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BB2 Revision 8 Flashcards

1
Q

Describe the MoA of TCAs [2]

A
  • Inhibit reuptake of amines on the presynaptic terminal, so 5HT or NA cannot be taken back into neuron
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2
Q

Important AEs of TCAs? [4]

A
  • 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!

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3
Q

Phenelzine, tranylcypromine belong to which drug class? [1]

A

Irreversible MONOAMINE OXIDASE INHIBITORS

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4
Q

Describe the MoA of monoamine oxidase inhibitors such Phenelzine, tranylcypromine [1]

Which type of food interact with MOIs? [1]

A

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

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5
Q

Which is the most selective SSRI?

citalopram
sertraline
fluoxetine
paroxetine

A

Which is the most selective SSRI?

citalopram
sertraline
fluoxetine
paroxetine

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6
Q

Moclobemide belongs to which drug class? [1]

A

REVERSIBLE MONOAMINE OXIDASE INHIBITOR

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7
Q

Which is the safest monoamine oxidisase inhibitor?

Moclobemide
Phenelzine
Tranylcypromine

A

Which is the safest monoamine oxidisase inhibitor?

Moclobemide (reversible MOAIs)
Phenelzine (irreversible MOAIs)
Tranylcypromine (irreversible MOAIs)

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8
Q

Describe MoA of Agomelatine [2]

Why is this potentially a really good drug? [2]

A

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’

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9
Q

The treatment with the SNRI [] reduces the increased Default Mode Network
connectivity seen in depression

A

The treatment with the SNRI duloxetine reduces the increased Default Mode Network connectivity seen in depression

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10
Q

Apart from inhibiting the reuptake of amines, which other receptors do TCAs bind to? [3]

Why is this problematic? [1]

A

Bind to:
* H1 receptors
* muscarinic receptors
* α1 and α2 adrenoceptors

Causes wide ranging side effects

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11
Q

What is the benefit of using SSRIs (citalopram, fluoxetine, paroxetine) with regards to AEs [3]

A

No anticholinergic activity
No cardiotoxic effects
Safe in overdose

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12
Q

AEs of SSRIs?

A

· Nausea vomiting

· Dry mouth

· Headache

· Asthenia

· Dizziness

· Anorexia

· Weight loss

· Nervousness

· Tremor

· Convulsions

· Sexual dysfunction

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13
Q

What are the different targets for reverible MAOIs compared to irreversible MOAIs? [2]

Describe the benefits of reversible MAOIs compared to irreversible MAOs [2]

A

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

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14
Q

Depression drugs

Name a noradrenaline reuptake inhibitor used for depression treatment [1]

A

Reboxetine

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15
Q

Depression Drugs

Name a serotonergic antagonist and reuptake inhibito (SARI) [1]

A

Trazodone

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16
Q

Depression drugs

Name a noradrenergic and specific serotonergic antidepressant (NaSSA) [1]

A

Mirtazapine

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17
Q

Explain why there is a delayed action for anti-depressant drug action for TCAs [4]

A

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

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18
Q

Name two risks of using antidepressant drugs used in bipolar disorder to treat periods of depression? [2]

A

can precipitate manic episodes or mixed
affective states

induce an increased frequency
in mood change cycles

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19
Q

Name 4 non-pharmacological approaches for mood disorders

A

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)

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20
Q

Which area is the DBS target for treating depression? [1]

What the is the Broadmann area?

21
22
23
24
25

A

Which area is the DBS target for treating depression: subgenual cingulate cortex

What the is the Broadmann area?

21
22
23
24
25

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21
Q

Name two new therapeutic developments for depression [2]

What types of depression do they speficifically treat? [2]

What are their MoAs? [2]

A

Esketamine:
* NMDA glutamate receptor antagonist
* treatment-resistant depression

Brexanolone:
* progesterone-related compound, positive modulator of GABAA receptors
* approved for post-partum depression

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22
Q

Most common AE of SSRI? [1]

A

gastrointestinal symptoms are the most common side-effect:

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23
Q

30% schizophrenic patients do not respond to treatment. Which drug would you provied for those who have drug resistance? [1]

A

Clozapine

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24
Q

Name a risk of clozapine treatment [2]

A

agranulocytosis: increases chance of infection

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25
Non-pharmacological approaches for SCH? [3]
* Cognitive Behavioural Therapy * Cognitive remediation * Family therapy **These do not replace the pharmacological treatment**
26
The drugs used to treat schizophrenia are [] receptor [antagonists / agonists] [2] They can be divided into typical and atypical drug treatments; what are the difference between them?
The drugs used to treat schizophrenia are **D2 (dopamine) receptor antagonists** **Typical**:’ are older and cause generalised dopamine receptor blockade. **Atypical**: are more **selective** in their dopamine blockade and also block **serotonin 5-HT2A receptors**.
27
Atypical antipsychotic drugs target which receptor/s D1 receptors D2 receptors D1 & D2 receptors D1 & 5-HT2 receptors D2 & 5-HT2 receptors
Atypical antipsychotic drugs target which receptor/s D1 receptors D2 receptors D1 & D2 receptors D1 & 5-HT2 receptors **D2 & 5-HT2 receptors**
28
Name 5 typical antipyschotics
**chlorpromazine**, thioridazine, fluphenazine, **haloperidol**, flupenthixol
29
Describe the effect of typical anti-physchotics on positive and negative symptoms [1]
**Improve positive** symptoms Little/no efficacy on **negative symptoms**
30
Clozapine blocks [] receptors with high affinity Aripiprazole is a partial [] at presynaptic D2 receptors but an [] at D2 postsynaptic receptors
**Clozapine** blocks **D4** receptors with high affinity **Aripiprazole** is a partial **agonist** at **presynaptic** **D2** receptors but an **antagonist** at **D2 postsynaptic receptors**
31
Name 6 atypical anti-psychotics used to treat SCH [6]
risperidone, **olanzapine**, **clozapine**, quetiapine, paliperidone, **aripiprazole**
32
Atypical anti-psychotics target which receptors? [2]
Antagonists at: * D2 receptors * 5-HT2A receptors
33
Name 3 extrapyramidal effects that occur due to antipsychotic drugs. [3] Why do these occur? [1]
Extrapyramidal effects (EPS): * **acute dystonias** * **parkinsonism** * **tardive dyskinesia** Approx. **60% D2 receptor occupancy** required for **antipsychotic** efficacy; if **>80% D2 receptors are blocked**, then potential for **EPS**
34
Explain why antipsychotic drugs may cause sexual dysfunction, galactorrhoea or amenorrhoea?
Block dopamine receptors; causes a rise in prolactin
35
Which anti-psychotics can be adminstered by IM injections? [2]
**fluphenazine** decanoate **haloperidol** decanoate
36
Describe the difference in AEs between atypicals and typical anti-pyschotics
**Atypicals** * Less EPS * Less cardiac toxicity (QT segment prolongation) * Less hyperprolactinaemia * Weight gain * Hyperglycaemia, diabetes * Insulin resistance * Dyslipidaemia * Cardiovascular disease **Typicals**: EPS (dystonia, parkinsonism…) Tardive dyskinesia Weight gain QT interval prolongation Sudden death Hyperprolactinaemia
37
Describe the difference in AEs between atypicals and typical anti-pyschotics
**Atypicals** * Less EPS * Less cardiac toxicity (QT segment prolongation) * Less hyperprolactinaemia * Weight gain * Hyperglycaemia, diabetes * Insulin resistance * Dyslipidaemia * Cardiovascular disease **Typicals**: EPS (dystonia, parkinsonism…) Tardive dyskinesia Weight gain QT interval prolongation Sudden death Hyperprolactinaemia
38
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
39
Describe what neuroleptic malignant syndrome is a combination of [6]
Due to typical anti-psychotics hyperpyrexia muscle rigidity tremor confusion autonomic instability
40
Explain what future SCH drug targers are [3]
The NMDA glutamate receptor: * Decreased glutamatergic transmission in SCH- hypoglutamatergic state in cortex * May be possible to potentiate activity of glutamatergic receptors in future
41
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**
42
Label A-E
A: **cingulate gyrus** B: **corpus callosum** C: **fornix** D: **parahippocampal gyrus** E: **subcallosal area**
43
Label A-F
A: **Fornix** B: **Cingulate cortex** C: **Thalamus** D: **Mamilllary body** E: **Hippocampus** F: **Amygdala**
44
Label A-C
A: **Anterior commissure** B: **Amygdala** C: **Hippocampal**
45
Label 14-17
14 Pulvinar of thalamus 15 Mamillary body 16 Optic tract 17 Anterior commissure
46
Label 18-22
18 **Fornix** 19 Longitudinal stria 20 **Dentate gyrus** 21 **Hippocampal** fimbria 22 Pes **hippocampi**
47
What are primary reinforcers?
Gene specified goals for action (for rewarding or punishment) A Primary Reinforcer is a stimulus that is biologically important to an organism, such as food, water, sleep, shelter, safety, pleasure, and sex
48
What is the role of the insula? [1]
Recieves data from cortex and amygdala. Has to make exec **decision** on whether the experience was **worth remembering.**
49
What is this structure? [1]
Nucleus accumbens
50
State the main function of the: Hippocampus [1] Parahippocampal gyrus [1] Amygdala: [1] Septal nucleus [1] Cingulate cortex [1]
**Hippocampus** = Memory acquisition and recall, formation of long-term memory. **Formation of memory** not storage **Parahippocampal gyrus**: storage and conversion of new experiences into memories **Amygdala** = Emotional content of stimuli: fear, anxiety and danger **Septal nucleus** = Pleasure and reward **Cingulate cortex** = Affective significance
51
Describe the route of Papez's circuit
Cingulate cortex --> parahippocampal cortex --> hippocampus --> fornix --> mamillary bodies --> hypothalamus -> anterior thalamus --> cingulate cortex.
52
Name the extremely fast response to an unexpected loud noise in babeies? [1]
**Acoustic startle reflex / Moro reflex**
53
What is the difference in role between anterior and posterior cingulate cortex? [1]
**Anterior cingulate cortex:** * monitors quality of pain continously; activates strategies to remove pain * Evaluates the degree of pain / ppleasure experienced **Posterior cingulate cortex:** * Recalling **emotional memories** - NOT involved in non-emotional memories
54
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**
55
What is 8? Corpus Callosum Hippocampus Subthalamic nuclei Nucleus accumbens Putamen
What is 8? Corpus Callosum Hippocampus Subthalamic nuclei **Nucleus accumbens** Putamen
56
What is 8? Anterior commissure Fornix Lateral ventricle Putamen Nucleus accumbens
What is 8? Anterior commissure **Fornix** Lateral ventricle Putamen Nucleus accumbens
57
What is 5? Hypothalamus Fornix Amygdala Hippocampus Thalamus
What is 5? Hypothalamus Fornix Amygdala **Hippocampus** Thalamus
58
What is 13? Hypothalamus Fornix Amygdala Hippocampus Thalamus
What is 5? Hypothalamus Fornix **Amygdala** Hippocampus Thalamus
59
What is 3? Hypothalamus Fornix Amygdala Hippocampus Thalamus
What is 3? **Hypothalamus** (mamilliary body) Fornix Amygdala Hippocampus Thalamus
60
What is 10? Hypothalamus Fornix Amygdala Hippocampus Thalamus
What is 10? Hypothalamus **Fornix** Amygdala Hippocampus Thalamus
61
Label A-D
A:Cingulate cortex nuclei B: Anterior thalamic C:Mammillary bodies D: hippocampus
62
A firefighter, with a history of traumatic brain injury after falling from a ladder, presents to the clinic for follow-up. He complains of anterograde amnesia ever since the accident. Magnetic resonance imaging reveals damage to the hypothalamic structure involved in memory. What thalamic nucleus receives input from the affected structure? A. Midline nucleus B. Dorsomedial nucleus C. Anterior nucleus D. Lateral dorsal nucleus
A firefighter, with a history of traumatic brain injury after falling from a ladder, presents to the clinic for follow-up. He complains of anterograde amnesia ever since the accident. Magnetic resonance imaging reveals damage to the hypothalamic structure involved in memory. What thalamic nucleus receives input from the affected structure? A. Midline nucleus B. Dorsomedial nucleus C.** Anterior nucleus** D. Lateral dorsal nucleus
63
An MRI of a 56-year-old man shows a lesion in the amygdala. Which relevant pathway involving the amygdala has been proposed as a substrate for the human ability to infer the intentions of others from their language, gaze, and gestures? A. Dorsal route via stria terminalis B. Ventral part via amygdalofugal pathway C. Via the amygdala's connections to the hypothalamus D. The basolateral circuit
An MRI of a 56-year-old man shows a lesion in the amygdala. Which relevant pathway involving the amygdala has been proposed as a substrate for the human ability to infer the intentions of others from their language, gaze, and gestures? A. Dorsal route via stria terminalis B. Ventral part via amygdalofugal pathway C. Via the amygdala's connections to the hypothalamus **D. The basolateral circuit**

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