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

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

25
MESS: \* what are the role of basal ganglia? [3] \*
Motor Program switching Inhibit antagonistic and unnecessary movement Role in attention and cognition
26
what is normal function of substancia nigra releasing dopamine?
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
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?
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
MESS questions: 6. Schizophrenia occurs because of an excess of which neurotransmitter? 7. Name 2 side effects of antipsychotics
6. Schizophrenia occurs because of an excess of which neurotransmitter? * *Dopamine** 7. Name 2 side effects of antipsychotics * *Extrapyramidal effects – acute dystonia, parkinsonism's, tardive dyskinesia. Hyperprolactinaemia**
29
8. Which 2 neurotransmitters are associated with depression ? 9. What is the mechanism of action of TCAs? 10. Why do they have more side effects than SSRIs
8. Which 2 neurotransmitters are associated with depression * *Low level of noradrenaline and serotonin at the level of receptor** 9. What is the mechanism of action of TCAs * *Antagonise noradrenaline and serotonin reuptake** 10. 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
Mechanism of action of cocaine and ecstasy? What is the MOA of disulfiram and how would you classify this therapy?
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**