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Pharmacology 2 > Final Exam Review > Flashcards

Final Exam Review Flashcards

1
Q

Broth Dilution Test-

A

Bacteria are grown in a series of tubes containing different concentrations of different antibiotics. We can establish:

A. Minimum Inhibitory Concentration (MIC)- Lowest concentration of an antibiotic that produces complete inhibition of bacterial growth.

B. Minimum Bactericidal Concentration (MCB)- lowest concentration of drug that produces a 99.9% decline in the number of bacterial colonies.

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2
Q

Minimum Inhibitory Concentration (MIC)

A

Lowest concentration of an antibiotic that produces complete inhibition of bacterial growth.

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3
Q

Minimum Bactericidal Concentration (MCB)-

A

lowest concentration of drug that produces a 99.9% decline in the number of bacterial colonies.

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4
Q

Spontaneous Mutation-

A

random changes in a bacterial DNA. Leads to low level resistance. Additional mutation leads to greater resistance.

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5
Q

CONJUCATION-

A

BACTERIA SEX- where bacteria “communicate” to one another and share/transfer DNA that leads to resistance (sometimes multi-drug resistance).

Can even share with our normal flora. Takes place primarily with GRAM-NEGATIVE BACTERIA.

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6
Q

Bactericidal-

A

bacteria killers

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7
Q

Bacteriostatic-

A

supress growth, but don’t kill

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8
Q

Disk Diffusion Test-

A

inoculating an agar plate, then place discs that contain different ABX on the agar plate.

The degree of sensitivity is proportional to the size of the bacteria free zone around the disk.

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9
Q

Postantibiotic Effect

A

bactericidal activity persists several hours after serum levels have dropped below MBC.

Seen in Aminoglycosides: Drugs: Gentamicin, Tobramycin, Amikacin

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10
Q

Two Drug Bug?

A

PSEUDOMONAS- usually nonpathogenic. Very resistant. TWO BUG DRUG.

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11
Q

Prophylactic Antibiotic Use-

A

ALMOST NEVER INDICATED EXCEPT

  1. Surgery- ex Cefazolin pre surgery
  2. Bacterial Endocarditis- individuals with congenital, valvular heart disease, or prothetic valves take antibiotics before dental procedures and surgery
  3. Neutropenia- ex Bactrim DS in AIDS Patients to prevent Pneumonia
  4. Influenza Outbreaks- Amantadine/ Ramantadine
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12
Q

Signs of a worsening vs resolving infection?

A

A. Monitoring Clinical Response

  1. Fever Curves
  2. WBC: Bands
  3. Regression of Erythema (For Tissue Infections)
  4. Improvement in Chest Xray for Pneumona
  5. General Improvement in health Status
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13
Q

Name 2 Gram positive Cocci

A

Enterococcus & Staph A.

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14
Q

Name 1 Gram Negative Cocci

A

Neisseria Gonococcus

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15
Q

Name 2 Gram Negative Rods

A

E-Coli & Psudomonas

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16
Q

Anti-staph penicillin-

A

NAFCILLIN

-INDICATED for PCNase producing staph (staph aureus and staph epi)

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17
Q

CLAVULANIC ACID

AZOBACTAM,

AND SULBACTAM

A

E.BETA LACTAMASE INHIBITORS (not ABX)

MOA: Inhibits beta lactamase. Combined with PCNs to extend their spectrum to some beta lactamase bacteria (staph aureas, Staph Epi, B. Frag, Proteus, H.Flu).

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18
Q

ntibiotics with excellent anaerobic coverage-

A

Clindamycin-

Metronidazole-

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19
Q

Selective toxicity**

A

the ability of a drug to injure a target cell or organism without injuring other cells or organisms that are not targeted**

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20
Q

Name the 3 ways that Selective toxicity** works by:

A

Disruption of the Bacterial Cell Wall:

Inhibition of enzymes unique to the bacteria:

Disruption of protein synthesis:

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21
Q

Bacteriostatic-

A

supperss growth, but don’t kill

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22
Q

Pathogen-

A

overgrowth or introduction of a new bacteria that causes an infectious response to the host

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23
Q

Superinfection-

A

secondary infection with resistant bacteria.

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24
Q

Nosocomial infection-

A

infection acquired in hospital/ nursing home. Typically very drug resistant.

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25
Q

Common upper respiratory pathogens-

A

H.Flu / Moraxella / Strep Pneumo

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26
Q

Antibiotics that are significant inhibitors and inducers of CYP450

A

inhibitors- Increases Warfarin
Erythromycin, Ciprofloxacin, LevoFloxacin, Moxifloxacin, Quinupristin / Dalflopristin

inducer- Decreases Warfarin
Rifampin

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27
Q

Safe in PCN allergic patients.

A

Quinupristin / Dalflopristin (Synercid)

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28
Q

MRSA- Severe PCN Allergy- Give

A

Vancomysin

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29
Q

________ IS THE ONLY ONE THAT HAS EXCELLENT PSEUD COVERAGE, AND EXCELLENT CNS PENETRATION.

A

CEFTAZIDIME

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30
Q

1st vs 4th generation cephalosporins. What are the differences?

A

AS one progresses from 1st generation to 4th generation

  1. Increased activity against G- rods
  2. Increased resistance to beta lactamase
  3. Increased ability to penetrate the CNS (Meningitis).
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31
Q

Counseling for trimethoprim-sulfamethoxazole therapy

A

drink 8-10 glasses of water a day while taking it.

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32
Q

Tolerance

A

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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33
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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34
Q

What causes Parkinson’s disease?

A

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

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35
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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36
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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37
Q

What is the main neurotransmitter in the peripheral nervous system?

A

Acetylcholine

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38
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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39
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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40
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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41
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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42
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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43
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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44
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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45
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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46
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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47
Q

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

A

levodopa

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48
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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49
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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50
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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51
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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52
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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53
Q

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

A

Levodopa/carbidopa

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54
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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55
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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56
Q

True or False

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

A

True

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57
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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58
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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59
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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60
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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61
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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62
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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63
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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64
Q

Name two dopamine agonists.

A

Pramipexole and Robinirole

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65
Q

What is the method of action of Pramipexole and Robinirole.

A

They bind selectively to central dopamine receptors.

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66
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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67
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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68
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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69
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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70
Q

Name the COMT inhibitors.

A

Entacopone and Tolcapone

The Al Capones of Pharmacology

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71
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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72
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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73
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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74
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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75
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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76
Q

MOA of MAO-A-

A

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

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77
Q

Name a MAO-B inhibitor.

A

Selegiline

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78
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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79
Q

Central acting anticholinergic drugs means?

A

(simply means they are active in the brain)

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80
Q

Name a central acting anticholinergic drug.

A

Benztropine

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81
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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82
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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83
Q

Name the 5 classes of Parkinson’s Drugs

A 
Levadopa
Levadopa/Carbidopa
Dopamine Agonists
COMT Inhibitors
MAO-B Inhibitors
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84
Q

Carbidopa = ________% more Levadopa in the system

A

75

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85
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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86
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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87
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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88
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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89
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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90
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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91
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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92
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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93
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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94
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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95
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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96
Q

What is the MOA of Acetylcholinesterase?

A

It metabolizes Acetylcholine

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97
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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98
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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99
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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100
Q

What class of drugs do Cholinesterase inhibitors interact with?

A

Anticholinergic drugs,

Antidepressants, Tylenol PM

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101
Q

Name the specific Cholinesterase inhibitors

A

Tacrine
Donepezil
Rivastigmine
Galantamine

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102
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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103
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
104
Q

What is the MOA of rivastigmine?

A

IRREVERSIBLE Cholinesterase inhibitor

105
Q

What is the MOA of Galantmine?

A

Reversible Cholinesterase inhibitor

106
Q

What are the cautions for Galantmine?

A

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

107
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

108
Q

What is the MOA of Memantine?

A

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

109
Q

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

A

Memantine

110
Q

What is Glutamate?

A

It is the major excitatory neurotransmitter in the brain

111
Q

What is the major neurotransmitter in the periphery?

A

Acetylcholine

112
Q

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

A

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

113
Q

True or False

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

A

True

114
Q

What drugs are used to treat Mild to Moderate Alzheimers?

A

Cholinesterase Inhibitors

Alzheimers progresses from Mild to Moderate to Severe over time.

115
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.

116
Q

Carbamazepine

serum target level

A

is 4-12 mcg/ml

MOA- inhibits sodium channels

117
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.

118
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.

119
Q

Adverse drug reactions of Carbamazepine-

A

Ataxia,

**hematologic Depression (need to monitor CBC),

agranulocytosis,

SIADH (check serum sodium, concentrates urine),

120
Q

Drug interactions of Carbamazepine-

A

Inducer of CP450. Makes double pac man.

Long 1/2 life, tolerance lessens over time.

121
Q

Phenobarbitol serum sodium target

A

20-40 mcg/ml

122
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.

123
Q

Pharmacokinetics of Phenobarbitol-

A

Enzyme Inducer.

124
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.

125
Q

ADR’s of Valproic Acid-

A

Hepatoxicity and pancreatitis are rare but possible

126
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.

127
Q

Name the Antiseizure medications that are Enzyme Inducers:

A

Phenytoin, Phenobarbitol, and Carbamazepine.

Decrease Target Medication

128
Q

Name the Antiseizure Medication that is an Enzyme Inhibitor.

A

Valproic Acid.

Inhibitor Increases

129
Q

Gabapentin-

A

also used for neuropathic pain

130
Q

Topiramate-

A

used for weight loss now

131
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.

132
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.

133
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

134
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.

135
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)

136
Q

MAO-A

A

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

137
Q

MAO-B

A

Inactivates or breaks down dopamine (Used in parkinsons)

138
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

139
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

140
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

141
Q

Lithium is effected by sodium levels in the body

A

and is eliminated renally

142
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
143
Q

Therapeutic Lithium levels

A

0.4 - 1

144
Q

Plasma levels of lithium while being treated for mania

A

0.8 - 1.4

145
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

146
Q

Adverse effects of Lithium during toxicity

A 
Confusion
EKG changes
Fasciculations
seizures
hypotension
coma
death
147
Q

Valporic Acid has replaced Lithium and is now

A

the drug of choice for Bi-Polar Disorder

148
Q

Adverse Effects of High potency Antipsychotics (Haloperidol)-

A

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

149
Q

Adverse Effects of Low potency Antipsychotics (Chlorpromazine)-

A

Peripheral side effects such as anticholinergic side effects and sleepyness.

150
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.

151
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.
152
Q

The treatment for neuroleptic malignant syndrome:

A

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

153
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.

154
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)-.

155
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.

156
Q

High potency (Haloperidol)-.

A

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

157
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.

158
Q

Tricyclic Antidepressants

A

Amitripyline
Desipramine
Nortriptyline

MOA= increases norepinepherine in the brain

these were the first antidepressants on the market

159
Q

Amtriptyline (Tricyclic Antidepressant)

A

MOA= increases norepinepherine in the brain

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

160
Q

Desipramine (Tricyclic Antidepressant)

A

least anticholinergic of tricyclics so use on older people

161
Q

Nortriptyline (Tricyclic Antidepressant)

A

least orthostatic of the tricyclics

162
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.

163
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

164
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.

165
Q

Phenobarbitol serum sodium target

A

20-40 mcg/ml

166
Q

The treatment for neuroleptic malignant syndrome:

A

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

167
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.

168
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.

169
Q

Atypical antipsychotic medications method of action:

A

dopamine and serotonin blockade.

170
Q

Clozopine MOA -

A

dopamine and serotonin blockade.

171
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.

172
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.

173
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.

174
Q

Atypical antipsychotics cause weight gain:

A

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

175
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.

176
Q

Respiridone-

A

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

177
Q

Atypical Antidepressants

Trazodone

A

causes Priapism

very sedating (sleep aid)

178
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.

179
Q

Clinical Features of Schizophrenia-

A

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

180
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.

181
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.

182
Q

Cognitive Symptoms-

A

disordered thinking, memory difficulties, and focusing abilities.

183
Q

Eitology of Schizophrenia-

A

not exactly known.

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

184
Q

Conventional Pharmacologic agents:

A

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

185
Q

Conventional Antipsychotics-

A

are the more historic medications such as Haloperidol and Chlorpromazine.

186
Q

Bi-Polar Disorder

A

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

187
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

188
Q

Types of mood episodes in Bi-Polar disorder

A

Pure Manic

Major Depressive

189
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

190
Q

Major Depressive

A

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

191
Q

Patterns in Bi-Polar

A

very random

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

192
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

193
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

194
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

195
Q

Epidemiology of Hyperlipidemia

A

In the US by far, the leading cause of death is coronary artery disease. It accounts for over 500,000 deaths per year.

196
Q

Why do we have Cholesterol?

A

Physiological cholesterol is:

  1. A component of our cell membranes.
  2. Important in the synthesis of hormones.
  3. It also makes up the majority of our Bile Acids which are squirted out by the gall bladder to help digest food.
  4. It is also part of the biophospholipid layer of the skin. This helps to protect the body from stuff that is trying to get in, but also keeps stuff in that could otherwise get out.

This is why we cannot lower cholesterol to zero. It has important roles within the body.

197
Q

** Production of Cholesterol

A

we do get some of our cholesterol from nutritional intake, however the vast majority of cholesterol is endogenously produced by the liver.

198
Q

Is TLC as effective in Hyperlipidemia as it is in Hypertention?

A

No

Unlike HTN, where we have TLC that is just as effective as Pharmacotherapy, this is not the case with Hyperlipidemia. Especially as it pertains to bad cholesterol.

TLC is not nearly as effective for patients who have had an MI and think that they can eat their way to an exceptable cholesterol level. It cannot be done because it is part of your genertic make-up.

199
Q

There are 6 major classes of plasma lipoproteins. Out of the 6, which 3 have the most CLINICAL relevance?

A
  1. VLDL
  2. LDL
  3. HDL
200
Q

What does VLDL stand for?

A

Very Low Density Lipoproteins (VLDL)

201
Q

What does LDL stand for?

A

Low Density Lipoprotiens (LDL)

202
Q

What does HDL stand for?

A

High Density Lipoproteins (HDL)

203
Q

What are Very Low Density Lipoproteins (VLDL)?

A

**The majority of Very Low Density Lipoproteins (VLDL) is Triglycerides.

Back in the day, they thought that Triglycerides were way to big to have a DIRECT effect on your risk for coronary artery disease ect…But, we have found out more recently that they do have a direct effect on your risk.

Therefore, we are starting to pay more attention to Triglycerides.

**Triglycerides ARE considered a INDEPENDENT risk factor for Coronary Artery Disease,

204
Q

What are Low Density Lipoprotiens (LDL)?

A

**Low Density Lipoprotiens (LDL) are the most important BY FAR.

The role of LDL is to DELIVER cholesterol away from the liver to NON-Hepatic Tissues.

So essentially it is a deliverer of Cholesterol.

This is notoriously called the “BAD” cholesterol.

The Higher your LDL, there is a DIRECT correlation with risks of diseases caused by cholesterol.

For every 1% REDUCTION in LDL, there is a 1% reduction of risk for cardiovascular disease. (Direct Correlation)

205
Q

What are High Density Lipoproteins (HDL)?

A

High Density Lipoproteins (HDL) are kind-of like a vacuum cleaner. It runs around and picks up cholesterol remnants, and takes them back to the liver to be metabolized.

HDL instead of delivering cholesterol, it grabs it and RETURNS it to the liver.

This is the good stuff. We call this the “GOOD” cholesterol.

The HIGHER your HDL, the better off you are going to be. For instance, probably the best reason that women typically live longer than men because they naturally have a higher HDL level.

** The HIGHER your HDL level, the LOWER your risk is of having Cardiovascular Disease.

206
Q

What is the role of LDL in Atherosclerosis?

A

LDL can pass freely from the arterial lumen into the sub-endothelial space,

In the sub-endothelial space, LDL can become Oxidized.

Oxidation attracts macrophages, which go into the sub-endothelial space and engulf the oxidized LDL and eventually become to fat to come back into the lumen. They then are white foam cells.

An accumulation of these foam cells causes a fatty streak within the artery which eventually herniates inward (stenoses). This makes a rough fibrous cap.

Which causes a supply and demand mismatch because not enough blood can flow through. (Angina).

If sheer forces occur, such as from sexual activity, elevated Blood Pressure, constipation,sudden stress, the fibrous cap can tear off (like a scab) and lipid contents can spill out causing a thrombus formation that can lead to a complete bloackage.

This causes an infarct of the area that the artery supplied.

207
Q

What does NCEP stand for?

A

National Cholesterol Education Program (NCEP)

208
Q

What does the National Cholesterol Education Program (NCEP) do?

A

They make the guidelines (bible) that Doctors follow in order to properly manage a patients cholesterol.

209
Q

What is the first step that the NCEP recommends that patients follow?

A

Screening:

The first step is educating patients to get their initial screening at 20 years of age or older.

This should be a FASTING lipid panel .

Once they have their initial screening, they need to repeat it every 5 years or so.

210
Q

Who is at greatest risk for hyperlipidemia?

A

Patients who already have established CHD (coronary heart disease)

Always ask the patient if they have any kind of heart disease or previous MI. (including people the had by-pass, stents ect)

211
Q

What is secondary prevention?

A

This refers to a person who already has Established CHD (coronary heart disease)

212
Q

What is primary prevention?

A

People that have RISK EQUIVALENTS for CHD but to NOT have CHD yet.

213
Q

What are the 5 risk equivalent categories?

A

Patients with:

  1. Peripheral Vascular Disease
  2. Carotid Artery Disease
  3. Type 2 Diabetes
  4. AAA
  5. Framingham of <20% risk

These patients, along with pre-existing CHD are at greatest risk for an MI

214
Q

According to NCEP, first we identify patients according to PMHx, then risk equivalents such as AAA, PVD, T2DM, and CAD. At this stage, if we have not found anything, what do we look for next?

A

screen for Major Risk factors.

The order of screening is:

  1. Past history of CHD
  2. Risk Equivalents
  3. Risk Factors

The higher on the list you are, the more likely you are to have problems.

215
Q

What are the Major Risk Factors that NCEP has you screen for?

A
  1. Cigarette Smoking- 1 cig within the last month would count.
  2. HTN- 140/90 - even if on BP meds and well controlled.
  3. LOW HDL- if less than 40
  4. Positive Family History for CHD
  5. Age- male 55, female 65

This is the one negative risk factor. (meaning it is a good thing)

  1. If HDL >= 60
216
Q

If your patient already has existing CHD, do you need to screen them for risk equivalents or risk factors?

A

No, if they have existing CHD, they go straight to the top of the list.

(Secondary Prevention)

217
Q

If your patient does not have existing CHD but they do have a risk equivalent, do you need to screen them for risk factors?

A

No, even though they do not have existing CHD, if they have a risk equivalent it takes them to the top of the list

(Primary Prevention)

218
Q

If you have evaluated your patent and they do not have existing CHD, they do not have any risk equivalents, but they do have 2 or more major risk factors, what would you complete next?

A

If 2 or more risk factors are present, calculate Framingham 10 year risk assessment and place the patient in the correct category of risk.

219
Q

What is FRAMINGHAM?

A

it is an estimation of 10 Year risk for CHD for men and women.

220
Q

What are the major factors in FRAMINGHAM? (5 of them)

A
  1. Age
  2. Smoking
  3. Systolic BP
  4. Total Cholesterol
  5. HDL

These are the things that you need to know in order to evaluate the patients risk. There is a different sheet to use for men and women. What you do is plug these variables in and it comes out with some sort of risk. This is used to categorize the patient. This is important in determining how aggressive you will treat the patient as well as what medication and dose they should be on.

221
Q

What are the categories of risk in Framingham?

A

Patient Populations are:

  1. High Risk
  2. Moderate Risk
  3. Low Risk
222
Q

Who falls into the High Risk Population in a Framingham assessment and what is their treatment goal?

A

High Risk Patient Population includes:

Patients with CHD and CHD risk equivalents.

(10 year risk of MI of >20%)

Their LDL goal is <100

223
Q

Who falls into the Moderate Risk Population in a Framingham assessment and what is their treatment goal?

A

Moderate Risk Patient Population includes:

Multiple 2+ risk factors

(10 year risk of MI of 10-20%)

Their LDL goal is < 130

224
Q

Who falls into the Low Risk Population in a Framingham assessment and what is their treatment goal?

A

Low Risk Patient Population includes:

0-1 Risk Factor

(10 Year risk of <160

225
Q

Patients with:

  1. Peripheral Vascular Disease
  2. Carotid Artery Disease
  3. Type 2 Diabetes
  4. AAA
  5. Framingham of
A
226
Q

Once we establish the risk establishment goals from the framingham assessment, What is the next thing that we do?

A

We look for secondary causes of dyslipidemia BEFORE initiation of various therapies.

Just like in HTN, we learned that diseases such as Pheocromocytoma can be a secondary cause of HTN and if you fix it, it can resolve the patients HTN.

Patients can also have secondary causes to their dyslipidemia that if fixed could resolve it.

227
Q

What are the secondary causes of Dyslipidemia?

A
  1. Uncontrolled Diabetes
  2. Hypothyroid Disease
  3. Protein Wasting Syndromes
  4. Certain Medications such as anabolic steroids and certain progesterone types of medications.

If you identify a secondary cause, you MUST try and control it first.

In most cases it is not caused by secondary issues.

228
Q

TRUE OR FALSE

TLC in patients with Dyslipidemia is just as effective as Pharmacotherapy, like TLC in HTN was

A

False

TLC may only lower the Patients LDL about 10% even if they ate like a bird.

It is generally not enough to keep the patient from having to utilize pharmacotherapy.

Any reduction is better than nothing so we do teach the patient about TLC.

229
Q

Therapeutic Lifestyle Changes (TLC) are non-drug measures used to positively impact the lipid panel.

What do they consist of?

A
  1. Diet- reduce saturated fat and cholesterol in the diet by drinking low fat milk, trimming the fat off of meat ect.. and also increasing your fiber.
  2. Weight Reduction
  3. Increasing Physical Activity.
230
Q

What are the normal triglyceride levels

A

< 150

231
Q

What are borderline triglyceride levels

A

150 - 199

232
Q

What are high triglyceride levels?

A

200 - 499

233
Q

What are Very high triglyceride levels?

A

<= 500

234
Q

When triglycerides are over 500 what are you at risk for?

A

Pancreatitis.

When over 500, VLDL becomes your primary target because if pancreatitis is not treated it can cause a septic like syndrome and the patient can die.

Once the triglycerides are back below 500, the primary target goes back to LDL.

235
Q

When a patients LDL has been treated and is at goal, what do you perform next?

A

You re-evaluate the patients triglycerides.

If they are greater than 200, you need to calculate a NON-HDL calculation.

This is done by taking the patients Total Cholesterol and subtracting the HDL.

That number should be less than 30 points higher than the patients LDL goal.

236
Q

If the patient has an LDL goal of < 100, what is their NON-HDL goal?

A

130

237
Q

What are the secondary targets of therapy for CHD?

A

Metabolic Syndrome
Hypertriglyceridemia if <200
Low HDL

238
Q

TRUE OR FALSE

Triglycerides respond great to TLC

A

TRUE

If you eat right, your triglycerides go down

if you exercise, your triglycerides go down

If you control your diabetes, your triglycerides typically improve.

If you drink excessive alcohol, your triglycerides will improve.

239
Q

What is Low HDL defined as

A

< 40.

Patients that have high triglycerides have low HDL.

240
Q

TRUE OR FALSE

Through randomized controlled trials, we actually found that using pharmacotherapy to manipulate a persons HDL makes a huge impact in CHD

A

FALSE

It actually showed no evidence that it even makes a difference.

HDL also responds to TLC so better to use that instead of Pharmacotherapy

241
Q

True or False

The lower you get someones LDL, the better off they will be

A

True

Studies proved that significantly lowering a patients LDL especially after the patient has already had By-pass or stents placed, the better off they are

we have yet to figure out how low is too low.

patients are now being kept below 70 even though they are at their LDL of less than 100.

Some people have decreased all the way to 30 and are fine.

This only pertains to secondary prevention patients.

242
Q

What is The most effective and widely used cholesterol medication that we have?

A

Statins:

The most potent LDL reducers that we have that is what makes them the most effective.

They can reduce events by up to 30-35%

It is prolonging how long we live.

243
Q

What is the MOA of Statins?

A

hydroxymethylglutaryl coenzyme A (HMG-CoA) Reductase Inhibitor.

This is an enzyme that is critical in the synthesis of cholesterol. So if we wipe this enzyme out, out body cannot make an adequate amount of cholesterol.

244
Q

If you wipe out (HMG-CoA) Reductase and the body needs more cholesterol, what does the liver do?

A

it sucks it out of the blood stream because it cannot make it,

This is how it lowers LDL

245
Q

Are statins linear or non linear drugs?

A

Non- Linear

This means that you get a big bang for your buck at the lowest doses.

This means that if you double your dose, it will not lower your LDL any more than like 6%.

246
Q

What are the net results of Statin therapy?

A

It can lower your LDL up to 60%

can lower VLDL by like 3%

247
Q

What are the Kinetics of Statin therapy

A

SAL

Simvastatin
Atorvastain
Lovastatin

are metabolized by CYP3A4

These have significant drug interactions

248
Q

What is the category for pregnancy for statins?

A

x

Not safe during pregancy

249
Q

What are the side effects of Statin therapy?

A
  1. Myalgia (1-5%)- myalgia simply means that something is going on with the muscles.
  2. Myositis- (Moderate elevation in CPK) Inflammation of the muscles.
  • Large muscles like thighs and butt, back.
  • Is terrible, like being beaten with a bat.
  • It is BILATERAL, usually associated with a fever.
  • Older people show signs of weakness and less pain
  1. Rhabdomyolysis- this is where muscles start to break down. It can lead to kidney failure. (Very rare)
  2. Transaminase Elevation- Approx 0.5-2%.- which is AST/ALT. When these are elevated it means that the liver is inflamed or irritated. Not indicative of function. Very Rare.
    - For Liver function we test- Albumin is low, Billirubin is high, PT/INR is high. Those are indicative of liver function.
250
Q

What is the MOA of Niacin?

A

Decreases production of VLDL.

**Increases HDL

Decreases LDL

This is the one drug that does everything correctly.

***It is THE BEST HDL increaser.

It is the 2nd Best LDL reducer (2nd to statins)

It is the 2nd best VLDL reducer

251
Q

If a patient cannot take a Statin due to true Myosytis, than which drug are you going to put them on to lower their LDL?

A

Niacin

Reduces LDL by about 35%

252
Q

To what percent does Niacin lower VLDL?

A

up to 40%

253
Q

To what percent does Niacin increase HDL?

A

up to 35%

254
Q

What are the adverse effects of Niacin?

A

Flushing (More common with IR)

GI Toxicity

Hepatoxicity (more common with SR)

Hyperglycemia - only 1/3 of diabetics will require any adjustment in dose

Hyperuricemia- (can cause gout)

255
Q

What is your counseling for Niacin?

A

**1. Start low and go slow

**2. Take it with food.

**3. Take an NSAID or Aspirn 30 min before Niacin

**4. Avoid taking with alcohol and hot or spicy foods or beverages.

**5.After a week or 2, you will become tolerant to that dose. Teach them to take IR at night.

**6. Avoid Interruption of therapy. If you run out of it, you have to start over with your tolerance level. (flushing, burning, itching)

  1. 2 grams per day cap on SR niacin. Not a cap on IR Niacin
256
Q

What are the fibrates?

A

Gemfibrozil and Fenofibrate (Tricor)

Pharmacology 2 (7 decks)

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