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Fluids, Nutrition and Metabolism > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

What is the Warburg effect?

A

All tumours show an increased rate of glucose uptake and glycolysis.
Indicates that the cancer will be more aggressive.

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2
Q

What is the function of 18F-fluorodeoxyglucose?

A

This is used to identify metastasised tumours through which parts of the body are using up more glucose than they need.

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3
Q

List 2 drugs that inhibit glycolysis?

A

GADPH inhibitor

3-bromopyruvate

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4
Q

How does inhibiting glycolysis show anti cancer effect?

A

This inhibits the growth of the cancer cells as they have no source of glucose.
It also increases the sensitivity of drugs that can directly affect cancer cells.

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5
Q

Name a drug that inhibits ATP synthase

A

Oligomycin

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6
Q

How do weak acids effect the electron transfer chain?

A

They allow H+ to enter the matrix without doing any work, which leads to the generation of heat rather than ATP. Common in brown adipose tissue.

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7
Q

What is an example of a weak acid that used to be used for weight loss?

A

Dinitrophenol (has adverse effects)

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8
Q

What do mitochondrial diseases affect?

A

The electron transport chain

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9
Q

What are some common symptoms of mitochondrial diseases?

A

Increased lactic acid and alanine concentration in the blood. (higher rate of glycolysis)

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10
Q

Which cycle does a deficiency of glucose 6-P dehydrogenase affect?

A

The pentose phosphate pathway

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11
Q

What occurs to RBCs in glucose 6-P dehydrogenase deficiency?

A

There is less NADPH so less protection against oxidative stress for erythrocytes, resulting in haemolytic anaemia.

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12
Q

How does lack of glucose 6 phosphatase affect glycogen storage?

A

Liver cannot break down glycogen to release circulating glucose into the bloodstream.
Liver may become enlarged.

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13
Q

What happens when there is liver phosphorylase deficiency?

A

The body cannot mobilise liver glycogen, liver becomes enlarged there is mild hypoglycaemia.

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14
Q

What is the function of FOX01 genes?

A

They inhibit the transcription of gluconeogenesis genes.

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15
Q

How does lack of insulin signalling affect gluconeogenesis?

A

Lack of insulin signalling means that gluconeogenesis is not inhibited by FOX01, so it continues at high levels even when in the fed state (which is bad)

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16
Q

What does MACD stand for?

A

Medium chain co-acyl A dehydrogenase deficiency

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17
Q

What occurs in MACD?

A

Body cannot metabolise the medium chain fatty acids, resulting in an accumulation of them in the plasma and in urine.
Cannot change metabolism accordingly therefore has hypoglycaemia and is hypoketotic when fasting.

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18
Q

How is MACD treated?

A

Low fat diet, carnitine supplements, avoid fasting.

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19
Q

Which is more regulated, fructose or glucose metabolism?

A

Fructose metabolism is less regulated than glucose metabolism.

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20
Q

Why is fructose metabolism being less regulated a negative thing?

A

The pancreas does not have a GLUT 5 transporter, so fructose does not increase the release of insulin or leptin. Means that the brain receives no messages to control its appetite.

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21
Q

What is glycogen synthase deficiency?

A

Inability to form glycogen so there is no storage of glycogen.
Means patient will be hypoglycaemic, has a need for frequent snacking to maintain a high blood glucose, tires easily in exercise.

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22
Q

What is glycogen branching enzyme deficiency?

A

An accumulation of unbranched, insoluble glycogen chains, especially in heart and liver.
Can cause liver cirrhosis.

23
Q

What is there a deficiency of in Beri Beri disease?

A

Thiamine B1 deficiency

24
Q

What occurs in thiamine deficiency?

A

Body is unable to make a cofactor of pyruvate dehydrogenase. Means pyruvate cannot be metabolised.
Can result in tingling snd confusion as the nervous system is most affected by this.

25
Q

What are the symptoms of pyruvate dehydrogenase deficiency?

A

Delayed development, reduced muscle tone, seizures.

26
Q

Why is pyruvate dehydrogenase deficiency bad?

A

Pyruvate cannot produce ACoA for fatty acid oxidation.
And increased production of lactate as it cannot enter the citric acid cycle.
High pyruvate and lactate levels in the plasma.

27
Q

How is pyruvate dehydrogenase deficiency treated?

A

With a ketogenic diet with minimum carbohydrates (5%).

Ensures that cells use ACoA from fat metabolism not from pyruvate.

28
Q

What do fluoroacetates do?

A

Causes suicide inhibition as fluoroacetyl CoA reacts with citrate synthase (instead of normal ACoA), which produces fluorocitrate that then permanently inhibits aconitase in the next part of the cycle.
Citrate then accumulates, further inhibiting glycolysis and fatty acid oxidation.

29
Q

What is the result of fluoroacetates?

A

The body starves its cells as it does not think it needs to metabolise ACoA.

30
Q

What is the treatment of fluoroacetates?

A

Ethanol is given which is metabolised to acetate, so it can compete with the fluorocitrate to slow down the rate of inhibition.

31
Q

What happens if there is too much (excess) citrate/AcoA for the enzymes?

A

The excess citrate will be released into the cytosol, indicating that the body is breaking down more fuel than it actually needs.
In liver and adipose tissue this stimulates fatty acid synthesis, in muscles it inhibits glycolysis and fatty acid oxidation (as there is already enough).

32
Q

What happens if there is an inadequate amount of oxaloacetate?

A

This means there is more ACoA than what can react with the oxaloacetate. The excess ACoA is used for ketogenesis instead.

33
Q

What are 3 ways in increase the activity of the citric acid cycle?

A

1) Increase activity of the 3 regulated enzymes
2) Increase supply of ACoA
3) Increase the concentration of intermediates

34
Q

What are the 3 regulates enzymes for the citric acid cycle?

A

Citrate synthase
Isocitrate dehydrogenase
Alpha ketoglutarate dehydrogenase

35
Q

In the fed state where is most ACoA supplied from?

A

Glycolysis

36
Q

In the fasting state where is most ACoA supplied from?

A

From fatty acids (glycolysis is inhibited)

37
Q

During exercise where is most ACoA supplied from?

A

Glycolysis and fatty acids, and the concentration of intermediates is increased

38
Q

Why do there have to be multiple sources of ACoA?

A

The oxaloacetate used in the citric acid cycle is the same as the one made as a result of the citric acid cycle.
Means that other compounds have to be metabolised to generate more oxaloacetate.
You cannot use ACoA to make more intermediates than were present to start off with.

39
Q

What is the short term regulation of the urea cycle?

A

The concentration of Glutmate and ACoA stimulates the activity of N-Acetylgultamate therefore increasing the production of Carbomoyl phosphate, which is the first step in the urea cycle.

40
Q

What is the long term regulation of the urea cycle?

A

The urea cycle enzymes are transcriptionally regulated.

Hormones involved in this are glucagon, adrenaline and glucocorticoids.

41
Q

Can you detect urea cycle deficiencies in a foetus?

A

No, can only detect after the child is born.

42
Q

What are common symptoms indicating urea cycle disorders?

A

Hyperammonaemia, vomiting, lethargy, mental retardation, accumulation of nitrogenous compounds.
(Usually seen clearly in situations with a high protein turnover eg. a car accident)

43
Q

What are the main 3 methods of controlling urea cycle defects?

A

1) Decreasing protein intake and avoiding catabolic states such as fasting.
2) Provide alternative routes for nitrogen excretion.
3) Supplement nitrogen compounds as is needed due to altered metabolism.

44
Q

Name 2 substances that can be used to provide an alternate route for nitrogen excretion

A

1) Phenyl acetate

2) Benzoate

45
Q

What is the result of carbomoyl P synthetase deficiency in the urea cycle?

A

Ammonium levels of the blood increase, as this enzyme is the first step in removing NH4+ from the body.

46
Q

Is ornithine transcarbomoylase a hereditary disorder?

A

Yes, it is an X linked hereditary disorder.

47
Q

What substances accumulate in ornithine transcarbomoylase deficiency?

A

Orotate and nitrogen (in the form of glycine and glutamine) accumulates.

48
Q

What is arginosuccinate synthetase deficiency also called?

A

Citrullinaemia (accumulation of citrulline)

49
Q

How is citrullinaemia treated?

A

Arginine supplementation helps to produce ornithine, so ammonium can still be excreted to some extent in the form of citrulline.

50
Q

How is is arginosuccinase deficiency treated?

A

Supplementation of arginine, as this will go through the urea cycle and produce urea up until the production arginosuccinate.

51
Q

What is arginase deficiency also called?

A

Hyperargininaemia

52
Q

Does arginase deficiency have a great effect on the body?

A

No, arginine can be excreted in the urine, so supplementation of arginine is not needed.

53
Q

What are the symptoms of NAGS deficiency?

A

NAG stimulates/regulates carbomoyl P synthetase, therefore lack of NAG will also result in severe hyperammonaemia.

54
Q

How is NAGS deficiency treated?

A

Treated with N-carbamoyl glutamate (does not stimulate CPS as efficiently as NAGS)

Fluids, Nutrition and Metabolism (6 decks)

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