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Biochemistry > Practical MCQ > Flashcards

Practical MCQ Flashcards

1
Q

who is the disease gout associated with

A

the disease of the kings because gout was experienced by people who were wealthy

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2
Q

what causes the turnover of DNA and RNA? and why is it important?

A

endonucleases turnover RNA and DNA molecules. this is important people, in DNA repair of double strands break, you need the cleaning of the double-strand break before the DNA can be repaired.

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3
Q

where are endonucleases prepared

A

on oligonucleotides

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4
Q

what do phosphodiesters give?

A

they give bases with the sugar units still attached.

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5
Q

what can be phosphorylated to nucleoside triphosphates

A

free bases

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6
Q

what can be done with nucleoside triphosphate

A

they can be reused

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7
Q

what are the 2 different pathways of nucleotide catabolism

A

1- re-usage of bases
this is the energy-efficient pathway
2- degradation
this pathway is taken when necessary
there is usually a balance between the 2 pathways

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8
Q

in the pathway of purine degradation, what does adenosine deaminase do?

A

it is an enzyme deaminating adenosine into inosine

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9
Q

in the pathway of purine degradation, what does guanine deaminase do?

A

it is an enzyme deaminating guanine into xanthine

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10
Q

in the pathway of purine degradation, what does xanthine oxidase do?

A

it changes hypoxanthine into xanthine

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11
Q

what does xanthine oxidase produce?

A

it produces uric acid from xanthine.
uric acid is either excreted by urine or reabsorbed by the kidneys.
in the practical, we looked at uric acid production by the enzyme xanthine oxidase

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12
Q

in the pathway of purine degradation, what has double-ring structure

A
  • adenosine
  • guanosine
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13
Q

in the pathway of purine degradation, what are the bases

A
  • hypoxanthine
  • xanthine
  • guanine
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14
Q

what is associated with hyperuricaemia

A

uric acid is associated with hyperuricaemia.
uric acid is the end product of purine degradation

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15
Q

what is the normal amount of serum urate and whats the high amount of serum urate

A

Normal amount is 4.5 +/- 1.2 mg/dl in males
the high amount is exceeding 7 mg/dl

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16
Q

what is hyperuricaemia associated with

A
  • impaired uric acid excretion
  • secondary hyperuricaemia
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17
Q

what happens when there is a high concentration of urate in the bloodstream

A

urate salts precipitate

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18
Q

what happens due to crystals of urate salt in the joints

A

it may precipitate gout.
this leads to polyarthritis and nephropathy (problems with the kidneys)

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19
Q

how do urate salts look like

A

quite pointy, they look like needle-shaped crystals

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20
Q

what happens when urate salts precipitate

A

-when urate salts precipitate, they attract macrophages because they are in places they shouldn’t be
- the macrophages absorb/eat they crystals
- these crystals stimulate an inflammatory reaction. this is because when the macrophages eat the crystals, they call for help by releasing cytokines.
- these cytokines induce more inflammatory cells to differentiate
- they start the destruction of the underlying bone tissue and cause inflammation in the joint capsule.
middle age men have more incidents of gout

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21
Q

what is the treatment for gout

A

-dietary
they look at the diet, advice the patients how to improve their diet, especially reduction of purine-rich foods.
- xanthine oxidase inhibitors
because xanthine oxidase is the enzyme producing uric acid

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22
Q

what is incorporated into cellular nucleic acids in a small percentage

A

only small percentage of ingested nucleic acids is incorporated into cellular nucleic acids

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23
Q

what is dietary purines generally converted into and by what

A

dietary purines are usually converted to uric acid by intestinal mucosal cells

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24
Q

what happens to most of the uric acid that is produced

A

it enters the blood and is eventually excreted in the urine

25
Q

what happens if we eat food that is rich in purine, like eggs and meat

A

then there will be a subsequent increase of uric acid in the circulation

26
Q

how are attacks of gout described/compared to

A
  • the agony of childbirth
  • its like being jabbed with a ‘million tiny white-hot needles’
27
Q

what food items increase the chance of gout attacks

A
  • meat, because it contains a lot of cells including DNA and RNA
  • alcohol, alcohol leads to dehydration, if you are dehydrated then you will have higher precipitation of uric acid and its also leads to a gout attack.
28
Q

which 5 disease’s is hyperuricemia a risk factor to

A
  • Atherosclerosis
  • Hypertension
  • cardiovascular diseases
  • chronic kidney disease
  • stoke
29
Q

what are the 2 forms of hyperuricaemia?

A
  • primary
  • secondary
30
Q

what is primary hyperuricaemia caused by

A

it is caused by either:
- overproduction of uric acid
- impairment of renal secretion

31
Q

what is secondary hyperuricaemia caused by and with example

A

it is caused by underlying diseases, mostly diseases with increased cell turnover, e.g. psoriasis, and malignancies.
Example
tumour lysis syndrome, this is when chemotherapy is initiated and there is a lot of tumour cell death. these cells will then release their internal contents into the bloodstream. then this leads to an increase in uric acid.

32
Q

what % of patients with gout are overproducers or have impaired renal uric acid secretion

A

15-25% are overproducers
75-85% of patients have impaired renal uric acid secretion

33
Q

what happens in the kidneys with uric acid

A

uric acid is first reabsorbed before actively secreted in the tubular system

34
Q

what leads to the formation of kidney stone

A

both a decrease in reabsorption and an increase in secretion

35
Q

what is urate pool dependent on, and how is it balanced

A

urate pool is dependent on:
- dietary purine intake
- tissue nucleic acids
- endogenous purine synthesis

how is the urate pool balanced by:
- gut excretion
- renal excretion

36
Q

what leads to hyperuricaemia in uric acid metabolism

A

overproduction of urate pool
underexcretion of urate pool
if the production of the urate pool is broken, which leads to overproduction or underexcretion then it leads to hyperuricaemia

37
Q

what can hyperuricaemia cause

A

it can be asymptomatic
it can cause acute gout attack or chronic tophaceous gout
the main problem it can cause is renal manifestations

38
Q

what are the 3 main benefits of uric acid

A
  • uric acid is an important factor in lengthening primate lifespans as it protects against reactive oxygen species
  • antioxidants are compounds such as vitamins A, C and E, uric acid is thought to be another antioxidant.
  • urate microcrystals are immunostimulatory
    uric acid was shown to be a principal endogenous danger signal released from injured cells. eliminating uric acid in vivo inhibits the immune response to antigens associated with injured cells except for antigens presented by activated dendritic (antigen-presenting) cells.
39
Q

where is xanthine oxidase present in large amounts

A
  • liver
  • intestinal mucosa
  • milk
40
Q

what are the 2 forms of xanthine enzyme

A
  • xanthine dehydrogenase (XD)
    uses NAD+ as an electron acceptor
    predominant in normal tissue
  • xanthine oxidase (XO)
    it is the proteolytically processed form
    uses O2 (oxygen) as an electron acceptor
41
Q

what does the xanthine enzyme process

A

the enzyme processes
- FAD
- nonheme Fe-S centers
- molybdenum cofactor as electron transferring group, from MO4 to MO6

42
Q

what does xanthine oxidase catalyse hypoxanthine and xanthine to and what is the byproduct

A

xanthine oxidase catalyses hypoxanthine into xanthine
it then catalyses xanthine into uric acid. it produces O2- as byproduct, which is reduced by NAD+ (XD)

43
Q

what happens to O2- than is produced by xanthine oxidase

A

O2- is detoxified by superoxide dismutase and catalase/ glutathione peroxidase

44
Q

what is allopurinol and what does it do

A

allopurinol is an inhibitor of xanthine oxidase
it inhibits xanthine oxidase because it remains tightly bound to the active site of the enzyme

45
Q

other than allopurinol, what is another inhibitor of xanthine oxidase

A

Febuxostat is a non-purine-selective, non-competitive inhibitor of xanthine oxidase

46
Q

what is reperfusion injury

A

it is tissue and cellular damage that occurs when inadequate blood is supplied to a region of the body, followed by the resumption of blood flow

47
Q

what does inadequate perfusion lead to

A

it leads to a lack of oxygen, depletion of high energy molecules (e.g. ATP) and build-up of toxic metabolites

48
Q

what is the consequence of reduced blood supply

A

reduce blood flow leads to the conversion of xanthine dehydrogenase to xanthine oxidase because of the increase of calcium that activates protease. this results in the production of O2- instead of NADH which leads to reperfusion.

49
Q

what happens with the onset of reperfusion

A

with the onset of reperfusion, there is an increase in reactive oxygen species (ROS)

50
Q

in reperfusion injury of the heart, what is it called when there is no later blood flow and what is the infarct size

A

myocardial ischemia in absence of reperfusion
infarct size - 70%

51
Q

what is myocardial ischemia with reperfusion

A

it means there is reperfusion, which can be because of a stent or drugs which dissolve the block. this leads to a reduction in the infarct size by 40% but this has a 30% of infarct size because of lethal reperfusion injury which is preventable

52
Q

what is myocardial ischemia with reperfusion and cardioprotection

A

it inhibits the release of the reactive oxygen species, which then lowers the infarct size.
the amount of damaged tissue is much lower, there is a further decrease of 25% with cardioprotective as it inhibits the increase in reactive oxygen species when there is reperfusion.

53
Q

what are 2 buffers used in the practical

A
  • hypoxanthine
  • xanthine
54
Q

how did we look at the release of oxygen reactive species in the practical

A

we looked at the release of oxygen reactive species when hypoxanthine is catalysed to xanthine

55
Q

what did we measure in the practical

A

we measured the appearance of 02- (oxygen reactive species) and the appearance of uric acid.
uric acid can be measured by itself but 02- can’t be measured by itself thus you need to add cytochrome C to measure 02-

56
Q

in the practical, what did we measure at 550nm and 300nm

A

at 550nm, we looked at what was happening to cytochrome C to see the appearance of 02-
at 300nm, we measured the appearance of uric acid

57
Q

what does allopurinol do in purine degradation
why do you add superoxide dismutase in purine degradation

A

you add allopurinol as it is an inhibitor of xanthine oxidase
you also add superoxide dismutase as it is an important enzyme in the detoxification of reactive oxygen species (ROS). superoxide dismutase with catalase gets rid of 02-

58
Q

in the practical, how do we measure cytochrome C

A

there is a colour change after 3 mins from the starting material to the end product after the enzyme has done its duty.
we measure the colour change using a spectrophotometer for 3 minutes.

59
Q

what is the overview of the practical and how should the results/graph look like in the 2nd experiment

A

we have 2 buffers:
- xanthine
- hypoxanthine
in the practical, to both xanthine and hypoxanthine, you add superoxidase dismutase (SOD) and allopurinol.

in the 2n experiment,
when there is no inhibitor added (which is experiment 1,4 and the first mins of all the other experiments), then the line in the graph should be linear and rising.
when the inhibitor is added, then you should see a flat line because the enzyme is no longer able to convert.

Biochemistry (9 decks)

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