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psychotherapeutic drugs Flashcards

1
Q

psychotherapeutic drugs

A

treatment of emotional and mental health disorders
- can range from occasional depression or anxiety to constant emotional distress
- inability to carry on normal daily living

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2
Q

how to establish effectiveness of drug therapy?

A
  • subjective reporting of symptoms
  • verbal reports and observations
  • tools (hamilton depression rating scale, self administered rating scales)
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3
Q

anxiety

A

unpleasant emotional state
- perception of real or perceived dangers

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4
Q

mood (affective) disorders

A
  • mania (abnormally pronounced emotions)
  • depression (abnormally reduced emotions
  • bipolar disorder- - periodic swings
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5
Q

psychosis

A

major emotional disorder that impairs the mental function of the affected individual to the point that the individual cannot participate in everyday life
- loss of contact with reality

  • schizophrenia
  • depressive and drug-induced psychoses
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6
Q

complexity of psychotherapeutic drugs

A
  • drugs used to treat mood disorders often take weeks to take full effect
  • probably reflects adaptive responses to drugs
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7
Q

psychotherapeutics: pathophysiology

A

biochemical imbalance theory: over simplistic description underlying mental health conditions
- coordination of neuronal activity play an important role in maintaining mental health

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8
Q

mood

A

sustained emotional attitude
- patient self report

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9
Q

affect

A

way the patient’s emotional state is conveyed
- others perception of the patient’s emotional state, responsiveness

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10
Q

mood (affective) disorders

A
  • depression
  • mania
  • both (bipolar)
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11
Q

symptoms of depression

A
  • sad, anxious, empty mood
  • loss of interest or pleasures in activities once enjoyed
  • eating habit change
  • sleep habit change
  • restless
  • worthless
  • difficulty thinking
  • suicidal ideation
  • decreased energy
  • physical symptoms

diagnosed by observation

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12
Q

monoamine neurotransmitters and depression

A

catecholamines: NE
indolamines: serotonin (5-HT)
- irregularities in these NTs tied to depression

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13
Q

anti-depressant drugs

A

newer (safer) :
- selective serotonin reuptake inhibitors (SSRIs)
- mixed serotonin and NE reuptake inhibitors (SNRI)
- NE reuptake inhibitors

  • tricyclic antidepressants (TCA)
  • monoamine oxidase inhibitors (MAOIs)
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14
Q

SSRI example

A

sertraline (zoloft)

most commonly prescribed drugs for depression

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15
Q

SSRIs moa

A

selectively inhibit 5-HT reuptake
- increased serotonin concentration in synapse
- little-no effect on NE or DA reuptake

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16
Q

SSRI advantages

A

advantages over tricyclics and MAOIs: little to no effect on CV system
- safer
- overdose won’t lead to death

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17
Q

SSRI indications

A
  • major depressive disorder
  • bipolar affective disorder (with other drugs)
  • eating disorders
  • obsessive-compulsive disorders
  • panic attacks
  • myoclonus (quick, involuntary muscle jerk)
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18
Q

SSRI adverse effects

A

can take 4-6 weeks for benefit but adverse effects happen quick

CNS: headache, nervousness, insomnia fatigue

GI: nausea

other: sexual dysfunction, weight gain (which can lead to other problems)

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19
Q

what is serotonin syndrome

A

happens when interfering with serotonin neurotransmission
- exaggerated effect of 5-HT
- more likely when two drugs in combination

within 2-72 hours:
- cognitive: confusion, agitation, restlessness
- autonomic: tachycardia, hypertension, hyperthermia, sweating
- neuromuscular: clonus, hyperreflexia, tremour

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20
Q

SNRI and examples

A

serotonin and norepinephrine reuptake inhibitors
- venlafaxine (effexor)

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21
Q

why are SSRI and SNRI more likely used

A
  • no more effective than older TCAs and MAOIs
  • fewer adverse effects than TCAs (anticholinergic) and MAOIs (cheese reaction)
  • few drug-drug or food-drug interactions
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22
Q

tricyclic antidepressant drugs and example

A
  • second line
  • for clients who fail with SSRIs or other newer-generation antidepressants
  • amitriptyline
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23
Q

TCA indications

A

depression

  • childhood enuresis (uncontrolled urination: imipramine)
  • OCD: clomipramine
  • adjunctive analgesics
  • trigeminal neuralgia
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24
Q

TCA moa

A
  • blockade of NE reuptake
  • blockade of 5-HT reuptake
  • also receptor block of: muscarinic receptors, a1 adrenoceptors, h1 receptors
  • can lead to adverse effects
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25
Q

TCA adverse effects

A
  • sedation: CNS h1 receptor blockade (wears off after 1-2 weeks)
  • anticholinergic effects: blurred vision, dry mouth, constipation, urinary retention, tachycardia
  • orthostatic hypotension: a1 adrenoceptor blockade

serious:
- people who have cardiac dysrhythmias: anticholinergic effect, slows conduction on bundle of his
- seizures: excessive excitability of brain neurons

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26
Q

TCAs in overdose

A

can be lethal
- 70-80% die before reaching the hospital
- death results from seizures or cardiac dysrhythmias

no antidote for acute toxicity:
- decrease drug absorption with activated charcoal
- speed elimination by alkalinizing urine
- manage seizures and dysrhythmias with drugs
- basic life support

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27
Q

monoamine oxidase inhibitors (MAOIs)

A
  • not first line anymore
  • used in treatment when people aren’t responding to other drugs
  • potential to cause hypertensive crisis when taken with tyramine (cheese effect)
  • phenelzine
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28
Q

MAOI moa

A

inhibit MAO enzyme:
- in CNS and periphery
- enzyme metabolizes monoamine (DA, 5-HT, NE) neurotransmitters

with MAOIs there is reduced breakdown of neurotransmitters

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29
Q

MAOI adverse effects

A

orthostatic hypotension
- dizzy, light-headed
- tachycardia

CNS stimulation: insomnia, anxiety

30
Q

MAOIs and the cheese effect

A

food and drug interactions with tyramine
- lead to hypertensive crisis
- severe headache, hypertension, tachycardia
- possible cerebral hemorrhage, stroke, death

happens because tyramine in the body is broken down by MAO and without it then it will be taken up by NE neurons and so there is excess NE in the synapse (which leads to hypertensive crisis)

31
Q

food containing tyramine

A
  • aged cheeses (cheddar, blue, swiss)
  • smoked/pickled or aged meats: fish, sausage
  • yeast extracts (marmite)
  • red wines
  • italian broad beans
32
Q

switching from SSRIs to MAOIs (avoiding serotonin syndrome)

A

must be a 2-5 week wash out drug free period
(if switching from MAOI to other antidepressant do the same and maintain diet restriction for 2 weeks)

33
Q

depression drugs: client care implications

A
  • may take 2-4 weeks to see therapeutic effects
  • monitor client during time before effectiveness (suicidal ideation)
  • sedation often occurs with tricyclic therapy
34
Q

therapeutic effects: drugs for depression

A

depends on person and their symptoms of depression:
- improved sleep/nutrition
- increased self esteem
- decreased hopelessness
- increased interest in self
- increased interest in daily activities
- fewer depressive manifestations or suicidal thoughts or ideations

35
Q

anxiety disorders

A

psychological components: fear, apprehension, dread, uneasiness

physical components: tachycardia, palpitations, trembling, sweating, shortness of breath

treatment when persistent and disabling

36
Q

major anxiety disorders

A
  • generalized anxiety disorder
  • social anxiety disorder
  • obsessive-compulsive disorder
  • PTSD
  • panic disorder
  • phobia
37
Q

anxiolytic drugs

A

benzodiazepines
- barbiturates

drugs initially used in depression (SSRIs, SNRIs)

buspirone in GAD (takes weeks for effect)
- 5-HT agonist

drugs used for seizures in GAD
- valproate, gabapentin

antipsychotics in GAD and PTSD
- olanzapine, risperidone

38
Q

benzodiazepines

A

depress activity in brainstem and limbic system
- immediate relief
- used sparingly long term
- CNS depressant (sedative-hynotic)

39
Q

benzodiazepine doses

A

increasing dosage:
1) anxiolytic
2) sedation (extreme calm, no care)
3) hypnotic (promote sleep)
4) stupor (near unconsciousness or insensibility)

40
Q

benzodiazepines indications

A

anxiety

  • sedations
  • muscle relaxation
  • seizure control
  • adjuvant therapy for depression
  • alcohol withdrawal
41
Q

benzodiazepines as anxiolytic examples

A

lorazepam (ativan)

alprazolam
diazepam
clonazepam

42
Q

benzodiazepines moa

A

GABA reduces excitability of neurons
- fewer action potentials in neurons

benzodiazepines enhance effect of GABA (allow GABA to work better)
- decreased neuronal excitability
- depressed CNS activity

43
Q

advantage of benzodiazepines (compared to barbiturates)

A

barbiturates used to be top CNS depressant drugs

benzodiazepines much safer in overdose
- little respiratory depression when given PO
- respiratory depression may happen when given IV or combined with opioids, alcohol, barbiturates
- antidote

barbiturates do not have antidote
- also effects metabolism and liver enzymes

44
Q

benzodiazepines AE

A

decreased CNS activity
- drowsy, loss of coordination, dizziness, confusion, effects manual skills

potentially habit-forming and addictive
- less than barbiturates

45
Q

anxiolytic therapeutic effects

A
  • improved mental alertness, cognition and mood
  • fewer anxiety and panic attacks
  • improved sleep patterns and appetite
  • less tension and irritability, fewer feelings of fear, impending doom, and stress
  • more interest in self and others
46
Q

bipolar disorder

A
  • mania: enthusiasm, rapid thought and speech patterns, extreme self confidence, impaired judgement, risk taking
  • depression

different from psychosis (schizophrenia): disturbances in thoughts

47
Q

bipolar disorder drugs

A

mood stabilizers (prevent highs and lows)
- lithium carbonate
- drugs used for other indications

48
Q

lithium as a mood stabilizer

A

first line treatment
- acute episodes and maintenance
- may be used with other meds to stabilize mood
- poor understanding of mechanism

49
Q

about lithium

A

chemically similar to Na
- body processes it very similarly
- not metabolized

50
Q

lithium therapeutic range

A

narrow therapeutic range
- blood tests often
- range should be 0.4-1.5 mmol/L
- toxicities about 2 mmol/L, death at 2.5 mmol/L
- maintenance treatment around 0/6-0.8 mmol/L range
- take a few days to work

51
Q

lithium adverse effects (<1.5mmol/L)

A
  • fine finger tremor
  • polyuria and thirst
  • GI upset (transient)

long term:
- renal impairment
- goiter & hypothyroidism

monitor kidney function, drink water to avoid dehydration

52
Q

lithium toxicity (>1.5 mmol/L)

A

can happen from Na depletion, volume depletion

  • persistent GI upset (early warning sign)
  • coarse hand tremor
  • CNS effects: confusion, sedation, incoordination, seizures, coma
53
Q

other bipolar drugs

A
  • valproate (first line like lithium)
  • carbamazepine
    (these were used for seizures)
  • atypical antipsychotics
  • antidepressants (not used alone)
54
Q

psychosis

A

-mental disorder characterized by abnormal perceptions and emotions
- loss of contact with reality
- severe disorganization in personality, thought, emotion, behaviour

55
Q

psychotic disorders

A
  • schizophrenia
  • schizoaffective disorder
  • depressive or drug-induced psychoses
56
Q

schizophrenia symptoms

A

positive (exaggeration): delusions, paranoia, hallucination, disorganized or catatonic behaviour

negative symptoms: flat emotions, withdrawal from social contact, lack of speech, more self care, avolition

cognitive symptoms: disorganized thoughts and speech, memory and learning difficulties

57
Q

antipsychotics

A
  • aka neuroleptics
  • drugs for psychosis
  • make be used for other indications
58
Q

indications for antipsychotics

A

treatment of serious mental illnesses:
- schizophrenia
- bipolar affective disorder
- depressive and drug induced psychoses
- autism

movement disorders (tourettes)

other:
- N&V
- intractable hiccups

59
Q

objectives of schizophrenia drug therapy

A
  • suppression of acute episodes
  • reduce relapse
  • maintenance of the highest possible level of functioning
60
Q

adjunctive drugs for schizophrenia with antipsychotics

A
  • benzodiazepines
  • antidepressants
61
Q

timescale of schizophrenia treatment

A
  • initial effects in 1-2 days
  • substantial improvement ~2-4 weeks
  • full effects may not develop for several months

positive symptoms may respond better than negative symptoms or cognitive dysfunction to e drug therapy

62
Q

antipsychotics: classification of drugs

A

1st generation (typical):
- chlorpromazine (also antiemetic)
- haloperidol
2nd generation (atypical):
- clozapine

63
Q

typical antipsychotics (1st gen) moa

A

dopamine receptor antagonists (D2)

  • block receptors in CNS: limbic system and basal ganglia (emotion, cognitive function, motor function). nigrostriatal pathway (motor function)

can also bind to other receptors (chloropromazine):
- histamine
- cholinergic receptors
- a1 adrenoceptors

64
Q

typical antipsychotics adverse effects: extrapyramidal motor disturbances

A
  • DA receptor antagonisms (motor disturbances): responsible for most serious adverse effect

extrapyramidal motor disturbances :

  • early onset effects of drugs: acute dystonias (abnormal muscle tension - neck, face, tongue, eyes), pseudoparkinsonism (rigidity, tremors, bradykinesia), akathisia (motor restlessness)
  • tardive (slow or delayed) dyskinesia: oral and facial muscles, speaking and eating problems. these happen after months or years of drugs treatment and are mostly irreversible

extrapyramidal motor disturbances = extrapyramidal symptoms

65
Q

how to reduce early onset extrapyramidal motor disturbances

A
  • give an anticholinergic drug (benztropine, diphenhydramine)
66
Q

typical antipsychotics adverse effects: neuroleptic malignant syndrome

A

usually 4-14 days after therapy starts
- lead pipe rigidity
- sudden high fever (>41)
- CV problems (BP irregularities, cardiac dysrhythmias)
- may end in seizures or coma

therapy: removal of typical antipsychotic drug. antipyretics, bromocriptine

67
Q

overview of typical antipsychotics adverse effects

A

neurological: extrapyramidal motor disturbances (EPD/EPS)

other CNS: sedation, delirium

CV: orthostatic hypotension, syncope, dizziness, ECG changes (long QT)

dermatological: photosensitivity, skin rash, hyperpigmentation, pruritus

68
Q

atypical/2nd gen antipsychotics

A

clozapine (little EPD)

69
Q

atypical antipsychotics moa

A

block 5-HT receptors
- less effect on DA receptors than typical antipsychotics (less motor disturbances)

other receptor effects:
- block histamine receptors (sedation)
- block muscarinic receptors (anticholinergic: constipation)
- block a1 adrenoceptors (hypotension)

equal efficacy to typical antipsychotics (more expensive)

also used to treat anxiety and bipolar

70
Q

atypical antipsychotics adverse effects

A

varies with drug

clozapine:
- hematological: agranulocytosis (low WBC), anemia, take regular blood counts
- drooling: ophthalmic atropine eye drops SL

71
Q

all antipsychotics adverse effects

A
  • weight gain
  • disturbances in metabolism (blood glucose management, plasma lipids)
  • extent varies with drug (generally atypical drugs)
72
Q

client care implications: antipsychotics

A
  • do not take alcohol or other CNS depressants with these medications
  • monitor for EPD: long term haloperidol therapy may result in tremors or shaking of small muscle groups
  • monitor for therapeutic effects: improved mood/affect, alleviation of psychotic symptoms and episodes, decrease in hallucination, paranoia, delusions, garbled speech and inability to cope

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