Pharm quiz 7
Terms in this set (71)
A severe mental disturbance that involves a profound misinterpretation of perceptions or loss of contact with reality
Leads to inappropriate ability to interact with others or with the environment
Psychotic features/symptoms are present in various disorders
Hallucinations-anything that really isn't there. Seeing things, hearing things, smelling things.
Delusions-any thing that you have a firm belief in. Persecutory- being spied on, mind control. The belief that you have superpowers.
Disorganized Speech-inability to utlilize conventional speech.
Disorganized or Catatonic Behavior-decreased expression of the range of emotions we typically have.
Epidemiology of Schizophrenia
Approximately 1% of the US population
Onset: Late adolescence to early adulthood
- "First Break"
Males = Females
No ethnic differences
--We cant find any links that put people at increased risk for schizophrenia.
Course of illness-shizophrenia
Ideal case: Initial psychotic episode is quickly detected and treated and further illness is prevented by prophylactic treatment
-Schizophrenia never goes away, there's no cure its just managed. The goal is for them to reenter society.
-Other disorders you can cure.
CHRONIC RELAPSING CASE
-Chronic relapsing condition with each psychotic exposure decreasing global function
--many homeless people experience this chronic relapse.
Symptoms of Schizophrenia-positive
Something added to a patient's normal presentation
- Persecutory, Grandiose, Thought Broadcasting, Bizarre
Grossly disorganized or catatonic behavior
Symptoms of Schizophrenia-Negative
Something taken away from a patient's normal presentation
Impaired outward display of emotions
Decreased speech fluency
Lack of motivation or "drive"
Loss of interest or pleasure
Lacking the capacity for social interaction
Symptoms of Schizophrenia-cognitive
Decreased cognitive functioning
Inability to plan
Difficulty executing tasks
Impaired decision making
**-Not everyone in the prodromal phase will be psychotic
Lose touch with reality
Flat or inappropriate affect
Difficulty with self-care
Diagnosis for psychosis
Symptoms associated with significant social/occupational dysfunction
Impairment in one or more major areas of functioning
Treatment Goals for psychosis
Prevent harm to self and others
Prevent side effects
Integrate back into community and improve social functioning
Improve overall quality of life
Pathophysiology of Schizophrenia
Imbalance in dopamine
- Increased dopamine in certain areas of the brain leads to symptoms of psychosis
Other neurotransmitters likely play a role as well
Dopamine and Serotonin blockade
Dopamine (D2) Receptor Blockade
Improved positive symptoms of psychosis
Worsening of negative symptoms and cognition
Extrapyramidal movement disorders (EPS) and tardive dyskinesia (TD)
*Typical 1st generation antipsychotic.
Dopamine and Serotonin Receptor Blockade
Reduced EPS and risk of TD
Possible improvement in negative symptoms and cognition
*-2nd generation atypical antipsychotics.
-Downside they are going to be on these drugs for the rest of their life, so sedation and weight gain worries us.
Treatment of Schizophrenia
First Generation (Typical) Antipsychotics
Second Generation (Atypical) Antipsychotics
Typical Antipsychotics (FGA)
**-Just know there are low, mid and high potency.
-High potency- have to know haloperidol and Fluphenazine. Only one we need to know the actual drug names for.
Extrapyramidal Symptoms (EPS)
Sustained muscle contractions
Twisting, repetitive movements or abnormal postures
Can look like a tremor or seizure
Painful and scary
Typically involve tongue, jaws, eyes, neck, limbs or
Usually occur 24-96 hours after a dose
Diphenhydramine, benztropine (Cogentin®), benzodiazepines
Akinesia, bradykinesia, slowed speech
Pill rolling tremor
Usually reversible within weeks of discontinuation
Persists or worsens in 10-40%
*-Drug induced Parkinson's disease.
-Akinesia- frozen, unable to move
-have trouble starting and stopping movements.
Motor restlessness or inability to sit still
Occurs in 20-30% of patients on typical antipsychotics
EPS Treatment Strategies
Decrease antipsychotic dose
Switch from high- to low-potency typical antipsychotic
Switch from typical to atypical antipsychotic
Use adjunctive medication
*-High potency tends to cause EPS.
-Can switch from a 1st to a 2nd generation.
Tardive Dyskinesia (TD)
Involuntary abnormal movements which generally occur after long-term antipsychotic therapy
Face, tongue, lips, neck, trunk common
Early signs may be reversible
If not detected early, may be irreversible
Even with drug discontinuation
Tardive Dyskinesia (TD) Treatment
Symptoms may interfere with ability to speak, chew, swallow
Prevention: most important intervention
AIMS scale every 3-6 months
Switch to atypical antipsychotic
-Valbenazine (Ingrezza) and Deutetrabenazine( Austedi)
Decreases presynaptic dopamine
Modest symptom improvement
Sedation and dry mouth > 5%.
Atypical Antipsychotic (SGA)
*-You avoid the EPS and tardive dyskinesia with these.
Decreases negative symptoms
Movement disorders (EPS)
Can cause tardive dyskinesia but much less of it.
What is "Atypical"?
Reduced risk for EPS
Reduced risk for TD
Potentially better at improving negative symptoms
Potentially better at improving cognition
Greater risk of metabolic ADRs
-2nd generation atypical anti psychotic.
Unique effectiveness for treatment for:
Persistent psychotic symptoms
1-2% develop agranulocystosis
Blood monitoring required weekly for first 6 months, every 2 weeks for 6 months, then monthly thereafter
Must be part of national registry
Reserved for treatment resistant patients
*Works better at treating psychosis than any other antipsychotic!
-It has dangerous side effects that's why we don't give it to everyone. Can cause agranulocytosis a life threatening blood disorder.
Atypical Black Box Warning
Increased rate of death in elderly patients with dementia receiving atypical antipsychotics for the treatment of behavioral disorders.
Chemical restraints (Meds) were used with patients with dementia.
-Behavioral symptoms- throwing things, yelling.
Antipsychotics Dosage Forms
Tablets or capsules
Long acting-depot injections of antipsychotic that lasts for weeks and months.
Time course of therapy for schizophrenia
1-7 days= decreased agitation/hostility, decreased aggression /anxiety. normalization of sleep and appetite.
1-2 weeks= improvement in socialization and mood
3-6 weeks or greater= improvement in thought disorder.
Residual sx= fixed delusions and hallucinations. is as good as they'll ever get.
Summary for shizophrenia
Schizophrenia is a complex disease with significant implications for patients and their families
Antipsychotics are the DOC
Typical antipsychotics decrease positive symptoms, but can cause movement disorders
Atypical antipsychotics have less risk for EPS, but increased risk for serious metabolic effects
Epidemiology of depression
17% of US population reports a major depressive episode in their lifetime
Depression occurs in women > men, about 2:1
Average age of onset: mid-20s
>50% of patients have first episode by age 40 years
Duration: 6 months-2 years if left untreated
-Episodes continue in up to 80% of untreated patients.
No correlations between any particular ethnicity, socio-economic class or lifestyle and depression
Depression is Serious
Most common diagnosis associated with psychiatric hospitalization
Lifetime Suicide Risk:
2% MDD treated as outpatient
4% MDD treated as inpatient
8% MDD with suicidal ideation/attempt treated as IP
Depression associated with increased mortality rates in individuals 50+ years old
Depression correlated to worse outcomes in chronic medical conditions such as diabetes mellitus
-Unipolar Depression= leading cause of disability
Economic Burden of depression
Estimated to be $30-60 billion
Economic burden can result from
Increased healthcare system utilization
What does depression look like
Depressed mood and/or anhedonia are hallmark symptoms
Some patients present as sad, guilt-ridden, and hopeless
Other patients will appear nervous, irritable, or agitated
Some will complain of somatic problems
Psychosis can accompany depression
*Anhedonia-inability to get pleasure from things that used to bring you pleasure.
*Somatic problems-stomach pain, headaches.
SIG E CAPS (depression)
-types of questions to ask when screening for depression
Causes of Depression
Depression associated with medical conditions
Stroke, heart attack
Depression associated with drugs
Substance abuse - MDMA, cocaine
Pathophysiology of Depression
Etiology not fully understood
Most likely related to a combination of 3 factors:
46% concordance rate among monozygotic twins vs. 20% rate among dizygotic twins
Genetic difference in receptors and transporters expression and function
Adverse life experiences
Biogenic amines (NE, 5HT, DA)-helps explain why we use the drugs we do.
Non-monoamine compounds (CRF)
Biogenic Amine Theory
A chemical substance released from a neuron that transmits a nerve impulse across a synapse
3 primary neurotransmitters thought to be involved in depression (the monoamines)
Biogenic Amine Theory-Monoamine reuptake transporters
Monoamine reuptake transporters:
Responsible for removing NTs from the synapse
Inhibition of these transporters → increases levels of NT in the synapse
Specific transporters for 5HT, NE, DA
Metabolizes monoamines → decreases NT levels
Inhibition of this enzyme → increases NT levels
**Monoamine reuptake-allows you to reuse the neurotransmitter, by taking it back from the synapse.
Monoamine oxidase-destroys the neurotransmitters out in the synapse.
-We are trying to increase the level of neurotransmitters (serotonin, dopamine, norepi) in the synapse
Biochemical Theories of Depression
Biogenic Amine Hypothesis
Low monoamine NT levels result in depression
5-HT alteration disposes individual to mood disorder
NE alterations determine type of mood d/o (depression or mania)
Receptor Dysregulation Hypothesis
Inefficiency of monoamine signal transmission results in depression
Antidepressants "kick start" the system
Hypothalamus-Pituitary-Adrenal (HPA) axis
Glucocorticoid receptor dysregulation
Attempts to account for genetic, biological and environmental factors
Cognitive behavioral therapy
Electroconvulsive therapy (ECT)
**Pharmacotherapy and psychotherapy are equally effective, and they work better when they are used together.
-A lot easier to take a pill than go to therapy sessions.
Potential Drug Targets-for depression
**Serotonin, norepi, and dopamine transporters- needs to be inhibited to increase levels of neurotransmitter in the synapse.
Selective Serotonin Reuptake Inhibitors (SSRIs)
Serotonin Norepinephrine Reuptake Inhibitors (SNRIs)
Tricyclic Antidepressants (TCAs)
Monoamine Oxidase Inhibitors (MAOIs)-Stops the enzyme that's destroying monoamines. therefore increasing level of nt in the synapase.
What are the Selective Serotonin Reuptake Inhibitors (SSRIs)
Paroxetine controlled-release (Paxil CR®)
Selective Serotonin Reuptake Inhibitors (SSRIs)-MOA
-Inhibit serotonin transporter
Most frequently used antidepressants
Generally dosed once a day
Typically given in the morning, but can be taken any time of day
No data conclusively demonstrates that any one SSRI is more effective than any other on a population basis
*Increasing the amt of serotonin in the synapse-SSRI.
Side effects related to increased serotonergic stimulation as well as nonselective receptor profiles of some agents
Serotonergic side effects
Activation or sedation-Activation is seen early in therapy, and sedation will be seen late.
Sexual side effects
Serotonin Norepinephrine Reuptake Inhibitors (SNRIs)
Inhibit neuronal reuptake of 5HT (serotonin) and NE
5-HT reuptake inhibition across dosage range
NE reuptake inhibition at doses >200mg/day
Dose related increases in blood pressure
XR - dosed once daily
IR - dosed two to three times daily
Nausea, GI complaints, insomnia, sexual side effects
Increased blood pressure, sweating, agitation
*Serotonin-At low doses it blocks reuptake a little bit, at high doses it blocks even more.
Norepi-needs to be at a dose of greater than 200 mg to block reuptake
Active metabolite of venlafaxine
Similar to venlafaxine
GI, nausea, blood pressure, sexual dysfx, etc.
*Venlafaxine= pro drug --> Desvenlafaxine= active drug
Balanced NE and 5HT reuptake inhibition across dosage range
FDA approved for neuropathic pain associated with DM
Similar to venlafaxine
Significant rates of nausea (dose and schedule)
*-At low doses it blocks same amount of serotonin and Norepi.
MOA: Inhibition of DA and NE reuptake
Also FDA approved for smoking cessation (Zyban®)
Lowers seizure threshold
Lower incidence of sexual side effects
-most commonly used in those who are on SSRI's and SNRI's that are having a lot of sexual side effects, they switch to bupropion for the less sexual side effects.
-do not give this to people who already have seizure disorders.
MOA: Enhances NE and 5HT activity
Sedating antihistaminic effect
Taken at bedtime
Useful for when insomnia is part of presentation
More common at lower doses
» Increased NE activity at higher doses
Significant weight gain
Low rate of sexual dysfunction
-Doesn't inhibit, but increases activity of serotonin and norepi.
-at lower doses we have very little activation of norepi, but increased sedating antihistaminic effect.
-at higher doses we are getting more norepi effect, decreasing the sedating effect.
-MOST SEDATING EFFECT AT THE LOWER DOSES OF THE DRUG.
-the significant weight gain is the reason we don't want to give this drug long term.
MOA: enhances 5HT activity
Very sedating - used to treat insomnia
Doses <300 mg used for insomnia
Antidepressant activity at higher doses
Sedation, nausea, GI upset, priapism
**-Used a lot more for insomnia, not so much for depression because you would just make them sleep more than they already are.
-75 mg dose for insomnia.
-300 mg or greater being used for depression
What are the Tricyclic Antidepressants
*Just as effective as SSRI's and SNRI's.
MOA: inhibition of NE and 5HT reuptake
Potency and selectivity vary among various agents
Lethal in overdose (as little as 3x daily dose)
Effect many other receptor systems, making for an unfavorable side effect profile
Anticholinergic - dry mouth, dry eyes, constipation, blurred vision
Alpha-adrenergic - orthostasis
Weight gain, glucose dysregulation, effects on cardiac conduction
**-Basically an SNRI, except they have other chemical properties that are dangerous.
-First things these drugs do are make you feel better, give you energy. This is what we worry about because now they can actually accomplish suicide.
-Don't use these drugs as much anymore!
-usually die from cardiac conduction problems or arrhythmias.
-at low doses for neuropathic pain, and also used for those with insomnia.
Monoamine Oxidase Inhibitors (MAOIs)
Reserved for treatment of •
Limit foods high in tyramine
Aged cheese, cured meats, sauerkraut, beer...
Only going to be used if nothing else has worked. The side effects limit their usability.
-Just know that high tyramine can cause hypertensive crisis.
Significant reduction in, but not complete resolution of depressive symptoms
-symptoms are getting better
Complete resolution of depressive symptoms
(get all the way back to where they have no symptoms anymore)
Sustained remission of at least 6 months
Return of depressive symptoms within 6 months of achieving remission
(anytime someone gets worse on drug therapy before recovery.)
Successive episode of MDD after recovery from initial episode of MDD
(is relapse after they have reached recovery. It's a whole new episode potentially starting).
Phases of Treatment for depression
Initial 6-12 weeks of treatment
Treatment bridging remission to recovery
Typically 6-9 months
Continuation of antidepressant at full therapeutic dosage
Antidepressant may be discontinued at the conclusion of the continuation phase
**-Once they have reached remission they are still in an episode and are going to be in the continuation phase.
-Until you reach recovery (remission for 6 months) then you are done with the episode, and can stop therapy.
-Maintenance phase is once you have reached recovery but want to still keep getting the drug therapy
Maintenance Phase of depression
Continuation of an antidepressant at full therapeutic dosage for extended periods of time, perhaps indefinitely
Not necessary for all patients
May be beneficial in patients at high risk of relapse or recurrence
-Patients with history of recurrence and/or risk factors for recurrence
**-Two types of patients that are going to be on maintenance therapy: their episode is so severe that we fear they are going to die if they have another one, another type is if they keep having more episodes, the more episodes they have the more likely they are going to have another one.
Risk of reccurence -depression
After 1 depressive episode= 60%
After 2 depressive episodes=70%
After 3 depressive episodes=90%
Choosing an Antidepressant
On a population basis, all antidepressants are equally effective
Individually, response to specific agents is generally unpredictable
Past history of response to a particular agent may predict future response
History of family member with response to a particular agent may predict response
*-We tend to use the drug that worked before, use it again.
Choice of antidepressant based on:
Past history of response
Side effect profile
Comorbid psychiatric or medical conditions
Potential for drug interactions
Remission is the goal of treatment for MDD
Treating to remission:
Results in improved overall functioning
Decreases the risk of experiencing another episode of depression
Increases amount of time until another episode in those who experience recurrence
Managing ADRs - Insomnia (antidepressants)
Caffeine??--Analyze caffeine consumption
Morning dosing-Take in the morning because if drug is causing insomnia they are going to be actively awake during the day.
Reduce dose-maintaining effect of antidepressant, but lowering the insomnia
Adjunct with a sleep medication--Adjunct is one drug used to treat the side effects of another drug. May use it for a few weeks only.
Managing ADRs - Anxiety (antidepressants)
Anxiety may be transiently increased with initiation of antidepressant treatment
Minimize or avoid caffeine intake
Reduce dose and titrate gradually
Beta-blocker or benzodiazepine
Benzo's are frequently used in the first few weeks to reduce the anxiety side effect.
Beta blockers- block the physical manifestations of anxiety, but not blocking the anxiety itself. They are safer to use than benzos and are not addictive.
Managing ADRs - Nausea (antidepressants)
Start low, titrate dosage up
Take with food
Serotonin is linked to nausea.
Take with food-helps to slow the absorption of the drug. (SSRI's and SSNRI's).
-You can use adjunct med to help treat the nausea.
Managing ADRs - Sexual (Antidepressants)
Wait to see if the patient builds up a tolerance to the side effect
Decrease antidepressant dose
Switch to another antidepressant
Add on a medication
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