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Flashcards in Turco 3 Deck (37)
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1
Q

Glc gives up how many total pairs of electron

A

12 pairs
1 in glycolysis to pyruvate
5 from pyr to CO2

2
Q

Step of glycolysis giving up electrons

A

Glyceraldehyde 3P —-> 1,3 BPGT

3
Q

Pyruvate dehydrogenase complex

A

Takes pyruvate to acetyl CoA
Located in Mitochondria
Releases pair of electrons

4
Q

Isocitrate dehydrogenase

A

Takes isocitrate to alpha ketoglutarate

Creates NADH from NAD

5
Q

Regulation of isocitrate dehydrogenase

A

Turned off by high levels of ATP and NADH…this will increase concentration of citrate that then inhibits PFK1 of glycolysis in EXTRAhepatic cells

6
Q

Creatine and ATP

A

ATP cannot be stored in cells so phosphate added to creatine for storage

7
Q

Creatine kinase isoforms

A

Skeletal muscle - MM
Brain - BB
HEart - MM and MB isoform

8
Q

Importance of MB isoform

A

Indicative of heart attack…creatine kinase will spill out into the bloodstream and be present for about 24 hours

9
Q

Creatine metabolism

A

Creatine converted to creatine phosphate using ATP

Creatine phosphate turns into creatinine nonenzymatically with release phosphate

10
Q

In very short burts?

A

ATP levels stay relatviely the same (enzyme that takes 2 ADP to ATP+AMP)
Creatine-P will decrease dramatically

Also lactic acid

11
Q

Intermediate energy expenditure

A

Mix of fatty acid and aerobic

12
Q

Long term energy expenditure

A

Glycogen is gone so increased fatty acid metabolism

13
Q

TG metabolism in adipose

A

HSL activated by epinephrine and cortisol, decreased by insulin
Phosphorylated enzyme takes TGs to Glycerol and FAs

14
Q

TG metabolism in liver

A

Glycerol moved into liver and taken to glucose via gluconeogenesis (activated by glucagon and cortisol)
FA moved into liver and unergo B-oxidation to AcCoA
AcCoA either goes to krebs or undergoes ketogenesis to form ketone bodies

15
Q

When will TG metabolism start

A

90 minutes after last carb

16
Q

No receptor for glucagon in

A

Adipose tissue

17
Q

Insulin, epinephrine, and cortisol mech of HSL

A

Insulin - dephosphorylate
Epi - phosphorylate
Cortisol - genomic level

18
Q

Why is B-oxidation important?

A

Creates energy necessary to drive gluconeogenesis

19
Q

Why would defect in B-oxidation cause SIDS?

A

Can’t drive gluconeogenesis so hypoglycemia

20
Q

Ketogenesis, B oxidation and gluconeogensis locations

A

Keto and gluco in liver only

B-oxidation can be in other cells

21
Q

Atkins diet rationale

A

Keep insulin low by decreasing carbs in diet…this means HSL always active

22
Q

Problem with atkins diet

A

Used muscle proteins from glucogenic amino acids to make appropriate glucose

23
Q

Other probs with atkins

A

Excessive N secretion (kidney)

Body is in long term ketosis

24
Q

FA transport into matrix for oxidation

A

CoA added to FA when bringing in through outer membrane…CoA then removed and FA transferred to carnitine by CAT…moved through inner membrane…CAT 2 removes carnitine and makes FA-CoA again

25
Q

FA-CoA in the matrix

A

Processed by LCAD, MCAD, or SCAD and forms FADH2…also form NADH…2 carbons removed in form of Ac-CoA
This is repeated until down to four and then split into 2 Ac-CoA

26
Q

KB metabolism

A

2 acetyl CoA get to acetoacetate
Acetoacetate forms B-hydroxybutyrate with NADH OR decarboxylated to form acetone

Acetoacetate and B-hydroxybutyrate moves out of blood

27
Q

How are ketone bodies used

A

Broken down into 2 acetyl CoA inside extrahepatic cells

28
Q

Hallmarks of ketosis

A

INcreased KBs leads to ketonemia (bad bc pH will drop)
Increased KBs in urine leads to ketonuria….bad because dehydration
Acetone breath (fruity odor)

29
Q

Myopathic canitine deficiency presentation

A

Elevated muscles TGs and reduced muscle carnintine onyl…muscle weakness severe during exercise

30
Q

Myopathic carnitine deficiency pathology

A

Could be defect of CAT enzymes, transporters, or error in carnitine creation

FAs will stay in the muscle cell and TGs cannot exit the muscle

Epinephrine activates adipose tissue and triggers HSL…TGs breakdown and enter cells…FA cannot go into matrix to be burned

31
Q

MCAD def presentation

A

Hypoglycemia and hypoketonemia
Dicarboxylic acidemia (from omega oxidation)
C8/C10 acylcarnitines in blood

32
Q

MCAD def pathology

A

Hypoglycemia because without MCAD, cannot power gluconeogenesis…normally hypoglycemia means hyperketonemia

33
Q

Propionate metabolism

A

5 carbon fragment split to acetyl CoA and proprionyl CoA (3 carbons)
Propionyl CoA carboxylase takes propionyl CoA to methylmalonyl CoA using (ATP, biotin, CO2)
Methylmalonyl CoA mutase takes methylmalonyl CoA to succinyl CoA using coenzyme form of Vit B12

34
Q

Propionyl CoA also made from

A

Val, Met, Ile, and Thr

35
Q

If priopionyl CoA carboxylase borken

A

Propionic acid in the urine and blood

36
Q

Defect in methylmalonyl CoA mutase

A

Causes methylmalonic acidemia and gives rise to peripheral neuropathy as integrated into myelin sheaths

37
Q

Causes of methylmalonyl CoA mutase def

A
B12 def
IF def (binds to B12 to absorb)
Mutase defect
Defect in coenzyme form of B12 (can't convert