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ESA 1 > Metabolism > Flashcards

Metabolism Flashcards

1
Q

What is the first enzyme in glycolysis?

A

Hexokinase/ glucokinase

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2
Q

What is the name of the process that converts glucose to glycogen stores?

A

Glycogenesis

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3
Q

Name the two enzymes involved in glycogenesis

A

After hexokinase, the two enzymes specific to glycogenesis are phosphoglucomutase and branching enzyme

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4
Q

Describe the process of glycogenolysis

A

Glycogen to glucose molecules. De-branching enzyme then phosphoglucomutase then glucose-6-phosphatase to create free glucose molecules

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5
Q

Describe the pathophysiology of Von Gierke’s disease

A

Absence or defect of glucose-6-phosphatase, meaning glycogen cannot be broken down to glucose. Results in excessive glycogen storage in the liver (hepatomegaly) and hypoglycaemia

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6
Q

Name the enzyme used in lipogenesis (creation of fatty acids)

A

Acetyl carboxylase. Allosterically regulated by citrate (promotes) and AMP (decreases)

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7
Q

Give the most commonly encountered free radicals in the body

A

Nitric oxide and hydroxyl groups

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8
Q

Give the two enzymes that work to reduce the effects of ROS

A

Superoxide dismutase (SOD) and catalase

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9
Q

Which molecule replenishes GSH from GSSG?

A

NADPH

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10
Q

Why is glutathione (GSH) such a good defence against ROS?

A

Has a very high reducing power

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11
Q

Why is nitric oxide produced by the body?

A

For its vasodilator effects. Created from arginine

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12
Q

Through which channels does glucose pass into beta cells in the islets of Langerhans?

A

GLUT 2

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13
Q

Glucagon is produced from which cells of the pancreas?

A

Alpha cells in the islets of Langerhans

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14
Q

Name the layers of the cortex of the adrenal glands

A

Zona glomerulosa (mineralocorticoids), zona fasciculata (glucocorticoids) and zona reticularis (androgens)

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15
Q

Where are catecholamines e.g. adrenaline and noradrenaline produced and by what cells?

A

Medulla of the adrenal glands by chromaffin cells (stimulated by sympathetic innervation)

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16
Q

Give the effects of aldosterone

A

Acts on the distal convoluted tubule to upregulate Na/K ATPase and increase ENaC expression. Keeps water/sodium and excretes potassium

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17
Q

Give the effects of cortisol

A

Stimulates gluconeogenesis, protein breakdown and distribution of fat to a central position in the body

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18
Q

Give the hypothalamic-pituitary axis for cortisol production

A

Hypothalamus secretes corticotropic releasing hormone (CRH) to act on the pituitary and secrete ACTH. ACTH stimulates the zone fasciculata of the cortex of the adrenals to secrete cortisol.

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19
Q

When are cortisol levels at their highest?

A

The morning. Lowest at night. Part of the normal circadian rhythm

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20
Q

Give some cushingoid signs

A

Hyperpigmentation of the skin, dorso-cervical fat pad, weight gain, muscle atrophy and striae.

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21
Q

Why does hyperpigmentation occur in high cortisol levels?

A

ACTH is produced from the precursor, POMC, which also gives alpha-MSH which stimulates melanocytes to pigment the skin

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22
Q

What channel is responsible for iodine uptake in the thyroid?

A

Sodium-iodine symporter (NIS). Sodium is extruded from the cell by Na/K ATPase and the gradient allows iodine uptake

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23
Q

Which cells of the thyroid produce thyroxine?

A

Thyrocytes. Excreted into the surrounding colloid

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24
Q

What is the precursor molecule to thyroxine?

A

Thyroglobulin

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25
Q

Where is T4 converted to T3?

A

The peripheral circulation

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26
Q

In what form is thyroxine produced by the thyroid?

A

T4

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27
Q

Which blood proteins bind thyroxine?

A

Thyroid binding globulin (TBG) and albumin

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28
Q

How, in simple terms, is thyroxine produced?

A

Iodide is added to free tyrosine residues on thyroglobulin by thyroid peroxidase and this is secreted

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29
Q

Give the pathophysiology of Graves’ exophthalmos

A

The reason is two-fold. Circulating antibody stimulates the thyroid receptors to stimulate thyroxine production to increase metabolism and vitreous production. The same antibody stimulates the extraocular muscles to push the eye out of the socket

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30
Q

Give the difference between Hashimoto’s disease and cretinism

A

Hashimoto’s is autoimmune destruction of the thyroid gland causing hypothyroidism. Cretinism is the result of hypothyroidism from birth, resulting in mental retardation, stunted growth and delayed sexual development

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31
Q

In what bone is the pituitary found?

A

Sella tursica of the sphenoid bone

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32
Q

What tissue does the anterior pituitary derive from?

A

Gut tissue (the infundibulum)

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33
Q

Name the hormones produced by posterior pituitary (neurohypophysis)

A

ADH and oxytocin

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34
Q

Name the hormones produced by the anterior pituitary (adenohypophysis)

A

ACTH, GH, TSH, GnRH and prolactin

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35
Q

ACTH is produced in a paraneoplastic syndrome of which cancer?

A

Small cell lung carcinoma

36
Q

What test is performed in someone with a high cortisol level?

A

Dexamethasone suppression - a pituitary tumour secreting ACTH will reduce the ACTH produced in response to dexamethasone but an ectopic production will not respond to dexamethasone. An overactive adrenal will also not respond to dexamethasone. Used to identify the cause of the high cortisol

37
Q

Define pharmacokinetics and pharmacodynamics

A

Kinetics - what the body does to the drug

Dynamics - what the drug does to the body

38
Q

Give the four stages of pharmacokinetics

A 
Absorption
Distribution
Metabolism
Elimination 
ADME
39
Q

What is phase 1 of drug metabolism?

A

Oxidation, reduction or hydrolysis of the compound to expose the active site

40
Q

Why do some drugs not go through phase 1 metabolism?

A

They have their active site already exposed when absorbed

41
Q

What is phase 2 drug metabolism?

A

The conjugation of the drug so that it can be excreted. This is normally by glucuronidation or glutathione conjugation

42
Q

Give the antidote for paracetamol overdose

A

N-acetyl cysteine

43
Q

How does paracetamol overdose lead to hepatocellular damage?

A

Phase 1 and 2 pathways are saturated so an alternative phase 1 pathway is used. NAPQI is produced by the conjugation by glutathione, depleting glutathione stores and making the liver susceptible to ROS attack

44
Q

Give the two enzymes used in alcohol metabolism

A

Alcohol dehydrogenase to form acetaldehyde

Acetaldehyde dehydrogenase to form acetic acid

45
Q

Give the mechanism of action for disulfiram

A

Blocks aldehyde dehydrogenase to cause a build up of aldehyde and cause awful hangover symptoms

46
Q

Which three stages of glycolysis are considered to be the most important?

A

1 (hexokinase), 3 (phosphofructokinase) and 10 (pyruvate kinase)

47
Q

What happens to pyruvate in the absence of oxygen?

A

Converted to lactate by lactate dehydrogenase and NADH. Reversed in the heart or liver by the reverse reaction

48
Q

What is the function of the pentose phosphate pathway?

A

To create pentose sugars that can be used to create the sugar phosphate backbone of DNA

49
Q

What is the key enzyme for the pentose phosphate pathway?

A

Glucose 6 phosphate dehydrogenase (G6PD) to convert G6P to the pentose sugar and NADPH.

50
Q

Why does a G6PD deficiency cause haemolysis?

A

G6PD is an important producer of NADPH, which is used to replenish GSH from GSSG. GSSG aggregates accumulate in the erythrocytes as Heinz bodies and cause haemolysis

51
Q

Which enzyme creates acetyl CoA?

A

Pyruvate dehydrogenase from pyruvate molecules

52
Q

How does acetyl CoA enter the mitochondria?

A

Via the carnitine shuttle

53
Q

Give the products of the Kreb’s cycle

A

3 NADH, 2 FADH2 molecules and 2 CO2

54
Q

What is the final electron acceptor of the electron transport chain?

A

Oxygen. Creates water

55
Q

Which enzyme creates ATP in the electron transport chain?

A

ATP synthetase

56
Q

What is the function of thermogenin?

A

Produced in brown adipose tissue and uncouples the electron transport chain to produce heat from the diffusion of hydrogen molecules down the concentration gradient

57
Q

How does cyanide cause death?

A

It binds to cytochrome c in the electron transport chain so that electrons cannot pass through and ATP cannot be made

58
Q

How do chylomicrons reach the systemic circulation?

A

Produced in the enterocytes, enter the lacteals of the villi into the lymphatic system and enters the blood through the thoracic duct in the left subclavian vein

59
Q

Where are LDLs produced?

A

The liver

60
Q

How are LDLs taken up by the tissues?

A

They express apoprotein b100 on their surface, which binds to the cell membrane of the tissues and allows uptake of the LDLD

61
Q

Why are HDLs deemed to be bad?

A

They take excess cholesterol from the tissues and deposit it in the liver

62
Q

Give the structure of triacylglycerols (TAGs)

A

Glycerol backbone and three fatty acid chains. Stored in adipose tissue

63
Q

Fatty acids are hydrophobic, so how do they enter the mitochondria?

A

They are activated by a molecule of CoA and enter via the carnitine shuttle

64
Q

Fatty acid oxidation (and break down) by FAD and NAD is known as what?

A

Beta oxidation

65
Q

How many calories are produced per gram of fat and glucose?

A

Fat - 9

Glucose - 4

66
Q

How can acetyl CoA produce ketone bodies?

A

By first forming HMG and then being reduced by HMG CoA reductase to form ketones. This enzyme is blocked by statin medications

67
Q

What is the main source of nitrogen in the body?

A

Breakdown of amino acids

68
Q

What is transamination?

A

Moving the amine group of an amino acid to another compound in the liver by alanine transaminase (ALT) or aspartate transaminase (AST)

69
Q

What is deamination?

A

Complete removal of the amine group of an amino acid to form ammonia (and then urea in the urea/ ornithine cycle)

70
Q

Explain the basics of the urea/ ornithine cycle

A

Ammonia or glutamate enters the cycle as nitrogen compounds and are converted to arginine. Arginine is broken down to urea and ornithine. Urea is released into the blood and excreted whilst the ornithine recycles and mops up ammonia/ glutamate

71
Q

Describe the problems with feeding a previously starved person with a high protein diet

A

This is refeeding syndrome. The urea cycle enzymes are very low in starvation and so they cannot cope with the sudden rise in nitrogen from amino acids and so the person suffers neuro deficits

72
Q

Give the region of the brain that is responsible for appetite control

A

Arcuate nucleus in the satiety centre of the hypothalamus

73
Q

Describe the suppression of appetite

A

POMC is secreted from the primary neurones in the satiety centre to stimulate PYY from the secondary neurones to suppress appetite

74
Q

How is appetite stimulated?

A

Neuropeptide Y is secreted from the primary neurones of the satiety centre to stimulate ghrelin release from the secondary neurones to stimulate the appetite

75
Q

How does a high level of adipose tissue suppress the appetite?

A

Adipose tissue secreted leptin, which is an inhibitor of the arcuate nucleus in the satiety centre to reduce the appetite. Leptin production is proportional to adipose content

76
Q

Which two enzymes can be deficient in galactosaemia and which is worse of the two?

A

Galactokinase and galactose-1-phosphate uridyl transferase. The second is worse because it’s substrate (G1P) is toxic

77
Q

How does galactosaemia lead to cataracts?

A

Enzyme deficiency leads to a build-up of galactose. This is converted to galactitol by aldose reductase. Aldose reductase requires NADPH and so there is an NADPH depletion. NADPH keeps disulphides bridges from forming in proteins and so protein aggregates form in the eyes as cataracts. NADPH also replenishes GSH from GSSG so these people are more susceptible to ROS

78
Q

What enzyme is deficient in phenylketonuria?

A

Phenylalanine hydroxylase

79
Q

Why does phenylketonuria cause CNS defects?

A

Phenylalanine hydroxylase normally converts phenylalanine to tyrosine. Tyrosine is the precursor to dopamine. The deficiency in this leads to a build up of phenylalanine, which is converted to phenylpyruvate. Lack of dopamine affects CNS development. Excess phenylalanine blocks the amino acid transporter at the blood-brain barrier. Phenylpyruvate competitively inhibits pyruvate so there is an energy deficiency

80
Q

Which enzyme is defective in homocystinuria?

A

Cystathione beta synthase

81
Q

In homocystinuria, what is the excess homocysteine converted to?

A

Methionine

82
Q

How is creatinine produced?

A

Spontaneous breakdown of phosphocreatine and creatine in the muscles

83
Q

Which enzyme converts creatine and Pi to phosphocreatine?

A

Creatine kinase. This reaction is reversible

84
Q

What is the function of phosphocreatine?

A

To replenish ATP stores when these levels are depleted

85
Q

When is phosphocreatine created?

A

When there is an excess of ATP molecules. Acts as a phosphate store

86
Q

What condition can serum creatine kinase diagnose?

A

Myocardial infarction

ESA 1 (4 decks)

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