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General Pathology > Cell Adaptations > Flashcards

Cell Adaptations Flashcards

0
Q

Is BAX Pro or anti-apoptosis?

A

Pro

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1
Q

Is Bcl-2 Pro or anti-apoptosis?

A

Anti-apoptosis

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2
Q

Is BAK Pro or anti-apoptosis?

A

Pro

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3
Q

Is Bcl-XL Pro or anti-apoptosis?

A

Anti

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4
Q

Is MCL-1 Pro or anti-apoptosis?

A

Anti

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5
Q

Is BAD Pro or anti-apoptosis?

A

Pro

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6
Q

Is BID Pro or anti-apoptosis?

A

Pro

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7
Q

Is PUMA Pro or anti-apoptosis?

A

Pro

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8
Q

P53 activates which apoptosis mediators & effect?

A

BAX & PUMA

Pro-apoptosis

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9
Q

Transcription factors activated during myocardial hypertrophy

A

GATA4
NFAT
MEF2

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10
Q

What molecule type is affected in atrophy?

A

Proteins

Reduced synthesis and increased degradation

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11
Q

BH3-Only sensors

A 
Bim
Bid
Bad
Puma
Noxa
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12
Q

What do activated BAX & BAK do?

A

Form channels in mitochondria membrane -> cytochrome C leakage -> intrinsic apoptosis

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13
Q

What happens to cytoplasmic cytochrome c?

A

Binds to Apaf-1 -> forms apoptosome -> activates Caspase 9

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14
Q

Intrinsic apoptosis pathway Caspase

A

Caspase 9

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15
Q

Extrinsic apoptosis pathway Caspase

16
Q

Molecules in Complex that activates necroptosis

A

RIP1
RIP3
Caspase 8

17
Q

What key feature distinguishes extrinsic apoptosis from necroptosis?

A

Caspases are not activated in necroptosis

18
Q

What goes wrong in Niemann-Pick type C

A

Lysosomal storage disease due to abnormal cholesterol trafficking

19
Q

Tay-Sacs

Type and deficiency

A

GM2 gangliosidosis

Hexosaminidase a-subunit deficiency

20
Q

Niemann-Pick Dz A& B

A

Sphingomyelinase defect

21
Q

Neimann-Pick Type C

A

NPC gene mutations

Defective lipid transport -> ganglioside accumulates in neurons

22
Q

Globoid cell Leukodystrophy

A

B-Galactocerebrosidase Deficiency

23
Q

GM1

A

B-galactosidase deficiency

General Pathology (6 decks)

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