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Genes 3670 > Lecture 20 > Flashcards

Lecture 20 Flashcards

1
Q

hippocratic medicine

A

melancholic - water - glum
choleric - fire - irritable
phlegmatic - earth - slow
sanguine - air - healthy

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2
Q

psychosurgery during 16th century

A

excising stone of folly (madness)
(trepanation)

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3
Q

what amount of US population report symptoms of major psychosis

A

1/3

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4
Q

depression more prevalent in

A

women

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5
Q

factors that influence likeliness of developing psychiatric disorders

A

race, age, gender, environment, genetics

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6
Q

the word schizophrenia means

A

split mind

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7
Q

psychosis =

A

general lack of contact w/ reality

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8
Q

prevalence of schizophrenia =

A

1-2 % of population

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9
Q

schizophrenia accounts for ___ of all admissions to mental hospitals

A

1/2

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10
Q

positive symptoms =

A

abnormal behaviours that are gained
- hallucinations (mainly auditory)
- delusions
- erratic motor behaviour

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11
Q

paranoid delusions vs persecution delusions

A

paranoid = people talking about you persecution = people out to get you

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12
Q

negative symptoms =

A

loss of functions
- slow thought/speech
- emotional/social withdrawal
- blunted emotions
- chronic, do not respond well to drugs

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13
Q

Disorganized schizo.

A

Incoherence, grossly disorganized behaviour, bizarre thinking, and flat or inappropriate emotions

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14
Q

Catatonic schizo.

A

Marked by stupor, unresponsiveness, posturing and mutism

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15
Q

Paranoid schizo.

A

Preoccupation with delusions; also involves hallucinations that are related to a single theme, especially grandeur or persecution

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16
Q

Undifferentiated schizo.

A

don’t fit into any of the above

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17
Q

Stress-vulnerability hypothesis

A

combination of environmental stress and inherited susceptibility to cause schizophrenic disorders
- genetics, family environment, psychological trauma, deviant communication, etc.

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18
Q

_____ activity excessive in schizophrenic brain

A

dopamine

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19
Q

______ ventricles evident in schizo.

A

enlarged

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20
Q

twins have ____% concordance rate

A

48% - significant genetic component, but not entirely

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21
Q

T/f: patients w/ schizo. have perturbed eye behaviour

A

ture - amygdala?

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22
Q

structural changes with schizophrenic brain

A
  • enlarged cerebral ventricles (especially in males)
  • smaller hippocampus + amygdala
  • pyrimidal cells in hippocampus in disarray
  • loss of gray matter
  • cotical thinning
  • thicker corpus callosum
  • decreased frontal lobe activity
  • higher dopamine amounts
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23
Q

DISC1 gene

A

disrupted in schizophrenia 1
- appears in one schizophrenic family
- mice w/ mutated version develop enlarged ventricles

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24
Q

T/F: they have trouble w/ wisconsin card sorting task

A

yes

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25
Q

drugs can effect

A

Ca2+ channels, survival of NTs. reuptake/release of NTs, binding NT to receptors, etc

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26
Q

competitive ligand (antagonist)

A

binds to same receptor site as endogenous transmitter

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27
Q

noncompetitive ligand (antagonist)

A

binds to a modulatory site on
the receptor

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28
Q

agonists

A

activate receptors, mimic endogenous substance

29
Q

binding affinity

A

degree of chemical attraction btwn ligand and receptor

30
Q

efficacy

A

the ability of the bound
ligand to activate the receptor

31
Q

dose-response curve

A

graph of the relationship between drug doses and their effects

32
Q

ED(50) =

A

50% effective dose

33
Q

a drug w/ same effects at lower dose is more

A

potent

34
Q

a lower maximal effect =

A

partial agonist

35
Q

therapeutic index =

A

seperation between effective dose and lethal dose
- a smaller therapeutic index is a more dangerous drug

36
Q

LD = lethal dose, LD(50) =

A

50% of animals that took this dose died

37
Q

efficacy of drugs is largely ________ in past 50 or so years

A

unchanged

38
Q

Amphetamine psychosis

A

caused by repeated use of amphetamines; resembles schizophrenia with paranoia, delusions and auditory hallucinations

39
Q

brain area important w/ dopamine + schizophrenia/addiction

A

VTA

40
Q

how some antipsychotic (neuroleptic) drugs work for schizo. and amphetamine psychosis

A

block dopamine D2 receptors

41
Q

But, dopamine and _____ pathways have large overlap, so maybe its not dopamine

A

serotonin

42
Q

mismatch hypothesis of disease

A

epigenetic alterations done early in life that alter gene expression may get the expected environment wrong, therefore are now maladaptive and can increase risk of disease

43
Q

bee fed royal jelly as larvae (vs. beebread) =

A

queen bee, even though genetically identical

44
Q

royal jelly silences _____, allows queen bee fertile genes to be activated

A

Dnmt3

45
Q

Dnmt3 is ______ in normal bees, silencing queen genes

A

active

46
Q

queen bee example shows

A

how nutrition affects epigenetic (postnatal) methylation and affect outcomes

47
Q

tail kinking nutritional effect

A

methy donor groups in diet = increased 5mC at Axin(Fu) = silenced cryptic promoter expression = decreased tail kinking
- mid-gestation effect
- not early embryonic

48
Q

agouti mice, methyl donor depleted diet (BPA)

A

more tumorgenic offspring, obese, yellow coat, diabetic

49
Q

IAP (agouti mice)

A

retrotransposon, inserts into genome near other genes, affects gene transcription and phenotype
- normally silenced via methylation
- metastability renders them susceptible to nutritional influences
- is transcribed, reverse transcriptase produces double stranded copy, inserted into DNA

50
Q

Wild type agouti mice have

A

brown fur bc of agouti (A) expression

51
Q

Banded fur =

A

brown, agouti (A)

52
Q

non-banded fur =

A

yellow, non-agouti

53
Q

A(vy/a) mom + methyl supplements =

A

more brown coat offspring, + IAP methylation

54
Q

The A(vy) metastable epiallele results from

A

the insertion of an IAP upstream of the transcription start site of the Agouti (A) gene

55
Q

normal, banded mice _______ agouti (A) gene

A

express

56
Q

IAP inserted just before agouti gene =

A

continually produce yellow phaeomelanin, making yellow, non banded mice.
- can be partially silenced with the degree of methylation on cryptic promoter region, this is how we get mottled mice.

57
Q

lower methylation (agouti mice)

A

more yellow

58
Q

yellow coat = non cyclical = ectopic

A

yes

59
Q

pseudo-agouti = cyclical = only in hair follicles

A

yes

60
Q

w/ control diet, most offspring coats are

A

slightly mottled

61
Q

high maternal methylation =

A

pseudo-agouti, brown, lean, healthier

62
Q

low A(vy) DNA Methylation =

A

yellow

63
Q

high agouti (A) expression =

A

brown

64
Q

high A(vy) expression =

A

yellow

65
Q

Avy = A (agouti) +

A

IAP, upstream

66
Q

cryptic promoter LTR (of IAP) expressed =

A

yellow

67
Q

cryptic promoter LTR (of IAP) highly methylated =

A

pseudo-agouti
- suppression associated w/ metylation

68
Q

more BPA in moms diet (agouti mice) =

A

more yellow

69
Q

BPA + methyl donors (agouti mice) =

A

same as control diet (mostly slightly mottled)

Genes 3670 (13 decks)

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