Ppal99 Dissecting The Usmle 1,2,3 Anabolic/glycolysis/fructose

Front 1

what are Catabolic Pathways? what pathways are catabolic?

Back 1

create energy (mitochondria) ''ABC"
• AcetylCoA production
• β-oxidation
• Citric acid cycle

Front 2

what are Anabolic Pathways:? what pathways are anabolic?

Back 2

store energy (cytosol) "EFGH"
• Endoplasmic Reticulum
• Fatty acid synthesis
• Glycolysis
• HMP shunt

Front 3

what pathways are both Anabolic+ Catabolic Pathways:

Back 3

"HUG"
• Heme synthesis
• Urea cycle
• Gluconeogenesis

Front 4

what energy does the brain use during
Normal/Stress/Extreme Stress:

Back 4

Normal/Stress/Extreme Stress
Glucose/ glucose/ Ketones

Front 5

what energy does the Heart use during
Normal/Stress/Extreme Stress:

Back 5

Normal/Stress/Extreme Stress:
free FA/ glucose/ Glucose

Front 6

what energy does the Muscles use during
Normal/Stress/Extreme Stress:

Back 6

Normal/Stress/Extreme Stress:
Glucose/ Free FA/ free FA

Front 7

what energy does the RBCs use during
Normal/Stress/Extreme Stress:

Back 7

Normal/Stress/Extreme Stress: Glucose/ Glucose/ Glucose

Front 8

what does hypoglycemia affect first and why? (RBC connection)
what other pathway does the RBC have?

Back 8

• RBC's use only glucose for energy.
• Hypoglycemia will always affect RBCs first, causing a hemolytic anemia.
• The only other pathway RBC's have is the Pentose Phosphate Pathway for making NADPH to maintain the membrane.

Front 9

The most active pathway in your body.

Back 9

Glycolysis:

Front 10

glycolysis is catabolic and anabolic in what locations?

Back 10

Catabolic in all cells except the liver, where it is anabolic.

Front 11

Catabolic State:
who controlls the catabolic state:
system, hormone and pathway

Back 11

• Controlled by the sympathetic system
• Second messenger is cyclic AMP
• Controlled hormonally by Epinephrine and Glucagon

Front 12

Energy Use·
2-4 hrs:
24-28 hrs
>36 hrs

Back 12

2-4 hrs: plasma glucose
24-28 hrs: liver glycogen
>36 hrs: proteolysis, ketogenesis and lipolysis

Front 13

Glucose ⇨G6P:
enzyme
location
km
energy

Back 13

Glucokinase:
Found in hepatocytes and β cells of pancreas
High Km
ATP ⇨ ADP + Pi

Front 14

Hexokinase:
where is it found
Km
energy

Back 14

• Found everywhere else
• Low Km
• ATP ⇨ADP + Pi

Front 15

G6P⇨F6P

Back 15

Phosphoglucose lsomerase

Front 16

F6P⇨F1,6DP
enzyme
activators (2)
inhibitors (2)
energy

Back 16

• PFK-1:
• Activators: AMP and F2,6DP (low energy)
• Inhibitors: ATP and Citrate (high energy)
• Uses ATP

Front 17

F6P⇨F1,6DP
enzyme
uses what for energy

Back 17

PFK2:
• Forms F2,6DP (the allosteric activator of PFK-1)
• Uses ATP

Front 18

F1,6DP⇨DHAP and G3P:
enzyme
enzyme from DHAP to G3P
where does G3P go

Back 18

• Aldolase A
• Triose phosphate isomerase (med conversion of DHAP to G3P and v.v.)
• DHAP
• Glycerol-3-phosphate shuttle
• Triglyceride synthesis

Front 19

G3P⇨G1,3DP:
enzyme
describe its active site
what blocks this reaction
what does it make?

Back 19

• Glyceraldehyde 3 phosphate dehydrogenase
1. Sulphur active site
2. Blocked by mercury poisoning
• NAD+⇨NADH

Front 20

Mercury Toxicity:
enzyme blocked
MCC (2)
what cell is affected first?
what part of the body is affected the most?

Back 20

• MCC: (1) tuna and (2) Biting into a thermometer
• Blocks Glyceraldehyde 3 phosphate dehydrogenase
• RBCs- affected first; brain affected the most.

Front 21

G1,3DP⇨G2,3DP:
enzyme
importance of this rxn

Back 21

• Bisphosphoglycerate mutase
• Shifts curve to the right decreasing affinity of hemoglobin to oxygen

Front 22

G1,3DP⇨3PG:

Back 22

• Phosphoglycerate Kinase
• ADP +Pi⇨ATP (substrate level phosphorylation)

Front 23

3PG⇨2PG:

Back 23

phosphoglycerate mutase

Front 24

2PG ⇨PEP:
enzyme

Back 24

• enolase
• Enol group (phosphate group next to a double bond)

Front 25

PEP ⇨ Pyruvate:
enzyme
what does it make?

Back 25

• pyruvate Kinase
• ADP + Pi⇨ATP (substrate level phosphorylation)

Front 26

Fluoride Poisoning:
enzyme blocked
cause
why is it rare now
clue

Back 26

• Blocks the enzyme Enolase
• Caused in the past by eating-rocks of Fluoride
• Rare today since fluoride. added to water and-toothpaste
• Clue: extra white teeth and bones

Front 27

Gluconeogenesis:
hormones that control it (2)
2nd messanger
organ it occurs (2)

Back 27

• Controlled by Epinephrine and Glucagon
• Second messenger is cyclic AMP
• Occurs only in the liver (90%) and adrenal cortex (10%)

Front 28

Gluconeogenesis:
what part of the cell it is in, when does it run?

Back 28

• Occurs while other tissues are running glycolysis
• Occurs in the mitochondria and cytoplasm

Front 29

Gluconeogenesis Enzymes

Back 29

• Pyruvate carboxylase (rate limiting)
• PEP Carboxykinase
• F16DPase
• G6Pase

Front 30

Pyruvate + C02 ⇨ OAA:
Pyruvate Carboxylase:
• Anapleuritic
• Cofactor:
• Activator:
• Inhibitor:

Back 30

Pyruvate Carboxylase:
• Anapleuritic
• Cofactor: Biotin
• Activator: Acetyl CoA
• Inhibitor: glucose, ADP

Front 31

OAA⇨PEP:
what does it bypass
how many GTP is required?
describe

Back 31

• PEP carboxykinase
• Bypasses Pyruvate kinase
• 1 molecule of GTP is required
• Decarboxylated

Front 32

F1,6BP⇨ F6P:
enzyme

Back 32

• F-1 ,6DPase

Front 33

G6P ⇨ Glucose:
where does this rxn occur? (2)
only place it does not occur? consequence

Back 33

G6Pase:
Missing in muscles, so unable to raise blood sugar
Only in liver and adrenal cortex

Front 34

Starvation State:
what pathway does the liver use?
what pathway does the tissues use?

Back 34

• Liver ⇨ Gluconeogenesis
• Tissues ⇨ glycolysis

Front 35

Well-fed State:
what does you liver go through and tissues

Back 35

• Liver ⇨ Glycolysis
• Tissues ⇨ gluconeogenesis

Front 36

GLUT 1:

Back 36

glucose transporters of all tissues

Front 37

GLUT 2:

Back 37

glucose transporters of liver, pancreatic and β cells

Front 38

GLUT 3

Back 38

glucose transporters of all tissues

Front 39

GLUT 4

Back 39

glucose transporters of fat, skeletal muscle, heart

Front 40

Glycolysis Irreversible Enzymes:

Back 40

• hexokinase (only hexokinase is feedback inhibited by G6P)
• PFK1
• PK

Front 41

Gluconeogenesis Irreversible Enzymes:

Back 41

• G6Pase (liver,adrenals) = "reverse glucokinase"
• F1,6Dpase = "reverse PFK-1"
• Pyruvate carboxylase + biotin (pyruvate ⇨ OAA)
• PEP carboxykinase + ATP (OAA ⇨ PEP)

Front 42

Lactate =>Glucose

Back 42

Cori cycle

Front 43

Pyruvate + NH4 +=> Glucose
cycle and activator

Back 43

Ala cycle
(Activator = AcCoA)

Front 44

Glycerol => Glucose
how is this converted?

Back 44

DHAP

Front 45

Glucose=>2 pyruvate + 2 ATP + 2 NADH
enzyme, inhibitor and activator

Back 45

PFK1
Activator: F2,6BP ,PFK-2)
(Inhibitors: citrate and ATP)

Front 46

how do yo Detect Sugars in the urine and stool

Back 46

• Urine: Clinitest
• Stool: Reducing substances

Front 47

Fructose: when does it enter the cycle.
diabetics
dieters

Back 47

• Enters Glycolysis after PFK1
• Diabetics: least likely to raise blood sugar
• Dieters: fruits eaten at late night can still be metabolized

Front 48

Fructose ⇨ F1P:
enzyme
energy

Back 48

• Fructokinase
• Requires ATP

Front 49

Fructosuria:
pathogenesis
test
presentation

Back 49

• Fructokinase enzyme is missing; Hexokinase fills in
• Fructose in the urine (positive Clinitest)
• Polyuria, polydypsia

Front 50

F1P ⇨ DHAP +Glycerol:
enzyme

Back 50

Aldolase B

Front 51

what are A and B enzymes>
Sucrose⇨Fructose+ Glucose⇨A⇨F1P⇨B⇨DHAP or Glyceraldehyde

Back 51

Fuctokinase and aldolase

Front 52

Essential Fructosuria:

Back 52

>Causes excreted fructose (still have hexokinase)
>fructokinase deficiency

Front 53

Fructosemia "Fructose Intolerance":

Back 53

• Aldolase. B-deficiency
• Fructose-1-phosphate is trapped within cells causing cellular-swelling and-Lysis

Front 54

Galactose Metabolism:
Galactose⇨Gal-1-P:
enzyme
energy

Back 54

• galactokinase
• Requires ATP

Front 55

Galactosuria:
enzyme deficiency
how is this overcome
test
presentation (2)

Back 55

• Galactokinase deficiency
• Hexokinase fills in for galactokinase
•galactose in the urine (clinitest positive)
• Polyuria; polydypsia

Front 56

Gal-1-P + UDP-Glu ⇨ UDP-Gal-1-P⇨ what happens next

Back 56

The glucose will enter glycolysis

Front 57

UDP-GAL-1-P⇨ Glu-1-P
enzyme

Back 57

UDP galactose-4-epimerase

Front 58

Glu-1-P ⇨ Glu-6-P

Back 58

Phosphoglucomutase

Front 59

what are the A and B enzymes?
Lactose⇨Galactose + Glucose ⇨A⇨Gal-1P⇨B⇨G-6P

Back 59

galactokinase and uridyl transferase

Front 60

Galactosemia:
enzyme defieciency
pathogenesis
management for the baby
presentation

Back 60

• uridyltransferase deficiency
• Galactose-1-phosphate builds up in the cells, causing cellular swelling and lysis
• Screened for early, due to galactose in lactose
• cataracts, mental retardation and liver damage

Front 61

Galactose Deficiency:
presentation

Back 61

Cataracts (still have hexokinase)