Biochem- Neuropsychiatric Disorders Flashcards

1
Q

Which receptor does the antibodies target in myasthenia gravis?

A

NmAchR

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2
Q

Which subunit of the NmAchR does the antibodies target in Myasthenia Gravis?

A

α1-subunit

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3
Q

In Huntingtons, there is an excess release of which NT?

A

Glutamate

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4
Q

The excess glutamate in Huntingtons causes the binding of which receptor?

A

NMDA

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5
Q

The excess binding of the NMDA receptor causes a toxic influx of which ion?

A

Ca++

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6
Q

The excess Ca++ causes what in the nerve cell?

A

intracellular Ca++ activates nucleases, proteases and phospholipases –> cell death

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7
Q

How can strokes lead to cellular death by Ca++?

A

Ischemia from blockage or hemorrhage triggers glutamate release from oxygen-starved neurons –> toxic levels of Ca++ enter through the NMDA receptor –> this causes exocytosis of additional glutamate from the NMDA stimulated neuron (amplification) –> intracellular Ca++ activates nucleases, proteases and phospholipases –> cell death

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8
Q

The excess Ca++ in strokes causes the release of which 2 factors which worsens the disease?

A

platelet-activating factor and the release of arachidonic acid, which causes vasoconstriction, and thus worsens the thrombosis.

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9
Q

There is a degeneratiuon of which part of the brain in Parkinsons?

A

substantia nigra

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10
Q

Death of the substantia nigra causes a decreasse in which NT?

A

Dopamine

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11
Q

A decrease in DA causes an increase in what other NT?

A

Ach

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12
Q

To treat parkinsons, which drug(s) do you need?

A. Dopamine
B. L-Dopa
C. L-Dopa + carbidopa
D. Physostigmine + L-Dopa
E. Red red winnneeeeee. stay close to meeeeeee.
A

C. L-Dopa and carbidopa

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13
Q

Why do you need Carbidopa in addition to the L-dopa?

A

Otherwise L-dopa would be rapidly degraded by dopa decarboxylase in the periphery before it passes the BBB

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14
Q

Does carbidopa pass the BBB with L-dopa?

A

No.

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15
Q

What forms in the cortex and hippocampus in Alzheimers pts?

A

Amyloid plaques

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16
Q

What are amyloid plaques made of?

A

a clump of amyloid beta peptides (AbP)

17
Q

Where are AbP’s derived from?

A

the proteolysis of amyloid precursor protein (APP)

18
Q

What happens in neurofibillary tangles?

A

the helical filament stabilizer tau is modified, which tangles and kills the cell

19
Q

How can AbP plaques cause excessive Ca++ stimulation?

A

AbP plaques are insoluble in the extracellular space where it is made from APP. It can therefore stimulate excessive Ca++, leading to the activation of protein kinases, induced phosphorylation of tau, and eventually cell death. AbP is therefore neurotoxic (kinda like glutamate for Huntingtons)!

Really good video: https://www.youtube.com/watch?v=NjgBnx1jVIU

20
Q

Genereally, what happens with dopamine in schizophrenia?

A

there is evidence for excess dopamine production in schizophrenia by an icnrease in D2 activity