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Semester 1 > Metabolism > Flashcards

Metabolism Flashcards

1
Q

Define: Anabolism

A

This process uses energy, reducing power and raw materials to build up molecules for growth and maintenance.

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2
Q

Name the 3 components of total energy expenditure.

A
  1. Basal metabolic rate
  2. Diet induced thermogenesis
  3. Physical activity level
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3
Q

Why is FAT an essential component of the diet?

A
  1. Needed to absorb fat soluble vitamins
  2. Can be used as an alternative energy source.
  3. Source of fatty acids
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4
Q

Why are CARBOHYDRATES an essential component of the diet?

A
  1. Major energy source for the body.
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5
Q

Why are PROTEINS an essential part of the diet?

A
  1. Provide amino acids for use in proteinsynthesis.

2. Maintain nitrogen balance

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6
Q

Why are VITAMINS an essential part of the diet?

A
  1. Prevents vitamin deficiencies.
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7
Q

Why are IONS an essential part of the diet?

A
  1. Act as cofactors for enzymes.

2. Can setup ion concentration gradients.

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8
Q

What is Marasmus? Symptoms? Cause?

A

A disease caused by starvation; the individual will have muscle wastage and a very starved look. Caused by a lack of protein and other food components in the diet. NO OEDEMA.

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9
Q

What is Kwashiokor? Symptoms? Cause?

A

This is a disease caused by a low protein, high carbohydrate diet. Normally found in young children taken off breast milk diets and fed with cassava. Symptoms include lethargy and a large oedema on the stomach. Due to high carbohydrate intake, fats build up in the liver; as there are reduced amounts of proteins to transport this fat from the liver, the patient gets a fatty liver. Hepatomegaly = swelling of liver

Also, due to reduced protein levels, the serum albumin level is low and therefore the oncotic pressure in the blood is reduced - this increases tissue fluid flow into the tissues, causing an oedema.

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10
Q

BMI Equation?

A

BMI = (Weight) / (Height)^2

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11
Q

How would you classify an individual with a BMI score of:

A

Underweight

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12
Q

How would you classify an individual with a BMI score of:

18 - 24.9

A

Normal/Ideal weight

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13
Q

How would you classify an individual with a BMI score of:

25 - 29.9

A

Overweight

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14
Q

How would you classify an individual with a BMI score of:

30-34.9

A

Obese

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15
Q

How would you classify an individual with a BMI score of:

> 35

A

Severely obese.

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16
Q

What is the problem with BMI calculations?

A

Doesn’t consider the individual’s build - they be very muscly. Muscle is heavier than fat.

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17
Q

What is an alternative method to the BMI calculation.

A

Hip to waist ratio.

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18
Q

Which is better as a body shape, apple or pear?

A

Pear is said to be a better body shape.

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19
Q

Define: Homeostasis

A

The maintenance of a constant internal environment.

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20
Q

What does the hypothalamus control?

A

Controls endocrine systems.

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21
Q

What does the medulla oblongata control?

A

Regulates systems such as the respiratory and cardiovascular systems.

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22
Q

Name the essential amino acids.

A 
If - Isoleucine
Learnt - Lysine
This - Threonine
Huge - Histidine
List - Leucine
May - Methionine
Prove - Phenylalanine
Truly - Tryptophan
Valuable - Valine
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23
Q

Define: Catabolism

A

This is the breaking down of molecules to release energy and reducing power.

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24
Q

Define: Cell metabolism

A

The highly integrated network of chemical reactions which occur in cells.

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25
Q

What does cell metabolism produce?

A
  1. Energy for cell function
  2. Building block molecules
  3. Reducing power
  4. Organic precursor molecules (eg. Acetyl coA)
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26
Q

Where do cell nutrients in the blood come from?

A
  1. Diet
  2. Synthesis in the body
  3. Released from storage
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27
Q

Where do cell nutrients end up?

A
  1. Degradation to release energy
  2. Synthesis
  3. Storage
  4. Inter-conversion into other nutrients
  5. Excretion
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28
Q

Why do cells need a continuous supply of energy?

A

So that the cell is able to perform it’s functions.

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29
Q

Define: Exergonic reactions

A

Energy releasing reactions.

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30
Q

What is the creatine phosphate reaction that can occur in muscles? When does it occur?

A

Creatine + ATP –> Creatine phosphate + ADP

Catalyst = Creatine kinase

Occurs when muscle cells require immediate high energy amount.

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31
Q

Equation of reduction of NAD+?

A

NAD+ + 2H+ + 2e- —-> NADH + H+

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32
Q

Is ATP a high or low energy signal?

A

High energy signal.

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33
Q

Is ADP/AMP a high or low energy signal?

A

Low energy signal.

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34
Q

Which readily crosses cell membranes?

Hydrophillic or hydrophobic molecules

A

Hydrophobic.

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35
Q

Which monomers make up sucrose?

A

Glucose + Fructose

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36
Q

Which monomers make up Lactose?

A

Glucose + Galactose

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37
Q

Which monomers make up maltose?

A

Glucose + Glucose

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38
Q

Define: Polysaccharides

A

Structures made by multiple monosaccharides joined together by glycosidic bonds.

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39
Q

Describe the structure of glycogen.

A

A highly branched polymer of glucose. Includes alpha 1,4-glycosidic bonds which join monomers and alpha 1,6-glycosidic bonds which cause branching.

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40
Q

Describe the structure of cellulose. Why can’t human digest cellulose?

A

A polymer of glucose monomers joined by Beta-1,4-glycosidic bonds.

Humans can’t digest this bond so we don’t digest cellulose.

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41
Q

Name three tissues/cells which are glucose dependent.

A
  1. Erythrocytes
  2. Lens of the eye
  3. Kidney Medulla
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42
Q

What energy source does the CNS have preference towards?

A

Glucose as an energy source.

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43
Q

Name three enzymes which catalyse irreversible steps in glycolysis.

A
  1. Hexokinase
  2. Phosphofructokinase-1
  3. Pyruvate kinase
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44
Q

Is CO2 produced in glycolysis?

A

No

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45
Q

What does glucose get made into by glycolysis? What type of reaction is it?

A

Glucose —> Pyruvate by oxidation reactions.

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46
Q

What happens in anaerobic glycolysis? Why is it important? What can happen to the lactate?

A

Glucose —> Pyruvate —> Lactate
The enzyme Lactate dehydrogenase performs the pyruvate to lactate.

Oxidises NADH to produce NAD+ which is required for glycolysis to continue. The lactate is dissolved into the blood and either becomes CO2 in the heart or glucose in the liver. The lactate can also be converted by into pyruvate (reversible reaction - using the enzyme lactate dehydrogenase).

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47
Q

Which enzyme is missing/defective in lactose intolerant people?

A

Lactase

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48
Q

Which enzymes may be defective/missing in those with galactosaemia.

A
  1. Galactokinase

2. Galactose-1-phosphate Uridyl Transferase

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49
Q

What happens to galactose which accumulates in tissues?

A

Galactose is reduced to Galactitol by the enzyme Aldo Reductase. This reduction requires the use of NADPH;as NADPH depletes, disulphide bonds are able to form - this can cause cataracts in the lens of the eye.

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50
Q

What’s the importance of the Pentose Phosphate pathway and what enzyme catalyses it?

A

Glucose-6-phosphate + NADP+
–> Pentose sugar phosphate + NADPH + CO2

Catalysed by: Glucose-6-phosphate dehydrogenase

Importance: Creates NADPH which is used to prevent disulphide bonds from forming (prevents Heinz bodies + cataracts). Also, produces pentose sugars which are used for nucleotides.

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51
Q

How are Heinz Bodies formed?

A

Due to a lack of NADPH in the body (eg. due to glucose-6-phosphate dehydrogenase deficiency), disulphide bonds form between red blood cells and other proteins, this forms Heinz bodies which are insoluble. Leads to haemolysis.

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52
Q

How is pyruvate prepared to enter TCA cycle?

A

Pyruvate cannot enter the TCA cycle, it must be converted into acetyl coA. This is done in the Link’s reaction using the enzyme Pyruvate dehydrogenase. This is an irreversible reaction.

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53
Q

What happens in the TCA cycle. How is it regulated?

A

Acetyl coA enters the cycle and undergos multiple reactions producing: 3 NADH, 2 CO2, 1 GTP, 1 FADH2.

Regulated by Isocitrate dehydrogenase which responds to high and low energy signals.

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54
Q

Where does the electron transport chain occur?

A

Inside mitochondria + mitochondria inter-membrane space.

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55
Q

What forced H+ through ATP synthase?

A

Proton Motive Force

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56
Q

In the ETC, what is the role of oxygen?

A

Terminal electron acceptor

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57
Q

How are the ETC and ATP synthase tightly coupled?

A

Only way for H+ to return back into the mitochondria is by ATP synthase.

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58
Q

Why/How does the ETC and ATP synthase become uncoupled?

A

Uncoupling proteins cause the membrane of the mitochondria to become more permeable meaning that H+ ions can move back into the mitochondria rather than through ATP synthase. Energy is released as heat energy instead, this is deliberately done in brown adipose tissue as non-shivering thermogenesis.

Alternatively, toxins such as Dinitrophenol and Dinitrocresol increase the permeability of the mitochondrial membrane so H+ ions can return into the matrix without passing through ATP synthase.

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59
Q

Give 4 comparisons of Oxidative and Substrate level phosphorylation.

A
  1. Oxidative phosphorylation requires membrane association whereas substrate level does not.
  2. Oxidative phosphorylation uses indirect energy coupling (PMF) whereas substrate level phosphorylation uses direct energy coupling.
  3. Oxidative phosphorylation cannot occur in the absence of oxygen whereas substrate level phosphorylation can, to an extent.
  4. Oxidative phosphorylation produces a lot of ATP whereas substrate level phosphorylation produces a little.
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60
Q

Name the three classes of lipids.

A
  1. Fatty acid derivatives
  2. Hydroxy-methyl-glutaric (HMG) acid derivatives
  3. Fat soluble vitamins
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61
Q

Name the three Ketone bodies made in the body.

A
  1. Acetoacetate
  2. Acetone
  3. Beta-Hydroxybutyrate
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62
Q

Give the name for:

  • Ketones lost in urine
  • Ketones being acidic in plasma
A

Urine: Ketonuria
Acid: Ketoacidosis

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63
Q

AcetylCoA can become either Ketone bodies or cholesterol. Name the enzymes involved and say what regulates which product is made.

A

Ketone bodies - Enzyme = HMGcoA lyase

Cholesterol - Enzyme = HMGcoA reductase

The Insulin/Glucagon ratio regulates which enzyme is inhibited.
High insulin/glucagon ratio = Cholesterol
Low insulin/glucagon ratio = Ketone bodies

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64
Q

Acetyl CoA is the hub of several reactions - name 3 products it could become.

A
  1. Fatty acids (eg. goes to triacylglycerol)
  2. CO2 (kreb’s cycle)
  3. HMG acids (eg. goes to ketone bodies)
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65
Q

Define: Glycogenesis

A

Glycogen synthesis

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66
Q

Define: Glycogenolysis

A

Breakdown of Glycogen

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67
Q

Give the equations + enzymes for glycogenesis

A
  1. Glucose + ATP –>Glucose-6-phosphate + ADP (Hexokinase)
  2. Glucose-6-phosphate
    • ->Glucose-1-phosphate (Phosphoglucomutase)
  3. Glucose-1-phosphate + UDP + H2O –> UDP Glucose + 2Pi
  4. (Glycogen)n + UDP Glucose –> (Glycogen)n+1 + UDP
    (Glycogen synthase + Branching enzyme)
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68
Q

Give the equations + enzymes for glycogenolysis.

A
  1. Glycogen + Pi –> Glucose-1-phosphate
    (Glycogen phosphorylase + debranching enzyme)
  2. Glucose-1-phosphate
    • -> Glucose-6-phosphate (Phosphoglucomutase)
  3. Muscles use Glucose-6-phosphate in glycolysis.
    However, in the liver:
    Glucose-6-phosphate + H2O –> Glucose + Pi
    (Glucose-6-phosphatase)
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69
Q

Compare liver and muscle glycogen.

A

Liver: For all tissues in the body (makes into glucose)

Muscle: Only to be used by muscle (makes into glucose-6-phosphate)

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70
Q

Define: Gluconeogenesis

A

The production of glucose from non-carbohydrates

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71
Q

Name 4 substrates for gluconeogenesis

A
  1. Lactate
  2. Amino acids (glucogenic)
  3. Glycerol
  4. Pyruvate
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72
Q

When does gluconeogenesis occur?

A

When glycogen stores are depleted.

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73
Q

What are the two key enzymes in gluconeogenesis?

How are they regulated?

A
  1. PEPCK
  2. Fructose 1,6-bisphosphatase.

Both are activated by glucagon and both inhibited by Insulin.

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74
Q

What is the name for the formation of triacylglycerols from glycerol + fatty acids?

A

Esterification

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75
Q

What is the name for the breakdown of triacylglycerols into glycerol + fatty acids?

A

Lipolysis.

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76
Q

What is the enzyme which converts Acetyl coA into Malonyl coA in liver lipogenesis?

A

Acetyl coA carboxylase

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77
Q

What complex does malonyl coA enter to produce fatty acids?

A

Fatty acid synthase complex.

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78
Q

What type of lipoprotein transports glycerol from the small intestine to tissues and the liver? What vessels does it travel in?

A

Chylomicrons. From the small intestine, these travel in the lymphatic system up to the left subclavian vein where the chylomicron then travels in the bloodstream.

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79
Q

What is the name for fatty acid degradation and how does it occur?

A

Beta Oxidation. Occurs in the mitochondria - through a series of reactions, 2 carbon molecules are removed and this cycles until the fatty acid is entirely broken up. The 2 carbon molecules become acetyl coA which can be used in a variety of ways.

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80
Q

How do fatty acids enter the mitochondria?

A

Fatty acids must first be activated by Acetyl CoA which forms Fatty acyl coA.

Activated fatty acids can’t cross mitochondrial membrane so carnitine shuttle transport must occur. Here, Fatty acyl coA joins with carnitine to form acyl carnitine. This passes through the membrane where the acyl group then leaves carnitine.

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81
Q

Name of fatty acid synthesis? How does it occur?

A

Lipogenesis.

Acetyl coA becomes malonyl coA due to the enzyme acetyl coA carboxylase. Malonyl coA then enters the fatty acid synthase complex where it produces a fatty acid.

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82
Q

Comparison of Fatty acid synthesis and Fatty acid oxidation.

A
  1. FAS adds 2C whilst FAO removes 2C.
  2. FAS adds Acetyl coA whilst FAO removes Acetyl coA
  3. FAS in cytoplasm whilst FAO in mitochondria
  4. FAS requires a lot of ATP whilst FAO requires only a little.
  5. FAS - Insulin activate whilst in, FAO inhibited.
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83
Q

First step of catabolism is to remove amino group. Which two ways can this happen? Describe.

A
  1. Transamination - the amino group is transferred from an amino acid to a keto acid. This uses aminotransferase enzymes. Alanine amino transferase produces Glutamate whilst Aspartate amino transferase produces Aspartate. Both Glutamate and Aspartate are then involved in producing Urea in the urea cycle.
  2. Deamination - The amino group is removed from an amino acid to produce a free ammonia. This is highly toxic and has to be transported to the kidney for removal as urea.
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84
Q

Name an example for each amino acid:

  1. Glucogenic
  2. Ketogenic
  3. Both
A 
Glucogenic = Alanine
Ketogenic = Lysine
Both = Threonine
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85
Q

What is Phenylketonuria?

A

When a person cannot convert Phenylalanine into Tyrosine due to a defect in the Phenylalanine hydroxylase enzyme. This causes a build up in Phenylalanine which becomes Phenylketones - these are excreted in the urine. This autosomal recessive condition can lead to brain damage.

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86
Q

What is Homocystinuria?

A

This is a condition where homocysteine cannot be converted into cystathionine due to a defect in the Cystathionine-Beta-synthase enzyme. The homocysteine converts back into methionine and can become oxidised into homocystine which can be lost in the urine. Autosomal recessive disease which can lead to delayed development and faults in the fibrillin-1 protein.

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87
Q

What is the importance of measuring Creatinine in the blood and urine?

A

Creatinine is the product of the breakdown of Creatine phosphate; the amount of Creatinine is proportional to the amount of muscle in an individual. If there are high levels of creatinine in the blood but low levels in the urine, we can also know learn there may be kidney failure.

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88
Q

How can ammonia be transported in the blood?

A
  1. NH3 + Glutamate form Glutamine which travels in the blood to the kidney where it enters the urea cycle.
  2. Pyruvate + NH3 becomes Alanine by transamination. Travels to liver where transamination occurs again to produce pyruvate and NH3. NH3 then binds with Glutamate to move to the kidney for the urea cycle.
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89
Q

Symptoms of inherited diseases of urea cycle? Eg. Hyperammonaemia. Why is it normally only a defect rather than a complete failure? Treatment?

A

-Mental retardation, seizures, coma

If it were a complete failure, urea cycle could not occur and this would not be compatible with life.

Treat with low protein diet.

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90
Q

Treatment of Phenylketonuria and Homocystinuria?

A

Low protein diets.

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91
Q

What is the function of Chylomicrons?

A

Transport fats from the small intestine to the tissues and liver.

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92
Q

What is the function of VLDLs?

A

Transport the fats from the liver to other tissues.

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93
Q

What is the function of IDLs?

A

Transport cholesterol from the liver to tissues.

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94
Q

What is the function of LDLs?

A

Transport cholesterol from the liver to the tissues.

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95
Q

What is the function of HDLs?

A

Transport cholesterol from tissues back to the liver.

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96
Q

Which enzyme removes triacylglycerols from lipoproteins?

A

Lipoprotein lipase.

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97
Q

What does LCAT do?

A

Converts cholesterol in HDLs into Cholesterol esters for transport. If this fails, cholesterol builds up in tissues -atherosclerosis can be a result.

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98
Q

How do tissues receive cholesterol from LDLs?

A

Receptor mediated endocytosis. Lysosomes then digest LDL to release contents.

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99
Q

How do tissues receive cholesterol from HDLs?

A

Scavenger receptors receive the HDLs and cholesterol is transferred to the tissue.

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100
Q

What methods can be used to tackle hyperlipoproteinaemia?

A
  1. Diet and lifestyle change
  2. Statins
  3. Bile Salt Sequestrants
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101
Q

What is the enzyme which converts releases triacylglycerol from adipose tissue for transport to tissues? Effects of insulin and glucagon?

A

Hormone Sensitive Lipase

Insulin - Inhibit
Glucagon - Stimulate

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102
Q

How can free radicals be found in the mitochondria? What can happen?

A

Electrons passing in the electron transport chain can leak out between protein carriers - this electron can then join a molecule such as oxygen to form a free radical. Eg. Superoxide.

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103
Q

What does ROS stand for?

A

Reactive Oxygen Species

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104
Q

How can superoxide become hydrogen peroxide?

A

Superoxide can react with 2 H+ and an e- to form hydrogen peroxide.

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105
Q

What does catalase do?

A

Catalase is an enzyme which breaks hydrogen peroxide into water and oxygen.

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106
Q

How are hydroxyl radicals formed?

A

Hydrogen peroxide can react with H+ and e- to form water + hydroxyl radical.

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107
Q

How can the immune system create free radicals?

A

Phagocytic cells contain NADPH oxidase which converts NADPH to NADP+ and converts O2 to superoxide. This O2 radical can then form hydrogen peroxide which can lead to the formation of HClO radical (bleach) for use to kill bacteria.

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108
Q

Describe the production of free radicals by nitric oxide synthase

A

Nitric oxide synthase is an enzyme which catalyses the reaction of Arginine to Citrulline and nitric oxide. This nitric oxide can also react with oxygen to form peroxynitrite.

109
Q

Describe 3 defence mechanisms by the cell to protect from ROS.

A
  1. Superoxide dismutase converts superoxide into hydrogen peroxide and then catalase reacts with hydrogen peroxide to produce water and oxygen.
  2. Glutathione in the form of GSH can donate an electron to a ROS. If two GSH do this, we can get GSSG. This conversion uses the enzyme Glutathione Peroxidase.
    We can then get electrons from NADPH to convert GSSG back into GSH using the enzyme Glutathione Reductase.
  3. Vitamins C and E are free radical scavengers.
110
Q

What effect does Oxidative stress have on cancer?

A

Causes DNA damage.

111
Q

What is Oxidative stress?

A

When the amount of ROS is too much for the cell defences to cope with.

112
Q

How does Oxidative stress affect Rheumatoid arthritis?

A

Causes joint inflammation by ROS.

113
Q

Name 3 macrovascular complications of DM.

A
  1. Increased risk of strokes
  2. Increased risk of MIs
  3. Poor circulation to periphery
114
Q

Name 4 microvascular complications of DM.

A
  1. Retinopathy
  2. Nephropathy
  3. Neuropathy
  4. Diabetic foot
115
Q

Common 3 symptoms of Type 1 DM?

A
  1. Polyuria
  2. Polydipsia
  3. Weight Loss
116
Q

Common 5 symptoms of Type 2 DM?

A
  1. Polyuria
  2. Polydipsia
  3. Weight Loss
  4. Lethargy
  5. Persistent infections
117
Q

Ketone Bodies - Type 1 or Type 2 DM?

118
Q

Oxidative or Reduction?

Catabolism

119
Q

Oxidative or Reductive?

Anabolism

120
Q

What can be measured to calculate skeletal muscle mass?

A

Creatinine levels.

121
Q

What does it mean if we have high blood creatinine levels but low urine levels of creatinine?

A

Suggests that there is kidney failure as the kidneys are normally good at filtering out creatinine.

122
Q

Sugars are partially oxidised - what benefit does this give sugars compared to fatty acids as fuels?

A

Sugars require less oxygen to be fully oxidised compared to fatty acids.

123
Q

GLUT receptors in Erythrocytes?

124
Q

GLUT receptors in Liver?

125
Q

GLUT receptors in neurones (brain)?

126
Q

GLUT receptors in skeletal + cardiac muscle and adipose tissue?

127
Q

How do those with lactose intolerance get diarrhoea?

A

Lactose cannot be digested by enzymes so moves into the lumen of the colon where bacteria begin to feed on it. This increases osmotic pressure so water moves by osmosis into the lumen. This causes diarrhoea.

128
Q

Name three clinical signs of hypercholesterolaemia.

A
  1. Xanthalasma = Yellow/white lumps around eyes
  2. Tendon Xanthoma = Lumps around tendons
  3. Corneal Arcus = White ring around eye.
129
Q

Which enzyme has failed in Homocystinuria?

A

Cystathionine Beta synthase

130
Q

Which enzyme has failed in Phenylketonuria?

A

Phenylalanine Hydroxylase

131
Q

Name 3 functions of apoproteins

A
  1. Package lipids for transport in the body
  2. Activate enzymes
  3. Recognise cell surface receptors
132
Q

How do bile salt sequestrants work?

A

Bind to bile salts meaning that they can’t be reabsorbed and are lost in faeces. Cholesterol is used to make bile salts so this in turn causes more cholesterol to be used.

133
Q

Describe what happens in paracetamol overdosing.

A

Body produces NAPQI which is highly toxic to hepatocytes. NAPQI can conjugate with glutathione - this causes a depletion of GSH which can lead to oxidative stress and damage to liver cells.

134
Q

How can we treat paracetamol overdosing?

A

Give acetylcysteine within 8 hours to replenish levels of GSH so NAPQI can be metabolised by the liver safely.

135
Q

Give the equations for the metabolism of alcohol in the body.

A

Alcohol –(Alcohol dehydrogenase) –> Acetaldehyde –(Aldehyde dehydrogenase) –> Acetate –> Acetyl CoA

136
Q

How does Disulfiram work for alcoholics?

A

Inhibites Aldehyde dehydrogenase meaning that there is a build up of acetaldehyde which causes hangover symptoms.

137
Q

Insulin or glucagon?

Released when blood sugars are low

138
Q

Insulin or glucagon?

Causes an increased glucose uptake by cells.

139
Q

Insulin or glucagon?

Promotes glycogenesis

140
Q

Insulin or glucagon?

Promotes gluconeogenesis

141
Q

Insulin or glucagon?

Promotes protein synthesis?

142
Q

How do we treat refeeding syndrome? Why?

A

To treat refeeding syndrome, we give an increasing diet beginning very small. This is because, the individual’s body has gotten use to metabolising little food (eg. producing little urea) - if we give them normal sized meals, they could die.

143
Q

Name the 5 important features of any control system.

A
  1. Communication
  2. Control centre
  3. Receptors
  4. Effectors
  5. Feedback
144
Q

What does paracrine mean?

A

Hormones are released locally and act locally

145
Q

What does autocrine mean?

A

Hormones affect cells from which they are released from.

146
Q

Afferent or Efferent?

Peripheral nervous system towards the brain.

147
Q

Afferent or Efferent?

Peripheral nervous system away from the brain.

148
Q

Which nucleus controls the biological clock?

A

Suprachiasmatic nucleus

149
Q

Which nucleus control appetite

A

Arcuate nucleus

150
Q

Which nucleus controls oxytocin release?

A

Supraoptic nucleus

151
Q

Which nucleus controls Anti-diuretic Hormone?

A

Paraventricular nucleus.

152
Q

Name the 4 types of hormones in the body and describe whether they are hydrophobic or hydrophillic. Give examples for each.

A
  1. Polypeptide/Peptide hormones -Hydrophillic-Insulin, GH
  2. Glycoprotein homones - Hydrophillic - FSH, LH
  3. Amino acid derivatives - Mixed - T3, T4, Adrenaline (adrenaline = hydrophillic; T3 + T4 = hydrophobic)
  4. Steroid hormones - Hydrophobic - Testosterone, Aldosterone
153
Q

How do hydrophobic hormones travel in the blood?

A

Have to use specific protein transporters. Only the unbound hormones are biologically active.

154
Q

How do hydrophillic hormones travel in the blood?

A

Can dissolve into the blood.

155
Q

How do hydrophobic hormones affect receptors?

A

They can travel phospholipid bilayer into cells and bind to receptors inside the cells.

156
Q

How do hydrophillic hormones affect receptors?

A

Can’t cross lipid bilayer so binds to surface receptors which triggers a second messenger inside the cell to perform a task.

157
Q

Name 2 possible effects a binding hormone could have on a cell

A
  1. Change activity of an enzyme

2. Alter gene expression

158
Q

Name 3 ways in which hormone secretion can be controlled

A
  1. Negative feedback/Positive feedback
  2. Tropic hormones
  3. Inactivation of hormones (in liver, kidneys and some target tissues).
159
Q

How are steroid and protein hormones inactivated in the liver, kidneys or target tissues?

A

Steroid - Small changes which make them hydrophillic so they can dissolve into water and be lost in the urine.

Protein - Multiple complex interactions to degrade proteins into amino acids which can be recycled in the body.

160
Q

Primary neurones in the arcuate nucleus can be excitatory or inhibitory. Give examples for both.

A

Excitatory - NPY or AgRP

Inhibitory - POMC = Beta endorphins, ACTH, alpha-MSH

161
Q

Some hormones give feedback about appetite state in the body. Give examples.

A

Ghrelin - Stimulates appetite from an empty stomach. Full stomachs stretch and this inhibits the release of ghrelin.

PYY - Released from small intestine and suppresses appetite.

Leptin - From adipose tissue and suppresses appetite.

Insulin - Suppresses appetite by inhibiting stimulatory and activating inhibitory.

162
Q

What is metabolic syndrome?

A

Collection of symptoms including:

  • Insulin resistance
  • Dyslipidaemia
  • Glucose intolerance
  • Hypertension
  • Central obesity

They all inter-link and this syndrome is becoming more and more recognised/accepted.

163
Q

What is the Develomental Origins of Health and Disease Theory?

A

Correlation between adulthood diseases (eg. Type 2 diabetes) and a low birth weight. Suggested that this is due to epigenetics where DNA methylation is causing suppression of gene transcription.

164
Q

Which type of diabetes mellitus requires immediate treatment with insulin?

165
Q

Give 5 signs/symptoms of type 1 DM.

A
  1. Polyuria
  2. Polydipsia
  3. High blood glucose
  4. Weight loss
  5. Ketoacidosis
166
Q

Give 5 signs/sympotoms of type 2 DM.

A
  1. Polyuria
  2. Polydipsia
  3. High blood glucose
  4. Weight loss
  5. Lack of energy
167
Q

Give 5 symptoms of hypoglycaemia

A
  1. Shaking
  2. Confusion
  3. Sweating
  4. Drowsiness
  5. Palpitations
168
Q

Give 5 symptoms of hyperglycaemia

A
  1. Polyuria
  2. Polydipsia
  3. Weight loss
  4. Fatigue
  5. Dry/itchy skin
169
Q

Treatment approach for type 2 DM?

A
  1. Diet/lifestyle change
  2. Drugs to increase insulin sensitivity
  3. Insulin
170
Q

Name 2 reactions that Aldose Reductase catalyses.

A
  1. Galactose –> Galactitol

2. Glucose + NADPH + H+ –> Sorbitol + NADP+

171
Q

Why can we measure glycosylation of haemoglobin?

A

With chronic hyperglycaemia, glucose binds to valine in haemoglobin through glycation. This forms glycated haemoglobin (HbA1c). We can measure the percentage of glucose attached to see how glucose control over the past 2-3 months has been. Normally

172
Q

Give 3 macrovascular implications of DM.

A
  1. Increased risk of stroke
  2. Increased risk of MI
  3. Poor periphery circulation.
173
Q

Give 4 microvascular implications of DM.

A
  1. Diabetic eye (Retinopathy)
  2. Diabetic kidneys (Nephropathy)
  3. Diabetic Neuropathy
  4. Diabetic foot
174
Q

Why do we get diabetic foot?

A

Poor circulation + nephropathy + slow healing of infections can cause infected ulcers on feet.

175
Q

How is the B-cell adapted for insulin synthesis?

A
  • Contains rough endoplasmic reticulum for protein synthesis
  • Contains signal peptidase to convert pre-proinsulin into proinsulin
  • Protein disulphide isomerase in RER for disulphide bonds in proinsulin
  • Contains golgi apparatus for packaging proinsulin into vesicles
176
Q

How can measuring C-peptide levels be useful in those who inject insulin?

A

Tells us how much endogenous insulin they are producing. Injections do not have C-peptide so all C-peptide present is from insulin made in body.

177
Q

Name the 5 hormones released by the anterior pituitary gland.

A
  1. ACTH
  2. TSH
  3. Growth hormone
  4. FSH/LH
  5. Prolactin
178
Q

What do mineralocorticoids do?

A

Promote resorption of water and Na+ in the kidneys and cause K+ to be lost.

179
Q

What do glucocorticoids do?

A

Promote the production of glucose and breakdown of proteins as well as the redistribution of fats.

180
Q

What do androgens do?

A

Give genders their male or female characteristics.

181
Q

What does adrenaline do?

A

Prepares for fight or flight.

Increased cardiac output + supply to muscles
Increased mental alertness
Increased glycogenesis
Increased lipolysis

182
Q

How do steroid structures vary?

A

Have different:

  • Number of carbons
  • Functional groups
  • Distribution of C=C double bonds
183
Q

How does cortisol affect its target tissues?

A

Crosses plasma membrane and binds to receptor inside of the cell. The hormone/receptor complex enters the nucleus to a specific part of the DNA to alter the rate of transcription.

184
Q

How does adrenaline affect its target tissues?

A

Cannot cross plasma membrane so binds to surface receptor. Secondary messenger then affects the cell activity.

185
Q

What is the condition where there are low cortisol levels?

A

Addison’s Disease

186
Q

How do you treat an Addisonian crisis?

A

Time critical - IV fluids + IV cortisol

187
Q

Which condition can cause pigmentation due to ACTH?

A

Addison’s disease - due to low cortisol levels, there is little feedback so ACTH levels increase. ACTH can cause ACTH-mediated melanocyte stimulation.

188
Q

What is the name of the syndrome where there is an over secretion of Cortisol?

A

Cushing’s Syndrome

189
Q

Describe what happens in the body in Cushing’s disease

A

Tumour in the pituitary gland causing over secretion of ACTH so a lot of cortisol is released. The tumour means that the pituitary is not sensitive to the cortisol negative feedback so continues to release ACTH.

190
Q

Describe what happens in the body in adenoma.

A

Tumour in the adrenal cortex means that a lot of ACTH is released causing high cortisol levels. Tumour does not respond to negative feedback of cortisol.

191
Q

Describe what happens in the body in ectopic tumours.

A

Tumour in the body produces ACTH which means that high cortisol levels are caused.

192
Q

Describe what happens in the body in addison’s disease.

A

Can be due to disorders in the pituitary or hypothalamus meaning that low levels of ACTH or CRH are released and hence a reduced level of cortisol is released. Alternatively, could have autoimmune damage to adrenal cortex so cortisol is not released from adrenal cortex.

193
Q

What is the dextamethasone suppression test?

A

Dextamethasone is a strong steroid which can cause negative feedback to the pituitary (even when cortisol can’t). This causes the pituitary to release less ACTH and therefore cortisol levels lower. This test shows that the individual has Cushing’s disease.

194
Q

What is the Synacthen test?

A

Synacthen acts like ACTH and will trigger cortisol to be released in response. If this response is not seen, the individual has Addison’s disease.

195
Q

Why can cortisol (a glucocorticoid) have mild mineralocorticoid and androgen effects?

A

Binding receptors have similarities meaning that glucocorticoids can bind to mineralocorticoid and androgen receptors mildly with a low affinity.

196
Q

Give the 3 layers of the adrenal cortex and describe what each layer secretes.

A

Zona Glomerulosa - Mineralocorticoid
Zona Fasciculata - Glucocorticoid
Zona Reticularis - Androgens

197
Q

Describe the location of the thyroid gland.

A

Front and base of the neck. Anterior to the upper trachea and inferior to the thryoid cartilage.

198
Q

What is the name of a swollen thyroid gland?

199
Q

True or False:

The thyroid is highly vascularised.

A

True - 3 arteries and 3 veins supply it.

200
Q

How can a horse-like voice occur following a thyroidectomy?

A

There are two nerves lying next to the thyroid gland (recurrent and superior laryngeal nerves) which supply the larynx - if these are cut, the voice box is affected.

201
Q

What shape is the thyroid? What are the components?

A

Butterfly shape - central isthmus with two lateral lobes.

202
Q

Name the 2 cell types in the thyroid.

A

Follicular cells + Parafollicular cells (C Cells)

203
Q

Name the 3 hormones synthesised in the thyroid

A
  1. Triiodothyronine (T3)
  2. Thyroxine (T4)
  3. Calcitonin
204
Q

What type of hormone is calcitonin?

A

Polypeptide

205
Q

How is T3 and T4 synthesised?

A
  1. Iodine is transported against the concentration gradient into follicular epithelial cells.
  2. Thyroglobulin is synthesised in epithelial cells and is then transported into the lumen (colloid).
  3. Thyroglobulin is iodinated to form MIT or DIT.
    MIT + DIT = T3
    DIT + DIT = T4
  4. This is stored in the colloid.
206
Q

How is T3 and T4 released from storage?

A

When needed, thyroglobulin moves into the epithelial cell by vesicles (endocytosis). Proteolytic cleavage then occurs to release T3 and T4 which then diffuse into circulation.

207
Q

How is T3 and T4 transported in the blood?

A

Thyroid hormones are hydrophobic so can be transported in the blood by a carrier protein called Thyronine Binding Globulin (TBG). T4 has a higher affinity to the carrier than T3 so there is more free T3 in the blood than T4.
ONLY THE FREE HORMONES ARE BIOLOGICALLY ACTIVE.

208
Q

Which has a shorter half life? T3 or T4?

A

T3 - therefore the body stores T4 which is then converted into T3.

209
Q

Describe the HPA axis to release T3 and T4.

A

Hypothalamus releases TRH which stimulates the pituitary gland to release TSH. The TSH then triggers the release of thyroid hormones from the thyroid.

210
Q

How can TSH cause a goitre?

A

TSH can have trophic effects on the thyroid causing it to swell in size when TSH accumulates, causing a goitre.

211
Q

Can goitres form even when TSH levels are low?

A

Yes, if there is high levels of T3 and T4, a goitre can also form.

212
Q

T3 + T4 effect:

On BMR

A

Increase BMR rate

213
Q

T3 + T4 effect:

On heat production

A

Increase heat production

214
Q

T3 + T4 effect:

On Bone mineralisation

A

Increase bone mineralisation

215
Q

T3 + T4 effect:

On heart rhythm

A

Can cause tachycardia

216
Q

T3 + T4 effect:

On GI tract

A

Increased mobility of the GI tract.

217
Q

True or False:

T3 and T4 are needed for ovulation

A

True - FSH and LH are under the permissive control of T3 and T4.

218
Q

How do thyroid hormones act?

A

They are hydrophobic so they can cross the plasma membrane of target cells. They bind to receptors in the nucleus or mitochondria and cause a change in the rate of transcription and hence protein translation.

219
Q

How can the conversion of T4 to T3 go wrong?

A

Instead of the 5’-iodine, the 3’-iodine may be removed from T4 causing rT3 to be formed. This does not trigger target receptors but can bind, causing it to be a competitive inhibitor to T3.

220
Q

Name a condition which can cause hyperthyroidism and give 4 symptoms.

A

Grave’s Disease

  1. Weight loss
  2. Heat intolerance
  3. Hyper mobility of GI tract
  4. Tachycardia
221
Q

Name a condition which can cause hypothyroidism and give 4 symptoms.

A

Hashimoto’s Disease

  1. Weight gain
  2. Cold intolerance
  3. Constipation
  4. Bradycardia
222
Q

Give 2 other causes of hypothyroidism other than hashimoto’s disease

A
  1. Post-surgery

2. Radioactive Iodine

223
Q

Give 2 other causes of hyperthyroidism other than Grave’s disease.

A
  1. Excess Iodine

2. Over treatment with oral T4 therapy

224
Q

Give a method of treatment for somebody with Grave’s disease.

A

Carbimazole - Inhibits thyroid peroxidase which iodinates thyroglobulin

225
Q

Give a method of treatment for somebody with Hashimoto’s disease.

A

Oral T4 - Alter dose by titrating it up.

226
Q

In adults and children, a deficiency of thyroid hormone in the brain can cause…

A

Children: Cretinism which is irreversible if not treated within the first few weeks of life.

Adults: Poor concentration, poor memory and poor initiative.

227
Q

What are the name of the antibodies which stimulate tyroid gland in Grave’s disease?

A

Thyroid Stimulating Immunoglobulin (TSI)

228
Q

Give the 3 forms that calcium can exist as in the body.

A
  1. Free ionised species
  2. Bound to serum proteins
  3. Complexed with low weight organic anions.
229
Q

Why is phosphate and calcium regulation closely related?

A
  1. Both are found in bone stored as hydroxyapatite crystals

2. Both are regulated by PTH, Calcitriol and Calcitonin

230
Q

Give the full name of calcitriol

A

1,25-dihydroxyvitaminD

231
Q

How is PTH regulated?

A

Chief cells in the parathyroid have calcium receptors on them. High calcium concentration causes high negative feedback which suppresses PTH release whilst low calcium concentration causes low negative feedback.

232
Q

Explain how calcitriol is formed.

A

Vitamin D is formed in the skin or absorbed from dietary sources. Vitamin D has a short half life so is converted into calciferol (25-hydroxyvitaminD) in the liver, which has a half life of around 2 weeks. This can be stored until calcitriol is needed to be released - calciferol is then converted into calcitriol (1,25-hydroxyvitaminD) in the kidneys.

233
Q

Describe the effects of calcitriol

A
  • Increase absorption of calcium from the gut
234
Q

Describe the effects of PTH

A
  • Increase resorption of calcium from bone
  • Increase resorption of calcium from kidneys
  • Increase conversion of calciferol –> Calcitriol
235
Q

Describe the effects of calcitonin

A

Lowers calcium levels

236
Q

Give 5 features of hypocalcaemia

A
  1. Hyper-excitability of neuromuscular junctions
  2. Paraesthesia (pins + needles)
  3. Tetany
  4. Convulsions
  5. Paralysis
237
Q

Give 5 features of hypercalcaemia

A
  1. Tiredness
  2. Depression
  3. Dehydration
  4. Constipation
  5. Kidney stones
238
Q

Discuss how tumours which affect calcium balance work.

A

Tumours release rPTH which have the same functions as PTH except that it doesn’t activate calcitriol from calciferol. Can lead to Humeral Hypercalcaemia of Malignancy which is associated with mortality.

239
Q

Describe the two phases of pregnancy

A

Phase 1: Anabolic stage - preparing for growth of the baby, birth and then lactation.

Phase 2: Catabolic stage - supply the foetus.

240
Q

Give 4 reasons why there are changes in metabolic activity during pregnancy.

A
  1. Supply range of nutrients needed by foetus
  2. Supply nutrients at the right time to the foetus
  3. Have minimal disruption on mother’s nutrient homeostasis.
  4. Buffer the foetus from any disruptions in mother’s nutrient supply.
241
Q

What is the name of the unit which connects mother and foetus?

A

Foetal-placental unit

242
Q

Give 3 ways in which nutrient concentration is kept high in circulation.

A
  1. Convert mother to use fatty acids rather than glucose
  2. Circulate nutrients in blood for longer after eating
  3. Release nutrients from stores build in phase 1 of pregnancy
243
Q

Does insulin levels decrease in the second phase of pregnancy?

A

No. Insulin levels remain high however anti-insulin levels increase so the insulin/anti-insulin levels lower.

244
Q

Give the name of 3 anti-insulin hormones produced in the placenta.

A
  1. Human Placental Lactogen
  2. Progesterone
  3. Corticotropin Releasing Hormone (CRH)
245
Q

How is an increase in insulin caused in pregnant women?

A

Hypertrophy + Hyperplasia of beta cells as well as increasing the rate of insulin synthesis in the beta cells.

246
Q

What is the name of the condition in pregnant women when they cannot produce sufficient insulin.

A

Gestational Diabetes

247
Q

Give 4 reasons why the body must have a metabolic response to exercise.

A
  1. Meet muscle demands with fuel
  2. Minimal disturbance to homeostasis
  3. Ensure glucose supply to brain is kept
  4. Remove end products ASAP.
248
Q

Give three main energy sources in the body.

A
  1. Creatine Phosphate
  2. Glycogen stores
  3. Triacylglycerols
249
Q

How is the use of fatty acids limited? Give 4 reasons.

A
  1. Carrying capacity of blood for fatty acids
  2. Rate of lipolysis
  3. Fatty acids need more oxygen than ATP.
  4. Cannot be used in anaerobic conditions.
250
Q

Which fuel sources are used in 100m sprints?

A
  • Creatine phosphate

- Anaerobic glycogen

251
Q

Which fuel sources are used in 1500m runs?

A 
Phase 1: 
- Creatine phosphate
- Anaerobic glycogen
Phase 2:
- Aerobic glycogen
Phase 3:
- Anaerobic glycogen
252
Q

What fuel sources are used in marathons?

A
  • Aerobic glycogen

- Triacylglycerols/Fatty acids

253
Q

Give 6 benefits of exercise

A
  1. Body composition changes (more muscle, less fat)
  2. Glucose tolerance increases
  3. Insulin sensitivity increases
  4. Blood pressure lowers
  5. Blood triacylglycerols lower(less LDL+VLDL, more HDL)
  6. Sense of well being
254
Q

Give 5 changes that occur with more exercise training.

A
  1. Heart beats slower for same cardiac output
  2. More 2,3-bisphosphoglycerate production
  3. More of an opportunity for fatty acid metabolism
  4. Increased GLUT 4 in cell membrane
  5. Increased glycogen stores.
255
Q

Name the enzyme which catalyses this reaction:

2ADP –> ATP + AMP

A

Adenylate Kinase

256
Q

What is the enzyme which catalyses:

Creatine+ ATP Creatine Phosphate + ADP

A

Creatine Kinase

257
Q

For fructose metabolism, name the two enzymes involved.

A
  1. Fructokinase

2. Aldolase

258
Q

What are the consequence of:

  1. Fructokinase deficiency
  2. Aldolase deficiency
A
  1. Fructose can’t be broken down into fructose-1-phosphate so fructose is lost in urine. No negative effects.
  2. Without Aldolase, fructose-1-phosphate levels build up. This is toxic to the liver.
259
Q

Give an example of a Glucogenic amino acid

260
Q

Give an example of a Ketogenic amino acid

261
Q

Give an example of an amino acid which is Glucogenic and Ketogenic

262
Q

Name the drug to treat alcoholism

A

Disulfiram - inhibits aldehyde dehydrogenase

263
Q

Name the hormone which inhibits growth hormone release

A

Somatostatin

264
Q

Name the hormone which inhibits growth hormone release

A

Somatostatin

265
Q

Name a hormone released by the placenta which gives an anti-insulin effect on maternal metabolism

A

Corticotropin Releasing Hormone

266
Q

Give 2 important glycolysis intermediates and say how they are used. Give equations.

A
  1. DHAP –> Glycerol Phosphate (Glycerol-3-phosphate dehydrogenase) - Glycerol phosphate used in lipid synthesis in the liver.
  2. 1,3-Bisphosphoglycerate –> 2,3-Bisphosphoglycerate (Bisphosphoglycerate mutase) - 2,3-BPG used in RBC to decrease oxygen affinity eg. at high affinity.
267
Q

Name a hormone released by the placenta which gives an anti-insulin effect on maternal metabolism

A

Corticotropin Releasing Hormone

268
Q

What is it in ATP which allows for it be an immediate energy source?

A

Contains a “high energy of hydrolysis” phosphate group. ATP can be reduced to release energy.

Semester 1 (4 decks)

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