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Lecture 1 Flashcards

1
Q

How many units of alcohol are recommended for men and women?

A

14 units/week spread over at least three days for both men and women

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2
Q

What is a unit of alcohol?

A

8g of pure ethanol which equates to 10ml of ethanol or roughly half a pint or a small 125ml glass of wine

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3
Q

How quickly is alcohol eliminated?

A

7g per hour and its elimination kinetics are linear and constant meaning that excess alcohol cannot be removed more quickly.

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4
Q

How is alcohol metabolised.

A

Alcohol is converted to acetaldehyde by alcohol dehydrogenase. Acetaldehyde is converted to acetate through aldehyde dehydrogenase. Acetate is then converted to acetyl Co-A.

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5
Q

What causes a hangover?

A

Buildup of acetaldehyde as well s dehydration due to the inhibition of ADH.

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6
Q

What causes liver damage?

A

Build up acetaldehyde as well as alcohol metabolism using up lots of NAD+ and excess acetyl Co-A production.

Excess acetyl Co-A often used to make fatty acids and ketone bodies as not enough NAD+ available for oxidation.

Liver damage occurs in the form of fatty liver, alcoholic cirrhosis and alcoholic hepatitis

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7
Q

What causes fatty liver in alcoholism?

A

Excess acetyl Co-A used to make ketone bodies and fatty acids. Impaired liver function means that lipoproteins used for fat transportation re not produced properly. This results in fat accumulating around the liver.

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8
Q

What are the main effects of alcohol oxidation?

A

Lactic acidosis, rate crystal accumulation resulting in gout, hypoglycaemia, fatty liver and oedema

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9
Q

How does alcohol oxidation lead to lactic acidosis?

A

NAD+ is required to convert lactic acid to pyruvate. NAD+ is used up in alcohol oxidation and so lactic acid is not converted leading to lactic acidosis.

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10
Q

How does alcohol oxidation lead to gout?

A

Urate and lactic acid use the same transporter in kidney. Excess lactate leads to poor urate transport and its subsequent build up. The Uris crystals accumulate in tissues and produce gout.

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11
Q

How does alcohol oxidation lead to hypoglycaemia?

A

Inadequate NAD+ for glycerol metabolism and inadequate pyruvate for gluconeogenesis as it cannot be converted from lactate due to lack of NAD+.

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12
Q

What causes oedema and lower lipoprotein synthesis in alcohol oxidation?

A

Liver function is impaired through the accumulation of fat and acetaldehyde etc so it fails to produce adequate amounts of lipoprotein and albumin.

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13
Q

What causes fatty liver?

A

Excess acetyl co-A results in fatty acid synthesis and impaired liver function results in lack of lipoprotein synthesis. This leads to fatty acid accumulating around the liver.

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14
Q

What is the name of the drug used to treat alcoholism and what does it do?

A

Disulfiram. It inhibits the aldehyde dehydrogenase enzyme which results in buildup of acetaldehyde which results in hangover symptoms on consumption of alcohol.

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15
Q

What is oxidative stress?

A

An imbalance between free radicals and cell defences (antioxidants). Either free radicals outnumber cell defences or cell defences are reduced so that free radicals outnumber ability of cell defences to combat them

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16
Q

What are some of the diseases that oxidative stress contribute to?

A

Cardiovascular disease, alzeihmers, cancer, rheumatoid arthritis, COPD, pancreatitis, Parkinson’s, MS etc

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17
Q

What are free radicals?

A

Atoms of molecules that have one or more unpaired electrons and is capable of independent existence

18
Q

What is the problem with free radicals?

A

They are very reactive and will take an electron from other molecules. Reaction with a free radical typically results in another free radical which propagates the damage

19
Q

What type of free radicals are there?

A

Reactive oxygen species and reactive nitrogen species. ROS and RNS.

20
Q

How is ROS formed?

A

Oxygen gains an electron to produce superoxide.

Superoxide can then form hydrogen peroxide which can form the hydroxyl radical which is highly reactive and damaging.

21
Q

How is RNS formed?

A

Nitric oxide is a free radical used in signalling but is toxic at high concentrations. Can also combine with oxygen to form peroxynitrite which not a free radical but is a powerful oxidant that can damage cells.

22
Q

What does ROS commonly damage?

A

DNA

Proteins

Lipoproteins

23
Q

How does ROS damage proteins?

A

Can react with bases which can lead to misspairing and mutation

Can react with sugar backbone which can cause strand break and mutation on repair.

24
Q

How can you measure DNA damage in cells through ROS?

A

Amount of 8-oxo-dG present

25
How does ROS damage proteins?
Damages backbone which leads to fragmentation and degradation. Reacts with sidechains resulting in disulphide bond formation etc which changes protein structure and can lead to loss of function and degradation or gain of function.
26
How does ROS damage lipids?
Free radical takes hydrogen from fatty acid in membrane lipid. Lipid radical formed and resulting chain reaction leads to hydrophobic environment of bilayer disrupted and membrane integrity fails. This is seen in atherosclerosis.
27
What endogenous and exogenous sources of biological oxidants are there?
Endogenous- electron transport chain, nitric acid synthase, NADPH oxidises etc Exogenous- ionising radiation eg uv and x rays. Pollutants, drugs and toxins such as the herbicide paraquat
28
How does the electron transport chain contribute to ROS?
Electron escapes chain early and reacts with O2 to form superoxide. This occurs in mitochondria
29
How does nitric oxide synthase contribute to RNS?
INOS eNOS and nNOS all synthesise nitric oxide for various functions in the body. Eg eNOS is located in the endothelium and the nitric oxide it produces plays a role in vasodilation. Nitric oxide is toxic at high levels however
30
How does respiratory burst contribute to RNS and ROS?
Neutrophil and monocytes use free radicals to destroy pathogens. NADPH oxidase in the cell uses NADPH to convert oxygen to superoxidase. This then becomes hydrogen peroxide and then hypochlorite through myeloperoxidase. Hypochlorite is the scientific term for bleach. This bleach is used to kill bacteria. Superoxide can also be combined with nitric oxide to form peroxynitrate which also kills bacteria.
31
What is chronic granulomatous disease?
Genetic defect in NADPH oxidase which prevents respiratory burst from occurring. The formation of superoxide in monocytes and neutrophils and they lose the ability to kill bacteria through free radicals. Leaves the sufferer susceptible to bacterial infections such as cellulitis, pneumonia and abscesses
32
What are the cellular defences against free radicals?
Superoxidase mutase and catalase Glutathione Free radical scavengers
33
What do superoxidase mutase and catalase do?
Superoxidase (SOD) converts superoxidase to hydrogen peroxide and oxygen and then catalase converts hydrogen peroxide to water and oxygen.
34
What may cause grey hair?
Lack of catalase in hair follicles which means that hydrogen peroxide gets converted to peroxynitrate by myeloperoxidase like it does in immune cells instead of water and oxygen.
35
How does glutathione act as a defence against free radicals?
Glutathione has a cysteine residue which donates an electron to free radical instead of it taking one from elsewhere. Two glutathione then form a disulphide bond. NADPH can then be used to regenerate the two glutathione molecules for use again. Lack of G6PDH means that the pentose phosphate doesnt work and NADH synthesis is impaired which means glutathione is not regenerated. This causes cataracts and other protein damage etc.
36
Role of pentose phosphate pathway in cellular defence against free radicals?
Produces NADH to regenerate glutathione.
37
What is the importance selenium in the diet?
Required by glutathione peroxidase to regenerate glutathione.
38
What is the role of free radical scavengers in the body?
Vitamin E which fat soluble protects against lipid peroxidation (protects cell membranes) Vitamin C plates a role in regenerating vitamin E from its reduced form
39
What contributes to cataracts in galactosaemia?
NADPH is used up to make galactitol from galactose. Glutathione cannot be regenerated and so disulphide bonds form in lens of eye.
40
Contribution of G6PDH deficiency oxidative stress?
Regents pentose phosphate pathway from operating which is a key source of NADH. Results in lower glutathione as regeneration cannot happen.
41
Why are HEINZ bodies formed and what are they?
Haemoglobin aggregates formed by crosslinking due to lack of glutathione. HEINZ bodies are a sign of G6PDH deficiency.
42
Paracetamol metabolism?
Excess results in NAPQI formation which uses up glutathione and results in toxicity damaging proteins and DNA. Treat with acetylcysteine which regenerates glutathione and allows NAPQI to be mopped up

MEH (17 decks)

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