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Foundations 8 > Turco 2 > Flashcards

Turco 2 Flashcards

1
Q

Complete pyruvate kinase defect

A

kills you

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2
Q

Diabetes glucose curve

A

Higher peak and takes longer to come back down…diabetic will get hungry before it ever comes back down all the way and will eat more…extra glucose in the blood for extended periods of time

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3
Q

Pathology of diabetes from

A

Glucose concentration in the blood

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4
Q

Insulin effect of GLUT4

A

GLUT 4 premade and sits in vesicles…insulin will cause vesicles to open and move to the membrane…more GLUT4 on surface means higher Vmax so more glucose entering

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5
Q

Type 1 vs type 2

A

1 - insulin scretion problem

2 - receptor problem

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6
Q

Obesity receptor effect

A

Leads to decreased eceptors

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7
Q

INsulin dependent tissues in body

A

Muscle (GLUT4)
Adipose tissue (GLUT4)
Liver (different effects)

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8
Q

Insulin effect on muscle of adipose

A

Increase uptake of glucose

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9
Q

IMpact of insulin on liver

A

Tells the liver to trap it using glucokinase…run glycolysis and create fatty acids ,etc.

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10
Q

Hemoglobin effect of hyperglycemia

A

Aldehyde from glucose reacts with amine group of hemoglobin to create A1C (glycosylated hemoglobin)

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11
Q

Values of A1C

A

6% or less is normal
7% or over is diabetic
6-7 is pre

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12
Q

Glucose effect on kidney

A

Binds transporters and renders them non-functional

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13
Q

Glucose effect on collage

A

Binds collagen and extends 1/2 life…means that capillary beds are restricted…why amputations occur

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14
Q

Glucose effect of brain

A

Hyperosmolar edema (draws water)

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15
Q

Glucose reaction with hemoglobin is

A

Non-enzymatic, irreversible

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16
Q

Formation of F2,6P

A

Formed from F6P by PFK2 using ATP

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17
Q

Location of F2,6P

A

Liver ONLY

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18
Q

WHere does F6P come from?

A

Glycolysis

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19
Q

PFK2 regulation

A

Positively by insulin

Negatively by glucagon

20
Q

PFK2/PFK1 relationship

A

If one is active, the other will be active…F2,6P increases activity of PFK1 by overriding any other inhibitors

21
Q

F2,6P other regulation

A

Turns off F1,6bisphosphatase of gluconeogenesis

22
Q

All cells except liver after high carb

A

Glucose becomes pyruvate through glycolysis

Increase ATP, decreased PFK1, Decreased glycolysis

23
Q

IN liver after high carb meal

A

Glucose becomes pyruvate
INsulin leads to increase in PFK2, increased in F2,6P, increase in PFK1, and increase in glycolysis

Leads to production of fatty acid synthesis

24
Q

IN short, F2,6P activates what and inhibits what?

A

Activates glycolysis and inhibitsa gluconeogenesis

25
Q

Without F2,6P

A

You would not be able to overcome inhibition of PFK1 and would never make fatty acids

26
Q

Effects of diabtetes on hepatic glycolysis

A

No PFK2 means decrease in PFK1 means decreased glycolysis
Increased F6P means increased G6P means decreased hexokinase activity and can’t keep glucose in the liver
No glucokinase activity because no insulin so no glucose trapping

27
Q

NAD+

A

Only small amounts

Converted to NADH in catabolic reactions and makes ATP

28
Q

NADP

A

Converted to NADPH and NADPH used for anabolic reactions

29
Q

Where does NAD come from?

A

Niacin

30
Q

NAD and NADP relationship with enzymes

A

Noncovalently bound to enzymes

31
Q

Cholera toxin mech

A

ADP ribosylation uyses NAD as substrate to create ADP ribose

32
Q

NADPH particularly importasnt in

A

NADPH oxidase of inflammation

33
Q

Are NAD and NADP interchangeable?

A

No

34
Q

Aerobic fate of pyruvate

A

2 pyruvate converted to 2 acetyl-CoA with loss of 2 CO2…2 acetyl CoA converted to 4CO2 and 4H2O and create a bunch of ATP

35
Q

Anaerboci fate of pyruvate

A

Create lactate (in vigourously contracting muscles, erythroicytes)

36
Q

Other fate of pyruvate

A

Converted to alanine

37
Q

Aerobic glycolysis equation

A

Glc + 2ADP+2NAD —-> 2 pyr + 2ATP + 2 NADH

NADH—-> more ATP via oxidative phosphorylation

38
Q

Anaerboic glycolysis

A

Blc —-> 2 lactate and 2 ATP (substrate level phosphorylation)

39
Q

Pyruvate conversion to lactate reactions

A

Lactate dehydrogenase using NADH

In muscle and liver cytoiplasm

40
Q

In conditions of high demand

A

INcreased ATP need, increased rate of oxidative catabolic reactions and increased NADH generated

41
Q

Point of exercise

A

Trying to condition lungs ot bring in more O2 and make more ATP

42
Q

Smokes

A

Will produce more lactic acid because less oxygen uptake

43
Q

What is the point of the lactic acid pathway?

A

Recycles NAD

44
Q

How long does it take to recover from lactic acid production?

A

About an hour

45
Q

Cori cycle

A

Glycogen converted to glucose…glucose undergoes glycolysis to pyruvate…pyruvate goes to lactate…lactate moved to blood to liver…in liver, lactate to pyruvate to glucopse via gluconeogenesis…glucose moved bacxk to muslce through blood

46
Q

Alanine cycle

A

Similar to lactate cycle except no pH effect on the blood

47
Q

Why does body prefer Cori cycle to alanine cycle?

A

LDH regenerates the NAD for glycolysis

Foundations 8 (13 decks)

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