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Flashcards in MEH Deck (40)
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1

Name low energy signals

NAD, inuslin, ADP, pyruvate

2

Name high energy signals

NADH, citrate, acetyl CoA, ATP

3

ADP + Pi --> ATP

Substrate level phosphorylation

4

When do we use LDH

To rexoxidise NADH to NAD when we can't carry out ETC or don't have enough oxygen (RBCs, exercising muscle)

5

Which proton carrier can be damaged by CO?

PTC IV- has a haem group to bind O2 and convert to H2O

6

What are uncouplers?

Uncouple electron transport from ATP synthesis. UCPs do this

7

Which is higher energy, FADH2 or NADH?

NADH

8

Brown adipose contains

UCP1 (thermogenin), an uncoupler

9

Name types of lactase deficiency

Primary is lack of lactase persistance allele, found in adults.
Secondary is due to SI injury and is reversible e.g. IBD, coeliac
Congenital is very rare AR can't digest breast milk

10

Name enzymes that if deficient would cause galactosemia

Galactokinase, UDP-galactose epimerase or uridyl transferase

11

Deficiency in which enzyme would cause fructosuria and which would cause fructose intolerance?

Essential fructosuria: fructokinase
Fructose intolerance: aldolase (F1P accumulates in liver to cause liver damage)

12

Which pathway makes NADPH and ribose?

Pentose phosphate pathway

13

What is used for GSH regeneration?

NADPH from pentose phsphate pathway

14

If you're starving, what activates ketone production?

Low insulin:glucagon activates lyase (enzyme in ketone production) and low glucose causes FA release from tissues to make acetyl CoA for ketones

15

How does alcohol change liver metabolism?

Uses up NAD in metabolising alcohol so then no NAD to break down FAs so they accumulate to give fatty liver. No NAD to break down glycerol for gluconeogenesis so hypoglycemia. No NAD to convert lactate to pyruvate so lactic acidosis and also build up of uric acid to causes gout.

16

What drug treats alcoholism

Disulfiram- inhibits aldehyde dehydrogenase so aldehyde builds up

17

Name some sources of free radicals

NADPH oxidase, ETC, radiation

18

Name three protectors of free radical damage

SOD: converts O2- --> H202 + O2
Glutathione: ROS react with it and form safe disulphide bonds, recycled back using NADPH
Catalase: H202 --> H20 + O2

19

Name some anti-oxidants

Vitamin E (regenerated by vitamin C) is a free radical scavenger

20

Consequences of galactosemia? (or indeed G6PDH deficiency!)

Galactose has to be converted to galctitol which uses up NADPH so NADPH not available to regenerate glutathione so prone to oxidative damage so cataracts
G6PDH needed for pentose phosphate pathway which produces NADPH so also get oxidative stress plus HEINZ bodies

21

What are Heinz bodies?

G6PDH deficiency sign- dark staining in RBCs frpm precipitated Hb. Forms a blister cell, spleen removes them to make a bite cell --> haemolysis

22

Describe metabolism of paracetamol

Metabolised to NAPQI (toxic metabolite), made safe by glutathione

23

Treatment for paracetamol OD

acetylcysteine- precursor to glutathione that makes NAPQI safe

24

Name ketogenic and glucogenic amino acids

Ketogenic: lysine and leucine (essential)
Glucogenic: alanine, glycine
Both: tyrosine, tryptophan

25

What hormones stimulate glucose production and which inhibit?

Insulin and growth hormone

26

What is transamination?

Transfer an amine group from an amino acid to a keto acid (and a keto acid gains an amine group to become an amino acid)

27

What's a keto acid?

An amino acid without an amine group

28

Name enzymes in gluconeogenesis

PEPCK, F16BPTase, G6Ptase

29

What goes into the urea cycle

Ammonia from deamination, CO2 and aspartate and glutamate from transamination

30

What is phenylketonuria

Deficiency AR in phenylalanine hydroxylase which converts phenylalanine to tyrosine, which we need to make NA, adrenaline, dopamine, thyroid hormones, melanin (so get intellectual disability, hypopigmentation, microcephaly)