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Physiology > Section 3 Lecture 4 > Flashcards

Section 3 Lecture 4 Flashcards

1
Q

Which portion of the brain is the BG in?

A

Forebrain

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2
Q

BG is involved in:

A

M control, cognitive fxn, and emotional or affective fxn

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3
Q

Fxn of the BG in terms of what info travels through and to where:

A

To control excitatory drive to cortex

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4
Q

What is the extrapyramidal system:

A

BG (does not operate independent of cortex, this is an old view)

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5
Q

What is the striatum composed of?

A

Caudate and putamen

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6
Q

What is the BG composed of?

A

Caudate, putamen and Globus pallidus

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7
Q

T or F? The substantia nigran and the subthalamic nucleus are both part of the BG.

A

F. Neither are.

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8
Q

Main fxn of SN:

A

dopamine released, altering the functional level of the striatum

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9
Q

Damage to BG:

A

involuntary moves or slowness of movement (bradykinesia)

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10
Q

BG diseases or disorders:

A

PD, ADHD, tourette’s, Restless Leg syndome, Tardive dyskinesia, Huntington’s, dystonias

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11
Q

PD facts:

A

typical onset: 60+, more men than women, progressive, but slow, can live for 20+ yrs

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12
Q

There is degeneration of this in PD:

A

substantia nigra

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13
Q

Specific cell population affected in PD:

A

substantia nigra degeneration of neurons, loss of dop input to striatum, caudate and putamen

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14
Q

Causes of PD:

A

unknown, genetic factors? Not a single gene mutation, would be genetic contribution or influence

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15
Q

Post-infectious PD:

A

got it after a flu virus, some viral influence (in this case at least)

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16
Q

Biochemical link to PD:

A

depression

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17
Q

Cognitive affects of PD:

A

dementia, sometimes

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18
Q

Motor symptoms of PD:

A

combo of + and - effects: tremor AT REST (esp hands and mouth), bradykinesia, akinesia

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19
Q

cerebellar lesions lead to:

A

tremors when movements are activated

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20
Q

Symptoms of PD:

A

motor, affective (depression), cognitive (dementia), tremor, brdykinesia, akinesia

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21
Q

Absence of movement, especially self-initiated moves, i.e. lack of facial expression, swinging arms when walking):

A

Akinesia

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22
Q

Are the motor symptoms connected to PD pos or negative?

A

both

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23
Q

How to induce PD in animals:

A

MPTP

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24
Q

BG is especially important in what type of moves?

A

self initiated movements

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25
Q

The ability to walk and swing arms with legs (assoc moves) is lost with the disease:

A

PD

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26
Q

T or F? Excitation and inh are intrinsic properties of dopamine.

A

F. They are not

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27
Q

Is PD slow or fast progressing?

A

slow prog

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28
Q

What is DBS and explain how it works.

A

deep brain stimulation: electrodes, subthalamus n., like a pacemaker

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29
Q

What led to the discovery of MPTP and what does it damage?

A

attempts to make heroin,MPTP damages SN

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30
Q

Effects of MPTP:

A

destroys neurons in substantia nigra

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31
Q

T or F? Most neurogenic disease aren’t found in animals.

A

T

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32
Q

Death of neurons in the sub nigra lead to what?

A

gradual loss of dopamergic input to caudate and putamen

33
Q

Cause of PD:

A

not known

34
Q

Tx for PD:

A

l-dopa, tissue/stem cell implants, lesion in pwy, or DBS

35
Q

Why can’t we give dopamine to tx PD?

A

bc it wont pass BB barrier, give a precursor

36
Q

Experimental procedure to tx PD:

A

Implant cells that will synthesize dopamine,

37
Q

Goal in the tx of PD:

A

block or reduces abnormal drive to MC, disrupt abnormal activity in the BG

38
Q

What happens w the removal of dopamine?

A

too much excitation in one place, too little in another.

39
Q

Recent development that will help our understanding of PD:

A

we now have animal models of PD

40
Q

PD involves the synapse bw:

A

SN to striatum

41
Q

Transporter protein takes up:

A

serotonin, dopamine

42
Q

Stimulant drugs act by:

A

changing dop levels, reuptake of dop at synapse is terminated by a “transporter” i.e. coin works on dop transporter

43
Q

T or F? Dopamine is involved only in the M system.

A

F. other cell groups synthesize and release dop

44
Q

Lack of sufficient dopamine reuptake can be related to:

A

transmitter concentrations, receptors, or transporters

45
Q

How do the serotonin levels in depressed people compare with those of non-depressed people?

A

the same, receptor function may be inhibited

46
Q

Subtypes of dopamine receptors:

A

D1-D5

47
Q

Which subtypes of dopamine receptors are found in the hypothalamus?

A

D3 and D5

48
Q

Which subtypes of dopamine receptors are found in the corpus striatum?

A

D1 and D2

49
Q

What is neurological basis of shizophrenia:

A

too much dopaminergic action in the frontal lobe (hypothesis)

50
Q

Dopamine receptor blockers:

A

neuroleptics, used to be tx for schizo, i.e. Chlorpromazine (Thorazine) and Haloperidol (Haldol)

51
Q

Long term use of neuroleptic drugs for schizo can lead to:

A

motor disorders: tardive dyskinesia (invol mouth, face and hand moves) or tardive dystonia (abnormal m. tone or postures)

52
Q

Which lobes of the brain are implicated in schizo?

A

frontal

53
Q

Newer drugs for schizophrenia:

A

atypical antipsychotics, act on dop receptors in cerebral cortex (frotal lobe) and not subsets in the BG (tx cortical and does not interfere with M systems use of dopamine) Also used to tx bipolar disorder

54
Q

Symptoms of atypical antipsychotics:

A

weight gain and diabetes

55
Q

List of atypical antipsychotic Dx:

A

Risperdal (Risperidone), Olanzapine (Zyprexa), Quetiapine (Seroquel), Ziprasidone (Geodon), Aripiprazole (Abilify), Paliperidone (Invega), Lurasidone (Latuda)

56
Q

T or F? ADHD is a M system disorder.

A

F.

57
Q

What NT is implicated in ADHD?

A

dop, fxnal dopamine deficiency (hypothesis)

58
Q

T or F? ADHD is a lifelong disorder

A

F, mainly. “symptoms MAY continue into adulthood”

59
Q

Fxn of ritalin (methylphenidate) or adderall:

A

increase dopamine levels (adderral increases NE as well)

60
Q

What is the biomarker for ADHD?

A

There isn’t one

61
Q

Rital fxns by:

A

acting on the dop transporter

62
Q

Adderall fxns by:

A

inc the release of dop and NE

63
Q

Tourette’s is a movement disorder assoc w this part of the brain:

A

BG

64
Q

T or F? The tics that come with Tourett’es an be suppressed and controlled.

A

F. Can’t control but can suppress

65
Q

T or F? Tourette’s is a single gene disorder

A

F. Hereditary, but not a single gene

66
Q

Is Tourettes’ more prevelant in men or women?

A

Men 3:1

67
Q

What is the neurological basis of Tourette’s?

A

Too much functional dopamine (hypothesis)

68
Q

Tx or Tourette’s

A

dopamine receptor blockers, ie Haldol (still?)

69
Q

Typical age of onset of Tourette’s:

A

childhood, often w ADHD

70
Q

T or F? Restless Leg Syndrome has M symptoms only.

A

F. Sensory and motor symptoms

71
Q

RLS is a disorder of what part of the brain?

A

BG (hypothesis)

72
Q

Tx for RLS:

A

increase synthesis of dopamine (L-dopa carbidopa = Sinemet) or mimic the action of dopamine (ropinirole, pramipexole, and rotigotine)

73
Q

Symptoms of RLS are more pronounced:

A

at night

74
Q

Who are affected by RLS more, men or women?

A

Women

75
Q

What portion of the brain is involved with Huntington’s?

A

BG disease:

76
Q

T or F? Huntington’s a dopamine disorder.

A

F

77
Q

What is going wrong in the brains of pts with Huntington’s?

A

Death of cells in caudate and putamen (the striatum)

78
Q

Does Huntington’s have a genetic basis?

A

Yes, 1 in 10,0000

79
Q

How is Huntington’s passed geneticlally:

A

Autosomal dominant

Physiology (55 decks)

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