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NEUR1005 > CNS disorders (Prof. Dickenson) > Flashcards

CNS disorders (Prof. Dickenson) Flashcards

1
Q

What CNS disorders are linked to an increase in CNS fct ?

A
  • Pain
  • Epilepsy
  • Anxiety
  • Schizoprenia +ve symptoms
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2
Q

What CNS disorders are linked to decreased CNS activity ?

A
  • Depression
  • Parkinson’s
  • Alzheimer’s
  • Schizoprenia -ve symptoms
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3
Q

Do we have knwon treatments for:

  • strokes ?
  • PD ?
  • AD ?
A
  • Strokes: could be anywhere
  • PD –> known pathway, DA treatable
  • AD –> known regions, ACh but poorly controlled
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4
Q

What are the 4 steps of the life of a NT ?

A
  1. Synthesis
  2. Release
  3. Effects
  4. Removal
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5
Q

How could epilepsy be treated ?

A
  • Epilepsy = excess activity –> need to restore balance
  • Increase inhibition (GABA)
  • Reduce excitation –> block ion channels (NA+ and Ca2+), block Glu receptors etc.
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6
Q

How could pain be treated ?

A
  • Pain = excess activity
  • Increase inhibition –> opioids
  • Reduce excitation –> block ion channels / Glu receptors / peripheral pain mediators (prostoglandins) etc.
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7
Q

How could PD be treated ?

A

Add L-DOPA (=DA precursor) or a DA2R agonist + prevent DA breakdown:

  • Selegiline –> blocks DA breakdown in the CNS
  • Carbidopa –> blocks L-DOPA breakdown outside the CNS
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8
Q

How could depression be treated ?

A

Block reuptake of excitatory NTS.

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9
Q

How could Schizophrenia be treated ?

A

Add a DA antagonist (+ Glu agonist ?)

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10
Q

How do cocaine and NMDA work ?

A

By blocking excitatory NT reuptake.

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11
Q

How do heroin, nictotine, cannabis and LSD work ?

A

Mainly on post-synaptic inhibitory receptors.

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12
Q

What are the problems w/ CNS drug therapy ?

A
  • Multiple receptors for NTs
  • Actions at multiple sites
  • Receptor up/down regulation to drugs
  • Blood brain barrier
  • Long term changes
  • Co-existence of NTs
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13
Q

What are the symptoms of epilepsy ?

A
  • Generalized seizures
  • Partial seizures
  • Absence seizures
  • Movement
  • Stiffness
  • Jerking
  • Consciousness
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14
Q

What causes epilepsy ?

Which drugs could be used treat it ?

A

Abnormal activity (excess excitation + lack of inhibition) in parts of the brain that control mvnt.
Enhancing inhibition:
Barbiturates –> phenobarbital: Cl- channel open
Benzodiazepines –> diazepam: modulates R, blocks GABA uptake/breakdown
Reducing excitation:
Na channel blockers –> carbamazepine, phenytoin
Ca channel blockers –> gabapentin

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15
Q

What is the main risks associated w/ epileptic drug therapy ?

A

Sedation.

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16
Q

What are the different (negative) forms that anxiety can take ?

A
  • Panic
  • Phobias
  • Obsessive-compulsive disorders
  • Post-traumatic stress
17
Q

How can anxiety be treated ?

A
  • Enhance GABA-A fct –> benzodiazepines

- enhance 5-HT inhibitory fct –> buspirone

18
Q

What are the symptoms of Schizophrenia ?

What causes this symptoms ?

A

Agitation, paranoia, hallucinations, delusions, withdrawal, poverty of speech,catatonia
Comes from an excess of DA

19
Q

How could Schizophrenia be treated ?

A

Reducing DA fct:

  • DA 2 receptor blockers –> chlorpromazine
  • clozapine –> 5-HT also ?
20
Q

What are the risks of Schizophrenia drug therapies ?

A

Motor disorders, sedation, flatness of mood, and may trigger PD like effects…

21
Q

What are the symptoms of PD ?

What is the cause of the disease ?

A

Motor disorder: tremor, rigidity.

Reduced DA fct.

22
Q

What are the risks of PD drugs therapies ?

A

They can cause nausea and psychosis.

23
Q

What are the symptoms of AD ?

A
  • Loss of neurons (Amyloid-beta plaques, neurofibrillary tangles)
  • Loss of memory
  • Cognition
  • Loss of comprehension
  • Speech disorders
  • Agitation
24
Q

What is the issue w/ ACh treatments in AD ?

A

Tachrine blocks AChesterases (AChE).

But these drugs affects NM and autonomic fcts as well.

25
Q

What are the 3 major affective disorders ?

A

Major depression (endogenous), bipolar disorder and mania.

26
Q

What are the symptoms of depression ?

A

Mood disorders: withdrawal, no drive, flatness,

lack of interest, fatigue, worthlessness etc.

27
Q

What are the causes of depression ?

How could it be cured ?

A

Reduced NA and 5-HT fct, leads to altered cortical processing.
Treatment –> increase NA + 5-HT activity –> block their reuptake or breakdown;
- fluoxetine = SSRI
- amytryptiline = TCA (Tricyclic Antidepressant) and SNRI, blocks reuptake of 5-HT (strongly) and NA (moderately)

28
Q

How does morphine work ?
Why do we have morphine receptors ?
Where are these located ?

A

Morphine acts on inhibitory MORs in the spinal cord and midbrain to block NT release, reduce sensory neuron activity and switch on descending inhibitions.
The receptor is present for the endogenous opioid peptides NTs. These are located in the brain and spinal chord.

29
Q

How do aspirin and ibuprofen work ?

A

Inhibition of prostoglandins/prostanoids (periphery).

30
Q

How does Lidocaine work ?

A

By blocking Na+ channels (periphery).

31
Q

What are the relative roles of the limbic system and cortex in pain experience ?

A

Limbic system: fear and aversion

Cortex: localization and intensity

32
Q

How do antidepresants work ?

A

By increasing levels of NA and 5-HT and switching on descending inhibitions.

33
Q

What are the side effects of morphine ?

A
  • Respiratory depression
  • Anti-cough
  • Sleep
  • Constipation - peripheral
  • Nausea and vomiting
  • Dependence
34
Q

What is the most common morphine antagonist used for clinical purposes ?

A

Naloxone.

35
Q

How can CNS therapies overlap ?

A

Ca2+ channel modulation: pain, epilepsy and anxiety
Na+ channel blockers: pain and epilepsy
Antidepressants 5-HT and NA: anxiety and depression

36
Q

How do genes play an important role in CNS disorders ?

A
  • Can be induced/suppressed by NTs
  • Ca2+ influx –> NMDA R as example
  • Mouse strains –> anxiety, pain, epilepsy
  • Genes for R, enzymes, transporters
  • Basis for individual differences
  • Protect or predispose
  • Ca2+ channel mutation –> migraine
  • Na+ channel mutation –> pain
  • GABA neurones - Huntingdon’s Chorea

NEUR1005 (31 decks)

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