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Stage 2 Basic Pharmacology > BP.18 Antidepressants and antipsychotics > Flashcards

BP.18 Antidepressants and antipsychotics Flashcards

1
Q

Name the monoamine neurotransmitors involved in

depression and anxiety

A

1) 5-Hydoxytryptamine (5-HT, serotonin)
Depression, anxiety

2) Noradrenaline (NA)

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2
Q

Name the monoamine neurotransmitors involved in

Schizophrenia,

A

dopamine

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3
Q

1) Describe reaction pathway leading to formation of 5-HT:
2) How is 5-HT released into synapse?
3) How does 5-HT re-enter the neurone?
4) how does the initial substrate enter the neurone?

A

1) -Tryptophan converted into 5-HTP by TPH
- Converted into 5-HT by AADC and stored in vesicles
2) -Released in response to an action potential
3) via SERT transporter
4) tryptophan enters neurone via LNAA

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4
Q

1) Describe reaction pathway leading to formation of Dopamine:

A

1) Tyrosine → L DOPA by TyOH

L DOPA converted into DOPA via DOPA decarboxylase

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5
Q

What is associated with schizophrenia?

A

Excess dopamine release , increased DA function

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6
Q

The 3 main dopamine pathways in the brain:

A

Nigrostriatal pathway
Mesolimbic and memocortical projections
Tuberoinfundibular

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7
Q

Where do the dopamine pathways go from and to:
1) Nigrostriatal
2 Mesolimbic and memocortical projections
3) Tuberoinfundibular

A

1) Substantia nigra → dorsal striatum
2) - VTA ( tegmentalis ventralis) → frontal cortex/ventral striatum
3) Hypothalamus → pituitary stalk

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8
Q

Function of dopamine pathways:
1) Nigrostriatal
2 Mesolimbic and memocortical projections
3) Tuberoinfundibular

A

1) Control of fine movement (EPS)
2) Cognition/mood (cortex)
Reward/addiction (ventral striatum)
3) Tonic inhibition of prolactin secretion (endocrine role)

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9
Q

Which dopamine pathway is dysfunctional in parkinsons:

A

nigrostriatal

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10
Q

Dopamine prevents further release of __a__ from the __b___ when not suckling/ prevents woman from continually ___c___

A

a) prolactin
b) pituatry
c) lactating

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11
Q

What released by hypothalamic nuclei stimulates prolactin release from the anterior pituitary?

2) what inhibits this?
3) Why is it tonic?
4) What stimulates lactation of mammary tissues?
5) Why changes does 4 cause?

A

prolactin releasing factor (hormone)
2) dopamine (Prolactin releasing inhibiting Factor (PRIF)
(tonic)
3) always released
4) prolactin
5) Milk production
proliferation & differentiation of mammary tissue during pregancy, maternal behaviour

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12
Q

3 symptoms of parkinsons?

A

Tremor
Muscle rigidity
Loss of facial expression

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13
Q

4 symptoms of Tardive dyskinesia:

A

Repetitive rhythmical involuntary movements,
lip smacking, chewing,
rocking, rotation of the ankles or legs,
marching in place, and
repetitive sounds such as humming or grunting

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14
Q

What is an effective antipsychotic?

2) why does it work?

A

1) D2 antagonists are effective antipsychotics

2) Use D2 antagonists to counteract this increase in DA function

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15
Q

D2 antagonism in the ___A___ DA pathway causes __B___ side effects (EPS)

A

A) nigrostriatal

B) extrapyramidal

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16
Q

D2 antagonism in the tuberoinfundibular DA pathway causes _____

A

hyperprolactinaemia

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17
Q

hyperprolactinaemia has 2 conditions:

A

Galactorrhoea,

Gynaecomastea

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18
Q

Antipsychotics also have affinity for ___A__ receptors . name 3 receptors:

A

A) nondopaminergic
B) Histamine receptors, Muscarinic, Adrenergic

,

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19
Q

A) What do TCAs inhibit?

B) unfortunatly , what do they also block? (3)

A

A) Inhibit 5-HT and NA uptake

B) 1) M1 receptors

2) H1 receptors
3) alpha 1 receptors

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20
Q 
TCAs block 
1) M1 receptors
2) H1 receptors
3) alpha 1 receptors
what is the unwanted/side effect of this?
A

1) Dry mouth, blurred vision, constipation, urinary retention
2) Sedation, weight gain
2) Postural hypotension

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21
Q

Which receptor blocking by TCA causes the following side effects:
A Sedation, weight gain
B Postural hypotension
C Dry mouth, blurred vision, constipation, urinary retention

A

A H1 receptors
B alpha 1 receptors
C M1 receptors

22
Q

side effects of Phenothiazines

1) group 1
2) group 2
3) group 3

A

Group I : Sedation (affinity for H1)
Group II :Anticholinergic (affinity for M1)
Group III :extrapyramidal side effects (EPS) (predomantly D2)

23
Q

What group of phenothiazinedoes the following fall into:

Chlorpromazine

A

group 1

24
Q

What group of phenothiazinedoes the following fall into:

Thioridazine

A

group 2

25
Q

What group of phenothiazinedoes the following fall into:

Fluphenazine

A

group 3

26
Q

Name antipsychphotic classes:
1)
2)
3)

A

1) Phenothiazine
2) Thioxanthenes
3) Butyrophenones

27
Q

What are Butyrophenones
selective to..
2) Why do they not cause sedation?
3) Are extrapyramidal side effects (EPS) a problem?

A

1) selective to D2
2) Lack muscarinic and antihistamine activity (no sedation)
3) yes , D2!

28
Q

4 Limitations Of Classical Antipsychotics

A

Approximately one-third of patients with schizophrenia fail to respond
Limited efficacy against negative symptoms
High proportion of patients relapse
Side effects and compliance issues

29
Q

What are the 2 types of symptoms of schizophrenia?

2) what symptoms arew within each group:

A

1) positive and negative
2) positive= Disorders of thought/disorganised behavior
Hallucinations (aural and visual)
Paranoia

negative= sBlunted emotions/anhedonia
Social withdrawal
Apathy/loss of energy

30
Q

Atypical antipsychotics

1) compare EPS profile to antipsychotics:
2) What is closapine associated with?
3) main difference between 2nd generation antipsychotics to 1st

A

1) has Better EPS side effect profile (without loss of antipsychotic efficacy)
2) agranulocytosis (acute condition involving a severe and dangerous leukopenia)

3) fewer side effects

31
Q

How do antidepressants work?

2) Why do Tricyclic antidepressants (TCAs) have side effects?
3) Why do MAOIs have side effects?
4) compare 2n generation and 1st

A

1) Block reuptake of monoamines (Inhibit 5-HT and NA uptake) OR block metabolism by MAO a/b.
2) Side effects of TCA due to action on other receptors, block M1 receptors, block H1, block alpha
3) have stimulant effects (dangerous in overdose, new ones more selective to MAOa btw)
4) 2nd generation: fewer side effects than 1st generation

32
Q

Effect of blocking M1 receptors:

A

Dry mouth, blurred vision, constipation, urinary retention

33
Q

Effect of blocking H1 receptors:

A

Sedation, weight gain

34
Q

Effect of blocking alpha1 receptors:

A

postural hypotension

35
Q

Clinical uses of TCAs: (3)

A

Severe treatment resistant depression
Where sedation is also required
Where disease history indicates efficacy and tolerance

36
Q

SSRI

stands for

A

SSRI: selective serotonin reuptake inhibitor

37
Q

SNRI stands for

NARI stands for

A

SNRI: serotonin/ noradrenaline reuptake inhibitor (venlafaxine)
NARI noradrenaline reuptake inhibitor (reboxitine)

38
Q

What are 2nd generation antidepressants selective to:

A

2nd generation antidepressants:

Selective for 5-HT or NA transporter and do not have affinity for postsynaptic receptors (fewer side effects)

39
Q

What are the 2nd generation of antidepressants:

A

SSRIs (have a better adverse side effect profile than TCAs (1st generation).

40
Q

What side effects do SSRIs have ?(3)

2) What side effects do they not cause

A

Sexual dysfunction (impotence)
Gastrointestinal (upper GI bleeds)
Precipitate anxiety
Do not cause sedation or anticholinergic side effects

41
Q

What is the hypothesis of the mechanism of aciton of atypical antipsychotics:

A

Atypicals do have affinity for D2 receptor, however they have a much faster dissociation rate from the D2 receptor (Koff) (loose binding)

These drugs can be displaced by physiological phasic bursts of DA transmission (important in DA striatal pathways)

Results in less distortion of physiological DA signalling in striatal pathways

Cannot exclude the role of 5-HT2

42
Q

Which one is typical and which is an atypical antipsychotic drug:

1) greater incidence of extra pyramidal side effects
2) greater efficacy in treating treatment resistant patients
3) greater efficacy against negative symptoms

A

1) typical
2) typical
3) atypical (as lower affinity for D2, higher for D3 and D4 and 5-HT2a receptor)

43
Q

SSRIs are used as antidepressants, what else can they be used to treat:

A

panic disorder,
obsessive compulsive disorder,
eating disorders

44
Q

Which is a TCA and which is an SSRI:

1) greater antidepressatn efficacy
2) better adverse side effect profile
3) has a lag time before onset of therapeutic effect

A

1) neither, equal
2) SSRI
3) SSRI

45
Q

What are 2 isoforms of MAO that MAOIs block, for each isoform what is broken down:

A

Two isoforms of MAO

1) MAOA breaks down 5-HT & NA ( and a bit of DA)
2) MAOB breaks down DA

46
Q

What groups are TCAs not used in:

A 
Elderly 
Cardiac patients (increase chance of conduction abnormalities)
Hepatic insufficiency
Suicidal patients (overdose)
Drivers (sedation)
Workers (sedation)
47
Q

What does MAOI stand for:

A

Monoamine oxidase inhibitors (

48
Q

which is (A) the old MAOI and which is (B) the new:

1) block both isofroms irreversibly
2) are reversible inhibitors
3) less stimulant effect
4) safer (less dangerous in overdose)

A

1) A
2) B
3) B
4) B

49
Q

What drug can cause the chees effect?

2) What is it?

A

1) MAOI
2) hypertensive crisis, resulting from and excess of dietary tyramine (either activating sympathetic nervous system themselves or displacing endogenous amines from vesicles and indirectly activating sympathetic nervous system)

50
Q

What causes Serotonin syndrome?

2) what is it?

A

1) MAOI & SSRIs (releasing agents)

2) hyperthermia,

51
Q

What can anitparkinson drugs cause? (these are MAIOs)

A

severe hypertension

52
Q

Name 3 antidepressant drug classes:

A

Tricyclic antidepressants (TCA’s)

Selective serotonin reuptake inhibitor (SSRI’s) - (2nd generation)

Monoamine oxidase inhibitors

Stage 2 Basic Pharmacology (16 decks)

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