Overall Things I Keep Getting Wrong Flashcards

1
Q

Mnemonic for heme sythesis

A

Ala pros hyd meth under corporations power houses

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2
Q

Where does lead poisoning act

A

It inhibits
Ala dehydratase enzyme so you’ll have a build up of ala

And
Ferrochelatase

Competes with ca2+

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3
Q

What does glycogen phosphorylase need

A

PLP

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4
Q

Which end of glycogen does glycogen phosphorylase attack

A

Non reducing end

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5
Q

Glycogen phosphorylase when its phosphorylated

A

ACTIVE
FAST state

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6
Q

Glycogen synthase when its NOT phosphorylated

A

ACTIVE
FED state

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7
Q

Symptoms of acute intermittent porphyria

A

5 P’s
Painful abdomen
Port wine urin
Polyneuropathy
Psychological disturbances
Precipitated by drugs alcohol and starvation

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8
Q

How do you treat AIP

A

Glucose and heme

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9
Q

Most common porphyria inhibits what enzyme

A

Uroporphyrinogen decarboxylase

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10
Q

What path is G6P dehydrogenase apart of

A

PPP

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11
Q

Malate to OAA makes and conversely

A

NADH

OAA to malate uses NADH

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12
Q

What pathway is pyruvate dehydrogenase in/ what does it do

A

Pyruvate——>Acetyl CoA

TCA

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13
Q

What pathway is pyruvate carboxylase apart of what does it do

A

Pyruvate —>OAA
TCA
GNG

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14
Q

What does pyruvate carboxylase need with it

A

CO2
ATP
Biotin

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15
Q

Alanine aminotransferase does what and where

A

Pyruvate<—>alanine
Cytoplasm

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16
Q

Acetyl can go to make

A

FA
Cholesterol
TCA cycle

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17
Q

Pyruvate<-?->lactate
Where

A

Lactate dehydrogenase
Cytoplasm
RBC
During strenous muscle activity

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18
Q

What does pyruvate<—>lactate make

A

regenerates NAD+

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19
Q

what can inhibit pyruvate dehydrogenase

A

NADH from FA

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20
Q

First barrier to cross in GNG all the enzyme names

A

Pyruvate —pyruvate carboxylase—> OAA

OAA —PEP carboxykinase—>PEP

If it goes

pyruvate > OAA —malate dehydrogenase—> malate

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21
Q

Fructose 1,6 bisphosphate -?-> fructose 6 phosphate

And vice versa

A

Fructose 1,6 bisphosphatase

PFK1

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22
Q

Glucose 6 phosphate -?-> glucose

And vice versa

A

Glucose 6 phosphatase

Hexokinase/glucokinase

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23
Q

Glucose 6 phosphatase and fructose 1,6 bisphosphatase are both

A

Inducible by glucagon

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24
Q

Glucose 6 phosphatase is used where

A

GNG and glycogen pathway

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25
Q

Tyrosine effects with def in dihydrobiopterin reductase or dihydrobiopterin synthetase

A

Decreased catecholamines

26
Q

Tyrptophan effects with def in dihydrobiopterin reductase or dihydrobiopterin synthetase

A

Decreased serotonin

27
Q

Trigger for all alcohol problems

A

Excess NADH

28
Q

How does NADH inhibit TCA cycle

A

Inhibits is citrate dehydrogenase
And
Inhibits α-ΚG dehydrogenase
And
It favors the production of Malate NOT OAA

29
Q

When NADH is high from drinking which does it favor OAA or Malate

What does this result in

A

Malate

Results in decreased GNG = hypoglycemia

30
Q

Why do alcoholics have lactic acidosis

A

Bc their body has way too much NADH so it needs to regenerate more NAD+. IT does this by utilizing pyruvate>lactate path bc this takes NADH and makes NAD+. The result is a ton of lactate

31
Q

What is an activator of acetyl CoA carboxylase and what does it do

A

Citrate is an activator

Acetyl-CoA —-acetyl CoA Carboxylase—> malonyl CoA—— β oxidation

32
Q

What does insulin do in the adipose tissue

A

Dephosphorylation of pyruvate dehydrogenase and lipase in adipose tissue

33
Q

What does insulin do in muscle

A

Dephosphorylates glycogen synthase and glycogen phosphorylase

34
Q

Glycolysis RLE

A

PFK1

35
Q

GNG RLE

A

Fructose 1,6 bisphosphatase

36
Q

TCA RLE

A

Isocitrate dehydrogenase

37
Q

Glycogen synthesis RLE

A

Glycogen synthase

38
Q

glycogenolysis RLE

A

Glycogen phosphorylase

39
Q

HMP shunt RLE

A

Glucose 6 phosphate dehydrogenase (G6PD)

40
Q

De novo pyrimidine sythesis RLE

A

Carbamoyl phosphate synthetase II

41
Q

De novo purine sythesis RLE

A

Glutamine PRPP amidotransferase
Aka
AMIDOPHOSPHORIBOSYL transferase

42
Q

Urea cycle RLE

A

Carbamoyl phosphate synthetase I

43
Q

Fatty acid sythesis RLE

A

Acetyl CoA carboxylase (ACC)

44
Q

Fatty acid oxidation RLE

A

Carnitine acyltransferase I

45
Q

Ketogenesis RLE

A

HMG CoA synthetase

During ketogenesis you can have a lot of KiSs chocolate

46
Q

Cholesterol sythesis RLE

A

HMG CoA reductase

She you make a lot of cholesterol you’re fat and angry and you “see (C) Red”

47
Q

β cells release what vs α cells

A

β = insulin

α = glucagon

Glucagon has an a so glucagon is alpha

48
Q

When you’re fasting what is increasing

A

Glucagon
Triglyceride hydrolysis
Glycogen degration
GNG
KB production
Release of AA

49
Q

When you are fed what is being synthesized

A

Triglycerides
Glycogen
FA
VLDL
Protein - replenish any protein degraded during previous post absorptive period

50
Q

When you see insulin think

A

DEPHOSPHORYLATION by activating phosphatase

51
Q

Which enzymes does insulin work INdirectly on what do they do

A

PFK2 and fructose 2,6bisphosphatase

Increases level of fructose 2,6 bisphosphate which activates PFK1 and continues glycolysis

52
Q

When you see glucagon think

A

PHOSPHORYLATION by PKA (protein kinase)

53
Q

What are they key enzymes glucagon phosphorylates

A

Pyruvate kinase
Glycogen sythase
Glycogen phosphorylase
Acetly CoA carboxylase

54
Q

What + activates PEP>Pyruvate

A

Fructose 1,6 bisphosphate

55
Q

What do insulin and glucagon act on in β oxidation

A

Hormone sensitive lipase

56
Q

glucagon receptor is what and what does it do

A

G protein coupled receptor
Increases adenylate cyclase
Which turns ATP to cAMP
Which activates kinase a
Which PHOSPHORYLATES

57
Q

Insulin receptor is what and what does it do

A

Tyrosine kinase receptor
It triggers protein phosphatases
Which will DEPHOSPHORYLATE

58
Q

What are all the enzymes in FA synthesis insulin induces and which are the ones that have a special function

A

Malic enzyme - NADPH
G6PDH - increase NADPH
FA sythase
Acetly CoA carboxylase
Citrate lyase

59
Q

LPL in response to insulin and glucagon and why

A

Insulin increases it in adipose BC we want to break down triglycerides into FA for storage

Glucagon decreases it in adipose BC we don’t want that

60
Q

Fight of flight in the liver vs skeletal muscle

A

Liver will have phosphorylation of PFK2 and F2,6bisphosphatase. The result is to decrease glycolysis here and increase GNG.

Muscle will have phosphorylation of PFK2 and F2,6 bisphosphatase. This will result in an increase of glycolysis here.