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G.Parslows Learning Objectives > Endocrine biochem > Flashcards

Endocrine biochem Flashcards

1
Q

Iodine is an element commonly found in high abundance in which areas?

A

in the sea

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2
Q

What is the RDI for iodine

A

150ug

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3
Q

What is TRH? where is it released from?

A

Thyrotropin releasing hormone - released from the hypothalamus

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4
Q

What is cretinism? what is it caused by?

A

A congenital condition caused by maternal iodine deficiency, worlds most common form of mental retardation and growth retardation

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5
Q

Radiation from I (-131) can be used to what?

A

destroy the thyroid

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6
Q

What kind of receptors do thyroid hormones operate via?

A

membrane receptors and cause direct activation of genes in DNA

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7
Q

What is the atomic number of iodine?

A

53

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8
Q

Where is cholesterol found in the body?

A

free in membranes and as esters in storage

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9
Q

Where are human steroids derived from?

A

dietary steroids or are made from acetyl-coA in the liver

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10
Q

Corticosteroids refers to which two groups of steroids?

A

Glucocorticoids (eg cortisol) and mineralocorticoids (aldosterone)

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11
Q

Where are oestrogen and progesterone made primarily

A

ovary and also placenta during pregnancy

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12
Q

Where is testosterone primarily produced?

A

testes

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13
Q

Tamoxifen blocks what steroid action?

A

blocks oestrogen receptors and is used in the treatment of breast cancer

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14
Q

What is the effect of leuprolide?

A

lowers testosterone - used in treatment of prostate cancers

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15
Q

What are the actions of anabolic steroids?

A

interact with androgen receptors to increase muscle and bone synthesis

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16
Q

Where does the name cholesterol originate from?

A

greek chole- (bile) and stereos (solid)

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17
Q

What is cholesterol?

A

a waxy steroid metabolites

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18
Q

What is cholesterols role in cell membranes?

A

required for proper membrane permeability and fluidity (makes membrane LESS fluid)

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19
Q

What is a lipoprotein? What is their function?

A

biochemical assembly that contains proteins and lipids. Carry cholesterol in the blood

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20
Q

What are some examples of lipoproteins?

A

chylomicrons, low density lipoprotein (LDL), very low density lipoprotein (VLDL) and high density lipoprotein (HDL)

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21
Q

Arteriolosclerosis is promoted by excess levels of which lipoprotein?

A

LDL

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22
Q

What did Goldstein and Brown win a nobel prize for?

A

Identifying the LDL receptor on the liver which carries LDL and VLDL into the liver via receptor mediated endocytosis - this process is essential for feedback inhibition of HMG-CoA Reductase, muatations in this receptor lead to familial hypercholesterolaemia

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23
Q

Apart from its role in cell membranes what other roles (3) does cholesterol have?

A
  1. precursor to steroid hormones such as testosterone, cortisol, aldosterone, 2. component of bile salts 3. Vit D production
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24
Q

how many carbons does cholesterol have?

A

27

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25
Q

How many more times energy does NADPH have compared to ATP

A

7 times more

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26
Q

Where are human steroids derived from?

A

Cholesterol -> dietary or made in the liver from Acetyl-CoA

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27
Q

What is the most abundant steroid in the body?

A

cholesterol

28
Q

Where is oestrogen and progesterone made?

A

Ovary and placenta

29
Q

How are steroids eliminated?

A

by CYP3A4 in the liver endoplasmic reticulum which adds a OH group

30
Q

What is Cyproterone acetate? what is it used for?

A

Inhibitor of the andreogen receptor. Used to treat Hirsuitism in females, male-to female gender change, prostate cancer, benign prostatic hyperplasia, priapism and hypersexuality (chemical castration)

31
Q

What protein does cortisol bind in the blood?

A

transcortin

32
Q

Hb makes up what percentage of RBC dry content?

A

97%

33
Q

carbon dioxide can bind to Hb and form what? what proportion of the total respiratory CO2 is in this form?

A

forms carbaminohaemoglobin

15% of total

34
Q

Hb carries nitric oxide bound to what molecule on globin?

A

thiol group of globin

35
Q

Why does Hb carry nitric oxide?

A

releases it at the same time as oxygen to relax vascular walls and enhance gas diffusion

36
Q

Kendrew and Perutz one a nobel price for doing what regarding Hb?

A

solving its protein structure (the first protein structure solved)

37
Q

What is the structural difference between adult and foetal Hb?

A

Foetal: alpha2-gamma2
Adult:alpha2-beta2

38
Q

Mutations in amino acid sequences cause hundred of whats (in relation to Hb)?

A

haemaglobinopathies

39
Q

What was Christian Bohrs contributed to our knowledge about Hb?

A

described the sigmoid binding character of Hb-O2

40
Q

What is the structure of haemaglobin?

A

Tetramer of globin subunits (proteins) with 4 haem groups inserted into each

41
Q

What colour is Hb-CO?

A

bright red

42
Q

What colour is De-oxy Hb?

A

dark red

43
Q

What colour is HbO2?

A

scarlet red

44
Q

What binds better to Hb O2 of CO?

A

CO binds 200x better than O2

45
Q

What is Met Hb?

A

Hb with Fe3+ in the haem due to oxidation = found in aged RBCs

46
Q

Haem inserts into the globin via a locking mechanism involving binding of histidine residues F8 and E7. One is always bound whilst the other can be displaced - which is which?

A

F8 is always locked (think its FATE for globin and haem to be together)

E7 can be displaced by O2, CO and cyanide

47
Q

What is the role of Bisphosphoglycerate (BPG)

A

stabilises Deoxy-Hb via 8 salt bonds which makes this form rigid (tense) and stops Oxygen binding back to Hb in the tissues. It is displaced when O2 levels are high (in the lungs)

48
Q

Oxygen binding to Hb shows cooperativity - what does this mean?

A

When the first Oxygen binds to Hb it induces a change in the quaternary structure of Hb which changes the affinity of the other Oxygen binding sites - this means with only small increases in the concentration of O2 it is much easier to saturate the rest of the Hb molecule

49
Q

What happens to the Hb-Oxygen binding curve in the presence of acid (bohr effect)? What functionally is the relevance of this?

A

graph is shifted to the right- meaning Hb has LESS affinity for O2, the relevance of this is that working tissues produce lactic acid and they require more O2 so we want the DeOxy-Hb form to be more stabilized so more oxygen is given up in the tissues - this is achieved via bonding to histidine residues

50
Q

How does altitude alter the Oxygen-Hb binding curve? how is this achieved?

A

shifts it to the right -> giving more O2 to the tissues compensates for less O2 being picked up in the lungs. At altitude RBCs produce more BPG

51
Q

Why does foetal Hb have higher affinity for O2 than adult hb?

A

gamma subunits have 6 positive charges (not 8) so BPG is bound less avidly so deoxy-form is stabilised less

52
Q

What was Archibald Garrods field of study?

A

inborn errors of metabolism

53
Q

The major burden of pathology in australia from genetic diseases is due to what disease?

A

Cystic Fibrosis

54
Q

________was the first disease to be routinely tested for at birth and treated as required

A

phenylketonuria (PKU)

55
Q

Genetic testing is usually carried out using what technique?

A

PCR

56
Q

What is the most common x-linked recessive disorder? give some other examples

A

red-green colour blindess is the most common, others are haemophilia Am duchenne muscular dystrophy, Lesch-Nyhan syndrome

57
Q

What happens in children affected by PKU?

A

they lack phenylalanine hydroxylase leading to a build up of Phe which gets converted to phenylpyruvate (a ketone) which damages the brain and affects melanin synthesis

58
Q

What is the incidence of CF in australia?

A

in in 2500 births

59
Q

What is the carrier rate of the CF gene in Australia?

A

1 in 25

60
Q

What is the most common CF mutation?

A

Delta F506 in the CFTR protein (chloride channel)

61
Q

What is Ehlers Danlos syndrome?

A

Inherited connective tissue disoder - mostly autosomal dominant condition due to mutations in genes that encode the structure, production or processing of COLLAGEN or proteins that interact with collagen -> those affected have hypermobile joints, hyper-elasticity of the skin but also affects arteries.

62
Q

What is Marfan Syndrome?

A

mutation in fibrillin gene leading to bone overgrowth and joint laxity, with disproportionately long extremities compared to the size of the trunk

63
Q

What enzyme is important in melanin formation?

A

tyrosinase

64
Q

Is the inheritance of skin colour mono or polygenetic?

A

polygenetic -> 40 genes influence skin colour

65
Q

If you lack tyrosinase what colour is your skin?

A

NO melanin = albinism

G.Parslows Learning Objectives (1 decks)

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