BB2 Revision 8 Flashcards
Describe the MoA of TCAs [2]
- Inhibit reuptake of amines on the presynaptic terminal, so 5HT or NA cannot be taken back into neuron
Important AEs of TCAs? [4]
- Dangerous (cardiotoxic) in overdose
- Anti-cholinergic: dry mouth; blurred vision, constipation, urinary retention, aggravation of narrow angle glaucoma, fatigue, postural hypotension, dizziness, loss of libido, arrhythmias
- Antihistaminic: sedation, weight gain.
- Block alpha 1 adrenoreceptors: orthostatic hypotension - blood pressure drops on standing, cardiac effects
As a result aren’t the first choice!
Phenelzine, tranylcypromine belong to which drug class? [1]
Irreversible MONOAMINE OXIDASE INHIBITORS
Describe the MoA of monoamine oxidase inhibitors such Phenelzine, tranylcypromine [1]
Which type of food interact with MOIs? [1]
Irreversible inhibition of the enzyme monoamine oxidase [1]
Interactions with tyramine-containing food (mature cheese, pickled fish and meat, red wine, beer, broad bean pods, yeast extract)- restrictions continue at least 2 weeks after discontinuation
Which is the most selective SSRI?
citalopram
sertraline
fluoxetine
paroxetine
Which is the most selective SSRI?
citalopram
sertraline
fluoxetine
paroxetine
Moclobemide belongs to which drug class? [1]
REVERSIBLE MONOAMINE OXIDASE INHIBITOR
Which is the safest monoamine oxidisase inhibitor?
Moclobemide
Phenelzine
Tranylcypromine
Which is the safest monoamine oxidisase inhibitor?
Moclobemide (reversible MOAIs)
Phenelzine (irreversible MOAIs)
Tranylcypromine (irreversible MOAIs)
Describe MoA of Agomelatine [2]
Why is this potentially a really good drug? [2]
MoA:
* Agonist at melatonin MT1 & MT2 receptors: important for sleep control
* Antagonist of 5-HT2 receptors
Benefits of Agomelatine:
* improves sleep quality
* less sexual dysfunction than SSRIs;
* anxiolytic effects
* no ‘discontinuation syndrome’
The treatment with the SNRI [] reduces the increased Default Mode Network
connectivity seen in depression
The treatment with the SNRI duloxetine reduces the increased Default Mode Network connectivity seen in depression
Apart from inhibiting the reuptake of amines, which other receptors do TCAs bind to? [3]
Why is this problematic? [1]
Bind to:
* H1 receptors
* muscarinic receptors
* α1 and α2 adrenoceptors
Causes wide ranging side effects
What is the benefit of using SSRIs (citalopram, fluoxetine, paroxetine) with regards to AEs [3]
No anticholinergic activity
No cardiotoxic effects
Safe in overdose
AEs of SSRIs?
· Nausea vomiting
· Dry mouth
· Headache
· Asthenia
· Dizziness
· Anorexia
· Weight loss
· Nervousness
· Tremor
· Convulsions
· Sexual dysfunction
What are the different targets for reverible MAOIs compared to irreversible MOAIs? [2]
Describe the benefits of reversible MAOIs compared to irreversible MAOs [2]
Drug targets:
* Reversible MAOI targets: MOA-A
* Irreversible MAOI targets: MAOA versus MAOB
Differences:
* Reversible is safer than irreversible MAOIs
* Can switch drug classes quicker
Depression drugs
Name a noradrenaline reuptake inhibitor used for depression treatment [1]
Reboxetine
Depression Drugs
Name a serotonergic antagonist and reuptake inhibito (SARI) [1]
Trazodone
Depression drugs
Name a noradrenergic and specific serotonergic antidepressant (NaSSA) [1]
Mirtazapine
Explain why there is a delayed action for anti-depressant drug action for TCAs [4]
The immediate increase in synaptic concentration of amines
may lead to activation of somatic neuronal autoreceptors
The activated autoreceptors decrease firing of the neurones
During the first weeks of treatment the autoreceptors desensitize
The neurones will return subsequently to the normal firing rate
The inhibition of reuptake continues and the level of amines
continues to be high, resulting in full efficacy
Name two risks of using antidepressant drugs used in bipolar disorder to treat periods of depression? [2]
can precipitate manic episodes or mixed
affective states
induce an increased frequency
in mood change cycles
Name 4 non-pharmacological approaches for mood disorders
Electroconvulsive therapy (treatment-refractory severe depression with suicide risk)
Cognitive behavioural therapy (CBT) (can augment the effects of pharmacological treatment)
Vagal nerve stimulation (especially in chronic depression)
Deep brain stimulation (DBS); subcallosal cingulate white matter – Brodmann area 25)
Which area is the DBS target for treating depression? [1]
What the is the Broadmann area?
21
22
23
24
25
Which area is the DBS target for treating depression: subgenual cingulate cortex
What the is the Broadmann area?
21
22
23
24
25
Name two new therapeutic developments for depression [2]
What types of depression do they speficifically treat? [2]
What are their MoAs? [2]
Esketamine:
* NMDA glutamate receptor antagonist
* treatment-resistant depression
Brexanolone:
* progesterone-related compound, positive modulator of GABAA receptors
* approved for post-partum depression
Most common AE of SSRI? [1]
gastrointestinal symptoms are the most common side-effect:
30% schizophrenic patients do not respond to treatment. Which drug would you provied for those who have drug resistance? [1]
Clozapine
Name a risk of clozapine treatment [2]
agranulocytosis: increases chance of infection
Non-pharmacological approaches for SCH? [3]
- Cognitive Behavioural Therapy
- Cognitive remediation
- Family therapy
These do not replace the pharmacological treatment
Explain what tardive dyskinesia is and the length of the AE [2]
Involuntary movements of the lips, jaw, face; grimacing, constant chewing, tongue thrusting; rapid involuntary limb movements
typical antipsychotics,
taken for longer than a few months/years
In some patients it may be possible to overcome it
The cingulate gyrus and parrahippocampal gyrus are continuous via a bundle of white matter called the []
The cingulate gyrus and parrahippocampal gyrus are continuous via a bundle of white matter called the cingulum
Label A-E
A: cingulate gyrus
B: corpus callosum
C: fornix
D: parahippocampal gyrus
E: subcallosal area
Label A-F
A: Fornix
B: Cingulate cortex
C: Thalamus
D: Mamilllary body
E: Hippocampus
F: Amygdala
Label A-C
A: Anterior commissure
B: Amygdala
C: Hippocampal
Label 14-17
14 Pulvinar of thalamus
15 Mamillary body
16 Optic tract
17 Anterior commissure
Label 18-22
18 Fornix
19 Longitudinal stria
20 Dentate gyrus
21 Hippocampal fimbria
22 Pes hippocampi
What is this structure? [1]
Nucleus accumbens
Describe the route of Papez’s circuit
Cingulate cortex –> parahippocampal cortex –> hippocampus –> fornix –> mamillary bodies –> hypothalamus -> anterior thalamus –> cingulate cortex.
Name the extremely fast response to an unexpected loud noise in babeies? [1]
Acoustic startle reflex / Moro reflex
Describe the pathway in which amygdala controls the startle reflex [4]
Sensory information feeds into the basolateral amygdala
Feeds into the central amygdala
Central amygdala sends output to the central gray area of the midbrain
Information is relayed to the nucleus in the pons responsible for the startle reflex
What is 8?
Corpus Callosum
Hippocampus
Subthalamic nuclei
Nucleus accumbens
Putamen
What is 8?
Corpus Callosum
Hippocampus
Subthalamic nuclei
Nucleus accumbens
Putamen
What is 8?
Anterior commissure
Fornix
Lateral ventricle
Putamen
Nucleus accumbens
What is 8?
Anterior commissure
Fornix
Lateral ventricle
Putamen
Nucleus accumbens
What is 5?
Hypothalamus
Fornix
Amygdala
Hippocampus
Thalamus
What is 5?
Hypothalamus
Fornix
Amygdala
Hippocampus
Thalamus
What is 13?
Hypothalamus
Fornix
Amygdala
Hippocampus
Thalamus
What is 5?
Hypothalamus
Fornix
Amygdala
Hippocampus
Thalamus
What is 3?
Hypothalamus
Fornix
Amygdala
Hippocampus
Thalamus
What is 3?
Hypothalamus (mamilliary body)
Fornix
Amygdala
Hippocampus
Thalamus
What is 10?
Hypothalamus
Fornix
Amygdala
Hippocampus
Thalamus
What is 10?
Hypothalamus
Fornix
Amygdala
Hippocampus
Thalamus
Label A-D
A:Cingulate cortex nuclei
B: Anterior thalamic
C:Mammillary bodies
D: hippocampus
