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Pharmacology 2 > Test 1 > Flashcards

Test 1 Flashcards

1
Q

What does the central nervous system act upon?

A

the brain and the spinal cord

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2
Q

Is the central nervous system and open or a closed system?

A

closed

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3
Q

There are a bunch of neurotransmitters in the central nervous system at least _______ have been identified and there are a lot more that are suspected.

A

21

There are a lot more keys floating around in our head then there are in the periphery.

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4
Q

____________, there are a bunch of them, their precise function is not clear, it is difficult to know exactly how central nervous system drugs work.

A

Neurotransmitters

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5
Q

Passage through the blood brain barrier is limited to what?

A

lipid soluble agents,

drugs that are able to cross via active transport system

also any highly protein-bound drugs generally cannot cross.

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6
Q

What are the characteristics that a drug needs to have in order to pass freely through the body?

A

Nonionized, non polar, lipophylic, and minimal protein-bound are the characteristics that allow drugs to pass freely through the body.

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7
Q

Drugs that are not able to be _______ _______ are difficult to get into the brain because of the blood brain barrier.

A

actively transported

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8
Q

Why is the blood brain barrier a mixed blessing?

A

it protects our brain, but when the brain is diseased it makes it extremely difficult to get medication into the brain.

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9
Q

What is dopamine?

A

Dopamine is Catecholamine. This prevents it from crossing the blood brain barrier.

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10
Q

In Parkinson’s disease, the problem is that the brain does not have enough ___________.

A

dopamine, but the dopamine is hard to get into the brain because it’s a Catecholamine.

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11
Q

Describe Central Nervous System Adaptation

A

When the central nervous system is exposed to drugs on a chronic basis, adaptive changes occur over time.

In essence you may see effects later as opposed to earlier. So oftentimes you need to be patient when you’re talking about central nervous system type drugs.

For example if a person is depressed, and they are put on an antidepressant and they start feeling good in about a week, that is called the placebo effect because the medication has not had enough time to cause adaptation in the brain.

The same thing applies for schizophrenia medications, anxiety medications, seizure medication and Parkinson’s disease medications.

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12
Q

What are some characteristics that you see with central nervous system adaptation?

A

Some of the things that you can see with central nervous system adaptation are increased therapeutic effects, decreased side effects, tolerance and physical dependence.

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13
Q

Are increased therapeutic effects seen earlier or later when taking a central nervous system medication?

A

Increased therapeutic effects are often seen later when taking the medication such as the person’s depression gets better the person seizures are better controlled the person has less anxiety etc. as well as we will see less side effects.

An example of this would be a person that takes morphine for the first time or any opioid will have nausea and vomiting, but the more that they take it and are exposed to it the nausea and vomiting will subside.

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14
Q

What is tolerance?

A

Tolerance, is a reduced responsiveness with prolonged exposure.

For example a person that has chronic pain such as cancer pain, their pain medication will stop working with prolonged exposure so it is absolutely appropriate for the doctor to crank up the dose to help them not be in pain.

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15
Q

What is physical dependance?

A

Physical dependence, a state where abrupt discontinuation results in withdraw.

The brain, due to the adaptive changes, needs the medication to function properly and cannot be stopped abruptly.

Physical dependence does not always mean that the patient is abusing the medication. It just means that the brain has adapted to the medication, and the medication needs to be weaned off.

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16
Q

What is Parkinson’s Disease?

A

Parkinson’s disease is a neurologic disease. Parkinson’s disease- disease of extrapyramidal system characterized by dyskinesias (tremors, rigidity, postural instability and bradykinesia).

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17
Q

What causes Parkinson’s disease?

A

Results from an imbalance of dopamine (inhibitory) and acetylcholine (excitatory) in the striatum.

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18
Q

How do people with parkinson’s disease present?

A

Parkinson’s disease presents with a masked face, sometimes drooling, shuffling gait, stooped over, cogwheeling, off balanced and they can fall easy.

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19
Q

What is the goal of therapy for Parkinson’s disease?

A

The goal of therapy is to improve the patient’s ability to carry out activities of daily living.

There is no cure for Parkinson’s disease.

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20
Q

What is the main neurotransmitter in the peripheral nervous system?

A

Acetylcholine

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21
Q

About how many people does parkinson’s effect?

A

Parkinson’s disease affects over 1 million Americans, it is second to Alzheimer’s disease. It is the most common degenerative disease of neurons.

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22
Q

How can you establish balance in a Parkinson’s patients brain?

A

In Parkinson’s disease, since you don’t have enough dopamine you need to reestablish balance between dopamine and acetylcholine.

You can do this by adding more dopamine, or by taking away some of the acetylcholine.

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23
Q

What is the pharmacotherapy goal for Parkinson’s?

A

Pharmacotherapy goal is to restore balance between acetylcholine and dopamine in the brain.

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24
Q

What is Wearing-Off?

A

Wearing off, this is almost like a light switch. It happens at the end of the dosing interval, And indicates sub therapeutic levels of dopamine in the brain.

When this happens symptoms begin to reemerge.

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25
Q

What could you do to prevent the wearing off of a drug?

A

One thing that you can do, is to shorten the dosing interval.

This would mean instead of giving it twice a day you would give it three times a day. This causes there to be less peaks and valleys associated with it.

You can give a drug that prolongs the dopamine half-life.

You could give a direct acting dopamine agonist. These go directly to the brain and stimulate dopamine production in the brain.

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26
Q

What does on/off Mean in Parkinson’s disease?

A

When the person is on and the medication is working correctly, that the person is functional and you can hardly tell that there something wrong.

When the patient is off, the medication is not working and sometimes the patient can even be catatonic.

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27
Q

Levodopa, is capable of entering the brain via ________.

A

active transport

Remember, the problem with dopamine is that dopamine is a catecholamine.

Catecholamines cannot be actively transported into the central nervous system, but levodopa can.

Levodopa is a pro drug this means that it is not in its active form until after it gets into the brain and is metabolized. This makes it active.

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28
Q

What is a pro drug?

A

A pro drug is a drug that is inactive when it is given to the patient and the body metabolizes it and makes it become active.

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29
Q

What is the name of the enzyme that metabolizes dopamine?

A

Dopamine is metabolized by an enzyme called dopa-decarboxylase.

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30
Q

Dopa-decarboxylase metabolizes _______ and turns it into the active form of dopa.

A

levodopa

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31
Q

Why can’t you give dopamine and its active form to treat Parkinson’s disease?

A

You cannot give dopamine to treat Parkinson’s disease because it has a short half life, it cannot cross the blood brain barrier, and it cannot be absorbed.

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32
Q

What are the kinetics of levodopa?

A

The vast majority of levodopa is metabolized in the periphery because Dopa-decarboxylase is also in the periphery.

This causes an increase of dopamine in the periphery. This can cause problems such as tachycardia arrhythmias blood pressure issues.

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33
Q

How much Levodopa actually passes through the blood brain barrier?

A

Less than 2% of levodopa gets past the blood brain barrier so 98% of levodopa stays in the periphery.

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34
Q

What are the stimulant properties of dopamine?

A

At really low doses it can stimulate dopamine receptors in the periphery, at moderate doses it can stimulate beta-1 receptors, And at high doses it can stimulate Alpha-1 receptors.

Dopamine->Beta1->Alpha1

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35
Q

What are the adverse drug affects of levodopa?

A

It can cause nausea, dyskinesias, (it is used to treat dyskinesias but also can cause them) Grimaces, head bobbing, arrhythmias,tachycardia, psychosis such as vivid dreams, hallucinations, or cause the patient to become paranoid.

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36
Q

What is the most successful drug that is used for Parkinson’s disease?

A

Levodopa/carbidopa

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37
Q

What is the method of action of levodopa?

A

Levodopa is a pro drug that delivers dopamine to the brain.

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38
Q

What is the method of action of levodopa carbidopa?

A

carbidopa has no therapeutic effects alone. This means that you can give somebody a boat load of carbidopa and it will not do anything.

It inhibits dopa-decarboxylase in the periphery which allows more of the inactive form of levodopa to cross through the blood brain barrier where it is then metabolized into dopa, thus increasing the dopamine levels in the brain.

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39
Q

True or False

Carbidopa only works in the periphery and it cannot into the brain.

A

True

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40
Q

What are the kinnetics of levodopa/Carbidopa?

A

They allow reduction of levodopa by 75%.

This is because there is less levodopa being transformed to dopamine in the periphery so more of it gets into the brain because only the inactive form can get into the brain due to the blood brain barrier.

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41
Q

What are the side effects of levodopa/carbidopa?

A

The side effects that are produced by levodopa such as nausea, dyskinesias, grimacing, head bobbing, arrhythmias, tachycardia, are minimized by decreasing dopamine levels in the periphery.

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42
Q

What form does levodopa/carbidopa come In?

A

It comes in immediate release tablets, and now comes in extended release tablets.

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43
Q

What is the method of action of dopamine agonist?

A

They caused direct activation of dopamine receptors in the brain.

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44
Q

What are the drugs of choice for patients with Mild to Moderate symptoms of Parkinson’s Disease?

A

A dopamine agonist is considered the drug of choice for patients with mild or moderate symptoms of Parkinson’s disease. They are less effective than levodopa carbidopa but have some advantages.

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45
Q

What are the advantages of dopamine agonist?

A

They are not dependent on enzymatic conversion, which means that they are not pro drugs. And the affects don’t wane as much overtime.

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46
Q

Will the effects of Levodopa/Carbidopa last forever?

A

Nothing works as well as levodopa carbidopa for Parkinson’s disease, however the effects of levodopa carbidopa will decrease overtime (works 5-7 years) thus making it ineffective.

This is why you do not start a patient on levodopa carbidopa first you would try other methods such as dopamine agonist first.

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47
Q

Name two dopamine agonists.

A

Pramipexole and Robinirole

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48
Q

What is the method of action of Pramipexole and Robinirole.

A

They bind selectively to central dopamine receptors.

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49
Q

What are the adverse drug reactions of Pramipexole and Robinirole?

A

These do not cause movement disorders such as dyskinesia but they do cause nausea and hallucinations.

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50
Q

Besides Parkinson’s disease what is Pramipexole and Robinirole also used to treat.

A

These dopamine agonists are also used to treat restless leg syndrome.

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51
Q

MOA of COMT-

A

(catechol-O-methyltransferase) are responsible for the metabolism levodopa in the periphery along with dopadecarboxilase as well as catecholamines in general.

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52
Q

MOA of COMT inhibitors-

A

Work By blocking catechol-O-methyltransferase or COMP from metabolizing levadopa…..so that the levels of levodopa can rise in the periphery without having to increase the dose.

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53
Q

Name the COMT inhibitors.

A

Entacopone and Tolcapone

The Al Capones of Pharmacology

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54
Q

Actions and therapeutic usage of COMT inhibitors?

A

Indicated only for use with Levadopa. Prolongs the half life of Levadopa by about 50 to 75 percent.

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55
Q

Why can’t you give catecholamines orally?

A

You cannot give them or orally because they get metabolized too fast by enzymes such as COMT and Dopadecarboxilase so they don’t have the ability to be absorbed.

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56
Q

MOA of MAO- Monoamine Oxidase

A

is an enzyme responsible for breaking down some of our neurotransmitters. So if we block MAO our neurotransmitters will increase.

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57
Q

MOA of MAO-B- Monoamine Oxidase-B

A

is responsible for breaking down or metabolizing dopamine in our brain. It can metabolize endoginous dopamine as well as dopamine created by Levadopa.

So inhibitting MAO-B will essientially increase dopamine levels in the brain.

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58
Q

MOA of MAO-B inhibitors-

A

supress the metabolism of endoginous and dopamine created by levadopa in the brain thus allowing dopamine levels to rise without increasing the amount of Levadopa given.

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59
Q

MOA of MAO-A-

A

metabolizes norepinepherine and seritonin in the brain and is used to treat depression disorders.

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60
Q

Name a MAO-B inhibitor.

A

Selegiline

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61
Q

What is the MOA of Selegiline?

A

Suppresses the destruction of dopamine in the brain. This can be endoginous dopamine or dopamine created by Levadopa.

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62
Q

Central acting anticholinergic drugs means?

A

(simply means they are active in the brain)

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63
Q

Name a central acting anticholinergic drug.

A

Benztropine

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64
Q

What is the MOA of Benztropine?

A

Relieves symptoms of Parkinson’s disease by blocking muscarinic receptors in the brain, thus restoring balance. (brings normal level of Acetylcholine down to match depleted level of dopamine)

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65
Q

What are the side effects of Benztropine?

A

Opposite of muscarinic man. So dry mouth, blurred vision, tachycardia, constipation, urinary retention, dilated eyes ect,.

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66
Q

Name the 5 classes of Parkinson’s Drugs

A 
Levadopa
Levadopa/Carbidopa
Dopamine Agonists
COMT Inhibitors
MAO-B Inhibitors
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67
Q

Carbidopa = ________% more Levadopa in the system

A

75

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68
Q

What medication would you give in adjunct to Levadopa/Carbidopa to a person who is having lots of On-Off Periods?

A

COMT Inhibitors (Entacopone, Tolcapone) because they prolong the 1/2 life of the dose, so that you do not have to raise the dose of Levadopa/Carbidopa.

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69
Q

What is the pathophysiology of Alzheimer’s disease?

A

It effects over 4.5 Million Americans, and kills over 400,000 people a year. It is the 4th leading cause of death behind cancer and strokes from hypertension. It is caused by:

Early: degeneration of neurons in the hippocampus, which serve in a significant role in memory formation. As these neurons begin to deteriorate your short term memory begins to fail initially.

Late: degeneration of neurons in the cerebral cortex, which is central to things such as speech, higher reasoning, perception, and higher functioning within the brain. As it continues to wrech the cerebral cortex within the brain, patients lose the ability to communicate, they lose bowel and bladder function wich results in death over time.

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70
Q

In Alzheimers Patients, what begins to fail initially? (EARLY STAGE)

A

Their short term memory.

This indicates that the disease progression is in the hippocampus

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71
Q

In Alzheimers Patients, What begins to fail when the disease process moves from the hippocampus to the cerebral cortex? (LATE STAGE)

A

degeneration of neurons in the cerebral cortex, which is central to things such as speech, higher reasoning, perception, and higher functioning within the brain.

As it continues to wrech the cerebral cortex within the brain, patients lose the ability to communicate, they lose bowel and bladder function wich results in death over time.

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72
Q

What are the 3 features of Alzheimer’s disease?

A
  1. Acetylcholine declines (can target from a pharmacological standpoint). Patients with Alzheimers have about 90% less Aceytalcholine than healthy patients. Acetylcholine is important in the role of memory formation, so by increasing this in the brain it could help them with memory loss.
  2. Beta-amyloid neuritic plaques (protein fragments in the brain seen upon autopsy)
  3. Neurofibrillary tangles- normally the brain is orderly. Autopsy of an Alzheimers patient’s brain shows a tangled mess.
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73
Q

What is the number 1 risk factor for Alzheimer’s disease?

A

Advanced age. It is also hereditary. 90% of the time patients are over the age of 65. After the age of 65, the risk factor doubles every 10 years.

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74
Q

What are the symptoms of Alzheimer’s disease?

A 
Memory loss and confusion
Impaired judgement
Personality changes
Aggressive
combative
Sundowning
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75
Q

What is sundowning?

A

Alzheimers patients do not sleep at night. They can be paranoid ect. When the sun goes down, they become wide awake. This is referred to as sundowning.

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76
Q

Which 2 of these symptoms are the classic cause of an Alzheimer’s patient to be placed into a nursing home?

Memory loss and confusion
Impaired judgement
Personality changes
Aggressive
combative
Sundowning
A

Aggressive

Combative

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77
Q

How can a definitive diagnosis of Alzheimer’s disease be made?

A

A definitive diagnosis can only be made at death upon autopsy.

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78
Q

What is the only class of drugs used for Alzheimer’s disease that is FDA approved to help with memory loss?

A

Cholinesterase inhibitors.

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79
Q

What is the MOA of Acetylcholinesterase?

A

It metabolizes Acetylcholine

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80
Q

What is the MOA of Cholinesterase inhibitors?

A

Prevents the breakdown of acetylcholine in the brain by Acetylcholinesterase, thus increasing the availability at the muscarinic receptors.

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81
Q

What is the goal of therapy for Alzheimer’s disease?

A

To slow progression and Slow memory loss to try and preserve independant function.

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82
Q

What is the side effect of Cholinesterase inhibitors?

A

The elevation of Acetylcholine levels in the periphery.

As a result, it makes muscarinic man. (increased snot and spit production, heart slows down, beady eyes, bowels and urine increase, bronchoconstriction, makes asthma and peptic ulcer disease worse***)

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83
Q

What class of drugs do Cholinesterase inhibitors interact with?

A

Anticholinergic drugs,

Antidepressants, Tylenol PM

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84
Q

Name the specific Cholinesterase inhibitors

A

Tacrine
Donepezil
Rivastigmine
Galantamine

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85
Q

What is the MOA of Tacrine and its important characteristics?

A

Cholinesterase inhibitor, HEPATOXICITY, short half life requiring 4 times a day dosing. (not an ideal drug)

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86
Q

What is the MOA of Donepezil and it’s important characteristics? (Second Alzheimers Drug)

A 
Cholinesterase inhibitor,
VERY EXPENSIVE,
dose is 5-10mg a day,
Nonhepatoxic
Better tolerated than tacrine
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87
Q

What is the MOA of rivastigmine?

A

IRREVERSIBLE Cholinesterase inhibitor

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88
Q

What is the MOA of Galantmine?

A

Reversible Cholinesterase inhibitor

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89
Q

What are the cautions for Galantmine?

A

Use with caution in pulmonary disease or COPD, avoid in severe hepatic or renal impairment.

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90
Q

True or False

Donepezil
Rivastigmine
Galantamine

Are all Cholinesterase inhibitors used to treat Alzheimers disease that are used interchangeably because there is not any evidence that one is any better than the other.

A

TRUE

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91
Q

What is the MOA of Memantine?

A

Modulates Glutamate or Glutamic Acid which is the major excitatory neurotransmitter in the brain

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92
Q

What drug is used for moderate to severe Alzheimer’s Disease?

A

Memantine

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93
Q

What is Glutamate?

A

It is the major excitatory neurotransmitter in the brain

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94
Q

What is the major neurotransmitter in the periphery?

A

Acetylcholine

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95
Q

What are some additional non-traditional Alzheimer’s drugs?

A

Vitamin E
Selegiline
NSAIDS (May help if taken at a young age)
Estrogens

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96
Q

True or False

Studies show that combining Memantine with a Cholinesterase inhibitor does not really prove to be signifiant.

A

True

97
Q

What drugs are used to treat Mild to Moderate Alzheimers?

A

Cholinesterase Inhibitors

Alzheimers progresses from Mild to Moderate to Severe over time.

98
Q

What is the result of Cholinesterase inhibitors?

A

Memory is spared due to the activation of the muscarinic receptors in the brain.

This has a very low response rate.

It does not stop the progression of Alzheimers, but it can slow it.

25 to 30% will respond to the medication and the response is shortlived.

99
Q

Epilepsy seizures are caused by synchronous high frequency discharge from a group of hyperexcitable neurons called a _______.

A

focus or focal area.

The focus is where the abnormal electrical stimulus comes from in the brain,.

100
Q

What causes a focus in the brain?

A

The focus could be caused from trauma, tumor, and unknown causes (genetical defect ect)

101
Q

2-3 Million people have epilepsy. 60-70% op people can be rendered seizure free, which means that 30-40% of patients cannot.

What are some things that can lower someone’s seizure threshold?

A

When patients get sick (vomiting diahrrhea, something that may cause their absorption to be off) it can lower the persons siezure threshold.

Sometimes medication can lower seizure threshold, illnesses, electrolyte abnormalities as well.

102
Q

What are the two main types of seizures?

A

Partial and generalized.

The choice of your pharmacotherapy really is chosen by what type of seizure that the patient is having.

103
Q

What is the best way to differentiate between a partial and a generalized seizure?

A

The best way to differentiate between a partial and a generalized seizure is that partial seizures do not lose consiousness.

104
Q

Partial seizures-

A

Begin at the focus but the spred is limited. Does not go to both hemispheres of the brain.

105
Q

What are the types of partial seizures?

A

Simple partial
and
Complex partial seizure

106
Q

Simple partial-

A

no loss of conciousness and they may have a discrete symptom depending on what area of the brain is actually involved.

For example- twitching, smelling something that is not there, hallucinations ect.

107
Q

Complex partial seizure-

A

impaired conciousness (they do not lose it, just impaired) and they have lack of responsiveness.

108
Q

If a person is partly conscious, are they having a generalized seizure?

A

No, a Complex partial seizure-

109
Q

Generalized-

A

produce an immediate loss of conciousness.

It effects both hemispheres of the brain.

There are different types of generalized seizures: Tonic-Clonic, 
Absence, 
Atonic, 
Myoclonic, 
Status Epilepticus, 
and Febrile.
110
Q

Tonic Clonic-

A

major convulsions, rigidity, and muscle jerks.

Tonic stands for the rigidity and this is usually what happens first.

Clonic means jerking.

These patients cry out right before it happens because the body contracts including the diaphragm which forces air out at a very rapid rate. (makes crying sound)

These patients can fall, bite their tongue, be really sore afterwords.

Have postictal period, when they wake up they are confused (may sound drunk).

The brain needs rest afterwords. Patients will generally go into a deep sleep and will be hard to wake up. This is a classic seizure.

111
Q

Absence-

A

brief loss of conciousness, could experience 100 atacks per day.

Mild symmetric facial activity like blinking eyes over and over or nystagmus.

Patients zone out and have no clue what is going on around them.

Could last for approximately 15-20 seconds.

112
Q

Atonic-

A

sudden loss of muscle tone, could be limitted or total body.

They call this drop syndrome (kid camps where they wear helmets).

Can be limmited to just the head or leg drop attacks (jellyfish legs).

113
Q

Myoclonic-

A

sudden, rapid muscle contractions.

Generally bilateral.

Basically it is the clonic phase of a tonic clonic. No rigidity just jerking.

114
Q

Status Epilepticus-

A

seizure lasting more than 30 min.

Most seizures are gennerally self limitting (stop themselves).

However if a sezure continues for a certain amount of time and does not stop, it is a medical emergency.

It is life threatening.

115
Q

Febrile seizure-

A

occurs at 6 months to 5 years of age and are NOT at risk for developing a seizure disorder later in life.

116
Q

Drug therapy:

Mechanisms of actions of seizure medications:

A

suppression of sodium influx,
suppression of calcium influx,

antagonism of glutamate,

and potentiation of GABA.

117
Q

suppression of sodium influx

A

decreases the ability of neurons to fire at high frequency. Slows down the focal area and surrounding neurons.

118
Q

suppression of calcium influx

A

if you suppress calcium influx it can supress neurotransmission.

119
Q

antagonism of glutamate

A

**Glutamate is the primary neurotransmitter in the CNS.

If you block the action of glutamate it decreases the neuronal excitement that can occur.

(Glutamate Excites)

120
Q

potentiation of GABA,

A

**GABA is the main inhibitory neurotransmitter in the CNS.

Several different drugs work to increase the levels of GABA.

(GABA Suppresses)

121
Q

General Therapeutic Considerations of Seizure disorders:

Therapeutic goal-

A

reduce seizures to an extent that enables the patient to live as normal of a life as possible.

122
Q

General Therapeutic Considerations of Seizure disorders:

Diagnosis and drug selection-

A

in general you have to have proper match of drug with the proper seizure, so often selection of drug therapy depends on what type of seizure the patient is having.

It also depends on what type of side effects that the patient is expericing and can handle.

Only one drug is effective for all types of seizures and that is Valproic Acid.

Expertise- Neurology, very specialized area.

Physical/Neurological/Laboratory evaluations can be used to pick a medication for a patient such as EEG (common in mapping the brain), CT, MRI ect. all used to find the focal point.

Thorough History- this is probably where pharmacists and nurses get more involved.

Basically asking the patient subjective things such as the onset of the seizures, frequency, duration, precipitating factors (antihistmamines ect.) Prodromal symtoms (before the seizure hits) such as numbness of the tongue ect.. gives you a chance to lay down or pull over while driving.

123
Q

General Therapeutic Considerations of Seizure disorders:

Drug evaluation-

A

once a drug is selected, you have to have a trial period to see if the drug is going to help.

Due to the adaptive changes in the brain, you have to give the medication a sufficient amount of time to work.

Until control is confirmed, people have to avoid things such as driving or opporating heavy machinery.

Maintaining a seizure frequency chart is important for nurses to help the patients do. This helps determine if the medication is working.

124
Q

General Therapeutic Considerations of Seizure disorders:

*****Monitor plasma levels-

A

this is important, especially in the traditional seizure medications (Phenytoin, Carbamazepine).

Effective plasma levels are firmly established for some of these antiseizure medications.

Which essientally means that if you can get a plasma level, the plasma levels can equate to brain efficacy.

125
Q

General Therapeutic Considerations of Seizure disorders:

**Promoting Compliance-

A

it is estimated that 50% of all treatment failures are secondary to patient non compliance.

Nurses should stress to the patient about how important it is to comply and the consequences on non-compliance.

126
Q

General Therapeutic Considerations of Seizure disorders:

***Withdrawing the medication

A

TAPER over six weeks to several months.

Due to CNS adaptations, the brain requires the medication to work normally. If you abruptly discontinue the medication, you can cause status epilepticus.

If you are on multiple medications for seizures, you never stop both of them at the same time. (taper off one at a time).

127
Q

General Therapeutic Considerations of Seizure disorders:

**Suicide risks-

A

patients on seizure medications have about twice the risk of committing suicide.

So as a nurse, monitor for depression and suicidal ideation.

128
Q

Drugs-

Traditional vs. Newer AED’s.-

A

Newer anti epileptic drugs are much cleaner, do not have as many side effects, they are not as concerning for birth defects, don’t have to monitor their plasma levels.

Traditional antiseizure medications are the nasty ones. However, even though the newer drugs appear to be cleaner, most people do not use them as much because they don’t have as much history with the newer ones.

Traditional drugs: have more experience with them, less expensive, but more side effects, nasty drug interactions ect.

129
Q

Phenytoin-

A

most widely used antiepileptic drug.

First drug that was developed that did not suppress the entire CNS.

Prior to Phenytoin, doctors prescribed barbituates such as phenobarbitol (tranqulizing effects).

130
Q

**Phenytoin serum target

A

10-20 mcg/ml

Subtherapeutic = seizures. Above therapeutic = toxic.

131
Q

MOA of Phenytoin-

A

inhibits sodium channels.

132
Q

Phenytoin is available as an oral and an IV medication.

A

***if you administer it through an IV, you can not infuse more than 50mg/min.

If you do, it will kill the patient.

Because of this, they came out with a prodrug called fosphenytoin.

This is an IV prodrug that is converted to phenytoin in the body.

It is way more expensive then phenytoin, but you can infuse it at 150mg/min.

This is used if you need to get the medication in the patient fast.(like status epilepticus)

133
Q

Unique Pharmacokinetics of Phenytoin-

A

MM- mecalus mentin, small dosage adjustments can make tremendous jumps once it reaches the saturation point.

Which means that the metabolizing capacity of the liver has a saturation point and after it reaches that point the medication goes straight into the blood stream.

So you have to be very careful when dosing this medication.

134
Q

ADR’s of Phenytoin-

A 
sedation, 
sleepy, 
lethargic, 
gingival hyperplasia, 
horizontal nastagmus with toxic levels, 
double vision, 
ataxia (heel to toe walking to check), 
significant cognitive impairments..

With really toxic levels, it can cause seizures, ahrrithmias,

135
Q

Drug interactions of phenytoin-

A

phenytoin is a significant inducer of CP450 (very important)

When you place someone on this medication, you have to evaluate all other drugs that they take.

Induction means double pac-man. Increases the metabolism. Liver gobbles up everything.

So if you are on other drugs like warfarin or birthcontrol you have to increase the dose because the levels will go down due to double pacman metabolizing it.

136
Q

Carbamazepine

serum target level

A

is 4-12 mcg/ml

MOA- inhibits sodium channels

137
Q

Unique Pharmacokinetics of Carbamazepine-

A

it causes autoinduction.

Over time, the drug causes induction of itself.

so the metabolism causes the liver to eat iself(carbamazepine) faster.

Can make 1/2 life go from 50 hours to 15.

138
Q

Adverse drug reactions of Carbamazepine-

A

Ataxia,

**hematologic Depression (need to monitor CBC),

agranulocytosis,

SIADH (check serum sodium, concentrates urine),

139
Q

Drug interactions of Carbamazepine-

A

Inducer of CP450. Makes double pac man.

Long 1/2 life, tolerance lessens over time.

140
Q

Phenobarbitol serum sodium target

A

20-40 mcg/ml

141
Q

There are two reasons we don’t use Phenobarbitol much anymore:

A
  1. it is very sedating

2. potentially lethal due to suicide risks.

142
Q

Pharmacokinetics of Phenobarbitol-

A

Enzyme Inducer.

143
Q

Valproic Acid-

is good for all types of seizures. The serum target is

A

is 50-150 mcg/ml.

MOA- works through Sodium, Calcium, and GABA.

144
Q

ADR’s of Valproic Acid-

A

Hepatoxicity and pancreatitis are rare but possible

145
Q

Unique Pharmacokinetics of Valproic Acid-

A

Significant Enzyme Inhibitor - meaning it will cause the metabolism of other drugs to slow, causing them to rise to toxic levels.

146
Q

Name the Antiseizure medications that are Enzyme Inducers:

A

Phenytoin, Phenobarbitol, and Carbamazepine.

147
Q

Name the Antiseizure Medication that is an Enzyme Inhibitor.

A

Valproic Acid.

148
Q

Gabapentin-

A

also used for neuropathic pain

149
Q

Topiramate-

A

used for weight loss now

150
Q

Seizure treatment during pregnancy-

A

This is one of those disease states where the risk to the fetus is greater from having uncrontrolled seizures than from taking the medication.

Medication is still a concern though.

Might try not to take as much especially in the first trimester.

151
Q

Status Epilepticus-

A

when seizures persist for more than 30 min. Medical Emergency,

leads to acidosis, tachycardia, hyperthermia, hypertensive crisis,

Status Epilepticus Supportive care- protect the airway, initiate IV.

Give benzodiazapine first followed by IV Phenytoin or fosphenytoin for long term.

works through the GABA pathway.

If it doesn’t work, have to induce coma in the patient to shut CNS down.

152
Q

Schizophrenia-

A

is a chronic psychotic illness characterized by disordered thinking and reduced ability to comprehend reality.

Usually hits in the 20’s (early teens to 20’s).

Effects about 1% of the population, and before meds were available these patients had to live in institutions.

153
Q

Clinical Features of Schizophrenia-

A

Symptoms can be sub-divided into 3 groups: positive, Negative, and cognitive.

154
Q

Positive Symptoms-

A

exageration or distortion of normal function such as hallucinations, delusions, paranoia, aggitation, combativeness, disorganized speech ect.

Much easier to treat with drugs.

155
Q

Negative Symptoms-

A

loss of normal function such as: social withdrawl, emotional withdrawl, lack of motivation, poor self care, poor judgement, poverty of speech, flat affect, ect..

Meds don’t help.

156
Q

Cognitive Symptoms-

A

disordered thinking, memory difficulties, and focusing abilities.

157
Q

Eitology of Schizophrenia-

A

not exactly known.

Deathly excess activation of dopamine is part of it, but reducing dopamine can cause parkinsons.

158
Q

Conventional Pharmacologic agents:

A

Positive symptoms respond very well to the medications, however, cognitive and negative symptoms do not.

159
Q

Conventional Antipsychotics-

A

are the more historic medications such as Haloperidol and Chlorpromazine.

160
Q

There are two divisions of Conventional Antipsychotics and they are classified by potency.

(does not mean that one effects symptoms better than another, it refers to how much they effect the dopamine receptors)

A

Low potency (Chlorpromazine)-

High potency (Haloperidol)-.

161
Q

Low potency (Chlorpromazine)-

A

This has more peripheral type side effects with it (outside of the CNS) such as sleepyness, or anticholinergic side effects.

162
Q

High potency (Haloperidol)-.

A

This is cleaner, but have more movement disorders associated with it. Such as psudoparkinsonism.

163
Q

When deciding which Schizophrenic medication to use, you typically base it off of what type of side effects do you want the patient to have.

A

For example: if a patient is agressive, you might want to give them a Low Potency (Chlorpromazine) because it will make them sleepy thus helping the agression.

You might use a high potency agent (Haloperidol) if a patient has urinary retention problems because the low potency agents have more anticholinergic side effects that would thus make the urinary retention worse.

164
Q

Mechanism of Action of Conventional Antipsychotics-

A

blocks many receptors, but mainly blocks dopamine receptors.

165
Q

Efficacy of Conventional Antipsychotics-

A

You do see some intital efficacy within the first couple of days,

example, Haloperidol might calm someone down intitially, but it will take months for the drug to work fully because of the adaptive nature of the brain. (takes time to adapt).

166
Q

**With traditional antipsychotics, positive symptoms respond very well but negative and cognitive symptoms do not.

A

Can make them quit hallucinating, but cannot make them be normal functioning beings in society.

Treatment for Schizophrenia is not a cure, but it can help if taken properly.

167
Q

Adverse Effects of High potency Antipsychotics (Haloperidol)-

A

has more Extraparamital Side Effects such as: Acute Distonia,
Parkinsonism,
Akathisia,
***Tardive Dyskinesia.

168
Q

Adverse Effects of Low potency Antipsychotics (Chlorpromazine)-

A

Peripheral side effects such as anticholinergic side effects and sleepyness.

169
Q

Acute Distonia,

A

typically happens quickly after administration of an antipsychotic agent.

You might hear a patient cry out and look over at them and they are twisted with their tongue hanging out.

It is a severe spasm of the tongue, face, neck, and upper torso. It is very painful.

Treatment is IM anticholenergic such as Benydryl, or Benztropine. These work very quickly.

170
Q

Parkinsonism

A

iatrogenic (meaning we gave it to them with medication)

classic symptoms are bradykinesia, drooling, masked face, cogwheeling, shuffling their feet ect.

171
Q

Akathisia-

A

an uncontrollable urge to be in motion. (his wife getting out of the car after sugery)

Usually develops within the first couple of months after starting the medication.

172
Q

***Tardive Dyskinesia-

A

the most troubling EPS that we have. I

t occurs in about 15-20% of patients on long term high potency antipsychotic therapy.

Risk is directly related to the dose and the duration. So the higher the dose, the greater the risk.

**This is an IRREVERSIBLE movement disorder that is characterized by involuntary Choreoathetioid (snakelike movements) movements. Usually starts in the facial area like the tongue. Over time it progresses to the rest of the body.

Use AIMScale to determine if the patient is getting it.

No reliable management after the patient gets this.

Newer antipsychotics dont cause this as much, but they cause diabetes..

173
Q

Neuroleptic malignant syndrome:

A

rare but serious, risks are worse with high potency drugs such as haloperidol.

The symptoms of neuroleptic malignant syndrome are:
leadpipe rigidity, 
high fever, 
sweating, 
autonomic instability, 
dysrhythmias, 
altered consciousness, 
seizures, 
coma 
death.
174
Q

The treatment for neuroleptic malignant syndrome:

A

supportive measures. *****And immediate withdraw of antipsychotic agents.

175
Q

Minimizing the recurrence of neuroleptic malignant syndrome:

A

do not reinitiate antipsychotic agents for at least two weeks or more.

Consider the lowest dose possible, and possibly switching to an atypical antipsychotic agent.

176
Q

Anti-cholinergic affects traditional antipsychotics:

A

anti-cholinergic side effects are from muscarinic blockade.

You are more likely to see these effects with low potency agents like Chlorpromazine.

These effects are opposite of muscarinic man. No spit, urinary retention, blurred vision, constipation, tachycardia, and cannot sweat.

177
Q

Traditional antipsychotics can cause orthostasis.

A

These drugs are nonselective, so they end up blocking alpha-1 receptors.

Orthostasis can be caused by Venodilators such as the “sin” drugs and diuretics as well.

178
Q

Sedation is caused from

A

histamine blockade.

179
Q

Neuroendocrine effects of traditional antipsychotics:

A

increased levels of prolactin, leads to Gynocomastia, galactorrhea which is the production of breast milk, even in guys.

180
Q

All antipsychotics can lower a persons seizure threshold

True or False

A

true

181
Q

**Sexual dysfunction:

A

50 to 60% of the time sexual dysfunction is caused by traditional antipsychotics and has a higher rate of incident with lower potency antipsychotics like Chlorpromazine.

182
Q

**Dysrhythmias,

A

torsade, which is the distinct EKG finding due to prolonged QT intervals, can cause the heart to quiver and go into VFIB.

(caused by traditional antipsychotics)

183
Q

Contrasting atypical antipsychotic agents from conventional antipsychotic agents:

A

atypicals have the same effect on positive symptoms of schizophrenia, but they do seem superior for cognitive and negative symptoms.

It also appears that they have fewer extraparametal side effects such as tardive dyskinesia, but they can cause big fat diabetic people that have coronary artery disease or metabolic syndrome.

184
Q

Atypical antipsychotic medications method of action:

A

dopamine and serotonin blockade.

185
Q

Clozopine MOA -

A

dopamine and serotonin blockade.

186
Q

Clozopine adverse effects:

A

sedation because of blockade of histamine receptor, orthostasis because of blockade of alpha-1 receptor, anti-cholinergic effects due to blockade of muscarinic receptor,

extraparametal symptoms: much safer for this, less tardive dyskinesia found.

187
Q

Clozapine causes agranulocytosis:

A

very specific to Clozapine. This is why people do not use it. Neutropenia, (neutrophils plummet), 1 to 2% of patients are affected. Have to check a weekly CBC, initially. Happens within the first six months of therapy.

188
Q

Atypical antipsychotics cause diabetes:

A

diabetes can develop or be exacerbated by atypical antipsychotics.

Causes metabolic syndrome. The hallmark signs of metabolic syndrome are overweight, high blood pressure, low HDL, high sugar, and their triglycerides are high.

This increases the patient’s risk for coronary artery disease because diabetics are 4 to 5 times more likely to develop coronary artery disease than normal patients.

189
Q

Atypical antipsychotics cause weight gain:

A

weight gain can be significant such as 30 to 50 pounds. Creates big fat diabetic people.

190
Q

Aripiprazole MOA

A

(atypical antipsychotic) partial agonist, stimulates the receptor but not as much as an agonist. This drug has no weight gain, it’s cleaner, and it’s just as effective.

191
Q

Respiridone-

A

do not give an old people because it causes significant orthostasis and they could fall.

192
Q

Depression:

A

most common psychiatric disorder.

It is estimated that 30% of all people experience clinical depression at some point in their life. A lot of people do not seek treatment for this.

Twice as likely in women compaired to men.

It is vastly undertreated.

It is estimated that only 30% of clinically depressed people actually seek treatment.

193
Q

Clinical features of depression

A

principle symptoms of depression are:

depressive mood,
Loss of pleasure or interest,
loss of concentration,
feelings of guilt and worthlessness,
can have insomnia
can have hypersomnia,
they can have anorexia,
they can also eat everything in sight (hyperplasia?)
Suicide
194
Q

Pathogenesis of depression

A

not completely understood

after Resirpine came out, they figured out that low levels of norepinepherine causes depression

later, they realized that low levels of serotonin actually contribute to depression as well.

195
Q

Suicide and Depression

A

patients who are treated with antidepressants have an increased suicide risk.

Also, because some antidepressants such as tricyclic can be very toxic, it makes it very easy for people to use them to overdose.

196
Q

Tricyclic Antidepressants

A

Amitripyline
Desipramine
Nortriptyline

MOA= increases norepinepherine in the brain

these were the first antidepressants on the market

197
Q

Amtriptyline

A

MOA= increases norepinepherine in the brain

Kinetics- very long 1/2 life so dose once a day

198
Q

Desipramine

A

least anticholinergic of tricyclics so use on older people

199
Q

Nortriptyline

A

least orthostatic of the tricyclics

200
Q

Tricyclic Antidepressants ADR’s

Amitripyline
Desipramine
Nortriptyline

A

Orthostasis: from alpha1 blockade

Anticholinergic Side Effects: from muscarinic Blockade

Sedation: from histamine Blockade

Cardiac Toxicity- overdose and you die of ahrhythmia

Seizures: lowers the seizure threshold

Mania: not for use alone in a Bi-Polar Patient. Must have a mood Stabilizer with it.

201
Q

Toxicity of Tricyclics

Amitripyline
Desipramine
Nortriptyline

A

8 times the therapeutic dose.

If you give more than 8 days at a time, the patient will be able to overdose if suicidal.

common way to commit suicide, especially in women

go to sleep and never wake up

202
Q

Dosage of Tricyclics

Amitripyline
Desipramine
Nortriptyline

A

never start on high doses, start low and go slow.

Dose by clinical response and side effects.

Selection is made off of side effect profile:

example, if the patient has insomnia, you would pick the one that is more sedating.

203
Q

Serotonin is usually _____ into the synapse.

A

Recycled

204
Q

Selective Serotonin Reuptake Inhibitors MOA

fluoxetine

A

Keep serotonin out of the synapse longer so that it has more time to interact with the receptors

205
Q

Fluoxetine (SSRI)

A

came after Tricyclics, and is more safe than tricyclics

Kinetcs: does have a long 1/2 life. Dose once a day

Is an INHIBITOR, so will prevent the breakdown of other medications allowing them to build up to toxic levels within the body

206
Q

Fluoxetine (SSRI) major side effects

A

***sexual dysfunction happens up to 70% of the time for men and women
: Impotence
: Delayed or absent orgasm
: Loss of interest

**Weight Gain

** Serotonin Syndrome

207
Q

**What are the signs and symptoms of serotonin syndrome and what should you do to fix it?

A

occurs within the first 3 days of initiating therapy and can kill you. Symptoms are:

Altered Mental Status
Incoordination
Myoclonus (seizure)
Hyperreflexia
Excessive Sweating
Tremor
Fever

**If these symptoms happen. must stop the SSRI immediately.

208
Q

SSRI’s and Withdrawl

A

the medication must be tapered down slowly if on it for a long time.

It can cause withdrawl symptoms such as:
Dizziness
Tremor
Headache
Nausea
209
Q

Serotonin / Norepinepherine Reuptake Inhibitors

Venlafaxine

Duloxetine MOA:

A

Powerful Blockade of serotonin and Norepinepherine, so that more can hang out in the synapse and stimulate the receptor sites.

210
Q

Venlafaxine

A

MOA: Powerful Blockade of serotonin and Norepinepherine, so that more can hang out in the synapse and stimulate the receptor sites.

**Can potentiate weight loss, but also elevates blood pressure (so need to monitor)

NOT FDA APPROVED FOR NEUROPATHIC PAIN

211
Q

Duloxetine

A

MOA: Powerful Blockade of serotonin and Norepinepherine, so that more can hang out in the synapse and stimulate the receptor sites.

***Initially an antidepressant, but IS APPROVED FOR NEUROPATHIC PAIN (peripheral neuropathy)

212
Q

If you increase norepinepherine, you are going to stimulate what receptors?

A

Alpha 1
Alpha 2
Beta 1

This is why antidepressant drugs that elevate norepi can cause high blood pressure

213
Q

Monoamine Oxidase MOA

A

is found in the gut and intestines, as well as the post ganglionic nerve terminal (where serotonin and norepinepherine is stored and released)

It is responsible for the breakdown of serotonin and norepinepherine.

214
Q

MOA of Monoamine Oxidase inhibitors (MAOI)

Phenelzine

A

by blocking the breakdown of serotonin and norepinepherine in the synapse, the concentrations are going to elevate which allows more stilulation at the receptor sites.

(these are considered a 3 line antidepressant because of their life threatening side effects)

215
Q

MAO-A

A

inactivates or breaks down serotonin and norepinepherine (used in depression)

216
Q

MAO-B

A

Inactivates or breaks down dopamine (Used in parkinsons)

217
Q

Monoamine Oxidase inhibitors (MAOI)
Phenelzine

ADR’s

A

CNS excitation
Orthostasis

***Hypertensive Crisis- there are certain drugs and food interactions that can cause increased levels or norepinepherine to be released into the body (causing ahrythmias and death)

Foods containing TYRAMINE are a trigger, and include Wines, aged meats and cheeses

These people have a strict diet

218
Q

Monoamine Oxidase inhibitors (MAOI)
Phenelzine

Drug interactions

A

Ephedrine and Amphetamine- causes hypertensive crisis

Tricyclic Antidepressants

SSRI’s- leads to serotonin syndrome

Meperidine (demerol) leads to hyperpyrexia

219
Q

Atypical Antidepressants

Bupropion

A

effective antidepressant

more of a stimulant action

effective for craving things such as cigs

less sexual effects

weight loss capabilities

220
Q

Atypical Antidepressants

Mirtazapine

A

new class

claim to fame is it blocks alpha 2 (whoa receptors) and by blocking these it allows for a contiual release of serotonin and norepinepherine

221
Q

Atypical Antidepressants

Trazodone

A

causes Priapism

very sedating (sleep aid)

222
Q

Bi-Polar Disorder

A

Formally known as manic depressive disorder. Effects about 3-7% of the population. Does require long term treatment.

223
Q

Characteristics of Bi-Polar Disorder

A

Alternating episodes of the mood that are abnormally elevated or abnormally depressed, separated by periods when the mood is relatively normal.

Symptoms generally begin in teens to early adulthood

Without treatment, the cycles of either mania or depression can last for months at a time almost like they are stuck in that phase.

Etiology is unknown

224
Q

Types of mood episodes in Bi-Polar disorder

A

Pure Manic

Major Depressive

225
Q

Pure manic

A 
hyperactive
flight of ideas
excessively enthusiastic
have little need for sleep
excessively social and talk alot
over confident
grandiose ideas
delusions of importance
potentially high risk sexual activities
endulge in high risk activities

Kicker is that they do all of this without giving any thought to what they are doing

226
Q

Major Depressive

A

deppressed mood and loss of pleasure or interest in all or nearly all of ones activities

227
Q

Patterns in Bi-Polar

A

very random

can be manic then normal then back to manic to normal then depressed. just cycles randomly

228
Q

Drug Treatment for Bi-Polar people

A

mood stabilizers such as Valproic Acid and Carbamazepine
- Relieve symptoms during manic and depressive episodes

  • Prevent recurrence of symptoms
  • Do not worsen symptoms

Also antipsycotics and antidepressants as needed

229
Q

Antidepressants and Bi-Polar Disorder

A

may be needed during depressive episodes but..

**** always have to be given with a mood stabilizer or will cause patient to become very manic

230
Q

Adherance in Bi Polar Disorder

A

It is difficult to get them to take their medication because they do not see themselves as sick.

They like being manic and do not want to be normal

231
Q

Lithium in Bi-Polar Disorder

A

used since the 70’s.

Structure is similar to sodium so our body treats it like sodium

Kinetics- short 1/2 life, which requires multiple daily dosing in an already non compliant population

Lithobid is dosed twice a day due to sustaned release

232
Q

Lithium is effected by sodium levels in the body

A

and is eliminated renally

233
Q

What can cause lithium levels to rise in a patient

A 
Age due to loss of kidney fuction
NSAIDS
Cold Medications
Dehydration
Diuretics
And Low Sodium Diets
234
Q

Therapeutic Lithium levels

A

0.4 - 1

235
Q

Plasma levels of lithium while being treated for mania

A

0.8 - 1.4

236
Q

Adverse effects of Lithium during therapeutic Levels

A 
GI issues (transient)
Polyuria
Polydipsia
Mild Tremor
Renal Toxicity
***** Hypothyroid disease- Medication induced

Pregnancy category D- Not that great

237
Q

Adverse effects of Lithium during toxicity

A 
Confusion
EKG changes
Fasciculations
seizures
hypotension
coma
death
238
Q

Valporic Acid has replaced Lithium and is now

A

the drug of choice for Bi-Polar Disorder

Pharmacology 2 (7 decks)

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