Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
82 Cards in this Set
- Front
- Back
What was the first drug used to treat psychosis?
|
Chlorpromazine
|
|
What are the 4 categories of Psychotropic Drugs?
|
Antipsychotics
Anti-anxiety-sedative Antidepressants Mood-stabilizing drugs |
|
What are the two types of Sx's associated with Schizophrenia?
|
Positive
Negative |
|
Which type are more easily controlled?
|
Positive
|
|
What are Schizophrenia's positive symptoms?
|
Formal Thought Disorder (babbling)
Delusions (often paranoia) Hallucinations (usually auditory) |
|
What is the example of Negative Symptoms in Schizophrenia?
|
Blunted Affect (lack of or inappropriate emotion; withdrawal; autism)
|
|
Biological Hypothesis for Schizophrenia?
|
Over-activity of Dopamine in the limbic system and cerebral cortex
|
|
What are the 3 main categories of DA Neurons?
|
1) ultra short neurons w/in amacrine cells of retina and periglomerular cells of olfactory bulb
2. intermediate length neurons w/in tuberobasal ventral hypothalamus that innervate median eminence and intermediate lobe of pituitary 3. long projections between DA neurons in substantia nigra and ventral tegmentum and their targets in the striatum, limbic zones of cerebral CTX, and other major limbic regions |
|
What is the focus of the different types AP drugs?
|
different DA receptors
|
|
Where are D3 receptors primarily located?
|
Limbic Regions
|
|
Which type of receptor is Clozapine most specific for?
|
D4 receptors
|
|
Since clozapine is a solid AP, which dopamine receptors likely play the biggest role in Schizophrenia?
|
D3 and D4
|
|
Then why are D2 receptors still important?
|
SIDE EFFECTS
|
|
What else do second generation AP's target too?
|
5HT2 receptors, muscarinic, H1 histaminergic, alpha1-adrenergic receptors
|
|
What is the "neuroleptic syndrome?"
|
Decreased Spontaneous Movements
Decreased Complex Behavior Intact Spinal Reflexes Intact Pain Avoidance Lack of Initiative Disinterest in the Environment Reduced Emotion and Affect Drowsy but Arousable and able to answer questions No ataxia or incoordination Reduced psychotic agitation, less withdrawn, decreased agression, and gradual decline in delusions and hallucinations |
|
Two Types of First Generation Antipsychotics
|
Low Potency
High Potency |
|
Who are the Low Potency First Generation AP's?
|
Chlorpromazine (thorazine)
Thioridazine |
|
Side Effects of Low Potency, First Gen AP's?
|
Autonomic SE's (e.g. orthostatic hypotension)
Sedation |
|
Who are the High Potency, First Gen AP's?
|
Haloperidol
Fluphenazine |
|
SE's of High Potency, First Gen AP's?
|
Less Sedation
Greater Frequency of Extrapyramidal SE's |
|
Clinical Uses of AP's
General Characteristics |
Rx is highly individualized
No real difference in effectiveness among agents Positive Sx's respond better than Negative Sx's Poor Compliance |
|
Other uses of AP's?
|
N&V
Huntington's Cognitive Disorders (dementia/delirium) Parkinson's Mania (along with lithium or anticonvulsants) Depression (along w/ antidepressant) |
|
Who are some of the 2nd Generation AP's?
|
Clozapine
Risperidone (in low doses) Quetiapine Olanzapine Ziprasidone Aripiprazole |
|
Clozapine Selectivity
|
5HT-2, D4, and D3 > D2
Also H1, alpha1, and M1 B/c of D3, it likes limbic sites |
|
Selectivity for Risperidone
|
5HT2 > D2
Also H1, M1, alpha1 |
|
Clozapine and Risperidone
Side Effects? |
Limited EP SE's
Wt gain in clozapine Agranulocytosis with clozapine |
|
Quetiapine's Selectivity
|
5-HT2 > D2
Also H1, alpha1, and alpha2 |
|
Olanzapine Selectivity
|
D1, D2, and D4
5-HT2, 5-HT3 H1, alpha1, M1 |
|
Side Effects of Olanzapine and Quetiapine?
|
Somnolence
Dizziness Constipation Postural Hypotension Dry Mouth WEIGHT GAIN Cataracts with Quetiapine |
|
Which drug has the least wt gain?
|
Quetiapine
|
|
Selectivity of Ziprasidone?
|
Potent 5-HT2A antagonist
High affinity agonist for 5-HT1A, 5-HT1D, and 5-HT2C receptors Less alpha1, H1, and M1 than clozapine |
|
Why is the potency for 5-HT2A antagonism important?
|
It may limit the EP SE's
|
|
Why is Ziprasidone's high affinity agonism of 5-HT1A's important?
|
May produce better anxiolysis and/or antidepressant actions
|
|
Why is ziprasidone's low affinity for alpha1's important?
|
It may produce less cognitive impairment in the elderly
|
|
Aripiprazole's Selectivity
|
Partial Agonist for D2 and 5-HT1A
Antagonist at 5-HT2A Antagonist at alpha1-adrenergic's |
|
Aripiprazole SE's
|
Orthostatic Hypotension (possibly via alpha1's antagonism)
|
|
Other Indications for Aripiprazole?
|
Acute Manic and Mixed Episodes (that come with Bipolar)
|
|
Aripiprazole contraindicated for?
|
dementia-related psychosis
|
|
Backtracking, generally, what are the side effects of 2nd Gen Antipsychotics as compared to 1st Gen?
|
Lower incidence of EP SE's
|
|
When are 2nd Gen's often subbed in for 1st's?
|
When tardive dyskinesia appears
|
|
Special indications for 2nd Gen AP's?
|
Levodopa-induced and AD-related psychoses
|
|
What should we usually use to treat psychoses in the elderly? why?
|
2nd Gen
b/c they have fewer EP SE's which can be extra bad for the elderly |
|
What are the main categories of Extrapyramidal SE's?
|
Dystonias
Akathisia Iatrogenic Parkinsonism Neuroleptic Malignant Syndrome Perioral Tremor Tardive Dyskinesia |
|
What are dystonias?
|
Maintenance of abnormal posture for seconds (phasic) or hours or longer (tonic)
|
|
When do dystonias usually occur?
|
within 72 hours of initiating AP therapy
|
|
Clinical Course of dystonias?
|
they are usually not a health hazard and patients will gain tolerance to the SE
|
|
How many AP patients get dystonias? preferentially who?
|
10%
many of who are young males |
|
What is Akathisia?
|
subjective feeling of restlessness
|
|
What is akathisia dependent upon?
|
the DOSE of the drug
|
|
When does akathisia normally occur?
|
from the first day and then for weeks after first Rx
|
|
What is the clinical course of Akathisia?
|
Patients don't often gain tolerance to this SE
Often mistaken for psychotic agititation |
|
What type of drugs can be used for dystonias and akathisia?
|
Antiparkinson agents
|
|
What also may help with akathesia?
|
BZD's
Propranolol |
|
Iatrogenic Parkinsonism
onset? |
5-30 days after starting AP Rx
|
|
Most common PD-like Sx's in Iatrogenic Parkinsonism?
|
Bradykinesia
Rigidity Not tremors/postural issures |
|
What's one sign of Iatrogenic Parkinsonism that helps with diagnosis in children?
|
presntation
|
|
What is Neuroleptic Malignant Syndrome?
|
Very severe Parkinsonism
+Catatonia +Fluctuating Tremor Autonomic Instability Stupor Elevation of plasma Creatine Occasionally Myoglobinemia |
|
Mortality frate NMS?
|
10%
|
|
when can perioral tremor arise?
|
late in Rx (months-->years)
|
|
when does Tardive Dyskinesia arise?
|
Late in Rx
|
|
Prevalence of Tardive Dyskinesia?
|
10-25% in chronically psychotic patients w/ a small remission rate
|
|
Tardive Dyskinesia=?
|
repetitive
painless tick-like movements or face, eyelids, mouth, tongue, extremities, etc |
|
Three temporal events of Dyskinesia?
|
1. disappears in sleep
2. vary in intensity over time 3. depend on arousal or stress |
|
Rx for tardive dyskinesia?
|
Typically Clozapine
But potent AP's or reserpine can be used too (but more SE's) |
|
Other locations of AP Side Effects
|
Hypothalamus
Tuberoinfundibular System Anticholinergic receptor antagonist Antiadrenergic (alpha 1 blockers) Antihistaminergic Jaundice Agranulocytosis Medullary Emetic Center (the CTZ) |
|
What's up with the hypothalamus side effects?
|
Dopamine plays a key role in temperature regulation.
AP's can basically turn us into cold-blooded animals where our body temp varies with outside temp |
|
What is up with the Tuberoinfundibular System and AP Side Effects?
|
Dopamine serves as a prolactin inhibitor. Blocking dopamine leads to increased prolactin activity. That means impotence and gynecomastia or galatorrhea or amenorrhea
|
|
What is up with the anticholinergic SE's?
|
All AP's (except Risperidone) have weak antimuscarinic activity.
This leads to: dry mouth blurred vision pee retention tachycardia constipation impotence and sometimes: memory disturbance euporia delirium |
|
Who is the most potent anticholinergic AP?
|
Clozapine
|
|
Who is characteristic of the less potent antimuscarinics?
|
Haloperidol
|
|
What is up with the antiadrenergic SE's?
|
All the AP's have weak alpha1 blocking activity.
Most commonly causes orthostatic hypotension chlorpromazine>risperidone>haloperidol |
|
How bout them Antihistaminergic SE's?
|
Primary SE is sedation
increased appetite and wt gain may be associated with this guy too |
|
Most potent Antihistaminergic's?
|
Clozapine
Clorpromazine |
|
Less potent Antihistaminergics?
|
Haloperidol
Risperidone |
|
Jaundice with AP's?
|
Low Potency AP's can cause jaundice during 2nd to 4th week of therapy due to hypersensitivity reaction
|
|
Who causes Agranulocytosis?
|
Clozapine>>Chlorpromazine>Haloperidol
|
|
What's up with the Medullary Emetic Center?
|
its where certain dopamine blockers can block N&V
|
|
Which guys are good antiemetics?
|
Metoclopramide
Trimethobenzamide The Phenothiazines except Thioridazine |
|
What can the Phenothiazines and thioxanthenes do?
|
Potentiate CNS depressants like booze, sedatives, antihistamines, etc
|
|
What can phenothiazines ans sympatholytic agents do?
|
they can have unpredictable effects on the cardiovascular system
|
|
What can the anti-muscarinic effects of Clozapine and Thioridazine do?
|
Induce Tachycardia
Enhance peripheral and central effects of other anticholinergics (think delirium, confusion) |
|
What effect on AP's do drugs like Phenobarbital and phenytoin have?
|
They enhance their metabolism via induction of microsomal drug-metabolizing enzymes
|