Ppal99 Dissecting The Usmle 1,2,3 Pyruvate And Kreb Cycle

Front 1

pyruvate has three complexes what are its complexes?

Back 1

• αKG dehydrogense
• Branched chain dehydrogense
• PDH complex

Front 2

pyruvate has three complexes what are its cofactors?

Back 2

TPP
lipoic acid
coenzyme A
NAD
FAD

Front 3

TPP: what does it do? vitamin?

Back 3

decarboxylation
vitamin B1 (thiamine)

Front 4

Iipoic acid: vitamin, function

Back 4

Accepts Acetyl group
lipoic acid (B4)

Front 5

function of Coenzyme A? vitamin?

Back 5

Final acceptor =>AcCoA
Panthenoic acid (B5)

Front 6

NAD: what does it oxidize? end product? vitamin?

Back 6

oxidizes FADH2 => NADH
Niacin (B3)

Front 7

FAD: what does it oxidizes? what is the end product?

Back 7

oxidizes Lipoic Acid => FADH2 Riboflavin(B2)

Front 8

5 fates of pyruvate

Back 8

1) Lactate
2) Alanine
3) Acetate
4) OAA
5) Acetyl CoA

Front 9

Lactate: aerobic/anaerobic? what does it use? NADH =>?

Back 9

• Anaerobic
• Uses LDH
• NADH => NAD+

Front 10

Alanine: aerobic/anaerobic, when is it formed?, what transaminase does it use?, when is it increased?

Back 10

• Anaerobic, formed due protection from overproduction of lactic-acid
• Uses ALT
• increases during exercise leaks"into-blood

Front 11

Acetate: ethanol=>?, NAD+=>, enzyme

Back 11

Ethanol => Acetaldehyde
NAD+=>NADH
Alcohol dehydrogenase

Front 12

Acetaldehyde⇨Acetate: NAD+, enzyme, what drug block this enzyme and what does it lead to?

Back 12

• NAD+⇨-NAD
Acetaldehyde dehydrogenase
• Disulfuam and Metronidazole inhibit this enzyme⇨ Acetaldehyde⇨N /V

Front 13

Macrosteatosis: (4), how do alcoholics get heart failure?

Back 13

• large fat droplets
• Atherosclerosis
• High Ketone
• Acetone smell
• Acidosis⇨GABA connection⇨heartfailure

Front 14

Microsteatosis:

Back 14

• Reye's syndrome
• Acetaminophen
• Pregnancy

Front 15

Alcoholics pathogenesis of fatty liver

Back 15

• High NADH; body thinks you're in a high energy state
• Inhibits gluconeogenesis, causing hypoglycemia
• Then use fat, leading to hyperlipidemia/fatty liver

Front 16

Alcoholics: tx

Back 16

• Tx: thiamine +Glucose (to prevent lactic acidosis)
• Thiamine deficient alcoholics: have even less AcCoA ⇨ more lactic acid

Front 17

OAA: enzyme, cofactor, describe

Back 17

• Anapleuritic
• Pyruvate Carboxylase
• Cofactor: Biotin

Front 18

Acetyl CoA: when does it work, function, uses what enzyme and NAD =>

Back 18

• If 02 is present
• removes CO2
• Uses Pyruvate Dehydrogenase
• NAD+ ~ NADH

Front 19

Pyruvate Dehydrogenase:
structure, # of proteins,steps and cofactors

Back 19

• Quaternary
• Three proteins
• Five steps
• Five cofactors
• Five vitamins

Front 20

Pyruvate Dehydrogenase:
• Allosteric Activator:
• Allosteric Inhibitor:
• Rate limiting enzyme for
• rxn

Back 20

• Allosteric Activator: pyruvate
• Allosteric Inhibitor: Acetyl CoA
• Rate limiting enzyme for Krebs cycle
• NAD+ ~ NADH

Front 21

4 fates of acetyl CoA

Back 21

FA
ketones
cholesterol
kreb cycle

Front 22

Acetyl CoA ⇨ FA

Back 22

acetyl CoA decarboxylate

Front 23

Acetyl CoA ⇨ ketones

Back 23

HMG coA synthase

Front 24

Acetyl CoA ⇨ cholesterol

Back 24

HMG CoA reductase

Front 25

Acetyl CoA ⇨ kreb cycle

Back 25

isocitrate dehydrogenase

Front 26

Kreb Cycle Components:

Back 26

"Cindy Is Kinky, So She Forniates More Often"
• Isocitrate
• αKG
• Succinyl CoA
• Succinate
• Fumarate
• Malonate
• OAA

Front 27

Isocitrate
inhibits what enzyme

Back 27

inhibits PFK-1

Front 28

αKG
rxn involved in

Back 28

transamination

Front 29

Succinyl CoA
make what and how

Back 29

-uses odd-chain FA, makes ringed structures (Ex: heme)

Front 30

AcetylCoA:
what pathway it uses it?

Back 30

FA synthesis; ketogenesis

Front 31

Isocitrate Dehydrogenase

Back 31

rate limiting enzyme

Front 32

Succinate Dehydrogenase: location, another name and energy it makes

Back 32

attached to mitochondria wall, ETC II (FADH2)

Front 33

TCA Substrates: Pyruvate

Back 33

Gly, Ala, Ser "Elastase victims"

Front 34

TCA Substrates: Acetyl-CoA

Back 34

Lys, Leu, "Bulkies" (Phe,Tyr, Trp)

Front 35

TCA Substrates: OAA

Back 35

Asp, Asn

Front 36

αKG

Back 36

glu and gln

Front 37

fumarate

Back 37

Phe and tyr

Front 38

OAA + AcCoA ⇨ Citrate:

Back 38

citrate synthase

Front 39

Citrate ⇨ Isocitrate: enzyme, function of citrate, what is the citrate shuttle?

Back 39

• Uses aconitase
• Citrate: Allosteric Inhibitor of PFK. Allosteric activator for FA synthesis
• Citrate shuttle: feeds acetyl CoA into fatty acid-synthesis

Front 40

αKetoglutarate ⇨Succinyl-CoA: enzyme, what does it release? NAD+ =>

Back 40

• Uses αKetoglutarate Dehydrogenase
• Releases C02
• NAD+⇨NADH

Front 41

Isocitrate ⇨ α-Ketoglutarate: enzyme, what does it do? and reaction

Back 41

• Uses isocitrate Dehydrogenase
• Regulatory step
• Releases CO2
• NAD+⇨NADH

Front 42

αKetoglutarate

Back 42

is the intermediate for all transaminase reactions
α-Ketoglutarate + Ala ⇨ glu + pyr

Front 43

what builds up in concentration during periods of high transamination

Back 43

glutamate, Aspartate, Alanine

Front 44

what happens during amino acid breakdown?

Back 44

Glutamate is still increasing, holding area for amine groups until shunted into Urea cycle.

Front 45

what transaminase in the most important?

Back 45

20 transaminases, one for each amino acid; AST/ALT most important

Front 46

All transaminases uses what vitamin as a cofactor? presentation if there is a deficiency?

Back 46

Vit B6 as a cofactor. if there is a deficiency, it causes neuropathy

Front 47

Succinyl-CoA ⇨ Succinate: enzyme, function

Back 47

• Uses succinyl CoA Synthetase
• Split sulphur bond to make GTP

Front 48

Succinyl CoA is responsible for: (6)

Back 48

1. Heme synthesis
2. Porphyrin ring substrate
3. Odd chained fatty acids feed into Succinyl-CoA.
4. Odd numbered fats break down into Propionic acid
5. Propionic CoA carboxylated becomes Methylmalonic acid CoA, which is then mutated to succinyl-CoA via Methylmanonyl mutase
(vit B12 factor) .

Front 49

Succinate ⇨ Fumarate: enzyme, what does it form?

Back 49

• Succinate Dehydrogenase is the only Kreb Cycle enzyme firmly anchored to the inner mitochondial membrane; attached to Complex II
• Forms FADH2

Front 50

Fumarate ⇨ Malate: enzyme, what is added?

Back 50

• Uses Fumarase
• Adds H20

Front 51

Malate ⇨ OAA: enzyme, rxn

Back 51

• Uses malate dehydrogenase
• NAD+⇨NADH

Front 52

ATP count:
Glycolysis:
Kreb:
G-3P shuttle:
Malate-Asp shuttle

Back 52

Glycolysis: 8 ATP "8 hrs = 1 work-day"
Kreb: 24ATP "24 hrs = 1 day"
G-3P shuttle: 4 ATP
Malate-Asp shuttle 6 ATP

Front 53

Malate-Asp shuttle: where do products end up? when is it used?

Back 53

Product ends up in cytosol, This shuttle is dominant since the G3P shuttle-is wastefull

Front 54

G-3P shuttle: when is it used?

Back 54

Used a great need of energy is needed; i.e. the need supercedes the waste
• Rapid Growth: Ages 0-2,4-7; puberty
• Rapid Division: pregnancy, cancer, burns, crush injuries

Front 55

OAA => Aspartate: enzyme, what is added, how does the cycle work?

Back 55

AST- aspartate Transaminase
Add NH3
Asp travels out to cytoplasm and gets converted back to OAA by AST

Front 56

OAA => Malate: rxn, how does the cycle go? energy wasted?

Back 56

• NADH => NAD+
• Malate travels back into mitochondria; converts to OAA; regains NADH
• No energy wasted

Front 57

Viral Hepatitis:

Back 57

Virus destroys cell membrane => 1 AST, 1 ALT leak out

Front 58

Alcoholic Hepatitis:

Back 58

Alcohol dissolves all membranes => 1 ALT, 2 AST leak out

Front 59

Glycerol 3-Phosphate Shuttle:
DHAP => G-3-P:

Back 59

glycerol 3 dehydrogenase
NAD=>NADH+

Front 60

G-3-P => DHAP: what is formed? ATP lost? why is it 36-38 ATP made?

Back 60

• FADH is formed
• 2 Atp is lost due to running the cycle twice.
• The reason for 36-38 ATPs per mole glucose in textbooks depends on which shuttle is used