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Mechanism of Drug Action > Neuropharmacology (Conditions) > Flashcards

Neuropharmacology (Conditions) Flashcards

1
Q

What are the different types of strokes?

A
  1. Occlusion: Caused by blockage of cerebral vasculature due to embolus or atherosclerosis.
  2. Haemorrhage: Haemorrhaging of cerebral vessel increases local pressure, occluding vessels nearby.
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2
Q

What are transient ischaemic attacks (TIAs)?

A

Brief interruption to cerebral blood supply that resolves within 24 hours, followed by full recovery.

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3
Q

What is the anatomy of area of brain affected by stroke?

A
  1. Ischaemic core: Neurones immediately adjacent to occluded vessel die very quickly following occlusion and cannot be saved.
  2. Penumbra: Neurones in region further out from point of occlusion are compromised, but are able to recover after restoration of blood flow
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4
Q

How can strokes be treated?

A
  1. Clot-busting drugs
  2. Hypothermia
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5
Q

How can ischaemia cause raised [Ca2+]i?

A

Direct:

  1. Reduced ATP results in reduced activity of PMCA and SERCA.
  2. Reduced ATP results in reduced activity of Na+/K+-ATPase causing increased [Na+]i and reducing activity of NCX.

Indirect (excitotoxicity):

  1. Release of Glu from pre-synaptic cells causes opening of NMDA channels resulting in Ca2+ influx.
  2. mGluRs activate IP3 that cause release of intracellular Ca2+.
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6
Q

How can toxicity be caused by raised [Ca2+]i?

A
  1. Activation of intracellular enzymes that cause direct cell damage, including:
    - Proteases: Cytoskeleton breakdown
    - Lipases: PLA breaks down membrane phospholipids
    - NOS
  2. Activation of caspases that drive apoptosis
  3. Production of free radicals that cause protein/DNA damage that drive apoptosis/necrosis
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7
Q

Aside from Ca2+, what are the other mechanism that can cause damage during stroke?

A
  1. Zn2+ neurotoxicity: Zn2+ in NT vesicles is released during ischaemia and causes toxicity
  2. Inflammation
  3. Ischaemic reperfusion injury
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8
Q

What are the ways in which nerve death due to ischaemia can be reduced?

A
  1. NMDA receptor antagonists
  2. Glycine receptor antagonists
  3. Free radical scavengers
  4. Anti-inflammatory compounds
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9
Q

What are the types of anxiety disorders?

A
  1. Phobias
  2. Panic disorders
  3. Post traumatic stress disorders (PTSDs)
  4. General anxiety disorders
  5. Obsessive compulsive disorders
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10
Q

What are the risk factors for insomnia?

A
  1. Stress
  2. Ageing
  3. Shift work
  4. Drug/alcohol abuse
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11
Q

What is the likely cause of narcolepsy?

A

Destruction of hypothalamic neurones producing orexin, which promotes wakefulness.

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12
Q

What are the types of epileptic seizures?

A
  1. Generalised seizures: Involvement of both hemispheres. There are 2 variants:
    - Non-convulsive
    - Convulsive
  2. Simple seizures: No effect on consciousness or memory
  3. Complex seizures: Loss of consciousness or memory
  4. Status epilepticus: Seizure lasting more than 5 minutes
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13
Q

What are the types of convulsive seizures?

A
  1. Tonic: Rigidity of extremities
  2. Clonic: Jerking of extremities
  3. Tonic-clonic (grand mal): Tonic followed by clonic
  4. Myoclonic: Bilateral jerking of specific muscle group bilaterally
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14
Q

What are the types of non-convulsive seizures?

A

Absence seizure (petite mal)

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15
Q

What is the pathophysiology of absence seizures?

A
  1. Activation of T-type Cavs in thalamocortical neurones causes activation of neurones.
  2. Thalamocortical neurones stimulate cortex and reticular thalamic nucleus.
  3. After period of time, T-type Cavs in thalamocortial neurones inactivate.
  4. GABA neurones from reticular thalamic nucleus inhibit thalamocortical neurones and causes re-activation of Cavs.
  5. Cycle continues
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16
Q

What are the negative effects of taking anti-epileptics in women specifically?

A
  1. Some anti-epileptics induce Cyp3A4 and so enhance metabolism of oral contraceptives
  2. Some anti-epileptics are teratogenic
  3. Some anti-epileptics may cause vitamin K deficiency in newborn
17
Q

Why should MAOIs and SSRIs not be used in combination?

A

Causes dangerous rise in levels of 5-HT to cause:

  1. Confusion
  2. Dizziness
  3. Hyperthermia
18
Q

What evidence is there to support involvement of dopamine in Schizophrenia?

A
  1. There is strong correlation between affinity of antipsychotic drugs for D2 receptor and effective dose
  2. D2 antagonists relieve positive symptoms
  3. Increased levels of dopamine by amphetamines/L-DOPA causes Schizophrenia-like symptoms
19
Q

What evidence is there against involvement of dopamine in Schizophrenia?

A
  1. D2 antagonism by antipsychotics is fast but their effects are slow to manifest
  2. D2 antagonists are less effective against negative symptoms
  3. Antipsychotic drugs don’t work on all schizophrenics
20
Q

What evidence is there to support involvement of Glu in Schizophrenia?

A
  1. NMDA receptor antagonists produce psychosis.
  2. Patients with schizophrenia have lower levels of Glu receptors in brain
21
Q

What evidence is there to support involvement of 5-HT in schizophrenia?

A

Agonists of 5-HT receptors cause psychosis (e.g. LSD is agonist for 5-HT2A)

22
Q

What are examples of typical (1st generation) anti-psychotics?

A
  1. Chlorpromazine
  2. Haloperidol
23
Q

What is the main side effect of typical anti-psychotics?

A

Extrapyramidal motor (Parkinson-like) side effects

24
Q

What are examples of atypical (2nd generation) anti-psychotics?

A
  1. Clozapine
  2. Risperidone
  3. Olanzapine
25
Q

What is the main side effect of atypical anti-psychotics?

A

Metabolic side effects (e.g. weight gain, type II diabetes)

26
Q

What causes Alzheimer’ disease?

A

Formation of amyloid plaques extracellularly and neurofibrillary tangles (NFT) intracellularly disrupts function of neurones

27
Q

How does plaque formation in Alzheimer’s disease occur?

A
  1. Amyloid precursor protein (APP) is cleaved by β-secretase (instead of usual α-secretase to give soluble APP)
  2. Intermediate then cleaved by γ-secretase to give β-amyloid 40/42 that aggregate to form plaques
28
Q

What is the general strategy for treatment of Alzheimer’s?

A

Cholinergic neurones in the basal forebrain are vulnerable to degeneration in Alzheimer’s and mediate memory. Improving cholinergic transmission may improve symptoms of Alzheimer’s.

Mechanism of Drug Action (28 decks)

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