Lecture 9 = Mental Health Flashcards

1
Q

describe issues with the brain

A

physical or chemical issues with brain

results in mental illness and corresponding change in behaviour

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2
Q

when is behaviour not easily controlled?

A

when you have a mental illness because persons brain is not functioning the way it is supposed to

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3
Q

is there a genetic basis for personality and mental illness?

A

yes

some mental illnesses are more likely to occur in some families

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4
Q

what were original beliefs/treatments surrounding mental illness?

A

thought to be caused by demons

mentally ill were tortured, institutionalized, and underwent trepanation

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5
Q

what is trepanation

A

common treatment in early days
consisted of drilling hole in head to fix brain

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6
Q

what did it mean if someone was institutionalized for mental health? how did this differ in Europe vs. Middle Easy and Africa

A

put into mental asylums and prison and were hidden away from populations

Middle East and Africa were slightly more accepting and didn’t necessarily exile people

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7
Q

What did Freud do?

A

developed psychotherapy in 1896

was first time a scientific approach was taken towards treating mental health issues

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8
Q

what was lobotomy and when did it take place

A

involve sticking needle in persons brain to severe connection between to parts

thought to make behaviour more manageable

didn’t do much for person will illness - just the people around them

1940s-1950s

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9
Q

describe electroshock therapy and when it took place

A

strap down a person and send large voltage through them

would sometimes reduce symptoms

common in 50s, but still performed today

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10
Q

when did asylums become mental hospitals? what else happened during this time

A

1950s

people weren’t exiled as much, but were put into mental institutions instead to get care

attitudes towards mental health changed a bit

first drugs for mental illnesses came out during this time

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11
Q

describe schizophrenia

A

lots of psychosis

auditory hallucinations, confused thinking, false beliefs, magical thinking, anxiety disorders, lack of emotion, etc.

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12
Q

describe how first schizophrenia drug was discovered

A

discovered by accident when trying to find drugs to reduce nerves for surgical patients

antihistamines tended to have an anxiety reducing effect

led to use of Thorazine for schizophrenia (because anxiety is a characteristic of disorder)

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13
Q

describe Thorazine

A

1952 - first effective schizophrenia treatment

reduced overall symptoms (reduced feelings of anxiety, and amount of psychotic episodes)

25% achieved remission

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14
Q

describe side effects of Thorazine

A

wasn’t a clean drug

had some strong/permanent effects such as uncontrollable facial expressions (similar to Parkinsons)

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15
Q

describe the theory that high dopamine activity is related to schizophrenia and what this means for Thorazine drug and amphetamines

A

believed that high dopamine was related to schizophrenia

thorazine was dopamine antagonist - so decreased dopamine signals - therefore symptoms of schizophrenia reduced (specifically psychosis)

amphetamines raise dopamine in the brain - so could produce psychosis similar to schizophrenia

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16
Q

what are the 5 dopamine receptor subtypes and what do they do? which is most important

A

range from D1 to D5

allow dopamine in different parts of the brain

create different pathways for dopamine to transfer information

D2 most important

17
Q

what type of agonist/antagonist were all early antipsychotics? were they clean?

A

all D2 antagonists

not very clean + had lots of side effects

18
Q

how were subsequent drugs discovered

A

identified through animal studies

researchers identified patterns of behaviour that drugs produce

main improvements were reducing side effects (not necessarily efficacy)

19
Q

what was the main atypical antipsychotic? describe

A

1972 - Chlozapine

was a weak D2 antagonist and strong serotonin agonist (5-HT)

different chemical structure than most regular D2 antagonists

less likely to cause motor control disabilities

cleaner side effect pattern

20
Q

what type of drug is Imipramine and what does it treat?

A

tricyclic antidepressants (1951)

depression

21
Q

how does imipramine (tricyclic antidepressant) work? how was it discovered

A

accidentally discovered when trying to treat schizophrenia

works by blocking serotonin reuptake by pre-synaptic cell (nerve still resets self, but doesn’t allow serotonin back in)

net effect is amplifying serotonin signals for elevated mood

22
Q

what are the side effects of imipramine

A

inhibits serotonin reuptake (intended)

inhibits norepinephrine reuptake

dopamine/acetylcholine/histamine antagonist

not clean drug

23
Q

what is Iproniazid

A

originally a tuberculosis drug

found to have antidepressant effects

works by inhibiting/blocking monoamine oxidase (MAO) leading to an increase in amount of serotonin in brain

24
Q

how to monoamine oxidase drugs work (ex. Iproniazid)

A

inhibits monoamine oxidase (which typically destroys serotonin)

allows for the destruction of serotonin to slow down

leads to increase in levels of serotonin inside the brain

25
what drugs "elevate" moods and how do they do it
tricyclic drugs = prevent serotonin reuptake MAO inhibitor = reduce serotonin destruction both antidepressant drugs that increase serotonin amounts
26
what are SSRI's? what was the first one
selective serotonin reuptake inhibitor first was Prozac
27
why are SSRI's better than previous drugs (such as MAO inhibitors and serotonin reuptake inhibitors)
similar effectiveness much cleaner side effect profile so less harm no effet on acetylcholine
28
what are the side effects of Prozac? are they common?
anxiety, sleep disturbances, sexual dysfunction, and suicidal thoughts very uncommon
29
what drugs may work for OCD?
drugs associated with elevated serotonin activity such as Prozac (SSRI) or MAO inhibitors
30
what likely causes OCD
low serotonin function because drugs that help are associated with elevated serotonin
31
what did John Cade believe? describe experiments
believed that bipolar was caused by toxins injected guinea pigs with urine from manic people - but they died tried again + neutralized urine with lithium carbonate caused calming effect on pigs found that lithium calmed bipolar patients 1949
32
describe Lithium as a drug for bipolar
has very narrow therapeutic window = difference between effective and dangerous dose is small hard to design new drugs using structure = because it is only one atom mechanisms are not known (does lots of things)
33
what is a drug other than lithium used for bipolar?
valproic acid anticholinergic drug (inhibits acetylcholine) mechanism not known
34
what were the first anxiety drugs? explain
barbiturates (1864) not clean - addictive and lots of side effects are GABA agonists: - GABA receptor inhibits neural function - because they are GABA agonists, they amplify this causing a calming effect
35
what was the 2nd type of anxiety drug after barbiturates? describe
Miltown (1967) = benzodiazepines first big seller anxiety drug cleaner version of barbiturates alleviated anxiety without side effects works by increasing GABA signalling (increases sensitivity of GABA Receptors + activates GABA ion channels)
36
what are common criticisms of psychiatric drugs
alter brain chemistry similar to placebo limited effectiveness side effects are addictive all true - but taken out of context
37
why don't psychiatric drugs work better?
brain very complex animal experiments hard = can't fully control, hard to transfer to humans, brains not same, not always ethical
38
what are me-too drugs
process when drugs are made from old drugs by implementing minimal changes
39
what are the main challenges for patient compliance?
misunderstanding side effects resisting treatment false beliefs financial