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Foundations 8 > Turco 6 > Flashcards

Turco 6 Flashcards

1
Q

Things that use glucose as primary source of energy

A

Kidney, testis, RBCs, embryonic tissue

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2
Q

Under starvation, MUST

A

Drink water because of ketone bodies

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3
Q

SOurces of glucose

A

Diet
Gluconeogenesis
Glycogen

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4
Q

Gluconeogenesis occurs in

A

Liver (and a little in kidney)

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5
Q

Sources of carbon for glucose

A

Lac/Pyr
Glycerol (from TG breakdown, but NOT FA)
Glucogenic AAs - all but leucine and lysine

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6
Q

Bypass rxn 1 + 2

A

Pyruvate carboxylase and PEP carboxykinase

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7
Q

Pyruvate carboxylase rxn

A

Takes pyr to OAA (ABC enzyme)…regulated by acetyl-CoA (obligate activator)

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8
Q

ABC enzymes

A

Propionyl carboxylase
pyruvate carboxylase
acetyl-CoA carboxylase

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9
Q

PEP carboxykinase rxn

A

OAA to PEP…gives off CO2 and uses GTP

Increased by glucagon and cortisol at genomic level

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10
Q

PEP carboxykinase rxn equilibrium

A

CO2 produced is breathed out and drvies formation of products

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11
Q

Bypass reaction 2

A

Fructose-1,6-bisphosphatase takes F-1,6-P to F-6-P and Pi
Regulated allosterically by F2,6P (turns off)
Turned on by ATP

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12
Q

Bypass reaction 3

A

Glucose-6-phosphatase

G-6-P to glucose and Pi

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13
Q

Metformin

A

Used for type 2 diabetes by inhibiting gluconeogenesis

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14
Q

PDH

A

Pyruvate dehydrogenase produces CO2

Takes pyruvate to AcCoA…decreased by AcCoA and increased by thiamine (cofactor)

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15
Q

Pyruvate can come from

A

Lactate/alanine/glycolysis

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16
Q

TG mobilization/FA-beta oxidation effects of gluconeo and glycolysis

A

Increases ATP which activates F-1,6-bisphosphatase and inactivates PFK1
Glycerol can form Glyceraldehyde-3-phosphate that can bypass first set of bypass rxns
FA-beta oxidation produces AcCoA that activate pyruvate carboxylase and inhibits PDH

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17
Q

Glucagon effect on glycolysis/gluconeogenesis

A

Glucagon will decrease PFK2 activity which will decrease F,2,6P which will decrease PFK1 activity
Glucagon increases activity of PEP carboxykinase

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18
Q

INsulin effect on glycolysis/gluconeogenesis

A

Insulin activates glucokinase and PFK2

19
Q

Liver reserves of glycogen have enough storage for ____ hours

A

12 hours resting

1 hour exercising

20
Q

Why do glycogenolysis and gluconeogenesis occur simultaneously?

A

Gluconeogenesis is regulated on a genomic level so it takes a long time…if you waited for all of glycogen stores to be depleted, would have period of time where you would not be able to make any glucose

21
Q

Fasting effects

A 
Decrease glycogen synthesis and increase breakdown via phosphorylation 
Decrease glycolysis because of increased ATP (from FA) and decreased F2,6P (because of decreased insulin)
Increase gluconeogenesis (obligate, allosteric, hormonal regulation)
22
Q

Liver energy source during fasting

A

FA

Glucose reserved from brain and other important cells

23
Q

Peroxisome major functions

A

Oxidation of VLCFA (generates H2O2)
Oxidation of branched chain/hydroxylated FAs (into phytanic acid)
Conversion of cholesterol to bile acids
Synthesis of plasmalogens (ether lipids)

24
Q

VLCFA oxidation

A

Undergoes alpha oxidation
Attached to CoA and brought into peroxisome…inside, converted to SCFA-CoA and MCFA-CoA (FADH2 produced is converted to H2O2)…SCFA attached to carnitine and brought into mitochondria…inside mitochondria, CAT 2 removes the carnitine and undergoes Beta-oxidation just as any other would

25
Q

Oxidase and catalase

A

Oxidase forms H2O2 from O2 using FADH2

Catalase takes H2O2 to H2O

26
Q

Zellweger syndrome

A

Defect in peroxisome biogenesis
Accumulation of VLCFA and hydroxylated/branched FAs
Defects primarily in liver and brain (incorporated into myelin sheaths)

27
Q

Adrenoleukodystrophy

A

Defect in FA trasnporters in peroxisome membrane
X-linked rec
Defect primarily in brain (myelin sheaths)

28
Q

Refsum dz

A

Defect in alpha oxidation of phyanoyl-CoA
Control with low phytanoic acid diet
Neuro probs

29
Q

Tx of peroxisomal disorders

A

Fibrates - PPAR alpha
Thiazolidinediones - PPAR gamma
Both turn on peroxisomes

30
Q

Reye’s Syndrome

A

Associated iwht fatty acid oxidation defect…can be cause of SCID
Will find fatty droplets in the liver
Vomiting, mental stauts change, seizures
No cirrhosis, just TG accumulation

31
Q

Aspirin metabolites

A

Decrease Beta-oxidation of fatty acids…why you can’t give them with Reye’s Dz

32
Q

Hemosiderin deposits

A

Indicate iron problem

33
Q

Mallory bodies

A

Seen in alcoholic cirrhosis

34
Q

Why should you not exercise then drink alcohol?

A

Lactic acid will leave muscle and go to liver where converted back to pyruvate using NAD
Alcohol metabolism reuqires NAD…if alcohol metabolism using NAD, then lactate concentration will increase and pH will drop

35
Q

Alcohol metabolism

A

Alcohol converted to acetaldehyde using alcohol dehydrogenase
Acetaldehyde converted t oacetic acid using acetaldehyde dehydrogenase
Both use NAD
Acetaldehyde causes damage

36
Q

Femopizole

A

Inhibits alcohol dehydrogenase
Tx for methanol or ethylene glycol poisoninig
Methanol accumulates and is excreted

37
Q

Disulfiram

A

Inhibits acetaldehyde dehydrogenase which causes acetaldehyde to accumulate and makes patient sick

38
Q

Acetaldehyde dehydrogenase deficiency ethnic

A

Asians from pacific rim

39
Q

Exercise induced hypoglycemia effect

A

GLUT 4 transported to membrane of monocytes due to increased concentrations of AMP…this causes hypoglycemia in the blood

40
Q

Cramping/muscle pain caused by

A

Inadequate delivery of oxygen

41
Q

Ketotic hypoglycemia

A

Hypoglycemia with ketonuria and ketonemia

This means there is a problem with protein catabolism

42
Q

Error in FA metabolism leads to

A

Hypoketosis

43
Q

Hypoglycemia without ketosis (with low blood pH)

A

Answer could be increased circulating levels of insulin…would cause blood glucose to decrease

44
Q

Increased A1C seen

A

Chronically

Foundations 8 (13 decks)

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