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IPAP Class 21-2 > Pharmacology 3 > Flashcards

Pharmacology 3 Flashcards

1
Q

Def of neuromodualtor

A

Any substance that has an effect on neurotransmission

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2
Q

What are the types of transmission in the brain

A

Chemical and voltage

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3
Q

What is essential for CNS drugs

A

Selectivity

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4
Q

What influx signals NT’s

A

Calcium

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5
Q

Two methods of NT action

A

Degradation via enzymes

Reputable into the presynaptic neuron

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6
Q

What activates para and sympathathetic systems and is degraded by acetylcholinesterase

A

ACH

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7
Q

What amino acids are degraded by transaminase?

A

GABA (sedative)
Glutamate/aspartame (stimulating)
Glycine/taurine (INHB /+ Excitatory)

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8
Q

Amines degraded by Monoamine Oxidase

A

Dopamine
NE
Serotonin
Histamine

[Excitatory or Inhibitory based on class]

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9
Q

Neuropeptides degraded by peptidses

A

Opioid

Techykins

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10
Q

Define sensitization

A

Up regulation of receptors, caused by long term antagonism or reduction of NT release

** may be more sensitive to medications **

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11
Q

Define desensitization

A

Down regulation of receptors, caused by sustained release or slower elimination of NT’s

Examples = Opioids

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12
Q

What defines a major depressive episode

A

Period of 2 weeks with 5 or + depressive symptoms

*Depressed mood
*Anhedonia (inability to feel pleasure)
Insomnia
Hypersomnia
Change in appetite or weight
Psychomotor retardation or agitation
Low energy
Poor concentration
Thoughts of worthlessness or guilt
Recurrent thoughts about death or suicide

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13
Q

Patients that had one major depressive episode and do not have a history of mania or hypomania.

A

Unipolar Major Depression or MDD

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14
Q

Depression that lasts 2 or more years with symptom-free periods being less than 2 consecutive months. (May include periods of MDD)

A

PDD or dysthymia

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15
Q

What causes mood disorders and how do we try to fix it?

A

Nearly all mood disorders are caused by an abnormal functional activity of neurotransmitters in the brain

By enhancing or blocking the presence (effect) of the neurotransmitters in the synaptic cleft, we are attempting to change or “normalize” the mood

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16
Q

3 main types of depression

A

Reactive or Secondary (Most Common): response to grief, illness, drugs, alcohol, senility

Unipolar: genetically determined and unable to experience ordinary pleasure or cope with life events (Major Depressive Disorder)

Bi-Polar Affective: depression associated with mania (manic-depressive

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17
Q

When are Psychotherapy and Exercise recommended

A

Recommended as monotherapy as initial treatment in patients with mild to moderate MDD
Cognitive Behavioral Therapy (CBT

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18
Q

When would we use electroconvulsive therapy

A

Option for refractory depression, depression in pregnancy, psychotic depression, and other conditions for which medications may not be optimal or effective
Cycle is three treatments/week

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19
Q

What preg category are most antidepressants

A

Cat C

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20
Q

What happens in the absence of a serotonin reputable inhibitor

A

serotonin (5-hydroxytryptamine, or 5-HT) is released from raphe neurons that project to limbic structures.

Serotonin activates postsynaptic and presynaptic 5-HT receptors and undergoes reuptake into the presynaptic neuron

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21
Q

What class of antidepressants blocks retake of 5-HT

A

TCA
SSRI
SNRI

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22
Q

What happens with continued use of a TCA SSRI or SNRI

A

increased synaptic concentrations of 5-HT cause the down-regulation of presynaptic autoreceptors and an increase in the firing rate of raphe neurons.

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23
Q

What is the efficacy of Benzo’s

A

Not classified as an anti-depressant

Used short-term in acute anxiety management while SSRIs are initiated

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24
Q

What are the tertiary TCA’s and their role?

A

More potent at blocking reuptake of serotonin > norepinephrine

Include: 
amitriptyline, 
clomipramine, 
doxepin, 
imipramine
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25
Q

What are the secondary TCA’s and their role?

A

More potent in blocking reuptake of norepinephrine > serotonin

Include:
nortriptyline,
desipramine,
protriptyline

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26
Q

MOA of TCA’s

A

Block the reuptake of norepinephrine and serotonin (precursors to SNRI) into the presynaptic neuron which increases the concentrations of monoamines in the synaptic cleft (debated theory

Also block alpha adrenergic, histamine and muscarinic receptors (anticholinergic side effects

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27
Q

Clin use of TCA’s

A

Depression
(Not first line)

Anxiety Disorders

Numerous off labeled uses such as:
Treatment for pain syndromes: useful in chronic pain but the reason is not clear
Migraine prophylaxis

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28
Q

TCA Pharmacokinetics / Warnings

A

Dosage adjustments upward will be needed due to low and inconsistent bioavailability and adverse effects

Cautions/Warnings:
Most commonly used drug in an overdose
Can produce serious, life-threatening cardiac arrhythmias, delirium, coma, seizures, and psychosis

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29
Q

ADE’s of TCA’s

A

Anticholinergic Effects: dry mouth, urinary retention, constipation, blurred vision

Dry mouth is a suggested link to weight gain due to the tendency for patients to drink excessive caloric beverages

The anticholinergic effects will make BPH worse

α receptors antagonist: orthostatic hypotension

Antihistaminic effects: sedating

Cardiovascular:
Can worsen arrhythmias due to quinidine like effect
Use with caution in ischemic heart disease, arrhythmias or conduction disturbances

Withdrawal Syndrome (if discontinued quickly)

Symptoms:
GI complaints, dizziness, insomnia and restlessness
Flu like symptoms

COMMON DRUG INTERACTIONS

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30
Q

Which TCA’s have high sedation and anti-cholinergic affects? (3)

A

Amitriptyline

Doxepin

Clomipramine

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31
Q

Which TCA’s have low sedation and anti-cholinergic affects and alpha blockade? (2)

A

Desipramine

Nortiptyline

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32
Q

COMMON SSRI’S and others (2)

A 
Fluoxetine
Fluvoxamine
Paroxetine
Sertraline
Citalopram
Escitalopram

Vilazodone
Vortioxetine

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33
Q

MOA of SSRI’S

A

Inhibit serotonin reuptake, without affecting reuptake of norepinephrine or dopamine into the presynaptic neuron

SSRI’s do not significantly effect histamine, muscarinic or other receptors

** Onset of action takes 3-8 weeks (or even longer in some cases**

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34
Q

Clin use of SSRI’S

A 
Depression
Obsessive Compulsive Disorder
Panic Disorder
Social Phobia
PTSD
Premenstrual Dysphoric Disorder (PMDD) 
Generalized Anxiety Disorder

** Low cost and best tolerability**

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35
Q

Pharmacokinetics of SSRI’S

A

Elimination half-life of SSRI’s is about 1 day
Fluoxetine has the longest half-life at 1-3 days for parent drug and active metabolites are 4-16 days
Fluvoxamine is the shortest with half-life at 15 hours

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36
Q

Which SSRI’S do not interact with CYP 450?

A

citalopram and escitalopram

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37
Q

ADE’s of SSRI’S

A

Gastrointestinal: nausea, diarrhea, constipation

CNS: agitation, anxiety, tremor, or panic may be seen in during the early phase of therapy

Most activating: fluoxetine and sertraline
Avoid in patients having trouble sleeping and give in the morning

Most sedating: paroxetine and fluvoxamine
Dose in the evening
Weight Gain (paroxetine is the worst)

Sexual Dysfunction

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38
Q

What are the three most severe ADE of SSRI’S

A

Serotonin Syndrome
Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH)

EPS side effects:
Include akathisia, dystonias, and parkinsonian symptoms
Reported with all SSRI’s, but paroxetine has the most reported

Especially with elderly

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39
Q

Treatment for Serotonin Syndrome

A 
Withdraw offending agent(s)
Supportive care
Anxiety/seizures 
benzodiazepines
Hyperthermia
ice, cooling blankets
Cyproheptadine 
1st generation antihistamine, and 5HT1A and 5HT2 antagonist
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40
Q

Which SSRI does not cause withdrawal symptoms

A

Fluoxetine

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41
Q

Common drug interactions of SSRI’S

A 
Bleeding Risk
Aspirin products
NSAIDS
Variable CYP interactions
Monoamine oxidase inhibitors (MAOIs)
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42
Q

Indication for Fluoxetine

A

PTSD
MDD

Premenstrual dysphoric disorder

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43
Q

Indication for Sertraline

A

PTSD

MDD

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44
Q

Indication for Paroxetine

A

PTSD
Panic Disorder
MDD
* Not rec for children *

CAN CAUSE CARDIAC SEPTAL DEFECTS IN 1ST TRI EXPOSURE

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45
Q

Indication for Fluvoxamine

A

Clinical Use: MOSTLY Obsessive-Compulsive Disorder
Considered sedating and more serotonin selective than most of the other SSRIs
Potent 2D6 Inhibitor

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46
Q

At what dose should Citalopram not be used and why

A

Citalopram should no longer be used at doses > 40mg/day due to the potential to cause QT prolongation and other cardiovascular electrical abnormalities.

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47
Q

What drug is an analog but more potent than citalopram

A

Escitalopram (Lexapro)

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48
Q

Vortioxetine Indication

A

MDD

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49
Q

Vortioxetine Drug Interactions

A

Strong inhibitor of CYP2D6
(Reduce the dose)

Substrate of CYP2D6 and CYP3A4
(Increase the dose)

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50
Q

Main and Other SNRI’s

A

Main SNRI medications
Duloxetine (Cymbalta)
Venlafaxine (Effexor)
Desvenlafaxine (Pristiq)

Other SNRI medications
Levomilnacipran (Fetzima)
Milnacipran (Savella)

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51
Q

MOA of SNRI’s

A

inhibit the reuptake of 5HT and NE, increasing their levels; little activity for alpha adrenergic, cholinergic, or histamine receptor

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52
Q

Which SNRI’s are associated with elevated diastolic blood pressure at higher doses

A

Venlafaxine, desvenlafaxine, and duloxetine

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53
Q

Drug interactions of SNRI’s

A

Both substrates and mild to moderate inhibitors of CYP2D6

SNRIs should not be used with MAOIs or other serotonergic agents

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54
Q

What is the clin use of Venlafaxine

A

Severe or treatment-resistant depression
Generalized anxiety disorder (GAD)
PTSD (1st line agent along with SSRIs)
Benefits:

Safer than TCAs in overdoses

Not as activating as fluoxetine

Unique MOA so it can be used when SSRIs have failed

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55
Q

What is unique about the dosage of venlafaxine

A

Works as an SSRI at doses ~75mg/day; SNRI at >225mg/day.

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56
Q

Venlafaxine is contrained in what two cases?

A

MAOIs inhibitors and triptans

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57
Q

Clin use of Des venlafaxine

A 
Clinical Use:
2nd line agent for MDD
No advantage over Venlafaxine
Adverse Effects: same as venlafaxine
Contraindication: same as venlafaxine
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58
Q

Clin use of Duloxetine

A 
Severe or treatment-resistant depression
Generalized anxiety disorder
Diabetic peripheral neuropathy
Fibromyalgia
Chronic musculoskeletal pain caused by chronic lower back pain or osteoarthritis pain
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59
Q

What patients should not take duloxetine

A

Should NOT be used in patients with hepatic insufficiency, end-stage renal disease requiring dialysis, or severe renal impairment

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60
Q

What is unique about levomilnacipran / its clin use / and ADE’s

A

Mechanism of Action:
Stronger inhibitor of norepinephrine reuptake than duloxetine (Cymbalta) or venlafaxine (Effexor)

More active isomer of the SNRI milnacipran (Savella)
Milnacipran (Savella) approved for fibromyalgia, not depression

Clinical Use: only for depression

Adverse Effects:
May cause hyponatremia and increase bleeding risk
Blood pressure elevation and orthostatic hypotension can occur

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61
Q

What are the drug interactions of Levomilnacipran

A

CYP3A4 substrate

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62
Q

Drug class of BUPROPION and MOA

A

NDRI

dopamine and norepinephrine reuptake (at high doses) inhibitor with minimal activity on serotonin

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63
Q

Clin use and ADE of Bupropion

A

Clinical Use:
MDD
Brand Name Zyban indicated for smoking cessation
Unlabeled Use: adjunctive agent in ADHD in children and adolescents

Adverse Effects:
Headache, insomnia, irritability, nausea, vomiting, decreased appetite
Weight loss ~4kg
Increased risk of seizures

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64
Q

What is contrained with use of bupropion

A

Alcohol Benzos and MAOI’s

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65
Q

SRA’s and common effects

A

Medications:
Trazodone
Mirtazapine
Nefazodone

Common effects:
Antagonists of 5HT2 family of receptors
Antagonists of α1 receptors
Antagonists of Histamine1 (H1) receptors – causes drowsiness

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66
Q

What receptors are inhibited by Trazodone

A

5HT2A, H1, and α1 receptors

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67
Q

Clin use of Trazadone and main ADE

A

Clinical Use:
Can be used for depression, but usually in combination with SSRI/SNRI in patients with sleep disorders
At low doses used as an agent for sleep
Compared to TCAs, has fewer anticholinergic side effects and fewer effects on the cardiac system

Drowsiness

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68
Q

Receptors inhibited by Mertazapine

A

5HT2A, 5HT3, H1, α1 and α2

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69
Q

Clin use and clearances of Mirtazapine

A

MDD in combo w SSRI’S

Renally cleared

Profound sedative efffect

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70
Q

MOA of Nefazodone

A

: Inhibits 5HT2 family of receptors, α1 receptors, and reuptake of serotonin + norepinephrine

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71
Q

Clinical use of nefazodone

A

Anxious depression

or in SSRI use that is too activating/sexual dysfunction
Considered a 2nd or 3rd line agent

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72
Q

ADE’s (5) and Black box warning for Nefazodone

A

Common: GI complaints, dry mouth, constipation, confusion, and light-headedness

Risk of liver failure

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73
Q

Drug interactions of Nefazodone

A

INHB of 3A4

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74
Q

MOA of MAOI’s

A

blocks the enzyme responsible for the break down of norepinephrine, dopamine and serotonin

which increases the stores of these transmitters in the neurons

Two Forms: MAO-A and MA

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75
Q

Clin use and Interactions of MAOI’s

A

Clinical Use:
Atypical depression (hypersomnia, hyperphagia, and mood reactivity)
Patients refractory to other anti-depressant agents

Interactions: the infamous food-drug interactions caused by these medications occur because they inhibit MAO in the GI track that normally breakdown tyramine

Can cause hypertensive crisis

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76
Q

What are the MAOI’s

A

‘Phenelzine

Selegilne

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77
Q

What are the regards for switching from an antidepressant to an MAOI

A

Wait 2 weeks after discontinuing antidepressant before initiating the MAOI

Except Fluoxetine waiting period should be 5-6 weeks

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78
Q

Clin use of Selegiline

A

MDD

MAO-B Inhibitor

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79
Q

What is the adequate trial of an antidepressant agent

A

full therapeutic doses for 2-8 weeks and in some cases for up to 12 weeks

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80
Q

Define response and remission

A

usually defined as a 50% reduction in symptoms

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81
Q

What antidepressant are likely to cause sexual dysfunction

A

SSRI’S

SNRI’s

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82
Q

What antidepressant are likely to cause Weight gain

A

Most all antidepressants

**except bupropion and fluoxetine

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83
Q

What antidepressant are likely to cause somnolence

A

TCA’s misrtazapine aroxetine trazadone

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84
Q

What antidepressant are likely to cause an increase in energy

A

Bupropion or an SNRI

Fluoxetine and Sertraline

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85
Q

What antidepressant are likely to cause anxiety

A

Bupropion

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86
Q

What antidepressant are likely to cause a reduction in pain

A

Duloxetine venlafaxine

amitriptyline and imipramine

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87
Q

What patients would you consider Vortioxetine in?

A

Overweight
Sexual dysfunction
Psychomotor slowing

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88
Q

What two antidepressants/anxiety meds do not require tapering when discontinuing

A

Fluoxetine

Bupropion

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89
Q

What are thyroid stimulants good for

A

Resistant depression

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90
Q

What atypical antipsychotics have approval as augmentations to antidepressant therapy

A

Aripiprazole and Quietiapine

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91
Q

What antidepressant can cause heart defects in pregnant patients newborn

A

Paroxetine

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92
Q

Mania vs/ Hypomania

A

Mania: the affective opposite of depression; characterized by at least 1 week of an abnormal and persistently elevated mood

Hypomania: similar to a manic episode, but it exists for 4 days or longer; not severe enough to warrant hospitalization, does not impair social or occupational functioning, and is not associated with psychosis

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93
Q

Cyclothymic disorder

A

Several periods of hypomania and mild depression that do not meet criteria for mania or MDD

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94
Q

BPI vs BPII

A

Bipolar I (BPI):
Chronic disorder marked by one or more manic or mixed episodes and major depressive episodes
Recurrent manic or mixed manic episodes more frequent and severe compared to depressive episodes; more hospitalizations

Bipolar II (BP II):
Chronic disorder marked by one or more major depressive episodes, accompanied by at least one hypomanic episode
Recurrent major depressive episodes alternating with hypomanic episodes; no mania, less hospitalizations, more common in females, more often rapid cycling

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95
Q

Define rapid cycling

A

four or more episodes of mania, hypomania, mixed mania, or depression in a one-year period; need to assess thyroid function

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96
Q

What overproduction is likely to cause a manic episode

A

NE and serotonin

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97
Q

Clin use of Lithium

A

Effective for manic and depressive components

Anti-manic effects can occur in 1-2 weeks

*discontinue after resolves

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98
Q

Discuss monitoring with lithium treatment

A

Narrow therap. Index
Half Life 20-24 hours
CBC, electrolyte, thyroid Preg Test

anything that alerts GFR affects its clearance

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99
Q

If pt has a tremor with lithium use, what do you do?

A

Reduce dose and add Beta blocker

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100
Q

If pt has CNS toxicity what should yo do with the lithium prescription

A

Reduce dose

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101
Q

If pt has GI issues on lithium what should you do

A

Reduce dose and try extended release product

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102
Q

If pt has hypothyroidism on lithium what should you do

A

Discontinue or give levothyroxine

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103
Q

Discuss lithium and sodium concentrations

A

If NA+ is not reabsorbed and hyper depleted remaining sodium and lithium are reabsorbed from proximal tubules and can increase concentration

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104
Q

Interaction of Lithium and NSAIDs

A

Decreased Li excretion causes increased Li serum levels; avoid use to reduce toxicity

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105
Q

What are the anticonvulsants

A

Valproic Acid derivatives
Carbamazepine (Tegretol, Equetro)
Lamotrigine (Lamictal)
Topiramate (Topamax)

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106
Q

When is valproic acid better than lithium

A

Rapid cycling
Comorbid substance abuse
Secondary bipolar disorder
Mixed mania

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107
Q

Preg Cat of Valproic acid and Divalproex

A

D

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108
Q

Clin use of Carbamazepine

A

Effective for acute mania and maintenance therapy
Used for long-term management

Can be added to lithium for patients who have not responded to monotherapy

Carbamazepine (Equetro) approved by the FDA for acute manic/mixed episodes

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109
Q

ADE’ s of carbamazepine

A

Hyponatremia, including SIADH can occur
Rash/Steven’s Johnson Syndrome
Agranulocytosis

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110
Q

Which anticonvulsant is effective for the depressed phase of bipolar disorder

A

Lamotrigine

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111
Q

If you give lamotrigine with carbamazepine what should you do

Primary concern of lamotrigine

A

Double the dose of lamotrigine

RASH

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112
Q

Use of BZD’s in bipolar disorder

A

Useful for insomnia, hyperactivity, and agitation

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113
Q

What are the acutely used BZD’s

A

Lorazepam, Diazepam

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114
Q

When is clonazepam used

A

Brief behavior symptoms

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115
Q

What two antipsychotics can control agitation and psychosis

A

Haloperidol

Olanzapine

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116
Q

What two antipsychotics are approved as mono therapy in bipolar disorder

A

Olanzipine and Aripiprazole

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117
Q

What is happening physiologically in Parkinson’s

A

Dopamine normally inhibits GABA in substantia nigra

Acetylcholine excites GABA in substantia nigra

In Parkinson’s there is a gradual loss of dopaminergic neurons

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118
Q

How does Parkinson’s affect mental status

A

Depression (50%)
Dementia (25%)
Psychosis
*May be precipitated or worsened by drugs

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119
Q

What are the secondary symptoms of Parkinson’s

A

Cognitive Dysfunction: amnesia, anxiety, dementia, confusion in the evening hours

Autonomic Dysfunction: dribbling of urine or leaking of urine
Speech Disturbances: impaired voice, soft speech, or voice box spasms

Micrographia “small handwriting”: handwriting appears cramped in patients with Parkinson’s

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120
Q

What are the drug induced dopamine antagonists

A

[Antipsychotics]
Prochloroperazine (Compazine)

Chlorpromazine (Thorazine)

Trifluoperazine (Stelazine)

Thioridazine (Mellaril)

Haloperidol (Haldol)

[Antiemetics]

Metoclopramide (Reglan)

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121
Q

What disease can induce Parkinson’s dz

A

Viral encephalitis

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122
Q

What drug can improve Parkinson’s motor disability

Drug that can Lessen motor complication?

A

Levodopa

Dopamine

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123
Q

What type of Parkinson’s pt receives monoamine oxidase inhibitor or dopamine agonist first

A

Younger
Bio fit
Mild symptomatics

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124
Q

What type of Parkinson’s pt receives L-DOPA therapy first

A

Bio unfit
Co-morbid
Cognitively impaired

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125
Q

If a Parkinson’s pt is experiencing the following symptoms what do you do

Dyskinesia

Motor Fluctuations

Tremors

A

Reduced L-DOPA

Subcutaneous aporphibe or duodopa

Deep brain stimulation

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126
Q

First line Txm in Parkinson’s dz

A

Dopamine agonist

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127
Q

Which drug has the greatest effect on bradykinesia and rigidity

A

Levodopa

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128
Q

Dopamine Agonists

A

Bromocriptine (Parlodel)
Pramipexole (Mirapex)
Apomorphine (Apokyn
Ropinirole (Requip)

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129
Q

Muscarinic antagonists

A

Benztropine (Cogentin)

Trihexyphenidyl (Artane)

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130
Q

NMDA Inhibitor

A

Amantadine (Symmetrel)

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131
Q

COMT Inhibtors

MAO Inhibitors

A

Catechol-O-Methyl-Transferase (COMT) Inhibitors:

Tolcapone (Tasmar)
Entacapone (Comtan)
Carbidopa/levodopa/entacapone (Stalevo)

Monoamine Oxidase (MAO) Inhibitors:

Selegiline (Eldepryl, Zelapar, Deprenyl)
Rasagiline (Azilect) (Therapeutic effects are not robust)

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132
Q

MOA and main receptor for Dopamine agonists

A

Act directly on postsynaptic dopamine receptors
Do not require enzymatic conversion

D2 family receptors (D2, D3 and D4): stimulation of D2 family improves rigidity and bradykinesia

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133
Q

Treatment of this drug Delays levodopa for years and advantages

A

Dopamine agonists

Advantage: less dyskinesia and fluctuations than levodopa; long half-life results in less dyskinesias
Not oxidized into free radicals

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134
Q

What pt symptoms worsen with dopamine agonists

A

Psychotic and/or dementia pts

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135
Q

non selective dopamine agonists

A

Bromocriptine

Rotigotine
Transdermal

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136
Q

Non selective dopamine agonist ADE’s

A 
Pleuropulmonary and/or cardiac fibrosis is a concern
Chest x-ray with abnormal pulmonary exam
Postural hypotension, dizziness
Hallucinations, mental confusion
GI disturbances
Digital vasospasm and leg cramps
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137
Q

D2 and D3 selective agonists

A

Pramipexole (Mirapex)

Ropinirole (Requip)

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138
Q

ADE’s and contraindications of D2 and D3 selective agonists

A

Adverse Effects:
Postural hypotension (at the initiation of therapy)
GI problems
Mental confusion
Dizziness
Hallucinations
Somnolence (all dopamine agonist can cause daytime sleepiness)

Contraindications:
History of psychotic illness
Recent myocardial infarction (MI)
Active peptic ulceration

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139
Q

Clin use of pramipexole (4 things)

A

Clinical Use:
Effective as monotherapy for mild parkinsonism and in patients with advanced disease

Allows the dose of levodopa to be reduced and smoothing out response fluctuations in advance disease.

Possible neuro-protective effect

Ability to scavenge hydrogen peroxide and enhance neurotrophic activity

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140
Q

Clin use of ropinirole

A

Clinical Use:
Affective as monotherapy in patients with mild disease
Allows the dose of levodopa to be reduced and smoothing out response fluctuations in advance disease

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141
Q

D2 Selective agonist

A

Apomorphine (short acting)

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142
Q

Clin use of apomorphine

A

Clinical Use: acute, intermittent treatment of “off” episodes associated with advanced Parkinson disease; recurring hypomotility, “off” episodes

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143
Q

Most severe ADE and treatment of apomorphine

A

Severe Nausea/vomiting (98%)

Treatment: prophylaxis with trimethobenzamide (anti-emetic) 3 days prior to initiating apomorphine and continued for the first month of therapy, if not indefinitely

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144
Q

Contraindications of apomorphine

A

5-hydroxytryptamine-3 antagonists (5-HT3) antagonists

IV use (thrombus formation)

Sulfite sensitivity (preservative)

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145
Q

MOA of carbidopa

A

Aromatic Inhibtor that DOES NOT CROSS THE BBB

Prevents peripheral conversion of levodopa to dopamine

Increases avail of levodopa to cross into the CNS

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146
Q

Levodopa MOA

A

Mechanism of Action:
Precursor to dopamine that has the ability to cross the BBB and replenish depleted dopamine in the brain
Converted into dopamine in the periphery

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147
Q

Clin effects of levodopa

A

Clinical effects:
Improvement in disability and possibly mortality
Greatest effect on bradykinesia and rigidity; less effect on tremor and postural instability

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148
Q

How long is the honeymoon stage of levodopa

A

3-5 years

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149
Q

Main ADE of Carbidopa/Levodopa

A

Dyskinesias (excessive dopamine):

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150
Q

What dz is contrained or has precautions for the use of C/L

A

Contraindications:
psychotic illness, narrow-angle glaucoma, use of non-selective MAOI’s

Precautions:
Peptic Ulcer Disease (PUD)
Malignant Melanomas: levodopa is a precursor of skin melanin and conceivably may activate malignant melanoma

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151
Q

When should a pt take selegiline

Which is more potent selegiline or rasagiline

A

Early afternoon to prevent insomnia

[in conjunction with levodopa]

RASAGILINE MORE POTENT

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152
Q

MOA OF COMT INHB and Clin use

A

Mechanism of Action: prevents the breakdown of dopamine, more levodopa available to cross blood-brain barrier

Clinical Use:
Manage motor fluctuations (“wearing-off” effect)
Adjunct to levodopa/carbidopa in patients with response fluctuations or who have failed or can not use other therapies

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153
Q

Most commonly noticed ADE of Entacapone (COMT-INHB)

A

Orange Urine

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154
Q

COMT Inhibitors

A

Tolcapone [ EXTREME HEPTATOXICTY ]

Entacapone [ USE WITH C/L / DOES NOT CROSS BBB ]

Stalevo [ C/L/ENTACAPONE ]

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155
Q

Anticholinergic MOA and Clin use

A

Mechanism of Action: block the excitatory neurotransmitter acetylcholine to try and restore balance with dopamine
Clinical Use:
Most effective on tremors and rigidity
DOC for drug-induced (anti-psychotics) parkinsonism
Does not relieve symptoms of tardive dyskinesia

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156
Q

Anticholinergics

A

Benztropine [ controls EPS symptoms ]

Trihextphenidyl

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157
Q

N-methyl-D-aspartate (NMDA) Receptor Inhibitor / Clin Use

A

Amantadine

Clinical Use:
Posses symptomatic benefits and may reduce dyskinesias caused by levodopa or dopamine agonists
Not as effective on bradykinesia, rigidity, tremor and dyskinesia as anticholinergics

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158
Q

Most common ADE of Amantadine

A

Livedo Reticularis (rash)

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159
Q

Two categories of seizures

A

Generalized - originates at some point within and then engages neural networks

Focal - involves only a portion of the brain impaired consciousness or awareness

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160
Q

Tonic

Vs.

Clonic

Vs.

Myoclonic

Vs.

Atonic

A

Tonic: flexion and/or extension

Clonic: rhythmic, repetitive, jerking muscle movements

Myoclonic: brief, lightning-like jerking movements of the entire body or the upper and occasionally lower extremities

Atonic:
Characterized by a loss of muscle tone

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161
Q

What is an absent seizure

A

Typical seizures are brief and abrupt, last 10-30 seconds, and occur in clusters
Usually results in a short loss of consciousness, or the patient may stare, be motionless, or have a distant expression on his or her face

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162
Q

What is an epileptic seizure

A

2 or more seizures

Epileptic Seizure: clinical manifestation presumed to result from abnormal and excessive discharge of a set of neurons in the brain that results in abnormal movements or perceptions

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163
Q

Discuss cause and treatment of primary vs secondary epilepsy

A 
Primary Epilepsy: no specific anatomic cause 
Drug treatment (MAY) be for life

Secondary Epilepsy: reversible disturbances responsible for seizures
Tumors, trauma, hypoglycemia, alcohol withdrawal
Drug treatment is used until the primary cause of the seizure can be corrected

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164
Q

When do you perform Venus nerve stimulation

A

For difficult to manage partial seizures

Implanted stimulator delivers stimuli on a regular basis and patients can use “on demand” stimulation

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165
Q

When can we attempt withdrawal from seizure therapy

A

Seizure free for 2-5 years

Single seizure type

Normal neurological exam and IQ

Normal electroencephalogram (EEG) with medication treatment

withdraw slow and one at a time

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166
Q

MOA of anticonvulsants (3 mechanisms)

A

blocking the initiation or preventing the spread of electrical discharge by several mechanisms

1) Enhancement of GABAnergic transmission
2) Diminution of excitatory transmission (i.e. Glutamate)
3) Modification of ionic conductance (i.e. Calcium, Sodium

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167
Q

What two drugs have a narrow spectrum in absent seizures

A

Ethosuximide

Valproate (alternative)

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168
Q

MOA and Clin Use of Phenytoin

A

Mechanism of Action: fast sodium channel blocker

Clinical Use:
Generalized tonic-clonic (not 1st line)

Simple or complex partial seizures with or without generalization (not 1st line)

Status Epilepticus

**DO NOT USE in Absence seizures

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169
Q

Administration Considerations of Phenytoin = (Dilantin, Phenytex)

A

IV Formulation: very basic product
Prepare only in normal saline solution

Oral suspension: shake well; adheres to feeding tubes and is bound by enteral nutrition products

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170
Q

Non dose related ADE’s of phenytoin

Vs.

Dose related

A

Non Dose:
Sexual dysfunction
Hirsutism (excessive hair growth), gingival hyperplasia (40-90%)
Long term use causes coarsening of facial features

Dose:
Nystagmus (rapid eye movement), ataxia, drowsiness, cognitive impairment

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171
Q

Preg Cat of Phenytoin

A

Preg Cat D

172
Q

Drug interaction of Phenytoin on

1) Anticoagulants
2) Contraceptives

A

Anticoagulants (oral): may increase phenytoin serum concentration; decreased/increased anticoagulant effects

Contraceptives: reduces efficacy of estrogen-containing contraceptives, oral progestin-only contraceptives, and the etonogestrel implant

173
Q

Kinetics of Phenytoin

A

Zero-Order Kinetics: drug concentration changes with respect to time at a constant rate;

174
Q

MOA for Fosphenytoin ; ADVANTAGES?

A

Mechanism of Action: PRODRUG for phenytoin; fast sodium channel blocker

Advantages over phenytoin:
Preferred when parenteral administration is needed (reduced extravasation, faster load)

1mg of phenytoin = 1.5 mg of fosphenytoin

175
Q

MOA and Clin use of Carbamazepine

A

Mechanism of Action: fast sodium channel blocker
** CYP3A4 inducer and auto inducer (self induction)**

Clinical Use:
Only available orally
Primary generalized tonic-clonic, simple or complex partial
Newer anticonvulsants are beginning to displace it from this role
Other uses: trigeminal neuralgia and bipolar disease

176
Q

Common ADE’s of carbamazepine

A

Diplopia
Rash
SIADH

177
Q

Serious ADE’s of Carbamazepine

A

Hyponatremia

Bone marrow suppression (mild leukopenia)

Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis (especially patients of Asian heritage with HLA-B 1502 mutation)

Multi-organ hypersensitivity: potentially fatal reaction characterized by cutaneous eruption, fever, lymphadenopathy, hematologic abnormalities, and visceral manifestations

Hepatotoxicity (Very rare)

Osteomalacia

178
Q

Drug interactions and pregnancy category of Carbamazepine

A

Pregnancy Category: D; teratogenic, neural tube defects

Drug Interactions: CYP 3A4 substrates
Lamotrigine may also increase carbamazepine epoxide levels
Reduces efficacy of estrogen-containing contraceptives

179
Q

Genetic testing recommendations for carbamazepine

A

HLA-B*1502 is common in Asians ancestry (>15% of populations in Hong Kong, Malaysia, the Philippines, and Thailand)

HLA-A*3101 occurs more frequently in patients of African-American, Asian, European, Indian, Arabic, Latin American, and Native American ancestry

180
Q

MOA : Fast sodium channel blockers

A

Oxcarbamazepine

Carbamazepine

Fosphenytoin

Phenytoin

181
Q

Clin use of Oxcarbamazepine

A

General tonic clonic
Trigminal neuralgia
Bipolar

Good for pts who do not tolerate carbamazepine*

182
Q

What is more common in oxcarbamazepine than carbamazepine?

A

Hyponatremia

183
Q

Carbamazepine or Phenytoin?

A

Carbamazepine FIRST!

  • LESS SEDATING
  • NO HIRSUTISM/ ACNE/ HYPERPLASIA
  • NO LEARNING IMPAIRMENT
184
Q

MOA of Phenobarbital and Primidone

A

Increases GABA mediated chloride influx

185
Q

Clin use phenobarbital / preg category / ADE’s

A

Clinical Use:
Generalized tonic-clonic seizures, simple or partial seizures
Refractory status epilepticus; tried for virtually every seizure type, especially when attacks are difficult to control

Adverse Effects: sexual dysfunction, hyperactivity and cognitive impairment

Pregnancy category: D

186
Q

Primidone special MOA characteristic

A

Metabolized to phenobarbital and phenylethylmalonamide

may be used with carbamazepine and phenytoin

187
Q

Most common Benzo’s

A

Diazepam (Valium)*
Lorazepam (Ativan)*
Clonazepam (Klonopin)

188
Q

What effect does high dose Benzo’s cause

A

Higher doses may cause ataxia (shaky movements and gait) and behavior changes

189
Q

MOA of Gabapentin and Clin Use

A

MOA:
Inhibition of α2δ subunit of voltage-dependent calcium channels
An analog of GABA, but does not directly impact GABA receptor

Clinical Use:

Partial onset seizures
Neuropathic pain and post herpetic neuralgia pain
Spasmolytic
Diabetic neuropathy (off-label)

190
Q

Pharmacokinetics of Gabapentin

And ADE’s

A

Eliminated renally

Drowsiness, fatigue, dizziness, headache, weight gain, and tremor during initiation

191
Q

Pregabalin MOA

A

Inhibition of α2δ subunit of voltage-dependent calcium channels.

GABA derivative similar to gabapentin that binds pre-synaptically to the alpha-2-delta subunit

192
Q

Main Clin use of Pregabalin

A

Non-epileptic: neuropathic pain

193
Q

Ethosuximide Clin Use

A

DOC in absence seizures

194
Q

Serious ADE’s of Ethosuzimide

A

Neutropenia (rare, 7%)

Transient leukopenia (common)

Hematologic toxicity (extremely rare)

195
Q

Derivatives of Valporic Acid (2)

A

Valproate (Depacon injection),

Divalproex (Depakote

196
Q

What is the parenteral use of valporic acid

A

Parenteral Use: FDA indication only for replacement of oral dosing;

sometimes used for status epilepticus = [ seizure lasting longer than 5 minutes ]

197
Q

ADE’s of Valporic acid

A

Common: alopecia, N/V, interferes with platelet aggregation, pancreatitis, sedation, weight gain (average of 2 kg after one year), rash

Serious:

Thrombocytopenia
Multi-organ hypersensitivity
Black box warning for hepatic failure fatalities

198
Q

Preg category for Valporic Acid in migraine prophylaxis

A

X

Substantial increase in the incidence of spina bifida

199
Q

Describe Valporic Acid Overdose

A

Can lead to CNS depression: somnolence and deep coma

** Naloxone may reverse CNS depressant effects, theoretically it can have a convulsant effect**

200
Q

MOA of Lamotrigine

A

Decreases glutamate and aspartate release

Delays repetitive firing of neurons

Blocks fast sodium channels

201
Q

How can yo avoid the Steven Johnson Syndrome Rash when administering Lamotrigine?

A

Titration should be done slowly upward

202
Q

Clin use of Topiramate / Preg Cat

A

Primary generalized tonic-clonic seizures, simple or complex partial with or without generalization
Absence seizure (adjunct)
Lenox-Gastaut
Non-epileptic: migraine prophylaxis

Preg Cat D

203
Q

Common and Serious (Common and Serious) ADE of Topiramate

A

Common
:Memory Impairment

Serious
:Metabolic Acidosis

204
Q

What can decrease Topiramate levels by 50%?

A

Carbamazepine and Phenytoin

Reduced efficacy of Contraceptives

205
Q

Clin use of Levetiracetam

A

Myoclonic seizures 12 yrs and older
Lenox-Gastaut [severe childhood epilepsy]
General tonic clonic/epilepsy 6 yrs and older

206
Q

What is another word for disorganized schizophrenia

A

Hebephrenia,

Extreme expression of disorganization syndrome, 1/3 factor of 3 factors of schizo. Others are :

  • Delusions/hallucinations
  • Psychomotor poverty (absence)
207
Q

Paranoid vs. Residual vs. Undifferentiated Schizo

A

P = Delusions of deceit

R = Blunted inappropriate emotion

U = Prominent psychotic symptoms without top 3 factors

208
Q

Primary NT’s of psychological abnormalities

A

Dopamine
5-hydroxtryptamine (5HT; serotonin)
Glutamate

209
Q

Pneumonic for 1st gen Antipsychotics

A

-Zine, -Xene, -Xapine + Halodol

210
Q

Pneumonic for 2nd gen Antipsychotics

A

-prazole, -pine, -done

211
Q

Max treatment response rate in atypical antipsychotics

A

Response to medications is NOT immediate, maximal treatment response may take 6 months or longer to be observed

212
Q

Which antipsychotic is common for and how does it exert anti emetic effect

A

(Most Typical Agents): due to blockage of D2 in the chemoreceptor trigger zone of the medulla

Prochlorperazine

213
Q

Hiccups longer than 2 days can be treated with what antipsychotic

A

Chlorpromazine

214
Q

Rapid acting Formulations of Antispychotics vs Long Acting Formulation use?

A

Rapid Acting Formulations: used to handle acutely agitated and disruptive behavior

Long Acting Formulations: used in patients that lack compliance

215
Q

Brief Explanation of EPS symptoms

A

Dystonia: abnormal tonicity; severe muscle spasm of the head, neck and tongue

Tardive Dyskinesia (may not be reversible)
Syndrome of involuntary movements of the face, mouth, tongue, trunk and limbs

Akathesia (most common EPS)
Desire to be in constant motion (inability to sit still, pacing).

216
Q

What drugs can cause Tardive Dyskinesia

A

High affinity D2 receptor drugs Ex: Haloperidol

217
Q

How can you treat Akathesia

A

Low dose propranolol

Dose reduction

218
Q

Black Box Warning of Antiphyschotics

A

increase mortality in elderly patients with dementia-related psychosis

219
Q

Typical 1st Gen MOA

A

Competitive blockers of dopamine receptors D2 in the mesolimbic pathway
ALSO histamine, muscarinic, alpha receptors

Less effective at negative symptoms

220
Q

Characteristics of Low Potency D2 Receptor Agents (3)

A

Low affinity for dopamine receptors, anticholinergic, a-adrengergic blocking

Less EPS

Highly sedative autonomic ADE’s

221
Q

Characteristics of High Potency D2 Receptor Agents (2)

A

High affinity for the dopamine receptors; thus higher rates of extrapyramidal symptoms (EPS)

Less potency at the other receptors

222
Q

High anticholinergic effects =

A

Fewer EPS symptoms

223
Q

Pseudo Parkinsonism pharmaco TXM

A

Anti-cholinergic: Trihexyphenidyl or Benztropine

Antihistamine: Diphenhydramine (Benadryl) IM/IV

224
Q

Typical Antipsychotic ADE’s (6)

A

Worse Neg Symptoms

Prolonged QT interval

Postural hypotension

Weight Gain

Anticholinergic

Sedation

225
Q

Define Neuroleptic Malignant Syndrome

A

High Potency induced agitation, fever, techs, hypertension

MOST SEVERE REACTION TO 1st GEN’S

226
Q

Hyperprolactinemia

A

Blocked Dopamine = prolactin elevation

Women = galactorrhea and menstrual irregularities

Men = gynecomastia, sexual dysfunction and decreased fertility

227
Q

Low Potency Antipsychotics

Vs

High Potency Antipsychotics

A

Chlorpromazine (Thorazine) IV/ PO
Thioridazine (Mallari) PO

Trifluoperazine (Stelazine) PO
Fluphenazine (Prolixin) IM
Haloperidol (Haldol) IV/IM/PO

228
Q

Which med has the highest occurrence of sedation

A

Thioridazine

229
Q

What is the most important ADDE of Chlorpromazine

A

May cause pigmentary deposits on the retina and corneal opacity

230
Q

Which antipsyhcotic is affective in generalized non psychotic anxiety but can produce long term tardive dyskinesia

A

Trifluoperazine (Stelazine) PO

231
Q

Which antipsychotic can mange prolonged paranteral neuroleptic therapy

A

Fluphenazine decanoate (Prolixin)

232
Q

Clin use of Haloperidol

A

Clinical Use: management of schizophrenia, acute agitation, and for the control of tics and vocal utterances of Tourette’s Disorder

233
Q

IV Halodol has been linked to toxicity including what dz?

A

torsade’s de pointes

234
Q

MOA of 2nd Gen Antipsychotics

A

Dopamine antagonists, but also block 5HT2A receptors (block 5HT to a greater extent than dopamine)

Exception: Aripiprazole is a partial agonist at D2 and 5HT1A agonist and a 5HT2A antagonist

235
Q

What are the common ADE’s of 2nd gen atypicals

A

Weight Gain

Hyperglycemia

Diabetes Mellitus

Lipid abnormalities

236
Q

What is the oldest atypical agent most effective in reserved patients resistant to 2 or 3 agents including typical and atypicals

A

Clozapine

237
Q

Black box warning of Clozapine

A

Agranulocytosis

238
Q

Abrupt discontinuation of clozapine can cause what

A

Fatal myocarditis

239
Q

Serious ADE of Olanzipine

A

Excessive weight gain, sedation, and hypotension compared to the other atypical agents

240
Q

Risperidone clin use

A

Schizophrenia acute psychosis and prevention

Bipolar mania and maintenance therapy

More effective at combating the positive symptoms

Children 10-17 yrs old

241
Q

Which antipsychotic has the MOST prolactin elevation

A

Risperidone

242
Q

Risperidone is similar to what analog?

A

Paliperidone

243
Q

What antipsychotic is a good choice for psychosis occurances with Parkinson’s Disease

A

Quetiapine

**also schizophrenia, bipolar, depression

244
Q

ADE’s of quetiapine (3)

A 
Very sedating (antihistamine effects)
Significant orthostatic hypotension should monitor BP
Cataracts
245
Q

Advantage and Disadvantage of Ziprasidone

A

Advantage: lower risk of metabolic syndrome and prolactin elevation
Disadvantage: Higher risk of QTc prolongation and cataracts

246
Q

Aripiprazole Clin Use

A

Schizophrenia maintenance and acute agitation

Manic or mixed Bipolar disorder

Depression in combination with SSRI or other antidepressants

247
Q

MOA, Clin Use, and Advantage of Asenapine

A

Mixed serotonin-dopamine antagonist

Clinical Use:
Schizophrenia maintenance and acute agitation
Manic or mixed Bipolar disorder

Adverse Effects:
Medium risk of sedation, tardive dyskinesia and EPS

248
Q

MOA and Clin Use of iloperidone

A

Mechanism of Action: mixed D2/5-HT2antagonist activity

Clinical Use: schizophrenia only

249
Q

Major ADE’s (3) of iloperidone

A

Higher risk of orthostatic hypotension and QTc prolongation

Esophageal dysmotility/aspiration

250
Q

MOA no Clin Use of Lurasidone

A

Mechanism of Action: mixed serotonin-dopamine antagonist activity

Clinical Use: schizophrenia and bipolar disorder only

251
Q

Sedative vs. Hypnotic

A

Sedative (anxiolytic): reduces anxiety and exerts a calming effect with little or no effect on motor or mental function

Hypnotic: produces drowsiness and encourages the onset and maintenance of a state of sleep resembling natural sleep

252
Q

Two major classes of sedatives

A

Two major historical classes were benzodiazepines and barbiturates

253
Q

What happens when GABA binds to the GABA receptor

A

relaxation and sedation

254
Q

What type of binding do sedatives and hypnotics exert

A

Allosteric binding , enhanced inhibitory effect of GABA

-increases chloride influx

255
Q

Disadvantages of barbiturates

A

ability to cause coma in toxic doses, physical dependence, and severe withdrawal symptoms

256
Q

Which short acting barbiturate does not end in -barbital?

A

Methohexital

257
Q

What can Phenobarbital treat?

A

Anticonvulsant: sedation, management of seizures & eclampsia

258
Q

Barbiturates ADE’s

A

CNS depression
Hangover
Withdrawal symptoms
Overdose TXM

Preg Cat D

259
Q

Phenobarbital MOA and Clin Use

A

Mechanism of Action: increases GABA mediated chloride influx

Clinical Use:
Generalized tonic-clonic seizures, simple or partial seizures
Refractory status epilepticus
Can be tried for virtually every seizure type

260
Q

Short, Long, Intermediate Benzos

A

Short Acting Agents
Midazolam (Versed)
Oxazepam
Triazolam (Halcion)

Long Acting Agents
Chlordiazepoxide (Librium)
Clonazepam (Klonipin)
Diazepam (Valium)
Flurazepam (Dalmane)
Quazepam (Doral)
Intermediate Acting Agents
Alprazolam (Xanax)
Estazolam (ProSom)
Lorazepam (Ativan)
Temazepam (Restoril)
261
Q

Longer half life Benzo’s =

Short Half Life (Quick) Benzo’s =

A

More hangover symptoms

High tolerance for hypnotic effect/common withdrawal

262
Q

Clin use of Benzo’s

A

Anxiolytic (Sedative)

Hypnotic: all benzodiazpines induce sleep if high enough doses are given

Muscle Relaxation

Anticonvulsant

Anesthesia/Amnesic actions

263
Q

How do benzos exert relaxation

A

Central Action

264
Q

What Benzo’s are best for alcohol withdrawal

A

Oxazepam, Lorazepam, Diazepam

265
Q

What BZD’s are good for anxiety

A

Clonazepam and lorazepam and diazepam [ short term use ]

266
Q

What BZD’s are good for panic attacks

A

Clonazepam, Alprazolam, Oxazepam

267
Q

What is a good agent for PTSD

A

SSRI - 1st line

268
Q

Short acting BZD’s for sleep induction

A

Triazolam

269
Q

Intermediate acting sleep maintenance BZD (2)

A

Temezepam and Estazolam

270
Q

Long acting BZD to reduce sleep, time, awakenings and increase duration

A

Flurazepam and Quazepam

271
Q

Long acting coverage of alcohol withdrawal

A

Chlordiazepoxide

Diazepam

272
Q

3 common complaints of BZD’s

A

Residual daytime sedation

Rebound insomnia

Anterograde amnesia

273
Q

How long should you use BZD’s as Txm

A

3-4 months

274
Q

Drugs that increase CNS depression

A

Alcohol

Antihistamines

Antipsychotics

Antidepressants

Opioids

275
Q

CYP3A4 interactions are minimal with which drugs

A

lorazepam, oxazepam, and temazepam (weak substrate)

276
Q

BZD’s are _____ recommended for peds geriatrics

A

NOT

LOT, if you must.

277
Q

Shorter half life leads to ______ dependence liability and more withdrawal

A

Higher

278
Q

BZD rescue agent

A

Flumazenil

279
Q

Buspirone MOA most common Clin Use

A

Mechanism of Action: (Not fully understood)
Has high affinity for serotonin receptors
Has moderate activity at D2 receptors

Clin use
Often used as a second line agent or when BZD should avoided to manage anxiety

280
Q

Zolpidem MOA and Clin Use

A

Mechanism of Action: acts on the benzodiazepine receptor by enhancing GABA activity (not chemically related to BZD)

Clinical Use: Only use is for insomnia
IR for difficulty going to sleep
CR for sleep maintenance issues

281
Q

(3) Common ADE’s of Zolpidem

A

Depression and suicidal ideations

Associated with abnormal thinking and behavior changes:
Decreased inhibition, aggression, bizarre behavior, agitation, hallucinations, and depersonalization

Causes functional dependence but no physical cravings

282
Q

Eszopiclone ADE common

A

Metallic taste

283
Q

Zaleplon MOA and Clin Use

A

Mechanism of Action: acts on BZD receptor, but is chemically not related to BZD

Clinical Use:
Short-term treatment of insomnia

284
Q

Which hypnotic is least likely to cause daytime somnolence?

A

Zaleplon

285
Q

Suvorexant MOA and Clin Use

A

Mechanism of Action: orexin-receptor antagonist

Clinical Use: treatment of insomnia

286
Q

MOA of Ramelteon

A

Mechanism of Action: melatonin receptor agonist. [Melatonin maintains circadian rhythm (sleep-wake cycle)]

287
Q

Tasimelteon MOA and Clin Use and ADE

A

Mechanism of Action: melatonin receptor agonist

Clinical Use:
Non-24-hour sleep-wake disorder that is generally present in blind patients due to lack of stimulus from the sun

Adverse Effects:
Headache and abnormal dreams

288
Q

Antihistamines can do what for insomnia and act on what receptors?

Examples of 2?

A

(H1 antagonists)

Diphenhydramine or Doxylamine

Sedating and anticholinergic effects

289
Q

Anxiety disorder acute management

A

benzodiazepines are the drug of choice for short term use

290
Q

Buspirone and Pregabalin can be used for what

A

Second line Agents for augment of SSRI or SNRI if low response in GAD treatment

291
Q

What Benzo’s is preferred for Panic Disorder Txm

A

Clonazepam

292
Q

What subtype of Social Anxiety Disorder uses propranolol?

A

Performance anxiety

293
Q

First line agent for OCD, what can be used to augment Txm

?

A

SSRI’S

Antipsychotics ; Halodol and 2nd Gen’s

294
Q

What antipsychotics are approved for PTSD Txm and what is first line

A

quetiapine, olanzapine, and risperidone

First line = SSRI’S

295
Q

What MDD med is significant for seizures?

A

Bupropion

296
Q

What BAC level achieved in 2 hours is significant for binge drinking

A

0.08g/dL

297
Q

What is the most severe form of alcohol withdrawal? When does it occur?

A

Delirium Tremens

1-10 days after last drink

298
Q

What is a good Benzo’s for alcohol withdrawal?

A

Diazepam

299
Q

What two benzos are associated with propylene glycol poisoning?

A

Lorazepam and Diazepam

300
Q

What is Wernicke’s Encephalopathy?

A

Presence of neurological symptoms, a triad of confusion, ataxia and ophthalmoplegia associated with ethanol withdraw due to chronic alcoholism

Depleted B-Vit Reserves = CNS lesions

301
Q

First line TXM of Alcohol dependence

A

Naltrexone and Acamprosate

302
Q 
What can Disulfiram (Antabuse)
Topiramate (Topamax)
Gabapentin (Neurontin)
Baclofen (Lioresal)
SSRI’s
Be used to treat?
A

2nd line for alcohol dependence

303
Q

Naltrexone MOA and main Clin Use

A

Mechanism of Action: Derivative of naloxone. Competitive antagonist at opioid receptor sites, showing the highest affinity for mu receptors.
Clinical Use:

Reduces alcohol dependence, cravings and consumption

304
Q

Naltrexone can have what effect on opioids?

A

Blocks effects of opioids

Will precipitate opioid withdrawal
If a patient is on Depo dose, opioids will not be adequate for pain control

305
Q

Acampasate is similar to what? And must be taken how often?

A

GABA

3 times a day

reduce or stop if renal insufficient

306
Q

MOA of Disulfiram

A

Inhibits aldehyde dehydrogenase (ALDH), blocking the metabolism of ethanol at the acetaldehyde step.

307
Q

What accumulates in a disulfiram reaction?

A

Acetalaldehyde

308
Q

What two drugs may also help in alcohol abuse?

A

Baclofen and Gabapentin

309
Q

What supplements (2) can help with ADHD Txm?

A

Iron , if deficient

And Zinc

310
Q

How do drugs increase learning potential and productivity of adhd pts? (3)

A

Decreasing motor activity
Increasing coordination
Improving ability to attend to task

311
Q

Stimulants for ADHD use (4)

A

Amphetamines
Dextroamphetamine
Methylphenidate/ Dexmethylphenidate
Lisdexamfetamine

312
Q

Non Stimulants for ADHD

A 
Atomoxetine (Strattera) 
Clonidine XR (Kapvay)
Guanfacine XR (Intuniv)
313
Q

Class of amphetamines and derivatives

A

Class 2

314
Q

MOA and Clin use of Amphetamines and derivatives

A

Mechanism of Action:
Promote release of catecholamines (primarily dopamine and norepinephrine) from their storage sites in the presynaptic nerve terminals
May have some effect on decreasing reuptake also

Clinical Uses:
Attention-deficit Hyperactivity Disorder (ADHD)
Narcolepsy
Obesity

315
Q

How do amphetamines effect the sympathetic nervous system?

A

Alpha and Beta

Increased BP
Increase in heart rate
Weak bronchodilation

316
Q

Addererall is mix of what?

A

Dextroamphetamine + Amphetamine

317
Q

Lisdexamfetamine is converted to what?

A

Dextroamphetamine in the blood stream

318
Q

What is preferred stimulants or non-stimulants?

A

Stimulants are preferred to non-stimulants;

have a rapid onset of action and long record of safety and efficacy

319
Q

First line non stimulant drug for ADHD and MOA

A

Atomoxetine

Blocks repute of NE

320
Q

MOA of clonidine , treats what two main dz’s?

A

Central a2 agonist

Impulsive behavior and Tourette’s

321
Q

Guanfacine MOA and is indicated for what children?

A

Central a2 agonist

Children with tic disorders

322
Q

What drug class is efficient for ADHD with depression

A

TCA’s

Impramine
Desipramine

323
Q

Clinical Use: improve wakefulness in adult patients with excessive sleepiness associated with obstructive sleep apnea (OSA), narcolepsy or shift work disorder (SWD)

A

Modafinil

324
Q

What is a mehtylzanthine antagonist of adenosine receptors that increases cAMP and equally response to CO2

A

Caffeine

325
Q

BMI’s for obesity

A

Overweight = BMI 25 to 29.9kg/m2
Obesity = BMI ≥ 30kg/m2
Severe obesity = BMI ≥ 40kg/m2

326
Q

When should yo discontinue use of weight loss mediations?

A

advise discontinuing medication if at least 5% weight loss is not achieved after 12 weeks of use

327
Q

Orlistat can do what?

A

Reduce fat and absorption and digestion

328
Q

Amphetamines can do what for obesity?

A

Suppress appetite

Increase thermogenesis

Can lead to rebound binge eating

329
Q

SSRI’S can do what for obesity?

A

Suppress appetite

330
Q

MOA of phentermine

A

promotes appetite suppression and decreased food intake secondary to its sympathomimetic activity

331
Q

When should you take the combo of phentermine and Topiramate?

A

In the morning to avoid insomnia

332
Q

Naltrexone and Bupropion can be used to do what?

A

Reduce cravings and appetite

333
Q

How does orlistat inhibit lipase?

A

by inhibiting GI lipase activity in the small intestine

30% of fat excreted in feces

334
Q

GLP -1 agonist for Type 2 Diabetic TXM

A

Liraglutide

335
Q

How is gastric acid secretion regulated

A

Proton pup o activation at parietal cell

Acetylcholine
Histamine
Gastrin

336
Q

What is a good start Txm after dietary and lifestyle mods;;;; and if that doesn’t work?

A

Start with H2 inhibitors in addition with antacids for breakthrough GERD symptoms

Make sure H2 is at max dose then after 4 weeks —> PPI

more freq GERD starts with PPI

337
Q

Common causes of PUD (4)

A

H. Pylori

NSAID

Stress Ulcers or Stress- Related Mucosal Damage

Zollinger Ellison Syndrome

338
Q

Gastric ulcer pain is worse when?

Duodenal ulcer pain is worse when?

A

G : When eating

D : At night, relieved by eating

339
Q

Noninvasive Diagnostic tests for H. Pylori

A

Recall antigen assay

Urea breath testing

Serologic testing

340
Q

Anti-secretory Txm for H. Pylori;;;;;; 1st and 2nd line therapies.

A

PPI

1st : Clarithromycin + Amoxicillin (or metronidazole)

2nd : tetracycline + metronidazole + bismuth subsalicylate

341
Q

What happens after Txm for h.pylori?

A

Confirmation of Erradication:

Must be done on all patients treated

Urea-breath test (UBT) or stool antigen tests are preferred

Must be off PPI for 1-2 weeks prior to the test
Can wait to confirm until after completion of the PPI course

342
Q

Two ways NSAIDs can induce mucosal injury

A

Direct irritation of gastric epithelium

Systemic inhibition of mucosal prostaglandin synthesis

343
Q

Cyclooxygenase (COX):

A

rate-limiting enzyme in the conversion of arachidonic acid to prostaglandins and is inhibited by NSAIDS

344
Q

Role of COX-1

A

Produces PG that

Increase blood flow to gastric mucosa and kidneys
Increase platelet aggregation via thromboxane A2 pathway

345
Q

Role of COX -2

A

Increase renal blood flow

Makes PG that activate and sensitize nociceptors (increased pain)

346
Q

What is a last line treatment for nsaid induced ulcers?

A

Celecoxib (Celebrex):

Should be reserved as last line
Associated with cardiovascular risk
Medical co-therapy with PPI (once daily) or misoprostol

347
Q

Stress ulcer prophylaxis

A

Proton Pump Inhibitors (PPI)

Histamine-2 Receptor Antagonists (H2RA)

348
Q

MOA of Antacids and Clin indication

A

Mechanism of Action:
Weak bases that neutralize gastric acid
Reacts with hydrochloric acid to form a salt and water

Clinical Indication:
1st line therapy for intermittent symptoms (less than twice weekly)
Breakthrough therapy for those on PPI/H2RA therapy

349
Q

ADE’s of antacids

A

Adverse Effects: constipation (aluminum & calcium), diarrhea (magnesium), accumulation of aluminum or magnesium in renal disease with repeated dosing

350
Q

What drug class can cause Chelation (fluroquinolones, tetracyclines); avoid giving at the same time as other drugs due to interactions

A

Antacids

351
Q

What effect do antacids have on pH and absorption? And what drugs are common for these?

A

Reduced ph:

ketoconazole, itraconazole, iron, atazanavir, delavirdine, indinavir, nelfinavir

Increased absorption:

raltegravir, saquinavir

352
Q

Sodium bicarbonate does what with HCL?

A

Reacts with HCL to produce carbon dioxide and sodium chloride.
CO2 results in gastric distention and belching

Long term = METABOLIC ALKALOSIS

353
Q

What caution do calcium carbonates have?

A

Caution:
excessive doses with other calcium-containing dairy products and renal insufficiency may cause

  • Metabolic alkalosis
  • Hypercalcemia
354
Q

Magnesium hydroxide reacts with HCL and has what ADE’s?

A

osmotic diarrhea caused by unabsorbed magnesium saltsosmotic

355
Q

Aluminum Hydroxide reacts with HCL and has what ADE’s (2)

A

Aluminum salts cause constipation

Aluminum is also absorbed and excreted in the kidneys (Renal insufficiency: should not take long-term)

356
Q

What is commonly admin together to minimize impact on bowel fax

A

Aluminum and Magnesium

357
Q

What is the action of Simethicone?

A

relieves flatulence with defoaming action (gas bubbles combine and are more easily freed)

358
Q

What contains aligned acid and creates a foamy layer above the stomach contents (reduces reflux)?

A

Aluminum Hydroxide and Magnesium Trisilicate (Gaviscon tablets & liquid)

359
Q

H2RA antagonist MOA

A

competitively block the binding of histamine to H2 receptors on the parietal cell, inhibiting gastric acid secretion induced by histamine

360
Q

What are clinical uses of H2RA

A

Peptic ulcers, GERD, non-ulcer dyspepsia, Zollinger-Ellison syndrome, and prevention of bleeding from acute stress-related gastritis ulcers

less effective than PPI’s at healing erosive esophagitis

361
Q

Prolonged cimetidine is associated with what?

A

Gynecomastia

362
Q

Drug interactions common with H2RA

A

May affect the absorption of drugs dependent on lower gastric pH or increases in absorption leading to potential toxicity (raltegravir, saquinavir)

363
Q

What drugs are dependent on lower gastric pH (6)

A

ketoconazole, itraconazole, iron, atazanavir, delavirdine, and nelfinavir

364
Q

Which H2RA acts as an anti androgen and competes with creatinine for tubular secretion in the kidney?

A

Cimetidine

365
Q

Low percentage of side effects nad good efficacy for duodenal ulcer GERD and gastric ulcers

A

Ranitidine

366
Q

H2RA antagonists end in what?

A

-tidine

367
Q

___ most effective for managing GERD and what are examples? (7)

A

PPI’s

-prazole

Rabeprazole (Aciphex)
Esomeprazole (Nexium)
Dexlansoprazole (Dexilant)

Pantoprazole (Protonix)
Omeprazole (Prilosec)
Omeprazole/Bicarbonate ion (Zegrid)
Lansoprazole (Prevacid)

368
Q

MOA of PPI’s and administration guidelines

A

Irreversibly binds to the H+/K+ ATPase enzyme system (proton pump) of the cells suppressing secretion of hydrogen ions

30-60 mins before meals; longer duration than H2RA’s

369
Q

4 common risks of PPI’s

A

Fx

Hypomagnesaemia

C diff

Community acquired pneumonia

370
Q

PPI use is associated with a high risk of what?

A

CKD “chronic kidney disease”

371
Q

What are FDA recommendations for Omeprazole and why

A

AVOID! CYP2C19 INHB

use pantoprazole instead

372
Q

pH-dependent absorption PPI’s

A

Ketoconazole
Itraconazole
Protease inhibitors

373
Q

Sucralfate is a mucousal protective agent that has what MOA

A

Covers the ulcer site and protects it against acid
Stimulates prostaglandin release

NO ADVERSE AFFECTS

Multi dose daily = limited use.

374
Q

If you are concerned for nosocomial pneumonia what can you use for stress related bleeding

A

Sucralfate

375
Q

Mechanism of Action:
Prostaglandin Analog
Synthetic, oral prostaglandin E1 analog that has both antisecretory and mucosal protective properties

A

Misoprostol

376
Q

Clin use of Misoprostol most common ADE / preg cat

A

Prevent NSAID induced ulcers

LOTS of diarrhea

Preg Cat D

377
Q 
Bismuth Subsalicylate (Pepto-Bismol) and Bismuth Subcitrate Potassium (Pylera)*
Avail as combo product of what?
A

metronidazole and tetracycline for the treatment of H. pylori

378
Q

Clinical Use:
Nonspecific treatment of dyspepsia and acute diarrhea
Prevention of traveler’s diarrhea
Used in quadruple drug regimens for H. pylori eradication

What med?

A

Bismuth Subsalicylate and BSPotassium

379
Q

What are the ADE’s of Bismuth Subsalicylate (Pepto-Bismol) and Bismuth Subcitrate Potassium (Pylera) (2)

A

Harmless blackening of stool (may be confused with GI bleed)
Harmless darkening of tongue (liquid formulations)

can lead to salicylate toxicity

380
Q

What metabolic disturbances occur at the chemoreceptor trigger zone, and medications are used?

A

Serotonin (5-HT3), dopamine (D2) receptors, histamine (H1) and muscarinic (M1) and substance P/neurokinin 1; and opioid receptors

Metabolic Disturbances: uremia, diabetic ketoacidosis, hypercalcemia, hypoxemia

Medications: opiate, dopamine agonists, digoxin, chemotherapeutic agents, macrolides, general anesthetics

381
Q

Vomiting center is stimulated by what 4 different sources of affront input?

A

1) Solitary Tract Nucleus: (Visceral Stimuli: dopamine and serotonin (5-HT3) receptors located in afferent vagal and splanchnic fibers
2) Gastric irritants
3) Non-gastric stimuli (biliary or GI distention, mucosal or peritoneal irritation and infection)
4) Chemotherapeutic agents

382
Q

Vomiting undigested food one to several hours after ingestion suggests

A

Gastroparesis

Gastric outlet obstruction

383
Q

Vomiting immediately after meals suggests

A

Bulimia

Psychogenic causes

384
Q

Morning vomit suggests

A

Pregnancy
Uremia
Alcohol Intake
Increased Intracranial Pressure

385
Q

General nausea & vomiting

A

Phenothiazines and serotonin antagonists

386
Q

Chemotherapy induced anti - emetics

A

Serotonin antagonists, phenothiazines, NK1 antagonist, dronabinol

387
Q

Postoperative anti-emetics

A

Serotonin antagonist scopolamine

388
Q

Motion sickness Anti-emetics

A

Antihistamine and scopolamine

389
Q

Anti emetics for pregnancy

A

Phosphorylation carb, pyridoxine, antihistamines

390
Q

Anti emetics for gastroparesis

A

Metoclopramide

391
Q

5HT3 antagonist MOA

A

Mechanism of Action: block presynaptic serotonin receptors on sensory vagal fibers in gut wall as well as central blockade in the vomiting center and CTZ

392
Q

ADE’s of 5HT3

A

Adverse Effects:
Well tolerated; most common is headache, dizziness, and constipation
QTc prolongation; small but statistically significant prolongation of QT interval (most pronounced with dolasetron)

393
Q

5HT3 antagonists and ends in what?

A

-setron

Ondansetron (Zofran) IV/PO
Orally disintegrating tablet available.
Ondansetron has become a popular antiemetic associated with pediatric gastroenteritis as well as general adult nauseous and general post-op surgery nausea and vomiting

Granisetron (Kytril) IV/PO
Dolasetron (Anzemet) IV/PO
Palonosetron (Aloxi) IV/PO

394
Q

1st gen Antihistamines

A 
Meclizine (Antivert,Bonine)
Diphenhydramine (Benadryl) 
Dimenhydrinate (Dramamine)
Doxylamine (Unisom)
Doxylamine/pyridoxine (Diclegis)
Pyridoxine = vitamin B6
Approved for women who do not respond to conservative management

Preg Cat A

395
Q

MOA and Clin u se of Prochlorperzine (Typical Antipsychotic)

and Promethazine (1st Gen Antihistamine)

A

Phenothiazines
Mechanism of Action:
Block dopamine, muscarinic, and histamine receptors in Chemoreceptor Trigger Zone (CTZ)
Sedation is due to their anti-histamine activity

Clinical Use: effective oral, injectable, and rectal anti-emetics for inpatient and outpatient use

396
Q

MOA and Clin use of Scopolamine

A

Mechanism of Action: cholinergic antagonist with greater central (more lipophilic; blocks muscarinic receptors in the vestibular system) than peripheral effects

Clinical Indication: motion sickness; surgical adjunct (blocks short-term memory and decreases saliva)

397
Q

Droperidol MOA and Clin use

A

Mechanism of Action: blocks dopamine receptors in chemoreceptor trigger zone (CTZ) of the CNS

Clinical Use:
Butyrophenone antipsychotic, no longer used as antipsychotic
Indicated for Postoperative Nausea/Vomiting (PONV)
Most often used for sedation in endoscopy and surgery, in combination with opioids or benzodiazepines

398
Q

Acid reducer : METOCLOPRAMIDE MOA

A

Dopamine and Serotonin antagonist ; enhances response to Acetylcholine

399
Q

ADE’s of Acid Reducers

A

CNS are most common and it usually causes drowsiness but may also cause restlessness

Extrapyramidal effects (dystonias, akathisia, parkinsonian features)

400
Q

Mechanism of Action:
Block emetic impulses in the chemoreceptor trigger zone (CTZ)
Does not cause extrapyramidal symptoms like metoclopramide
Clinical Use:
Used for apomorphine pre-treatment in Parkinson’s patients

A

Trimethobenzamide(Tiguan)

401
Q

How can corticosteroid treat nausea and vomiting (DM)

A

Use in Chemotherapy Induced Nausea and Vomiting (CINV) with 5HT3 Antagonists
Corticosteroids improve the response rates of serotonin-receptor antagonists (5-HT3) by 15-30% when combined

Products:
Dexamethasone (IV/PO)
Methylprednisolone (IV)

402
Q

Clinical Use: used before the initiation of chemotherapy to reduce anticipatory nausea and vomiting caused by anxiety

Products:
Lorazepam (Ativan)
Diazepam (Valium)

A

BZD’s

403
Q

Mechanism of Action:
Synthetic cannabinoid
Targets central endogenous cannabinoid receptors

Clinical Use:
Nausea associated with chemotherapy (not responding to conventional therapy)
Anorexia associated with weight loss in AIDS patients
Drug Interactions:
May potentiate the clinical effects of other psychoactive agents

A

Dronabinol

404
Q

NAbilone C-2 MOA and Clin use

A

Mechanism of Action:
Synthetic cannabinoid
Targets central endogenous cannabinoid receptors

Clinical Use:
Nausea associated with chemotherapy that is refractory to other anti-emetics

405
Q

NK1 Agents (3)

A

-pitant

Aprepitant

Fosaprepitant

Netupitant/Palosetron

406
Q

Secretory Diarrhea

A

Large watery volume with HIGH electrolytes

407
Q

Altered Motility

A

Autonomic nerve dysfunction

408
Q

Osmotic diarrhea

A

Hypersmolar gradients in intestinal lumen

409
Q

Inflammatory diarrhea

A

Infiltration/invasion of intestinal mucosa

410
Q

Mild Mod Severe Diarrhea and TXM

A

Mild Diarrhea: ≤ 3 unformed stools/day, minimal symptoms

Moderate Diarrhea: ≥ 4 unformed stools/day and/or systemic symptoms

Severe Diarrhea: ≥ 6 unformed stools/day and or temp > 101F, blood, or fecal leukocytes

Treatment:
Mild Diarrhea: rehydration fluids + lactose free diet, avoid caffeine
Moderate Diarrhea: anti-motility agents and rehydration fluids

411
Q

ABX therapy for travelers diarrhea

A

Fluoroquinolones
Azithromycin
Rifaximin (Xifaxan) only works in the colon
Rifamixin treats IBS-diarrhea dominant

412
Q

C diff Txm

A

C. difficile

Treatment: metronidazole or oral vancomycin

413
Q

Opioid antidiarrheal action

A

Activates presynaptic opioid receptors (mu receptors) in the enteric nervous system

Inhibit presynaptic cholinergic nerves in the submucosal and mesenteric plexuses

Lead to increase colonic transit time and fecal water absorption

Decreases mass colonic movement and the gastrocolic reflex

414
Q

LOPeramide MOA, does it cross BBB?

A

Mu opioid agonist; activates opioid receptors in the enteric system, leading to inhibition of acetylcholine release and decreased peristalsis

Does not cross the BBB

No analgesic properties

415
Q

Loperamide (Imodium) controls what?

A

Mild to mod symptoms of non invasive diarrhea

416
Q

Osmotic laxative MOA

A

Rapid movement of water into the distal small bowel and colon, leads to high volume of liquid stool
Increase volumes leads to bowel distension and reflex urge to defecate
Followed by rapid relief of constipation

intermittent constipation relief

417
Q

Osmotic Laxatives (4)

A 
Magnesium Sulfate (EpSOM salt)
Magnesium Citrate
Non-absorbable salt
Magnesium Hydroxide (Milk of Magnesia; MOM)
Non-absorbable salt
Sodium Phosphate (Fleets)
418
Q

Which osmotic laxative has a caution with existing electrolyte abnormalities

A

Sodium phosphate (Fleets)

419
Q

Lactulose and Sorbitol are what?

A

Non-absorbable semisynthetic disaccharide sugars

That,
metabolize by colonic bacteria, producing increased osmotic pressure causing fluid accumulation, severe flatus, cramps, and defecation

420
Q

What lax has severe flatulence an cramps

A

LActulose and 70% sorbitol

421
Q

Pre op prep for endoscopic or radiologic procedures

A

Polyethylene Glycol (PEG) solutions (GoLyte, GoLYTELY)

safe in renal and hepatic dz and pregnancy

422
Q

What lax is approved for IBS constipation dominant?

A

PEG 3350 powder (Miralax)

safe hepatic/preg/renal

423
Q

Lubricating Agents

A

Glycerin Suppository - think peds

Mineral Oil

424
Q

Bulk Forming Laxative that absorb and retain water in stool

A

Natural

  • Psyllium(Metamucil)
  • Wheat Dextrin(benefiber)

Synthetic

Calcium polycarbophil

Methyl cellulose

Bran powder

425
Q

What do Bulk forming laxatives promote and require?

A

Peristalsis and requires adequate water intake

IPAP Class 21-2 (12 decks)

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