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general psych Flashcards

1
Q

major depressive disorder:Diagnosed based on ____, _____ and ______ , change in level of function and interest in patient activities.

A

on DSM-V, severity & duration of symptoms

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2
Q

what does “SIGECAPS” stand for? (kinda weeds)

A 
clinical features of depression: 
Sleep disturbances
Interest in usual activities is decreased
Guilt
Energy level changes
Concentration impairment
Appetite decreased (most common) or increased
Psychomotor impairment
Suicide (thoughts, ideation, attempt)
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3
Q

three types of therapy options for major depressive disorder. which take longest to be effective? which are best to prevent relapse?

A
  1. pyschotherapy - longer for effect, prevents relapse
  2. pharmacotherapy - shorter for effect, incr. risk relapse
  3. electroconvulsive therapy

*best combine pyscho and pharm.

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4
Q

7 general classes of drugs for major depressive disorder

A
  1. Tricyclic Antidepressants (TCAs)
  2. MAOIs
  3. SSRIs
  4. SSNRI
  5. Norepinephrine Dopamine Reuptake Inhibitor (NDRI)
  6. Serotonin Modulators
  7. Tetracyclic
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5
Q

how does the MOA of TCAs, SSRI, SNRI and alpha block work?

A

in general, they all block the reuptake of Serotonin or norepi into presynaptic, keeping it in synaptic cleft longer

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6
Q

what are the 5 TCA drugs. which are secondary and which are tertiary?

A 
Imipramine -
Desipramine -
Amitriptyline -
Nortriptyline - 
Clomipramine
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7
Q

what are the tertiary and secondary TCA drugs, what does this mean?

A

tertiary: imipramine, amitripyline
secondary: desipramine, nortriptyline
* tertiary converted to secondary when metabolized

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8
Q

what is the one TCA that has a specific indication for OCD?

A

clomipramine

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9
Q

are TCAs used much for depression?

A

no, the higher dose needed for depression txt has too many ADRs, more likely used in low doses for other things. (i.e. chronic pain, incontinence)

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10
Q

PKs of TCAs (maybe weeds)

A

Extensive first pass metabolism, active metabolites

Highly protein bound, lipophilic, and long half-lives

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11
Q

tertiary TCAs are more effective on which receptor? what about secondary?

A

tertiary (imipramine, amitriptyline) : Serotonin reuptake

secondary (desipramine, nortriptyline) : norepi reuptake

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12
Q

what are the most significant ADRs with imipramine? what are the receptor?

A 
orthostatic hypotension (alpha)
cardio tox (Na+ channel on purkinje fibers )
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13
Q

what are the most significant ADRs with amitriptyline? what are the receptors?

A

anticholinergic (muscarinic)

sedation (histamine)

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14
Q

which TCA has the lowest chance of anticholinergic and sedation?

A

desipramine

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15
Q

which TCA has the lowest chance of orthostatic hypotension?

A

norptriptyline

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16
Q

what are the “3 Cs” of TCAs?

A

convulsions, coma, cardiotox

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17
Q

what is the antidote to an overdose of TCA?

A

cardiotox major concern- replace Na+ with SODIUM BICARB

*(increase the amount of Na+ that can get through even with blocked channels- cause we’re flooding the channel)

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18
Q

what is the MOA or MAOIs?

A

block the monoamine oxidase enzyme which normally breaks down serotonin, NE, and dopamine = more of these NTs in the synaptic cleft.

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19
Q

selective vs nonselective MAOIs (maybe weeds)

A

MAO-A: preferably metabolizes serotonin
MAO-B: preferably metabolizes dopamine
selective- targets MAO- A or MAO- B
nonselective- targets A and B

nardel & parnate: nonselective
selegiline: selective- B (why its good to txt parkinson’s too)

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20
Q

what are the 3 MAOI drugs?

A

Phenelzine (Nardel)
Tranlcypromine (Parnate)
Selegeline (Eldepryl)

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21
Q

what 2 things do we use MAOIs for?

A
  • reserve for severe depression

- Parkinson’s disease (selegeline)

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22
Q

what are the 4 potential ADRs of MAOI drugs?

A
  1. hypotension
  2. insomnia
  3. drug- drug: HTN crisis
  4. drug-drug: serotonin syndrome
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23
Q

how can MAOI cause HTN crisis?

A

tyramine- comes from food- (fermented food, wine and cheese)
increase in tyramine and SSRIs (increase in serotonin) - will cause increase serotonin, NE and can lead to HTN crisis

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24
Q

txt for HTN crisis from MAOI?

A

nitrates and CCBs (to vasodilate)

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25
Q

txt for serotonin syndrome from MAOI?

A

txt supportive (cooling blanket)

  • benzo or anti-convulsants
  • nifedipine (for HTN)
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26
Q

given an MAOI and pt has muscle rigidity, agitation, increased temp. what is this?

A

serotonin syndrome!

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27
Q

if someone is on an MAOI and you want to put them on an SSRI, TCA, miperidine, dextomorphine, levodopa… what MUST you do first? why?

A

2 week washout period (to avoid serotonin syndrome)

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28
Q

SSRI MOA short-term vs longterm

A

short term- more available in cleft - take advantage of inhib effect of 5HT1

long-term- feedback to 5HT1 - continually till it down-regulates, then it will cause more serotonin released into cleft
overall: takes time to get full effect of agent

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29
Q

what are the 6 SSRI agents?

A 
Fluoxetine (Prozac)
Sertraline (Zoloft)
Paroxetine (Paxil)
Citalopram (Celexa)
Escitalopram (Lexapro)
Fluvoxamine (Luvox) -
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30
Q

which SSRI is reserved for OCD b/c of significant hepatotox ADR?

A

fluvoxamine (luvox)

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31
Q

what is the SSRI with the longest half life, what does this mean?

A

fluvoxamine (luvox) - 75hr 1/2 life. once-a-week pill

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32
Q

what is the metabolism of SSRIs?

A

Hepatic metabolism
CYP2D6 inhibition – fluoxetine (prozac) , paroxetine (paxil)
CYP3A4 inhibition – fluvoxamine (weakly)

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33
Q

which SSRIs are more stimulating? which are more sedating? which have no effect on sleep?

A

fluoxetine (prozac) and sertraline (zoloft) - more stimulating
paroxetine (paxil) and fluvoxamine - more sedating
if you dont wanna effect sleep at all- “loprams” (celexa, lexapro)

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34
Q

7 uses for SSRIs ?

A 
Major Depression
Anxiety disorders
Panic disorder
OCD
PTSD
Eating disorder
Perimenopausal vasomotor symptoms
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35
Q

what are the 3 most significant ADRs of SSRIs?

A
  1. Weight gain (5-10 lbs)
  2. Anxiety, initially - can be from 7-10 days. usually stabilize after this time period
  3. serotonin syndrome
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36
Q

4 other ADRs of SSRIs

A

GI upset
Insomnia
Drowsiness
Sexual dysfunction: Decreased libido, anorgasmia

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37
Q

are SNRIs more of less selective than TCAs?

A

more- which means less ADRs

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38
Q

5 SNRI drugs

A 
Duloxetine (Cymbalta)
Venlafaxine (Effexor)
Desvenlafaxine (Pristiq)
Milnacipran (Savella)*
Levomilnacipran (Fetzima)
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39
Q

which two SNRIs are reserved for fibromyalgia?

A

“-ciprans”

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40
Q

which SNRIs have renal elimination ?

A

“-ciprans”

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41
Q

hepative clearance of SNRIs- cymbalta, effexor and pristiq

A

cymbalta and effexor - phase 1 - cyp450

pristiq- phase 2 - glucuronidation

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42
Q

Venlafaxine (effexor) metabolism produces active metabolite ________

A

desvenlafaxine (pristiq)

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43
Q

4 uses for SNRIs

A

Major depression
Chronic pain disorders (diabetic neuropathy)
Fibromyalgia - duloxetine
Perimenopausal symptoms - venlafaxine for vasomotor symptoms

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44
Q

which SNRI would you use for perimenopausal symptoms?

A

venlafaxine (effexor) for vasomotor symptoms

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45
Q

which hepatic phase is better for elderly?

A

2- so give them pristiq

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46
Q

3 ADRs of SNRIs

A

Anticholinergic side effects: Anti-SLUDGEM
Sedation
Hypertension

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47
Q

CYP2D6 inhibition- which SNRI?

A

cymbalta

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48
Q

SNRIs, at low doses target what? at high doses? which causes PSNS effects?

A

low doses- more of an effect on SE, higher doses more effect on NE (where ADRs come from)
-target of NE - PSNS effects

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49
Q

general MOA or serotonin receptor modulators

A

they hit multiple receptors

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50
Q

what are the “serotonin receptor modulator” drugs?

A

“-zodones” and vortioxetine

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51
Q

MOA of trazadone?

A

Postsynaptic 5-HT2A antagonist
α1 receptor antagonist
H1 receptor antagonist

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52
Q

ADR of trazadone?

A

ADR - priapism (longterm erection)- from alpha blockade

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53
Q

is trazadone stimulating or sedating?

A

sedating

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54
Q

what are the serotonin modulators used for?

A

Major Depression

Sedation/hypnosis (trazodone)

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55
Q

4 ADRs of serotonin receptor modulators?

A 
Orthostatic hypotension (trazodone, nefazodone)
Sedation (trazodone)
Priapism (trazodone)
Liver toxicity (nefazodone)
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56
Q

drug/drug with serotonin modulators (kinda weeds)

A 
CYP2D6 substrate (Vortioxetine)
CYP3A4 inhibitor (nefazodone)
CYP3A4 substrate (vilazodone)

*“substrate” - no effect on other drugs

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57
Q

A 56 year old truck driver is on a disability for a back injury he sustained while making a delivery 3 months ago. He has been on several opioid drugs but continues to complain of “nagging back pain.” The pain specialist he sees decides to try treating him with an antidepressant approved for the management of chronic pain. Which of the following would be an effective option.

A

Duloxetine - helps with neuropathy

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58
Q

what does wellbutrin target?

A

target NE and dopamine transporters (NDRI)

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59
Q

what are the 2 uses for wellbutrin?

A

Major depression

Smoking cessation

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60
Q

what is the major ADR with wellbutrin? how can we avoid this?

A

increased risk of seizure- avoid by titrating the dose

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61
Q

wellbutrin is a stimulating agent and therefore can cause what other 3 ADRs?

A

Nervousness, HA, insomnia

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62
Q

what are the 2 benefits of using wellbutrin for major depression over other agents?

A

Rarely produces cardiovascular effects or sexual dysfunction

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63
Q

what is our one tetracyclic agent?

A

Mirtazepine (Remeron)

64
Q

MOA or remeron?

A

CENTRALLY ACTING Alpha 2 blocker
alpha 2 receptor in the CNS - reuptakes NE and inhibits release of NE and serotonin…
mirtazepine antagonizes it = consistent or increased release of NE and serotonin

65
Q

3 uses for remeron

A

Major depression
Appetite stimulant
Sedation

66
Q

ADRs of remeron: at low doses _____, at high doses _____

A

Sedation at low doses

Insomnia at higher doses

67
Q

what is one potentially beneficial ADR of remeron?

A

Increased appetite/weight gain

68
Q

A 36 year old man has been smoking 2 packs of cigarettes a day for the last 20 years. He is concerned that his health has deteriorated, and he has a persistent hacking cough. He also states that he doesn’t want to “get lung cancer and die, like my father did.” He has tried nicotine patches with no success and wants to know if there is any “pill” he could try. What medication could the physician recommend?

A

Bupropion (wellbutrin)

69
Q

how long do you usually have to wait for full effect of anti-depression drug?

A

4-8 weeks

70
Q

what are the two major considerations when selecting a drug for depression?

A

drug/drug interaction, other concomittant diseases

71
Q

“response” vs “remission”

A

Response is defined as 50% reduction in symptoms

Remission is a return to normal mood

72
Q

what is the general guideline for prescribing these drugs, as far as how long to wait for response, how long to stay on after?

A

4-8 weeks for full response
then stay on for 6-9 months
(not meant for lifetime but some pts may need it)

73
Q

CYP 450 enzyme: which 2 are “very high” inhibitor potential for 2D6 ?

A

Fluoxetine (prozac) , paroxetine (paxil)

74
Q

CYP 450 enzyme: which is “very high” inhibitor potential for 34A

A

nefazadone

75
Q

CYP 450 enzyme: which is “very high” inhibitor potential for 1A2

A

fluvoxamine (luvox)

76
Q

antidepressant discontinuation guidelines

A

Rapid discontinuation or missed doses can produce withdrawal symptoms
Taper antidepressants over 2-3 weeks

77
Q

what must we monitor when initiating anti-depressant or with does increases?

A

suicidal ideation:
Increased thought/behavior (not completions) in child, adolescent, and young adults age <25). but risk is smaller than we thought. ALL have this boxed warning.

78
Q

smoking cessation: ___ is useful.

A

bupropion (most likely due to dopamine effect)

79
Q

epilepsy: ____ increases risk in these pts (more than _____ or ____)

A

bupropion

more than SSRI or SNRI

80
Q

chronic pain- _____ or _____ can be effective in reducing chronic pain.

A

SNRI and TCA can be effective in reducing chronic pain (fibromyalgia, diabetic neuropathy)

81
Q

HTN- ___ more likely to cause dose-related increase in BP and HR.

A

SNRI

82
Q

anxiety: _____ and ____ are more effective than _____ for longterm treatment of anxiety disorders.

A

SSRI and SNRI are just as or more effective than benzodiazepines for long term treatment of anxiety disorders

83
Q

Sexual dysfunction: ____ and _____ increase incidence while _____and _____don’t have an effect

A

SSRI and SNRI increase incidence of sexual dysfunction;

bupropion and mirtazapine

84
Q

_______ therapy May decrease doses of individual agents leading to fewer AE

A

combo drug therapy

85
Q

4 augmentation therapies for depression (maybe weeds)

A
  1. Lithium: helps in treatment-resistant depression
  2. Thyroid: effective for treatment-resistant depression; dose usually is 25 mcg/day
  3. Buspirone
  4. Second-generation antipsychotics
86
Q

A 22 year old woman is being treated with sertraline for depression. She, and her family, should be cautioned about not seeing a therapeutic effect for…?

A

3 to 4 weeks (may see some 7-14 days)

87
Q

After suffering from an MI, a 52 year old male experiences depression and a psychiatrist prescribes fluoxetine. At a follow up visit the patient reluctantly tells the psychiatrist that he has not been taking his medication because of side effects. Of the following side effects, which is likely to be the most bothersome?

A

Sexual dysfunction

88
Q

How does venlafaxine differ from other antidepressants?

A

venlafazine SNRI - targets serotonin and NE - more selective than TCAs

89
Q

what are the two types of bipolar disorder?

A

Bipolar I: presence of manic episodes with major depressive episodes
Bipolar II: presence of major depressive episodes and hypomanic episodes

90
Q

what does the proposed mechanism of lithium involve?

A

MOA not well known - inositol monophosphate is targeted. regulates neuronal firing - increase serotonin release.

91
Q

what is lithium used for?

A

Bipolar disorder-to help prevent mood swings

92
Q

what is the half life of lithium?

A

20 hrs

93
Q

what is the excretion of lithium?

A

Renal excretion (1/2 of oral dose excreted within 12 hours, remainder is excreted our 1-2 weeks)

94
Q

2 significant ADRS of lithium at therapeutic levels

A

Diabetes insipidus - ADH not working properly - increased urination
Weight gain - significant

95
Q

2 ADRs of lithium at supratherapeutic levels

A

Mild toxicity: N/V, confusion, dizziness

High toxicity: seizures, coma

96
Q

other ADRs of lithium at therapeutic levels (5)

A 
GI side effects
Tremor
Edema
Polydipsia &amp; Polyuria
hypothyroidism
97
Q

lithium is very structurally similar to what?

A

Na+ (body exchanges them often)

98
Q

how to txt: hypothyroidism caused by lithium

A

stop lithium, give levothyroxine

99
Q

how to txt: polyuria/polydypsia caused by lithium

A

Reduce dose, manage intake, try amiloride or HCTZ (know that HCTZ will increase lithium concentration)

100
Q

what trimester should lithium be avoided b/c of teratoginicity ?

A

1st

101
Q

how to txt: tremor caused by lithium

A

reduce dose, add alpha blocker

102
Q

how to txt: GI upset from lithium

A

reduce dose, try ER product

103
Q

how to txt: rash or psoriasis from lithium

A

stop lithium temporarily or permanently

104
Q

which drugs increase lithium?

A

TZDs, NSAIDs, ACEs

105
Q

what situations increase lithium?

A

dehydration, salt loss

decreased renal functions

106
Q

which drug decreases lithium?

A

theophylline

107
Q

pregnancy in 2nd/3rd trimester has increased GFR and therefore what effect on lithium?

A

decrease

108
Q

aging effect on lithium

A

decrease GFR = dec. lithium requirements

incr. sensitivity to ADR = incr. risk lithium tox.

109
Q

lithium with NM block, neuroepileptic drugs, carbamazepine… what are the effects of each combo?

A

NM block- Li prolongs action
neuroEp- Li increases seizure risk
carb- increased CNS tox risk

110
Q

alternative bipolar txt: anti-epileptic drugs

A

Divalproex (Depakote)
Carbamazepine (Tegratol)
Lamotrigine (Lamictal)
Topiramate (Topamax)

111
Q

alternative bipolar txt: anti-pyschotic drugs

A 
Haloperidol
Atypical antipsychotics (2nd generation)
112
Q

alternative bipolar txt: Benzodiazapines

A

Lorazepam or diazepam for agitation

113
Q

what are the four dopamine pathways of schizophrenia?

A
  1. mesolimbic
  2. mesocortical
  3. nigrostriatal
  4. tuberohypophyseal
114
Q

mesolimbic pathway (increase/decrease) dopamine which results in (positive/negative) symptoms?

A

increases dopamine

positive symptoms

115
Q

mesocortical pathway (increase/decrease) dopamine which results in (positive/negative) symptoms?

A 
decrease dopamine 
negative symptoms (and cognitive deficits)
116
Q

which pathway do dopamine antagonists target? what is the effect?

A

mesolimbic, prevents positive symptoms

117
Q

which pathway do 5HT2 receptor antagonists target? what is the effect?

A

mesocortical, increase dopamine - prevent negative symptoms

118
Q

what pathway (s) are targeted to treat schizophrenia?

A

BOTH the mesolimbic and mesocortical

119
Q

hitting what pathway causes the EPS (parkinson-like) ADRs

A

nigrostriatal

120
Q

hitting what pathway causes hyperprolactinemia ADRs?

A

tuberhypophyseal

121
Q

what part of the brain regulates prolactin levels? imbalance of what here causes ADRs?

A

hypothalamus

dopamine and serotonin

122
Q

what are the two groups of anti-pysc. agents used to txt schizophrenia ?

A
  1. typical (1st gen)

2. atypical (2nd gen)

123
Q

what are the two types of typical (1st gen) anti-psyc agents? what is significant about the difference

A

low potency and high potency

- similar efficacy but difference in ADRs

124
Q

LOW potency 1st gen anti-pysc drugs have (low/high) risk of EPS symptoms and (low/high) risk of anticholingeric, sedation, ortho hypotension?

A

low potency
low risk EPS
high risk: anti-chol, sedation, orthostatic hypotension

125
Q

HIGH potency 1st gen anti-pysc drugs have (low/high) risk of EPS symptoms and (low/high) risk of anticholingeric, sedation, ortho hypotension?

A

high potency
high risk EPS
low risk: anti-chol, sedation, orthostatic hypotension

126
Q

are 1st gen (typical) or 2ng gen (atypical) drugs a better “go-to” for SCZ?

A

2nd generation (less risk of ADRs)

127
Q

when would 1st gen (typical) be used for SCZ?

A

only for an acute phase SCZ, b/c they don’t take as long to take effect BUT have more ADRs.

128
Q

what are the low potency 1st gen antipysch drugs?

A

Chlorpromazine (Thorazine)

Thioridazine

129
Q

what are the high potency 1st gen anti-pysch drugs?

A 
Fluphenazine (Prolixin)
Haloperidol (Haldol)
Loxapine (Loxitane)
Perphenazine
Prochlorperazine (Compazine)
Thiothixene (Navane)
Trifluoperazine (Stelazine)
130
Q

what are the atypical (2nd gen) anti-psyc drugs?

A 
Clozapine (Clozaril)
Olanzapine (Zyprexa)
Quetiapine (Seroquel)
Asenapine (Saprhis)
Risperidone (Risperdal)
Paliperidone (Invega)
Ziprasidone (Geodon)
Aripiprazole (Abilify)
Lurasidone (Latuda)
Iloperidone (Fanapt)
Aripiprazole (Abilify)
Pimavanserin (Nuplazid)
Brexpiprazole (Rexulti)
131
Q

what is the MOA of typical (1st gen) anti-pysc drugs?

A

decrease the positive symptoms by antagonizing dopamine receptors
- also hit alpha, muscarinic, histamine = ADRs

132
Q

what are the three uses for “typical” (1st gen) anti-pysc drugs?

A
  1. schizophrenia
  2. bipolar disorder (occassionally used)
  3. antiemetic (chlorpromethazine)
133
Q

what is the metabolism of typical anti-pysc drugs?

A

large 1st pass metabolism

134
Q

what are the ADRs of tyical (1st gen) anti-pysc drugs?

A
  • anti-chol, sedation, orthostatic hypotension
  • corneal/retinal deposits
  • metabolic- dyslipidemia, hyperglycemia, weight gain
  • QT PROLONGATION
  • HYPER-PROLACTINEMIA
  • EPS
  • TARDIVE DYSKINESIA (jaw muscles)
135
Q

what three things are included in the EPS ADRs?

A
  1. parkinsonism: bradykinesia, rigid, tremor
  2. dystonia: torticolis, laryngospasm
  3. akathisia : restless
136
Q

what 4 agents can you give a pt to counteract the EPS symptoms from typical anti-pysc drugs?

A
  • anticholinergics (benztropine, trihexyphenadyl)
  • diphenahydramine (but can be sedating)
  • benzodiazepines (for parkinson-like)
  • propranolol (for tremors)
137
Q

tardive dyskinesia: diagnosed after only ___ months, difficult or easy to treat?

A

Diagnosed only after 6 months of therapy

difficult to treat, may not resolve when drug is removed

138
Q

can’t use _____ to txt tardive dyskinesia b/c it will make it worse.

A

anti-cholinergics

139
Q

effect on prolactin production: normally, dopamine is (inhibitory/stimulatory), and serotonin is (inhibitory/stimulatory) ?

A

dopamine- inhibitory

serotonin- stimulatory

140
Q

how can you get antipyschotic-induced hyperprolactinemia?

A

if you block dopamine = overactive serotonin receptor = increase prolactin level (hyperprolactinemia)
(see more with first generation, second generation has more of a balancing act)

141
Q

normal nigrostriatal pathway: dopamine effect is what?

A

Dopaminergic neurons in nigrostriatal pathway have an inhibitor effect on muscarinic neurons that regulate motor activity

142
Q

nigrostriatal pathway with Dopamine antagonist: effect is what?

A

double negative: D2 antagonist decrease the inhibitory effect of dopamine, leading to increased firing of cholinergic neurons, increased ACh release and EPS

143
Q

nigrostriatal pathway: balancing dopamine antagonist with anti-cholingeric: effect is what?

A

Benztropine can antagonize muscarinic transmission to reduce EPS

144
Q

what are the 4 uses for atypical (2nd gen) anti-pysc drugs?

A

Schizophrenia – improve positive and negative symptoms
Bipolar disorder
Major depression
Irritability associated with autistic disorder (for children)

145
Q

what are the ADRs of atypical antipyschotic drugs?

A
  • sedation, orthostatic hypotensions
  • EPS &anticholinergic (but less than typical)
  • metabolic: dyslipidemia, hyperglycemia, weight gain
  • **AGRANULOCYTOSIS
  • HYPERPROLACTINEMIA
  • QT PROLONGATION
146
Q

which atypical (2nd gen) drug in particular can cause agranulocytosis? when would you ever use this drug?

A

clozapine- depletes neutrophils (agranulocytosis)- MUST be monitored aka REMS policy
—> used only after pt has failed a 2nd gen, a 1st gen and have failed both

147
Q

which two atypical (2nd gen) drugs in particular cause hyperprolactinemia ?

A

risperidone & paliperidone

148
Q

which two atypical (2nd gen) drugs in particular cause metabolic issues?

A

“pines” (olanzapine, clozapine, quetiapine, asenapine)

149
Q

what is the boxed warning for atypical (2nd gen) drugs ?

A

Boxed warning-off label use with dementia in elderly- these people will have higher mortality risk (don’t know why this happens)

150
Q

what system and what type of blockade would cause: loss of accomodation, dry mouth, difficulty urinating and constipation?

A

ADR of antipysc drugs: Autonomic system, muscarinic block

151
Q

what system and what type of receptor block would cause: Orthostatic hypotension, impotence, failure to ejaculate?

A

ADR of antipysc drugs: Autonomic system, alpha block

152
Q

what system and what type of receptor block would cause: Parkinson’s syndrome, akathisia, dystonia?

A

ADR of antipysc drugs: CNS system, dopamine block

153
Q

what system and what type of receptor block would cause: confusion?

A

ADR of antipysc drugs: CNS system, muscarinic block

154
Q

what system and what type of receptor block would cause: Amenorrhea-galactorrhea, infertility, impotence?

A

ADR of antipysc drugs: endocrine system, dopamine block –> hyperprolactinemia

155
Q

what receptor block would cause weight gain?

A

not sure- possibly histamine (H1) or serotonin (5HT)

pharmacology (24 decks)

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