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ESA 1 > Metabolism > Flashcards

Metabolism Flashcards

To cover most Metabolism you are required to know for ESA 1 I take no responsibility for any of the flashcards featured here...mistakes/shit happens.

1
Q

Which two main hormones do the follicular cells of the thyroid release?

A

T3 (triiodothyronine) and T4 (thyroxine)

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2
Q

Which main hormone do the parafollicular cells of the thyroid release?

A

Calcitonin

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3
Q

What is the anatomical position of the thyroid gland?

A
  • Inferior to voice box

- Anterior to trachea

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4
Q

What type of epithelia can be found in the thyroid follicles?

A

Simple cuboidal

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5
Q

Briefly outline the production of thyroid hormones. (6 key points)

Hint: ATE ICE

A
  • Active transport iodide into the cytosol
  • Thyroglobulin synthesis by the follicular cells
  • Exocytosis to release vesicle of thyroglobulin into lumen
  • Iodination of tyrosine parts of thyroglobulin
  • Coupling of T1 (MIT) and T2 (DIT)
  • Endocytosis into follicular cytosol followed by cleavage to form mature T3/T4
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6
Q

What are the thyroid hormones bound to when travelling in the blood? Why?

A

The thyroid hormones are bound to thyroxine-binding globulin (TBG) as they are hydrophobic

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7
Q

List the main actions of thyroid hormones?

A
  • Increase BMR and temperature
  • Increase normal growth/development - heart muscle + bone mineralisation etc.
  • Ovulation
  • Increase protein synthesis and metabolism
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8
Q

How can T4 be converted to T3?

A

Cleavage of the 5’ iodide on the T4

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9
Q

Which hormone controls the release of thyroid hormones and where is it released from?

A

Thyroid stimulating hormone (TSH) which is released from the anterior pituitary

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10
Q

Which hormone controls the release of TSH and where is it secreted from?

A

Thyroid releasing hormone (TRH) is released from the hypothalamus and acts on thyrotrophs in the anterior pituitary

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11
Q

Why does TRH travel in blood through the hypophyseal portal vein?

A
  • Less hormone needed

- Faster response

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12
Q

What is the autoimmune cause of Grave disease and therefore main cause of hyperthyroidism?

A

Formation of an antibody that stimulates TSH receptors on the thyroid producing excess T3/T4

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13
Q

Name 3 other things that can be other causes of hyperthyroidism?

A
  • Ectopic thyroid
  • Excessive therapy of hypothyroidism
  • Excessive treatment of other conditions with drugs - amiodarone
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14
Q

What are the main symptoms of Grave’s disease?

A
  • Exopthalmos
  • Osteoporosis (due to excessive bone turnover)
  • Weight Loss
  • Heat intolerance
  • Intestinal hypermotility
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15
Q

What is the main treatment for Grave’s disease and how does it work?

A
  • Carbimazole which works by preventing the iodination of thyroglobulin.
  • Thyroid removal
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16
Q

What are the two main autoimmune causes of Hashimoto’s disease?

A
  • Antibody blocks a TSH receptor

- Destruction of follicles

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17
Q

What can be other causes of hypothyroidism?

A
  • Iodine deficiency (uncommon)

- Radiation

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18
Q

What are the main symptoms of hypothyroidism?

A
  • Weight gain
  • Tiredness
  • Cold intolerance
  • Alopecia
  • Decreased BMR
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19
Q

What is the main treatment for hypothyroidism?

A

Oral thyroxine

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20
Q

What does the parathyroid gland release and what does this control?

A

Parathyroid hormone which controls the level of calcium in the blood and in bones.

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21
Q

What are the four main functions of active calcium?

A
  • Muscle contraction
  • Nervous conduction
  • Enzyme activation
  • Hormonal secretion
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22
Q

In the blood which three ways can calcium be found?

A
  • Free biologically active
  • Bound to anionic sites on albumin
  • Forming complexes with anions like citrate
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23
Q

In what way are calcium and phosphate linked together?

A

Together they form calcium hydroxyapatite crystals which are minerals in bone

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24
Q

What are the symptoms of hypocalcaemia? How are they caused?

A
  • Convulsions
  • Arrythmia
  • Tetany (involuntary muscle contraction)
  • Paraesthesia (tingling)

Due to low calcium at neuromuscular junctions which leads to easier depolarisation

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25
Q

What are the symptoms of hypercalcaemia?

A

Stoans, moans and groans:

  • Kidney stones (renal calculi)
  • Depression and tiredness
  • Constipation and dehydration
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26
Q

What are the three hormones responsible for control of calcium levels?

A
  • Parathyroid hormone
  • Calcitriol
  • Calcitonin (less important)
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27
Q

What would an increase in the level of PTH and calcitriol result in?

A

An increased level of serum calcium

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28
Q

How is calcitriol formed? (3 stages)

A
  • Vitamin D absorbed in skin/gut
  • Hydroxylation of the vitamin D in the liver to form calciferol as it has a longer half life
  • Finally, calciferol is converted to calcitriol by hydroxylation in the kidney
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29
Q

What hormone regulates the formation of calcitriol?

A

Parathyroid hormone (PTH)

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30
Q

How are parathyroid hormone levels regulated by calcium?

A
  • Chief cells have G-protein calcium receptors which when calcium levels are high are stimulated
  • Causes the production of phospholipase C (PLC)
  • PLC causes the inhibition of adenylate cyclase which reduces cAMP and PTH
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31
Q

What is Parathyroid releasing peptide (PTHrP) produced from?

A

Tumours

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32
Q

What does PTHrP do? From this, what could it be expected to do but doesn’t?

A

It has similar effects to PTH as it:

  • increases calcium release from bone
  • decreased renal calcium excretion
  • decreased renal phosphate reabsorption

Therefore, it may be expected to increase renal C-1 hydroxylase activity, like PTH, but it doesn’t so has no effect on calicitriol concentration.

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33
Q

If there is too much PTHrP what can occur?

A

Humeral hypercalcaemia of malignancy

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34
Q

If the calcium level is low, what does the PTH do in the kidney?

A

Calcium reabsorption in the distal covoluted tubule of the kidney

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35
Q

If the calcium level is high what does the kidney do to phosphate? Why?

A

Phosphate is removed from circulation by the proximal tubule of the kidney to prevent the formation of calcium stones.

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36
Q

What is the outermost layer of the cortex called and what does it release?

A

Zona Glomerulosa which releases mineralcorticoids

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37
Q

What is the middle layer of the cortex called and what does it release?

A

Zona fasiculata which releases glucocorticoids

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38
Q

What is the innermost layer of the cortex called and what does it release?

A

Zona reticularis which releases androgens (and some glucocorticoids)

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39
Q

How is cortisol transported?

A

In the blood bound to proteins

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40
Q

What does an increase in cortisol production result in?

A
  • Increase in gluconeogenesis and glycogenolysis
  • Muscle proteolysis increases
  • Lipolysis increases (lipogenesis increases at very high levels)
  • Decreased immune system
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41
Q

Which clinical condition can be identified by a increased level of cortisol and ACTH caused by pituitary adenoma?

A

Cushings disease

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42
Q

Which clinical condition can be identified by a decreased level of cortisol due to adrenal adenoma?

A

Addisons disease

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43
Q

What is the difference between Cushings syndrome and disease?

A

Cushings syndrome relates to an elevated level of cortisol detected whereas Cushings disease relates to a tumour in the pituitary resulting in the elevated cortisol

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44
Q

What does a derease in cortisol production result in?

A
  • Muscle weakness
  • Hypotension
  • Hypoglycaemia
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45
Q

What group of chemicals does the adrenal medulla produce? Which cells are they stored in?

A

Catecholamines stored in medullary cells

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46
Q

What type of hormone is cortisol and how is it transported?

A

Steroid hormone which is lipophillic and has to be bound to protein and transported in blood

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47
Q

Where is ACTH released from?

A

Anterior pituitary

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48
Q

What are the two main roles of ACTH?

A
  • Activate cholesterol esterase - creating more free cholesterol
  • Stimulate steps in the conversion of cholesterol to cortisol
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49
Q

What is the function of aldosterone?

A

Stimulates Na+ reabsorption

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50
Q

Briefly describe how adrenaline is formed

A
  • Dopamine turned into noradrenaline

- Noradrenaline methylated creating adrenaline

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51
Q

What effects on the body does an increased adrenaline level have on the body?

A
  • Increased cardiac output
  • Increased alertness
  • Increased glycogenolysis
  • Increased lipolysis
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52
Q

List 4 clinical consequences of too much adrenaline

A
  • Hypertension
  • Sweating
  • Anxiety
  • Glucose intolerance
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53
Q

How does adrenaline bind to cells?

A

Binds to adenoreceptors on the outside of cells then uses a secondary messenger system

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54
Q

How does cortisol bind to cells?

A

Crosses plasma membrane and binds to cytoplasmic receptors causing some genes to be transcribed

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55
Q

How does ACTH bind to cells?

A

Binding to corticotrophin receptor on the fasiculata and reticularis then a secondary messenger system

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56
Q

Describe the steps in the creation of glycogen from glucose

A

1) Glucose to Glucose-6-Phosphate (hexokinase/glucokinase)
2) Glucose-6-P to Glucose-1-P (Phosphoglucomutase)
3) Glucose-1-P are polymerised (Braching enzyme and glycogen synthase)

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57
Q

How do you work out BMI?

A

Weight (kg) divided by height x height (m)

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58
Q

How is lactate produced?

A

By reacting NADH, pyruvate and H+ together

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59
Q

How is pyruvate kinase activated?

A

Dephosphorylation

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60
Q

How much energy does each food group provide?

A

Lipid - 37000 kj/kg
Alcohol - 29000 kj/kg
Protein - 17000 kj/kg
Carbohydrates - 17000 kj/kg

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61
Q

Outline the process of oxidative phosphorylation

A
  • Reduced coenzymes are reoxidised
  • Electrons pass along the ETC until they are accepted by O2 at end
  • Energy from electrons drive H+ across membrane
  • Generation of a PMF
  • H+ renter through ATP synthase molecule causing the production of ATP
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62
Q

What are the anabolic roles of the TCA cycle?

A

Provides precursors for the synthesis of amino acids, fatty acids and glucose

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63
Q

What are the catabolic roles of the TCA cycle?

A

Produce NADH, FAD2H, GTP and CO2

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64
Q

What are the main cellular processes that use energy?

A
  • Biosynthetic work
  • Osmotic work
  • Mechanical work
  • Electrical work
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65
Q

What are the three irreversible steps of glycolysis?

A
  • Glucose to Glucose 6 phosphate (Hexokinase/glucokinase)
  • Fructose-1-Phosphate to Fructose-1,6-Bisphosphate (Phosphofructokinase)
  • Phosphoenolpyruvate to pyruvate (pyruvate kinase)
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66
Q

What are the three types of daily energy expenditure?

A
  • Basal metabolic rate
  • Diet induced thermogenesis
  • Voluntary physical activity
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67
Q

What enzyme converts fructose to fructose-1-phosphate?

A

Fructokinase

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68
Q

What enzyme converts fructose-1-phosphate to GALP?

A

Aldolase

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69
Q

What enzyme converts pyruvate to lactate?

A

Lactate dehydrogenase

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70
Q

What factors affect the basal metabolic rate?

A
  • Gender
  • Temperature
  • Endocrine status
  • Weight (surface area)
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71
Q

What is the effect of dinitrophenol (DNP) on oxidative phosphorylation?

A

It increases the permeability to H+ ions which leads to the uncoupling of electron transport from ATP synthesis

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72
Q

What is the function of brown adipose tissue?

A

It is a naturally occuring uncoupling protein which produces heat through non-shivering thermogenesis - allows H+ back into mitrochondria without passing through normal channels

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73
Q

What is the purpose of the pentose phosphate pathway?

A
  • Provide NADPH

- Synthesise 5 carbon sugars for DNA creation (pentose sugars)

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74
Q

Where does the link reaction occur?

A

Mitrochondrial matrix

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75
Q

Where is glycogen stored?

A

Muscle and liver

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76
Q

Which enzyme regulates glycogen degradation?

A

Glycogen phosphorylase

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77
Q

Which enzyme regulates glycogen synthesis?

A

Glycogen synthase

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78
Q

Which enzyme regulates the TCA cycle and what activates/inhibits it?

A

Isocitrate dehydrogenase - activated by ADP and inhibited by NADH

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79
Q

Which organs remove lactate from the blood?

A

Heart and liver

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80
Q

Which tissues have an absolute requirement for glucose?

A
  • Blood cells (Red and white)
  • Lens of the eye
  • Kidney medulla
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81
Q

Why are TAGs more efficient than glycogen?

A
  • Hydrophobic so can be packed anhydrously

- More reduced so yields more when oxidised

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82
Q

Why can’t the human body digest cellulose?

A

The human body cannot break the Beta 1-4 linkages in the polysaccharide.

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83
Q

Why is glycolysis done in so many steps?

A
  • Easier in small reactions
  • Can be controlled
  • Efficient energy conservation
  • Production of useful intermediates
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84
Q

Why are there two enzymes for breaking down glycogen? (Glycogen phosphorylase and debranching enzyme)

A

Glycogen phosphorylase breaks alpha 1-4 linkages whereas debranching enzyme breaks the alpha 1-6

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85
Q

What is the approximate energy expenditure for a 70kg man?

A

12,000 kj

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86
Q

What is the approximate energy expenditure for a 58kg female?

A

9,500 kj

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87
Q

Define obesity

A

Excess body fat has accumulated to the extent that it may have an adverse effect on health (BMI > 30), leading to reduced life expectancy and/or increased health problems.

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88
Q

Define homeostasis

A

Homeostasis is the maintenance of a stable internal environment in a dynamic equilibrium.

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89
Q

What are the main features of control systems in the body?

A
  • Communication
  • Control centre
  • Effector
  • Receptor
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90
Q

Which enzyme catalyses the creation and breakdown of creatine phosphate?

A

Creatine kinase

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91
Q

What is the minimum glucose requirement for an adult each day?

A

180g

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92
Q

Name two uses of NADPH

A
  • Lipid synthesis (important in liver/adipose)

- Used to prevent Heinz body formation in red blood cells

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93
Q

What are the 4 key differences between the two types of phosphorylation in ATP synthesis?

A

Subs Level - soluble enzymes, energy coupling is direct, can be anaerobic, minor for ATP synthesis.

Oxid - membrane associated complexes, energy coupling is indirect, MUST be aerobic, major for ATP synthesis.

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94
Q

What are the 4 main hydroxy-methyl-glutaric acid derivatives? What are they for?

A
  • Ketone bodies are water soluble fuel
  • Cholesterol for membrane and steroid hormone synthesis
  • Cholesterol esters for cholesterol storage
  • Bile salts for lipid digestion
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95
Q

What are the 4 fat soluble vitamins?

A

A, D, E and K

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96
Q

What three things are required to hydrolyse TAGs in the small intestine?

A
  • Pancreatic lipase
  • Bile salts
  • Protein factor called colipase
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97
Q

When TAGs are hydrolysed what happens to the glycerol?

A

It enters the blood stream and is transported to the liver where it is metabolised

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98
Q

What are the three different ketone bodies?

A
  • Acetoacetate
  • Acetone
  • β-hydroxybutyrate
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99
Q

How is acetone formed?

A

Spontaneous non-enzymatic decarboxylation of β-hydroxybutyrate and acetoacetate

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100
Q

How are β-hydroxybutyrate and acetoacetate formed?

A

Synthesised in the liver from Acetyl~CoA

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101
Q

What level of ketone bodies in the blood is regarded as pathological ketoacidosis?

A

> 10mM

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102
Q

Why are ketone bodies able to be secreted in the urine? (ketonuria)

A

Water soluble

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103
Q

When does ketone body synthesis occur?

A

When glucose is low i.e. starvation

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104
Q

Which enzyme produces HMG-CoA from acetyl CoA?

A

HMG CoA Synthase

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105
Q

Which enzyme converts HMG CoA to acetoacetate?

A

HMG CoA Lyase

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106
Q

What other ketone body is β-hydroxybutyrate produced from?

A

Acetoacetate

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107
Q

How is the ketone body used as a fuel?

A

Converted to acetyl CoA

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108
Q

What ratio controls the rate of ketone body synthesis?

A

Insulin/glucagon ratio

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109
Q

What two things are required for ketone body synthesis to occur?

A
  • Fatty acids to be available for oxidation in the liver following excessive lipolysis in adipose tissue
  • The plasma insulin/glucagon ratio to be low, usually due to a fall in plasma insulin – this activates the lyase and inhibits the reductase
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110
Q

Describe the steps in the breakdown of glycogen.

A
  • Glycogen is broken into smaller sections by glycogen phosphorylase and debranching enzyme to form glucose-1-phosphate
  • Glucose-1-phosphate is converted to glucose-6-phosphate by phosphoglucomutase
  • In the liver the glucose-6-phosphate is converted to glucose by glucose-6-phosphatase
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111
Q

What is the main difference between muscle and liver glycogen?

A

Liver glycogen is used by all the body whereas muscle glycogen is only used by muscles

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112
Q

Why is glucose produced from non-carbohydrate sources?

A

Allows production of glucose when carbs are absent.

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113
Q

What is the main site of gluconeogenesis?

A

Liver

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114
Q

Name four substrates that can be used in gluconeogenesis?

A
  • Pyruvate
  • Lactate
  • Glycerol
  • Non-essential amino acids
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115
Q

In gluconeogenesis how are the irreversible steps bypassed?

A

1) Pyruvate -> Phosphoenolpyruvate - pyruvate carboxylase and PEPCK
2) Frustose 1,6-bisphosphate -> Fructose 6-phosphate - fructose 1,6-bisphosphatase
3) Glucose 6-phosphate -> Glucose - glucose 6-phosphatase

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116
Q

What two enzymes control the rate of gluconeogenesis?

A
  • Fructose-1,6-Bisphosphatase

- PEPCK

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117
Q

What is the effect of glucagon on PEPCK and Fructose-1,6-Bisphosphatase?

A

Increases the rate of both of them

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118
Q

What is the effect of insulin on PEPCK and Fructose-1,6-Bisphosphatase?

A

Decreases the rate of both of them

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119
Q

How is glycerol (from dietary TAGs) stored?

A
  • Enters the blood
  • Transported in chylomicrons
  • Stored as TAGs in adipose tissue
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120
Q

What is the name of the process that degrades fatty acids?

A

Beta oxidation

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121
Q

Describe the process of Beta oxidation of fatty acids

A

The pathway oxidises fatty acids by removing a C2 (acetate) each time it is cycled through

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122
Q

What three things does Beta oxidation require to function?

A
  • Oxygen
  • NAD+
  • FAD
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123
Q

What is the main substance produced from the Beta oxidation of fatty acids

A

Acetyl CoA

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124
Q

Where does fatty acid synthesis occur?

A

Cytoplasm

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125
Q

What is needed for fatty acid synthesis occur?

A
  • Fatty acid synthase complex
  • ATP
  • NADPH
  • Protons
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126
Q

Describe the process of fatty acid synthesis

A

Fatty acids are built up in a sequence by adding C2 each time in the form of malonyl CoA (loss of CO2)

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127
Q

How is Malonyl CoA produced?

A

From acetyl CoA using the enyme acetyl~CoA carboxylase and biotin

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128
Q

What enzyme controls the rate of fatty acid synthesis?

A

Acetyl~CoA carboxylase

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129
Q

What regulates the acetyl~CoA carboxylase enzyme?

A
  • Allosteric regulation - citrate activates and AMP inhibits
  • Covalent modification - Insulin activates by promoting dephosphorylation, Glucagon & Adrenaline inhibit the enzyme by promoting phosphorylation
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130
Q

Why do amino acids need to be broken down?

A

In a typical western diet more protein is eaten than is needed to supply the essential amino acids so excess amino acids are broken down

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131
Q

What are amino acids that produce acetyl-CoA described as?

A

Ketogenic

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132
Q

What are amino acids that produce TCA intermediates and pyruvate described as?

A

Glucogenic

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133
Q

What does measuring Creatinine give an indication of?

A

The breakdown of creatine, if it is constant, gives an indication of muscle mass and renal function

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134
Q

How can ammonia be detoxified?

A
  • Synthesis of N-compounds like glutamine
  • Conversion to urea

Both can be excreted in urine

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135
Q

How can glutamine be synthesised?

A

From ammonia, glutamate and ATP using the enzyme glutamine synthetase

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136
Q

How can glutamine be excreted?

A

Glutamine is transported to the liver and kidney where it is hydrolysed by glutaminase releasing ammonia that is disposed of in the urine (kidney) and converted to urea (liver).

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137
Q

What two things do all defects of the urea cycle result in?

A
  • Hyperammonaemia (high blood NH4+ concentration)

- Accumulation and/or excretion of a particular urea cycle intermediate

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138
Q

What happens to urea in the liver?

A

Diffuses from the liver cells to the blood and is carried to the kidney where it is filtered and excreted in the urine.

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139
Q

Briefly describe transamination.

A

Use of transaminases to transfer NH2- group from molecules like alanine and aspartate

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140
Q

Which enzyme turns galactose to galactitiol?

A

Aldose reductase

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141
Q

Briefly describe deamination

A

D-amino acid oxidases break down D amino acids so they aren’t use for protein synthesis (not normal for human body) produce NH3 and keto acids

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142
Q

What are pharmacokinetics?

A

What the body does to the drug

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143
Q

What are pharmacodynamics?

A

What the drug does to the body

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144
Q

What are the four components to pharmacokinetics? (ADME)

A
  • Absorption
  • Distribution
  • Metabolism
  • Elimination
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145
Q

What is the purpose of Phase 1 drug metabolism?

A

Exposes the reactive group by oxidation, reduction or hydrolysis

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146
Q

What is the purpose of Phase 2 drug metabolism?

A

Conjugation - addition of a water soluble group (Glucuronidation, sulphate conjugation, glutathione conjugation)

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147
Q

Name three metabolites that are more pharmacologically active than the original drug?

A

Phenobarbitone (from Primidone)
Norpethidine (from Pethidine)
Morphine (from Codeine)

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148
Q

What is the high energy cofactor needed for phase 2 of drug metabolism?

A

UDPGA - uridine diphosphate glucuronic acid

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149
Q

Give one drug that skips phase 1 metabolism and enters directly into phase 2?

A

Morphine

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150
Q

What enzyme system and cofactor does the phase 1 drug metabolism use?

A

Cytochrome P450 enzyme system and NADPH cofactor

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151
Q

Give two factors for variation in drug metabolism within the population

A
  • Genetic factors (levels of enzymes etc)

- Environmental factors (use of other drugs etc.)

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152
Q

What type of drug is paracetamol?

A

Antipyretic (suppresses fever)

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153
Q

At normal therapeutic levels how is paracetamol metabolised in the body?

A

It proceeds directly to phase 2 drug metabolism where it conjugates with glucuronide or sulphate

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154
Q

What occurs if a toxic dose of paracetamol is given?

A

It goes through a phase 1 pathway and forms the toxic product N-acetyl-p-benzo-quinone imine (NAPQI)

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155
Q

How does NAPQI damage the body?

A
  • Toxic to hepatocytes

- Undergoes Phase II conjugation with glutathione, which is an important anti-oxidant.

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156
Q

Where is the major site of alcohol metabolism?

A

Liver

157
Q

Which enzyme converts alcohol to acetaldehyde? Which converts acetaldehyde to acetate?

A 
Alcohol dehydrogenase (low specificity).
Aldehyde dehydrogenase.
158
Q

What converts acetaldehyde to acetate?

A

Aldehyde dehydrogenase

159
Q

What effect does excessive alcohol consumption have on the body?

A
  • Low NAD+
  • High Acetyl CoA
  • Decrease in liver function (due to cell damage from toxic acetaldehyde)
  • Effect on GI tract (impaired absorption of vitamins and minerals)
160
Q

What problems does a high amount of acetyl CoA in excessive alcohol consumption cause?

A
  • Production of ketone bodies - high blood acidity

- Production of fatty acids however not enough lipoproteins to move it causing fatty liver development

161
Q

What problems does a low NAD+ in excessive alcohol consumption cause?

A
  • Build up of lactate as NAD+ used for conversion from pyruvate to lactate.
  • Reduces kidneys ability to get rid of uric acid - you get urate crystal and gout
  • Gluconeogenesis can’t be activated
162
Q

What drug can be given as a treatment for excessive alcohol consumption? How does it work?

A

Disulfiram which works by inhibiting the enzyme aldehyde dehydrogenase causing the build up of acetaldehyde and therefore hangover symptoms

163
Q

What level of blood glucose classifies a patient as hypoglycaemic?

A

<3.0mM

164
Q

What level of blood glucose classifies a patient as hyperglycaemic?

A

> 7.0mM

165
Q

Give three acute effects of hypoglycaemia (note: there are a lot more)

A
  • Trembling
  • Sweating
  • Palpatations
166
Q

Give three acute effects of hyperglycaemia (note: there are a lot more)

A
  • Polydipsia
  • Polyuria
  • Weight loss
167
Q

Give four effects of insulin?

A
  • Increases glucose uptake and utilisation by muscle and adipose tissue
  • Promotes storage of glucose as glycogen in the liver and muscle
  • Promotes lipogenesis and storage of fatty acids as triacylglycerols in adipose tissues
  • Promotes amino acid uptake and protein synthesis in liver and muscle
168
Q

Give three effects of glucagon?

A
  • Gluconeogenesis to maintain supplies of glucose for the brain
  • Glycogenolysis in the liver to maintain blood glucose for glucose-dependant tissues
  • Lipolysis in adipose tissue to provide fatty acids for use by tissues
169
Q

What is a reaction described as if the energy release is greater than the input?

A

Exergonic

170
Q

How can you obtain a rough estimate of BMR?

A

Weight (kg) x 100

171
Q

Name three things that can increase the BMR.

A
  • Pregnancy
  • Lactation
  • Thyroid hormones
172
Q

What are clinicians increasingly using as opposed to BMI to give more accurate measure of risk of CV disease and obesity?

A

Waist to hip ratio

173
Q

Above what core temperature is considered to clinically be hyperthermia?

A

38 degrees celsius

174
Q

Below what core temperature is considered to clinically be hypothermia?

A

35 degrees celsius

175
Q

What is the importance of DHAP in glycolysis?

A

Synthesis of TAGs in liver and adipose for storage

176
Q

What is the function of superoxide dismutase (SOD)?

A

Turns reactive oxygen species into hydrogen peroxide

177
Q

What activates uncoupling proteins in brown adipose tissue?

A

Noradrenaline

178
Q

Name three defences against ROS?

A
  • Glutathione
  • NADPH
  • Catalase (conversion from H2O2 to H2O)
179
Q

Which is the most dense lipoprotein? What is its function?

A

HDL which transports cholesterol from tissues back to liver for disposal

180
Q

Which is the least dense lipoprotein? What is its function?

A

Chylomicron which transports TAGs from intestine to adipose tissue

181
Q

What is the function of LCAT?

A

Restores stability of lipoproteins by converting surface lipids to core lipids (cholesterol to cholesterol esters

182
Q

What is the function of LDLs?

A

Take cholesterol from liver to tissues

183
Q

What enzyme do neutrophils and monocytes use to cause an oxidative burst?

A

NADPH Oxidase

184
Q

What does the secretion of ACTH from the anterior pituitary lead to the release of?

A

Cortisol from the adrenals

185
Q

What is appetite controlled by?

A

Arcuate Nucleus in the hypothalamus.

186
Q

What nerve do the secondary neurones use to co-ordinate a response to appetite and metabolism?

A

Vagus nerve

187
Q

In the stimulation of appetite, what neuropeptide do stimulatory primary neurones release?

A

Agouti related peptide (AgRP) and Neuropeptide Y

188
Q

In the inhibition of appetite, what polypeptide do inhibitory primary neurones release?

A

Pro-opiomelanocortin (POMC)

189
Q

What 3 things (important in appetite) can the polypetide prohormone POMC be enzymatically cleaved to produce?

A
  • ACTH (Adrenocorticotrophin Hormone)
  • α-MSH (α-Melanocyte stimulating hormone)
  • β-endorphin
190
Q

What does α-MSH act on to suppress appetite?

A

Melanocortin 4 receptor

191
Q

What polypeptide is released when the stomach is full?

A

POMC

192
Q

What polypeptide/hormone is released when the stomach is empty? Which neurone does it stimulate?

A

Ghrelin stimulates primary stimulatory neurone

193
Q

What is the effect of increased PYY release? How is it released?

A

Stretching of the small intestine leads to PYY secretion which suppresses hunger.

194
Q

Where is Leptin released from and what is it’s function?

A

Released from adipocytes to suppress appetite

195
Q

What is the effect of insulin on appetite?

A

Suppresses it

196
Q

What are the two effects of Amylin release?

A
  • Suppresses appetite and glucagon secretion

- Slows gastric emptying

197
Q

Which neurone do both insulin, leptin and PYY inhibit?

A

The primary stimulatory neurone

198
Q

Which neurone do leptin and insulin stimulate?

A

The primary inhibitory neurone.

199
Q

Where are amylin and insulin released from?

A

β-cells

200
Q

Why is oxygen required for any step beyond glycolysis?

A

NAD+ needs to be reformed so the pyruvate is used to produce lactate

201
Q

How are TAGs from chylomicrons and VLDLs released into tissues?

A

The endothelial cells of capillaries have lipase attached to their cell membrane. Chylomicrons and VLDLs bind to these enzymes and the TAGs are cleaved into fatty acids and glycerol. The FA enters the tissue and the glycerol remains in circulation.

202
Q

How is cholesterol released from LDLs?

A

Cells have LDL receptors on their cell membrane which binds to the ApoB100 apoprotein. The LDL-receptor complex is taken into the cell. Lysosomes digest the lipoprotein, releasing cholesterol and breaking down cholesterol esters into cholesterol and FA.

203
Q

How does insulin secretion increase during pregnancy?

A

Pancreatic B-cells undergo hypertrophy and hyperplasia, they become more sensitive to glucose by the action of oestrogen and progesterone.

204
Q

Define endergonic.

A

An endergonic reaction has a higher energy input than the amount of energy released. An exergonic reaction has a higher amount of energy released than the energy input.

205
Q

Define feedback.

A

Feedback is a mechanism by which the output of the system has an effect on the control system

206
Q

Define metabolic syndrome.

A

A pattern of symptoms found in obese adults. It’s existence is disputed. Symptoms are:

  • insulin resistance
  • dyslipidaemia
  • impaired glucose tolerance
207
Q

Define metabolism.

A

The processes which derive energy and raw materials from the diet and use them to support repair, growth and activity of tissues.

208
Q

Describe how ammonium ions generated by deamination are disposed of.

A

1) Used to synthesise glutamine from glutamate
2) Glutamine can either directly release the ammonium ions at the kidneys (becoming glutamate)
Or
3) Transport it to the liver where it is used to synthesise urea in the ornithine cycle.

209
Q

Describe how cholesterol is derived and used in the body.

A

Cholesterol can be derived from the diet but can also be synthesised in the diet. It can be used to make cholesterol ester by esterification with a FA. It is a HMA acid derivative.

210
Q

Describe how energy is used in a 100m sprint.

A

1) ATP and creatine phosphate already present in muscle cells is used up.
2) Muscle glycogen is broken down to supply glucose-6-phosphate which then undergoes anaerobic respiration to supply more ATP.

211
Q

Describe how fuel stores are used in a 1500m race.

A

1) Initial sprint - ATP and creatine phosphate are used up.
2) Middle phase - aerobic respiration of G-6-P from muscle glycogen takes place, some fat is aerobically respired.
3) Final sprint - anaerobic respiration of G-6-P from muscle glycogen takes place.

212
Q

Where does Phase 1 of drug metabolism occur?

A

Mainly in microsomes in hepatocytes, but also in the GI tract, kidneys, lungs and blood plasma.

213
Q

Describe stage 1 of carbohydrate metabolism.

A

Enzymes are secreted into the GI tract - amylase (from saliva and pancreas), lactase and isomaltase. Glycosidic bonds in polysaccharides are broken to form monosaccharides. These are actively transported into the intestinal epithelial cells and then into the blood and from the blood to tissues via GLUT receptors.

214
Q

Describe the action of growth hormone on cells.

A

Growth hormone does not act directly on cells. It is converted to IGF-1 in the liver which acts on cells, usually promoting anabolism.

215
Q

How does ghrelin control appetite?

A

It stimulates appetite by activating the primary stimulatory neurone.

216
Q

How does insulin control appetite?

A

Suppresses appetite by both inhibiting primary stimulatory neurones and stimulating primary inhibitory neurones. (It’s less significant than leptin.)

217
Q

How does leptin control appetite?

A

Suppresses appetite by both inhibiting primary stimulatory neurones and stimulating primary inhibitory neurones.

218
Q

How does PYY control appetite?

A

It suppresses appetite by inhibiting primary stimulatory neurones.

219
Q

Describe the activation of FAs in stage 2 of FA metabolism.

A

FAs must be activated to undergo B-oxidation. This is done by linking the FA to CoA, forming acyl-CoA. This is catalysed by fatty acyl-CoA synthase.

220
Q

Describe the blood supply to the thyroid gland.

A

The thyroid gland has a very good blood supply because it’s an endocrine gland. It’s supplied by the superior and inferior thyroid arteries and the superior, middle and inferior thyroid veins.

221
Q

Describe the cellular defences against superoxide radicals.

A

The enzyme SOD converts superoxide radicals to H2O2. However, H2O2 is also a reactive oxygen species, so it is converted to H2O and O2 by catalase.

222
Q

Describe the first stage of lipid metabolism.

A

In the small intestine the lipid is digested by lipases, secreted by the pancreas, into FAs and glycerol which are then absorbed into the intestinal epithelial cells.

223
Q

Describe the general structure of a lipoprotein molecule.

A

A lipoprotein molecule consists of aggregates of lipid molecules contained within a micelle made up of phospholipids, apoproteins (ApoA to ApoH) and cholesterol. There are several classes of lipoprotein.

224
Q

Describe the histological structure of the thyroid gland.

A

The thyroid gland is arranged into follicles. Each follicle is lined by follicular cells (simple cuboidal) and has a lumen filled with colloid. Between the follicles there is CT which contains parafollicular cells.

225
Q

Describe the large-scale structure of the thyroid gland.

A

The thyroid has 2 lobes connected by as isthmus. Normally about 2-3cm across and has a very good blood supply.

226
Q

Describe the process of alcohol metabolism.

A

Alcohol is first converted to acetaldehyde by the enzyme alcohol dehydrogenase (this can also be done by a CYP enzyme). Acetaldehyde is then quickly converted to acetate by aldehyde dehydrogenase (which has a very low Km for acetaldehyde). Acetate is then linked with CoA to form acetyl CoA. Both the alcohol -> acetaldehyde and acetaldehyde -> acetate reactions reduce NAD+ to NADH

227
Q

Describe the process of deamination.

A

Deamination removes the NH2 group from an amino acid, forming ammonia, NH3. The ammonia is then converted to the ammonium ion, NH4. The ammonium ions are removed by the synthesis of glutamate or by the urea cycle.

228
Q

Describe the process of FA synthesis.

A

FAs are synthesised by a series of reactions in the cytoplasm that add 2-carbon units to the carbon chain from malonyl-CoA. These reactions require large amounts of NADPH and ATP. Malonyl-CoA is produced from acetyl-CoA by the enzyme acetyl-CoA carboxylase. Acetyl-CoA carboxylase is the enzyme that regulates FA synthesis.

229
Q

What is the difference between glycogenolysis in muscle and liver glycogen?

A

In muscle the glucose-6-phosphate is NOT converted to glucose. In the liver the glucose-6-phosphate is converted to glucose.

230
Q

Describe the role of glutathione and NADPH in cellular defence against reactive oxygen species.

A

Glutathione has an -SH group which can donate it’s H atom to ROS, thus acting as a reducing agent. It then becomes it’s oxidised form, glutathione disulfide. NADPH can reduce glutathione, regenerating glutathione that can be used to reduce more ROS.

231
Q

Describe B-oxidation

A

A series of reactions that each remove a 2-carbon unit (acetate) from the FA and produce 1 NADH and 1 FAD2H. The 2-carbon units are linked with CoA to form acetyl-CoA. These reactions continue until there are only 2 carbon atoms left.

232
Q

Describe how creatine phosphate is used to supply energy.

A

Creatine phosphate is formed from creatine when there are high levels of ATP present. When levels of ATP are low, the reverse reaction occurs. In this way creatine phosphate acts as an energy store and can sustain several seconds of activity in a muscle cell.
Creatine + ATP Creatine phosphate + ADP.

233
Q

Does gestational diabetes cause problems for the mother or the foetus?

A

Both

234
Q

Explain re-feeding syndrome.

A

When a person is fed a high-protein diet immediately after prolonged starvation. During prolonged starvation the activity of the urea cycle decreases because less protein is being catabolised, but when the person is fed a high-protein diet there’s a sudden influx of protein resulting in a lot of ammonia being produced when the amino acids are catabolised. The urea cycle doesn’t have a high enough activity to process all of the urea and the excess ammonia can cause death.

235
Q

Explain the concept of a HbA1c test and it’s use clinically.

A

A HbA1c test measures the proportion of HbA1c present in the blood. This is related to the average blood glucose concentration over the last 3 months (the lifespan of a rbc is 3 months). Clinically, a HbA1c test is used to access how well a diabetic is controlling their blood glucose. A measurement of over 10% HbA1c indicates poorly controlled diabetes.

236
Q

Explain the concept of nitrogen balance.

A

Nitrogen enters the body in the diet and is excreted in the urine. If the amount if nitrogen in equals the amount of nitrogen out, the individual is said to have zero nitrogen balance. If the nitrogen out > nitrogen in the individual is said to have negative nitrogen balance. If nitrogen out < nitrogen in the individual is said to have positive negative feedback.

237
Q

Explain the effects of excessive alcohol consumption on the body.

A

Depleted NAD+/NADH ratio means there’s inadequate NAD+ for FA oxidation, conversion of lactate to pyruvate and glycerol metabolism, causing accumulation of lactate in the blood and fasting hypoglycaemia. The increased level of acetyl-CoA and NADH causes FA production, which can’t be transported out of the liver, giving fatty liver. Ketone bodies may be produced which can cause ketoacidosis.

238
Q

Explain the purpose and process of the pentose phosphate pathway.

A

The PPP has 2 stages.
1) Glucose-6-phosphate is converted to a 5-carbon sugar and reduces NADP to NADPH.
2) 3 5-carbon sugars are converted to 2 fructose-6-phosphate molecules and glyceraldehyde-3-phosphate which can both re-enter glycolysis.
The PPP creates 5-carbon sugars for nucleotide synthesis and also generates NADPH.

239
Q

Explain the role of lactate with regard to glycolysis.

A

Lactate is created during periods of anaerobic respiration because the conversion of lactate to pyruvate regenerates NAD+ which is needed for glycolysis to occur but in anaerobic conditions it cannot be regenerated as part of oxidative phosphorylation. The reaction of pyruvate lactate is catalysed by lactate dehydrogenase.

240
Q

What is an essential amino acid?

A

An aa which can’t be synthesised by the body and must be taken in through the diet.

241
Q

Why is urea a suitable molecule for the transport and excretion of nitrogen?

A

Urea is highly soluble, inert, non-toxic and has a high hydrogen content.

242
Q

What does growth hormone (generally) promote?

A

Anabolism.

243
Q

Give 2 examples of biological rhythms.

A

The concentration of cortisol in the blood throughout the day (circadian rhythm) and the menstrual cycle.

244
Q

Give 4 functions of metabolism.

A
  • To produce energy in the form of ATP
  • To supply building block molecules for synthesis of larger cell components
  • To produce precursor molecules for interconversion of building block molecules
  • To create reducing power in the form of NADH, FAD2H, NADPH etc.
245
Q

Give 5 benefits of exercise.

A 
Better balance of lean tissue and fat in the body.
Lower blood lipids.
Lower blood pressure.
Increased glucose tolerance.
Increased muscle sensitivity to insulin.
246
Q

Example of a drug which is an oxidising agent.

A

The antimalarial primaquine.

247
Q

Give a hormone which is secreted from the zona reticularis.

A

Testosterone.

248
Q

Give an example of a mineralocorticoid.

A

Aldosterone

249
Q

Give examples of antioxidants (other than glutathione) that provide defence against ROS

A

Vitamins A, C, E, flavenoids such as polyphenols and carotene, minerals such as selenium and zinc.

250
Q

Give examples of diseases linked to oxidative stress

A

Cancer, CVD, emphysema, pancreatitis, Crohn’s, type 1 diabetes, Alzheimer’s.

251
Q

Give examples of inducing and inhibiting agents for drug metabolism.

A

Inducing agents include alcohol, barbiturates and nicotine. Inhibiting agents include grapefruit and cranberry juice.

252
Q

How and where is lactate dealt with?

A

Lactate is utilised either by conversion back into pyruvate for the Kreb’s cycle at the heart or used in gluconeogenesis at the liver. Lactate is also disposed of at the kidney by excretion in the urine.

253
Q

How are hydroxyl radicals produced?

A

By ionising radiation.

254
Q

How are the B-cells of the pancreas adapted for insulin production?

A

Extensive RER, well defined Golgi bodies, many mitochondria and well defined microtubules and microfilaments.

255
Q

How can ROS be used for the benefit of the body?

A

Certain immune cells such as neutrophils and macrophages can rapidly produce ROS in an oxidative burst, which kills pathogens as well as the immune cell itself. The ROS are produced by the enzyme NADPH oxidase.

256
Q

How do adrenaline levels change during a marathon? What effect does this have on insulin levels?

A

Adrenaline concentration increases rapidly. This decreases insulin concentration.

257
Q

How do blood glucagon concentrations change during a marathon?

A

Blood glucagon concentration increases steadily.

258
Q

What are the metabolic consequences of a decrease in insulin concentrations?

A

Reduces the amount of energy being stored and increases blood glucose concentration.

259
Q

How do carrier proteins affect the properties of the hormone they bind to?

A

They increase solubility and half-life when the hormone is bound.

260
Q

How do cortisol levels change during a marathon? What are the metabolic consequences of this?

A

Cortisol levels rise slowly throughout the marathon. This mobilises fat stores and stimulates gluconeogenesis.

261
Q

How do growth hormone levels change during a marathon? What is the metabolic consequence of this change?

A

They increase rapidly, which stimulates mobilisation of fat stores.

262
Q

How do hydroxyl radicals damage cells?

A

Very damaging to cell membranes and can cause the cell to lyse.

263
Q

How do you estimate the numerical value of diet-induced thermogenesis?

A

It’s about 10% of the energy content of the consumed food.

264
Q

How can you estimate the numerical value of energy expended by voluntary activity?

A

If a person is sedentary, it’s about 30% of BMR. If a person does moderate exercise, it’s about 60% of BMR. If a person does heavy exercise, it’s equal to BMR.

265
Q

How does acyl-CoA enter the mitochondria?

A

Acyl-CoA (activated FA) can’t enter mitochondria directly because they can’t pass through the inner membrane. Acyl-CoA is transported across the inner membrane via the carnitine shuttle. Acyl-CoA is converted to acyl carnitine which crosses the membrane. This reaction is reversible and inhibited by malonyl-CoA, which is involved in FA synthesis.

266
Q

How is 1,3-BPG created and what else can it be used for?

A

It is created by step 6 of glycolysis. It can be converted to 2,3-BPG which is the molecule that binds to Hb and decreases it’s affinity for oxygen, giving more efficient oxygen transport.

267
Q

How is cholesterol supply matched to demand?

A

The expression of LDL receptors on the cell surface membranes of cells is changed according to the concentration of cholesterol in the cell.

268
Q

How is nitric oxide produced?

A

Nitric oxide is synthesised in the body by nitric oxide synthases, in particular nitric oxide synthase which is an enzyme involved in inflammation. It has an important role in bodily control mechanisms but is also a ROS.

269
Q

List all of the hormones which feed back from the body to the primary neurones in the arcuate nucleus.

A

Ghrelin, PYY, leptin, insulin, amylin

270
Q

List all of the hormones that act in the excitatory primary neurones of the arcuate nucleus.

A

Ghrelin, PYY, leptin, insulin

271
Q

List all the hormones that act on the inhibitory primary neurones of the arcuate nucleus.

A

PYY, leptin, insulin

272
Q

What effects do glucagon have on target tissues?

A

Increase glycogenolysis in the liver.
Increase lipolysis in adipose tissue.
Increase gluconeogenesis in the liver.
Increase ketone body synthesis in the liver.

273
Q

List the major energy stores in an average 70kg man

A

TAGs: 15kg, glycogen: 0.4kg, protein: 6kg

274
Q

Name 3 anti-insulin hormones secreted in high amounts during pregnancy.

A

Oestrogen, progesterone and hPL

275
Q

List the 6 essential components of the diet.

A

Carbohydrate, protein, lipid, vitamins and minerals, fibre, water.

276
Q

Outline how a high level of LDLs in the blood is thought to cause atherosclerosis.

A

The LDLs are oxidised, then phagocytosed by macrophages in artery walls. As macrophages phagocytose more and more LDLs they become foam cells. The buildup of foam cells forms a fatty streak, which then turns into an atheroma.

277
Q

Outline the catabolism of amino acids.

A

The NH2 group is removed by transamination or deamination. The remaining carbon skeleton is converted to another molecule which depends on the type of amino acid. Ketongenic amino acids are converted to acetyl-CoA which is used to synthesise ketone bodies. Glucogenic amino acids can be converted to pyruvate, oxaloacetate, fumarole, a-ketoglutarate or succinate.

278
Q

Outline the mechanism by which insulin secretion is controlled by the blood glucose concentration.

A

Increased glucose concentration in the blood causes increased concentration in the extracellular fluid.
Glucose is transported into the B-cell by GLUT2.
Increased glucose concentration increases ATP/ADP ratio.
Increased ATP/ADP ratio causes depolarisation of the cell surface membrane.
Depolarisation causes influx of calcium ions via voltage-gated calcium channels.
Influx of calcium ions causes exocytosis of insulin.

279
Q

Outline the process of urea.

A

The urea cycle produces urea from ammonium ions. It occurs partly in the cytoplasm and partly in mitochondria. 5 enzymes are involved and there are several intermediates of the cycle. The cycle is not directly regulated but it’s inducible, so if there is more ammonium the turnover of the cycle will increase and if the is less ammonium the turnover will decrease.

280
Q

Outline the treatment for diabetic ketoacidosis.

A

Fluid replacement, insulin

281
Q

What are the 4 classes of hormone?

A
  • Polypeptide hormones - largest class of hormone, nearly all single chain polypeptides, varying in length, eg. insulin, glucagon, GH.
  • Glycoprotein hormones - all glycoprotein hormones have 2 polypeptide chains with a carbohydrate side chain, eg. FSH
  • Amino acid derivative hormones - derived from aas, eg. thyroid hormone, adrenaline.
  • Steroid hormones - derived from cholesterol, 4 ring part remains, but the functional group changes, eg. testosterone, oestrogen and cortisol.
282
Q

What are the 5 possible fates of nutrients?

A 
Degradation to release energy.
Synthesis of cell components.
Storage.
Interconversion to other nutrients.
Excretion.
283
Q

State the features of a control system which use hormones for communication.

A

Endocrine gland(s) to produce the hormone.
Transport of the hormone in the blood to the target cell.
Receptors for the hormone to bind to cause a response.
Inactivation of the hormone.

284
Q

What 3 main metabolic changes occur during starvation?

A

The brain becomes able to use ketone bodies as fuel.
The kidney cortex begins to contribute to gluconeogenesis.
BMR falls to a lower level.

285
Q

What are GLUT proteins and what is their function?

A

GLUT proteins are transport proteins that allow facilitated diffusion of monosaccharides from intestinal epithelial cells into the blood and facilitated diffusion from the blood into tissue cells. There are 5 GLUT proteins, some can be hormonally controlled eg. GLUT4 is inserted into the membrane in response to insulin.

286
Q

What are hyperlipoproteinaemias?

A

High levels of one or more type of lipoprotein in the blood. They are caused by over-production or under-removal of lipoproteins. This can be due to defective enzymes, receptors or apoproteins.

287
Q

What are superoxide radicals and how do they form?

A

Superoxide radicals (O2-) are a ROS. A superoxide radical is formed when an electron in the ETC doesn’t reach the end because it drops out. The electron reacts with oxygen, forming the superoxide radical.

288
Q

What are the 2 main things achieved by the metabolic changes that occur during pregnancy?

A

Higher levels of nutrients in the blood and increase in the amount of energy stores, particularly fats.

289
Q

What are the 3 classes of lipids?

A

FA derivatives, hydroxy-methyl-glut auric acid derivatives, vitamins.

290
Q

What are the 5 cell types of the anterior pituitary gland and what do they release?

A 
Thyrotrophs release TSH
Corticotrophs release ACTH
Somatotrophs release GH
Gonadotrophs release LH and FSH
Lactotrophs release prolactin
291
Q

What are the acute effects of hyperglycaemia?

A

Ketoacidosis, hyperosmolar non-ketotic syndrome.

292
Q

What are the chronic effects of hyperglycaemia?

A

Microvascular effects include nephropathy (kidney damage), retinopathy (diabetic eye disease), neuropathy (damage to peripheral nerves) and diabetic feet (caused by nerve damage, poor circulation and infection). Macrovascular effects include higher risk of stroke and MI caused by poor circulation to the periphery.

293
Q

What are the clinical consequences of hypothyroidism in newborn children?

A

Will cause cretinism if not treated within 3 weeks. Cretinism caused severe mental retardation, course features, decreased growth and decreased sexual development.

294
Q

What are the clinical consequences of inadequate glycogen storage?

A

Hypoglycaemia some time after meals and low exercise tolerance.

295
Q

What are the clinical consequences of too much glycogen storage?

A

Damage to muscle and liver due to the osmotic effect of glycogen.

296
Q

What are the different types of communication that a biological control system may use?

A

Nervous, endocrine, paracrine (local hormones), autocrine (hormones released by the cell that will be affected)

297
Q

What are the possible causes of hypercalcaemia?

A

Hyperparathyroidism due to an adenoma of the parathyroid gland, ectopic secretion of PTH or PTHrP (a molecule which mimics the action of PTH except for the stimulation of activation of vit D)

298
Q

What are the possible causes of hypocalcaemia?

A

Accidental surgical removal of the parathyroid glands, renal failure, hypothyroidism (rare)

299
Q

What are the target tissues of glucagon?

A

Mainly the liver.

300
Q

What are the target tissues of insulin?

A

Mainly the liver, skeletal muscle and adipose tissue.

301
Q

What are the target tissues of the thyroid hormones?

A

Virtually every tissue.

302
Q

What components of the cell can ROS damage?

A

DNA, lipids in cell membranes, proteins.

303
Q

What controls the synthesis and secretion of T3 and T4?

A

The hypothalamus produces and secretes TRH which acts upon the anterior pituitary gland and stimulates it to produce TSH. TSH acts on the thyroid gland and stimulates the production and secretion of thyroid hormone. TSH also stimulates growth of the thyroid gland itself. The secretion of TRH and TSH is controlled by negative feedback.

304
Q

What do LDL receptors bind to?

A

ApoB100

305
Q

What do the different types of neurone in the arcuate nucleus do?

A

Primary neurones sense the levels of glucose and FAs in the blood and respond to hormones. Excitatory primary neurones stimulate appetite and inhibitory primary neurones inhibit appetite.
Secondary neurones receive the input from primary neurones and co-ordinate a response via the vagus nerve.

306
Q

What do the hormones secreted by the posterior pituitary gland do?

A

ADH is involved in the control of water reabsorption in the kidneys, oxytocin stimulates maternal behaviour and romantic behaviour.

307
Q

What does the concept of Developmental Origin of Health and Disease (DOHaD) mean?

A

DOHaD states that birth weight is strongly linked to the incidence of adult disease eg. CHD, hypertension and type 2 diabetes incidence correlate with a low birth weight.

308
Q

What effects do high energy signals have on metabolism?

A

They promote anabolic reactions and inhibit catabolic reactions because they signal that the cell has ample energy.

309
Q

What effect do low energy signals have on metabolism?

A

They promote catabolic reactions and inhibit anabolic reactions because they signal that the cell has insufficient.

310
Q

What effect does PTH have on bone.

A

It stimulates osteoblasts to release cytokines that promote osteoclasts differentiation and activity, which increases the reabsorption of bone and causes a rise in serum calcium levels.

311
Q

What effect does PTH have on the kidneys?

A

It increases the amount of reabsorption of calcium in the kidneys so less is excreted. It also stimulate the conversion of vitamin D to it’s active form, calciferol, in the kidneys.

312
Q

What effect does vitamin D have on the gut?

A

Vitamin D stimulates the uptake of calcium from the diet in the gut.

313
Q

What effect does vitamin D have on the kidneys?

A

It stimulates reabsorption of calcium in the kidneys.

314
Q

What effect might renal failure have on serum calcium levels?

A

Renal failure could cause serum calcium levels to fall because of decreased calcium reabsorption.

315
Q

What factors affect the magnitude of a target cell’s response to a hormone?

A

The amount of hormone.
The amount of receptors for a hormone.
The affinity of receptors for the hormone.
The degree of amplification of the signal.

316
Q

What happens after phase 2 of drug metabolism?

A

The water-soluble drug-conjugate complex is excreted in the urine.

317
Q

What happens to remnants of VLDLs after they have offloaded TAGs at the target tissue?

A

They are removed by the liver or converted to other lipoprotein particles.

318
Q

What happens to T4 at it’s target tissues?

A

It’s converted to T3 by removal of an iodine group.

319
Q

What hormone inhibits the secretion of GH from the anterior pituitary gland?

A

Somatostatin.

320
Q

What hormone promotes release of GH from the anterior pituitary gland and where is this hormone secreted from?

A

GHRH (growth hormone releasing hormone), secreted from the hypothalamus.

321
Q

What hormones affect glycogenesis?

A

Insulin stimulates glycogenesis and glucagon inhibits it. (Insulin dephosphorylates the enzymes involved and glucagon phosphorylates the enzymes involved).

322
Q

What hormones affect glycogenolysis?

A

Glucagon and adrenaline both stimulate glycogenolysis.

323
Q

What is a biological rhythm?

A

A biological rhythm occurs when the set point of a control system is not fixed and varies according to time.

324
Q

What is a circadian rhythm?

A

A circadian (or diurnal) rhythm is a biological rhythm that varies over a 24 hour timescale.

325
Q

What is an adenoma?

A

A benign tumour of glandular tissue.

326
Q

What is an apoprotein?

A

A protein found in the micelle of a lipoprotein. There are several different apoproteins and each class of lipoprotein has specific apoproteins. Apoproteins have structural roles and functional roles such as enzyme activation and recognising cell surface receptors.

327
Q

What is creatinine?

What is it’s clinical significance?

A

Creatinine is the breakdown product of creatine and creatine phosphate. It’s produced by a spontaneous reaction at a constant rate so normally the blood concentration is very stable. Creatinine excretion over 24 hours is proportional to muscle mass. If there is muscle wasting, blood creatinine concentration increases.

328
Q

What is foetal programming? What theory is it a possilbe explanation for?

A

The idea that a foetus adapts to the conditions such as nutrient supply in utero and this is related to disease in adult life. Foetal programming is a possible explanation for DOHaD.

329
Q

What is the most common cause of hyperthyroidism?

A

Grave’s disease.

330
Q

What is the most common cause of hypothyroidism?

A

Hashimoto’s disease.

331
Q

What is POMC a precursor for? What do these molecules do?

A
  • ACTH = stimulates corticosteroid production and secretion
  • a-MSH = inhibits appetite
  • B-endorphin = part of the reward system and produces feelings of euphoria and tiredness.
332
Q

What is the cytochrome P450 system?

A

An enzyme system that catalyses part 1 of drug metabolism. There are polymorphisms of enzymes in the cytochrome P450 systems in the human population.

333
Q

What is the effect of aldosterone on the kidneys?

A

Acts on the distal tubules and collecting ducts of the kidneys to promote active reabsorption of sodium ions and secretion of potassium ions. The reabsorption of sodium ions causes water to be reabsorbed and thus blood pressure increases.

334
Q

What is the effect of glucose on Hb?

A

Glucose glycosylates Hb, forming HbA1c

335
Q

What is the enzyme that defends against hydroxyl radicals?

A

There isn’t one

336
Q

What is the first stage of the pentose phosphate pathway and which enzyme is it catalysed by?

A

Glucose-6-phosphate -> 5-carbon sugars, accompanied by the reaction of NADP -> NADPH.
Glucose-6-phosphate dehydrogenase.

337
Q

What type of hormone do all three layers of the adrenal cortex produce?

A

Steroid hormone.

338
Q

What is the general formula for carbohydrates?

A

(CH2O)n

339
Q

What is the minor hormone involved in calcium metabolism, where is it secreted from and what does it do?

A

Calcitonin is secreted from the parafollicular cells in the thyroid gland and it lowers serum calcium levels.

340
Q

What is the most common cause of excessive GH secretion?

A

A pituitary adenoma.

341
Q

What is the most common cell type of the anterior pituitary gland?

A

Somatotrophs

342
Q

What is the name for the covalent bond between monosaccharides and how is it formed?

A

Glycosidic bond, condensation reaction between OH and H groups, eliminating H2O

343
Q

What is the name of the axis that controls section of cortisol?

A

HPA axis

344
Q

What is the nett change in ATP during phase 2 of glycolysis?

A

4 molecules of ATP are made per glucose molecule during phase 2 by substrate level phosphorylation.

345
Q

What is the nett change in ATP molecules for phase 1 of glycolysis?

A

2 molecules of ATP are used up per glucose molecule.

346
Q

What is the normal blood concentration of ketone bodies?

A

1mM

347
Q

What is the normal blood concentration of lactate and at what concentration does it begin to cause acidosis?

A

The normal blood concentration is 1mM.

If the concentration is >5mM, it causes acidosis.

348
Q

What is the normal concentration of calcium in the blood (total and free)?

A

Total: 2.2 to 2.5mM
Free: 1.0 to 1.3mM

349
Q

What is the primary function of skeleton?

A

To buffer the level of calcium in the blood when it becomes low.

350
Q

What is the priority of metabolism during exercise?

A

To supply the brain with glucose.

351
Q

What is the purpose of the increased level of insulin during pregnancy?

A

To promote energy storage

352
Q

What is the relationship between anabolism and catabolism?

A

Anabolism uses the energy and reducing power released by catabolism.

353
Q

What is the role of pyruvate dehydrogenase?

A

Catalyses the conversion of pyruvate to acetyl-CoA. This is accompanied by the loss of CO2 so it is irreversible. The acetyl-CoA may then enter the Krebs cycle.

354
Q

What is the role of the control centre in a biological control system?

A

To analyse the incoming signals from receptors and coordinate a response. The control centre also decides the ‘set point’ as a reference for whatever is being controlled.

355
Q

What is the role of effectors in a biological control system?

A

To produce an effect when a signal from the control centre is received.

356
Q

What is the role of the receptors in a biological control system?

A

To detect stimuli and relay the information to the control centre.

357
Q

What is the route taken by chylomicrons to their target tissue and why is this route taken?

A

From the gut, they enter lacteals (small lymphatic vessels) and travel through the lymphatic system to the thoracic duct then into the left subclavian vein. This allows them to bypass the liver.

358
Q

What is the second stage of the pentose phosphate pathway?

A

3 5-carbon sugars are converted to 2 fructose-6-phosphate molecules and 1 glyceraldehyde-3-phosphate molecule.

359
Q

What parts of the body does PTH act on?

A

Bone and kidneys

360
Q

What parts of the body does vitamin D (calcitriol) act on?

A

Bone, gut and kidneys

361
Q

Where is the pituitary gland derived from?

A

The anterior pituitary gland is derived from gut tissue and the posterior pituitary gland is derived from nervous tissue.

362
Q

What processes make up stage 2 of FA metabolism?

A

Activation of FA, transport of FA into mitochondria and B-oxidation

363
Q

What stimulates glycogenolysis during a 1500m race?

A

Adrenaline

364
Q

What stimulates the release of CRH from the hypothalamus?

A

Physical chemical or emotional stress

365
Q

When are TAGs released from storage?

A

In stress ie. starvation, exercise or pregnancy and when the insulin/glucagon ratio is low

366
Q

Where and how are HDLs synthesised?

A

HDLs are synthesised in tissues either from shells (nascent HDL) in the liver or from VLDL remnants. Both types take up cholesterol in the tissues and convert into mature HDL particles, which then transport the cholesterol to the liver.

367
Q

Where are chylomicrons formed and what is their function?

A

Chylomicrons are formed in the epithelial cells which line the intestine. Their function is to transport TAGs (re-formed in the epithelial cells from absorbed FA and glycerol), and also cholesterol and lipid soluble vitamins from the intestine to tissues, especially adipose tissues.

368
Q

Where are LDLs synthesised and what is their function?

A

LDLs are synthesised in the liver. Their function is to transport cholesterol synthesised in the liver to tissues.

369
Q

Where are the hormones which stimulate the increase in energy stores during pregnancy secreted from?

A

Mainly the placenta, some from the ovaries.

370
Q

Where does stage 1 of carbohydrate metabolism take place?

A

In the GI tract, is it extracellular.

371
Q

Where is insulin produced?

A

In the B-cells of the islets of Langerhans in the pancreas.

372
Q

Where is the pituitary gland found?

A

In the brain, inferior to the optic chasm and connected to the hypothalamus via the pituitary stalk.

373
Q

Where is the body’s biological clock and what is involved in ‘setting it’?

A

The biological clock is found within the suprachiasmic nucleus in the hypothalamus. The hormone melatonin is involved in setting it. The time is kept up to date by detection of environmental factors called Zeitgebers.

374
Q

Which 2 classes of lipoprotein transport mainly TAGs?

A

Chylomicrons and VLDLs

375
Q

Which amino acid is adrenaline derived from?

A

Tyrosine

376
Q

Which hormone controls the long term regulation of serum calcium, and which the short?

A

PTH controls the short term

Vitamin D controls the long term

377
Q

Which molecules cause appetite to be stimulated when they are detected at the secondary neurones?

A

Neuropeptide Y and AgRP

378
Q

Which part of the adrenal gland is adrenaline secreted from?

A

The adrenal medulla

379
Q

Why can a high concentration of ACTH cause increased pigmentation of some parts of the body?

A

ACTH contains within it’s polypeptide sequence the sequence of a-MSH so ACTH can stimulate melanocytes to some extent, causing skin pigmentation.

380
Q

Why can’t fat stores be utilised during a 100m sprint?

A

Extra oxygen cannot be supplied to the muscles during a sprint and catabolism of fats (B-oxidation) requires oxygen.

381
Q

Why can’t pyruvate enter the TCA cycle directly?

A

It can’t pass through the impermeable inner mitochondrial membrane, whereas acetyl-CoA can.

382
Q

Why does cortisol have weak mineralocorticoid and androgen effects?

A

Because steroid receptors have sequence homologous in the binding regions of their steroid hormone receptors. This means mineralocorticoid and androgen receptors have a low affinity for cortisol and cortisol can bind to them

383
Q

Why is carbohydrate essential for the diet?

A

It’s needed to provide energy.

384
Q

Why is fibre essential to the diet?

A

It’s needed for healthy digestion.

385
Q

Why is lipid essential to the diet?

A

It supplies energy and essential FA.

386
Q

Why is protein essential to the diet?

A

Is supplies essential amino acids.

387
Q

Why is there a higher blood glucose level in a pregnant woman?

A

Despite the higher insulin level, the high anti-insulin levels ensures blood glucose remains high. Also, appetite is stimulated so more carbohydrates are taken in from the diet.

388
Q

Why is water essential to the diet?

A

It’s needed to replace the water lost in sweat, breath, urine and faeces.

389
Q

What is the reaction which converts pyruvate to acetyl-CoA?

A

Pyruvate + CoA + NAD+ —> acetyl-CoA + CO2 + H+

ESA 1 (9 decks)

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