Chapter 18 Flashcards
(121 cards)
1
Q
What is the most common treatment for opiate addiction?
A
Methadone
2
Q
Adding ___________________ to buprenorphine ensures the combination drug has no potential for abuse.
A
naloxone
3
Q
A study of male twin pairs showed abuse of every category of drugs except _________________ was influenced by genetic factors.
A
psychedelics
4
Q
A variant of the gene for alcohol dehydrogenase can cause an aversive reaction to alcohol. Where is this gene most prevalent?
A
Eastern Asia
5
Q
Cocaine and amphetamine are different in that __________________.
A
cocaine blocks dopamine reuptake, while amphetamine releases dopamine
6
Q
What drug can produce symptoms that closely resemble schizophrenia?
A
Amphetamines
7
Q
Which drug accounts for the most deaths?
A
Nicotine
8
Q
The compulsion to smoke is so strong that ________________ percent of people continue to smoke after having undergone a laryngectomy.
A
40
9
Q
Withdrawal from what drug can be fatal?
A
Alcohol
10
Q
The presence of _______________ in marijuana has a protective effect against dependence on cannabis.
A
cannabidiol
11
Q
What is an alarming effect of chronic abuse of cocaine?
A
Psychotic behavior
12
Q
Withdrawal symptoms produced by a drug are __________________________.
A
usually opposite to the effects of the drug itself
13
Q
__________ refers to a decreased sensitivity to a drug after repeated use.
A
Tolerance
14
Q
The common aspect of all natural reinforcers relates to ____________________.
A
the release of dopamine within the nucleus accumbens
15
Q
Which of the following refers to a compulsion to take a drug?
A
Craving
16
Q
Which of the following statements is NOT true of the opiates?
A
The most commonly abused opiate is morphine.
17
Q
Cravings for crack cocaine are a learned behavior. Dr. Rosenthal’s therapy puts a recovering addict in a virtual crack-related situation, which induces cravings. When the cravings are repeatedly not followed by the drug, the recovering addict’s learned response of craving will eventually be ________.
A
extinguished
18
Q
A diminished craving sensation is paired with a tone, so the addict learns to associate one with the other. When he later enters a real life crack-related situation, he can play the tone on his cell phone and it will serve as a(n) ___________ to evoke the reduced sensation of craving.
A
conditioned stimulus
19
Q
Research on treating addiction with virtual reality demonstrates that _______.
A
addiction can be controlled through learning new associations
20
Q
Heroin is in the class of drugs called _____.
A
opiates
21
Q
According to Dr. Obert, it is harder to kick the heroin habit because of _____.
A
the subculture that goes along with it
22
Q
According to Dr. Obert, heroin use has been ____.
A
glamorized
23
Q
The rise in heroin use came after the _____ epidemic.
A
cocaine
24
Q
Dr. Obert makes the observation that drug use in society usually occurs ____.
A
in cycles
25
What trait makes a person high risk for alcoholism?
being able to drink a lot without effect
26
Alcohol has the most devastating effect on fetal development during the brain growth spurt period, which is during the _______ of pregnancy.
last trimester
27
What enhances the craving for nicotine?
Endocannabinoids
28
Mary enrolled in a smoking cessation program. What are her chances of abstaining from smoking for one year?
20%
29
In a laboratory study, three groups of monkeys were given constant access to a lever that administered one of the following drugs: cocaine, heroin, or alcohol. Which group was most likely to self-administer a drug until it caused death?
The monkeys with access to cocaine
30
Administering an opiate for a lengthy period of time and then blocking its effects by injecting naloxone causes ___________________.
withdrawal symptoms
31
About _____ percent of people who try cocaine, become addicted to it.
15
32
Although the neural mechanism involved in reinforcement is not completely understood, it is apparent that ____ is a necessary condition for positive reinforcement to take place.
dopamine release
33
Abnormalities in the _______ cortex may play a key role in schizophrenia and drug abuse.
prefrontal
34
Why was Dave given naltrexone in the emergency room?
He had overdosed on heroin.
35
The site of action of the endogenous cannabinoids in the brain is the ______ receptor.
CB1
36
Which of the following is a drawback of methadone treatment?
It has a potential for abuse.
37
Genes that produce _____________ affect the addictive potential of cocaine.
sirtuins
38
Why do addicts sometimes have drug cravings for months, or even years, after abstinence from the drug?
Taking the drug for an extended period of time can produce long-lasting changes in the brain.
39
Hallucinations, delusions of persecution, mood disturbances, and repetitive behaviors are all possible effects of abuse of ________.
cocaine
40
Even though he had to have his jaw removed due to cancer from his addiction, Sigmund Freud continued to ______ after the procedure, which was the very thing that caused the cancer.
smoke
41
What were the results of a randomized, double-blind, placebo control study of bupropion and varenicline for treatment of smoking?
After 52 weeks, the smokers treated with varenicline were most likely to still be abstinent.
42
The experience of stress has been found to _____________________.
increase the amount of cocaine self-administered by rats
43
What is an effect produced by cocaine?
euphoria
44
The process of addiction begins in the ______, which then produces changes in other brain areas that receive input from these neurons
mesolimbic dopaminergic system
45
The capacity of opiates to produce analgesia is due to an action on ______ receptors within the ______.
mu; periaqueductal gray matter
46
What age is most vulnerable to drug addiction?
Adolescence
47
How much of the world's adult population smokes?
Approximately 33%
48
Why do drug users prefer heroin over morphine?
It has a more rapid effect.
49
Which of the following statements is true of cocaine and amphetamines?
They both act as strong dopamine agonists.
50
Chao recently moved from China to the United States to attend college. When he turned 21, he started going out to clubs with his friends. He enjoyed going to the clubs, but found that he had an unpleasant physical reaction to alcohol that was different from his western friends and he did not enjoy drinking. What most likely caused his adverse reaction?
A hereditary genetic variation
51
Deep brain stimulation was demonstrated by Mantione and associates (2010) to be effective as a method to stop _______.
smoking cigarettes
52
Opium is derived from ______ produced by ______.
a sticky resin; opium poppy
53
Hypothermia and sedation are effects of what drug?
Heroin
54
Why is freebase cocaine (crack) probably the most positive reinforcer of all drugs?
Its effects are potent and rapid.
55
Buprenorphine _________________ the effects of opiates and produces a __________ opiate effect.
blocks, weak
56
Why are drugs that block dopamine receptors not useful in treatment of cocaine abuse?
They produce unpleasant feelings.
57
(18.1-1) Positive symptoms of schizophrenia
Symptoms of schizophrenia that seem to represent an excessive typical function. Symptoms occur for 1 month, with at least one positive symptom.
Delusions; hallucinations; inappropriate affect; disorganized speech or thought; or odd behaviours.
58
Negative symptoms of schizophrenia
Symptoms of schizophrenia that seem to represent a reduction or loss of typical function.
Affective flattening, abolition (absence/reduction in motivation), catatonia.
Frequent reoccurrence of any two of the symptoms from one month is sufficient for a diagnosis of schizophrenia. One of the symptoms must be a positive symptom.
59
(18.1) Schizophrenia
A severe psychiatric disorder occurring in 1 % of the population. Typically, beginning in adolescence or early adulthood. There is an overlap with several different brain diseases. DSM 5 uses the label schizophrenia spectrum disorders.
60
(18.1-2) Experiential factors implicated in the development of schizophrenia
Not caused by a single gene; several genes are more strongly implicated acting in combination .
61
(18.1-3) Drugs developed in the treatment of schizophrenia
Chlorpromazine, reserpine -The first of many antagonist to be used in the treatment of schizophrenia.
The antipsychotic effect are manifested only after patient has been medicated for 2 to 3 weeks. Both drugs antagonize transmission of dopamine synapse but in different ways: R-by depleting the brain of dopamine, C- by binding to dopamine receptors
Haloperidol: A butyrophenone used as an antipsychotic. As one of the most potent antipsychotic drugs of its day it had relatively low affinity for dopamine receptors.
62
(18.1-3) Schizophrenia and Parkinson's Disease
The onset of psychotic affect is usually associated with the motor effects similar to Parkinson's disease. Similarities suggest the drugs are acting on the same mechanism as Parkinson's disease.
63
(18.1-1) Reserpine
Active ingredient is the snakeroot plant. However, it produces a dangerous decline a blood pressure of the doses needed for successful treatment
64
(18.1-2) The Neurodevelopmental theory of schizophrenia
1. Schizophrenia and autism share many of the same causal factors, genetic risk factors, and environmental triggers. (2) The study of 2/20 century families: The Dutch famine of 1944 to 1945, and the Chinese famine of 1959 to 1961. Foetuses who's pregnant mother suffered in those famines were more likely to develop schizophrenia as adults.
65
(18.1-2) genetic susceptibility for the onset of schizophrenia
Early experiences are thought to alter the normal cause of neurodevelopment leading to schizophrenia. Individuals who have genetic susceptibility, birth complications, maternal stress, prenatal infections, social economic factors, urban birth, or residing in an urban setting, and childhood adversity.
66
(18.1-4) D2 receptors and the degree of typical antipsychotics
Early experiences are thought to alter the normal cause of neurodevelopment leading to schizophrenia. Individuals who have genetic susceptibility, birth complications, maternal stress, prenatal infections, social economic factors, urban birth, or residing in an urban setting, and childhood adversity.
67
(18.1-4) D2 receptors and the degree of typical antipsychotics
```
Phenothiazine: A class of antipsychotic drugs that bind affectively to both D1 and D2 receptors (chlorpromazine).
Butyrphenomes: Antipsychotic drugs that form primarily to D2 receptors (haloperidol).
```
68
(18.1-5) LSD
Psychedelic drugs : drugs whose primary action is to altered perception, emotion, and cognition.
LSD is a classical hallucinogen along with dissociative hallucinogens and cannabinoids
69
Atypical antipsychotics
: drugs that are effective against schizophrenia, but do not bind too strongly to D2 receptors. Also known as second-generation antipsychotics
70
(18.2-1) Major depressive disorder
Clinical depression: depression severe enough to cause difficultly for the patient to meet the requirements essential for daily life. Conditions last two weeks or longer.
It is almost impossible to keep, or maintain social contacts, to eat, or maintain an acceptable level of personal hygiene. Sleep disturbances, and thoughts of suicide are common.
71
(18.2-1) peri/postpartum depression
The intense, sustained depression experienced by some females during pregnancy, after they give birth, or both.
A subtype of major depressive disorders. It appears to be associated with 19% of pregnancies.
72
(18.2-1) seasonal affective disorder
Type of MDD, episodes of depression usually occurs during the winter months. Light therapy is often effective in reducing the symptoms of SAD.
Incidences are higher in Alaska-at 9%. Whereas in Florida-1%, the winter days are longer and brighter.
73
(18.2-2) Ketamine
(Dissociative hallucinogen) a single low dose of ketamine rapidly reduces depression. Even for patients who had been experiencing a severe episode. However, ketamine has undesirable side effects. Researchers are trying to identify more selective NMDA-receptor antagonists with fewer side effects.
74
(18.2-2) atypical antidepressant
A catch-all class comprising drugs that have many different modes of action: the atypical antidepresants
For example, bupropion, has several effects on neurotransmission: It is a blocker of dopamine and norepinephrine reuptake, and a blocker of nicotinic acetylcholine receptors. Agomelatine—a melatonin receptor agonist.
75
(18.2-2) monomine oxidase inhibitor
MAO inhibitors, Accordingly, a new class of antidepressant medications emerged.
76
(18.2-2) tricyclic antidepressant
tricyclic antidepressants, and selective monoamine-reuptake inhibitors.
Tricyclic antidepressants block the reuptake of both serotonin and norepinephrine, thus increasing their levels in the brain. They are a safer alternative to MAO inhibitors.
Their chemical structures include threerings of atoms. Imipramine, the first tricyclic antidepressant, was initially thought to be an antipsychotic drug. However, when its effects on a mixed sample of psychiatric patients were assessed, it had no effect against schizophrenia but helped with some depression.
77
(18.2-2) NMDA-receptor antagonist
ANTAGONISTS. Beginning in the early 1990s. Several studies reported a positive effect of antagonizing the glutamate NMDA receptor on depressive disorders.
78
(18.2-2) SSRI's
Selective serotonin-reuptake inhibitors (SSRIs) are serotonin agonists that exert their agonistic effects by blocking the reuptake of serotonin from synapses
Fluoxetine (marketed as Prozac) is a slight variation of that of imipramine and other tricyclic antidepressants.
Fluoxetine is no more effective than imipramine in treating depression. Nevertheless, it was immediately embraced by the psychiatric community and has been prescribed in many millions of cases.
Fluoxetine and other SSRIs popularity is attributable to: (1) hey have fewer side effects than tricyclics and MAO inhibitors. (2) They act against a wide range of psychological disorders in addition to depression.
The success of the SSRIs spawned the introduction of a similar class of drugs. The selective norepinephrine-reuptake inhibitors (SNRIs). These (reboxetine) have proven to be just as effective as the SSRIs in the treatment of depression. Also effective against depression are drugs that block the reuptake of more than one monoamine neurotransmitter (e.g., venlafaxine).
79
(18.2-3)MRI studies of depressed patients
Consistent reductions and gray matter volume in the prefrontal cortex, hippocampus, amygdala and cingulate cortex have been observed. Gray matter in the medial prefrontal cortex and the amygdala. In a group of healthy volunteers generally predisposed to developing depression, had cell loss in the medial prefrontal cortex and the amygdala. White matter reductions are noted in several brain regions most reliably the frontal cortex
80
(18.2-4) Neuroplasticity theory of depression
Depression results from a decrease of neuroplastic processes and various brain structures like the hippocampus, this leads to neuron loss and other neural pathology.
Research shows stress and depression or associated with the disruption of various neuroplastic processes like a reduction in the synthesis of neurotrphins, a decrease in adult hippocampal neurogenesis. Research shows that antidepressant treatments are associated with an enhancement of neuroplastic processes like an increase in the synthesis of neurtrophins an increase in synaptoenesis, an increase in adult hippocampal neurogenesis .
81
(18.2-4) brain-derived neurotrophic factor
The decreased blood levels of DDF and might be a biomarker-a biological state that is protective of particular disorders for depression, and that increased blood levels of BDNF might be a biomarker for the successful treatment of depression. Does hypothesized that the increase of blood levels of BDNF and which increase certain neuroplastic processes-increase adult hippocampal neurogenesis, leading to an alleviation of depression.
82
(18.2-5) rTMS (high and low frequency)
Repetitive transcranial magnetic stimulation: a form of transcranial magnetic stimulation that involves the delivery of repetitive magnetic pulses at either high frequencies-5+ per second; high frequency RTMs. Low frequencies-less than one pulse per second; low-frequency RTMs to specific cortical areas
83
(18.3-1) Bipolar disorders
A category of psychiatric disorders that involves alternate bouts of depression and mania or hypomania
hypermania characterized by reduced need for sleep, high-energy, and positive affect. During periods of hypomania people are talkative energetic and positive, positive, and very confident. They can be very effective at certain jobs and can be great fun.
mania A state that has the same features as hypermania but take to an extreme; it also has additional symptoms, such as delusions of grandeur, overconfidence, and the distractibility. Mania usually involves psychosis.
psychosis loss of touch with reality
84
(18.3-1) bipolar disorder type one and two
Bipolar disorder type one: a psychiatric disorder that involves alternate bouts of depression and mania
Bipolar disorder type two psychiatric disorder that involves alternate bouts of depression and hypomania
Bipolar disorders do not involve rapid alterations in mood, rather, the mood episodes after last weeks to months. A subtype of bipolar disorder known as rapid cycling bipolar disorders-are defined as involving for a more mood episodes per year
85
(18.3-2) John Cade
Injected guinea pigs with the urine of various psychiatric inpatient and found that the urine in many manic patients was the most toxic.
He injected guinea pigs with lithium urea, and others with lithium carbonate to check whether it was a lithium or the uric acid that was protective. He found that lithium carbonate also protected the guinea pigs from the toxicity of Europe. Cade hypothesize that manic patients have lower levels of lithium the non-manic patients
There was a little interest because few drug companies had little interest
the therapeutic properties of a metallic ion that cannot be protected by a patent.
86
(18.3-3) Brain structures affected by bipolar
Specific brain structures are smaller in patients with bipolar disorders including the medial prefrontal cortex, the left anterior cingulate, the left superior temporal gyrus, and prefrontal regions and the hippocampus.
Hyperthermic-pituitary-adrenal axis HPA dysregulation in bipolar disorder's. Marked disruptions in circadian rhythm's in both patients with bipolar disorders and their non-bipolar relatives; and alteration in the GABA glutamate and monomane neurotransmission in patients with bipolar disorders
87
(18.3-4) fMRI studies of bipolar patients
FMRI studies of patients with bipolar disorders have found a typical activation in the frontal cortex, medial temporal lobe structures in the basal ganglia as well as a typical functional connectivity between some of these structures in a variety of cognitive states.
88
(18.3-5) BDNF levels are lower in bipolar patients
Brain-derived neurotrophic factor: BDNF levels are lower in patients with bipolar disorder's when they are either depressed or manic.
HPA axis dysregulation of bipolar disorder's, Mark to the disruptions in the circadian rhythm's and both patients with bipolar disorders and their non-bipolar relatives and GABA glutamate in mono Anamine new transmission in patients with bipolar disorders
89
(18.4-1) Anxiety disorders
Psychiatric disorder that involves anxiety that is so extreme and so pervasive that it disrupts normal functioning.
Anxiety is a chronic fear that persists in the absence of any direct threat
Anxiety disorders of the most problem DeVol psychiatric disorders. Between 14 and 34% of all people suffer from an anxiety disorder at some point in their lives and the incident it's twice as high for females.
Anxiety disorders include generalizing Zaidi disorder, specific phobias, ever phobia, panic disorder, panic attacks.
90
(18.4-1) anxiety disorder: generalized anxiety disorder
And anxiety disorder characterized by stress responses and extreme feelings of anxiety and worry about a large number of different activities or events
91
(18.4-1) anxiety disorders specific phobias
anxiety disorder that involves strong fear or anxiety about particular objects like birds or spiders or situations like in close spaces of darkness.
92
(18.4-1) gene's associated with anxiety disorders
No specific genes have yet been linked to anxiety disorders, significant genetic component to read ability estimates range from 30 to 50%
93
(18.4-2) Diazepam and anxiety disorders
Diazepam is a benzodiazepine: a class of GABAA agonist in and anolyxics sedatives and anticonvulsant properties.
94
(18.4-2) ketamine and anxiety disorders
Serotonin agonists like buspirone is used for the treatment of anxiety disorders. Please porn appears to have selective agonist affects on a subtype of serotonin receptor, the five-HT one a receptor. I made a vantage of it buspirone over benzodiazepines is it's specificity
95
(18.4-2) Chlorpromazine and anxiety disorders
Benzodiazepines are widely prescribed for treatment of anxiety disorders. They are also prescribed as hypnotics for sleep inducing drugs, anticonvulsants, and muscle relaxer and's.
Approximately 10% of adult North Americans are currently taking a benzodiazepine, if her side effects include sedation, ataxia or disruption of motor activity, tremor, nausea, and a withdrawal reactions that includes rebounding anxiety. Benzodiazepines are addictive and should only be prescribed for short term use. Behave real effects of benzodiazepines are thought to be mediated by their GABAA receptor's.
96
Plus maze tests
An animal bottle of anxiety; anxious rats tend to stay in the enclosed arms of the maze rather than venturing onto the open arms. The maze rests 50 cm above the floor. To arms have sides and two arms have no sides, and the measure of anxiety is the proportion of time the right spend in the enclosed arms rather than venturing onto the exposed arms.
97
(18.4-4) Risk assessment test and rats
An animal model of anxiety after a single brief exposure to a cat on the surface of a laboratory borough system, rat flea to the boroughs and freeze. Then they engage in a variety of risk assessment behaviors. The measure of anxiety in this test are the amounts of time spend freezing and risk assessments.
98
(18.4-5) anxiolytic drugs and agonist drugs
The elevated plus maze the defence burying, and the risk assessment test of anxiety show potential problem with the line of evidence. Existing animal models of anxiety may be models of benzodiazapine -sensitive anxiety rather then of anxiety in general, and models may not be sensitive to anxiolytic drugs that act on a different non-GABA mechanism. Example serotonin agonists buspirone does not have a reliable anxiolytic effect on the elevated plus maze test
99
(18.5-1) echolalia
Vocalize repetition of some or all of what has just been hard
100
(18.5-2) Tourettes disorder
A disorder of tics-involuntary, repetitive, stereotyped movements or vocalizations
Tics: involuntary repetitive stereotype movements or vocalizations; the defining feature of Tourette's disorder
Develops in 0.13 to 1% of the population, it is four times more frequent and male children then and female children but the sex differences not for found an adult patients. There is a significant genetic component: concordance rate or 50% from monozygotic twins and 10% for dizygotic twins.
Comorbidity with attention deficit hyper activity disorder, obsessive-compulsive disorder, or both.
Tic suppression is not inevitably followed by rebound and tics become worse than before
101
(18.5-3) Tourettes and brain structures
Cerebral pathology associated with Tourette's disorder has focused on the striatum (caudate plus putamen). Patients with this disorder tend to have smaller striatal volumes and when they suppress their tics, fMRI activity is recorded in both the prefrontal cortex and caudate nuclei
The decision to suppress tics comes from the prefrontal cortex (initiates the suppression by acting on the caudate nuclei).
For example, an MRI study of children with Tourette's disorder documented thinning in sensorimotor cortex gray matter that was particularly prominent in the areas that controlled the face, mouth, and larynx (voice box).
102
(18.5-4) cortical stratal thalamic-cortical brain circuits in Tourette's disorder
Dysfunctional dopaminergic and GABAergic signaling within the cortical-striatal- thalamic-cortical brain circuits in Tourette's disorder. This finding has been of particular interest because those brain circuits are implicated in motor learning—including habit formation
103
(18.5-5) drug treatment for Tourettes Disorder
Tics of Tourette's disorder are usually treated with antipsychotics. Antipsychotics can reduce tics by about 70 percent, but patients or their caregivers often refuse them because of the adverse side effects (e.g., weight gain, fatigue, dry mouth).
The success of antipsychotics in blockng Tourette's tics is consistent with the hypothesis that the disorder is related to changes in the cortical-striatal- thalamic-cortical circuit because that circuit relies heavily on dopaminergic singling
104
Clinical tries conducted in three operate phases
Translational research: Research designed to translate basic scientific discoveries into effective clinical treatments
Basic research
Discovery of the drug, development of efficient methods of synthesis, and testing with animal models
Application to begin clinical trials and the review of basic research by government agency
Human clinical trials
Phase 1: screening for safety and finding the maximum safe dose
Phase 2: establishing most effective doses and schedules of treatment
Phase 3: clear demonstration that the drug is therapeutic
Application to begin marketing and reviews of results of clinical trials by government agency
Selling to the public
Recovering development costs and continuing to monitor the safety of the drug
105
(18.6-1) PHASE 1: SCREENING FOR SAFETY.
The purpose of the first phase of a clinical trial is to determine whether the drug is safe for human use and, if it is, to determine how much of the drug can be tolerated.
106
(18.6-1) PHASE 2: ESTABLISHING THE TESTING PROTOCOL.
The purpose of the second phase of a clinical trial is to establish the protocol (the conditions) under which the final tests are likely to provide a clear result.
For example, in phase 2, researchers hope to discover which doses are likely to be therapeutically effective, how frequently they should be administered, how long they need to be administered to have a therapeutic effect, what benefits are likely to occur, and which patients are likely to be helped
107
(18.6-1) PHASE 3: FINAL TESTING.
Phase 3 of a clinical trial is typically a double-blind, placebo-control study on large numbers—often, many thousands—of patients suffering from the target disorder. The design of the phase 3 tests is based on the results of phase 2 so that the final tests are likely to demonstrate positive therapeutic effects if they exist.
108
(18.6-2) Clinical trials
Studies conducted on human volunteers to assess the therapeutic efficacy of an untested drug or other treatment
109
(18.6-3) Placebo
Phase 2 tests are conducted on volunteer patients suffering from the target disorder; the tests usually include placebo-control groups (groups of patients who receive a control substance rather than the drug), and their designs are usually double- blind—that is, the tests are conducted so that neither the pa- tients nor the physicians interacting with them know which treatment (drug or placebo) each patient has received.
110
(18.6-4) Orphan drugs
Drugs for which the market is too small for the necessary developmental research to be profitable
111
(18.6-5) double blind studies
Tests are conducted so that neither the patients nor the physicians interacting with them know which treatment (drug or placebo) each patient has received.
There can be no convincing evidence that the experimental treatment is effective until a double-blind, placebo-control trial has been completed. Because psychiatric disorders often improve after a placebo, a double-blind, placebo-control procedure is essential in the evaluation of any psychotherapeutic drug.
112
(18.6-5) placebo-controlled studies
At therapeutic doses, many drugs have side effects that are obvious to people taking them, and thus the par- ticipants in double-blind, placebo-control studies who receive the drug can be certain that they are not in the placebo group. This knowledge may greatly contribute to the positive effects of the drug, independent of any real thera- peutic effect. Accordingly, it is now widely recognized that an active placebo is better than an inert placebo as the control drug. Active placebos are control drugs that have no therapeutic effect but produce side effects similar to those produced by the drug under evaluation.
113
The first anti-schizophrenic drug to be widely marketed was
Chlorpromazine -the first antipsychotic drug. Developed as an antihistamine, to counteract swelling had a calming affect on some of his patients, he suggested that it might have a calming affect on different difficult to handle patients with psychosis.
Agitated patients with schizophrenia were called, and emotionally blunted patients with schizophrenia were activated by it. It often reduces the severity of symptoms enough to allow institutionalize patients to be discharged.
114
(18.6) schizophrenic patients often display long periods even in mobility and waxy flexibility a pattern commonly referred to as
Catatonia: a negative symptoms of schizophrenia.
115
The active ingredient of the snake root it is
Reserpine: An antipsychotic once used to treat schizophrenia. It is no longer used in the treatment because it produces a dangerous decline and blood pressure at the doses needed for successful treatment. It is similar to chlorpromazine because both drugs are manifested after the patient has been medicated for 2 to 3 weeks. And onset of antipsychotic effects is usually associated with motor effects similar to symptoms of Parkinson's disease.
116
(18.8) current dopamine theory at schizophrenia
Theory of schizophrenia suggested schizophrenia is caused by excessive activity at D2 receptors, rather than a dopamine receptor in general, or hyperactivity at D2 receptors
Typical antipsychotics bind to D2 receptors is highly correlated with their effectiveness and suppressing the symptoms of schizophrenia. Spirihas the greatest affinity for D2 receptors in the most potent antipsychotic affect.
The theory that schizophrenia is caused by too much dopamine and, conversely, that antipsychotic drugs exert their effects by decreasing dopamine levels.
The antipsychotic drugs (chlorpromazine and reserpine) are known to deplete the brain of dopamine and other monoamines by breaking down the synaptic vesicles in which these neurotransmitters are stored.
Anphetamine and cocaine can trigger a schizophrenic-like episodes and healthy users, were known to increase the extracellular levels of dopamine and other monoamines in the brain
117
(18.2-1) anti-depressant drugs
Five major classes of drugs have been used for the treatment of depression monamine oxidize inhibitors, tryicyclic antidepressants, selective monamine reuptake inhibitor's, atypical antidepressants, anti-NMDA receptor agonist's
Iproniazid: The first anti-depressant drug; a monamine oxidize inhibitor, used to treat patients with tuberculosis first. It is a monoamine agonist; it increases the levels of monoamine like norepinephrine and serotonin by inhibiting the activity of manna mean oxidized and a oh, the enzyme that breaks down monoamine neurotransmitters in the cytoplasm of the neuron.
MAO inhibitor's; antidepressant drugs that increase the inhibiting the action of the enzyme monoamine oxidase
Tricyclic antidepressants: drugs with an antidepressant action and a threering molecular structure
SSRIs: serotoniagonists that exert their agonistic effects by blocking the reuptake of serotonin from synapse
SNRIs: The selective norepinephrine reuptake inhibitor's, or effective as the SSRIs and treatment of depression. Also affective against depression or drugs that block three uptake of more than one monoanamine neurotransmitter
118
(18.3) lithium
A mood stabilizer, metallic ion the first drug found to act as a mood stabilizer. The discovery of lithium anti-mania action was discovered by accident
Considered to be the best mood stabilizer
I'll mood stabilizers act against bouts of mania, some at the gens depression, and some act against both. They do not illuminate all symptoms. Many carry an array of adverse side effects like weight gain, tremor, blurred vision, dizziness. Causing not adherence to medication
119
(18.15) Comorbid
The tendency for two or more health conditions to occur together in the same individual
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(18.2-1) Atypical anti-depressants
A catchall class of antidepressant drugs that do not fit into the other categories of antidepressants like monoamine oxidize inhibitors, try cyclic antidepressants. Each of the drugs in this class has its own unique mechanism of action.
Kata mean: a drug that is a type of dissociative hallucinogen, hello single-dose will rapidly reduce depression however, it has undesirable side effects.
121
Ketamine.
: a drug that is a type of dissociative hallucinogen, hello single-dose will rapidly reduce depression however, it has undesirable side effects
