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endocrine > Biochemistry and Physiology > Flashcards

Biochemistry and Physiology Flashcards

0
Q

Which iodine isotype can destroy the thyroid?

A

Iodine-131

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1
Q

What is cretinism?

A

Congenital condition caused by maternal iodine deficiency

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2
Q

What is the RDI of iodine?

A

150 micrograms

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3
Q

What goitrogens inhibit iodine uptake in the thyroid?

A
  • soy
  • broccoli
  • kale and cabbage
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4
Q

What are the effects of thyroid hormones?

A
  • control basal metabolic rate by activating gene transcription
  • increase mental alertness
  • stimulate brown adipose tissue to generate heat
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5
Q

What is the relationship between thyroid hormones and catecholamines?

A
  • elevate catecholamine receptors

- enhance catecholamine effects

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6
Q

What are the relative amounts and activity of T3 and T4?

A

Normal thyroid produces about 80% T4

T3 is about 4 times more active than T4

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7
Q

What is the effect of long term starvation on thyroid hormones

A

depressed levels

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8
Q

How are thyroid hormones synthesised?

A

T3 and T4 are tyrosine derivatives
Tyrosine is bound to protein, thyroglobulin which is in the follicular cell
Iodide is brought into follicular cell via Na/I symporter
Iodide oxidised by thyroperoxidase to iodine in the colloid
Iodine reacts with tyrosines on thyroglobulin (MIT and DIT) in colloid
Iodinated tyrosines undergo series of condensation reactions
Modified thyroglobulin (containing DIT, MIT, T3 and T4) is taken up into follicular cell via endocytosis
Proteases cleave T3 and T4 from thyroglobulin
T3 and T4 released into blood stream

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9
Q

How does uptake if iodide occur?

A

TSH binds to TSHR

Sodium-Iodide symporter driven by Na gradient created by Na/K/ATPase

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10
Q

What proteins bind thyroid hormones to allow for plasma transport?

A

Thyroid binding globulin, thranthyretin, serum albumin

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11
Q

How is T4 converted into T3?

A

Type 1 deiodinase activity in liver and kidney

Type 2 deiodinase activity in brain, brown adipose tissue and pituitary

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12
Q

How do thyroid hormones regulate metabolism?

A

Thyroid hormone binding to receptor is associated with transcriptional activation. Thyroid hormone regulates the rate of synthesis of proteins. Proteins involved in oxidative phosphorylation are upregulated to make more ATP

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13
Q

What are signs and symptoms of hyperthyroidism?

A
  • insomnia
  • heat intolerance
  • infertility
  • irritability
  • muscle weakness and fatigue
  • tachycardia
  • sweating
  • exophthalmos
  • frequent bowl movements
  • weight loss
  • nervousness
  • amenorrhea
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14
Q

What are signs and symptoms of hypothyroidism?

A
  • cold intolerant
  • depression
  • dry skin
  • fatigue
  • forgetfulness
  • heavy menstruation
  • weight gain
  • bradycardia
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15
Q

How does the nervous system compare to endocrine system?

A
  • structural continuity (wired) vs. glands and target cells dispersed (wireless
  • Neurotransmitter into synaptic cleft vs. hormone into blood
  • Diffusion across synaptic cleft vs. carried to distant organs
  • Rapid response vs. slow response
  • Brief duration of action vs. long duration of action
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16
Q

What are neurohormones?

A 
neurocrine secreted into bloodstream (chemicals released by nueonrs into blood for action at distant sites)
3 major groups:
-hypothalamus to anterior pit
-hypothalamus to posterior pit
-catecholamines
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17
Q

What are tropic hormones?

A

hormone that controls the secretion of another hormone

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18
Q

Which hormones have their receptors on the cell membrane?

A
  • peptide

- catecholamines

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19
Q

Which hormones have long half-life?

A
  • steriod

- thyroid

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20
Q

Which hormones have short half-life?

A
  • peptide

- catecholamines

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21
Q

Which hormones are made in advance and stored in vesicles?

A
  • peptide
  • catecholamines
  • thyroid
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22
Q

Which hormones are synthesised on demand?

A

steroid

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23
Q

Which hormones have their receptor in the nucleus?

A
  • steroid

- thyroid

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24
Q

What are examples of peptide hormones?

A
  • insulin

- PTH

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25
Q

What is the general target response of peptide hormones?

A
  • modify existing proteins

- induce protein synthesis

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26
Q

Which hormones activate second messenger systems?

A
  • peptide

- catecholamines

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27
Q

Which hormones dissolve in plasma during transport in blood?

A
  • peptide

- catecholamines

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28
Q

What are characteristics of peptide hormones?

A
  • made in advance and stored in vesicles
  • exocytotic release
  • dissolves in plasma
  • short half-life
  • receptor located on cell membrane
  • activates second messengers
  • e.g. insulin, PTH
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29
Q

Which hormones are bound to carrier proteins in blood?

A
  • steriod

- thyroid

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30
Q

Which hormones active gene transcription and translation?

A
  • steriod

- thyroid

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31
Q

Which hormones induce protein synthesis?

A
  • steroid

- thyroid

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32
Q

What are examples of steroid hormones?

A
  • oestrogen
  • androgens
  • cortisol
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33
Q

What are examples of catecholamines

A
  • Adr

- NA

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34
Q

How are peptide hormones synthesised?

A
  • Preprohormone cleaved into prohormone
  • Prohormone transported into secretory vesicles
  • Prohormone cleaved into active hormone in secretory vesicles
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35
Q

What are steroid hormones derived from?

A

Cholesterol

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36
Q

What are amine hormines derived from?

A

Tyrosine

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37
Q

Which hormones are hydrophilic?

A
  • peptide

- catecholamines

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38
Q

Which hormones are lipophilic?

A
  • steroid

- thyroid

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39
Q

How are steroid hormones removed?

A

conjugated and either excreted in urine or in bile

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40
Q

How are amine hormones removed?

A

enzymatic degradation

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41
Q

How are large peptide hormones removed?

A

receptor-mediated endocytosis

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42
Q

How are small peptide hormones removed?

A

via kidneys

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43
Q

What are causes of decreased hormone activity?

A
  • hyposecretion (primary or secondary)
  • increased removal from blood
  • abnormal tissue response
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44
Q

What are causes of increase hormone activity?

A
  • hypersecretion (primary or secondary)
  • decreased plasma protein binding
  • decreased removal from blood
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45
Q

What are the effects of secondary hypersecretion due to hypothalamic problem?

A

increased RH from hypothalamus to pituitary
increased SH from pituitary to target organ
increased hormone from target organ into blood

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46
Q

What are the effects of secondary hypersecretion due to pituitary problem?

A

increased SH from pituitary to target organ
increased hormone from target organ into blood
negative feedback to hypothalamus:
decreased RH from hypothalamus to pituitary

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47
Q

What are the effects of primary hypersecretion due to problem with target organ?

A

Increased hormone from target organ into blood
Negative feedback:
decreased RH from hypothalamus to pituitary
decreased SH from pituitary to target organ

48
Q

What is the origin of the posterior pituitary?

A

Nervous tissue - outgrowth of the brain

49
Q

What is the origin of anterior pituitary?

A

glandular epithelial tissue

50
Q

How does the posterior pituitary link to hypothalamus?

A

neural link

51
Q

How does anterior pituitary link to hypothalamus?

A

vascular link

52
Q

What hormones are released from posterior pituitary?

A
  • vasopressin/ADH

- oxytocin

53
Q

How are posterior pituitary hormones synthesised, stored and released?

A

Hormone made and packaged in cell body of neuron in hypothalamus
Vesicles transported down the axon
Vesicles stored in posterior pituitary
Hormones released into blood via vein

54
Q

What is the synthesis, storage and release of anterior pituitary hormones?

A 
trophic hormones (RH) are synthesised by neurons in hypothalamus
RH released into capillaries of portal system
portal veins carry RH directly to anterior pituitary
RH trigger release of SH by endocrine cells of the anterior pituitary
SH released into another set of capillaries to be distributed to the body
55
Q

What hormones are released by the anterior pituitary?

A
  • Growth hormone
  • TSH
  • ACTH
  • Gonadotropins (LH and FSH)
  • prolactin
56
Q

What trophic hormones are released by the hypothalamus to the anterior pituitary?

A
  • Corticotropin RH
  • Thyrotropin RH
  • Gonadotropin RH
  • Growth hormone RH
  • Growth hormone inhibiting hormone (somatostatin)
  • Prolactin releasing factor
  • Prolactin inhibitory hormone (dopamine)
57
Q

What is the function of prolactin?

A

Prolactin targets mammary glands to cause breast growth and milk secretion

58
Q

What is somatotrophin?

A

Growth hormone

59
Q

What is the effect of LH?

A

sex hormone production

60
Q

What is the effect of FSH?

A

gamete production (ova and sperm)

61
Q

What are the effects of GH?

A
  • increase FAs and glucose in blood (antagonise insulin)
  • hyperplasia and hypertrophy of soft tissues and skeleton
  • increase protein synthesis
  • sodium retention
  • stimulate liver to produce somatomedins (IGF)
62
Q

What are somatomedins?

A

Insulin-like growth factors (I and II) and polypeptide growth factor
GH stimulates synthesis by the liver

63
Q

What is the GH control pathway?

A

GHRH stimulates GH (somatotropin) release
GH stimulates somatomedin synthesis
Somatostatin inhibits GH release

64
Q

What are functions of the thyroid gland?

A

Secrete thyroid hormones to regulate metabolism

Secrete calcitonin to regulate calcium levels

65
Q

What is colloid?

A

Glycoprotein mix which contains thyroglobulin

66
Q

How is the thyroid gland organised?

A

Colloid is surrounded by follicular cells

C cells are in the interstitial spaces and secrete calcitonin

67
Q

What is the effect of cold in infants on thyroid hormone control pathway?

A

Only factor which increases TRH

68
Q

What is the effect of stress on thyroid hormone pathway?

A

decreases TRH

69
Q

What are the actions of thyroid hormones?

A
  • increase BMR (calorigenic and heat producing)
  • increase oxygen consumption
  • sympathomimetic effect (increases HR and CO)
70
Q

What is primary hypothyroidism?

A

Thyroid failure means that T3 and T4 release is low
This is fed back to hypothalamus and pituitary which increase their release of TRH and TSH
Results in goitre

71
Q

What is the effect of decreased dietary iodine?

A

insufficient iodine means decreased synthesis of T3 and T4
Fed back to hypothalamus and pituitary which increase release of TRH and TSH
Leads to goitre

72
Q

What is the effect of secondary hypothyroidism?

A

Either hypothalamic or pituitary failure/tumour
Decreased synthesis/release of TRH/TSH
results in decreased synthesis of T3 and T4
Hypothalamus/pituitary are unresponsive to feedback
No goitre

73
Q

What are the physiological effects of hypothyroidism?

A
  • decreased BMR and oxygen consumption
  • fatigue and decreased energy
  • weight gain
  • cold intolerance
  • bradycardia
  • decreased protein synthesis causes puffy face (myxedema)
74
Q

What is the effect of primary hyperthyroidism?

A

Grave’s disease (thyroid-stimulating immunoglobulin)
Increased stimulation of thyroid hormone receptors produce same effects as increased T3 and T4
Fed back to hypothalamus which decreases TRH
Decreased TRH decreases TSH
Goitre

75
Q

What is the effect of secondary hyperthyroidism?

A

Either hypothalamic or anterior pituitary excess
If hypothalamic excess, there will be increased release of TRH which increases release of TSH causing increased circulating T3 and T4. These are unable to feedback to hypothalamus
Leads to a goitre

76
Q

What is the effect of a hypersecreting tumour causing secondary hyperthyroidism?

A

Elevated T3 and T4
Feedback to hypothalamus to decrease TRH and TSH
No goitre

77
Q

What are physiological consequences of hyperthyroidism?

A
  • Increased BMR and oxygen consumption
  • increased appetite
  • weight loss
  • muscle weakness
  • heat intolerance
  • sweaty
  • tachycardia
  • anxiety
78
Q

What sort of gland is the adrenal medulla?

A

modified sympathetic ganglion

79
Q

What type of gland is the adrenal cortex?

A

true endocrine gland

80
Q

What hormones does the adrenal medulla release?

A

catecholamines

sex hormones

81
Q

What hormones does the adrenal cortex release?

A

steroids - glucocorticoids and aldosterone

82
Q

Which region of the adrenal medulla secrete sex hormones?

A

zona reticularis (and fasciculata)

83
Q

Which region of the adrenal cortex secretes glucocorticoids?

A

zona fasciculata (and reticularis)

84
Q

Which region of the adrenal cortex secretes mineralocortocoids?

A

zona glomerulosa

85
Q

Which adrenal hormones have crossover effects?

A

high cortisol has aldosterone-like effects

86
Q

What is the HPA pathways for the control of cortisol release?

A

circadian rhythm and stress stimulate hypothalamic release of CRH
acts on anterior pituitary to release ACTH
acts on adrenal cortex to release cortisol

87
Q

What are the effects of cortisol?

A
  • immune system suppresion
  • stimulates gluconeogenesis in the liver
  • stimulates proteolysis in the muscle
  • stimulates lipolysis in adipose tissue
  • negative Ca++ balance: decrease absorption, increase excretion, break down bone
88
Q

What peptides are yielded from POMC?

A

ACTH, beta endorphon, alpha MSH (melanocyte-stimulating)

89
Q

What are the effects of alpha-MSH?

A
  • melanin synthesis
  • decrease food intake
  • immune response
90
Q

What are the functions of cortisol?

A
  • protects against hypoglycaemia by stimulating catabolism of energy stores
  • permissive for glucagon and catecholamine actions
  • helps body to cope with long-term stress
91
Q

What is a consequence of long-term exogenous corticosteroid use?

A

Inhibition of ACTH due to negative feedback
Adrenal gland becomes desensitised to endogenous ACTH
Cells that secrete cortisol atrophy

92
Q

What are the effects of primary and secondary hyperaldosteronism?

A
  • hypernatremia
  • hypokalemia
  • hypertension
93
Q

What is Cushing’s disease?

A
  • secondary hypercortisolism

- pituitary tumour autonomously secretes ACTH

94
Q

What are the effects of hypercortisolism?

A
  • hyperglycaemia
  • muscle breakdown and lipolysis
  • abnormal fat distribution due to increased appetite (trunk obesity)
  • Na+ retention leading to hypertension
  • Osteoporosis
95
Q

What is the effect of secondary hypercortisolism due to hypothalamic problem?

A
  • increased CRH released from hypthalamus
  • increased ACTH released from anterior pituitary
  • increased cortisol released from adrenal medulla
  • no negative feedback occurs
96
Q

What is the effect of secondary hypercorisolism due to pituitary problem?

A
  • increased ACTH released from anterior pituitary
  • increased cortisol released from adrenal medulla
  • negative feedback to hypothalamus
  • decreased CRH
  • no negative feedback to anterior pituitary
97
Q

What is the effect of primary hypercortisolism due to problem with adrenal cortex?

A
  • increased cortisol released from adrenal medulla
  • negative feedback to hypothalamus
  • decreased CRH
  • negative feedback to anterior pituitary
  • decreased ACTH
  • no negative feedback to adrenal medulla
98
Q

What is Addison’s disease?

A
  • primary adrenal insufficiency (hyposecretion)
  • autoimmune destruction of adrenal cortex
  • hyposecretion of all adrenal steroid hormones
  • decreased aldosterone: retention of K+ (arrhythmias) and Na+ depletion (hypotension)
  • decreased cortisol: decreased stress response and hypoglycaemia
99
Q

What is the effect of secondary hypocortisolism?

A
  • either abnormal hypothalamus or pituitary
  • decreased ACTH
  • normal aldosterone
100
Q

What is the effect of defects in adrenal steroid enzymes?

A
  • lack of cortisol and aldosterone
  • increased androgens
  • adrenogenital syndrome
101
Q

What catecholamines does the adrenal medulla secrete?

A
  • Adr
  • NA
  • dopamine
102
Q

What are the metabolic effects of catecholamines?

A
  • increased glucose and FFA

- increased BMR

103
Q

What are the responses to acute and chronic stress?

A

Acute stress results in fight-or-flight reaction

Chronic stress elevates cortisol which suppresses immune response

104
Q

Where does the conversion of squalene to cholesterol occur?

A

Endoplasmic reticulum

105
Q

How are steroids eliminated?

A

Oxidised by CYP450 enzymes (mainly CYP3A4)

106
Q

What is the action of cyproterone acetate and what is it used to treat?

A

Synthetic steroid inhibitor of androgen receptor
Blocks synthesis of mRNA for androgenic proteins
treat hirsutism in women

107
Q

In what region of the adrenal gland is DHEA produced?

A

Zona reticularis of the adrenal cortex

108
Q

What are the actions of DHEA?

A
  • testosterone-like hormone (weak androgen)

- opposes the effect of cortisol

109
Q

What is the secretion signal for DHEA release?

A

ACTH

110
Q

What are the secretion signals for aldosterone release?

A

Angiotensin II, ACTH, high potassium

111
Q

What region of the adrenal cortex produces cortisol?

A

Zona fasciculata

112
Q

What is the action of leuprorelin and what is it used for?

A

analogue of GnRH
induces chemical castration by inhibiting FSH and LH release
suppresses oestrogen and progesterone from ovaries
suppresses testosterone from testes
Treats breast, ovarian and prostate cancers

113
Q

What protein do sex steroids bind to in plasma for transport in blood?

A

Sex hormone binding globulin

114
Q

What is the action of FSH in females?

A

FSH stimulates ovarian follicle to produce estradiol which prepares the uterus for embryo plantation

115
Q

What is the action of LH in females?

A

LH stimulates the mature ovarian follicle to degenerate to corpus luteum which produces progesterone
Surge of LH stimulates ovulation

116
Q

What cells produce testerone?

A

Leydig cells

117
Q

What are the effects of anabolic steroids on muscle mass?

A
  • increase production of actin and myosin
  • reduce exercise recovery time
  • increase BMR

endocrine (2 decks)

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