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physiology > Hormones 3 & 4 > Flashcards

Hormones 3 & 4 Flashcards

1
Q

what are the 2 key components of growth:

A

bone (height) and soft tissue (weight)

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2
Q

what is the continuous process of growth characterised by

A

spurts and ultimate arrest

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3
Q

what are the requirements for growth and their function

A

hormones - primarily growth hormone
decent diet - vitamins, minerals, energy, amino acids
extent of growth genetically determined

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4
Q

what happens in adolescence so that no further growth is possible

A

epiphyseal plate “closes” in adolescence

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5
Q

what is the function of chondrocytes and osteoblasts within different sections of the bone
top :
middle :
middle :
bottom :

A

top : diving chondrocytes add length to bone
middle : produce cartilage
middle : old (larger) start to disintegrate
bottom : is the osteoblasts, lay down bone on top of cartilage

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6
Q

what is the growth hormone release controlled by

A

GHRH and GHIH

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7
Q

what is pulsatile release

A

the circadian rhythm stress that causes the release growth of hormones

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8
Q

how many amino acid peptides within the growth hormone

A

191 amino acid peptides

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9
Q

how does the growth hormone atypically extend its half life

A

atypically has a plasma binding protein

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10
Q

what are the direct and indirect effects of growth hormone

A

D: on growth and metabolism
I: growth and
metabolism through stimulation of
insulin-like growth factor-1 (IGF-1), which is released from the liver

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11
Q

growth hormones release pattern

A

particularly high during sleep

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12
Q

describe the full effects of growth hormones function

A

stimulates differentiation of precursor cells in bone
(prechondrocytes → chondrocytes) – these produce IGF-1
*IGF-1 stimulates chondrocyte proliferation →new cartilage→new bone→ growth
*

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13
Q

where is GH and IGFs function

A

GH and IGFs stimulate protein synthesis in muscle and other tissues
IGFs : stimulate cell division

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14
Q

example of growth hormones cascade

A

GH stimulates cell maturation and IGF-1 production
then IGF-1 stimulates cell division and tissue growth

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15
Q

how do IGFs travel

A

as an auto/paracrine (local) & a hormone (travels in blood)

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16
Q

what are the effects of growth hormones GH metabolically

A

uptake of plasma amino acids (for protein synthesis)
- breakdown of fat (energy for growth)
- spares glucose stores (responsible hormone)

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17
Q

what are the effects of growth hormones, IGF-1 and insulin metabolically

A

uptake of plasma amino acids (for protein synthesis)
- glucose/energy substrate uptake into cells (for growth)

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18
Q

what are the effects of growth hormones, GH and IGF-1 together metabolically

A

together these hormones ensure tight regulation of energy reserves

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19
Q

what is the function of thyroid hormones in relations to growth

A

THs stimulate GH receptor expression
allows GH to have an effect, synthesis and regulation
anabolic, involved in synthesis reactions

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20
Q

what is the function of thyroid hormones in homeostasis

A

initiate changes in gene expression slowly
raises metabolic rate & produces heat
*provides substrates for oxidative metabolism (AA’s, FA’s & CHO)

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21
Q

what is the function of thyroid hormones in foetal brains

A

required for foetal brain development (deficiency = cretinism)
→ can be caused by dietary iodine deficiency in the mother
*important for nervous system function & cognition

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22
Q

role of insulin as a hormone

A

*required for growth
*enhances protein synthesis and amino acid uptake
*inhibits protein degradation
→ net increase in proteins
*promotes uptake of glucose into cells
*helps maintain energy balance

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23
Q

role of sex hormones

A

*co-ordinates pubertal growth spurt
*stimulate production of GH/IGF
*induce closure of epiphyseal plate (stops further growth)
*testosterone directly increases protein synthesis (anabolic steroids)

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24
Q

role of cortisol

A

Cortisol
*antagonistic in high concentration
*stimulates protein breakdown
*inhibits GH and growth processes
*arrests growth in favour of stress response

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25
Q

name the GH disorders

A

pituitary dwarfism, pituitary giant (gigantism), acromegaly

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26
Q

what causes Pituitary Dwarfism

A

childhood deficiency in GH, due to production/receptor problem

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27
Q

what is the course of treatment for Pituitary Dwarfism

A

treated using genetically engineered hGH

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28
Q

what are the limitations when treating Pituitary Dwarfism

A

*limited treatment window (before epiphyseal plate
closes)

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29
Q

what is the causes Pituitary Giant

A

childhood excess of GH caused by a benign, slow growing, GH-secreting anterior pituitary tumour

extensive growth of long bones – excessive height.

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30
Q

what is the course of treatment for Pituitary Giant

A

*treatment usually surgical removal of tumour
*alternatively can be treated with somatostatin-like drugs (inhibit GH release)

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31
Q

what is the causes Acromegaly

A

excess GH after epiphyseal plate closure caused by a benign, slow growing, GH-secreting anterior pituitary tumour

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32
Q

symptoms/features of acromegaly

A

*thickening of bones in hands, feet and head
(particularly the jaw)
*increased size of other soft tissues (e.g. heart) may
impair physiological function

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33
Q

what is the course of treatment for Acromegaly

A

*treatment usually surgical removal of tumour
*alternatively can be treated with somatostatin-like
drugs (inhibit GH release)

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34
Q

name the thyroid hormone disorders

A

hyperthyroidism vs hypothyroidism
- goiter

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35
Q

what type of hormone is the thyroid hormone

A

anterior pituitary hormone

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36
Q

describe thyroid gland a bit and where is it

A

bi lobed, 15-20g large gland at the base of throat

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37
Q

what is the thyroid gland made up of, name the 2 cell types and their function

A

2 endocrine cell types
follicular cells-secrete THs
clear (C) cells-secrete calcitonin

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38
Q

how the cells arranged within the thyroid gland

A

arranged in follicles
enclosed spherical structure
lined by follicular cells

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39
Q

what do the cells contain within the thyroid gland

A

contains colloid → sticky,
glycoprotein-rich matrix

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40
Q

where does TH synthesised from

A

tyrosine

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41
Q

is TH soluble in plasma and what are the implications

A

no it is not as it is lipophilic, hence require plasma binding proteins → thyroid-binding globulin (TBG

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42
Q

what is the half life of TH

A

T4 ~ 6 days; T3 ~ 1 day

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43
Q

how is T4 converted to T3

A

T4 converted to T3 in target tissue by tissue deiodinase (peripheral deiodination)

44
Q

where does T4 usually form

A

in plasma

45
Q

where are receptors for TH

A

receptors are intracellular, located in nuclei of most cells

46
Q

how is the TH pieced together

A

remain attached to
thyroglobulin backbone

47
Q

how is TH released and regulated

A

tonic release through hypothalamus- anterior pituitary-thyroid gland
through neg. feedback

48
Q

what is hyperthyroidism caused by

A

Tumour, nodules, too much

49
Q

symptoms of hyperthyroidsm

A

increased metabolic rate and heat production
→heat intolerance/weight loss
increased protein catabolism
→muscle weakness/weight loss
altered nervous system function
→hyperexcitable reflexes and psychological disturbances
elevated cardiovascular function
→increased heart rate/contractile force

50
Q

causes of hyperthyroidism

A

*hormone-secreting thyroid
tumour (rare) or nodules
*Graves’ disease (antibodies
produced that bind and activate the thyroid gland

51
Q

treatment for hyperthyroidism

A

*surgical removal of part of gland
*radioactive iodine treatment (destroys TH-producing follicular cells)
*thyrostatics (block TH synthesis)
*propylthiouracil (blocks T4 → T3)

52
Q

how to identify Thyroid Hormone Dysfunction - Goiter

A

significant enlargement
of the thyroid gland
*a mass such as this is termed a goiter

53
Q

how are goiters formed

A

goiter formation is caused by trophic action of TSH on
thyroid follicular cells
→results in hypertrophy (overgrowth) of thyroid gland

54
Q

causes of Hypothyroidism

A

deficiency in dietary iodine
*autoimmune attack of thyroid gland

55
Q

Hypothyroidism treatment

A

*oral thyroxine (T4)
*dietary iodine supplements e.g.
iodized salt

56
Q

key symptoms/features of Hypothyroidism

A

decreased metabolic rate and heat production
→cold intolerance/weight gain
disrupted protein synthesis
→brittle nails/thin skin
altered nervous system function
→slow speech/reflexes, fatigue
reduced cardiovascular function
→ slow heart rate/weaker pulse

57
Q

what are TSIs and what is their function

A

TSIs- trophic so stimulate thyroid overgrowth
Thyroid stimulating immunoglobulins (TSIs) mimic actions of TSH by binding it’s receptors and stimulating thyroid gland
causes Graves’ disease

58
Q

what is exophthalmia

A

immune-mediated
enlargement of eye muscles/tissues

59
Q

function of the adrenal medulla

A

rapid stress response – “fight or flight
electrolyte balance
minor role in development of sexual characteristics

60
Q

identify the 3 layers of adrenal cortex

A

➢glucocorticoids (cortisol)
➢adrenal androgens (low affinity)
➢mineralocorticoids (e.g. aldosterone) → renin-angiotensin release system

61
Q

function of adrenal cortex

A

layers and steroid biosynthesis

62
Q

what is hypercortisolism also known as

A

also known as Cushing’s syndrome

63
Q

hypocortisolism causes and alternative name

A

adrenal insufficiency/Addison’s disease

64
Q

what is the adrenal gland composed of

A

medulla and cortex

65
Q

key feature of medulla and cortex

A

medulla is neurohormonal and cortex is true endocrine

66
Q

where does the medulla arise from and what do they produce

A

arises from neural tissue
produces catecholamines (adrenaline)
~ ¼ of total mass

67
Q

where does the cortex arise from and what do they produce

A

arises from non-neural tissue
produces steroid hormones
cortisol, aldosterone and androgens
~ ¾ of total mass

68
Q

physiological effects of fight or flight response in adrenal medulla

A

→ glycogen breakdown
rapid glucose source
→ fat breakdown
more energy available
→ increased cardiac function
→ increased ventilation
all support/maintain physical activity

69
Q

composition of adrenal cortex

A

divided into 3 histological sections which produce distinct types of
steroid hormones
*not entirely exclusive, some cross over exists

70
Q

adrenal cortex : where are all steroid hormones synthesised from

A

*steroid hormones all synthesised from cholesterol via complex biosynthetic
pathway

71
Q

what does Steroid biosynthesis in the adrenal gland mean and involve

A

biosynthesis involves complex chemical modifications to cholesterol

72
Q

what are the 3 layers of the adrenal cortex and what type of hormones are in each

A

Zona glomerulosa: outside: Adrogens and sex hormones
Zona fasciculata: cortisol
Zona reticularis: inside : aldosterone

73
Q

what are Glucocorticoids

A

group of steroid hormones

74
Q

what is a primary Glucocorticoids

A

cortisol is the primary glucocorticoid and is vital for survival

75
Q

function of Glucocorticoids

A

strong diurnal rhythm of secretion → inducible in response to stress

76
Q

what does cortisol (Glucocorticoids) production show

A

cortisol production shows a circadian pattern
patterns change in
response to physical
and psychological
stress

77
Q

what does ACTH bind to and to relase what effect

A

ACTH binds membrane-bound receptors on cells of Zona fasciculata in the adrenal cortex
increases conversion of cholesterol→ cortisol

78
Q

what is cortisol used for

A

critical, long-term mediator of stress response
→ adrenalectomized animals die in response to stress
*protects against hypoglycemia (opposes insulin) and has both catabolic and
anabolic actions

79
Q

which is faster cortisol response or catecholamine stress response

A

cortisol actions much slower (60-90 mins) than catecholamine stress response (secs)

80
Q

metabolic functions of cortisol

A

1.stimulates gluconeogenesis
2.breaks down fat and uses fatty acids/breaks down protein into amino acids for use as energy sources
3.maintains plasma glucose levels and prevents hypoglycemia
4.mobilises energy to cope with, adapt to or escape stress

81
Q

Metabolic Functions of Cortisol: what does stimulates gluconeogenesis allow for

A

protects carbohydrate stores (glycogen) – eye on the long term
- can build-up or breakdown glycogen stores depending on stress levels

82
Q

Metabolic Functions of Cortisol: what does breaks down fat and uses fatty acids as energy source allow for

A

alternative to glucose

83
Q

Metabolic Functions of Cortisol: what does breaks down protein into amino acids for use as an energy source allow for

A

another alternative to glucose
- these amino acids are also used for gluconeogenesis

84
Q

function of cortisol in other systems :Brain function

A

mood regulation
learning and memory

85
Q

function of cortisol in other systems : Development

A

important for proper develop

86
Q

function of cortisol in other systems : how does the system comprise others to allow stress response

A

Other
reduces “non-essential” function
e.g. growth, reproduction
in favour of responding to stress

87
Q

function of cortisol in other systems: Suppresses inflammatory &
immune response

A

prevents harmful over-reaction

88
Q

what other systems does cortisol impact

A

brain, development, immune system

89
Q

what are the function of low affinity androgens

A

converted to testosterone or estrogen
from low activity to more potent sex steroids in other tissues

90
Q

Adrenal Androgens: function of estrogen and testosterone

A

development/maintenance of male/female sexual/reproductive characteristics

91
Q

Mineralocorticoids function

A

regulate minerals e.g. Na+ and K
by alter gene expression → increased expression of Na+ transporter proteins
*thereby influences levels of Na+ (and water) reabsorbed by the kidney

92
Q

example of mineralocorticoids and Glucocorticoids

A

M: aldosterone
G: cortisol

93
Q

describe mineralocorticoid receptors compared to adrenal androgens and Glucocorticoid receptors (cortisol )

A

G: membrane bound steroid recepors
A: low activity of androgens at receptors
M: steroid receptors (intracellular)

chexck later

94
Q

what is the aldosterone release controlled by

A
95
Q

aldosterone release: where is the renin released from and what is it stimulated by

A

from kidney cell
decrease blood volume (haemorrhage, dehydration)
▪ increase Na+ levels
→ detected by specialised sensor cells in kidney

96
Q

aldosterone release: what does the renin release result in

A

results in angiotensin II production
→ binds receptors on surface of zona glomerulosa cells
→ activates biosynthesis of aldosterone

97
Q

3 key Hypercortisolism causes

A

1.Primary hypercortisolism
2. Secondary hypercortisolism
3. Iatrogenic (physician-caused) hypercortisolism

98
Q

Hypercortisolism causes: Secondary hypercortisolism

A

excessive ACTH (trophic hormone) production
pituitary tumour that secretes ACTH and stimulates too much cortisol

99
Q

Hypercortisolism causes: PRIMARY hypercortisolism

A

adrenal glands (TUMOUR)
produces too much cortisol

100
Q

Hypercortisolism causes: Iatrogenic (physician-caused) hypercortisolism

A
  • occurs following glucocorticoid therapy for other conditions
  • glucocorticoids are commonly used topical and systemic anti-inflammatory drugs
101
Q

hypercortisolism treatment

A

surgical removal of tumour
* removal of glucocorticoid therapy – must be gradual to allow axis to adapt

102
Q

what happens biologically during Hypercortisolism (Cushing’s syndrome)

A

diabetagenic (hyperglycemia) → too much glucose in blood
* tissue wasting → muscle, fat and bone breakdown (breakdown of proteins/fat

103
Q

key symptoms of hypercortisolism

A

“plumping” of trunk and “moon face” → redistribution of fat
*mood disorder/immunosuppression/impaired inflammatory cascade

104
Q

name 2 key causes of Hypocortisolism

A

1.primary adrenal insufficiency (at level of adrenal gland
2.Secondary adrenal insufficiency (at level of anterior pituitary trophic hormone)

105
Q

causes of Hypocortisolism: primary adrenal insufficiency

A

loss of adrenal cortical function (up to 90% loss before symptoms apparent)
* can be caused by tuberculosis, invasive tumours, autoimmune attack, genetic disease
* sufferers at severe risk of “Addison’s crisis” following minor stress/illness
→ no cortisol → profound hypoglycemia → potentially fatal

106
Q

causes of Hypocortisolism: secondary adrenal insufficiency

A

pituitary disease → ACTH deficiency
* symptoms less dramatic – aldosterone not affected (not dependent on ACTH)

107
Q

treatment for Hypocortisolism

A

daily oral administration of glucocorticoids and mineralocorticoids
* careful dietary/fluid management
* treatment of causative disorder

physiology (10 decks)

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