Pharmacology Flashcards
4 Phases of schizophrenia
Prodromal (gradual - can go unnoticed)
Acute (crisis)
Stabilization (getting better)
Stable (declined or absent symptoms. Some residual might exist).
Negative symptoms
Supposed to be there but they’re aren’t.
Social withdrawal
Lack of motivation
Poor self care
Blunted affect
Three goals of schizophrenic drug therapy
Supression of acute episodes (pt goes back to daily life)
Prevention of remissions/acute exacerbation
Maintain highest possible level of functioning
Positive symptoms
Symptoms that ARE there that shouldn’t be
Hallucinations
Delusions
Hostility
Paranoia
Easier to suppress these with drug therapy (usually the target) as opposed to negative symptoms.
What are residual symptoms (schizophrenia)
Depression
Anxiety
Poor self-care
Remain even when schizophrenia is in remission
DSM-5 Criteria for schizophrenic diagnosis
Include: Delusions Hallucinations Disorganized speech Disorganized or catatonic behavior Negative symptoms
At least two symptoms for at least one month.
At least one should be delusions, hallucinations or disorganized speech.
What is a first line drug?
The drug that should be tried first (most preferred)
What is the first line drug for schizophrenia?
Atypical Antipsychotics (2nd generation)
How do first generation anti psychotics work?
Block receptors for dopamine in the CNS
What are the side effects for first generation antipsychotics?
Movement disorders - extrapyramidal symptoms
Second-generation antipsychotics
(AKA atypical antipsychotics)
Only partially block dopamine receptors, block serotonin even more.
We use these first.
Fewer Extrapyramidal Symptoms (movement disorders)
Black box warning
The strongest warning from the FDA.
All antipsychotics have this warning to NOT USE with older adults with dementia.
ALSO, there is a risk for increased risk of suicidal thinking in children, adolescents and young adults.
What can you assume if your patient is on both first and second generation antipsychotics?
That their symptoms weren’t easily controlled by the first line options.
QT prolongation
Longer intervals between Q and T.
Higher risk of ventricular arrythmias.
Be particularly careful if pt is on multiple drugs with this caution.
Early Extrapyramidal Symptoms
Akathesia (difficulty staying still. Subjective sense of restlessness)
Dystonia (involuntary muscle contractions - usually repetitive movement or abnormal postures)
Parkinsons-like symptoms (“drug-induced Parkinsonism)
Stooped posture.
Late EPS
Tardive diskinesia (involuntary, repetitive body movements)
Happens with long-term use (diagnosed in 20s or 30s and have been using meds for decades)
Neuroleptic malignant syndrome
Sudden elevated temperature (high fever - above 40C) Unstable blood pressure Profuse sweating Dyspnea Muscle rigidity Incontinence
Anticholinergic side effects
Dry mouth Blurred vision Photophobia Urinary hesitance Constipation Tachycardia
(Can’t see, can’t cry, can’t spit, can’t pee, can’t poop)
Adverse reactions for antipsychotics
EPS
Neuroleptic Malignant Syndrome
Anticholinergic effects
Orthostatic Hypotension
How does potency of antipsychotics relate to EPS?
If potency is high, likelihood of EPS is high.
How does potency of antipsychotics relate to anticholinergic effects, sedation and orthostatic hypotension?
Low potency means it’s more likely to hit other receptors, thereby creating these adverse effects in higher frequency.
When should Clozapine be used?
Only as a last resort. It’s the most potent and one of the best 2nd generation medications.
Must have tried and failed at least 1 first generation and 1 second generation medication.
What should we worry about with Clozapine?
Black box warnings: Severe neutropenia (high risk for infections) OH, bradycardia, syncope, cardiac arrest Seizures Myocarditis and cardiomyopathy
What does the patient have to remember with Lurasidone
Must be taken with at least 350 kcal of food for absorption.
Depot formulations (define)
Medication is available as an injectable for long-term therapy
Good for patients with compliance issues.
What does it mean if smoking is an inducer?
It “induces” the activity of the enzyme - metabolizes the drug faster, and it’s therefore less effective.
What enzyme does smoking interact with?
1A2
What enzymes are associated with drug interactions?
1A2
2D6
3A4
Major Depressive Disorder (MDD)
Criteria
Aka “unipolar disorder” or “depression”
At least five symptoms almost every day for at least two weeks
Depressed mood* (must have) Anhedonia Sleep disturbances Weight/appetite changes Decreased energy Guilt/worthlessness Psychomotor retardation/agitation Decreased concentration Suicidal ideation Interferes with ability to function* (must have)
Persistent Depressive Disorder
Aka dysthymia
Chronic depressed mood
More days than not
At least two years
(But doesn’t meet the criteria for MDD - might not have the same severity)
Monoamine hypothesis of depression
Depression caused by the functional insufficiency of monoamine transmitters (norepinephrine, serotonin, dopamine)
What are the five classes of antidepressants
Tricyclics (TCAs) SSRIs Serotonin/norepinephrine reuptake inhibitors MAO inhibitors Atypical antidepressants
TCAs/Trycyclic antidepressants
Effective, but have adverse effects Newer ones (the metabolites) have less
More often used for off-label problems (pain syndromes, migraine prevention, anxiety disorders).
Might not mean that the patient is depressed.
How do TCAs work?
They prevent the pump that pulls the NTs out of the synapse for recycling. Therefore, the NT stays in the synapse so it’s available for the post-synaptic neuron’s receptors.
