Cellular Homeostasis Flashcards

1
Q

Where are glut 1 receptos found?

A

everywhere but mainly in the brain and rbc

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2
Q

where are glut 2 receptors found?

A

liver and pancrease, this is how beta cells know how to secrete insulin

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3
Q

Where are glut 3 receptors found?

A

neurons

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4
Q

where are glut 4 receptors founf?

A

skeletal muscle tissue, heart, and adipose tissue

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5
Q

Which glut R is regulated by insulin?

A

glut 4

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6
Q

How many ATP are made from 1 molecule of glucose

A

34-36

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7
Q

what is the ultimate product of anaerobic glycolysis?

A

2 lactate and 2 NAD+

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8
Q

3 suppliers of glucose?

A

diet
glycogenolysis
gluconeogenesis

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9
Q

Fanconi Bickel Syndrome is caused by

A

inherited deficiency of glut 2 receptors in the liver, pancreas, and proximal renal tubule- so your body doesnt know to secrete insulin and stimulate the GLUT 4 in muscle and fat so the clearing of excess blood glucose

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10
Q

S/S of Fanconi Bickel Syndrome

A

hepatomegaly, stunted growth, hyperglycemia after a mean and hypoglycemia during fasting

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11
Q

Why does Fanconi Bickel Syndrome cause hepatomegaly?

A

because glycogen stored in the liver cannot get out

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12
Q

Rx for Fanconi Bickel?

A

ingestion of small meals throughout the day and supplementation of vitamin D (proximal tubular nephropathy prevents uptake and can lead to rickets)

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13
Q

Is the Glut 2 transporter uni or bi directional?

A

bidirectional depending on the concentration

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14
Q

High—— low—— system

A

capacity, affinity

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15
Q

How does gluoce sensing by Glut 2 work?

A

glucose is taken into the cell and ATP is made from it. Rishe in ATP closes K+ channels causing depolarization which opens voltage gated Ca++ channels. Influx of Ca++ triggers release of already synthesized insulin molecules and the synthesis of more insulin in a slow release pathway

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16
Q

What is the glucose tolerance test?

A

involves a patient ingesting a known amount of glucose followed by 8-12h. fasting period

17
Q

What is normal fasting glucose?

A

less than 6

18
Q

After 2 hours of eating normal gluc? diabetes?

A

11.1

19
Q

How is PEPCK regulated?

A

PEPCK takes pyruvate to OAA in the synthesis of glucose. Its synthesis is regulated by TF’s thyroxine and cortisol

20
Q

what do chaperones and enzymes do for newly made protein?

A

help it to fold properly

21
Q

What do Hsp70 and Hsp90 do?

A

chaperones that aid in proper folding of proteins

22
Q

What does the TOM complex do?

A

recognized the signal recognition sequence and binds precursor protein. It then allows protein into the intermembrane space of the mitochondria

23
Q

What does the TIM complex do?

A

TIM live in the inner membrane of mitochondria and allows protein tagged with a special signal to enter into the matrix for folding and modification

24
Q

4 types of PTM

A

Acetylation, glycation/glycosylation, phosphorylation, and ubiquitination

25
Q

2 methods to degrade proteins

A

lysosome (mainly used for intermembrane proteins and endocytosed agents)
proteasomes (mainly stuff in house)

26
Q

How are extracellular protein degraded?

A

proteoytic enzymes often secreted in their inactive form (zymogens)

27
Q

What is autophagy?

A

catabolism where dysfunctionl cellular components are degraded and other cellular components are recycled

28
Q

How are cells usually degraded?

A

autophagy and fusion with lysosome

29
Q

Which 4 things happen in mitochondria?

A

beta oxidation of fatty acids, TCA, urea cycle, and ctorage of Ca++

30
Q

Fusion of mitochondria happens when

A

a sick mitochondria fuses with a well mitochondria in order to mitigate healing

31
Q

fission of mitochondria happens when

A

we need to create new mitochondria, to remoe damaged mitochondria, and to facilitate apoptosis