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Foundations 8 > Turco 5 > Flashcards

Turco 5 Flashcards

1
Q

Glycogen bonds

A

Alpha 1,4 - most common

Alpha 1,6 - branch

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2
Q

All glycogen link to

A

Glycogenin protein

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3
Q

Why make a polymer vs free glucose?

A

Polymer will not draw as much water

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4
Q

Where is glycogen made?

A

Liver and muscle

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5
Q

Why branched vs linear glycogen?

A

Branched is more soluble because more terminal glucoses
Branched can make glycogen available more quickly…need to increase muscle contraction, need ATP, need to oxidize glucose, glucose needs to be available

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6
Q

Why not make more than 1 pound of glycogen?

A

Glycogen must have water so it would take up too much space

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7
Q

Glycogen problems often manifest as

A

___megalies

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8
Q

Advantage to TG storage

A

No water accompanies TGs

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9
Q

Glycogen synthesis process

A

Glucose enters via GLUT2/4
Made into G-6-P, then G-1-P then UDP-glc
Glycogen synthase forms alpha 1,4 bonds and branching enzyme forms alpha 1,6 bonds

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10
Q

Glucose-6-phosphate important

A

Can go to glycogen synthesis, pentose phosphate, or glycolysis

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11
Q

Glycogen syntahse regulation

A

Insulin will increase activity by dephosphorylating

Off by epinephrin and glucagon

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12
Q

Glycogen degradation

A

Glycogen phosphorylase uses INORGANIC PHOSPHATE to break alpha 1,4
Debranching enzyme hydrolyzes alpha 1,6
This forms glucose-1-P, then glucose-6-phosphate
G-6-P in liver ONLY, forms glucose via glucose-6-phosphatase

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13
Q

Muscle vs. liver with glycogen

A

Muscle will NOT release glucose back into bloodstream because no glucose-6-phosphatase…liver will

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14
Q

Glycogen phosphorylase mechnaism

A

Off by insulin via dephosphorylation

On by epinephrine and glucagon

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15
Q

In hard working muscle ONLY

A

AMP can allosterically activate glycogen phosphorylase

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16
Q

Allosteric effects of AMP in hardowrking muscle

A

Turn on glycogen phosphorylase
INcrease GLUT4 on muscle surface to increase glucose uptake
Turn on PFK1 to drive glycolysis

17
Q

Type 1 name, enzyme, structural/clinical consquences

A

von Gierke’s
G-6-Pase
Severe postabsorptive hypoglycemia, lactic acidemia, hyperlipidemia, hepatomegaly***

18
Q

Explanation for type 1 symptoms

A

Hypoglycemia because can’t mobilize glucose from liver
Hyperlipidemia because severe hypoglycemia so glucagon and cortisol secreted and turn on HSL which breaks down TGs and FAs released into blood

19
Q

Type 2 name, enzyme, clinical

A

Pompes
Lysosomal alpha galactosidase (acid maltase)
Glycogen grnaules in lysosome and cardiomegaly

20
Q

Explanation of Type 2

A

Alpha 1,4 glucosidase affected

21
Q

Type 3 name, enzyme, clinical

A

Cori’s
Debranching enzyme
altered glycogen structure and hypoglycemia

22
Q

Type 4 name, enzyme, clinical

A

Anderson’s
Branching enzyme
Altered glycogen structure

23
Q

Type 3 vs. 4

A

4 - structure will be linear like starch

3 - single glucose stubs that can’t be removed

24
Q

Type 5 name, enzyme, clinical

A

McArdle’s
Muscle phosphorylase
Excess muscle glycogen deposition, exercise induced cramps and fatigue

25
Q

Type 6 name, enzyme, clinical

A

Hers
Liver phosphorylase
Hypoglycemia (not as severe as von Gierke’s) and hepatomegaly

26
Q

Why is type 6 not as severe as type 1 hypoglycemia

A

Can make G-6-P from glycogen or gluconeogenesis
Type 6 interferes with just the glycogen degradation
Type 1 interferes with G-6-P conversion to glucose

27
Q

Type 5 mech

A

Child running around, epinephrine released, muscle targeted, glycogen synthase off and phosphorylase on and can’t break down

28
Q

Myopathic carnitine def vs. type 5

A

MC def - build up of TGs in muscle cytoplasm (Oil Red O or Sudan Black stain)
Type 5 - PAS stain will show glycogen in cytoplasm

29
Q

Liver glycogen supply

A

12 hours sitting

1 hour exercising

30
Q

RBCs cannot use

A

FAs or KBs

31
Q

Methylmalonyl CoA mutase presnetation

A

Peripheral neuropathy with methylmalonyl acidemia and aciduria

32
Q

MCAD presentation

A

Hypoglycemia and dicarboxylic acidemia

33
Q

Energy of fuels

A

Carbs - 4
Fat - 9
Alcohol - 7

34
Q

When does KB synthesis begin?

A

90 minutes after last meal

35
Q

FA glucose

A

FA cannot be made into glucose but can be made from glucose

36
Q

Where are KBs formed?

A

Liver

37
Q

Acylcarnitines indicate

A

MCAD

38
Q

Urea cycle and B-oxidation

A

B-oxidation powers urea cycle so if problem with B-oxidation then hyperammonia

Foundations 8 (13 decks)

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