Neuropharmacology Flashcards

1
Q

which part of the brain is affected by parkinsons? [1]

what do they have a deficit in? [1]

A

which part of the brain is affected by parkinsons? [1]
substantia nigra: produces dopamine (get a dopamine deficit)

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2
Q

what type of NT is dopamine? [1]

A

what type of NT is dopamine? [1]
monamine

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3
Q

what are potential treatment options for parkinson? [2]

why are they problematic? [2]

A

what are potential treatment options for parkinson? [2]
provide deficient dopamine
provide precursor L-Dopa

why are they problematic? [2]
dopamine cannot reach the brain !! :(
L-Dopa gets converted to dopamine outside of the brain (
also triggers vomiting lol)

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4
Q

what are two ways could treat / target parkinsons?

A

provide L-Dopa, but combine a peripheral inhibitor of the enzyme (L-aromatic amino acid decarboxylase) which doesnt have access to the brain: therefore L-Dopa is converted into dopamine only in the brain

OR

stimulate dopamine receptors with dopamine receptor agonists

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5
Q

what causes schizophrenia? [1]

what do schizophrenia drugs target? [1]

what is a problem with them? [1]

A

what causes schizophrenia? [1]
increased release of dopamine (hyperactivtity in the ventral striatum)

what do schizophrenia drugs target?
dopamine receptors: drugs are dopamine receptor antagonists

what is a problem with them? [1]
not very specific - causes AES

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6
Q

what can be adverse of antipyschotic drugs? (anti-schizophrenia) [4]

A

extrapyramdal effects (e.g. parkisnons):

  • rise in prolactin: breast enlargement & weight gain
  • allergic and toxic reactions
  • postural hypotension
  • anticholinergic effects (dry mouth)

all a consequence of the lack of specifity

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7
Q

depression is caused by a lack of ? [2]

what is treatment goal for treating depression?

A

depression is caused by a lack of ? [2]
serotonin & noradrenaline

what is treatment goal for treating depression?
inhibitors of transport / reuptake of monoamines

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8
Q

tricyclic are antidepressants that inhibit the reuptake of monoamines such as serotonin & noradrelanie.

However, they also cause AEs. What & Why?

A
  • have an affinity of binding to histamine H1 r, musc. cholinergic Rs, alpha 1 & 2 adrenoreceptors:
    a) dry mouth, loss of libido, blurred vision, constipation, weight gain, postural hypotension

also many patients dont like them !!

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9
Q
A
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10
Q

why might someone be resistant to antidepressant treatment ? [1]

A

genetic variations in drug transporters: e.g. ABCB1

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11
Q

why is treating addiction tricky? [3]

is it a single or multi target? [1]

A

drug treatments need to treat withdrawal of drugs of abuse too (but really hard!)
addiction changes the brain;
if multiple drugs of abuse = multiple changes to brain

is it a single or multi target? [1]
multi!

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12
Q

which of the following inhibits uptake of monoamines?

ketamine
cocaine
heroin
nicotine
ecstasy

A

which of the following inhibits uptake of monoamines?

ketamine
cocaine
heroin
nicotine
ecstasy

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13
Q

which of the following increases release of monoamines?

ketamine
cocaine
heroin
nicotine
ecstasy

A

which of the following increases release of monoamines?

ketamine
cocaine
heroin
nicotine
ecstasy

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14
Q

how can you treat:

heroin? [1]

cocaine? [1]

nicotine? [1]

alchohol [1]

A

how can you treat:

heroin? [1]
methadone (sub)

cocaine? [1]
cant really - antibodies agaisnt cocain in the future

nicotine? [1]
nicotine replacment

​alchohol [1]
disulifiram (makes u nauseaus after alchohol consumption)

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15
Q

what does the effectiveness of treating neurological pathologies depend on? [1]

how is this achieved/ [1]

A

what does the effectiveness of treating neurological pathologies depend on? [1]
needs to pass BBB

​how is this achieved? [1]
drug solubility in lipids - essential for crossing membranes

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16
Q

why may drug targets in the CNS may never be reached? [2]

A

intrinsic or acquired overexpression of multidrug transporters at the BBB restricts up take of drugs (e.g. ABC family - ATP binding cassette)

drug efflux is mediated by these transporters (drug is pumped out = drug resistance)

17
Q

how do you get over drug efflux as a cause of drug resistance? [1]

A

block the expression / activity of such transports

18
Q

which of the following are substrates for ABC transporters, which typically undergo drug efflux and restricts the brains uptake of drugs?

anti-deppresive
anti-addictive
anti-schizophrenic
anti-epileptic
anti-parkinson

A

which of the following are substrates for ABC transporters, which typically undergo drug efflux and restricts the brains uptake of drugs?

anti-deppresive
anti-addictive
anti-schizophrenic
anti-epileptic
anti-parkinson

19
Q

which is the largest dural fold (septa)?

falx cerebri
tentorium cerebelli
tentorial notch
falx cerebelli
infundibulum

A

which is the largest dural fold (septa)?

falx cerebri
tentorium cerebelli
tentorial notch
falx cerebelli
infundibulum

20
Q

which of the following is a gap through which the brainstem and blood vessels pass to enter the middle cranial fossa?

falx cerebri
tentorium cerebelli
tentorial notch
falx cerebelli
infundibulum

A

which of the following is a gap through which the brainstem and blood vessels pass to enter the middle cranial fossa?

falx cerebri
tentorium cerebelli
tentorial notch
falx cerebelli
infundibulum

21
Q

which of the following covers the posterior fossa structures (hindbrain) and supports the temporal and occipital lobes.

falx cerebri
tentorium cerebelli
tentorial notch
falx cerebelli
infundibulum

A

which of the following covers the posterior fossa structures (hindbrain) and supports the temporal and occipital lobes.

falx cerebri
tentorium cerebelli
tentorial notch
falx cerebelli
infundibulum

22
Q
A
23
Q

MESS:

what are the main motor symptoms of parkinsons? [5]

A

Resting Tremor

Bradykinesia

Rigidity

Frozen facial expression

Postural changes

Altered gait

Difficulty in starting and stopping movement

24
Q
A
25
Q

MESS:

* what are the role of basal ganglia? [3] *

A

Motor Program switching

Inhibit antagonistic and unnecessary movement

Role in attention and cognition

26
Q

what is normal function of substancia nigra releasing dopamine?

A

Substancia Nigra releases dopamine (DA)

Dopamine binds to Receptors in the striatum of the basal ganglia

Direct pathway – D1 receptors

Indirect pathway – D2 receptor

27
Q

MESS Questions:

  1. Which neurotransmitter is associated with Parkinson’s?
  2. What are the 3 main motor symptoms of Parkinson’s disease?
  3. Which area of the brain degenerates in Parkinson’s
  4. Treatments of Parkinson’s?
A
  1. Which neurotransmitter is associated with Parkinson’s?
    * *Dopamine**
  2. What are the 3 main motor symptoms of Parkinson’s disease?
    * *Resting Tremor, Bradykinesia, Rigidity**
  3. Which area of the brain degenerates in Parkinson’s
    * *substantia nigra pars compacta**
  4. Treatments of Parkinson’s?
    * *L-dopa + Dopa decarboxylase inhibitor or dopamine agonist**
28
Q

MESS questions:

  1. Schizophrenia occurs because of an excess of which neurotransmitter?
  2. Name 2 side effects of antipsychotics
A
  1. Schizophrenia occurs because of an excess of which neurotransmitter?
    * *Dopamine**
  2. Name 2 side effects of antipsychotics
    * *Extrapyramidal effects – acute dystonia, parkinsonism’s, tardive dyskinesia. Hyperprolactinaemia**
29
Q
  1. Which 2 neurotransmitters are associated with depression ?
  2. What is the mechanism of action of TCAs?
  3. Why do they have more side effects than SSRIs
A
  1. Which 2 neurotransmitters are associated with depression
    * *Low level of noradrenaline and serotonin at the level of receptor**
  2. What is the mechanism of action of TCAs
    * *Antagonise noradrenaline and serotonin reuptake**
  3. Why do they have more side effects than SSRIs
    * *TCAs also inhibit H1, muscarinic and alpha adreno receptors. SSRIs more specific to serotonin receptors**
30
Q

Mechanism of action of cocaine and ecstasy?

What is the MOA of disulfiram and how would you classify this therapy?

A

Mechanism of action of cocaine and ecstasy?
Ecstasy – increases release of monoamines
Cocaine – inhibits reuptake of monoamines

What is the MOA of disulfiram and how would you classify this therapy?

Aversion therapy
Inhibit aldehyde dehydrogenase – build up of acetaldehyde