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
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)
3
Q
three types of therapy options for major depressive disorder. which take longest to be effective? which are best to prevent relapse?
A
- pyschotherapy - longer for effect, prevents relapse
- pharmacotherapy - shorter for effect, incr. risk relapse
- electroconvulsive therapy
*best combine pyscho and pharm.
4
Q
7 general classes of drugs for major depressive disorder
A
- Tricyclic Antidepressants (TCAs)
- MAOIs
- SSRIs
- SSNRI
- Norepinephrine Dopamine Reuptake Inhibitor (NDRI)
- Serotonin Modulators
- Tetracyclic
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
6
Q
what are the 5 TCA drugs. which are secondary and which are tertiary?
A
Imipramine - Desipramine - Amitriptyline - Nortriptyline - Clomipramine
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
8
Q
what is the one TCA that has a specific indication for OCD?
A
clomipramine
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)
10
Q
PKs of TCAs (maybe weeds)
A
Extensive first pass metabolism, active metabolites
Highly protein bound, lipophilic, and long half-lives
11
Q
tertiary TCAs are more effective on which receptor? what about secondary?
A
tertiary (imipramine, amitriptyline) : Serotonin reuptake
secondary (desipramine, nortriptyline) : norepi reuptake
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 )
13
Q
what are the most significant ADRs with amitriptyline? what are the receptors?
A
anticholinergic (muscarinic)
sedation (histamine)
14
Q
which TCA has the lowest chance of anticholinergic and sedation?
A
desipramine
15
Q
which TCA has the lowest chance of orthostatic hypotension?
A
norptriptyline
16
Q
what are the “3 Cs” of TCAs?
A
convulsions, coma, cardiotox
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)
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.
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)
20
Q
what are the 3 MAOI drugs?
A
Phenelzine (Nardel)
Tranlcypromine (Parnate)
Selegeline (Eldepryl)
21
Q
what 2 things do we use MAOIs for?
A
- reserve for severe depression
- Parkinson’s disease (selegeline)
22
Q
what are the 4 potential ADRs of MAOI drugs?
A
- hypotension
- insomnia
- drug- drug: HTN crisis
- drug-drug: serotonin syndrome
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
24
Q
txt for HTN crisis from MAOI?
A
nitrates and CCBs (to vasodilate)
25
txt for serotonin syndrome from MAOI?
txt supportive (cooling blanket)
- benzo or anti-convulsants
- nifedipine (for HTN)
26
given an MAOI and pt has muscle rigidity, agitation, increased temp. what is this?
serotonin syndrome!
27
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?
2 week washout period (to avoid serotonin syndrome)
28
SSRI MOA short-term vs longterm
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
29
what are the 6 SSRI agents?
```
Fluoxetine (Prozac)
Sertraline (Zoloft)
Paroxetine (Paxil)
Citalopram (Celexa)
Escitalopram (Lexapro)
Fluvoxamine (Luvox) -
```
30
which SSRI is reserved for OCD b/c of significant hepatotox ADR?
fluvoxamine (luvox)
31
what is the SSRI with the longest half life, what does this mean?
fluvoxamine (luvox) - 75hr 1/2 life. once-a-week pill
32
what is the metabolism of SSRIs?
Hepatic metabolism
CYP2D6 inhibition – fluoxetine (prozac) , paroxetine (paxil)
CYP3A4 inhibition – fluvoxamine (weakly)
33
which SSRIs are more stimulating? which are more sedating? which have no effect on sleep?
fluoxetine (prozac) and sertraline (zoloft) - more stimulating
paroxetine (paxil) and fluvoxamine - more sedating
if you dont wanna effect sleep at all- “loprams” (celexa, lexapro)
34
7 uses for SSRIs ?
```
Major Depression
Anxiety disorders
Panic disorder
OCD
PTSD
Eating disorder
Perimenopausal vasomotor symptoms
```
35
what are the 3 most significant ADRs of SSRIs?
1. Weight gain (5-10 lbs)
2. Anxiety, initially - can be from 7-10 days. usually stabilize after this time period
3. serotonin syndrome
36
4 other ADRs of SSRIs
GI upset
Insomnia
Drowsiness
Sexual dysfunction: Decreased libido, anorgasmia
37
are SNRIs more of less selective than TCAs?
more- which means less ADRs
38
5 SNRI drugs
```
Duloxetine (Cymbalta)
Venlafaxine (Effexor)
Desvenlafaxine (Pristiq)
Milnacipran (Savella)*
Levomilnacipran (Fetzima)
```
39
which two SNRIs are reserved for fibromyalgia?
"-ciprans"
40
which SNRIs have renal elimination ?
"-ciprans"
41
hepative clearance of SNRIs- cymbalta, effexor and pristiq
cymbalta and effexor - phase 1 - cyp450
| pristiq- phase 2 - glucuronidation
42
Venlafaxine (effexor) metabolism produces active metabolite ________
desvenlafaxine (pristiq)
43
4 uses for SNRIs
Major depression
Chronic pain disorders (diabetic neuropathy)
Fibromyalgia - duloxetine
Perimenopausal symptoms - venlafaxine for vasomotor symptoms
44
which SNRI would you use for perimenopausal symptoms?
venlafaxine (effexor) for vasomotor symptoms
45
which hepatic phase is better for elderly?
2- so give them pristiq
46
3 ADRs of SNRIs
Anticholinergic side effects: Anti-SLUDGEM
Sedation
Hypertension
47
CYP2D6 inhibition- which SNRI?
cymbalta
48
SNRIs, at low doses target what? at high doses? which causes PSNS effects?
low doses- more of an effect on SE, higher doses more effect on NE (where ADRs come from)
-target of NE - PSNS effects
49
general MOA or serotonin receptor modulators
they hit multiple receptors
50
what are the "serotonin receptor modulator" drugs?
"-zodones" and vortioxetine
51
MOA of trazadone?
Postsynaptic 5-HT2A antagonist
α1 receptor antagonist
H1 receptor antagonist
52
ADR of trazadone?
ADR - priapism (longterm erection)- from alpha blockade
53
is trazadone stimulating or sedating?
sedating
54
what are the serotonin modulators used for?
Major Depression
| Sedation/hypnosis (trazodone)
55
4 ADRs of serotonin receptor modulators?
```
Orthostatic hypotension (trazodone, nefazodone)
Sedation (trazodone)
Priapism (trazodone)
Liver toxicity (nefazodone)
```
56
drug/drug with serotonin modulators (kinda weeds)
```
CYP2D6 substrate (Vortioxetine)
CYP3A4 inhibitor (nefazodone)
CYP3A4 substrate (vilazodone)
```
*"substrate" - no effect on other drugs
57
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.
Duloxetine - helps with neuropathy
58
what does wellbutrin target?
target NE and dopamine transporters (NDRI)
59
what are the 2 uses for wellbutrin?
Major depression
| Smoking cessation
60
what is the major ADR with wellbutrin? how can we avoid this?
increased risk of seizure- avoid by titrating the dose
61
wellbutrin is a stimulating agent and therefore can cause what other 3 ADRs?
Nervousness, HA, insomnia
62
what are the 2 benefits of using wellbutrin for major depression over other agents?
Rarely produces cardiovascular effects or sexual dysfunction
63
what is our one tetracyclic agent?
Mirtazepine (Remeron)
64
MOA or remeron?
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
3 uses for remeron
Major depression
Appetite stimulant
Sedation
66
ADRs of remeron: at low doses _____, at high doses _____
Sedation at low doses
| Insomnia at higher doses
67
what is one potentially beneficial ADR of remeron?
Increased appetite/weight gain
68
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?
Bupropion (wellbutrin)
69
how long do you usually have to wait for full effect of anti-depression drug?
4-8 weeks
70
what are the two major considerations when selecting a drug for depression?
drug/drug interaction, other concomittant diseases
71
"response" vs "remission"
Response is defined as 50% reduction in symptoms
| Remission is a return to normal mood
72
what is the general guideline for prescribing these drugs, as far as how long to wait for response, how long to stay on after?
4-8 weeks for full response
then stay on for 6-9 months
(not meant for lifetime but some pts may need it)
73
CYP 450 enzyme: which 2 are "very high" inhibitor potential for 2D6 ?
Fluoxetine (prozac) , paroxetine (paxil)
74
CYP 450 enzyme: which is "very high" inhibitor potential for 34A
nefazadone
75
CYP 450 enzyme: which is "very high" inhibitor potential for 1A2
fluvoxamine (luvox)
76
antidepressant discontinuation guidelines
Rapid discontinuation or missed doses can produce withdrawal symptoms
Taper antidepressants over 2-3 weeks
77
what must we monitor when initiating anti-depressant or with does increases?
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
smoking cessation: ___ is useful.
bupropion (most likely due to dopamine effect)
79
epilepsy: ____ increases risk in these pts (more than _____ or ____)
bupropion
| more than SSRI or SNRI
80
chronic pain- _____ or _____ can be effective in reducing chronic pain.
SNRI and TCA can be effective in reducing chronic pain (fibromyalgia, diabetic neuropathy)
81
HTN- ___ more likely to cause dose-related increase in BP and HR.
SNRI
82
anxiety: _____ and ____ are more effective than _____ for longterm treatment of anxiety disorders.
SSRI and SNRI are just as or more effective than benzodiazepines for long term treatment of anxiety disorders
83
Sexual dysfunction: ____ and _____ increase incidence while _____and _____don't have an effect
SSRI and SNRI increase incidence of sexual dysfunction;
| bupropion and mirtazapine
84
_______ therapy May decrease doses of individual agents leading to fewer AE
combo drug therapy
85
4 augmentation therapies for depression (maybe weeds)
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
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...?
3 to 4 weeks (may see some 7-14 days)
87
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?
Sexual dysfunction
88
How does venlafaxine differ from other antidepressants?
venlafazine SNRI - targets serotonin and NE - more selective than TCAs
89
what are the two types of bipolar disorder?
Bipolar I: presence of manic episodes with major depressive episodes
Bipolar II: presence of major depressive episodes and hypomanic episodes
90
what does the proposed mechanism of lithium involve?
MOA not well known - inositol monophosphate is targeted. regulates neuronal firing - increase serotonin release.
91
what is lithium used for?
Bipolar disorder-to help prevent mood swings
92
what is the half life of lithium?
20 hrs
93
what is the excretion of lithium?
Renal excretion (1/2 of oral dose excreted within 12 hours, remainder is excreted our 1-2 weeks)
94
2 significant ADRS of lithium at therapeutic levels
Diabetes insipidus - ADH not working properly - increased urination
Weight gain - significant
95
2 ADRs of lithium at supratherapeutic levels
Mild toxicity: N/V, confusion, dizziness
| High toxicity: seizures, coma
96
other ADRs of lithium at therapeutic levels (5)
```
GI side effects
Tremor
Edema
Polydipsia & Polyuria
hypothyroidism
```
97
lithium is very structurally similar to what?
Na+ (body exchanges them often)
98
how to txt: hypothyroidism caused by lithium
stop lithium, give levothyroxine
99
how to txt: polyuria/polydypsia caused by lithium
Reduce dose, manage intake, try amiloride or HCTZ (know that HCTZ will increase lithium concentration)
100
what trimester should lithium be avoided b/c of teratoginicity ?
1st
101
how to txt: tremor caused by lithium
reduce dose, add alpha blocker
102
how to txt: GI upset from lithium
reduce dose, try ER product
103
how to txt: rash or psoriasis from lithium
stop lithium temporarily or permanently
104
which drugs increase lithium?
TZDs, NSAIDs, ACEs
105
what situations increase lithium?
dehydration, salt loss
| decreased renal functions
106
which drug decreases lithium?
theophylline
107
pregnancy in 2nd/3rd trimester has increased GFR and therefore what effect on lithium?
decrease
108
aging effect on lithium
decrease GFR = dec. lithium requirements
| incr. sensitivity to ADR = incr. risk lithium tox.
109
lithium with NM block, neuroepileptic drugs, carbamazepine... what are the effects of each combo?
NM block- Li prolongs action
neuroEp- Li increases seizure risk
carb- increased CNS tox risk
110
alternative bipolar txt: anti-epileptic drugs
Divalproex (Depakote)
Carbamazepine (Tegratol)
Lamotrigine (Lamictal)
Topiramate (Topamax)
111
alternative bipolar txt: anti-pyschotic drugs
```
Haloperidol
Atypical antipsychotics (2nd generation)
```
112
alternative bipolar txt: Benzodiazapines
Lorazepam or diazepam for agitation
113
what are the four dopamine pathways of schizophrenia?
1. mesolimbic
2. mesocortical
3. nigrostriatal
4. tuberohypophyseal
114
mesolimbic pathway (increase/decrease) dopamine which results in (positive/negative) symptoms?
increases dopamine
| positive symptoms
115
mesocortical pathway (increase/decrease) dopamine which results in (positive/negative) symptoms?
```
decrease dopamine
negative symptoms (and cognitive deficits)
```
116
which pathway do dopamine antagonists target? what is the effect?
mesolimbic, prevents positive symptoms
117
which pathway do 5HT2 receptor antagonists target? what is the effect?
mesocortical, increase dopamine - prevent negative symptoms
118
what pathway (s) are targeted to treat schizophrenia?
BOTH the mesolimbic and mesocortical
119
hitting what pathway causes the EPS (parkinson-like) ADRs
nigrostriatal
120
hitting what pathway causes hyperprolactinemia ADRs?
tuberhypophyseal
121
what part of the brain regulates prolactin levels? imbalance of what here causes ADRs?
hypothalamus
| dopamine and serotonin
122
what are the two groups of anti-pysc. agents used to txt schizophrenia ?
1. typical (1st gen)
| 2. atypical (2nd gen)
123
what are the two types of typical (1st gen) anti-psyc agents? what is significant about the difference
low potency and high potency
| - similar efficacy but difference in ADRs
124
LOW potency 1st gen anti-pysc drugs have (low/high) risk of EPS symptoms and (low/high) risk of anticholingeric, sedation, ortho hypotension?
low potency
low risk EPS
high risk: anti-chol, sedation, orthostatic hypotension
125
HIGH potency 1st gen anti-pysc drugs have (low/high) risk of EPS symptoms and (low/high) risk of anticholingeric, sedation, ortho hypotension?
high potency
high risk EPS
low risk: anti-chol, sedation, orthostatic hypotension
126
are 1st gen (typical) or 2ng gen (atypical) drugs a better "go-to" for SCZ?
2nd generation (less risk of ADRs)
127
when would 1st gen (typical) be used for SCZ?
only for an acute phase SCZ, b/c they don't take as long to take effect BUT have more ADRs.
128
what are the low potency 1st gen antipysch drugs?
Chlorpromazine (Thorazine)
| Thioridazine
129
what are the high potency 1st gen anti-pysch drugs?
```
Fluphenazine (Prolixin)
Haloperidol (Haldol)
Loxapine (Loxitane)
Perphenazine
Prochlorperazine (Compazine)
Thiothixene (Navane)
Trifluoperazine (Stelazine)
```
130
what are the atypical (2nd gen) anti-psyc drugs?
```
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
what is the MOA of typical (1st gen) anti-pysc drugs?
decrease the positive symptoms by antagonizing dopamine receptors
- also hit alpha, muscarinic, histamine = ADRs
132
what are the three uses for "typical" (1st gen) anti-pysc drugs?
1. schizophrenia
2. bipolar disorder (occassionally used)
3. antiemetic (chlorpromethazine)
133
what is the metabolism of typical anti-pysc drugs?
large 1st pass metabolism
134
what are the ADRs of tyical (1st gen) anti-pysc drugs?
- anti-chol, sedation, orthostatic hypotension
- corneal/retinal deposits
- metabolic- dyslipidemia, hyperglycemia, weight gain
- QT PROLONGATION
- HYPER-PROLACTINEMIA
- EPS
- TARDIVE DYSKINESIA (jaw muscles)
135
what three things are included in the EPS ADRs?
1. parkinsonism: bradykinesia, rigid, tremor
2. dystonia: torticolis, laryngospasm
3. akathisia : restless
136
what 4 agents can you give a pt to counteract the EPS symptoms from typical anti-pysc drugs?
- anticholinergics (benztropine, trihexyphenadyl)
- diphenahydramine (but can be sedating)
- benzodiazepines (for parkinson-like)
- propranolol (for tremors)
137
tardive dyskinesia: diagnosed after only ___ months, difficult or easy to treat?
Diagnosed only after 6 months of therapy
| difficult to treat, may not resolve when drug is removed
138
can't use _____ to txt tardive dyskinesia b/c it will make it worse.
anti-cholinergics
139
effect on prolactin production: normally, dopamine is (inhibitory/stimulatory), and serotonin is (inhibitory/stimulatory) ?
dopamine- inhibitory
| serotonin- stimulatory
140
how can you get antipyschotic-induced hyperprolactinemia?
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
normal nigrostriatal pathway: dopamine effect is what?
Dopaminergic neurons in nigrostriatal pathway have an inhibitor effect on muscarinic neurons that regulate motor activity
142
nigrostriatal pathway with Dopamine antagonist: effect is what?
double negative: D2 antagonist decrease the inhibitory effect of dopamine, leading to increased firing of cholinergic neurons, increased ACh release and EPS
143
nigrostriatal pathway: balancing dopamine antagonist with anti-cholingeric: effect is what?
Benztropine can antagonize muscarinic transmission to reduce EPS
144
what are the 4 uses for atypical (2nd gen) anti-pysc drugs?
Schizophrenia – improve positive and negative symptoms
Bipolar disorder
Major depression
Irritability associated with autistic disorder (for children)
145
what are the ADRs of atypical antipyschotic drugs?
- sedation, orthostatic hypotensions
- EPS &anticholinergic (but less than typical)
- metabolic: dyslipidemia, hyperglycemia, weight gain
- **AGRANULOCYTOSIS
- HYPERPROLACTINEMIA
- QT PROLONGATION
146
which atypical (2nd gen) drug in particular can cause agranulocytosis? when would you ever use this drug?
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
which two atypical (2nd gen) drugs in particular cause hyperprolactinemia ?
risperidone & paliperidone
148
which two atypical (2nd gen) drugs in particular cause metabolic issues?
“pines” (olanzapine, clozapine, quetiapine, asenapine)
149
what is the boxed warning for atypical (2nd gen) drugs ?
Boxed warning-off label use with dementia in elderly- these people will have higher mortality risk (don’t know why this happens)
150
what system and what type of blockade would cause: loss of accomodation, dry mouth, difficulty urinating and constipation?
ADR of antipysc drugs: Autonomic system, muscarinic block
151
what system and what type of receptor block would cause: Orthostatic hypotension, impotence, failure to ejaculate?
ADR of antipysc drugs: Autonomic system, alpha block
152
what system and what type of receptor block would cause: Parkinson’s syndrome, akathisia, dystonia?
ADR of antipysc drugs: CNS system, dopamine block
153
what system and what type of receptor block would cause: confusion?
ADR of antipysc drugs: CNS system, muscarinic block
154
what system and what type of receptor block would cause: Amenorrhea-galactorrhea, infertility, impotence?
ADR of antipysc drugs: endocrine system, dopamine block --> hyperprolactinemia
155
what receptor block would cause weight gain?
not sure- possibly histamine (H1) or serotonin (5HT)
