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Pharmacology > Neuropharmacology > Flashcards

Neuropharmacology Flashcards

1
Q

Why is neuronal death an important event?

A

There is limited capacity for neurons to divide and re-establish synaptic contacts

Death produces largely irreversible changes in brain function

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2
Q

Common neurodegenerative conditions

A

Alzheimer’s

Parkinson’s

Huntington’s

Motor neuron diseases

Creutzfeld-Jakob disease

Acute brain ischaemia and stroke

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3
Q

Mechanisms underlying neurodegeneration

A

Excitotoxicity

Oxidative stress

Apoptosis

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4
Q

What is the main mechanism of excitotoxicity?

A

Glutamate-induced excitotoxicity

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5
Q

What is the main ion causing the damage seen in glutamate-induced excitotoxicity?

A

Calcium

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6
Q

Describe what happens following the excitation of glutamatergic neurons

A
  1. Glutamate activates AMP receptors, depolarising the plasma
  2. This leads to the opening of voltage-dependent calcium channels and unblocks NMDA channels
  3. Stimulation of NMDA receptors allows Ca2+ influx
  4. Stimulation of metabotropic receptors activates PLC which releases Ca2+ from the ER
  5. Cell membrane Na+/Ca2+ exchange further increases Ca2+ concentration
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7
Q

How does calcium lead to excitotoxicity?

A

The increase in Ca2+ concentration leads to activation of Ca2+-dependent enzymes

These cause degradation of proteins and membrane damage

Overloading of the mitochondria with Ca2+ interferes with their function

Leading to ROS production

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8
Q

What is another consequence of mitochondrial damage in glutamatergic neurons?

A

The malfunction of mitochondria following Ca2+ overloading means that the production of ATP decreases

There isn’t enough energy available for the pumps to work, so the mechanisms for increasing [Ca2+] become unopposed

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9
Q

Which molecules prevent elevations in ROS?

A

Anti-oxidants

These defense mechanisms are overwhelmed in neurodegenerative conditions

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10
Q

What are most potential drug targets aimed at in neurodegenerative disorders?

A

Calcium entry

Intracellular protease activation

Free radical damage

Inflammatory response

Membrane repair

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11
Q

Pathological mechanisms behind stroke

A

Brain ischaemia leads to rapid cell death in the hypoxic area

Followed by neurodegeneration in the adjacent areas

This leads to depolarisation in neurons, causing a release of glutamate

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12
Q

What drugs can help the prognosis of stroke?

A

Fibrinolytic drugs given at the correct time

Can improve blood flow and reduce further damage

Dependent on the stroke being thrombic, not haemorrhagic

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13
Q

Characteristics of Parkinson’s disease

A

Tremor at rest

Muscle rigidity

Difficult performing voluntary movements

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14
Q

An imbalance in which neurons is an important factor in PD?

A

Dopaminergic and cholinergic fibres of the striatum

Loss of dopamingergic fibres in the nigrostriatal pathway is coupled with an excessive activity of cholinergic fibres of the striatum

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15
Q

What causes the damage to nigrostriatal dopaminergic neurons in PD?

A

Excitotoxicity

Oxidative stress

Apoptosis

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16
Q

Common treatments of Parkinson’s

A

Levodopa

Dopamine receptor agonists

Amatidine

Muscarinic antagonists

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17
Q

What is main treatment for Parkinson’s?

A

Levodopa

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18
Q

Mechanism of action of Levodopa

A

Increases the concentration of dopamine in the basal ganglia

Given with carbidopa to prevent the systemic effects of dopamine

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19
Q

When does Levodopa work best?

A

When coupled with MAO-B or COMT inhibitors

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20
Q

Example of a MAO-B inhibitor

A

Selegiline

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21
Q

Example of a COMT inhibitor

A

Entacapone

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22
Q

Unwanted effects of Levodopa

A

Acute schizophrenia-like syndrome linked to increased dopamine concentration

Disorientation

Insomnia

Nightmares

23
Q

What is carbidopa?

A

A DOPA decarboxylase inhibitor

24
Q

When are dopamine agonists used?

A

In adjuncts to Levodopa

25
Q

Peripheral side effects of Levodopa

A

Postural hypotension

Nausea

26
Q

Mechanism of action of Amitidine

A

Antiviral agent

Increases neural release of dopamine

27
Q

Mechanism of action of muscarinic antagonists

A

Decreases the characteristic tremor in PD patients

28
Q

Side effects of Muscarinic antagonists

A

Sedation

Confusion

29
Q

What is Alzheimer’s?

A

Age-related dementia

30
Q

What is Alzheimer’s associated with?

A

Loss of neurons

Shrinkage of the brain tissue

31
Q

Underlying pathological mechanism behind Alzheimer’s

A

Amyloid plaques

Tau tangles

32
Q

The loss of which neurons are thought to be a key factor in Alzheimer’s?

A

Cholinergic receptors

33
Q

Drugs used in Alzheimer’s

A

Anticholinesterases

NMDA antagonists

34
Q

What is epilepsy?

A

Condition where intermittent high-frequency firing of a localised group of cerebral neurons cause seizures

Discharge can remain localised or spread to other regions of the brain

35
Q

What are the two types of seizures?

A

Partial seizures - abnormal discharge is localised to a relevant area

General seizures

36
Q

Example of partial seizures

A

Jerking of a limb

Complex behavioural change

37
Q

Is there loss of consciousness in partial seizures?

A

No

38
Q

What are the two major forms of general seizures?

A

Tonic-clonic or grand mal epilepsy

Petit mal epilepsy

39
Q

Describe grand mal epilepsy

A

Initial tonic convulsion followed by jerking of the whole body

Accompanied by sudden loss of consciousness

40
Q

Describe petit mal epilepsy

A

Episodic loss of consciousness

Otherwise known as absence seizures

41
Q

What is status epilepticus?

A

When generalised convulsions follow each other without consciousness being regained

Medical emergency

42
Q

How many patients respond well to antiepileptic drugs?

A

75%

43
Q

Why do antiepileptic drugs need to have as few side-effects as possible?

A

The drugs need to be taken lifelong

The fewer the side-effects, the better

44
Q

What are the three main mechanisms by which anti-epileptics work?

A

Inhibition of action potential generation through Na+ channels or T-type Ca2+ channel block

Enhancement of GABAergic transmission

Reduction of glutamatergic transmission

45
Q

Why is blocking Na+ and T-type Ca2+ channels an effective therapy for epilepsy?

A

Reduces the influx of positive ions into the cell, reducing the depolarisation of the neurons

Reduces the release of neurotransmitters from the presynaptic membrane

Reduces the propagation of the action potential in the post-synaptic membrane

46
Q

Targets on the neurons that reduce depolarisation

A

Na+ channels

Ca2+ channels

NMDA receptors

AMPA receptors

GABA receptors

47
Q

Targets on the neurons that reduce neurotransmitter release

A

Ca2+ channels

Na+ channels

48
Q

Mechanism of action of Carbamezapine

A

Binds to inactivated Na+ channels (hyperpolarisation)

Preventing them from returning to a normal state to allow for further action potential generation

49
Q

Unwanted effects of Carbamezapine

A

Narrow therapeutic index

  • Vertigo
  • Confusion
  • Sedation
50
Q

Mechanism of action of Ethosuximide

A

Inhibits T-type Ca2+ channels

51
Q

For which type of epilepsy is Ethosuximide prescribed for?

A

Used only for absence seizures

52
Q

Mechanism of action of Valproate

A

Increases GABA concentration in the brain through blocking the enzyme that degrades it pre-synaptically

53
Q

Mechanism of action of Benzodiazepine

A

Increases opening of GABA channels

Allows more Cl- to enter the cell

Hyperpolarising the cell

54
Q

Characteristic of newer antiepileptics

A

Can affect all types of epilepsy

Pharmacology (13 decks)

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