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Semester 1 > Metabolism Sessions 1-6 > Flashcards

Metabolism Sessions 1-6 Flashcards

1
Q

Which is the natural stereoisomer form of a monosaccharide?

A

D

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2
Q

How do carbohydrates exist?

A

As mono, di or polysaccharides

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3
Q

In a typical western diet, how many grams make up the carb intake?

A

300

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4
Q

What makes up 1% of wet weight in the body?

A

Carbohydrates

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5
Q

How is the energy from carbohydrates stored in the body?

A

First ~300g as glycogen, nucleic acids, glycolipids and glycoproteins then as TAGs in adipose tissue

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6
Q

At what level is glucose always present in the blood?

A

~5 mmol per litre

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7
Q

What can excessive dietary intake of galactose, fructose and glucose lead to respectively in the blood?

A

Galactosaemia
Fructose intolerance
Diabetes mellitus

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8
Q

What glucose level in the blood confers with diabetes?

A

> or equal to 7 mmol per litre

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9
Q

What bond is found in disaccharides?

A

O-glycosidic

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10
Q

What are the monomers of sucrose, lactose and maltose respectively?

A

Sucrose: glucose and fructose
Lactose: galactose and glucose
Maltose: 2x glucose

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11
Q

Where does maltose come from in the diet?

A

Digestion product of dietary starch

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12
Q

When is a disaccharide non-reducing?

A

If aldehyde and/or ketone groups of both monomers are involved in forming the glycosidic bond

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13
Q

Give an example of a non-reducing disaccharide.

A

Sucrose

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14
Q

What are mainly homopolymers?

A

Disaccharides

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15
Q

What is the structure glycogen?

A

Glucose units linked by alpha 1-4 and alpha 1-6 bonds which give a highly branched structure

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16
Q

Where is glycogen stored?

A

In granules in the liver and skeletal muscle

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17
Q

What is the structure of starch?

A

Amylose with alpha 1-4 binds and amylopectin with alpha 1-4 and alpha 1-6 bonds

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18
Q

What does hydrolysis of starch release in the GI tract?

A

Glucose and maltose

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19
Q

Why can the human body not digest cellulose?

A

It does not have the enzymes needed to break beta 1-4 bonds present between glucose molecules

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20
Q

If it can’t be digested, why do we need to eat cellulose?

A

Important for normal GI function

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21
Q

Where is starch and glycogen digested to dextrins?

A

In the mouth by salivary amylase

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22
Q

Where are dextrins digested to monosaccharides?

A

In the small intestine by pancreatic amylase

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23
Q

What is attached to the brush border membrane of epithelial cells to aid digestion?

A

Pancreatic amylase, isomaltase, sucrose and lactose

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24
Q

How does a low level of lactase cause diarrhoea?

A

Lactose remains in colon lumen and increase osmotic pressure to water moves into the lumen

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25
Q

How does a low level of lactose cause bloating?

A

Colonic bacteria digest the lactose present in the colonic lumen and produce hydrogen, carbon dioxide and methane

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26
Q

How are glucose, galactose and fructose absorbed into the blood?

A

Actively transported into absorbitive cells lining gut and then move by facilitated diffusion into blood and tissue

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27
Q

What does facilitated diffusion of glucose into the tissues require?

A

GLUT1-5

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28
Q

Which GLUT transporter is upregulated in response to high levels of insulin in skeletal muscle and adipose tissue?

A

4

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29
Q

Can all tissues remove glucose, galactose and fructose from the blood?

A

Yes

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30
Q

Where is the major site of fructose and galactose metabolism?

A

Liver

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31
Q

Roughly how much glucose is needed per day to supply the tissues who have an absolute need for glucose?

A

180 g

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32
Q

Which areas of the body have an absolute glucose requirement?

A 
RBCs
WBCs
Kidney
Lens of eye
CNS
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33
Q

What is the central pathway of glucose metabolism which happens in all tissues?

A

Glycolysis

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34
Q

What are the functions of glycolysis?

A

Oxidise glucose
Produce NADH
Net synthesis of 2 ATP
Produce glycerol phosphate and 2,3-BPG

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35
Q

What are the main features of glycolysis?

A

Exergonic
Oxidative
No loss of carbon dioxide
Irreversible pathway

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36
Q

What is the purpose of converting glucose to G6P during glycolysis?

A

Makes it ionic so that it doesn’t cross the membrane
Increases reactivity so can follow a different pathway
Allows formation of high phosphoryl-group transfer potential compounds

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37
Q

Why are steps 1 and 3 in the glycolytic pathway irreversible?

A

Have a very negative delta-G

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38
Q

Which step of the glycolytic pathway is the committing step to glycolysis?

A

3

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39
Q

What does the initial investment of energy in glycolysis do to glucose?

A

Makes it less stable so it is more easily catabolised

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40
Q

What occurs in the second phase of glycolysis?

A

C3 –> 2C3 which are interconvertible
Small amount of reducing power is captured
Substrate level phosphorylation allows for ATP synthesis

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41
Q

Which glucose metabolism pathway is cytosolic?

A

Glycolysis

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42
Q

Which glucose metabolism pathway is cytoplasmic?

A

Pentose Phosphate pathway

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43
Q

Where does the pentose phosphate pathway occur?

A

Liver
RBCs
Adipose tissue

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44
Q

What are the functions of the pentose phosphate pathway?

A

Produce NADPH for reducing power for anabolic processes

Produce C5 sugar ribose for nucleotide synthesis

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45
Q

What is the NADPH generated in the pentose phosphate pathway used for?

A

Lipid synthesis in liver and adipose tissue
Maintain free -SH groups on cysteine residues in RBCs
Detoxification

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46
Q

What are the features of the pentose phosphate pathway?

A

High activity in dividing tissues
Carbon dioxide produced so irreversible
Considered in two phases

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47
Q

What happens in the first phase of the pentose phosphate pathway?

A

G6P makes C5 sugar phosphate, NADPH, hydrogen ions and carbon dioxide

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48
Q

Which enzymes are involved in the first phase of the pentose phosphate pathway?

A

Glucose-6-phosphate dehydrogenase

6-phosphogluconate dehydrogenase

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49
Q

What happens in the second phase of the pentose phosphate pathway?

A

Complex series of reactions to convert unused C5 sugar phosphates to glycolysis intermediates

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50
Q

How is the second phase of the pentose phosphate pathway regulated?

A

Controlling activity of G6PD with NADP+ which activates it and NADPH which inhibits it

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51
Q

What are the products of the second phase of glycolysis?

A

ATP
1,3-BPG
Phosphoenolpyruvic acid

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52
Q

What is glycerol phosphate needed for?

A

TAG synthesis in liver and adipose tissue

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53
Q

What is glycerol phosphate produced from in adipose tissue?

A

Dihydroxyacteone phosphate

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54
Q

Why is TAG synthesis not as dependent on rate of glycolysis in the liver as it is in adipose tissue?

A

Liver has glycerol kinase which it can use to phosphorylase glycerol

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55
Q

What is 2-3 BPG produced from in RBCs?

A

1,3-bisphosphoglycerate

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56
Q

What is 2,3-BPG?

A

An important oxygen affinity regulator

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57
Q

What does muscle tissue possess that enables the high energy of hydrolysis phosphate bond in ADP to drive ATP synthesis in an emergency?

A

Myokinase

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58
Q

How is glycolysis regulated by ATP levels?

A

Inhibited when high

Stimulated when low

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59
Q

Why do most of the metabolic reactions in glucose metabolism not need to be regulated?

A

They are close to equilibrium

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60
Q

How can phosphofructokinase be regulated?

A

Inhibited by high ATP levels or glucagon

Stimulated by high AMP or insulin

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61
Q

What are the products of anaerobic glycolysis?

A

Lactate
ATP
Water

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62
Q

What normally produces ~50 g of lactate per day?

A 
RBCs
Skin
Brain
Skeletal muscle
GI tract
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63
Q

How is lactate dealt with once it has been released into the circulation?

A

Converted to glucose in liver and kidney

Converted back to pyruvate and oxidised to carbon dioxide in heart muscle

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64
Q

How does lactic acidosis occur?

A

If plasma lactate concentration >5 mmol per litre it exceeds renal threshold and affects buffers

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65
Q

What can cause lactic acidosis?

A 
Compromised circulation
Lack of thiamine
Shock
Strenuous exercise
Liver disease
Hearty eating
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66
Q

What appears in the urine in lactic acidosis?

A

Lactate

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67
Q

How is galactose liberated?

A

Digestion of lactose

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68
Q

Where is galactose metabolised?

A

Mainly liver but also kidney and GI tract by soluble enzymes

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69
Q

What are the products of galactose metabolism?

A

G6P and ADP

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70
Q

What does epimerase do?

A

UDP-glucose UDP-galactose

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71
Q

Why is it important for the epimerase reaction to be reversible?

A

So galactose can be formed during lactation

So galactose can form UDP-glucose in glycogen synthesis

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72
Q

Which two enzymes can patients with galactosaemia lack?

A

Kinase or transferase

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73
Q

Which is the more common enzyme deficiency in galactosaemia?

A

Transferase

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74
Q

What accumulates in the tissues of patients lacking kinase enzyme in galactosaemia?

A

Galactose

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75
Q

What accumulates in the tissues of patients lacking the transferase enzyme in galactosaemia?

A

Galactose and galactose-1-phosphate

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76
Q

What happens to the accumulated metabolites in transferase deficient galactosaemia?

A

Reduced by aldose reductase to galacitol which depletes NADPH

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77
Q

What are the consequences of NADPH reduction in transferase deficient galactosaemia?

A

Raised intraocular pressure –> blindness
Non-enzymatic glycosylation of lens proteins –> cataracts
Inappropriate disulphide bond formation –> cataracts

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78
Q

Why are the liver, kidney and brain damaged in transferase deficient galactosaemia?

A

Pi sequestered so not available for ATP synthesis

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79
Q

Why does galactose spill into pathways it is not normal seen in during galactosaemia?

A

High Km values

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80
Q

Why does treating galactosaemia patients with a galactose free diet not cause a galactose deficiency?

A

UDP-glucose is present and this can be converted by epimerase

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81
Q

How is fructose produced in the body?

A

Hydrolysis of sucrose and ingestion of fruit

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82
Q

How is fructose metabolised?

A

Soluble enzymes in the liver catalyse its conversion to glyceraldehyde 3-phosphate, an intermediate of glycolysis

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83
Q

What causes G6PD deficiency?

A

Point mutation causing an X-linked gene defect

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84
Q

Which populations is G6PD more prevalent in?

A

Mediterranean

Black USA males

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85
Q

What are the consequences of G6PD deficiency?

A

Insufficient NADPH levels
Inappropriate disulphide bridges form
Haemoglobin and other proteins become X-linked

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86
Q

What are Heinz bodies?

A

Insoluble aggregates of X-linked proteins in RBCs which cause haemolysis

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87
Q

What can cause acute haemolytic episodes in G6PD deficiency?

A

NADPH level reducing chemicals e.g. antimalarials, sulphonamides, glycosides

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88
Q

What happens to pyruvate before it can enter the TCA cycle?

A

Converted to acetyl CoA by pyruvate dehydrogenase

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89
Q

Why is pyruvate metabolism sensitive to vitamin B deficiency?

A

4 B vitamins are needed as cofactors for pyruvate dehydrogenase

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90
Q

Why is the PDH reaction irreversible?

A

Carbon dioxide is lost

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91
Q

What controls the PDH reaction?

A

PDH allosterically activated by ADP

PDH allosterically inhibited by acetyl-CoA, ATP and NADH

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92
Q

What does the allosteric inhibition of PDH by acetyl CoA allow?

A

Acetyl-CoA from beta-oxidation to be used instead of that from glycolysis under certain conditions

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93
Q

How does insulin activate PDH?

A

Promotes dephosphorylation

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94
Q

Where does the conversion of pyruvate to acetyl CoA take place?

A

Mitochondrial matrix after transportation of pyruvate from the cytoplasm

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95
Q

What does PDH deficiency lead to?

A

Lactic acidosis

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96
Q

Why is the TCA cycle unidirectional?

A

Conversion of removed acetyl to carbon dioxide which is lost

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97
Q

Why does the TCA cycle require NAD+ and FAD?

A

It is oxidative

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98
Q

Where does the TCA cycle take place?

A

Mitochondrial matrix

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99
Q

How does the TCA cycle produce energy?

A

ATP/GTP

Precursors for biosynthesis

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100
Q

What are the products of one molecule of glucose entering the TCA cycle?

A

6 NADH
2 FAD2H
2 GTP

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101
Q

Which molecules does the TCA cycle produce precursors of biosynthesis for?

A

Fatty acids
Amino acids
Haem
Glucose

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102
Q

How is the TCA cycle regulated?

A

Isocitrate dehydrogenase is allosterically activated by ADP and allosterically inhibited by NADH

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103
Q

Which enzyme in the catabolism of glucose must gluconeogenesis bypass?

A

PDH

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104
Q

What is the TCA cycle the central pathway of metabolism for?

A 
Sugars
Fatty acids
Ketone bodies
Amino acids
Alcohol
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105
Q

How do the intermediates of the TCA cycle act?

A

Catalytically - no net synthesis or degradation

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106
Q

Why are there no known genetic defects to the TCA cycle?

A

They would be lethal

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107
Q

How many molecules of ATP are produced per molecule of glucose in that has entered the TCA cycle?

A

32

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108
Q

Where does oxidative phosphorylation take place?

A

Inner membrane of the mitochondria

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109
Q

Why is oxygen required in oxidative phosphorylation?

A

Final electron acceptor

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110
Q

What happens to NADH and FAD2H in oxidative phosphorylation?

A

Re-oxidised

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111
Q

How is energy used in oxidative phosphorylation?

A

30% to move H+ across membrane

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112
Q

Why are humans warm blooded?

A

70% of the energy in oxidative phosphorylation is dissipated as heat

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113
Q

What creates the proton motive force in oxidative phosphorylation?

A

Anions left on inside of inner membrane create [H+] gradient

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114
Q

Why does ATP synthesis occur in oxidative phosphorylation?

A

Return of proteins is energetically favoured electrically and chemically but can only happen via ATP synthase

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115
Q

How is discharge of the proton gradient prevented?

A

Impermeable membrane

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116
Q

How much ATP is generated by oxidation of 2 moles of NADH?

A

5 moles

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117
Q

How much ATP is generated by oxidation of 2 moles of FAD2H?

A

3 moles

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118
Q

How does the transfer of electrons differ between FAD2H and NADH?

A

FAD2H is lower energy so transfers electrons at a lower energy complex

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119
Q

How is oxidative phosphorylation regulated?

A

High ATP means no substrate for ATP synthase –> inward H+ flow stops, proton gradient rises and feedback inhibition takes place so e- transport is stopped

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120
Q

How are oxidative phosphorylation and electron transport usually regulated?

A

By mitochondrial [ATP] as they are tightly coupled

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121
Q

How do cyanide ions and carbon monoxide interfere with the electron transport chain?

A

Bind to cytochrome oxidase and prevent transfer of e- to oxygen therefore the pmf is not established

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122
Q

What does cytochrome oxidase contain which allows it to be used in electron transport?

A

Haem group that can change oxidation state

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123
Q

What percentage of BMR can be attributed to proton leak?

A

~20-25%

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124
Q

How do uncouples work?

A

Increase permeability of the IMM to protons so the gradient is dissipated and there is no pmf for ATP synthesis

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125
Q

Why are overweight people warmer than lean individuals?

A

Fatty acids act as uncouplers so more energy is dissipated as heat due to leaky IMM

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126
Q

What are dinitrophenol and dinitrocresol examples of?

A

Uncouplers

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127
Q

What genetic defects can reduce electron transport and ATP synthesis?

A

PTCs and ATP synthase encoded by mtDNA

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128
Q

What affects the efficiency of energy transfer and can be varied in some tissues?

A

Tightness of oxidative phosphorylation and electron transport coupling

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129
Q

Where is brown adipose tissue found in newborns?

A

Around vital organs

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130
Q

What does brown adipose tissue contain that allows uncoupling of oxidative phosphorylation from electron transport?

A

Thermogenin (UCP1)

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131
Q

How does thermogenin in brown adipose tissue cause an independent in temperature?

A

NA stimulates lipase –> FA from TAGs oxidised –> UCP1 activated which transports H+ back to mitochondria causing energy of pmf to be released as heat

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132
Q

How do the proteins in oxidative phosphorylation compare to those in substrate level phosphorylation?

A

OP: membrane associated complexes
SLP: soluble enzymes in cytoplasm and mitochondrial matrix

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133
Q

How does energy coupling in oxidative phosphorylation compare to substrate level phosphorylation?

A

OP: indirectly through generation and utilisation of pmf
SLP: directly through formation of high energy of hydrolysis bonds

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134
Q

How does the ability of substrate level phosphorylation and oxidative phosphorylation compare?

A

OP: cannot occur in oxygen absence
SLP: occurs to limited extent in oxygen absence

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135
Q

Which is the major process for ATP synthesis in cells needing lots of energy?

A

Oxidative phosphorylation

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136
Q

Why do carbohydrates require less oxygen than fatty acids to be metabolised?

A

They are already partially oxidised

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137
Q

Why are lipids more reduced that carbohydrates?

A

They have less oxygen and more hydrogen atoms per carbon atom

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138
Q

What are the four fatty acid derivatives?

A

FA
TAGs
Phospholipids
Eicosanoids

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139
Q

What is the function of eicosanoids?

A

Transmitter b/w neighbours

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140
Q

What are the 4 derivatives of hydroxy-methyl–glutamic acid?

A

Ketone bodies
Cholesterol
Cholesterol esters
Bile acids and salts

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141
Q

What are cholesterol esters used for?

A

Cholesterol storage

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142
Q

Which hydroxy-methyl-glutamic acid derivative is used in lipid digestion?

A

Bile acids and salts

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143
Q

What does vitamin A deficiency cause?

A

Scaly skin

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144
Q

What does vitamin E deficiency cause?

A

Muscular dystrophy

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145
Q

What does vitamin K deficiency cause?

A

Haemorrhaging anaemic babies

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146
Q

What are TAGs?

A

Hydrophobic molecules stored in anhydrous form in fatty globules in adipose tissue until there is an increase in metabolic load

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147
Q

What stimulates reduced TAG storage?

A 
Glucagon
Adrenaline
Cortisol
Growth hormone
Thyroxine
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148
Q

What happens to the glycerol part of TAGs?

A

Hydrolysed in GI tract from TAG –> enters blood –> taken up by liver

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149
Q

What happens to the fatty acid part of TAGs?

A

Hydrolysed from TAG in GI tract –> carried by chylomicrons in blood –> taken up by adipose tissues

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150
Q

What are chylomicrons in the blood recognised by?

A

Tissues that need triglycerides

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151
Q

What is released by adipose tissue into the blood that can be taken up by muscles to provide energy?

A

Fatty acids

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152
Q

What are fatty acids carried by in the blood?

A

Plasma proteins e.g. Albumin

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153
Q

What happens to TAGs in the small intestine?

A

Hydrolysed by pancreatic lipase to release glycerol and FA using bile salts and colipase

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154
Q

What is colipase?

A

Protein factor

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155
Q

What happens to glycerol in the liver?

A

Turned into glycerol phosphate which can be used in glycolysis or TAG synthesis

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156
Q

What is the difference between saturated and unsaturated fatty acids?

A

Saturated: all single carbon bonds
Unsaturated: one or more double carbon bonds

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157
Q

Why are certain polyunsaturated fatty acids essential?

A

Mammals cannot introduce double carbon bonds beyond C9

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158
Q

What happens with lipolysis in stress response?

A

FA released and non-covalently bound to albumin and carried in blood to liver, heart and skeletal muscle for beta-oxidation
Glycerol is released into blood where it travels to the liver to be oxidised/converted to glucose/TAGs

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159
Q

Where does FA oxidation take place?

A

Cytoplasm

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160
Q

What is the function of fatty acyl CoA synthase?

A

Link FA to CoA by forming a high energy sulphide bond using ATP

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161
Q

Why do activated FAs not readily cross the IMM?

A

Hydrophobic acids w/a hydrophobic cofactor

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162
Q

How is the rate of FA oxidation controlled?

A

Need for cartinine shuttle to transport fatty-aceyl CoA across the IMM

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163
Q

What happens in the transport of fatty acetyl-CoA across the IMM?

A

Molecule modified into cartinine derivative which is recognised by the transporter –> into matrix where enzyme converts back to acetyl CoA so it is in its metabolic form

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164
Q

What prevents newly synthesised FA from being immediately oxidised?

A

Inhibition of fatty acyl-CoA transport by FA synthesis intermediate malonyl CoA

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165
Q

How do defects in the fatty acyl-CoA transport system present?

A

Poor exercise tolerance

Increase in fat droplets in muscle cells

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166
Q

What is acetyl CoA a catoabolism product of?

A

FA
Sugars
Alcohol
Amino acids

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167
Q

Why is beta-oxidation of a fatty acid said to be a spiral cycle?

A

Gets shorter w/each turn until there is only one C2 unit left

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168
Q

Why can beta-oxidation not occur in the absence of oxygen?

A

Requires mitochondrial NAD+ and FAD

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169
Q

Is there any direct ATP synthesis in beta-oxidation of FA?

A

Nope

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170
Q

What happens to all intermediates and carbon atoms in beta-oxidation of FA?

A

Intermediates linked to CoA

Carbon atoms converted to acetyl-CoA

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171
Q

Is more energy derived from FA oxidation or glucose oxidation?

A

FA oxidation

172
Q

What can be said about the substrate and product in beta-oxidation of FA?

A

Both activated

173
Q

Which ketone bodies are synthesised in the liver from acetyl CoA?

A

Acetoacetate

Beta-hydroxybutyrate

174
Q

How is acetone formed?

A

Spontaneous, non-enzymatic decarboxylation of acetoacetate

175
Q

Why are ketone bodies present in plasma and excreted in urine?

A

Soluble in water

176
Q

What occurs if ketone bodies are present in the blood above renal threshold?

A

Ketonuria

177
Q

At what concentration is the plasma lactate level kept son start at?

A
178
Q

Why level of ketone bodies is usually seen in the blood?

A
179
Q

What is physiological ketosis?

A

Ketone bodies at 2-10 mM in the blood, seen in starvation

180
Q

Why is pathological ketosis?

A

Ketone bodies at >10mM in blood seen in untreated type I diabetics with pear-drop smelling breath

181
Q

What happens in the fed state to HMG-CoA which has been formed from acetyl CoA?

A

Goes to form cholesterol to increase the insulin/glucagon ratio

182
Q

What happens in the starvation state to HMG-CoA?

A

Forms ketone bodies to decrease the insulin/glucagon ratio

183
Q

How do statins work to lower cholesterol?

A

Inhibit HMG-CoA reductase to prevent conversion of HMG-CoA to mexalonate and then cholesterol

184
Q

How are ketone bodies synthesised?

A

Acetyl CoA –> synthase –> HMG-CoA –> lyase —> acetoacetate –> beta-hydroxybutyrate

185
Q

How is ketone body synthesis controlled?

A

Isocitrate dehydrogenase which uses feed forward allosteric inhibition

186
Q

What is required for ketone body synthesis?

A

FA for oxidation in liver after excess lipolysis in adipose

187
Q

How can ketone bodies be used as a source of energy?

A

All tissues w/mitochondria (incl. CNS) convert to acetyl-CoA at a rate proportional to plasma concentration

188
Q

How is acetone transported around the body?

A

In blood as it is soluble

189
Q

What can beta-hydroxybutyrate carry?

A

Hydrogen

190
Q

Why are ketone bodies used in starvation/diabetes?

A

Prime aim is to spare glucose for brain

191
Q

What processes can spare glucose?

A

Glycogenolysis
Gluconeogenesis
Ketogenesis
Lipolysis

192
Q

Why does the body preferentially break down muscle in starvation?

A

It does not want to lose tissue mass

193
Q

What are the 4 basic stages of catabolism?

A

1: breakdown to building block molecules
2: breakdown to metaboli intermediates, release of reducing power and energy
3: TCA cycle, release energy and reducing power
4: conversion of reducing power to ATP

194
Q

What energy stores make up the textbook 70 kg man?

A

~15 kg TAGs
~0.4 kg glycogen
~6 kg muscle protein

195
Q

How do the typical energy stores change in obesity?

A

Glycogen and muscle protein masses stay the same but mass of TAGs greatly increases

196
Q

How long after a meal does glycogenolysis occurs?

A

2 hrs

197
Q

How long after a meal does gluconeogenesis occur?

A

8-12 hours

198
Q

Why doe glycogen have a minimal osmotic effect?

A

It’s structure

199
Q

What forms the straight chain alpha 1-4 bonds in glycogen?

A

Glycogen synthase

200
Q

What forms the branching alpha 1-6 bonds in glycogen?

A

Branching enzyme

201
Q

What ratio are the alpha 1-4 and 1-6 bonds present in?

A

10:1

202
Q

Why is the amount of glycogen stored in liver and skeletal muscle limited?

A

High polarity attracts a lot of water

203
Q

What can glycogen storage diseases cause?

A

Tissue damage w/excessive storage
Fasting hypoglycaemia
Poor exercise tolerance
Abnormal storage affecting liver and/or muscle

204
Q

Why is glycogen never completely degraded?

A

Small amount needed as primer

205
Q

What can the body not do in von Gierke’s disease?

A

Breakdown glycogen

206
Q

How is glycogen synthesised?

A

Glucose + ATP –> G6P –> G1P + UTP + water –> UDP-glucose –> add on to existing glycogen

207
Q

Which enzymes are needed for synthesis of glycogen?

A

Hexokinase/glucokinase
Phosphoglucomutase
Glycogen synthase/branching enzyme

208
Q

What inhibits glycogen synthesis?

A

Phosphorylation by glucagon or adrenaline

209
Q

What activates glycogen synthesis?

A

Dephosphorylation by insulin

210
Q

How is glycogenolysis controlled with respect to glycogen synthesis?

A

Reciprocally

211
Q

Which is the rate limiting step of glycogenolysis?

A

Conversion of glycogen to G1P by glycogen phosphorylase/de-branching enzyme

212
Q

Which enzyme converts G1P to G6P?

A

Phosphoglucomutase

213
Q

What is found only in the liver which can convert G6P from glycogenolysis into glucose?

A

Glucose-6-phosphatase

214
Q

What precursors are used mainly in the liver but also the kidney cortex for gluconeogenesis after 8 hours of fasting?

A

Non-carbohydrate

215
Q

Which enzyme controls the rate limiting step in galactose metabolism?

A

Fructose-1,6-bisphosphosphatase

216
Q

Which enzyme is used for galactose, fructose and glycerol in gluconeogenesis?

A

PEPCK

217
Q

How do the stimulators of gluconeogenesis act on the enzymes involved?

A

Increase expression and activity

218
Q

When can the energy from TAG storage in adipose be mobilised?

A

~20 mins of aerobic exercise
Stress
Starvation
Second half of gestation

219
Q

Why can FA not move through the blood-brain barrier to the CNS?

A

Endothelial cells in BV have very tight junctions

220
Q

What is acetyl CoA converted into using ATP and NADPH in the cytoplasm of liver cells?

A

Fatty acids

221
Q

How is acetyl-CoA transported out of the mitochondria if it is too big to pass through as it is?

A

Combines w/oxaloacetate to form citrate which can be transported, then reforms in cytoplasm

222
Q

How are FA synthesised once acetyl-CoA has been transported into the cytoplasm?

A

Acetyl-CoA converted to malonyl-CoA

Fatty acid synthase adds one C2 unit to growing FA per cycle

223
Q

What is the growing fatty acid linked to in FA synthesis?

A

Acyl carrier protein (ACP)

224
Q

Which enzyme controls the important regulatory step in FA synthesis?

A

Acetyl carboxylase

225
Q

How is acetyl carboxylase controlled?

A

Citrate and insulin activate
AMP, glucagon and adrenaline inhibit
(Hormones cause covalent modification)

226
Q

Are fatty acid oxidation and synthesis reversals of each other?

A

Nope

227
Q

Why is the catabolism and anabolism of the same substrate usually not just a reversal of the same process?

A

Allows greater flexibility, better control and thermodynamically irreversible steps can be bypassed

228
Q

What is special about lysine, isoleucine, leucine, threonine, valine, tryptophan, phenylalanine, methionine and under certain conditions histidine, arginine, tyrosine and cysteine?

A

They are essential

229
Q

What are amino acids used in the synthesis of?

A 
Proteins
Purines
Pyrimidines
Porphyrins
Creatine
Neurotransmitters
Hormones
230
Q

When is the nitrogen balance negative?

A

During starvation

231
Q

When is the nitrogen balance positive?

A

During growth

232
Q

What release free amino acids by breaking peptide bonds?

A

Proteases

Peptidase said

233
Q

What stimulates uptake of amino acids into skeletal muscle, adipose, and the liver as well as stimulating protein synthesis?

A

Insulin

Growth hormone

234
Q

Which hormone stimulates proteolysis and can be raised by steroid drugs?

A

Cortisol

235
Q

What happens to amino acids once they’ve been released from the polypeptide?

A

Amino group is removed and carbon skeleton enters TCA cycle

236
Q

What types of carbon skeleton can be left when the amino group is removed from a free amino acid?

A

Glucogenic

Ketongenic

237
Q

How do Ketongenic amino acids enter the TCA cycle?

A

Produce acetyl CoA which goes on to make ketone bodies

238
Q

How do goucogenic amino acids enter the TCA cycle?

A

Produce pyruvate, oxaloacetate, fumarate, alpha-ketoglutarate or succinate to undergo gluconeogenesis

239
Q

What is special about the catabolism of isoleucine, threonine, phenylalanine, tyrosine and tryptophan?

A

They can take either goucogenic or ketongenic pathways

240
Q

What two ways can be used to transform excess amino acids metabolised in the liver into a less toxic form?

A

Transamination

Deamination

241
Q

Which enzymes are used in transamination what can be used to measure liver function?

A

ALT

AST

242
Q

Why does transamination disrupt energy supply?

A

It reduces TCA cycle activity

243
Q

What does ALT convert?

A

Alanine to glutamate

244
Q

What does AST convert?

A

Glutamate to aspartate

245
Q

What stimulates transaminase in the liver?

A

Cortisol

246
Q

What happens to the amine group removed from amino acids at physiological pH?

A

Converted to very toxic and soluble ammonium ion

247
Q

Who can toxic ammonium ions be removed?

A

Via urea or glutamine

248
Q

What is required to form glutamine in order to remove toxic ammonium ions?

A

Glutamate
Ammonia
ATP

249
Q

Which enzyme is needed for glutamine synthesis?

A

Glutamine synthetase

250
Q

How is excess glutamine dealt with?

A

Released from cells into blood where it travels to the kidneys to enter urine and the liver to form urea

251
Q

Why is urea a good way to get rid of ammonium ions?

A

High N content
Non-toxic
V. water soluble
Chemically inert in humans

252
Q

What nitrogen containing compound can bacteria in the gut break down?

A

Urea

253
Q

What are the products of the urea cycle?

A 
Urea
Fumarate
ADP
AMP
Pi
254
Q

How may enzymes are there in the urea cycle?

A

5

255
Q

Why is the urea cycle not regulated by feedback inhibition?

A

Function is disposal so controlled by protein intake

256
Q

Where does the urea cycle take place?

A

Ornithine part in mitochondrial matrix and rest in cytosol

257
Q

What is the result of a complete loss of any one enzyme in the urea cycle?

A

Death

258
Q

Why does partial loss of an enzyme in the urea cycle cause vomiting, lethargy, irritability, mental retardation, seizures and coma?

A

Causes hyperanaemia which increases intermediates that interfere with the TCA cycle

259
Q

How is a deficiency of an enzyme in the urea cycle treated?

A

Low protein diet and replacing amino acids w/keto acids

260
Q

How is phenylketonuria detected?

A

Excess phenylketones excreted in urine and high levels in the blood

261
Q

What causes phenylketonuria?

A

Autosomal recessive defect of gene on chromosome 12 which causes lack of phenylalanine hydroxylase enzyme

262
Q

How is phenylketonuria treated?

A

Low phenylalanine diet

263
Q

Why is mental retardation seen in PKU?

A

Tyrosine is not formed which is needed to synthesise noradrenaline, adrenaline and dopamine for CNS development

264
Q

What causes homocystinuria?

A

Autosomal recessive defect on chromosome 21 causes complete deletion or reduced activity of cystathionine beta-synthase

265
Q

What is made instead of cystathionine in homocystinuria?

A

Methionine

266
Q

What does homocystinuria affect in the body?

A

Fibrillin-1 protein structure so tissue, muscle, CNS and CVS affected

267
Q

Symptoms of which other disease involving chromosome 21 are linked with homocystinuria?

A

Down’s syndrome

268
Q

What other disease presents similarly to homocystinuria and can be confused on diagnosis?

A

Marian’s

269
Q

How do the relative toxicities of methionine and homocysteine compare?

A

Methionine is harmful at high levels but less so than homocysteine

270
Q

What does cystathionine-beta-synthase need to function?

A

Active vitamin B

271
Q

What treatment is given in homocystinuria where there is reduced activity of CBS?

A

Vitamin B supplement

272
Q

Which important gas signalling molecule is linked with arginine?

A

Nitric oxide

273
Q

What functions does nitric oxide have?

A

Vasodilator - maintenance of B.P.
Neurotransmitter
Inflammatory mediator
Memory storage

274
Q

Which important gas signalling molecule is cysteine associated with?

A

Hydrogen sulphide

275
Q

What is the function of hydrogen sulphide?

A

Vasodilator
Neuromodulator
Cytoprotective agent against oxidation (it’s a reducing agent)

276
Q

What is creatinine?

A

Breakdown product of creatine and creatine phosphatase in muscle cells

277
Q

How does the release of creatinine vary?

A

Constant unless muscle is wasting when it becomes elevated

278
Q

What is the importance of creatinine excretion over 24 hrs by the kidneys being proportional to muscle mass ?

A

Means urine concentration is a stable marker of urine dilution, blood concentration and measure kidney function

279
Q

When is the level of urinary creatinine excretion over 24 hrs not proportional to the muscle mass of an individual?

A

If they are a carnivore or are wasting

280
Q

What are the five classes of lipids?

A 
Phospholipids
Cholesterol esters
Cholesterol
Fatty acids
Triacyglycerols
281
Q

What is cholesterol he precursor to?

A

Steroid hormones and bile acids

282
Q

What is the function of bile acids?

A

Emulsify fats in the GI tract

283
Q

Where does cholesterol come from?

A

Some from the diet but mainly synthesised in the liver

284
Q

How can a fatty acid be used to eliminate the polar part of a cholesterol molecule?

A

The OH on the cholesterol can be esterified with a FA

285
Q

What is the most abundant protein in the blood?

A

Albumin

286
Q

What does albumin carry?

A

~2% of lipids, mainly FA

287
Q

What is the problem with using albumin as transport for lipids?

A

It has a limited capacity of ~3 mmol per litre so becomes saturated if lipid levels are too high

288
Q

How is ~98% of lipid carried in the blood?

A

As lipoprotein particles

289
Q

What is a lipoprotein?

A

Particle mainly constructed in the liver consisting of a TAG and cholesterol hydrophobic core surrounded by a protein, phospholipid and cholesterol coat

290
Q

What is the function of the protein component of an apolipoprotein?

A

Stabilisation during transit

291
Q

What is the role of phospholipids and cholesterol in the apolipoprotein?

A

Structural integrity

292
Q

What is an apoprotein?

A

Specialised protein for lipid transport

293
Q

How do different types of lipoproteins vary?

A 
Size (5-100 nm)
Lipid and protein composition (2-55% protein)
Density
Surface charge
Function
294
Q

How can lipoproteins be separated?

A

Electrophoresis or ultracentrifugation

295
Q

What does each class of lipoprotein particle have?

A

Own set of specific apolipoproteins

296
Q

What are the two general functions of apolipoproteins?

A

Activate enzymes

Recognise CSM receptors

297
Q

Where can ApoA (I) be found and what is its function here?

A

Intestine

Structural HDL component

298
Q

Where is ApoB100 found and what is its function?

A

Liver

VLDL

299
Q

Where can ApoC be found and what is its function?

A

Liver

Cofactor activator of lipoprotein lipase/inhibits LPL

300
Q

Where is ApoD found and what is its function?

A

Brain and testes

HDL

301
Q

Where is ApoE found and what is its function?

A

Liver, binding to LDL receptors

302
Q

What is the function of ApoH?

A

Inhibits coagulation factors

303
Q

What happens if there are polymorphisms in LDL receptors?

A

Early onset CVD

304
Q

Order the classes of chylomicrons in increasing density.

A

VLDL
LDL
HDL

305
Q

What are chylomicrons?

A

Recombined TAGs and apoprotein

306
Q

What forms chylomicrons?

A

Enterocytes - simple columnar cells w/glycocalyx found on the intestinal lining

307
Q

What is the function of chylomicrons?

A

Combine dietary TAGs split by pancreatic lipase and reformed w/apoprotein so to carry lipids form the diet to tissues

308
Q

How long are chylomicrons usually present for in the blood following a meal?

A

4-6 hours

309
Q

Where are VLDLs formed?

A

In liver for energy store

310
Q

What are VLDLs rich in?

A

TAGs

311
Q

What is the function of VLDLs?

A

Combine TAGs synthesised in the liver w/specific apoproteins to carry lipids from liver to tissues

312
Q

Which is more important, the absolute LDL and HDL levels or the ratio between them?

A

Ratio

313
Q

Where are LDLs formed?

A

In the liver

314
Q

What are LDLs rich in?

A

Cholesterol

315
Q

What is the function of LDLs?

A

Combine liver cholesterol w/specific apoproteins (esp. apoB100) to carry it to the tissues

316
Q

What is the structure of an LDL?

A

Phospholipid she’ll w/lots of cholesterol, filled w/cholesterol esters

317
Q

What are high levels of LDLs associated with?

A

High risk of atherosclerosis

318
Q

Where are HDLs formed?

A

Tissues

319
Q

What is the function of HDLs?

A

Combine excess cholesterol in the tissues w/specific apoproteins to carry it to the liver so it cannot cause damage by being in the blood

320
Q

What enzyme do endothelial cells have on their outside?

A

Lipase

321
Q

What catches cholesterol and binds it?

A

Chylomicrons and VLDL

322
Q

What happens to VLDL remnants?

A

Removed by liver or converted to other lipoprotein particles

323
Q

What is necessary for recognition of cholesterol from LDL?

A

ApoB100

324
Q

What controls ApoB100 receptor expression in the cell?

A

[cholesterol]

325
Q

What happens when the LDL complex binds to the receptor on a cell?

A

Receptor/LDL complex taken in by endocytosis –> cholesterol ester is released and cleaved into cholesterol and FA

326
Q

How are HDL particles loaded?

A

Nascent HDL shells made in the liver and VLDL tenants sequester cholesterol from capillaries which then mature into HDL particles

327
Q

What is hyperlipoproteinaemia?

A

Raised levels of one or more lipoprotein classes

328
Q

What causes hyperlipoproteinaemia?

A

Problems w/receptors, lipase enzymes or ApoE (for example) which results in over production or under removal

329
Q

What lifestyle alterations can be sufficient to treat hyperlipoproteinaemia?

A

Reduce cholesterol and saturated lipid intake
Increase exercise
Stop smoking

330
Q

What drugs can be used to treat hyperlipoproteinaemia?

A

Statins

331
Q

What effects do statins have?

A

Inhibit HMG CoA reductase
Increase LDL receptor expression in hepatocytes
Increase vascular lipase secretion
Possible anti-inflammatory action

332
Q

What effects does hypercholesterolaemia have around the body?

A

Cholesterol deposited on eyelids (xanthelasma), on tendons, corneal arcus

333
Q

What is the pathogenesis of atherosclerosis?

A

Oxidised LDL in intima –> macrophages become foam cells –> accumulation in intima of BV walls –> fatty streak –> atheroma

334
Q

What are foam cells?

A

Fat filled macrophages

335
Q

What is an early warning sign of atherosclerosis?

A

Angina

336
Q

What happens if an atherosclerotic plaque ruptures?

A

Clotting cascade is initiated and thrombus forms

337
Q

Why do statins have a wide spectrum of side effects?

A

Pathway they act on is wide branching

338
Q

Give an example of a useful species produced by the cholesterol pathway.

A

Coenzyme Q10

339
Q

Why are statins taken before bed?

A

Most cholesterol is produced in the liver at night

340
Q

Are statins universally effective?

A

No, varies from patient to patient so trial and error for treatment plan

341
Q

What is the problem with statins and risk of CVD?

A

Statins save lives at high risk of CVD but controversy over whether to prescribe routinely for >10% risk

342
Q

What is a dangerous byproduct of ATP production?

A

Reactive oxygen species

343
Q

How are reactive oxygen species formed surfing ATP synthesis?

A

Electrons drop out of the electron transport chain and combine with oxygen

344
Q

What do superoxide radicals damage?

A

DNA and CSM

345
Q

How does superoxide dismutase (SOD) act as a defence mechanism against superoxide radicals?

A

Converts them to hydrogen peroxide which catalase can then turn into oxygen and water

346
Q

Where is catalase found?

A

Widely distributed in cells

347
Q

What ROS is produced by ionising radiation?

A

Hydroxyl radicals

348
Q

What do hydroxyl radicals cause in RBCs?

A

Haemolysis

349
Q

Why are antioxidants needed to eliminate hydroxyl radicals?

A

They cannot be removed enzymatically

350
Q

How is nitric oxide, which is a free radical, used physiologically in the body?

A

Used for signalling

351
Q

How is nitric oxide formed?

A

From arginine by inducible NO synthase

352
Q

What is formed if hydrogen peroxide combines with oxygen?

A

Peroxynitrite

353
Q

What is peroxynitrite involved in?

A

Inflammation

354
Q

What exogenous agents can overwhelm the tissue’s defence against oxidising agents?

A

Drugs e.g. antimalarials

Toxins e.g. paraquat

355
Q

What are the five most common reactive oxygen species?

A 
Superoxide
Hydrogen peroxide
Hydroxyl
Nitric oxide
Peroxynitrite
356
Q

What are the five cellular defences against ROS?

A 
SOD
Catalase
NADPH
Glutathione
Antioxidants e.g. those found in grapes
357
Q

Why is glutathione a very effective reducing agent?

A

Thiol group donates its hydrogen easily

358
Q

How does glutathione act as the first line of defence against ROS?

A

Donates H from thiol group –> oxidised to glutathione disulphide which can be reduced by GSH reductase to be constantly replenished to glutathione

359
Q

When can glutathione not be reformed in RBCs?

A

G6PDH deficiency

360
Q

How is NADPH mainly produced?

A

Pentose phosphate pathway

361
Q

What does NADPH use to act as a second line of defence against ROS?

A

G6PD

362
Q

What does NADPH replenish?

A

GSH

363
Q

What other types of antioxidants are there apart from glutathione and NADPH?

A

Dietary vitamins
Flavenoids
Minerals

364
Q

Which dietary vitamins are antioxidants?

A

A, C and E

365
Q

Give two examples of flavonoids which are found in coloured fruit and veg.

A

Polyphenols

Beta-carotene

366
Q

Name two minerals which may be required by some enzymes for antioxidant function.

A

Selenium

Zinc

367
Q

What is lipid peroxidation?

A

Reaction of unsaturated lipids w/ROS to form lipid peroxide so

368
Q

Why does lipid peroxidation lead to early stages of CVD?

A

Damages CSM and plaques form as macrophages recognise and engulf faulty lipids

369
Q

What is oxidative burst?

A

Rapid release of superoxide and hydrogen peroxide from leucocytes to kill local pathogens

370
Q

What is NADPH oxidase?

A

A very complex protein in CSM that fires rapidly produced ROS inwards

371
Q

What conditions are associated with oxidative stress?

A 
Cancer
Emphysema
Pancreatitis
CVD
Crohn's
RA
T1DM
Alzheimer's 
Ischaemia/reperfusion injury
372
Q

How does reperfusion injury cause oxidative stress?

A

Clot bust –> sudden increase in oxygen to ischaemic tissue –> increase in ROS

373
Q

What is pharmacodynamics?

A

What the drug does to the body

374
Q

What is pharmacology?

A

Study of how chemical agents affect the function of living organisms

375
Q

What is pharmacokinetics?

A

What the body does to the drug

376
Q

What four things does pharmacokinetics consider?

A

Absorption
Distribution
Metabolism
Elimination

377
Q

Are most drugs water soluble or lipid soluble?

A

Lipid

378
Q

Why is a large proportion of a penicillin dose lost in the urine?

A

It is water soluble

379
Q

Why can most drugs not be excreted directly by the kidney?

A

Lipid soluble so are filtered out by kidney but then reabsorbed so

380
Q

What path must drugs take to be excreted via the kidney?

A

Parent drug molecule –> polar, lipid insoluble, water soluble derivative –> excretion via kidney

381
Q

How does the pharmacological activity of metabolites usually compare to the parent drug molecule?

A

Less active

382
Q

What is special about prodrugs?

A

They must be metabolised to become active

383
Q

Why might patients belonging to the Chinese population not be able to be treated with codeine?

A

Lack conversion enzyme so cannot metabolise it to morhpine

384
Q

What is primidone metabolised to?

A

Phenoarbitone

385
Q

What is the toxic metabolite of pethidine?

A

Norpethidine

386
Q

What happens during phase I of drug metabolism?

A

Add or exposure of a reactive group by oxidation, reduction or hydrolysis

387
Q

What is the main site of phase I drug metabolism?

A

Microsomes on ER in hepatocytes

388
Q

Where, other than the liver, can phase I drug metabolism take place?

A

GI tract
Kidney
Lung
Plasma

389
Q

Why does heroin have such a short half life?

A

Its ester bonds are rapidly broken down by cholinesterase enzymes in the plasma

390
Q

Give an example of an opioid drug which skips phase I metabolism.

A

Morphine

391
Q

What is present in the microsomes of ER in hepatocytes that is used in phase I of drug metabolism?

A

Cytochrome P450 enzyme system (CYP)

392
Q

What accounts for ~55% of drug metabolism in the phase I pathway?

A

Isoform CYP3 A4

393
Q

What is abundant in hepatocytes which is a CYP cofactor that has both oxidative and reductive functions?

A

NADPH

394
Q

What happens in phase II of drug metabolism?

A

Conjugation - altered molecule is combined w/water soluble group so it can be eliminated by the kidney

395
Q

Where is the most common site of conjugation which uses cytosolic enzymes?

A

Liver

396
Q

What reactions can be used in phase II drug metabolism?

A

Glucuronidation
Sulphate conjugation
Glutathione conjugation

397
Q

What high energy form of metabolite is used as a cofactor for glucuronidation?

A

Uridine diphosohate glucuronic acid

398
Q

What is glucuronic acid?

A

Metabolite of glucose which is readily available to make drug molecules water soluble

399
Q

What genetic factors can vary drug metabolism in the population?

A

Polymorphisms
Lack main enzyme for acetylation in phase II - slow acetylators
Low levels of pseudocholinesterase

400
Q

What causes short term muscle relaxants to act for much longer in some individuals?

A

Have low levels of pseudocholinesterase in plasma

401
Q

What environmental influences vary drug metabolism in the population?

A

Metabolism of one drug can affect metabolism of another
Inhibition e.g. fruit juices
Induction by an agent of enzymes in the liver

402
Q

Why are smokers and drinkers problematic for anaesthetists?

A

Smoking and alcohol consumption induces enzymes in the liver so anaesthetics are more rapidly broken down

403
Q

What path do drugs take in the first pass effect?

A

Lumen of ileum –> venous blood –> hepatic portal vein –> liver

404
Q

What is the first pass effect?

A

Any drug absorbed into the blood is excessively metabolised by the liver

405
Q

Why are large doses of paracetamol needed?

A

90% is metabolised by first pass effect so only 10% of a dose is effective

406
Q

What is pharmacoepidemiology?

A

Study of drug effects in a large population

407
Q

What is pharmacovigilance?

A

Reporting of adverse drug reactions (ADRs) post-marketing

408
Q

Give two drugs and their effects that were significant to pharmacovigilance.

A

Thalidomide - affected limb buds which did not arise in animal testing
Mefloquine - no wide malarial resistance but causes lots of side effects

409
Q

What happens to a therapeutic dose of paracetamol?

A

Undergoes phase II metabolism only - glucuronidation and sulphation

410
Q

Why does paracetamol bypass phase I metabolism?

A

It already has an OH reactive group

411
Q

What happens in a toxic dose of paracetamol?

A

Glucuronidation and sulphation are saturated so paracetamol undergoes phase I metabolism

412
Q

What is formed when paracetamol undergoes phase I metabolism?

A

NAPQI, a toxic metabolite

413
Q

Why is NAPQI formation in paracetamol overdose so dangerous?

A

It is a toxic metabolite

It undergoes glutathione conjugation which kills liver cells by oxidative stress

414
Q

How is alcohol dealt with by the body?

A

90% metabolised

415
Q

What is alcohol converted to as it is metabolised?

A

Alcohol –> acetylaldehyde –> acetic acid

416
Q

Which enzymes are involved in alcohol metabolism?

A

Alcohol dehydrogenase
Aldehyde dehydrogenase
CYP2E1

417
Q

What causes hangovers?

A

Build up of toxic metabolite acetylaldhyde

418
Q

What can acetic acid from alcohol metabolism be used for?

A

FA and ketone body synthesis

419
Q

What is the metabolism rate for alcohol?

A

~7 g per hour

420
Q

What action of alcohol dehydrogenase can lead to excess fat deposition, decreased FA oxidation and therefore hypoglycaemia, gout and lactic acidosis?

A

Decreases NAD+ to NADH ratio

421
Q

What causes fatty liver in alcoholics?

A

Fat deposition and acetylaldehyde damage

422
Q

What can fatty liver lead to?

A

Alcoholic hepatitis

Alcoholic cirrhosis

423
Q

What treatment is given in severe alcohol dependency?

A

Disulfiram

424
Q

How does Disulfiram work?

A

Inhibits aldehyde dehydrogenase which causes a build up of acetaldehyde resulting in a week long hangover

425
Q

What do the cost and effects on the CNS in alcoholism cause?

A

Poor dietary habit which leads to GI tract disturbances such as folic acid deficiency leading to anaemia, vitamin deficiency, diarrhoea and lack of appetite

Semester 1 (7 decks)

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