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Clinical Neurology > Biochem- Neuropsychiatric disorders > Flashcards

Biochem- Neuropsychiatric disorders Flashcards

1
Q

What are the major clinical findings in myastenia gravis?

A
  • drooping eyelid
  • trouble swallowing
  • fatigue
  • blurred vision

**-recurrent muscle weakness ofter exercise **

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2
Q

Are men or women affected more by MG?

A

Women (3:2)

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3
Q

What nerves are chiefly affected? What is the treatment?

A
  • CN
  • Achestylcholinesterase inhibitors
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4
Q

Most cases of MG have serum antibodies against what?

A

N1 acetylchline receptors

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5
Q

What is the form of MG with antibodies against the E subunit? How about the gamma subunit?

A
  • slow channel syndrome
  • Neonatal MG (transient)
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6
Q

What drug is typicall used to test for MG?

A

Edrophonium: a short acting AChEi

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7
Q

What is Diisopropylflurophophate?

A

-an irreversible AChEi (toxic nerve gas)

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8
Q

Wha are some of the major symtoms of huntington disease?

A
  • Choreatic movements
  • death of certain neurons
  • Death ~15 years after onset
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9
Q

What is the genetic dominance of huntington disease?

A

Autosomal dominant

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10
Q

Neurons in the _____ ______ die and are replaced by _____ ______ in huntington disease.

A
  • Corpus striatum
  • Glial cells
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11
Q

A gene on chromosome __ encodes for a protein called _________. A repeat of ____ in this gene results in huntington disease.

A
  • 4
  • huntingtin
  • CAG trinucleotide
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12
Q

Huntington disease displays _______, which means that subsequent generations contract the illness at a younger and younger age.

A

Anticipation

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13
Q

The altered gene product huntintin results inthe excess release of what excitatory NT?

A

Glutamate

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14
Q

What are the five important excitatory channels stimulated by the exces glutamate?

A
  • NMDA
  • AMPA
  • Kainate
  • L-AP4
  • metabotropic

***the first four are cationic channels, the fifth stimulates the increase of IP3 and DAG which then stimulates cationic channels***

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15
Q

What kind of toxin is glutamate known as?

A

-Excitotoxin

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16
Q

What is the major treatment for the control of huntington disease?

A

-Bezodiazepines which increase GABA and reduce the choratic movements and seizures.

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17
Q

What is the role of glutamate in a stroke patient?

A

Induction

  • Ischemia causes **glutamate to be released from oxygen starved neurons **
  • Glutamate binds to NMDA
  • This causes a release of calcium to toxic levels

_Amplification _

-This continues as intracellular calcium causes the release of gutamate from the NMDA stimulated cell which contiues on to excite another neuron.

_Expression _

-activation of Ca dependant nucleases, proteases and phospholipase causes degrdation of cell components and death

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18
Q

How does the expression step of glutamate excitotoxicity further cause ischemic damage?

A

Degrdation of phopholipids leads to the formation of platelet-activating factor** and the release of **arachdonic acid

–>both cause vasoconstriction, worsening the thrombosis

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19
Q

How does the production of arachadonic acid in glutamate excitotoxicity lead to more cell damage?

A

-Arachdonic acid metabolism to eicosanoids lead to the production of free oxygen radicals which damage cell components further

20
Q

What is the siginificance of GABA receptors in alcohold withdrawl?

A

-Overactivation of GABAA receptors can lead to down regulation resulting in seizures.

21
Q

What are some characteristic signs of parkingson disease?

A

Tremors

Bradykinesia

Rigitidy

22
Q

Degeneration of the ____ _____ and the _____ _____ results in parkinson disease.

A
  • Substantia Nigra
  • Corpus Striatum
23
Q

Decreased levels of _____ and increased levels of _____ are observed in parkinson disease>

A
  • Dopamine
  • Acetylcholine
24
Q

After a loss of ____-____% of nigral cells, symtons of parkinson disease appear.

A

-80-90%

25
Q

What histological abnormaility is seen in the SN of parkinson patients?

A

Lewy Bodies

26
Q

What are the six steps in the dopamine pathway?

A
  1. sythesized from tyrosine
  2. stored in vesicles
  3. released via exoxytosis
  4. Binds to one of 5 receptors
  5. Reuptake by ATP transporter
  6. Degraded in the synaptic cleft of after reuptake by MAOB–> homovanillic acid
27
Q

What are the three treatment stratagies to managing parkinson disease?

A
  1. Increase the synthesis of dopamine by giving L-DOPA
  2. Block the degredation of dopamine
  3. Use dopamine receptor agonists
28
Q

Why is L-DOPA given as a treatment and not straight dopamine on the rocks?

A

L-DOPA can cross the BBB

29
Q

What two classes of drugs are used to block the degradation of dopamine?

A
  • MAO-Is
  • COMT-Is

Both work to increase the dopamine concentration in the synaptic cleft

30
Q

What is the name of a dopamine receptor agonist?

A

Bromocriptine

31
Q

What are the names of the two MAO-Is that are important?

A
  • Deprnyl
  • Selegiline

(if you don’t take your MAOI you will be in deep shit)

32
Q

Is there an identified genetic component to parkinson disease?

A

NO

33
Q

What is a dug that can exacerbate parkinson disease by inhibiting dopamine storage?

A

Reserpine

34
Q

What is a neurotoxin that can destroy dopamine secreting cells?

A

Street heroin–> MPTP

35
Q

Do MAO-Is potect against MPTP damage? What is the significance?

A

Yes. Can prevent future progession of PD.

36
Q

Why is it good to give cabidopa with L-Dopa in the treatment of PD?

A

-Carbidopa inhibits dopa decarxylase. This prevent dopa decarboxylase from converting L-Dopa to DA which does not cross the BBB

37
Q

What are some common characteristics of Alzheimer disease?

A
  • Onset generally> 65y
  • Progressive cognitive impairment accompanied by affective and behavioral disturbances
  • First sign is loss of memory–> final stage of incapacitation
38
Q

What are the two difinitive histological features of Alzheimer disease?

A

-Amyloid ß peptide Neurofibrillary plaques and tangles

39
Q

What microtube associated protein is hyperphosphorylated in neurofilbrillary plaques and tangles?

A

tau

40
Q

What two structures degenerate the most in Alzheimer disease?

A

-cortex and hippocampus

41
Q

What is the amyloid cascade hypothesis?

A

Amyloid b-protein, a peptide fragment of a transmembrane protein, is insoluble in the extracellular space.

-AbP may be neurooxic by stimulating excessive calcium uptake leading to activation of protein kinase and Tau–> cell death

42
Q

Whart are some characteristics of schizophrenia?

A

-psycotic symptoms: disturbances of thinking, feeling and behavior.

43
Q

What are positive symptoms of schizophrenia?

A

Hallucinations, delusions and bizzare behavior

44
Q

what are negative symptoms of schizophrenia?

A

Social withdrawl, emotional blunting

45
Q

What are some noted strcutural abnormalities in schizophrenic patients?

A
  • Altered orientation of hippocampal pyramidal cells
  • enlarged ventricles
46
Q

What is the dopamine hypothesis with respect to schizophrenia?

A

Hypoerdopaminergia detected by:

  • elevated dopamine in brain tissue
  • elevated homovanillic acid (HVA) in CSF
  • elevated numbers of D2 receptors in brain tissue
47
Q

what is the modified dopamine hypothesis?

A

there is abnormal, not necessarily excessive, dopaminergic activity in schizophrenia.

Clinical Neurology (8 decks)

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