psychotherapeutic drugs Flashcards
psychotherapeutic drugs
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
how to establish effectiveness of drug therapy?
- subjective reporting of symptoms
- verbal reports and observations
- tools (hamilton depression rating scale, self administered rating scales)
anxiety
unpleasant emotional state
- perception of real or perceived dangers
mood (affective) disorders
- mania (abnormally pronounced emotions)
- depression (abnormally reduced emotions
- bipolar disorder- - periodic swings
psychosis
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
complexity of psychotherapeutic drugs
- drugs used to treat mood disorders often take weeks to take full effect
- probably reflects adaptive responses to drugs
psychotherapeutics: pathophysiology
biochemical imbalance theory: over simplistic description underlying mental health conditions
- coordination of neuronal activity play an important role in maintaining mental health
mood
sustained emotional attitude
- patient self report
affect
way the patient’s emotional state is conveyed
- others perception of the patient’s emotional state, responsiveness
mood (affective) disorders
- depression
- mania
- both (bipolar)
symptoms of depression
- 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
monoamine neurotransmitters and depression
catecholamines: NE
indolamines: serotonin (5-HT)
- irregularities in these NTs tied to depression
anti-depressant drugs
newer (safer) :
- selective serotonin reuptake inhibitors (SSRIs)
- mixed serotonin and NE reuptake inhibitors (SNRI)
- NE reuptake inhibitors
- tricyclic antidepressants (TCA)
- monoamine oxidase inhibitors (MAOIs)
SSRI example
sertraline (zoloft)
most commonly prescribed drugs for depression
SSRIs moa
selectively inhibit 5-HT reuptake
- increased serotonin concentration in synapse
- little-no effect on NE or DA reuptake
SSRI advantages
advantages over tricyclics and MAOIs: little to no effect on CV system
- safer
- overdose won’t lead to death
SSRI indications
- major depressive disorder
- bipolar affective disorder (with other drugs)
- eating disorders
- obsessive-compulsive disorders
- panic attacks
- myoclonus (quick, involuntary muscle jerk)
SSRI adverse effects
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)
what is serotonin syndrome
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
SNRI and examples
serotonin and norepinephrine reuptake inhibitors
- venlafaxine (effexor)
why are SSRI and SNRI more likely used
- 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
tricyclic antidepressant drugs and example
- second line
- for clients who fail with SSRIs or other newer-generation antidepressants
- amitriptyline
TCA indications
depression
- childhood enuresis (uncontrolled urination: imipramine)
- OCD: clomipramine
- adjunctive analgesics
- trigeminal neuralgia
TCA moa
- blockade of NE reuptake
- blockade of 5-HT reuptake
- also receptor block of: muscarinic receptors, a1 adrenoceptors, h1 receptors
- can lead to adverse effects
TCA adverse effects
- 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
TCAs in overdose
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
monoamine oxidase inhibitors (MAOIs)
- 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
MAOI moa
inhibit MAO enzyme:
- in CNS and periphery
- enzyme metabolizes monoamine (DA, 5-HT, NE) neurotransmitters
with MAOIs there is reduced breakdown of neurotransmitters
MAOI adverse effects
orthostatic hypotension
- dizzy, light-headed
- tachycardia
CNS stimulation: insomnia, anxiety
MAOIs and the cheese effect
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)
food containing tyramine
- aged cheeses (cheddar, blue, swiss)
- smoked/pickled or aged meats: fish, sausage
- yeast extracts (marmite)
- red wines
- italian broad beans
switching from SSRIs to MAOIs (avoiding serotonin syndrome)
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)
depression drugs: client care implications
- may take 2-4 weeks to see therapeutic effects
- monitor client during time before effectiveness (suicidal ideation)
- sedation often occurs with tricyclic therapy
therapeutic effects: drugs for depression
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
anxiety disorders
psychological components: fear, apprehension, dread, uneasiness
physical components: tachycardia, palpitations, trembling, sweating, shortness of breath
treatment when persistent and disabling
major anxiety disorders
- generalized anxiety disorder
- social anxiety disorder
- obsessive-compulsive disorder
- PTSD
- panic disorder
- phobia
anxiolytic drugs
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
benzodiazepines
depress activity in brainstem and limbic system
- immediate relief
- used sparingly long term
- CNS depressant (sedative-hynotic)
benzodiazepine doses
increasing dosage:
1) anxiolytic
2) sedation (extreme calm, no care)
3) hypnotic (promote sleep)
4) stupor (near unconsciousness or insensibility)
benzodiazepines indications
anxiety
- sedations
- muscle relaxation
- seizure control
- adjuvant therapy for depression
- alcohol withdrawal
benzodiazepines as anxiolytic examples
lorazepam (ativan)
alprazolam
diazepam
clonazepam
benzodiazepines moa
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
advantage of benzodiazepines (compared to barbiturates)
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
benzodiazepines AE
decreased CNS activity
- drowsy, loss of coordination, dizziness, confusion, effects manual skills
potentially habit-forming and addictive
- less than barbiturates
anxiolytic therapeutic effects
- 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
bipolar disorder
- mania: enthusiasm, rapid thought and speech patterns, extreme self confidence, impaired judgement, risk taking
- depression
different from psychosis (schizophrenia): disturbances in thoughts
bipolar disorder drugs
mood stabilizers (prevent highs and lows)
- lithium carbonate
- drugs used for other indications
lithium as a mood stabilizer
first line treatment
- acute episodes and maintenance
- may be used with other meds to stabilize mood
- poor understanding of mechanism
about lithium
chemically similar to Na
- body processes it very similarly
- not metabolized
lithium therapeutic range
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
lithium adverse effects (<1.5mmol/L)
- fine finger tremor
- polyuria and thirst
- GI upset (transient)
long term:
- renal impairment
- goiter & hypothyroidism
monitor kidney function, drink water to avoid dehydration
lithium toxicity (>1.5 mmol/L)
can happen from Na depletion, volume depletion
- persistent GI upset (early warning sign)
- coarse hand tremor
- CNS effects: confusion, sedation, incoordination, seizures, coma
other bipolar drugs
- valproate (first line like lithium)
- carbamazepine
(these were used for seizures) - atypical antipsychotics
- antidepressants (not used alone)
psychosis
-mental disorder characterized by abnormal perceptions and emotions
- loss of contact with reality
- severe disorganization in personality, thought, emotion, behaviour
psychotic disorders
- schizophrenia
- schizoaffective disorder
- depressive or drug-induced psychoses
schizophrenia symptoms
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
antipsychotics
- aka neuroleptics
- drugs for psychosis
- make be used for other indications
indications for antipsychotics
treatment of serious mental illnesses:
- schizophrenia
- bipolar affective disorder
- depressive and drug induced psychoses
- autism
movement disorders (tourettes)
other:
- N&V
- intractable hiccups
objectives of schizophrenia drug therapy
- suppression of acute episodes
- reduce relapse
- maintenance of the highest possible level of functioning
adjunctive drugs for schizophrenia with antipsychotics
- benzodiazepines
- antidepressants
timescale of schizophrenia treatment
- 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
antipsychotics: classification of drugs
1st generation (typical):
- chlorpromazine (also antiemetic)
- haloperidol
2nd generation (atypical):
- clozapine
typical antipsychotics (1st gen) moa
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
typical antipsychotics adverse effects: extrapyramidal motor disturbances
- 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
how to reduce early onset extrapyramidal motor disturbances
- give an anticholinergic drug (benztropine, diphenhydramine)
typical antipsychotics adverse effects: neuroleptic malignant syndrome
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
overview of typical antipsychotics adverse effects
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
atypical/2nd gen antipsychotics
clozapine (little EPD)
atypical antipsychotics moa
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
atypical antipsychotics adverse effects
varies with drug
clozapine:
- hematological: agranulocytosis (low WBC), anemia, take regular blood counts
- drooling: ophthalmic atropine eye drops SL
all antipsychotics adverse effects
- weight gain
- disturbances in metabolism (blood glucose management, plasma lipids)
- extent varies with drug (generally atypical drugs)
client care implications: antipsychotics
- 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
