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482 Pharm > psychotherapeutics wk 4 notes > Flashcards

psychotherapeutics wk 4 notes Flashcards

1
Q

psychotherapeutics

A

Psychotherapeutics: treatment of emotional and mental health disorders.

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2
Q

benzodiazepines
how are they anxiolytic
what NTM do they work on

A

Benzodiazepines: exert their anxiolytic effects by depressing activity in brainstem and limbic system. They inc. action of GABA (neurotransmitter in brain that functions to inbibit nerve transmission in CNS)

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3
Q

how are antihistamines used as anxiolytics

A

Antihistamines: used as anxiolytics d/t ability to depress CNS by sedating pt.

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4
Q

what is the dysregulation hypothesis

A

Dysregulation hypothesis: a new leading theory. Depression and affective disorders are viewd not simply in terms of decreased or increased catecholamine activity but as a failure of the regulation of these systems.

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5
Q

what is challenging about measuring effieffectiveness of psychotropic drugs

how to bypass this

A
  • subjectivity of mental health disorder
  • verbal reports
  • dont know how long a psychotropic drug works

-use objective tools eg HAM-D

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6
Q

what is a spectrum disorder

A

• Patients that have ongoing symptoms that meet several criteria for several different disorders are said to have spectrum disorder. Ie. More than ½ of those who are chronically depressed also have concurrent personality disorder. 1/3 have concurrent anxiety disorder.

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7
Q

what are the 3 major classifications of emotional and mental health disorders

A

psychoses, affective disorders, and anxiety.

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8
Q

which NTM are catechoamines and which are indolamines

A

catecholamines (dopamine/ norepinephrine) and indolamines (serotonin and histamine).

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9
Q

almost no cards on anxiety, bipolar, depression

A

.

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10
Q

what NTM are involved in bipolar disorder

A

• Inc. activity of catecholamines (dopamine/norepi) may play role re: mania, and reduced levels may contribute to depression. Serotonin may stabilize catecholamine/inhibit dopamine release. GABA may play role in mania.

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11
Q

what is bipolar I vs bipolar II

A

• subtypes: bipolar disorder type 1 (major depressive disorder/manic/mixed episode), bipolar type ii major depressive/hypomania disorder

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12
Q

what characterizes a manic episode

A

• Manic episode includes symptoms of grandiosity, dec need for sleep or food, pressured speech, flight of ideas, distractibility, and involvement in pleasurable activities of ten resulting in neg consequences

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13
Q

what are the theories on the et of majore depression

A

biogenic amine hypothesis

  • downreulation of NE receptors
  • dysregulation hypothesis
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14
Q

the general MOA of all antianxiety drugs is (in relation to CNS)

A

• All reduce anxiety by diminishing over activity in CNS.

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15
Q

benzos: what are they ating on and what effect does it have

A

depress activity in brainstem/limbic system. Inc. action of GABA (functions to inhibit nerve transmission in CNS). Benzo’s have receptor proteins (receptor binding sites) in same areas of brain that govern release of GABBA. Binding of benzos with these receptor sites= anxiolytic effects/sedation.

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16
Q

wht are the drugs most safely used for aniolytics

A

• Benzo, antidepressants, and buspirone most effective/safe drugs re: ongoing anxiety disorders.

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17
Q

which of the aforementioned anxiolytics is non sedating and non habit forming

A

buspirone. Non sedating/non habit forming.

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18
Q

are barbiturates used much these days

A

less common becaue of newer/better drugs.

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19
Q

what kind of anxiety are benzos gen used for

do they have a small or lg impact on LOC

A

• Benzo’s most common for rapid relief of acute anxiety. Little effect on consciousness.

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20
Q

do benzos have a sm or lg adverse effect profile

do they interact much

A

Safe re: low adverse effect profile, and don’t interact with many drugs.

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21
Q

which benzo is used for mod sedation

A

• Midazolam: only available in injectable form, used as sedative/anaesthetic during sx. Used for “moderate sedation” Also used for agitation in CCU.

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22
Q

what kind of side effects do benzos have

A
  • hoTN (also caused by antihistamines, dec CNS activity
  • Benzo: paradoxical reactions include hyperactivity/aggressive behavior. Pretty uncommon, more likely to occur in children/teens/ patients with psychiatric disorders. -Benzos can be habit forming/addictive.
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23
Q

do antihistamines have an antidote

what might happen w overdose

A

Usually not severe but may be associated with excessive sedation, hypotension, seizures. No antidote.

if extreme might use cholinergic drug

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24
Q

consequences of benzo overdose

A

can be life-threatening. Don’t take with other sedating drugs/alcool, life-threatening resp. depression can occur. Can also occur r/t metabolism/elimination impaired d/t hepatic/renal dysfunction.

  • symptomatic/supportive if within 4 hours, decontamination of GI is indicated. Gastric lavage generally best/most effective means. Activated charcoal/saline cathartic may be administered after gastric lavage to remove remaining drug.
  • HD only if extreme
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25
Q

what is antidote to benzo and when is it used

A

flumazenil might be used

it is also used for reversing mod sedation

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26
Q

when treating bipolar what are the 3 states youre trying to address

A

acute mania, acute depression, maintenance.

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27
Q

bipolar: what is the drug of choice to manage mania and maintenance

how does it work

A

• Lithium is drug of choice to effectively alleviate mania and in maintenance. MOA: may poteniate serotonergic neurotransmission , inhibit dopamine synthesis/decrease nuber of b adrenergic receptors, and enhance GABA activity.

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28
Q

what is used as monotherapy for acute mania

A

quetiapine fumarate

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29
Q

• Drugs used as mood stabilizers / conjunction with lithium

A

high dose benzos, antiepileptic drugs, carbamazepine, divalproex sodium, dopamine receptor agonists, amino acid L-tryptophan, calcium channel antagonists.

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30
Q

which drug is better than lithium for o adults

A

• the mood stabilizer: Valproic acid: better than lithium for older adults because of narrow therapeutic index/monitoring needs of lithium.

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31
Q

what should youc onsider when selecting an antidepressant for the depression seen in bipolar

A

Choose ones that are les likely to evoke manic response.

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32
Q

t or f its better to be les invasive and see if depression will respond without pharm interventions

A

F

• Early/aggressive antidepressant tx increase chances for full remission.

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33
Q

HOW LONG SHOULD PT STAY On antideressant after remission of symptoms

A

• Individuals recommended to stay on antidepressants for 8-14 months after remission of symptoms.

34
Q

how is dose optimization of antidepressant done

A

• Dose optimization involves careful upward titration for several weeks. If one class of antidepressant does not work there is a 40 to 60% chance another class will.

35
Q

treatment resistnt depression is what

A

• Nonresponse to at least two trials is called: treatment resistant drepssion.

36
Q

when is the acute phase of depression and what are the goals

A

• First 6-8wks are acute phase where goals are to have response to drug therapy and improve symptoms

37
Q

what are the common drug categories for tx of affective disorders

A

selective serotonin reuptake inhibitors and 2nd and 3rd gen antidepressants. Less commonly used=tricyclic antidepressants (TCA) and MAOI(1st gen antidepressants)

38
Q

why are SSRIs considered better Tx for depression than Tca and MAOI

A

d/t their adverse effect profiles. Newer drugs have less anticholinergic and cardiovascular effects, less drug-drug-food interactions.
-• 2nd and 3rd gen drugs are less selective and act at dopamine and NE receptors. Aka multimodal or multireceptor drugs

39
Q

how long do newer antidep take for max clinical effectiveness

A

• Newer antidep also take 4-6wks for max clinical effectiveness

40
Q

how does SSR work

A

• SSRIs slow or inhibit the reuptake or serotonin into presynaptic terminals and inc levels of serotonin for NTmission at postsynaptic nerve endings
they do also have weak effects on NE and dopamine reuptake

41
Q

how do SSRIs affect sleep and appetite

A
  • The inc NTM conc in Cns leads to dec REM sleep.
  • SSRIs are assoc w wt loss and anorectic activity (appetitie inhibiting activity may come from inc in serotonin conc at nerve endings. This is why SSRIs are sometimes used as tx for eating disorders like bulimia that involve compulsive overeating
42
Q

indications of SSRIs

A

depression, BPD, obesity, eating disorders, OCD, panic attacks or disorders, social anxiety disorder, PTSD, premenstrual dysmorphic disorder, myoclonus

43
Q

contraindications for SSRIs

A

do not use sooner than 14 days after stopping MAOI therapy, sig hx of cardiac or seizure disorders (d/t rare side effects)

44
Q

most common SE of SSRI

A
  • Most common=insomnia, wt gain, sexual dysfx (mainly male impotence)
  • Less common= chest pain, palpitations and QT prolongation on ECG
  • Dec seizure threshold in susceptible pts
  • Risk of serotonin syndrome
45
Q

interaction for SSRI

A

• risk when combined with drugs like warfarin and phenytoin that, like SSRIs and NGAs, are highly bound to plasma proteins eg albumininc amount of free, unbound drug and inc effect

46
Q

what is the concern with TCA overdose

A

can cause fatal dysrhythmias following overdose (this is v risky considering depressed pts are inc suicide risk)
• TCA ODs are notoriously lethal and 70-80% of deaths occur before reaching hospital
• Mostly affects CNS and CV sstems
• No antidote

47
Q

when are tricyclic antidep used in r/t other antidep

A

• No longer first line therapy since SSRIs. 2nd line therapy for those who fail NGAs

48
Q

MOA of triclycic antidep

A
  • Believed to work by correcting imbal of NTM conc of serotonin and NE at nerve endings in CNS. Happens by bloking reuptake of NTMs (NE and serotonin) and causing them to accum in the nerve endings
  • May also reg malfx nerves (the dysregulation hypothesis)
49
Q

TCA side effects in r/t the receptors affected •

A
  • Mostly from muscarinic receptors-blockade of these receptorsanticholinergic effects most common=sedation, erectile dysfx, orthostatic HoTN
  • Dopaminergic receptors: Extrapyrimidal and endocrine adverse effects,
  • Histaminergic: sedation, wt gain, dry mouth
  • Muscarinic receptors: dry mouth, constipation, blurred vision, tachy, urinary retention, confusion
  • Norepinephrine reuptake: tremors, tachy, additive pressor effects w sympathomimetic drugs antidepressant
  • Serotonergic receptors: HoTN, alleviation of rhinitis
  • Serotonin reuptake: antidepressant, N, headache, anxiety, sex dysfx
50
Q

monoamine oxidase inhibitors

old or new antidep?
what is a major disadvantage of MAOI?

A
  • A first generation antidepressant
  • Serious disadvantage is possible hypertensive crisis when taken w substance that has tyramine (found in many foods and drinks). One of few drus that interacts with food. Tyramine is an amino acid.
51
Q

when is MAOI used in relation to other antidep

A

• Second or third line treatment for depression not responding to first line drugs

52
Q

how does MAOI work

A

By inhibiting the MAO enzyme system in the CNS of patients who have depression, amines such as dopamine, serotonin and norepinephrine are not broken down and therefore, higher levels occur, alleviating the symptoms of depression

53
Q

how long does it take to reach therapeutic levels with MAOI

A

1-4wks to reach theraeutic levle

54
Q

what drugs should be avoided when taking MAOI and for how long after d/cing them should they be avoided

A

• Drugs to be avoided while taking MAOIS (+up to 2 weeks after discontinuing use), Cough preparations, nasal decongestants, hay fever medications, sinus medication, asthma inhalants, anti appetite medications, weight reducing preparations, and L-tryptophan containing preparations

55
Q

MAOI OD

is it fast as TCA
s/s in gen

A
  • Symptoms of overdose don’t appear until 12 hours post ingestion
  • Primary signs are cardio and neuro changes (tachycardia, circulatory collapse, seizures and coma)
56
Q

foods w high tyramine content (interacts w MAOI) that are NOT PERMITTED

A
  • Mature aged cheese
  • Aged fermented meats
  • Red wine
  • Smoked or picled meats
  • Fava beans or sauerkraut
  • Brewers yeast
57
Q

foods w moderate amount of tyramine that pt can have LIMITED AMOUNTS OF

A

Moderate-limited amounts
• Meat extracts
• Pasteurized light and paLe beer
• Ripe avocado

58
Q

FOODS THAT ARE permissible because of low tyramine

A
  • Canadian and mozza chese
  • Chocolate and caffeinated beverages
  • Distilled spirits
  • Figs, bananas, raisins, grapes, pineapples, oranges
  • Soy auce
  • Yogurt, sour cream
59
Q

what are the adverse effects of MAOI

A
  • Adverse effects: CV=ortho HoTN, tachy, palpitations, dysrhtymias, edema.
  • CNS=dizziness, drowsy, restless, insomnia, headache, ataxia, hallucinations, seizures, tremors, confusion,
  • GI=anorexia, abdm cramps, N, dry mouth
  • Other=blurred viion, impotence, skin rashes, resp depression
60
Q

other old names for antipsychotics

A

• Antipsychotics have been called tranquilizers and neuroleptic, therse are old terms & not used much

61
Q

2/3 of antipsychotics are _____. what kind of effects are these assoc w and why

A

• 2/3 of all antipsychotics are phenothiazines. Theyre assoc w high incidence of anticholinergic effects as theyre closely r/t antihistamines

62
Q

what are newer antipsycotics called. do they have same MOA and side effects?

A

• In the past 6-7yrs new class of antipsychotics: atypical antipsychotics (AAPs) or second generation antipsychotic. Theyre diff from 1st geeration in MOA and side effects

63
Q

are older or AAP assoc w metabolic effects? what effects are these

A

• AAPs have been assoc w metb effects like inc risk of type 2 DM, abdm or visceral wt gain, and dyslipidemia. These metb side effects are assoc w dec life expectancy of 9-12yrs than gen population

64
Q

how should the risk between AAP and metb issues be managed (assessments and what kind of counseling would be given)

A

o Before therapy assess for hx/family hx of CV disease, HTN, dyslipidemia, obesity, DM, smoking
o Check BMI and wt at baseline and 4,8,12 wks after initiating therapy and q4 months. If pt has wt gain of >2.5kg gain may switch to another antipsych. Measure waist circumference at baseline and yearly
o BP, fasting glucose, and fasting lipid profile should be checked at baseline, 12wks and annually
o Nutrition/exercise counselling if obese/overwt

65
Q

in a psychotic pt do you want a inc or dec concentration of dopamine in the pt? what effect does this have?

A

• All antipsychotics block to some degree dopamine receptors in brain–>inc dopamine conc in CNS. This blocking–>tranquilizing effect in psychotic pt.

66
Q

what are the effects of antipsychtics

A

o block dopamine receptors in CNS (this can dec anxiety)
o Block alpha receptors HoTN and other CV effects
o Many side effects are from blocking histamine receptorsanticholinergic effects
o Can be Serotonin blockers (which in combo w dopamine blocking in CTZ is why can be used as antiemetic)
o Blocking dopamine receptors in brainstemanxiolytic
o Older first gen drugs can gynecomastia in men, in women prolactin release (milk secretion, swelling of breasts

67
Q

were the older generation antipsychotics more helpful with positive or negative symptoms of schizo

did these drugs cause EPS or is that just AAP

A

o 1st gen antipscyh are less effective for negative symptoms=apathy, social withdrawal, blunted affect, poverty of speech, catatonia (these neg symptoms cause most of social and vocational disability caused by schiz)
o All 1st gen cause extrapyrimidal symptoms

68
Q

what are extrapyrimidal symptoms (names only)

A

PSEUDOPARKINSONISM

  • AKATHISIA
  • DYSKINESIA
  • DYSTONIA
  • TARDIVE DYSKINESIA
  • CHOREOATHETOSIS
69
Q

what are

  • AKATHISIA
  • DYSKINESIA
  • DYSTONIA
A

akathisia (the feeling of inner restlessness and the urge to move as well as rocking while staning or sitting, lifting the feet as if marching on the spot and crossing and uncrossing legs while seated), dyskinesia (involuntary movement of tongue, lips, face, trunk, extremities) dystonia (movement disorder commonly head, neck, tongue).

70
Q

what is tardive dyskinesia and choreoathetosis

A

o tardive dyskinesia (tardive means late appearing this involves involuntary contractions of oral and facial muscles (eg tongue thrusting) and choreoathetosis (wavelike movements of extremities)

71
Q

are EPS symptoms more related to cholinergic, endocrine, or dopamine receptors

A

dopamine

72
Q

what are the side effects of»>? i think AAP but have to check

A
  • EPS
  • neuroleptic malignant syndrome (d/t acute dopamine depletion)
  • agranulocytosis, hemolytic anemia
  • cholinergic (o Blurred vision, dry mouth, tachycardia, constipation, urinary retention)
  • histamine receptors (Sedation, drowsiness, HoTN, wt gain)
  • endocrine (prolactin, sexual dysfx, menstrual changes)
73
Q

in what wasys are adverse effects of AAP better than older antipsychotics

A

refers to the advantageous properties of these drugs like dec effects on prolctin and improvement in the negative symptoms assoc w schizophrenia, dec risk of neuroleptic malignant syndrome and dec risk of tardive dyskinesia.

74
Q

AAPs: which receptors are responsible for the antimanic activity
what about orthostatic effect

A
  • Antagonistic activity in dopamine D1antimanic activity.

* Alpha 1 adrenergic activity is assoc w orthostatic effects

75
Q

AAPs: which receptors are assoc w antidepressant activity

what about sedating and appetite stim effects

A
  • Serotonergic activity and alpha2 adrenergic activity are assoc w antidepressant acitivty
  • Histamine receptor antagonist activity is assoc w sedative and appetitie stimulating effects (can result in obesity or worsen DM). Sedative effects may diminish with time
76
Q

are AAPs a good choice for controlling agitative behav in seniors

A

NO! this carries risk of death. they arent indicated for this although they are used for it

77
Q

what VS are you most concerned abt for depressed or pschotic pt and their meds

A

BP for HoTN esp from MAOI and TCAs)

78
Q

which of the aforementioned drug classes is most likely to cause wt gain

A

AAP

79
Q

how does fat % relate to antianxiety drugs and toxicity

A

• Obese elderly more at risk of toxicity as their fat is higher % of their body and the drug stays in longer

80
Q

what conditions in r/t pts BP and lytes would predispose pt to lithium toxicity

A

• Pt is at risk of lithium toxicity if hypovolemic or hyponatremic

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