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Pharmacology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What is the mortality of meningitis?

A

up to 25% depending on the organism

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2
Q

In 1995 ______ _____ was 47% of meningitis cases.

A

streptococcus pneumoniae

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3
Q

What 1986, _____ _____ was 45% of meningitis cases.

A

haemaphilus influenzae

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4
Q

What causes 8% of meningitis cases that is aerobic gram negative bacilli?

A

Listeria monocytogenes

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5
Q

What causes 53% of meningitis cases in neonates?

A

Streptococcus agalactiae

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6
Q

What pathogen causes meningitis with trauma or CSF shunts?

A

Staphylococcus aureus

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7
Q

What is the classic triad of meningitis?

A

fever
neck stiffness
change in mental status (confusion, lethargy, coma)

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8
Q

What fraction of patients with meningitis will present with the classic triad?

A

only 2/3

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9
Q

What are the long term effects of meningitis if not mortality? (4)

A

hearing loss (10%)
seizure disorders
learning difficulties
neurologic problems (spasticity, paresis, ataxia)

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10
Q

What patients with meningitis clinical presentation benefit from CT?

A 
immunocompromised
h/o CNS disease
new onset of seizures
papilledema
altered consciousness or focal neurological defect
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11
Q

How is meningitis diagnosed?

A

CSF examination by lumbar puncture

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12
Q

What is seen with meningitis lumbar puncture?

A

gram stain, C&S, cell counts with diff, CSF protein and CSF glucose

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13
Q

What are the CNF findings for bacterial meningitis for opening pressure?

A

> 180mm H2O

<20

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14
Q

What are the CNF findings for bacterial meningitis for WBC count?

A

1000-5000/mm3

0-10/mm3

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15
Q

What are the CNF findings for bacterial meningitis for % of neutrophils?

A

> 80%

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16
Q

What are the CNF findings for bacterial meningitis for protein?

A

100-500 mg/dl

10-45

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17
Q

What are the CNF findings for bacterial meningitis for glucose?

A

<40 mg/dl

50-100 (normally 2/3 plasma glucose level)

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18
Q

What are the CNF findings for bacterial meningitis for gram stain?

A

+ in 60-90%

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19
Q

What are the CNF findings for bacterial meningitis for culture?

A

+ in 70-85%

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20
Q

What antibiotics (empirical therapy) is used for meningitis?

A

ceftriaxone 2g IV Q12
Dexamethasone
Vancomycin
(1 month-50 years)

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21
Q

What is the dosage of ceftriaxone for meningitis empirical therapy?

A

2g IV Q12

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22
Q

What antibiotic is prescribed for empirical therapy for meningitis in someone over 50 years old, ETOH and other debilitating disease?

A 
Ampicillin 
\+
ceftriaxone
vancomycin
dexamethasone
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23
Q

What is someone greater than 50 years at increased risk of with meningitis?

A

increased risk of Listeria monocytogenes

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24
Q

What is the empiric therapy with a positive gram stain for Gram(+) diplococci S. pneumoniae?

A

Ceftriaxone 2g IV Q 12h
Vancomycin
dexamethasone 10mg Q6h x 4 days

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25
Q

What is the empirical therapy for a gram(-)diplococci meningitidis?

A

Pen G 4MU IV every 24 hours x5-7days

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26
Q

What is the empiric therapy for a gram (+) bacilli or coccobacilli : L. monocytogenes?

A

Ampicillin

Gentamicin

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27
Q

Why is gentamicin being used for empiric therapy for gram (+)?

A

SYNERGY against gram +

not for gram - effects

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28
Q

What are the findings of dexamethasone with meningitis? (3)

A
  1. reduction in unfavorable outcomes
  2. reduction in mortality
  3. even better findings in patients with S. pneumoniae meningitis
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29
Q

When should adjunctive dexamethasone be used for meningitis?

A

with documented or suspected S. pneumoniae

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30
Q

What is the dose of dexamethasone for meningitis?

A

10mg every 6 hours x 4 days

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31
Q

When should dexamethasone be given in related to antibiotic dose for meningitis?

A

Give with or 15 minutes prior to antibiotic dose

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32
Q

When should dexamethasone not be given to meningitis pts?

A

If antibiotic has already been started
If patient has septic shock
If NOT caused by s.pneumoniae

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33
Q

What is used to measure cognition for AD?

A

mini-mental status exam

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34
Q

What are the neurological changes seen in AD?

A

reduced:
acetylcholine (ACh)
acetylcholinesterase (AChE)

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35
Q

What are the two main objectives in pharm for AD?

A
  1. raise cortical acetylcholine levels

2. decrease glutamate-medicated neuronal cell death

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36
Q

What are the main goals of therapy?

A
  1. minimize behavioral disturbances

2. improve symptoms

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37
Q

what are 4 drugs FDA approved for managing AD?

A

donepezil (aricept)
rivastigmine (exelon)
galantamine (razadyne)
memantine (nameda)

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38
Q

what are the 3 acetylcholinesterase inhibitors for AD?

A

donepezil (aricept)
rivastigmine (exelon)
galantamine (razadyne)

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39
Q

What medication is a NMDA antagonist for AD?

A

memantine (Namenda)

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40
Q

What medication is most effective for treating AD?

A

Acetylcholinesterase Inhibitors (AChEIs)

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41
Q

How can Acetylcholinesterase Inhibitors (AChEIs) affect AD?

A

typically results in small improvements and symptoms
most studies involve mild to moderate symptoms
may improve cognition and behavior

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42
Q

What happens if side effects develop with Acetylcholinesterase Inhibitors (AChEIs)?

A

a switch can usually be initiated 24 hours after discontinuation of the first medicine

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43
Q

What are the adverse effects of Acetylcholinesterase Inhibitors (AChEIs) mostly related to?

A

increased ACh

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44
Q

What are the adverse reactions of increased Achievement from Acetylcholinesterase Inhibitors (AChEIs)? (6)

A 
depression
headache
anxiety
dizziness
stomach pain
insomnia
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45
Q

What are the Acetylcholinesterase Inhibitors (AChEIs) pronounced adverse effects on the the GI tract? (7)

A 
nausea
vomiting
diarrhea (N/V/D)
dehydration
decreased appetite
weight loss
stomach ulcers
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46
Q

Incidence and seriousness of Acetylcholinesterase Inhibitors (AChEIs), adverse effects are __________ _______.

A

dose related. and may require drug discontinuation

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47
Q

What methods are used for Acetylcholinesterase Inhibitors (AChEIs) to decrease incidence and seriousness of Acetylcholinesterase Inhibitors (AChEIs)?

A

minimize by starting low and dose titration

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48
Q

Who is at risk for dose related SE of Acetylcholinesterase Inhibitors (AChEIs)?

A

pts <50kg (110lbs)
elderly

both have increased incidence

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49
Q

What medication was the first agent approved for moderate to severe AD?

A

Donepazil (aricept)

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50
Q

What is the dosing of Donepazil (aricept)?

A

starting dose is 5mg daily
increase to 10mg daily after 4-6 weeks
may increase to 23mg daily after 3 months

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51
Q

What time of day should Donepazil (aricept) be given?

A

HS with or without food

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52
Q

What dosage of Donepazil (aricept) is available only brand name?

A

23mg Extended release Tablet

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53
Q

What medication is approved for mild to moderate AD?

A

Galantamine (Razadyne)

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54
Q

What are the MOI of Galantamine (Razadyne)? (2)

A

inhibits AChE & stimulates nicotinic receptors

stimulates at non-ACh site (allosteric modulation)

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55
Q

What is important to remember about renal adjustment for Galantamine (Razadyne) for AD?

A

moderate renal impairment: max dose of 16mg/day

DONT use with severe renal impairment

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56
Q

What is important to remember when converting to Galantamine (Razadyne) with poor tolerability with donepezil or rivastigmine?

A

wait until side effects subside or allow 7 days washout prior to giving Galantamine (Razadyne).

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57
Q

What is important to remember when converting to Galantamine (Razadyne) with no intolerance to donepezil or rivastigmine?

A

begin galantamine the day after stopping.

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58
Q

What is a transdermal patch approved for severe AD?

A

rivastigme (exelon)

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59
Q

How does rivastigme (exelon) compare to oral medication for AD?

A

less N/V/D
similar rates of bradycardia & syncope as oral forms
PATCH doses are immediately therapeutic (not oral-titrate)

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60
Q

How can allergic contact dermatitis be prevented with rivastigme (exelon)?

A

rotate application sites
don’t reuse the same site for 14 days
recommended: upper/lower back
alternate sites: chest/upper arm

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61
Q

What is the unique MOA of rivastigme (exelon)?

A

“pseudoirreversible”

Inhibits G1 AChE> G4 AChE

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62
Q

What is significant about the metabolism and elimination of rivastigme (exelon)?

A

results in fewer drug-drug interactions

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63
Q

What medication for AD is a N-methyl-D-aspartate (NMDA) antagonist?

A

mementine (nameda)

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64
Q

What medication was recently approved for mod-severe AD that results in cognitive improvement when added to ACHIs?

A

mementine (nameda)

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65
Q

mementbine (nameda) side effects are _____ and _____.

A

infrequent; mild

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66
Q

What is the dosage in renal impairment for mementine (nameda)?

A

mid to moderate: no adjustment

severe impairment: 5mg BID

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67
Q

What monoamine neurotransmitters changes are seen in the symptoms of depression? (3)

A

norepinephrine (NE)
Serotonin (5-hydroxytryptamine; 5-HT)
Dopamine (DA)

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68
Q

What agents block reuptake/metabolism of amines making them effective for depression?

A

Biogenic amine hypothesis

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69
Q

What are medical conditions that can cause depression? (5)

A 
Hypothyroidism
Addison or Cushings Disease
Pernicious Anemia 
Severe anemia
HIV/AIDS
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70
Q

What are the antihypertensives that can cause depression?

A

clonidine (Catapres)

Diuretics

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71
Q

What other mediations besides HTN meds that can cause depression?

A

oral contraceptives
steroids
ACTH

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72
Q

What are the factors that increase risk of suicide?

A 
suicidal plans/attempts
male genders (females attempt more but males succeed)
single or living alone
inpatient status
feelings of hopelessness
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73
Q

What should be done for patients that are high risk of suicide?

A

immediately refer

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74
Q

What are the 3 phases of depression treatment?

A

acute phase: 3 months
continuation phase: 4-9 months
Maintenance phase: 12-36 months (prophylaxis)

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75
Q

What does the duration of therapy for depression depend on?

A

Depends on risk of recurrence

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76
Q

How often should pt be evaluated for treatment in acute phase?

A

evaluate weekly or twice a month

continue until substantial improvement occurs

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77
Q

During the acute phase of depression what should happen with <50% improvement (non response, partial response) at 4 weeks?

A

change meds and consider non adherence

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78
Q

What amounts should be prescribed to patients in acute phase depression?

A

do not presribe large amounts to seriously depressed patients

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79
Q

All patients should complete this phase of depression( usually 3 months)

A

acute phase

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80
Q

During continuation phase what might be indicated by residual symptoms (partial remission)?

A

reccurence
early relapse
chronic course

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81
Q

How long is the continuation phase?

A

4 months minimum AFTER the acute phase. should continue treatment until symptoms have resolved

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82
Q

When should you consider discontinuation of depression treatment?

A

consider if no recurrence or relapse during continuation phase

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83
Q

What might be a side effect of early discontinuation of depression treatment?

A

higher risk of relapse

taper medication over several weeks

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84
Q

How long is the maintenance phase of depression treatment last? how does it effect recurrence?

A

12-36 months

decreases recurrence by 2/3

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85
Q

When is maintenance indicated for depression patients?

A 
yearly episodes
impairment from mild residual symptoms
chronic major depression
severe episodes
high risk of suicide
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86
Q

What is a non pharmacological therapy for depression?

A

psychotherapy to all those willing

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87
Q

When is psychotherapy 1st line for depression?

A

mild-moderate depression

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88
Q

The initial choice of antidepressants is made empirically based on: (7)

A 
previous response history
pharmacogenetics 
presenting symptoms (fatigue vs agitation)
drug-drug interaction potential
side effect profile
patient preference
cost
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89
Q

What class of medication is superior to other antidepressants for major depression?

A

Selective Serotonin Reuptake Inhibitors (SSRIs)

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90
Q

Why are Selective Serotonin Reuptake Inhibitors (SSRIs) considered 1st line for major depression?

A

due to overdose safety and tolerability

fewer anticholinergic and cardiovascular adverse effects than TCAs

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91
Q

What is a common side effect of Selective Serotonin Reuptake Inhibitors (SSRIs)?

A

decreased libido

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92
Q

What happens if Selective Serotonin Reuptake Inhibitors (SSRIs) are stopped abruptly?

A

withdrawal syndrome

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93
Q

What Selective Serotonin Reuptake Inhibitors (SSRIs) is less likely to cause withdrawal syndrome?

A

fluoxetine (prozac)- metabolite has longer half life; improves adherence

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94
Q

When are Selective Serotonin Reuptake Inhibitors (SSRIs) contraindicated?

A

patients on or recently (5-6 weeks) taken off MAOIs (Serotonin syndrome)

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95
Q

What is the first Selective Serotonin Reuptake Inhibitors (SSRIs) approved for children?

A

fluoxetine (prozac)

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96
Q

What is the black box warning of fluoxetine (prozac)?

A

increased suicidal ideation in children and adolescents

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97
Q

Why is fluoxetine (prozac) once daily dosing?

A

active metabolite with longer halflife than other SSRIs

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98
Q

When is fluoxetine (prozac) used with caution?

A

pts with bipolar disorder because one metabolite persists for weeks and may aggravate the manic state

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99
Q

What is the maximum dose od fluoxetine (prozac)?

A

80mg/daily

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100
Q

What SSRI blocks serotonin reuptake at lower doses; blocks domain reuptake at HIGHER doses?

A

paroxetine (Paxil)

sertaline (Zoloft)

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101
Q

Since paroxetine (Paxil) blocks dopamine reuptake at higher doses it may help contribute to its ______ action.

A

antidepression

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102
Q

What is the maximum dose of paroxetine (Paxil)?

A

50mg/daily

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103
Q

What is the maximum dose of sertaline (Zoloft)

A

200mg daily

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104
Q

What is one of the oldest SSRIs?

A

fluvoxamine (Luvox)

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105
Q

What SSRI may cause or worsen sexual dysfunction?

A

fluvoxamine (Luvox)

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106
Q

What is the maximum dose of fluvoxamine (Luvox)?

A

300mg daily

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107
Q

Medication that is FDA approved to treat symptoms of major depression?

A

citalopram (Celexa)

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108
Q

What was the FDA warning for citalopram (Celexa)?

A

> 40mg daily may prolong QT interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

When should citalopram (Celexa) be avoided?

A

congenital long QT syndrome
other drugs causing QT prolongation
or at high risk for Torsades de pointes

110
Q

What is the maximum dose of citalopram (Celexa)?

A

40mg daily (used to be 60mg)

111
Q

What is the S-isomer of citalopram?

A

escitalopram (Lexapro)

112
Q

What medication may help reduce the frequency and severity of hot flashes in perimenopausal women?

A

escitalopram (Lexapro)

113
Q

What is the maximum dose of escitalopram (Lexapro)?

A

20mg daily

114
Q

What are the newer 2nd generation agents for depression?

A

Mixed 5-HT/NE Reuptake inhibitors

115
Q

What class of medications are SNRIs?

A

Mixed 5-HT/NE Reuptake inhibitors

116
Q

What are the “dual action” antidepressants?

A

Mixed 5-HT/NE Reuptake inhibitors

117
Q

What medication can block monoamine uptake more selectively than TCAs WITHOUT cardiac conduction effects like TCAs

A

Mixed 5-HT/NE Reuptake inhibitors

118
Q

What are the Mixed 5-HT/NE Reuptake inhibitors agents? (3)

A

venlafaxine (Effexor)
duloxetine (cymbals)
desvenlafaxine (pristiq)

119
Q

What medication is superior for severe depression than other SSRIS or TCAs that is also effective for chronic pain?

A

venlafaxine (Effexor)

120
Q

What medication may double the risk of miscarriage?

A

venlafaxine (effexor)

121
Q

What is the O-desmethylvenlafaxine (metabolite) of venlafaxine?

A

desvenlafaxine (Pristiq)

122
Q

What medication is 10x more effective at blocking serotonin than NE uptake?

A

desvenlafaxine (Pristiq)

123
Q

Medication with higher rates of discontinuation syndrome?

A

desvenlafaxine (Pristiq)

124
Q

What is duloxetine (Cymbalta) FDA approved for? (3)

A

major depressive disorder
neuropathic pain
fibromyalgia pain

125
Q

Prescribers observed that duloxetine (Cymbalta) is not chosen a lot because there are so many other options given what side effect?

A

hepatic disorders and drug interactions

126
Q

When is duloxetine (Cymbalta) not recommended?

A

CrCl <30ml/min

with hepatic impairment

127
Q

What medication inhibits both NE & dopamine reuptake with NO action on serotonin?

A

bupropion (Wellbutrin)

128
Q

How does bupropion (Wellbutrin) compare to TCAs and SSRIs?

A

similar in efficacy to TCAs and SSRIs
less N/D, somnolence and sexual dysfunction than SSRIs
effective alternative or adjunctive for SSRI non responders

129
Q

What are mixed serotonin/NE reuptake inhibitors that are effective for all depressive subtypes?

A

Tricyclic antidepressants (TCAs)

130
Q

What are common side effects of Tricyclic antidepressants (TCAs) and why their use is limited?

A 
anticholinergic effects
sedation
orthostatic hypotension
seizures
cardiac conduction abnormalities
131
Q

What are the commonly available Tricyclic antidepressants (TCAs) agents?

A

tertiary amines
secondary amines
high risk of death with overdose

132
Q

What are the older 1st generation agents, irreversibly, non selecting binding MAO-A&B?

A

monoamine oxidase inhibitors (MAOIs)

133
Q

monoamine oxidase inhibitors (MAOIs), are antidepressants with similar effects to _____.

A

TCAs

134
Q

What are monoamine oxidase inhibitors (MAOIs) not considered 1st line?

A

due to risk of “serotonin syndrome”

numerous drug-drug interactions

135
Q

What are the common monoamine oxidase inhibitors (MAOIs)?

A

phenelzineu (Nardil)

selegiline (Eldepryl)

136
Q

What are the potentially life threatening adverse drug reactions of serotonin syndrome? (4)

A

therapeutic drug use with SSRIs
intentional self poisoning with SSRIs
Interaction between 2 drugs (SSRI + another drug)
tyramine-containing foods while on MAOIs

137
Q

Why is patient counseling critical for serotonin syndrome?

A

dietary and medication restrictions (for MAOIs)

early symptom recognition (pts and clinicians)

138
Q

What is the usual triad of serotonin syndrome?

A

mental status changes
autonomic hyperactivity
neuromuscular abnormalities

139
Q

How often does serotonin syndrome occur in SSRI overdoses?

A

14-16%

140
Q

what are the notable autonomic findings of serotonin syndrome?

A

shivering
diaphoresis
mydriasis

141
Q

What are the clinical presentations of serotonin syndrome besides the notable autonomic findings?

A

labile blood pressure/hypertension

hyperthermia >41C is critical

142
Q

What is the treatment for serotonin syndrome?

A

STOP precipitating agent!
TEMP
5-HT 2A antagonist; cyproheptadine
monitor & treat hypotension

143
Q

What should you do if temp is greater than 41C with serotonin syndrome?

A 
immediate sedation with benzodiazepines (diazepam)
neuromuscular paralysis (vecuronium-nondepolarizing)
orotracheal intubation
144
Q

What is significant about Triazolopyridines? (4)

A

newer, mixed- action agents
less sexual and sleep associated side effects
pharmacologically similar to TCAs
fewer anticholinergic side effects

145
Q

How does nefazodone (Serzone) work?

A

blocks 5-HT 2A receptor and serotonin reuptake
efficacy similar to SSRIs
less sexual and sleep related side effects

146
Q

What are the recent reports of nefazodone (Serzone) ?

A

hepatic toxicity

black box warning of possible liver failure

147
Q

What is significant of mirtazapine (remeron)?

A

efficacy is similar to the TCAs and SSRIs

fewer Uses especially sexual and sleep side effects

148
Q

What is significant about trazadone (desyrel)?

A 
less anticholinergic (dry mouth, constipation and tachycardia)
less sexual side effects than most TCAs
149
Q

Why is trazadone (desyrel) not associated with increased appetite and weight gain?

A

limited by dizziness, orthostatic hypotension & sedation

caused by potent alpha 1 blockade

150
Q

What medication is FDA apprised for adjunctive depression on 11/20/07, that was originally approved as an “atypical” antipsychotic agent

A

aripiprazole (abilify)

151
Q

What is the US lifetime prevalence of Schizophrenia?

A

1% (0.6-1.9%)

152
Q

What is the lifetime prevalence of suicide in Schizophrenia?

A

10%

153
Q

What is the genetic risk factor of schizophrenia if 2nd degree relative has it?

A

3%

154
Q

What is the genetic risk factor of schizophrenia if 1st degree relative has it?

A

10%

155
Q

What is the genetic risk factor of schizophrenia if BOTH parents have it?

A

40%

156
Q

What is the genetic risk factor of schizophrenia in monozygotic twins?

A

48%

157
Q

Schizophrenia is NOT ______

A

split personality

158
Q

What is schizophrenia?

A

a chronic disease of thought & affect (expression)

159
Q

What are the acute psychotic episodes of schizophrenia? (3)

A 
auditory hallucinations (especially voices)
delusions (fixed false beliefs)
Ideas of influence (external forces control their actions)
160
Q

What are the symptom classifications of schizophrenia? (3)

A

Positive (most obvious/dramatic)
Negative (functional impairment)
Cognitive

161
Q

What are the characteristics of positive schizophrenia?

A

suspiciousness, unusual thought content (delusions), hallucinations, conceptual disorganization

162
Q

What are the characteristics of negative schizophrenia?

A

affect flattening, logia(inability to speak, anhedonia(total loss of pleasure things, avocation(lack of desire, drive or motivation to pursue meaningful goals

163
Q

What are the characteristics of cognitive schizophrenia?

A

impaired attention, impaired working memory, impaired executive function

164
Q

What is the mainstay of treatment for schizophrenia?

A

pharmacotherapy

165
Q

What is the mainstay for non pharmacological treatment for schizophrenia?

A

psychosocial rehab

166
Q

What is included in the lab work up for schizophrenia prior to pharmacotherapy?

A 
vitals
CBC
electrolytes
LFTs
renal function
ECG
fasting glucose
lipid studies
thyroid function
urine drug screen
167
Q

Why is it important to do lab work up for schizophrenia prior to starting pharmacotherapy?

A

baseline

rule out medical or substance abuse causes

168
Q

What is the rational of “Dopamine Hypothesis” pharmacotherapy for schizophrenia?

A

acute psychotic episodes increase dopamine neurotransmission

results in hypersensitivity to stimuli

169
Q

What is the rational of “Dysregulation Hypothesis” for schizophrenia pharmacotherapy?

A

Since inhibitory neurons are modulated by dopamine, serotonin, acetylcholine norepinephrine; these became targets for the new antipsychotics

170
Q

In schizophrenia, antipsychotic efficacy is proportional to what?

A

dopamine (D2) affinity

171
Q

Non D2 (dopamine) receptors are associated with what?

A

side effects and adverse effects

172
Q

What was the MOA of the first generation antipsychotics?

A

Dopamine antagonism, especially D2

“typical antipsychotic”

173
Q

Older term applies to antipsychotic drugs with prominent D2-dopamine receptor antagonism and risk of adverse extrapyramidal symptoms

A

neuroleptic

174
Q

What is called the “typical” antipsychotic?

A

neuroleptic

175
Q

What is the MOA of “atypical” antipsychotics?

A

act on multiple receptors not just D2

Second Generation Antipsychotics-SGAs

176
Q

What is the preferred term of neuroleptics?

A

First Generation Antipsychotics (FGA)

177
Q

What are the first generation antipsychotics?

A

fluphenazine (Prolixin)
Haloperidol (Haldol)
long acting depot injection formulations available but highly potent

178
Q

What is the result of first generation antipsychotics (FGA)?

A

immediate D2 receptor blockade

179
Q

How long does it take for first generation antipsychotics (FGA) therapeutic effect to develop?

A

6-8 weeks

180
Q

What does the efficacy of FGAs correlate with?

A

decreased presynaptic release of dopamine

181
Q

For FGAs what is the result of greater than 60% D2 blockade?

A

clinical response

182
Q

For FGAs what is the result of greater than 70% D2 blockade?

A

hyperprolactinemia

183
Q

For FGAs what is the result of greater than 80% D2 blockade?

A

increased risk of extrapyramidal symptoms

184
Q

What are the adverse effects of FGAs?

A 
sedation
dystonias/parkinsonism movement disorders
anticholinergic effects
orthostatic hypotension
seizures
hyperprolactinemia
moderate weight gain
prolonged QT interval
185
Q

What are anticholinergic effects?

A 
constipation
urinary retention
blurry vision
tachycardia
dry eyes, mouth and throat
186
Q

What antipsychotics have the worst increase in QTc baseline to the least? (3)

A

Thioridazine (Mellaril)- worst
Ziprasidone (Geodon)
Haloperidol (Haldol)-least

187
Q

What are the early neurological effects of FGAs? (3)

A

Acute dystonia- muscle spasms of tongue, face, neck and back (mimic seizures)
Akathisia (motor restlessness, pacing foot tapping)
Parkinsonism (bradykinesia, rigidity, variable tremor)

188
Q

When is the maximal risk of acute dystonia associated with FGAs?

A

1-5 days

189
Q

What is acute dystonia treated with in FGA adverse effects?

A

diphenhydramine IM

benztropin IM

190
Q

When does akathisia present with FGA adverse effects?

A

5-60 days

191
Q

When does Parkinsonism present with FGA adverse effects?

A

5-30 days

192
Q

What are the late neurological effects of FGAs (3)?

A

Neuroleptic Malignant Syndrome
Tardive dyskinesia
Perioral tumor

193
Q

When does Neuroleptic Malignant Syndrome present with FGA adverse effects? What is the mortality?

A

weeks

10% mortality

194
Q

When does Tardive dyskinesia present as an adverse effect of FGAs?

A

after months- years of treatment

195
Q

What is rabbit syndrome? and when does it present as an AE of FGAs

A

Perioral tremor

months- years

196
Q

What is significant about Neuroleptic Malignant Syndrome treatment?

A

antiparkinson agents NOT effective

197
Q

When is Neuroleptic Malignant Syndrome more common?

A

pts on high potency FGAs
depot FGAs
dehydrated or exhausted patients

198
Q

What is the treatment for Neuroleptic Malignant Syndrome?

A

discontinue the antipsychotic
The DA agonist bromocriptine reduces rigidity, fever and CK in up to 94% of patients
Another DA agonist, amantadine works in up to 63%

199
Q

What is the antipsychotic recommended after neuroleptic malignant syndrome?

A

use only SGAs for rechallenge post NMS

200
Q

What are the second generation antipsychotics, early agents?

A 
clozapine (Clozaril)
rispeidone (Risperdal)
olanzapine (Zyprexa)
quetiapine (Seroquel)
ziprasidome (Geodon)
aripiprazole (Ability)
201
Q

What are the second generation antipsychotics, later agents?

A

palpiperidone (Invega)
Iloperidone (Fanapt)
asenapine (Saphris)
lurasidone (Latuda)

202
Q

What is the MOA of second generation antipsychotics?

A

all are B2 antagonists; less tightly bound
D1, D4 antagonism
Norepinephrine and Serotonin antagonism

203
Q

What is significant about second generation antipsychotics compared to first generation?

A

second generation have significantly less risk of extrapyramidal effects but tradeoff is increased risk of metabolic effects (especially weight gain)

204
Q

What is the benefit of second generation antipsychotics (atypical antipsychotics)?

A

-few or no acutely occurring extrapyramidal side effects
enhanced efficacy (especially for negative symptoms & cognition)
absence of tardive dyskinesia

205
Q

What is the only SGA to fulfill all criteria?

A

clozapine

206
Q

What are the side effects of second generation antipsychotics? (7)

A 
moderate to severe weight gain (olanzapine, clozapine)
diabetes mellitus
seizures (clozapine)
nocturnal salivation (clozapine)
agranulocytosis (clozapine)
myocarditis (clozapine)
lens opacities (clozapine)
207
Q

The first atypical antipsychotic drug that is FDA approved despite risk of agranulocytosis?

A

Clozapine (clozaril)

risk of death (0.013%)

208
Q

When is clozapine prescribes? What must be done if prescribed?

A

reserved for patients who fail on other agents

weekly CBCs x 6 months; then every 2 weeks

209
Q

What is significant about early 2nd generation antipsychotics?

A

virtually no EPS
reduced risk of tardive dyskinesia
especially good for “negative” symptoms
significantly less relapse than first generation

210
Q

What is the rate of relapse of second generation, risperidone?

A

25%

211
Q

What is the rate if relapse first generation anti psychotic?

A

40%

212
Q

What is the 9-OH metabolite of risperidone?

A

Paliperidone (Invega)

213
Q

What is the SGA that has increased risk of orthostatic hypotension

A

Iloperidone (Fanapt)

214
Q

What is the SGA oral dissolving sublingual tablet?

A

Asenapine (Saphris)

215
Q

How is Asenapine (Saphris), the SGA taken?

A

SL!

do not chew or swallow due to increased risk of anaphylaxis & angioedema

216
Q

What are the 3 phases of schizophrenia treatment?

A
  1. acute phase
  2. stabilization phase
  3. maintenance phase
217
Q

What is the initial goal for treatment of first (acute) psychotic episode?

A

to calm agitated patients

218
Q

Why is immediate treatment important in first (acute) psychotic episode?

A

immediate treatment improves long term outcome

219
Q

What so most psychiatrists usually prescribe for treatment of first (acute) psychotic episode?

A

SGA (other than clozapine)

decreased anger & anxiety usually seen in 24-48 hours

220
Q

When is maximal improvement seen in the treatment of first (acute) psychotic episode?

A

seen by 6-8 weeks

221
Q

Suicide risk _______, as other symptoms improve.

A

INCREASES

222
Q

What are the indications of clozapine use for schizophrenia?

A

lack of response with other SGAs

intolerable side effects of other antipsychotics

223
Q

When are FGAs usually prescribed for schizophrenia?

A

typically NOT 1st line therapy

may be used before a SGA if chronically ill patients had a precious satisfactory response

224
Q

What is the pharmacotherapeutic algorithm for stage 1?

A

only for patients with FIRST schizophrenic episodes

SGAs are considered 1st line

225
Q

What is the pharmacotherapeutic algorithm for stage 2?

A

chronically ill patients recently started on antipsychotics
or new onset patients with poor response to stage 1
mono therapy with a FGA or SGA (not clozapine)
choose a different antipsychotic than used in stage 1

226
Q

What is the pharmacotherapeutic algorithm stage 3?

A

switch to clozapine (mono therapy)
Increased efficacy for suicidal behavior
Consider earlier in suicidal patients
monitor CBC weekly for agranulocytosis

227
Q

What is the pharmacotherapeutic algorithm stage 4?

A

continue clozapine

add an additional antipsychotic (combination therapy)

228
Q

What is the pharmacotherapeutic algorithm stage 5?

A

trial of mono therapy AP

use a FGA or SGA not previously used

229
Q

pharmacotherapeutic algorithm stage 6?

A

consider combination therapy
when switching APs:
overlap 2nd agent for 1-2 weeks
taper & D/C 1st agent (taper clozapine slowly)

230
Q

What is combination therapy?

A

involves using 2 APs simultaneously

231
Q

What is augmentation treatment?

A

addition of a non antipsychotic drug to an antipsychotic drug

232
Q

What are the augmentation guidelines? (4)

A

use only in inadequately responding patients
augmentation agents are rarely effective for schizophrenia if used alone
Augmentation responders usually improve rapidly
If symptoms so not improve, D/C the augmentation agent

233
Q

What are the mood stabilizers? (3)

A

Lithium
Valproic acid
Carbamazepine

234
Q

What are the augmentation gents? (3)

A

mood stabilizers
selective serotonin reuptake inhibitors
beta- blockers

235
Q

What are the beta blockers used for augmentation agents?

A

anti-aggressive effect

propranolol
pindolol
nadolol

236
Q

What is important to know about the combination therapies (steps 4-6)

A

combo trails should be time limited to 12 weeks

if no improvement, taper 1 medication then discontinue

237
Q

In general a series of ______ is preferred over _______ combinations

A

mono therapies; AP

238
Q

What is important to note about stabilization (maintenance) treatment?

A

1st presentation may respond sooner
meds may reduce symptoms, but are not curative
all symptoms may not abate

239
Q

The stabilization (maintenance) treatment prevents relapse. What is the % of relapse vs drug and placebo?

A

18-32% on drug

60-80% on placebo

240
Q

How long should the stabilization (maintenance) treatment occur?

A

continue at least 12 months past remission

241
Q

When are long-acting depot injectable APs used?

A

recommended in unreliable (non adherent) patients
NOT used as 1st line therapy
look for side effects as a cause of non adherence

242
Q

What are the long acting depot injectable APs?

A

haloperidol decanoate-Haldol (FGA)
fluphenazine decanoate- Prolixin (FGA)
Risperidone microspheres- Risperdal (SGA)

243
Q

How is haloperidol decanoate prescribed? (sustained release)

A

use 10-15 times the oral daily dose
round dose up to nearest 50mg
give dose via deep IM (NOT IV) injection every month
Overlap with PO haloperidol for 1st month

244
Q

What is the immediate release of haldol injection?

A

haldol lactate

245
Q

How is fluphenazine decanoate (Prolixin) given?

A

use 1.2 times the oral daily dose
use 1.6 times PO dose for more acutely ill patients
Round dose up tp nearest 12.5 mg interval
Overlap with PO fluphenazine for 1 week

246
Q

What is the only SGA depot agent ; needs reconstitution

A

Risperidone microspheres (Risperdal)

247
Q

What is the optimum dose of risperidone microspheres (Risperdal)?

A

25-50mg

higher doses show no benefit but more EPS

248
Q

What type of bipolar disorder is associated with at least 1 episode of MANIA and affects 1% of the worldwide population?

A

Bipolar I Disorder

249
Q

What type of bipolar disorder is associated with at least 1 episode of HYPOMANIA?

A

Bipolar II Disorder

250
Q

What is important to rule out in bi-polar disorder?

A

amphetamine abuse

pheochromocytoma

251
Q

What was bipolar disorder originally called?

A

Manic-Depression

252
Q

What is the unique hallmark of bipolar disordeR?

A

mania

253
Q

What is bipolar disorder characterized by?

A

elevated mood
overactivity
lack of need for sleep
increased optimism

254
Q

What is sufficient for diagnosis of bipolar disorder?

A

a single manic episode not caused by amphetamine abuse or pheochromocytoma

255
Q

What are the types of bipolar disorder?

A

one manic episode then frequent depressive episodes
alternating episodes of mania and depression annually
mania every few years without a depressive episode

256
Q

What are rapid cyclers of bipolar disorder?

A

patients with > 4 manic or depressive cycles year

257
Q

What percentage of people with bipolar disorder have family history?

A

50%

258
Q

What is the risk of bipolar disorder in the siblings on affected patients?

A

10%

259
Q

What are the non-treatment endangers of acute mania? (medical emergency)

A

marriage job and patients life

260
Q

What treatment is effective in acute mania?

A

Antipsychotic drugs

261
Q

What treatment is important in acute mania with violent patients?

A

rapid onset drugs like short acting injectables

262
Q

What treatment is good in acute mania for patients that are compliant?

A

newer “atypical” secondary antipsychotic agents

263
Q

What are the mood stabilizers that can be used for acute mania?

A

lithium
valproic acid
carbamazepine

264
Q

What is the treatment for bipolar depression? (3)

A

SSRIs
TCAs
MAOIs

265
Q

What can happen when giving antidepressants in bipolar depression?

A

pt may switch from depression to mania

266
Q

When should antidepressants not be used in bipolar depression?

A

pts with h/o dangerous mania episodes

267
Q

Lithium is a classic mood stabilizer for prophylaxis of bipolar disorder and bipolar depression, what is the trough level for seizure and death?

A

> 2.5mEq/L

268
Q

How often should blood levels be drawn when starting lithium for bipolar disordeR?

A

2x per week until stable

269
Q

When should trough samples be collected for lithium in bipolar disorder pts?

A

just prior to next dose

270
Q

In bipolar disorder, _____ was found more more effective than ______ for suicide prevention

A

lithium prophylaxis; valproate

Pharmacology (17 decks)

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