Practical MCQ

Question 1

who is the disease gout associated with

Answer 1

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

Question 2

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

Answer 2

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.

Question 3

where are endonucleases prepared

Answer 3

on oligonucleotides

Question 4

what do phosphodiesters give?

Answer 4

they give bases with the sugar units still attached.

Question 5

what can be phosphorylated to nucleoside triphosphates

Answer 5

free bases

Question 6

what can be done with nucleoside triphosphate

Answer 6

they can be reused

Question 7

what are the 2 different pathways of nucleotide catabolism

Answer 7

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

Question 8

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

Answer 8

it is an enzyme deaminating adenosine into inosine

Question 9

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

Answer 9

it is an enzyme deaminating guanine into xanthine

Question 10

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

Answer 10

it changes hypoxanthine into xanthine

Question 11

what does xanthine oxidase produce?

Answer 11

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

Question 12

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

Answer 12

• adenosine
• guanosine

Question 13

in the pathway of purine degradation, what are the bases

Answer 13

• hypoxanthine
• xanthine
• guanine

Question 14

what is associated with hyperuricaemia

Answer 14

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

Question 15

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

Answer 15

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

Question 16

what is hyperuricaemia associated with

Answer 16

• impaired uric acid excretion
• secondary hyperuricaemia

Question 17

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

Answer 17

urate salts precipitate

Question 18

what happens due to crystals of urate salt in the joints

Answer 18

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

Question 19

how do urate salts look like

Answer 19

quite pointy, they look like needle-shaped crystals

Question 20

what happens when urate salts precipitate

Answer 20

-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

Question 21

what is the treatment for gout

Answer 21

-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

Question 22

what is incorporated into cellular nucleic acids in a small percentage

Answer 22

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

Question 23

what is dietary purines generally converted into and by what

Answer 23

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

Question 24

what happens to most of the uric acid that is produced

Answer 24

it enters the blood and is eventually excreted in the urine

Question 25

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

Answer 25

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

Question 26

how are attacks of gout described/compared to

Answer 26

- the agony of childbirth - its like being jabbed with a 'million tiny white-hot needles'

Question 27

what food items increase the chance of gout attacks

Answer 27

- 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.

Question 28

which 5 disease's is hyperuricemia a risk factor to

Answer 28

- Atherosclerosis - Hypertension - cardiovascular diseases - chronic kidney disease - stoke

Question 29

what are the 2 forms of hyperuricaemia?

Answer 29

- primary - secondary

Question 30

what is primary hyperuricaemia caused by

Answer 30

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

Question 31

what is secondary hyperuricaemia caused by and with example

Answer 31

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.

Question 32

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

Answer 32

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

Question 33

what happens in the kidneys with uric acid

Answer 33

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

Question 34

what leads to the formation of kidney stone

Answer 34

both a decrease in reabsorption and an increase in secretion

Question 35

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

Answer 35

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

Question 36

what leads to hyperuricaemia in uric acid metabolism

Answer 36

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

Question 37

what can hyperuricaemia cause

Answer 37

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

Question 38

what are the 3 main benefits of uric acid

Answer 38

- 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.

Question 39

where is xanthine oxidase present in large amounts

Answer 39

- liver - intestinal mucosa - milk

Question 40

what are the 2 forms of xanthine enzyme

Answer 40

- 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

Question 41

what does the xanthine enzyme process

Answer 41

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

Question 42

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

Answer 42

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

Question 43

what happens to O2- than is produced by xanthine oxidase

Answer 43

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

Question 44

what is allopurinol and what does it do

Answer 44

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

Question 45

other than allopurinol, what is another inhibitor of xanthine oxidase

Answer 45

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

Question 46

what is reperfusion injury

Answer 46

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

Question 47

what does inadequate perfusion lead to

Answer 47

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

Question 48

what is the consequence of reduced blood supply

Answer 48

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.

Question 49

what happens with the onset of reperfusion

Answer 49

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

Question 50

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

Answer 50

myocardial ischemia in absence of reperfusion infarct size - 70%

Question 51

what is myocardial ischemia with reperfusion

Answer 51

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

Question 52

what is myocardial ischemia with reperfusion and cardioprotection

Answer 52

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.

Question 53

what are 2 buffers used in the practical

Answer 53

- hypoxanthine - xanthine

Question 54

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

Answer 54

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

Question 55

what did we measure in the practical

Answer 55

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-

Question 56

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

Answer 56

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

Question 57

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

Answer 57

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-

Question 58

in the practical, how do we measure cytochrome C

Answer 58

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.

Question 59

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

Answer 59

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.