are the adverse effects of rivastigmine?

A

Acetylcholinergic effects (SLUDGE)
Bradycardia -> Fainting, Falls

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35
Q

What is the MOA of Memantine?

A

Blocks NMDA receptors and prevents excessive calcium accumulation in the neurons

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36
Q

What are the benefits of Memantine?

A

Slows decline
May improve symptoms

*** Does not modify the disease process

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37
Q

What drug combined with Memantine has a potentiated effect?

A

Donepezil + memantine

(Pts score better on cognitive function tests)

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38
Q

What is multiple sclerosis?

A

MS is a chronic, progressive, inflammatory, autoimmune disorder affecting the myelin sheath of the neurons on the spinal cord

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39
Q

Immunomodulators are indicated for?

A

All patients with relapsing-remitting subtype, and not just for MS

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40
Q

Immunomodulators can reduce the relapse rate of MS by?

A

Around 30%

*It only slows down the disease process, but is not a cure

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41
Q

What is one of the negatives to MS immunomodulators?

A

They are very expensive

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42
Q

What drug was the prototype for the immunomodulators?

A

Inferon Beta

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43
Q

What are the pharmacokinetics of Interferon Beta?

A

Slows inflammation of CNS myelin.
It is a syntheic form of an endogenously produced glycoprotein that supplements what the body is already doing.

Administered parenterally (SQ or IM)
Dosing interval varies depending on drug

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44
Q

What are the adverse effects of interferon beta?

A

Flu like symptoms (common)
Hepatotoxcitity
Bone Marrow suppression (Low RBC, WBC, Hb, Platelets)
Injection site problems
Headache

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45
Q

What type of drug for MS is less preferred than immunomodulators but has a stronger effect?

A

Immunosuppressants
-has stronger immunosuppression
-more toxic
-Effective against all subtypes of MS

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46
Q

When would immunosuppressants be used?

A

In patients that don’t respond to immunomodulators

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47
Q

What are the pharmacokinetics of Mitoxantrone?

A

Supresses production of immune cells
IV infusion every 3 months

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48
Q

What are the adverse effects of Mitoxantrone?

A

Hepatotoxicity
Bone Marrow Supression
Cardiotoxicity (looks like HF)
Teratogenic

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49
Q

What is something a patient taking Mitoxantrone should look out for?

A

Edema, pink frothy sputum, cough

can be signs of cardiotoxicity (looks like heart failure)

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50
Q

What is the treatment of acute MS Flares?

A

High-dose IV steroids for 3-5 days
This quickly reduces acute inflammation (rapid improvement in patient when pharmacological levels)

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51
Q

What is the treatment of acute MS Flares?

A

High-dose IV steroids for 3-5 days
This quickly reduces acute inflammation (rapid improvement in patient when pharmacological levels)

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52
Q

What are the 4 ways AEDs Work?

A

1)Suspression of sodium influx in cell membranes (Decreases ability of neurons to fire at high frequency)

2) Suppressionn of calcium influx in axon terminals (blocks channels to suppress transmission)

3) Antagonism of glutamate (A neurotransmitter)

4) Potentiation of GABA (a neurotransmitter)

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53
Q

What is the goal of antiepileptic drugs (AEDs)?

A

The goal is to decrease focal epileptic activity and prevent spread to other areas of the brain

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54
Q

What is one very important aspect about AED drugs for acheiving therapeutic response?

A

Adherence is very important for achieving therapeutic response because if they miss a dose they have a seizure

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55
Q

What are the 3 traditional Antieptileptic drugs?

A

Phenytoin
Phenobarbital
Valproic Acid

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56
Q

What is the newest epileptic drug?

A

Oxcarbazepine

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57
Q

What are the positives and negatives of the traditional AEDs?

A

Less expensive
Teratogenic
More interactions
More adverse effects

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58
Q

What are the positives and negatives of the newer AEDs?

A

More expensive $$$
Safer in pregnancy
Less Interactions
Less adverse effects

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59
Q

What is the MOA of Phenytoin?

A

Inhibits the sodium channels of hyperactive neurons

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60
Q

What are the Pharmacokinetics of Phenytoin?

A

NTI Drug- therapeutic levels are 10-20 mcg/mL

Highly Protein bound

Hepatotoxic

Half life dose dependent (8-60hr)

CYP enzyme inducer

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61
Q

What is the most widely used and first line medication for seizures?

A

Phenytoin

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62
Q

What are the Adverse effects of phenytoin?

A

CNS effects due to NTI levels
10-20: Mild headache, drowsiness, irratability

> 20: Nystagmus (eye jumping), sedation, ataxia, diplopia (double vision, cognitive impairment

Gingival hyperplasia

Rash (resembling measles)

Teratogenic (2 forms birth control)

Lots of drug interactions

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63
Q

What is the MOA of Valproic Acid?

A

Blocks Na and Ca Channels, may potentiate GABA

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64
Q

Which traditional AED drug in addition for use in seizure disorders is used for bipolar and migranes?

A

Valproic Acid

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65
Q

What are the adverse effects of Valproic Acid?

A

GI effects common

Rare hepatotoxicity

SERIOUS teratogen

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66
Q

What is the MOA of Phenobarbital?

A

Enhances and mimics the effets of GABA

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67
Q

What are the adverse effects of Phenobarbital?

A

Since it’s a barbituate and has sedation type effects, it has many adverse effects such as decrease in locus of control and effects respiration

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68
Q

What is the MOA of Oxcarbazepine?

A

MOA: Blocks overactive sodium channels

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69
Q

What is the MOA of Oxcarbazepine?

A

MOA: Blocks overactive sodium channels

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70
Q

What is a benefit of Oxcarbazepine, a newer AED prototype that gives it an advantage over Phenytoin?

A

No drug level monitoring is required for oxcarbazepine

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71
Q

What are the adverse effects of oxcarbazepine?

A

CNS (dizziness, drowsiness, double vision, nystagmus, headache, ataxia)

Hyponatremia (rare)

Serious skin reactions (SJS, toxic epidermal necrolysis)

Teratogentic

Lots of drug interactions

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72
Q

While oxcarbazepine is teratogenic, it can be given in pregnancy because the risk of seizures can be worse. What is the nursing education related to this?

A

The drug can cause low birth weights and women should be taking folic acid when taking the drug.

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73
Q

What is status epilepticus?

A

An extended period of continuous seizure activity that is often more than 20 minutes and is considered a medical emergency

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74
Q

What is the treatment in status epilepticus?

A

The goal is to intervene in the first 5 minutes to avoid permanent neurological damage and the treatment is to secure the airway, give IV benzodiazepine and follow up with antiepileptics

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75
Q

What is a spasm?

A

Involuntary contraction of a muscle or muscle group that limits function temporarily and can be painful

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76
Q

What is spasticity?

A

Prolonged muscle tightness or contraction, characteristic finding in movement disorders of CNS origin

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77
Q

What can cause muscle spasms?

A

Epilepsy
Hypocalcemia
Chronic Pain syndrome
Localized muscle injury

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78
Q

What can occur due to muscle spasticity?

A

Increased muscle tone, spasms, decreased fine motor control/dexterity usually also hyperactive DTRs

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79
Q

What can cause muscle spasticity?

A

Multiple sclerosis
cerebral palsy
stroke
traumatic spinal cord lesions

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80
Q

What is Cyclobenzaprine used for and which class of medications does it belong to?

A

Used for Spasm

Centrally acting muscle relaxers

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81
Q

What is Baclofen used for and which class of medications does it belong to?

A

Spasticity

Centrally acting muscle relaxers

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82
Q

What is Dantrolene used for and which class of medications does it belong to?

A

Spasticity

Direct Acting muscle relaxers

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83
Q

What is Diazepam used for and which class of medications does it belong to?

A

Spasticity

Benzodiazpine

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84
Q

Treatment of muscle spasms:
What medications are used?

A

Acetaminophen
Ibuprofen
Cyclobenzaprine

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85
Q

Treatment of muscle spasms:
Which types if Physical Therapy are used?

A

Stretching

Flexibility

Tens

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86
Q

Treatment of muscle spasms:
What type of heat therapy can be used?

A

Heating pad

Whirpool/warm bath

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87
Q

What are the therapeutic uses for cyclobenzaprine?

A

Relief of pain from acute muscle spasm to increase ROM

Not effective to treat spasticity

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88
Q

What are the adverse effects of cyclobenzaprine?

A

CNS effects (drowsiness, dizziness, sedation)
Anticholinergic effects (anti-sludge)

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89
Q

What are the interactions of cyclobenzaprine?

A

Alcohol and other CNS depressants (Additive effect ->increased drowsiness)
Antidepressants (risk for serotonin syndrome)

Tolerance and Dependence can develop

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90
Q

What drug is used to treat spasticity, and is a CNS drug that acts on the spinal cord to supress hyperactive reflexes?

A

Baclofen

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91
Q

What two drugs for spasticity must not be given together?
What is the adverse effect of both of these drugs?

A

Baclofen and Diazepam (Valium)

Both have sedation has an adverse effect

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92
Q

Where does the drug Dantrolene act?

A

Directly on skeletal muscle

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93
Q

Pharmacokinetics:
What is special about the routes of administration of Dantrolene?

A

The PO dosing is used for spasticity
The IV dosing is used for malignant hyperthermia

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94
Q

What is the adverse effect of Dentrolene?

A

Dose related heptaotoxicity

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95
Q

Which type of medications act by increasing the activity of CNS neurons and are used in ADHD and narcolepsy?

A

Stimulants such as:
Amphetamine
Methylphenidate
Methyxanthine

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96
Q

How do stimulants increase the activity of CNS neurons?

A

Some enhance neuronal excitation
Some suppress neuronal inhibition

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97
Q

What is the MOA of Amphetamine and Methylphenidate?

A

They release norepinephrine and dopamine and inhibit reuptake of both in the CNS and peripheral nervous system

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98
Q

What are the therapeutic effects of Amphetamine and Methylphenidate?

A

Increased alertness
Increased initiative
Reduced fatigue
Elevated mood

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99
Q

What are the adverse effects of Amphetamine and Methylphenidate?

A

Tolerance develops to mood elevation, appetite suppression and CV effects
High dependence and abuse potiential

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100
Q

What are the pharmacokinetics of Amphetamine and Methylphenidate?

A

Available PO in both short and long duration forms

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101
Q

What are the adverse effects of Amphetamine and Methylphenidate?

Which ones are common?

A

Common:
(insomnia)Excess CNS stimulation
(weight loss)Reduced Appetite
(HTN)Vasoconstriction
(dysrhythmias, angina) Cardiac excitation
Psychosis (with excess use)
Overdose can cause seizures/coma/death`

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102
Q

What is the MOA of Methylxanthine (caffeine)?

A

Blockade of adenosine receptors appears responsible for most effects

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103
Q

What are the therapeutic effects of Methyxanthine?

A

Decreased drowsiness
Decreased fatigue
Increased intellectual exertion
Headache relief (vasoconstriction)
Mild diuretic

When I drink alot of caffeine, I am not as tired and can focus on work. It also helps my headache go away but it does make me have to pee.

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104
Q

What are the adverse effects of Methyxanthine?

A

Nervousness
Insomnia
Convulsions (extreme doses)

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105
Q

What are some of the factors that can lead to drug abuse?

A

Reinforced qualities of the drug
Physical dependence
Psychological dependence
Social factors
Availability
Individual vulnerability

Quality Purple Pheasants All Indivually Sing

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106
Q

Knowledge of drug abuse enables nurses to?

A

Recognize abuse and toxicity
Participate in treatment and withdrawal
Educate patients who are struggling with addiction and recovery

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107
Q

What is the APA’s definition of substance use disorder?

A

A cluster of cognitive, behavorial and physiological symptoms indicating that the individual continues using the substance despite significant substance-related problems

***Important note: Their definition has no connection to physical dependence

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108
Q

The is the goal of the treatment of substance use disorder?

A

Goal is complete cessation with 40-60% reduce drug use

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109
Q

What is the definition of addiction?

A

A chronic, relapsing disease process (chronic brain disease) characterized by the continued use of a specific psychoactive substance despite the physical, psychological or social harm

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110
Q

What is tolerance?

A

Smaller and smaller responses from the same drug

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111
Q

What is cross tolerance?

A

Tolerance to one drug confers tolerance to another

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112
Q

What is psychological dependence?

A

An intense subjective need for another psychoactive drug

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113
Q

What is cross-dependence?

A

One drug dependence on another drug

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114
Q

What are the two main CNS effects of Alcohol (EtOH)?

A

GABA receptor activation
Glutamate inhibition

(Both these contribute to widespread CNS depression)

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115
Q

The effects of alcohol are?

A

Dose dependent->As concentration increases, “deeper” levels of the brain are effected

In high doses it can give a state of general anesthesia

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116
Q

What is the controlled substances act?

A

Federal legislation that categorized potentially addictive substances into five categories: Schedule I-V

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117
Q

Stage I drugs are?

A

Drugs that have the highest abuse potential and have no medical use

Heroin, LSD, and marjuana are all examples of stage I drugs

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118
Q

Stage II drugs are?

A

Drugs that require a typed or inked and signed prescription for a single RX no refills

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119
Q

Stage III & IV drugs are?

A

Drugs that can be prescribed by an oral, written or electronic prescription and have up to 5 refills

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120
Q

Stage V drugs are?

A

Drugs not requiring a prescription that can be dispensed by a PharmD with a record of tx
Must be 18 y/o

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121
Q

What are the Pharmacokinetics of Alcohol?

A

Absorption: 20% absorbed in stomach, 80% in large intestine

Distribution: Crosses BBB and placenta

Hepatic ‘constant’ metabolism

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122
Q

What does a constant rate of metabolism mean in regards to EtOH?

A

Alcohol is metabolized at a rate of 1 drink per hour

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123
Q

What are the adverse effects of Alcohol?

A

Encephalapothy
Cutaneous vasodilation
Elevation of BP
Respiratory Depression
Liver damage (Fatty liver->hepatitis->cirrhosis)
Erosive gastritis (heartburn)
Diuresis
Pancreatitis
Sexual Function
Cancer
Teratogen

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124
Q

What are the drug interactions with alcohol?

A

Other CNS depressants (due to sedation)
NSAIDs (stomach ulcers)
Acetaminophen (Liver toxicity)
Disulfiram (purposeful interaction to quit drinking)

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125
Q

What are the drugs used to treat alcohol abuse?

A

When facilitating withdrawal:
Benzodiazepines
Beta Blockers
Clonidine (off label use, lowers BP)
Antiepileptics (due to seizure risk)

To maintain abstinence:
Disulfiram

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126
Q

Chronic alcohol use builds significant tolerance, but not?

A

A tolerance to respiratory depression

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127
Q

What are the symptoms of alcohol withdrawl syndrome?

A

GI distress
SNS over-activiation
Hallucinations
Tonic-clonic seizures
Disorientation
Delirium
Tremors (Rare-vivid hallucinations)

Great Snakes Have ToxiC Terrible Domination

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128
Q

How long do symptoms of Alcohol withdrawl syndrome last?

A

12-72 hours up to one week

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129
Q

What is the MOA of Disulfiram?

A

Irreversibly inhibits aldehyde dehydrogenase causing acetaldehyde accumulation from ETOH ingestion

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130
Q

What is acetaldehyde syndrome?

A

ETOH + Disulfiram

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131
Q

What are the symptoms of acetaldehyde syndrome?

A

Vomiting, flushing, headache, sweating, blurred vision, hypotension

*If severe, can be life threatening

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132
Q

What are patient education points for Disulfiram (Antabuse) precautions?

A

Consuming ANY alcohol can cause a reaction
Only 7mL ETOH required
Includes transdermal absorption
Effects last two weeks past last dose

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133
Q

What is the MOA of Nicotine?

A

At low doses, activates nicotine receptors in the reward center which stimulate dopamine release

-the delivery system of inhalation through smoking is particularly addictive

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134
Q

What are the adverse effects of nicotine?

A

Cardiovascular stimulation
Nausea
Appetite suppression
Fetal Harm

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135
Q

What are the long-term increased risk of nicotine?

A

There is a long term increased risk of CV, several cancers, and COPD

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136
Q

How many people are killed from second hand smoke per year?

A

41,000

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137
Q

What are public health measures to decrease smoking?

A

Gradual changes in regulation of cigarette sales, advertising, and smoking ordinances and the public health measures

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138
Q

What are the nicotine replacement therapies?

A

Gum or lozenges
Patches
Nasal Spray
Inhaler

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139
Q

What type of nicotine replacement is not approved through the FDA?

A

e-cigarettes

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140
Q

What is the nicotine content in nicotine patches?

A

24% nicotine concetrations

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141
Q

What is the education for nicotine gum or lozenges?

A

No eating or drinking for 15 minutes

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142
Q

What is the education for nicotine patches?

A

Since they are steady release, you put on in the AM and take off in PM

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143
Q

What are the side effects of bupropion SR?

A

Dry mouth, insomnia, decreased appetite

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144
Q

In what demographic can wellbutrin/buproprion not be used?

A

In patients with risk of seizures, because wellbutrin can cause seizures due to CNS activity

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145
Q

What is Varenicline (Chantix)?

A

The most effective aid for smoking cessation-reduced cravings and intensity of symptoms with a 33% abstinence rate

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146
Q

What is the method of action of Varenicline?

A

A partial nicotinic receptor agonist, so it prevents most of the nicotine from binding

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147
Q

What is the MOA of methamphetamine?

A

Increases levels of norepinephrine and dopamine in the CNS

148
Q

What are the effects of methamphetamine?

A

Methamphetamine causes
arousal
improved mood
euphoria
decreased pain perception
decreased appetite and need for sleep

149
Q

What are the administration methods for methamphetamine?

A

Can be snorted, injected or smoked

150
Q

What are the adverse effects of methamphetamine?

A

Psychosis (delusions, paranoia, hallucinations)
Cardiac stimulation and vasoconstriction (HTN, angina, dsyrhythmias)
Weight loss (appetite suppression)
Tooth Decay
Pregnancy complications

151
Q

What types of household products can methamphetamine be produced from?

A

Drain cleaners
Acetone
Batteries
Many others

152
Q

What does the activation of the opiod receptor Mu do?

A

The activation of Mu causes
analgesia (pain relief)
respiratory depression
euphoria
sedation
decreased GI motility
eventual physical dependence

153
Q

What does the activation of the opioid receptor Kappa do?

A

The activation of Kappa causes analgesia, sedation and decrease GI motility but will not end up with physical dependence

154
Q

What does the activation of the opioid receptor Delta do?

A

The activation of delta has no effect

155
Q

What is an opioid?

A

Opioids

156
Q

Endogenous opioid peptides are?

A

Made by the body and found in the central nervous system and in the peripheral tissues and serve as neurotransmitters, neurohormones, and neuromodulators

157
Q

What are opioid pure agonists?

A

Agonists for Mu and Kappa receptors (these are divided into strong and mod-strong)

Morphine
Codeine
Meperidine (Demerol)

158
Q

What are opioid agonist-antagonists?

A

Antagonists for Mu
Agonist for Kappa Receptors
Pentazocine (Talwin)
Nalbuphine (Nubain)

159
Q

An agonist for Kappa receptor is considered a ___________________________ than an agonist for Mu.

A

Lower abuse risk

160
Q

What are the opioid pure antagonists?

A

Antagonists for Mu and Kappa
Naloxone (Narcan)
Naltrexone

Think overdose drugs

161
Q

Name the Drug Class:
Common drugs in the class include morphine, hydromorphone, fentanyl, merperidine (demerol), heroin, methadone.

A

Morphine

162
Q

What is the MOA of morphine?

A

Morphine mimics the endogenous opioids and activate mu and kappa receptors.

It is a STRONG opioid agonist

163
Q

What are the clinical used for morphine?

A

Relief of moderate to severe pain (post operative, cancer-related, labor/delivery, MIs)

164
Q

What are the absorption/distribution pharmacokinetics of morphine?

A

Can be given practically any route, onset and duration differ

Small amount crosses BBB

Scheduled is usually best, amount depends on pain severity

165
Q

What are the metabolism pharmacokinetics of morphine?

A

Affected by the first pass effect
Liver inactivation
Short half life

166
Q

What are the adverse effects of morphine?

A

-Respiratory depression (varies with route and is most serious)
-Constipation (common)
-Orthostatic hypotension
-Urinary retention
-Nausea/vomiting
-Cough suppression
-Toxicity

167
Q

What are the signs of a morphine toxicity?

A

Coma
Respiratory depression (2-4 breaths per min)
Pinpoint pupils (due to hypoxia)

168
Q

What drug interactions does morphine have?

A

CNS depressants (EtOH)
Anticholinergics
Antihypertensives
Agonist-Antagonists
Antagoinist (Narcan)

169
Q

What factors influence the withdrawl syndrome of morphine?

A

The intensity and duration of withdrawl depend on the T1/2 and degree of dependence on the drug

170
Q

How long is the intense withdrawl period of morphine?

A

7-10 Days

171
Q

What are the symptoms of morphine withdrawl?

A

Initial reactions include: yawning, rhinorrhea, and sweating
Following symptoms include:
Anorexia, irritability, tremor, gooseflesh, violent sneezing, N/V/D, abdominal cramping, muscle and bone pain, kicking movement

172
Q

Which drug is a strong opioid agonist that is around 100x more potent than morphine?

A

Fentanyl (Duragesic)

173
Q

What are the uses for Fentanyl?

A

Parenteral administration: Induction and maitenance of anesthesia

Transdermal administration: Post-operative pain and chronic pain*

*usually used for persistent and sever pain in patients who are opioid tolerant

174
Q

What is the metabolism of Fentanyl?

A

Hepatic metabolism by CYP3A4

175
Q

What are the adverse effects of Fentanyl?

A

The same as morphine

176
Q

What are the strong opioid agonists?

A

Morphine
Fentanyl

177
Q

What are the moderate-strong opioid agonists?

A

Codeine
Oxycodone
Hydrocodone

178
Q

What is the MOA of the moderate-strong opioid agonists?

A

The same MOA as the strong opioid agonists which is mimicing the endogenous opioids and activate mu and kappa receptors.

179
Q

What is the main differences between the strong opioid agonists and the moderate-strong opioid agonists?

A

The moderate-strong opioid agonists are less effective and they have a little less abuse potential

180
Q

What are the uses for Codeine?

A

Relief of pain, often co-formulated with acetominophen
Also used as a cough suppressant

181
Q

What are the administration pharmacokinetics of codeine?

A

PO is the most common method

182
Q

What are the metabolism pharmacokinetics of Codeine?

A

CYP2D6 enzymes metabolize codeine in the liver, and turns around 10% of codeine into morphine (likely how it produces anesthesia

Similar to prodrug

183
Q

How do CYP2D6 enzymes effect codeine?

A

The genetic differences in the enzyme affect analgesia from codeine

184
Q

What are the adverse effects of codeine?

A

Similar to morphine, increasing with higher dosages
Higher dosages required for significant pain relief, which can have dangerous side effects

185
Q

What receptor effect do Agonist-Antagonist opioids effect?

A

Activate kappa receptors, block mu receptors

186
Q

What are the benefits of the Agonist-Antagonist opioids?

A

Provide analgesia without as many side effects as pure agonists and have less potential for abuse

187
Q

If a Agonist-Antagonist opioid is used to replace a long-term opioid agonist it could?

A

Cause withdrawl symptoms due to the blocking of Mu

188
Q

What type of drug is Pentazocine (Talwin)?

A

A Agonist-Antagonist

189
Q

What is the MOA of Pentazocine?

A

Activates Kappa receptors causing analgesia, sedation, and limited respiratory depression

190
Q

What are the absorption pharmacokinetics of Pentazocine?

A

PO administration

191
Q

What are the metabolism pharmacokinetics of Pentazocine?

A

Short T 1/2 life; therefore frequent dosing is needed

(Around every 3-4 hours)

192
Q

What are the adverse effects of Pentazocine?

A

-Similar to morphine but less respiratory depression
-Increases cardiac workload***
-Physical dependence can develop but withdrawl is mild in comparison

**This is NOT a good choice for pain related to myocardial infarction

193
Q

What are the 3 post-op pain management dosing options?

A

PCA (kind of like a basal rate w/option to administer more)

Fixed Schedule

PRN

194
Q

What type of drug is Naloxone?

A

Known as the brand name Narcan, it is an opioid antagonist and is used to block the opioid receptora to reverse opioid overdose

195
Q

What are the administration pharmacokinetics of Naloxone?

A

Given parenterally or intranasally (Longer effects when given IM/SC)

196
Q

What are the metabolism pharmacokinetics of Naloxone?

A

Hepatic metabolism
T 1/2 around 2 hours

197
Q

What are the adverse effects of Naloxone?

A

None on its own, however if pt is dependent on opioids they can have immediate/severe withdrawl problems

198
Q

What occured involving the drug Naloxone and the FDA in 2023?

A

The FDA approved intranasal OTC availability

199
Q

What is the nurse’s role in the opioid epidemic?

A

Minimize physical dependence and abuse
-Assessing pain and administering dose sufficient for relief
-Administer lowest effective dose for shortest time needed
-Reduce dosing as pain decreases
-Advocate for pt to be switched to a nonopioid analgesic asap

200
Q

What are the 3 severe forms of headache?

A

Tension-type
Cluster
Migraine

201
Q

Cluster headaches are less common in what demographic?

A

Males (5:1)

202
Q

What are the symptoms of cluster headaches?

A

Normally occuring in a series of cluster attacks that last 15min-2 hrs they involve:
Unilateral pain near eye
Lacrimation
Ptosis (Droopy eye)
Nasal congestion
Rhinorrhea

203
Q

What are the abortive treatment for cluster headaches?

A

Oxygen
Sumatriptan

204
Q

What are the preventative methods for treatment of cluster headaches?

A

Betamethasone (Steriod)
Verapamil (CCB)
Lithium

205
Q

What is the most common type of severe headache?

A

Tension-type headache

206
Q

What are the symptoms of tension-type headaches?

A

“Headband” non-throbbing pain, tightness in head and neck

207
Q

What are the abortive medication for tension-type headaches?

A

Ibuprofen
Naproxen
Aspirin
Butalbital

208
Q

What are the preventative measures for tension-type headaches?

A

Coping & Relaxation skills
Amitriptyline

209
Q

What are the symptoms of a migraine headache?

A

A throbbing, moderate-severe pain that may be unilateral or bilateral that may last for days

Associated with nausea/vomiting, photo/phonophobia

210
Q

What are the visual symptoms that can accompany around 30% of migraines?

A

No aura (more common)

211
Q

Which demographic is more likely to experience migranes?

A

Females

212
Q

What is the pathology of migraine headaches?

A

Migraines are due to a neurovascular problem that involves vasodilation and inflammation of the cranial blood vessels

213
Q

What are some of the neurochemicals involved in migraines?

A

Calcitonin gene-related peptide-CGRP is a possible cause of migraines

Serotonin/5-HT suppresses migranes

214
Q

What are the drugs that is an abortive therapy for both migraines and cluster headaches?

A

Ergot Alkaloids
Triptans

215
Q

What is the MOA of Ergot Alkaloids?

A

Activation of serotonin receptors
Blockage of cranial inflammation
Cranial vasoconstriction

216
Q

What are the pharmacokinetics of administration for ergot alkaloids?

A

PO
SL
PR*
Inhalation*

*Best method for administration

217
Q

What are the pharmacokinetics of metabolism for the erogt alkaloids?

A

Metabolized by CYP3A4
T 1/2 of 2 hours

218
Q

What are the adverse effects of the ergot alkaloids?

A

Rare at therapeutic doses
Possible N/V
Risk of dependence

219
Q

What are the drug interactions for the ergot alkaloids?

A

Triptans cause vasospastic reactions (wait 24 hours)
CYP3A4 inhibitors raise to dangerous levels to cause vasospasm

220
Q

What are Triptans?

A

Serotonin 1B/1D receptor agonists that are used to treat migraines and cluster headaches

221
Q

What is the MOA of Triptans?

A

Bind to and activate specific subtypes of serotonin receptors in the brain causing vasoconstriction

222
Q

What are the administration pharmacokinetics of Triptans?

A

PO
SQ
Inhalation

223
Q

What are the metabolism pharmacokinetics of Triptans?

A

Hepatic metabolism
T 1/2 of 2.5 hrs

224
Q

What are the adverse effects of Triptans?

A

50% of pts experience chest “heaviness” but it is not angina

Coronary vasospasm*

Teratogen

*Should not be given to patients with heart problems

225
Q

What are the drug interactions with Triptans?

A

Ergot Alkaloids (cause Vasospasm, wait 24 hours)
SSRI/SNRI cause excessive serotonin syndrome

226
Q

What is one of the barriers to migraine prevention?

A

Patients tend to not like the daily dosing

227
Q

What are the 3 common options for preventative migraine therapy?

A

Beta Blockers-Propanolol

Antiepileptics

Tricyclic Antidepressants-Amitriptyline

228
Q

What are the adverse effects of giving Beta blockers as migraine prevention?

A

May cause tiredness or exacerbate asthma

229
Q

What are the adverse effects of antiepileptics such as topiramate for migraine prevention?

A

May cause fatigue and cognitive dysfunction

“Pts say they ‘feel stupid’”

230
Q

What are the adverse effects of Tricyclic antidepressants for migraine prevention?

A

May cause hypotension and anticholinergic effects

231
Q

Cox 1 is considered the _____________ receptor, while Cox 2 is considered the ________________ receptor.

A

Cox 1 is considered the good receptor while Cox 2 is considered the bad receptor.

232
Q

How do the Cox receptors work?

A

The Cyclooxygenase enzyme regulates multiple processes using prostaglandins

233
Q

COX Receptors:
What is the effect in the stomach?

A

Cox 1 protects the gastric mucosa

234
Q

COX Receptors:
What is the effect on platelets?

A

Cox 1 stimulates aggregation

235
Q

COX Receptors:
What is the effect on the Uterus?

A

Cox 1 causes contractions at term

236
Q

COX Receptors:
What is the effect on the kidney?

A

Cox 1 & 2 maintain renal blood flow

237
Q

COX Receptors:
What is the role in tissue injury?

A

Cox 2 promotes inflammation and pain

238
Q

COX Receptors:
What is the role in the vessels?

A

Cox 2 causes vasodilation

239
Q

COX Receptors:
What is the role in the brain?

A

Cox 2 mediates fever and perception of pain

240
Q

COX Receptors:
What is the role in the colon?

A

Cox 2 promotes colorectal cancer

241
Q

What is the first generation NSAID that is still used today?

A

Aspirin

242
Q

What are the uses of aspirin?

A

Reduction of pain, fever, inflammation

243
Q

What is the MOA of Aspirin?

A

Irreversibly inhibits COX-1 and COX-2
Desired effects from COX-2 inhibition
Adverse effects from COX-1 Inhibition

244
Q

What are the pharmacokinetics of administration of aspirin?

A

PO: plain, buffered, enteric-coated

245
Q

What are the pharmacokinetics of metabolism of aspirin?

A

Short T 1/2 and is quickly converted to salicylic acid an active metabolite

T 1/2 is concentration dependent

Excreted by the kidneys, dependent on pH

246
Q

What are the pharmacokinetics of distribution of aspirin?

A

Salicylic Acid is highly bound to albumin and crosses all membranes easily

247
Q

NSAIDs are excreted through the ________________ not the _____________.

A

Kidneys not the liver

248
Q

What are the adverse effects of aspirin?

A

GI distress, bleeding, ulcers
General bleeding
Renal impairment
Salicylism syndrome
Hypersensitivity

249
Q

What demographics is aspirin contraindicated in?

A

Children (Reye’s Syndrome)
Pregnant Women
Pts. with peptic ulcer disease, bleeding disorders, ASA/NSAID hypersensitivity

250
Q

What are the drug interactions with aspirin?

A

Other anticoagulants such as warfarin
Alcohol (will erode gastric mucosa)
Other NSAIDS (Antiplatelet effect)

251
Q

What is Salicylism Syndrome?

A

Develops as ASA levels climb above therapeutic range Symptoms are:
Tinnitus
Sweating
Headache
Dizziness

252
Q

How is Salicylism syndrome treated?

A

Witholding aspirin until s/s resolve, then reducing dose

In acute poisoning:
Treatment is supportive

253
Q

What are the signs and symptoms of acute aspirin poisoning?

A

Pt. will enter into respiratory alkalosis, which will lead to respiratory depression, acidosis, hyperthermia, sweating, dehydration, stupor, coma

Death can occur due to respiratory failure

254
Q

What is the MOA of Ibuprofen?

A

Reversible inhibition of COX-1 and COX-2

255
Q

What are the uses of ibuprofen?

A

The same as aspirin except:
Does not prevent MIs/CVAs
May increase the risk of CV events

Good choice for dysmenorrhea (period cramping) because it is selective for COX in the uterine muscle

256
Q

What are the benefits and risks of ibuprofen?

A

Benefits: Less gastric bleeding than aspirin
Negatives: Risk of renal impairment

257
Q

What is the MOA of Naproxen?

A

Fairly selective for COX-1

258
Q

What is the benefits of naproxen?

A

Less incidence of GI problems and MI/CVA than other non-ASA NSAIDs

Long half life so less dosing

259
Q

What is the pharmacokinetic metabolism of naproxen?

A

T 1/2 of 12-17 hours

260
Q

What is the MOA of Celecoxib?

A

Inhibits COX-2 only

261
Q

What are the uses for Celecoxib?

A

Arthritis
Acute Pain
Dysmenorrhea

262
Q

What are the benefits and risks of Celecoxib?

A

Less GI problems that 1st gen NSAIDS
Increased risk of MI/SVA
Can impair kidneys
Contraindicated for patients with heart disease

263
Q

What are the uses for Acetaminophen?

A

Analgesia
Antipyretic
No-anti inflammatory effects
Preferred for children

264
Q

What is the MOA of Acetaminophen?

A

COX inhibition, but thought to be limited to the CNS

265
Q

What are the pharmacokinetics of Administration?

A

PO
Regular Strength
Extra Strength
PR
IV

266
Q

What are the pharmacokinetics of the metabolism of acetominophen?

A

Metabolized in the liver via 2 pathways:
Major pathway-Simple, acetaminophen converted directly into nontoxic metabolites

Minor-CYP450 converts acetaminophen to a toxic metabolite, then glutathione is required to then convert the toxic metabolite to a non-toxic metabolite

267
Q

What is the 24 hour max for acetaminophen in adults?

A

4 grams

268
Q

Regular _____________ reduces the liver’s ability to metabolize excessive doses of acetaminophen.

A

alcohol consumption

269
Q

Why is alcohol contraindicated with acetaminophen?

A

Alcohol:
-induces CYP450
-depletes glutathione
-causes general liver damage

270
Q

What is alcohol recommendation when a pt cannot abstain from alcohol consumption?

A

Regular users of alcohol should limit their acetaminophen intake to 2g in a 24 hour time period instead of the regular 4 grams

271
Q

Which drug is responsible for 50% of acute liver failures?

A

Acetaminophen

272
Q

When do manifestations of liver injury (hepatic necrosis) appear after acetaminophen overdose?

A

48-72 hours

273
Q

What are the early signs of acetaminophen overdose?

A

N/V/D
Sweating
Abdominal pain/discomfort

274
Q

What are the late signs of acetaminophen overdose?

A

Hepatic failure
Coma
Death

275
Q

What is the antidote to acetaminophen overdose?

A

Acetylcysteine (Mucomyst)

276
Q

How does the antidote to acetaminophen overdose work?

A

It substitutes for glutathione and is 100% effective if given within 8-10 hours

277
Q

The diagnosis of schizophrenia is characterized by?

A

3 Types of symptoms: Positive, negative and cognitive

Acute episodes with periods of remission or semi-remission

278
Q

What are included in the positive symptoms of schizophrenia?

A

Hallucinations
Delusions
Agitation
Disordered Speech
Bizarre Behaviors

The delusional agitated man was experiencing hallucinations that made him talk act act weird, although he always remained positive.

279
Q

What are included in the negative symptoms of schizophrenia?

A

Social withdrawal
Poor Self care
Lack of motivation
Poverty of speech (Empty speech)
Blunted affect

The dishelved man didn’t have motivation to do self care or see his friends, and he answered questions like a robot.

280
Q

What are the cognitive symptoms of schizophrenia?

A

Disordered thinking
Lack of Focus
Learning disability
Memory problems

281
Q

What are the two main classes of antipsychotics?

A

FGAs (first generation antipsychotics)
SGAs (Second generation antipsychotics)

282
Q

What is the MOA of FGAs?

A

Block several receptors in the CNS
Acetylcholine
Histamine
Norepinephrine

283
Q

How long do FGAs take to go into effect?

A

2-4 weeks but several months for full effect

284
Q

What type of schizophrenia symptoms do FGAs inhibit best?

A

positive symptoms

285
Q

How are FGAs classified?

A

By potency
Low, medium, high

The potency contributes to severity of adversity of effects

286
Q

What are the categories of the FGAs adverse effects, also known as extrapyramidal symptoms?

A

Acute Dystonia
Parkinsonism
Akathisia
Tardive Dyskinesia

287
Q

What is the onset and effect of Acute Dystonia?

A

Hours to Days
Spasms of the tongue, face, neck and back muscles

288
Q

What is the onset and effect of parkinsonism?

A

Occurs within one month
Looks just like parkinson’s diagnosis (tremor, rigidity, shuffling, drooling)

289
Q

What is the onset and effect of akathisia?

A

Occurs within two months

Pacing, restlessness, agitated, squirming, need for constant motion

290
Q

What is the onset and effect of tardive dyskinesia?

A

Occurs months to years

Involuntary twisting, writhing movements of tongue and face, progresses to difficulty speaking, swallowing down the body

***** difficult to treat and can be permanent

291
Q

What are the other adverse effects of FGAs that are not part of extrapyramidal syndrome?

A

Neuroleptic malignant syndrome
Anticholingeric effects
Orthostatic hypotension
Neuroendocrine effects
Sedation (1st week)
Seizures
Sexual Dysfunction
Angranulocytosis
Dysthrythmias
Photosensitivity

292
Q

What is Neuroleptic Malignant Syndrome?

A

“Lead pipe” muscle rigidity
Sudden very high fever
Labile BP
Dysrhythmias

***If not treated can be fatal

293
Q

What are the drug interactions for FGAs?

A

Anticholinergic drugs
CNS depressants
Levodopa and direct dopamine receptor agonists
Overdose: Hypotension, CNS depression, EPs

294
Q

What is the MOA of Second-generation Antipsychotics?

A

Block dopamine and serotonin receptors in CNS, and take 2-4 weeks and several months for full effect

295
Q

What is a huge negative aside from adverse effects for SGAs?

A

They are very very expensive

296
Q

What are the adverse effects of SGAs that are DIFFERENT from FGAs?

A

Metabolic effects
-weight gain
-diabetes
-hyperlipidemia
Myocarditis (rare)

297
Q

What are the goals of therapy for schizophrenia?

A

Supress acute episodes
Prevent Exacerbations
Promote high quality of life and function

298
Q

What type of symptoms do SGAs inhibit best?

A

Both positive and negative symptoms

299
Q

Medications for depression can help-
_________ achieve full remission with medication.
_______ improve symptoms with medications.

A

30% achieve full remission
50% improve symptoms with medications

300
Q

What are the different treatment methods for depression?

A

Pharmacotherapy
Psychotherapy
Somatic Therapy (ECT or TMS)

301
Q

What are the 4 classes of antidepressants?

A

SSRI (Fluoxetine)
TCAs (Imipramine)
MAOIs (Phenelzine)
Atypical (Bupropion)

302
Q

What is the method of action of Fluoxetine?

A

SSRI-prevents 5-HT reuptake of serotonin

303
Q

What are the uses of Fluoxetine?

A

Depression
Panic Disorder
OCD

304
Q

What are the absorption pharmacokinetics of Fluoxetine?

A

PO
94% Protein-bound

305
Q

What are the metabolism pharmacokinetics of Fluoxetine?

A

Initially converted to norfluxetine and active metabolite
T 1/2 is around 9 days

306
Q

What are the adverse effects of fluoxetine?

A

Nausea and HA
Sexual Dysfunction
Weight gain
Withdrawal syndrome
Serotonin Syndrome

307
Q

What are the drug interactions of Fluoxetine?

A

Any drug that increases serotonin (MAOIs)
TCAs & Lithium (fluoxetine raises drug levels)
Antiplatelets and anticoagulents (Displaces warfarin)

308
Q

What is serotonin syndrome?

A

A group of symptoms caused by excessive accumulation of serotonergic transmission in the CNS that can develop in hours or days

309
Q

What are the symptoms of serotonin syndrome?

A

Altered mental status
Increased SNS activity
Can be fatal if not treated

310
Q

What would be considered an altered mental status from serotonin syndrome?

A

Agitation
Confusion
Disorientation
Hallucination
Poor concentration

311
Q

What would be considered increased SNS activity from serotonin syndrome?

A

Incoordination
Hyperreflexia
Excessive sweating
Tremor
Fever

312
Q

What is the treatment of serotonin syndrome?

A

Stop the SSRI immediately

313
Q

What is the MOA of Amitriptyline?

A

Tricyclic Antidepressant

Prevents reuptake of norepinephrine (NE) and/or 5-HT serotonin receptors
Also blocks histamine, acetylcholine and NE receptors

314
Q

What are the uses for Amitriptyline?

A

Depression
Insomnia
Pain

315
Q

What re the pharmacokinetics of amitriptyline?

A

PO

316
Q

What are the adverse effects of amitryptyline?

A

Orthostatic hypotension
Sedation (night dosing)
Anticholinergic effects
Diaphoresis
QT prolongation
Seizures
Hypomania
Suicide risk

Overdose can be deadly

317
Q

What are the drug interactions with amitryptyline?

A

MAOIs
Sympathomimetics (often used in nasal congestion)
Anticholinergics
CNS depressants

318
Q

What is the MOA of Phenelzine?

A

MonoAmine Oxidase Inhibitors

Irreversibly inhibits MAO (enzyme that degrades 5-HT, NE, and dopamine)

Allows more uptake of NE and serotonin

319
Q

What are the uses for Phenelzine?

A

Depression
OCD (not 1st or 2nd choice)

320
Q

What are the pharmacokinetics of Phenelzine?

A

PO

321
Q

What are the adverse effects of Phenelzine?

A

CNS stimulation
Orthostatic hypotension
Hypertensive crisis from dietary tyramine)

322
Q

What is tyramine?

A

A dietary substance that promotes the release of NE from sympathetic neurons

323
Q

What are the foods containing tyramine that should be avoided when taking Phenelzine (an MAOI)

A

Avocado
Raisins
Soy Sauce
Smoked Ham
Pizza (Pepperoni)
Wine
Cheese
Beer

324
Q

Why does dietary tyramine cause a hypertensive crisis when a patient is also taking an MAOI?

A

It won’ t be degraded and therefore can run through the body

325
Q

What are the interactions with Phenelzine?

A

Get ALL new medications approved (OTC & Rx)
TCAs and SSRIs
Meds for HTN
Dietary tyramine

326
Q

What are the signs of a hypertensive crisis?

A

Severe HA
Tachycardia
N/V
Confusion
Profuse sweating
BP 180/120

327
Q

What is the MOA of bupropion?

A

Prevents reuptake and NE and dopamine

328
Q

What are the pharmacokinetics of buproprion?

A

PO
Metabolized by the CYP P450 enzyme

329
Q

What are the adverse effects of buproprion?

A

Seizures
CNS stimulation

330
Q

What are the interactions with buproprion?

A

Some SSRIs (depending on CYP enzymes, use lowest dosage of buproprion)

MAOIs (can cause buproprion toxicity)

331
Q

What is bipolar disorder?

A

A chronic biological illness that is a problem with altered brain physiology with neuronal atrophy of perfrontal cortex (emotions) that requires lifelong treatment

332
Q

What are the alternating episodes of bipolar disorder?

A

Depression->Dysphoria->Normal mood->Hypomania->Mania

333
Q

The longer bipolar episodes go untreated, the?

A

Longer the episodes and the less normalcy

334
Q

What is the MOA of lithium?

A

A mood stabilizer that has an unclear MOA, but likely involves alterations of ions, neurotransmitters

335
Q

What are the uses for lithium?

A

Acute mania and long-term prevention of mania in BPD

336
Q

What are the pharmacokinetics of lithium?

A

PO
Short T 1/2 requires 2-4 times dosing
Excreted by kidneys
Na levels affect Lithium
NTI drug

337
Q

What are the NTI levels of lithium?

A

Therapueutic dose: 1-1.5 mEq/L

338
Q

At Lithium toxic levels 1.5-2 mEq, what are the symptoms?

A

Worse GI upset
Course hand tremors
Sedation
Confusion
Incoordination
ECG changes

339
Q

What are the adverse effects of lithium at the therapeutic dose?

A

N/V/D
Weakness
Fine hand tremor
Polydipsia/polyuria
Slurred Speech

No Wind Flows Past Sally.

340
Q

At Lithium toxic levels 2-2/5 mEq, what are the symptoms?

A

Ataxia
Polyuria
ECG changes
Clonic movements
Seizures
Stupor/coma
Hypotension

An Excited Pony Comes Swiftly Straight Here

341
Q

At Lithium toxic levels above 2.5 mEq, what are the symptoms?

A

Seizures
Oliguria
Death

342
Q

What are the interactions with lithium?

A

Thiazide & Loops diuretics (hypoatremia)
NSAIDS (made lithium reabsorb in kidney)
Anticholinergics

343
Q

What are the nursing considerations for lithium?

A

Give with food to lessen GI effects
Monitor NTI drug levels
Monitor Na, BUN, Creatine, GFR, thyroid and HCG

Warn of toxic side effects

344
Q

What are the 3 classes of sedatives/hypnotics?

A

Benzodiazepines
Benzodiazeine-like drugs
Barbiturates

345
Q

What is the MOA of Benzodizapines?

A

Potentiate the effects of GABA an inhibitory neurotransmitter

346
Q

What are the uses for Benzodiazapines?

A

Anxiety
Insomnia
Muscle Spasms
Seizures
ETOH withdrawal
Anesthesia Induction

347
Q

What are the pharmacokinetics of Benzodiazapines?

A

PO, IM & IV (IV can cause cardiac arrest)
Highly lipid soluble (Crosses BBB)
Metabolized by liver

348
Q

What are the expected CNS adverse effects of benzodiazapines?

A

Reduce anxiety
Promote sleep
Muscle relaxation

349
Q

What are the expected/adverse cardiac effects of Benzodiazapines?

A

PO has no effect
IV hypotension->cardiac arrest

350
Q

What are the expected/adverse respiratory effects of Benzodiazapines?

A

Mild in general
Can be significant for COPD, OSA

351
Q

What are the interactions with Benzodiazapines?

A

CNS depressants

352
Q

What schedule drug are Benzodiazapines?

A

Schedule IV

353
Q

What are the tolerance/dependance factors for Benzodiazapines?

A

No tolerance for anxiety or hypnotic effects

Significant tolerance to anti-seizure effects

Cross tolerance for those who have tolerance to barbituates, alcohol or opioids

Withdrawal likely in long term use

354
Q

What are the signs of an acute IV Benzodiazapine toxicity?

A

PO is very rare-IV is what to watch for.

Profound hypotension
Cardiac and Respiratory arrest

355
Q

What is the antidote for IV Benzodiazapine toxicity?

A

Flumazenil (Romazicon) a competitive benzo receptor antagonists

356
Q

How do you administer Flumazenil for Benzodiazapine overdose?

A

Rapid IV over 15 seconds

357
Q

What is important to remember about Flumazenil?

A

It has a short T 1/2 life->Frequent dosing
It reverses sedation but not respiratory depression so patient may be put on a ventilator
May cause seizures

358
Q

What are the 4 common Benzodiazapines to recognize?

A

Alprazolam (Xanax)
Clonazepam (Klonopin)
Diazepam (Valium)
Lorazepam (Ativan)

359
Q

What is the MOA of Zolpidem?

A

It is a Benzodiazapine-like drug

It potentiates the effects of GABA, an inhibitory neurotransmitter

360
Q

What is Zolpidem used for?

A

Insomnia (not anxiety)

361
Q

What are the adverse effects of Zolpidem?

A

Daytime drowsiness
Dizziness
Sleep related behaviors (Sleep eating, walking, etc)
No respiratory depression but do not combine with CNS depressants
Long term use can build tolerance and dependence (Schedule IV)

362
Q

What is the MOA of Phenobarbital?

A

A barbiturate
Enhances and mimics the action of GABA

363
Q

What are the uses for phenobarbital?

A

Seizure control and anesthesia

364
Q

What is the MOA of Buspirone?

A

Unclear but thought to bind to serotonin receptors (and some dopamine receptors)

365
Q

What are the benefits of buspirone?

A

Not as CNS depressant but just as effective
No abuse potiential
No cross dependence with benxos
Therapeutic effect takes one week

366
Q

What are the adverse effects of buspirone?

A

Nausea
Headache
Dizzness/lightheadedness
Sedation in some/excitment in others

367
Q

What are the drug interactions with buspirone?

A

Grapefruit juice (CYP inhibitor)
Erythromycin
Ketoconazole (increases buspirone levels)

Nurs 711 Pharmacology (6 decks)

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