Exam 4 Flashcards
1
Q
CNS neurotransmitters are?
A
Acetylcholine
Dopamine
Glutamate
GABA
2
Q
What balance of neurotransmitters are out in Parkinson’s Disease?
A
Too little Dopamine
Too Much acetylcholine
3
Q
What are the two types of medications for Parkinson’s?
A
Dopaminergic Agents
Anticholinergic agents
4
Q
Dopaminergic agents are used to?
A
Directly or indirectly activate dopamine receptors
5
Q
Anticholinergic Agents are used to?
A
Block receptors for acetylcholine
6
Q
How long does Parkinson’s Disease take to develop?
A
5-7 years
7
Q
What is Levodopa?
A
A drug used to treat Parkinson’s that is a dopamine replacement
8
Q
What type of drug is Levodopa?
A
A prodrug that is converted into it’s active form after crossing the BBB
9
Q
How much of Levodopa reaches the brain?
A
2%
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
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
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.
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
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
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)
16
Q
What is the MOA of carbidopa/levodopa?
A
Prevents decarboxylase action, allowing us to give a lower dose of levodopa
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
18
Q
What is the MOA of Entacapone?
A
Inhibits COMT enzyme from breaking down levodopa (catechol-O-methyltransferase)
19
Q
Which drug works directly to activate dopamine receptors in brain?
A
Pramipexole
20
Q
Which drug for Parkinson’s is often used in as the first line in the early stages?
A
Pramipexole
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
22
Q
What is Pramipexole added to after first line treatment is tried?
A
Levodopa/carbidopa
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
24
Q
Which neurotransmitters have low levels in Alzheimer’s Disease?
A
Acetylcholine
25
What are the two major drug classes to treat Alzheimer's Disease?
Cholinesterase inhibitors
NMDA antagonists
26
What is the MOA of Donepezil?
Prevents the breakdown of acetylcholine by the acetylcholinesterase enzyme in the CNS
27
What are the benefits of Donepezil?
Improved QOL
Memory
Reasoning
28
Donepezil ___________ __________ delay disease progression.
Donepezil does not delay disease progression.
29
What are the pharmacokinetics of Donepezil?
Available as ODT
96% protein bound
Long half life
30
What are the adverse effects of Donepezil?
The high acetylcholine causes cholinergic effects-> SLUDGE
31
What is the MOA of Rivastigmine?
Prevents the breakdown of acetylcholine by the acetylcholinesterase enzyme in the CNS
32
What are the benefits of Rivastigmine?
Improved QOL
Memory
Reasoning
33
What is the administration method for Rivastigmine?
Available as a transdermal patch
34
What are the adverse effects of rivastigmine?
Acetylcholinergic effects (SLUDGE)
Bradycardia -> Fainting, Falls
35
What is the MOA of Memantine?
Blocks NMDA receptors and prevents excessive calcium accumulation in the neurons
36
What are the benefits of Memantine?
Slows decline
May improve symptoms
*** Does not modify the disease process
37
What drug combined with Memantine has a potentiated effect?
Donepezil + memantine
(Pts score better on cognitive function tests)
38
What is multiple sclerosis?
MS is a chronic, progressive, inflammatory, autoimmune disorder affecting the myelin sheath of the neurons on the spinal cord
39
Immunomodulators are indicated for?
All patients with relapsing-remitting subtype, and not just for MS
40
Immunomodulators can reduce the relapse rate of MS by?
Around 30%
*It only slows down the disease process, but is not a cure
41
What is one of the negatives to MS immunomodulators?
They are very expensive
42
What drug was the prototype for the immunomodulators?
Inferon Beta
43
What are the pharmacokinetics of Interferon Beta?
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
44
What are the adverse effects of interferon beta?
Flu like symptoms (common)
Hepatotoxcitity
Bone Marrow suppression (Low RBC, WBC, Hb, Platelets)
Injection site problems
Headache
45
What type of drug for MS is less preferred than immunomodulators but has a stronger effect?
Immunosuppressants
-has stronger immunosuppression
-more toxic
-Effective against all subtypes of MS
46
When would immunosuppressants be used?
In patients that don't respond to immunomodulators
47
What are the pharmacokinetics of Mitoxantrone?
Supresses production of immune cells
IV infusion every 3 months
48
What are the adverse effects of Mitoxantrone?
Hepatotoxicity
Bone Marrow Supression
Cardiotoxicity (looks like HF)
Teratogenic
49
What is something a patient taking Mitoxantrone should look out for?
Edema, pink frothy sputum, cough
can be signs of cardiotoxicity (looks like heart failure)
50
What is the treatment of acute MS Flares?
High-dose IV steroids for 3-5 days
This quickly reduces acute inflammation (rapid improvement in patient when pharmacological levels)
51
What is the treatment of acute MS Flares?
High-dose IV steroids for 3-5 days
This quickly reduces acute inflammation (rapid improvement in patient when pharmacological levels)
52
What are the 4 ways AEDs Work?
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)
53
What is the goal of antiepileptic drugs (AEDs)?
The goal is to decrease focal epileptic activity and prevent spread to other areas of the brain
54
What is one very important aspect about AED drugs for acheiving therapeutic response?
Adherence is very important for achieving therapeutic response because if they miss a dose they have a seizure
55
What are the 3 traditional Antieptileptic drugs?
Phenytoin
Phenobarbital
Valproic Acid
56
What is the newest epileptic drug?
Oxcarbazepine
57
What are the positives and negatives of the traditional AEDs?
Less expensive
Teratogenic
More interactions
More adverse effects
58
What are the positives and negatives of the newer AEDs?
More expensive $$$
Safer in pregnancy
Less Interactions
Less adverse effects
59
What is the MOA of Phenytoin?
Inhibits the sodium channels of hyperactive neurons
60
What are the Pharmacokinetics of Phenytoin?
NTI Drug- therapeutic levels are 10-20 mcg/mL
Highly Protein bound
Hepatotoxic
Half life dose dependent (8-60hr)
CYP enzyme inducer
61
What is the most widely used and first line medication for seizures?
Phenytoin
62
What are the Adverse effects of phenytoin?
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
63
What is the MOA of Valproic Acid?
Blocks Na and Ca Channels, may potentiate GABA
64
Which traditional AED drug in addition for use in seizure disorders is used for bipolar and migranes?
Valproic Acid
65
What are the adverse effects of Valproic Acid?
GI effects common
Rare hepatotoxicity
SERIOUS teratogen
66
What is the MOA of Phenobarbital?
Enhances and mimics the effets of GABA
67
What are the adverse effects of Phenobarbital?
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
68
What is the MOA of Oxcarbazepine?
MOA: Blocks overactive sodium channels
69
What is the MOA of Oxcarbazepine?
MOA: Blocks overactive sodium channels
70
What is a benefit of Oxcarbazepine, a newer AED prototype that gives it an advantage over Phenytoin?
No drug level monitoring is required for oxcarbazepine
71
What are the adverse effects of oxcarbazepine?
CNS (dizziness, drowsiness, double vision, nystagmus, headache, ataxia)
Hyponatremia (rare)
Serious skin reactions (SJS, toxic epidermal necrolysis)
Teratogentic
Lots of drug interactions
72
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?
The drug can cause low birth weights and women should be taking folic acid when taking the drug.
73
What is status epilepticus?
An extended period of continuous seizure activity that is often more than 20 minutes and is considered a medical emergency
74
What is the treatment in status epilepticus?
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
75
What is a spasm?
Involuntary contraction of a muscle or muscle group that limits function temporarily and can be painful
76
What is spasticity?
Prolonged muscle tightness or contraction, characteristic finding in movement disorders of CNS origin
77
What can cause muscle spasms?
Epilepsy
Hypocalcemia
Chronic Pain syndrome
Localized muscle injury
78
What can occur due to muscle spasticity?
Increased muscle tone, spasms, decreased fine motor control/dexterity usually also hyperactive DTRs
79
What can cause muscle spasticity?
Multiple sclerosis
cerebral palsy
stroke
traumatic spinal cord lesions
80
What is Cyclobenzaprine used for and which class of medications does it belong to?
Used for Spasm
Centrally acting muscle relaxers
81
What is Baclofen used for and which class of medications does it belong to?
Spasticity
Centrally acting muscle relaxers
82
What is Dantrolene used for and which class of medications does it belong to?
Spasticity
Direct Acting muscle relaxers
83
What is Diazepam used for and which class of medications does it belong to?
Spasticity
Benzodiazpine
84
Treatment of muscle spasms:
What medications are used?
Acetaminophen
Ibuprofen
Cyclobenzaprine
85
Treatment of muscle spasms:
Which types if Physical Therapy are used?
Stretching
Flexibility
Tens
86
Treatment of muscle spasms:
What type of heat therapy can be used?
Heating pad
Whirpool/warm bath
87
What are the therapeutic uses for cyclobenzaprine?
Relief of pain from acute muscle spasm to increase ROM
Not effective to treat spasticity
88
What are the adverse effects of cyclobenzaprine?
CNS effects (drowsiness, dizziness, sedation)
Anticholinergic effects (anti-sludge)
89
What are the interactions of cyclobenzaprine?
Alcohol and other CNS depressants (Additive effect ->increased drowsiness)
Antidepressants (risk for serotonin syndrome)
Tolerance and Dependence can develop
90
What drug is used to treat spasticity, and is a CNS drug that acts on the spinal cord to supress hyperactive reflexes?
Baclofen
91
What two drugs for spasticity must not be given together?
What is the adverse effect of both of these drugs?
Baclofen and Diazepam (Valium)
Both have sedation has an adverse effect
92
Where does the drug Dantrolene act?
Directly on skeletal muscle
93
Pharmacokinetics:
What is special about the routes of administration of Dantrolene?
The PO dosing is used for spasticity
The IV dosing is used for malignant hyperthermia
94
What is the adverse effect of Dentrolene?
Dose related heptaotoxicity
95
Which type of medications act by increasing the activity of CNS neurons and are used in ADHD and narcolepsy?
Stimulants such as:
Amphetamine
Methylphenidate
Methyxanthine
96
How do stimulants increase the activity of CNS neurons?
Some enhance neuronal excitation
Some suppress neuronal inhibition
97
What is the MOA of Amphetamine and Methylphenidate?
They release norepinephrine and dopamine and inhibit reuptake of both in the CNS and peripheral nervous system
98
What are the therapeutic effects of Amphetamine and Methylphenidate?
Increased alertness
Increased initiative
Reduced fatigue
Elevated mood
99
What are the adverse effects of Amphetamine and Methylphenidate?
Tolerance develops to mood elevation, appetite suppression and CV effects
High dependence and abuse potiential
100
What are the pharmacokinetics of Amphetamine and Methylphenidate?
Available PO in both short and long duration forms
101
What are the adverse effects of Amphetamine and Methylphenidate?
Which ones are common?
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`
102
What is the MOA of Methylxanthine (caffeine)?
Blockade of adenosine receptors appears responsible for most effects
103
What are the therapeutic effects of Methyxanthine?
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.
104
What are the adverse effects of Methyxanthine?
Nervousness
Insomnia
Convulsions (extreme doses)
105
What are some of the factors that can lead to drug abuse?
Reinforced qualities of the drug
Physical dependence
Psychological dependence
Social factors
Availability
Individual vulnerability
Quality Purple Pheasants All Indivually Sing
106
Knowledge of drug abuse enables nurses to?
Recognize abuse and toxicity
Participate in treatment and withdrawal
Educate patients who are struggling with addiction and recovery
107
What is the APA's definition of substance use disorder?
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
108
The is the goal of the treatment of substance use disorder?
Goal is complete cessation with 40-60% reduce drug use
109
What is the definition of addiction?
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
110
What is tolerance?
Smaller and smaller responses from the same drug
111
What is cross tolerance?
Tolerance to one drug confers tolerance to another
112
What is psychological dependence?
An intense subjective need for another psychoactive drug
113
What is cross-dependence?
One drug dependence on another drug
114
What are the two main CNS effects of Alcohol (EtOH)?
GABA receptor activation
Glutamate inhibition
(Both these contribute to widespread CNS depression)
115
The effects of alcohol are?
Dose dependent->As concentration increases, "deeper" levels of the brain are effected
In high doses it can give a state of general anesthesia
116
What is the controlled substances act?
Federal legislation that categorized potentially addictive substances into five categories: Schedule I-V
117
Stage I drugs are?
Drugs that have the highest abuse potential and have no medical use
Heroin, LSD, and marjuana are all examples of stage I drugs
118
Stage II drugs are?
Drugs that require a typed or inked and signed prescription for a single RX no refills
119
Stage III & IV drugs are?
Drugs that can be prescribed by an oral, written or electronic prescription and have up to 5 refills
120
Stage V drugs are?
Drugs not requiring a prescription that can be dispensed by a PharmD with a record of tx
Must be 18 y/o
121
What are the Pharmacokinetics of Alcohol?
Absorption: 20% absorbed in stomach, 80% in large intestine
Distribution: Crosses BBB and placenta
Hepatic 'constant' metabolism
122
What does a constant rate of metabolism mean in regards to EtOH?
Alcohol is metabolized at a rate of 1 drink per hour
123
What are the adverse effects of Alcohol?
Encephalapothy
Cutaneous vasodilation
Elevation of BP
Respiratory Depression
Liver damage (Fatty liver->hepatitis->cirrhosis)
Erosive gastritis (heartburn)
Diuresis
Pancreatitis
Sexual Function
Cancer
Teratogen
124
What are the drug interactions with alcohol?
Other CNS depressants (due to sedation)
NSAIDs (stomach ulcers)
Acetaminophen (Liver toxicity)
Disulfiram (purposeful interaction to quit drinking)
125
What are the drugs used to treat alcohol abuse?
When facilitating withdrawal:
Benzodiazepines
Beta Blockers
Clonidine (off label use, lowers BP)
Antiepileptics (due to seizure risk)
To maintain abstinence:
Disulfiram
126
Chronic alcohol use builds significant tolerance, but not?
A tolerance to respiratory depression
127
What are the symptoms of alcohol withdrawl syndrome?
GI distress
SNS over-activiation
Hallucinations
Tonic-clonic seizures
Disorientation
Delirium
Tremors (Rare-vivid hallucinations)
Great Snakes Have ToxiC Terrible Domination
128
How long do symptoms of Alcohol withdrawl syndrome last?
12-72 hours up to one week
129
What is the MOA of Disulfiram?
Irreversibly inhibits aldehyde dehydrogenase causing acetaldehyde accumulation from ETOH ingestion
130
What is acetaldehyde syndrome?
ETOH + Disulfiram
131
What are the symptoms of acetaldehyde syndrome?
Vomiting, flushing, headache, sweating, blurred vision, hypotension
*If severe, can be life threatening
132
What are patient education points for Disulfiram (Antabuse) precautions?
Consuming ANY alcohol can cause a reaction
Only 7mL ETOH required
Includes transdermal absorption
Effects last two weeks past last dose
133
What is the MOA of Nicotine?
At low doses, activates nicotine receptors in the reward center which stimulate dopamine release
-the delivery system of inhalation through smoking is particularly addictive
134
What are the adverse effects of nicotine?
Cardiovascular stimulation
Nausea
Appetite suppression
Fetal Harm
135
What are the long-term increased risk of nicotine?
There is a long term increased risk of CV, several cancers, and COPD
136
How many people are killed from second hand smoke per year?
41,000
137
What are public health measures to decrease smoking?
Gradual changes in regulation of cigarette sales, advertising, and smoking ordinances and the public health measures
138
What are the nicotine replacement therapies?
Gum or lozenges
Patches
Nasal Spray
Inhaler
139
What type of nicotine replacement is not approved through the FDA?
e-cigarettes
140
What is the nicotine content in nicotine patches?
24% nicotine concetrations
141
What is the education for nicotine gum or lozenges?
No eating or drinking for 15 minutes
142
What is the education for nicotine patches?
Since they are steady release, you put on in the AM and take off in PM
143
What are the side effects of bupropion SR?
Dry mouth, insomnia, decreased appetite
144
In what demographic can wellbutrin/buproprion not be used?
In patients with risk of seizures, because wellbutrin can cause seizures due to CNS activity
145
What is Varenicline (Chantix)?
The most effective aid for smoking cessation-reduced cravings and intensity of symptoms with a 33% abstinence rate
146
What is the method of action of Varenicline?
A partial nicotinic receptor agonist, so it prevents most of the nicotine from binding
147
What is the MOA of methamphetamine?
Increases levels of norepinephrine and dopamine in the CNS
148
What are the effects of methamphetamine?
Methamphetamine causes
arousal
improved mood
euphoria
decreased pain perception
decreased appetite and need for sleep
149
What are the administration methods for methamphetamine?
Can be snorted, injected or smoked
150
What are the adverse effects of methamphetamine?
Psychosis (delusions, paranoia, hallucinations)
Cardiac stimulation and vasoconstriction (HTN, angina, dsyrhythmias)
Weight loss (appetite suppression)
Tooth Decay
Pregnancy complications
151
What types of household products can methamphetamine be produced from?
Drain cleaners
Acetone
Batteries
Many others
152
What does the activation of the opiod receptor Mu do?
The activation of Mu causes
analgesia (pain relief)
respiratory depression
euphoria
sedation
decreased GI motility
eventual physical dependence
153
What does the activation of the opioid receptor Kappa do?
The activation of Kappa causes analgesia, sedation and decrease GI motility but will not end up with physical dependence
154
What does the activation of the opioid receptor Delta do?
The activation of delta has no effect
155
What is an opioid?
Opioids
156
Endogenous opioid peptides are?
Made by the body and found in the central nervous system and in the peripheral tissues and serve as neurotransmitters, neurohormones, and neuromodulators
157
What are opioid pure agonists?
Agonists for Mu and Kappa receptors (these are divided into strong and mod-strong)
Morphine
Codeine
Meperidine (Demerol)
158
What are opioid agonist-antagonists?
Antagonists for Mu
Agonist for Kappa Receptors
Pentazocine (Talwin)
Nalbuphine (Nubain)
159
An agonist for Kappa receptor is considered a ___________________________ than an agonist for Mu.
Lower abuse risk
160
What are the opioid pure antagonists?
Antagonists for Mu and Kappa
Naloxone (Narcan)
Naltrexone
Think overdose drugs
161
Name the Drug Class:
Common drugs in the class include morphine, hydromorphone, fentanyl, merperidine (demerol), heroin, methadone.
Morphine
162
What is the MOA of morphine?
Morphine mimics the endogenous opioids and activate mu and kappa receptors.
It is a STRONG opioid agonist
163
What are the clinical used for morphine?
Relief of moderate to severe pain (post operative, cancer-related, labor/delivery, MIs)
164
What are the absorption/distribution pharmacokinetics of morphine?
Can be given practically any route, onset and duration differ
Small amount crosses BBB
Scheduled is usually best, amount depends on pain severity
165
What are the metabolism pharmacokinetics of morphine?
Affected by the first pass effect
Liver inactivation
Short half life
166
What are the adverse effects of morphine?
-Respiratory depression (varies with route and is most serious)
-Constipation (common)
-Orthostatic hypotension
-Urinary retention
-Nausea/vomiting
-Cough suppression
-Toxicity
167
What are the signs of a morphine toxicity?
Coma
Respiratory depression (2-4 breaths per min)
Pinpoint pupils (due to hypoxia)
168
What drug interactions does morphine have?
CNS depressants (EtOH)
Anticholinergics
Antihypertensives
Agonist-Antagonists
Antagoinist (Narcan)
169
What factors influence the withdrawl syndrome of morphine?
The intensity and duration of withdrawl depend on the T1/2 and degree of dependence on the drug
170
How long is the intense withdrawl period of morphine?
7-10 Days
171
What are the symptoms of morphine withdrawl?
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
Which drug is a strong opioid agonist that is around 100x more potent than morphine?
Fentanyl (Duragesic)
173
What are the uses for Fentanyl?
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
What is the metabolism of Fentanyl?
Hepatic metabolism by CYP3A4
175
What are the adverse effects of Fentanyl?
The same as morphine
176
What are the strong opioid agonists?
Morphine
Fentanyl
177
What are the moderate-strong opioid agonists?
Codeine
Oxycodone
Hydrocodone
178
What is the MOA of the moderate-strong opioid agonists?
The same MOA as the strong opioid agonists which is mimicing the endogenous opioids and activate mu and kappa receptors.
179
What is the main differences between the strong opioid agonists and the moderate-strong opioid agonists?
The moderate-strong opioid agonists are less effective and they have a little less abuse potential
180
What are the uses for Codeine?
Relief of pain, often co-formulated with acetominophen
Also used as a cough suppressant
181
What are the administration pharmacokinetics of codeine?
PO is the most common method
182
What are the metabolism pharmacokinetics of Codeine?
CYP2D6 enzymes metabolize codeine in the liver, and turns around 10% of codeine into morphine (likely how it produces anesthesia
Similar to prodrug
183
How do CYP2D6 enzymes effect codeine?
The genetic differences in the enzyme affect analgesia from codeine
184
What are the adverse effects of codeine?
Similar to morphine, increasing with higher dosages
Higher dosages required for significant pain relief, which can have dangerous side effects
185
What receptor effect do Agonist-Antagonist opioids effect?
Activate kappa receptors, block mu receptors
186
What are the benefits of the Agonist-Antagonist opioids?
Provide analgesia without as many side effects as pure agonists and have less potential for abuse
187
If a Agonist-Antagonist opioid is used to replace a long-term opioid agonist it could?
Cause withdrawl symptoms due to the blocking of Mu
188
What type of drug is Pentazocine (Talwin)?
A Agonist-Antagonist
189
What is the MOA of Pentazocine?
Activates Kappa receptors causing analgesia, sedation, and limited respiratory depression
190
What are the absorption pharmacokinetics of Pentazocine?
PO administration
191
What are the metabolism pharmacokinetics of Pentazocine?
Short T 1/2 life; therefore frequent dosing is needed
(Around every 3-4 hours)
192
What are the adverse effects of Pentazocine?
-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
What are the 3 post-op pain management dosing options?
PCA (kind of like a basal rate w/option to administer more)
Fixed Schedule
PRN
194
What type of drug is Naloxone?
Known as the brand name Narcan, it is an opioid antagonist and is used to block the opioid receptora to reverse opioid overdose
195
What are the administration pharmacokinetics of Naloxone?
Given parenterally or intranasally (Longer effects when given IM/SC)
196
What are the metabolism pharmacokinetics of Naloxone?
Hepatic metabolism
T 1/2 around 2 hours
197
What are the adverse effects of Naloxone?
None on its own, however if pt is dependent on opioids they can have immediate/severe withdrawl problems
198
What occured involving the drug Naloxone and the FDA in 2023?
The FDA approved intranasal OTC availability
199
What is the nurse's role in the opioid epidemic?
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
What are the 3 severe forms of headache?
Tension-type
Cluster
Migraine
201
Cluster headaches are less common in what demographic?
Males (5:1)
202
What are the symptoms of cluster headaches?
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
What are the abortive treatment for cluster headaches?
Oxygen
Sumatriptan
204
What are the preventative methods for treatment of cluster headaches?
Betamethasone (Steriod)
Verapamil (CCB)
Lithium
205
What is the most common type of severe headache?
Tension-type headache
206
What are the symptoms of tension-type headaches?
"Headband" non-throbbing pain, tightness in head and neck
207
What are the abortive medication for tension-type headaches?
Ibuprofen
Naproxen
Aspirin
Butalbital
208
What are the preventative measures for tension-type headaches?
Coping & Relaxation skills
Amitriptyline
209
What are the symptoms of a migraine headache?
A throbbing, moderate-severe pain that may be unilateral or bilateral that may last for days
Associated with nausea/vomiting, photo/phonophobia
210
What are the visual symptoms that can accompany around 30% of migraines?
No aura (more common)
211
Which demographic is more likely to experience migranes?
Females
212
What is the pathology of migraine headaches?
Migraines are due to a neurovascular problem that involves vasodilation and inflammation of the cranial blood vessels
213
What are some of the neurochemicals involved in migraines?
Calcitonin gene-related peptide-CGRP is a possible cause of migraines
Serotonin/5-HT suppresses migranes
214
What are the drugs that is an abortive therapy for both migraines and cluster headaches?
Ergot Alkaloids
Triptans
215
What is the MOA of Ergot Alkaloids?
Activation of serotonin receptors
Blockage of cranial inflammation
Cranial vasoconstriction
216
What are the pharmacokinetics of administration for ergot alkaloids?
PO
SL
PR*
Inhalation*
*Best method for administration
217
What are the pharmacokinetics of metabolism for the erogt alkaloids?
Metabolized by CYP3A4
T 1/2 of 2 hours
218
What are the adverse effects of the ergot alkaloids?
Rare at therapeutic doses
Possible N/V
Risk of dependence
219
What are the drug interactions for the ergot alkaloids?
Triptans cause vasospastic reactions (wait 24 hours)
CYP3A4 inhibitors raise to dangerous levels to cause vasospasm
220
What are Triptans?
Serotonin 1B/1D receptor agonists that are used to treat migraines and cluster headaches
221
What is the MOA of Triptans?
Bind to and activate specific subtypes of serotonin receptors in the brain causing vasoconstriction
222
What are the administration pharmacokinetics of Triptans?
PO
SQ
Inhalation
223
What are the metabolism pharmacokinetics of Triptans?
Hepatic metabolism
T 1/2 of 2.5 hrs
224
What are the adverse effects of Triptans?
50% of pts experience chest "heaviness" but it is not angina
Coronary vasospasm*
Teratogen
*Should not be given to patients with heart problems
225
What are the drug interactions with Triptans?
Ergot Alkaloids (cause Vasospasm, wait 24 hours)
SSRI/SNRI cause excessive serotonin syndrome
226
What is one of the barriers to migraine prevention?
Patients tend to not like the daily dosing
227
What are the 3 common options for preventative migraine therapy?
Beta Blockers-Propanolol
Antiepileptics
Tricyclic Antidepressants-Amitriptyline
228
What are the adverse effects of giving Beta blockers as migraine prevention?
May cause tiredness or exacerbate asthma
229
What are the adverse effects of antiepileptics such as topiramate for migraine prevention?
May cause fatigue and cognitive dysfunction
"Pts say they 'feel stupid'"
230
What are the adverse effects of Tricyclic antidepressants for migraine prevention?
May cause hypotension and anticholinergic effects
231
Cox 1 is considered the _____________ receptor, while Cox 2 is considered the ________________ receptor.
Cox 1 is considered the good receptor while Cox 2 is considered the bad receptor.
232
How do the Cox receptors work?
The Cyclooxygenase enzyme regulates multiple processes using prostaglandins
233
COX Receptors:
What is the effect in the stomach?
Cox 1 protects the gastric mucosa
234
COX Receptors:
What is the effect on platelets?
Cox 1 stimulates aggregation
235
COX Receptors:
What is the effect on the Uterus?
Cox 1 causes contractions at term
236
COX Receptors:
What is the effect on the kidney?
Cox 1 & 2 maintain renal blood flow
237
COX Receptors:
What is the role in tissue injury?
Cox 2 promotes inflammation and pain
238
COX Receptors:
What is the role in the vessels?
Cox 2 causes vasodilation
239
COX Receptors:
What is the role in the brain?
Cox 2 mediates fever and perception of pain
240
COX Receptors:
What is the role in the colon?
Cox 2 promotes colorectal cancer
241
What is the first generation NSAID that is still used today?
Aspirin
242
What are the uses of aspirin?
Reduction of pain, fever, inflammation
243
What is the MOA of Aspirin?
Irreversibly inhibits COX-1 and COX-2
Desired effects from COX-2 inhibition
Adverse effects from COX-1 Inhibition
244
What are the pharmacokinetics of administration of aspirin?
PO: plain, buffered, enteric-coated
245
What are the pharmacokinetics of metabolism of aspirin?
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
What are the pharmacokinetics of distribution of aspirin?
Salicylic Acid is highly bound to albumin and crosses all membranes easily
247
NSAIDs are excreted through the ________________ not the _____________.
Kidneys not the liver
248
What are the adverse effects of aspirin?
GI distress, bleeding, ulcers
General bleeding
Renal impairment
Salicylism syndrome
Hypersensitivity
249
What demographics is aspirin contraindicated in?
Children (Reye's Syndrome)
Pregnant Women
Pts. with peptic ulcer disease, bleeding disorders, ASA/NSAID hypersensitivity
250
What are the drug interactions with aspirin?
Other anticoagulants such as warfarin
Alcohol (will erode gastric mucosa)
Other NSAIDS (Antiplatelet effect)
251
What is Salicylism Syndrome?
Develops as ASA levels climb above therapeutic range Symptoms are:
Tinnitus
Sweating
Headache
Dizziness
252
How is Salicylism syndrome treated?
Witholding aspirin until s/s resolve, then reducing dose
In acute poisoning:
Treatment is supportive
253
What are the signs and symptoms of acute aspirin poisoning?
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
What is the MOA of Ibuprofen?
Reversible inhibition of COX-1 and COX-2
255
What are the uses of ibuprofen?
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
What are the benefits and risks of ibuprofen?
Benefits: Less gastric bleeding than aspirin
Negatives: Risk of renal impairment
257
What is the MOA of Naproxen?
Fairly selective for COX-1
258
What is the benefits of naproxen?
Less incidence of GI problems and MI/CVA than other non-ASA NSAIDs
Long half life so less dosing
259
What is the pharmacokinetic metabolism of naproxen?
T 1/2 of 12-17 hours
260
What is the MOA of Celecoxib?
Inhibits COX-2 only
261
What are the uses for Celecoxib?
Arthritis
Acute Pain
Dysmenorrhea
262
What are the benefits and risks of Celecoxib?
Less GI problems that 1st gen NSAIDS
Increased risk of MI/SVA
Can impair kidneys
Contraindicated for patients with heart disease
263
What are the uses for Acetaminophen?
Analgesia
Antipyretic
No-anti inflammatory effects
Preferred for children
264
What is the MOA of Acetaminophen?
COX inhibition, but thought to be limited to the CNS
265
What are the pharmacokinetics of Administration?
PO
Regular Strength
Extra Strength
PR
IV
266
What are the pharmacokinetics of the metabolism of acetominophen?
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
What is the 24 hour max for acetaminophen in adults?
4 grams
268
Regular _____________ reduces the liver's ability to metabolize excessive doses of acetaminophen.
alcohol consumption
269
Why is alcohol contraindicated with acetaminophen?
Alcohol:
-induces CYP450
-depletes glutathione
-causes general liver damage
270
What is alcohol recommendation when a pt cannot abstain from alcohol consumption?
Regular users of alcohol should limit their acetaminophen intake to 2g in a 24 hour time period instead of the regular 4 grams
271
Which drug is responsible for 50% of acute liver failures?
Acetaminophen
272
When do manifestations of liver injury (hepatic necrosis) appear after acetaminophen overdose?
48-72 hours
273
What are the early signs of acetaminophen overdose?
N/V/D
Sweating
Abdominal pain/discomfort
274
What are the late signs of acetaminophen overdose?
Hepatic failure
Coma
Death
275
What is the antidote to acetaminophen overdose?
Acetylcysteine (Mucomyst)
276
How does the antidote to acetaminophen overdose work?
It substitutes for glutathione and is 100% effective if given within 8-10 hours
277
The diagnosis of schizophrenia is characterized by?
3 Types of symptoms: Positive, negative and cognitive
Acute episodes with periods of remission or semi-remission
278
What are included in the positive symptoms of schizophrenia?
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
What are included in the negative symptoms of schizophrenia?
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
What are the cognitive symptoms of schizophrenia?
Disordered thinking
Lack of Focus
Learning disability
Memory problems
281
What are the two main classes of antipsychotics?
FGAs (first generation antipsychotics)
SGAs (Second generation antipsychotics)
282
What is the MOA of FGAs?
Block several receptors in the CNS
Acetylcholine
Histamine
Norepinephrine
283
How long do FGAs take to go into effect?
2-4 weeks but several months for full effect
284
What type of schizophrenia symptoms do FGAs inhibit best?
positive symptoms
285
How are FGAs classified?
By potency
Low, medium, high
The potency contributes to severity of adversity of effects
286
What are the categories of the FGAs adverse effects, also known as extrapyramidal symptoms?
Acute Dystonia
Parkinsonism
Akathisia
Tardive Dyskinesia
287
What is the onset and effect of Acute Dystonia?
Hours to Days
Spasms of the tongue, face, neck and back muscles
288
What is the onset and effect of parkinsonism?
Occurs within one month
Looks just like parkinson's diagnosis (tremor, rigidity, shuffling, drooling)
289
What is the onset and effect of akathisia?
Occurs within two months
Pacing, restlessness, agitated, squirming, need for constant motion
290
What is the onset and effect of tardive dyskinesia?
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
What are the other adverse effects of FGAs that are not part of extrapyramidal syndrome?
Neuroleptic malignant syndrome
Anticholingeric effects
Orthostatic hypotension
Neuroendocrine effects
Sedation (1st week)
Seizures
Sexual Dysfunction
Angranulocytosis
Dysthrythmias
Photosensitivity
292
What is Neuroleptic Malignant Syndrome?
"Lead pipe" muscle rigidity
Sudden very high fever
Labile BP
Dysrhythmias
***If not treated can be fatal
293
What are the drug interactions for FGAs?
Anticholinergic drugs
CNS depressants
Levodopa and direct dopamine receptor agonists
Overdose: Hypotension, CNS depression, EPs
294
What is the MOA of Second-generation Antipsychotics?
Block dopamine and serotonin receptors in CNS, and take 2-4 weeks and several months for full effect
295
What is a huge negative aside from adverse effects for SGAs?
They are very very expensive
296
What are the adverse effects of SGAs that are DIFFERENT from FGAs?
Metabolic effects
-weight gain
-diabetes
-hyperlipidemia
Myocarditis (rare)
297
What are the goals of therapy for schizophrenia?
Supress acute episodes
Prevent Exacerbations
Promote high quality of life and function
298
What type of symptoms do SGAs inhibit best?
Both positive and negative symptoms
299
Medications for depression can help-
_________ achieve full remission with medication.
_______ improve symptoms with medications.
30% achieve full remission
50% improve symptoms with medications
300
What are the different treatment methods for depression?
Pharmacotherapy
Psychotherapy
Somatic Therapy (ECT or TMS)
301
What are the 4 classes of antidepressants?
SSRI (Fluoxetine)
TCAs (Imipramine)
MAOIs (Phenelzine)
Atypical (Bupropion)
302
What is the method of action of Fluoxetine?
SSRI-prevents 5-HT reuptake of serotonin
303
What are the uses of Fluoxetine?
Depression
Panic Disorder
OCD
304
What are the absorption pharmacokinetics of Fluoxetine?
PO
94% Protein-bound
305
What are the metabolism pharmacokinetics of Fluoxetine?
Initially converted to norfluxetine and active metabolite
T 1/2 is around 9 days
306
What are the adverse effects of fluoxetine?
Nausea and HA
Sexual Dysfunction
Weight gain
Withdrawal syndrome
Serotonin Syndrome
307
What are the drug interactions of Fluoxetine?
Any drug that increases serotonin (MAOIs)
TCAs & Lithium (fluoxetine raises drug levels)
Antiplatelets and anticoagulents (Displaces warfarin)
308
What is serotonin syndrome?
A group of symptoms caused by excessive accumulation of serotonergic transmission in the CNS that can develop in hours or days
309
What are the symptoms of serotonin syndrome?
Altered mental status
Increased SNS activity
Can be fatal if not treated
310
What would be considered an altered mental status from serotonin syndrome?
Agitation
Confusion
Disorientation
Hallucination
Poor concentration
311
What would be considered increased SNS activity from serotonin syndrome?
Incoordination
Hyperreflexia
Excessive sweating
Tremor
Fever
312
What is the treatment of serotonin syndrome?
Stop the SSRI immediately
313
What is the MOA of Amitriptyline?
Tricyclic Antidepressant
Prevents reuptake of norepinephrine (NE) and/or 5-HT serotonin receptors
Also blocks histamine, acetylcholine and NE receptors
314
What are the uses for Amitriptyline?
Depression
Insomnia
Pain
315
What re the pharmacokinetics of amitriptyline?
PO
316
What are the adverse effects of amitryptyline?
Orthostatic hypotension
Sedation (night dosing)
Anticholinergic effects
Diaphoresis
QT prolongation
Seizures
Hypomania
Suicide risk
Overdose can be deadly
317
What are the drug interactions with amitryptyline?
MAOIs
Sympathomimetics (often used in nasal congestion)
Anticholinergics
CNS depressants
318
What is the MOA of Phenelzine?
MonoAmine Oxidase Inhibitors
Irreversibly inhibits MAO (enzyme that degrades 5-HT, NE, and dopamine)
Allows more uptake of NE and serotonin
319
What are the uses for Phenelzine?
Depression
OCD (not 1st or 2nd choice)
320
What are the pharmacokinetics of Phenelzine?
PO
321
What are the adverse effects of Phenelzine?
CNS stimulation
Orthostatic hypotension
Hypertensive crisis from dietary tyramine)
322
What is tyramine?
A dietary substance that promotes the release of NE from sympathetic neurons
323
What are the foods containing tyramine that should be avoided when taking Phenelzine (an MAOI)
Avocado
Raisins
Soy Sauce
Smoked Ham
Pizza (Pepperoni)
Wine
Cheese
Beer
324
Why does dietary tyramine cause a hypertensive crisis when a patient is also taking an MAOI?
It won' t be degraded and therefore can run through the body
325
What are the interactions with Phenelzine?
Get ALL new medications approved (OTC & Rx)
TCAs and SSRIs
Meds for HTN
Dietary tyramine
326
What are the signs of a hypertensive crisis?
Severe HA
Tachycardia
N/V
Confusion
Profuse sweating
BP 180/120
327
What is the MOA of bupropion?
Prevents reuptake and NE and dopamine
328
What are the pharmacokinetics of buproprion?
PO
Metabolized by the CYP P450 enzyme
329
What are the adverse effects of buproprion?
Seizures
CNS stimulation
330
What are the interactions with buproprion?
Some SSRIs (depending on CYP enzymes, use lowest dosage of buproprion)
MAOIs (can cause buproprion toxicity)
331
What is bipolar disorder?
A chronic biological illness that is a problem with altered brain physiology with neuronal atrophy of perfrontal cortex (emotions) that requires lifelong treatment
332
What are the alternating episodes of bipolar disorder?
Depression->Dysphoria->Normal mood->Hypomania->Mania
333
The longer bipolar episodes go untreated, the?
Longer the episodes and the less normalcy
334
What is the MOA of lithium?
A mood stabilizer that has an unclear MOA, but likely involves alterations of ions, neurotransmitters
335
What are the uses for lithium?
Acute mania and long-term prevention of mania in BPD
336
What are the pharmacokinetics of lithium?
PO
Short T 1/2 requires 2-4 times dosing
Excreted by kidneys
Na levels affect Lithium
NTI drug
337
What are the NTI levels of lithium?
Therapueutic dose: 1-1.5 mEq/L
338
At Lithium toxic levels 1.5-2 mEq, what are the symptoms?
Worse GI upset
Course hand tremors
Sedation
Confusion
Incoordination
ECG changes
339
What are the adverse effects of lithium at the therapeutic dose?
N/V/D
Weakness
Fine hand tremor
Polydipsia/polyuria
Slurred Speech
No Wind Flows Past Sally.
340
At Lithium toxic levels 2-2/5 mEq, what are the symptoms?
Ataxia
Polyuria
ECG changes
Clonic movements
Seizures
Stupor/coma
Hypotension
An Excited Pony Comes Swiftly Straight Here
341
At Lithium toxic levels above 2.5 mEq, what are the symptoms?
Seizures
Oliguria
Death
342
What are the interactions with lithium?
Thiazide & Loops diuretics (hypoatremia)
NSAIDS (made lithium reabsorb in kidney)
Anticholinergics
343
What are the nursing considerations for lithium?
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
What are the 3 classes of sedatives/hypnotics?
Benzodiazepines
Benzodiazeine-like drugs
Barbiturates
345
What is the MOA of Benzodizapines?
Potentiate the effects of GABA an inhibitory neurotransmitter
346
What are the uses for Benzodiazapines?
Anxiety
Insomnia
Muscle Spasms
Seizures
ETOH withdrawal
Anesthesia Induction
347
What are the pharmacokinetics of Benzodiazapines?
PO, IM & IV (IV can cause cardiac arrest)
Highly lipid soluble (Crosses BBB)
Metabolized by liver
348
What are the expected CNS adverse effects of benzodiazapines?
Reduce anxiety
Promote sleep
Muscle relaxation
349
What are the expected/adverse cardiac effects of Benzodiazapines?
PO has no effect
IV hypotension->cardiac arrest
350
What are the expected/adverse respiratory effects of Benzodiazapines?
Mild in general
Can be significant for COPD, OSA
351
What are the interactions with Benzodiazapines?
CNS depressants
352
What schedule drug are Benzodiazapines?
Schedule IV
353
What are the tolerance/dependance factors for Benzodiazapines?
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
What are the signs of an acute IV Benzodiazapine toxicity?
PO is very rare-IV is what to watch for.
Profound hypotension
Cardiac and Respiratory arrest
355
What is the antidote for IV Benzodiazapine toxicity?
Flumazenil (Romazicon) a competitive benzo receptor antagonists
356
How do you administer Flumazenil for Benzodiazapine overdose?
Rapid IV over 15 seconds
357
What is important to remember about Flumazenil?
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
What are the 4 common Benzodiazapines to recognize?
Alprazolam (Xanax)
Clonazepam (Klonopin)
Diazepam (Valium)
Lorazepam (Ativan)
359
What is the MOA of Zolpidem?
It is a Benzodiazapine-like drug
It potentiates the effects of GABA, an inhibitory neurotransmitter
360
What is Zolpidem used for?
Insomnia (not anxiety)
361
What are the adverse effects of Zolpidem?
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
What is the MOA of Phenobarbital?
A barbiturate
Enhances and mimics the action of GABA
363
What are the uses for phenobarbital?
Seizure control and anesthesia
364
What is the MOA of Buspirone?
Unclear but thought to bind to serotonin receptors (and some dopamine receptors)
365
What are the benefits of buspirone?
Not as CNS depressant but just as effective
No abuse potiential
No cross dependence with benxos
Therapeutic effect takes one week
366
What are the adverse effects of buspirone?
Nausea
Headache
Dizzness/lightheadedness
Sedation in some/excitment in others
367
What are the drug interactions with buspirone?
Grapefruit juice (CYP inhibitor)
Erythromycin
Ketoconazole (increases buspirone levels)
