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physiology > Hormones 3 & 4 > Flashcards

Hormones 3 & 4 Flashcards

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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
name the GH disorders
pituitary dwarfism, pituitary giant (gigantism), acromegaly
26
what causes Pituitary Dwarfism
childhood deficiency in GH, due to production/receptor problem
27
what is the course of treatment for Pituitary Dwarfism
treated using genetically engineered hGH
28
what are the limitations when treating Pituitary Dwarfism
*limited treatment window (before epiphyseal plate closes)
29
what is the causes Pituitary Giant
childhood excess of GH caused by a benign, slow growing, GH-secreting anterior pituitary tumour extensive growth of long bones – excessive height.
30
what is the course of treatment for Pituitary Giant
*treatment usually surgical removal of tumour *alternatively can be treated with somatostatin-like drugs (inhibit GH release)
31
what is the causes Acromegaly
excess GH after epiphyseal plate closure caused by a benign, slow growing, GH-secreting anterior pituitary tumour
32
symptoms/features of acromegaly
*thickening of bones in hands, feet and head (particularly the jaw) *increased size of other soft tissues (e.g. heart) may impair physiological function
33
what is the course of treatment for Acromegaly
*treatment usually surgical removal of tumour *alternatively can be treated with somatostatin-like drugs (inhibit GH release)
34
name the thyroid hormone disorders
hyperthyroidism vs hypothyroidism - goiter
35
what type of hormone is the thyroid hormone
anterior pituitary hormone
36
describe thyroid gland a bit and where is it
bi lobed, 15-20g large gland at the base of throat
37
what is the thyroid gland made up of, name the 2 cell types and their function
2 endocrine cell types follicular cells-secrete THs clear (C) cells-secrete calcitonin
38
how the cells arranged within the thyroid gland
arranged in follicles enclosed spherical structure lined by follicular cells
39
what do the cells contain within the thyroid gland
contains colloid → sticky, glycoprotein-rich matrix
40
where does TH synthesised from
tyrosine
41
is TH soluble in plasma and what are the implications
no it is not as it is lipophilic, hence require plasma binding proteins → thyroid-binding globulin (TBG
42
what is the half life of TH
T4 ~ 6 days; T3 ~ 1 day
43
how is T4 converted to T3
T4 converted to T3 in target tissue by tissue deiodinase (peripheral deiodination)
44
where does T4 usually form
in plasma
45
where are receptors for TH
receptors are intracellular, located in nuclei of most cells
46
how is the TH pieced together
remain attached to thyroglobulin backbone
47
how is TH released and regulated
tonic release through hypothalamus- anterior pituitary-thyroid gland through neg. feedback
48
what is hyperthyroidism caused by
Tumour, nodules, too much
49
symptoms of hyperthyroidsm
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
causes of hyperthyroidism
*hormone-secreting thyroid tumour (rare) or nodules *Graves’ disease (antibodies produced that bind and activate the thyroid gland
51
treatment for hyperthyroidism
*surgical removal of part of gland *radioactive iodine treatment (destroys TH-producing follicular cells) *thyrostatics (block TH synthesis) *propylthiouracil (blocks T4 → T3)
52
how to identify Thyroid Hormone Dysfunction - Goiter
significant enlargement of the thyroid gland *a mass such as this is termed a goiter
53
how are goiters formed
goiter formation is caused by trophic action of TSH on thyroid follicular cells →results in hypertrophy (overgrowth) of thyroid gland
54
causes of Hypothyroidism
deficiency in dietary iodine *autoimmune attack of thyroid gland
55
Hypothyroidism treatment
*oral thyroxine (T4) *dietary iodine supplements e.g. iodized salt
56
key symptoms/features of Hypothyroidism
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
what are TSIs and what is their function
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
what is exophthalmia
immune-mediated enlargement of eye muscles/tissues
59
function of the adrenal medulla
rapid stress response – “fight or flight electrolyte balance minor role in development of sexual characteristics
60
identify the 3 layers of adrenal cortex
➢glucocorticoids (cortisol) ➢adrenal androgens (low affinity) ➢mineralocorticoids (e.g. aldosterone) → renin-angiotensin release system
61
function of adrenal cortex
layers and steroid biosynthesis
62
what is hypercortisolism also known as
also known as Cushing’s syndrome
63
hypocortisolism causes and alternative name
adrenal insufficiency/Addison’s disease
64
what is the adrenal gland composed of
medulla and cortex
65
key feature of medulla and cortex
medulla is neurohormonal and cortex is true endocrine
66
where does the medulla arise from and what do they produce
arises from neural tissue produces catecholamines (adrenaline) ~ ¼ of total mass
67
where does the cortex arise from and what do they produce
arises from non-neural tissue produces steroid hormones cortisol, aldosterone and androgens ~ ¾ of total mass
68
physiological effects of fight or flight response in adrenal medulla
→ glycogen breakdown rapid glucose source → fat breakdown more energy available → increased cardiac function → increased ventilation all support/maintain physical activity
69
composition of adrenal cortex
divided into 3 histological sections which produce distinct types of steroid hormones *not entirely exclusive, some cross over exists
70
adrenal cortex : where are all steroid hormones synthesised from
*steroid hormones all synthesised from cholesterol via complex biosynthetic pathway
71
what does Steroid biosynthesis in the adrenal gland mean and involve
biosynthesis involves complex chemical modifications to cholesterol
72
what are the 3 layers of the adrenal cortex and what type of hormones are in each
Zona glomerulosa: outside: Adrogens and sex hormones Zona fasciculata: cortisol Zona reticularis: inside : aldosterone
73
what are Glucocorticoids
group of steroid hormones
74
what is a primary Glucocorticoids
cortisol is the primary glucocorticoid and is vital for survival
75
function of Glucocorticoids
strong diurnal rhythm of secretion → inducible in response to stress
76
what does cortisol (Glucocorticoids) production show
cortisol production shows a circadian pattern patterns change in response to physical and psychological stress
77
what does ACTH bind to and to relase what effect
ACTH binds membrane-bound receptors on cells of Zona fasciculata in the adrenal cortex increases conversion of cholesterol→ cortisol
78
what is cortisol used for
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
which is faster cortisol response or catecholamine stress response
cortisol actions much slower (60-90 mins) than catecholamine stress response (secs)
80
metabolic functions of cortisol
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
Metabolic Functions of Cortisol: what does stimulates gluconeogenesis allow for
protects carbohydrate stores (glycogen) – eye on the long term - can build-up or breakdown glycogen stores depending on stress levels
82
Metabolic Functions of Cortisol: what does breaks down fat and uses fatty acids as energy source allow for
alternative to glucose
83
Metabolic Functions of Cortisol: what does breaks down protein into amino acids for use as an energy source allow for
another alternative to glucose - these amino acids are also used for gluconeogenesis
84
function of cortisol in other systems :Brain function
mood regulation learning and memory
85
function of cortisol in other systems : Development
important for proper develop
86
function of cortisol in other systems : how does the system comprise others to allow stress response
Other reduces “non-essential” function e.g. growth, reproduction in favour of responding to stress
87
function of cortisol in other systems: Suppresses inflammatory & immune response
prevents harmful over-reaction
88
what other systems does cortisol impact
brain, development, immune system
89
what are the function of low affinity androgens
converted to testosterone or estrogen from low activity to more potent sex steroids in other tissues
90
Adrenal Androgens: function of estrogen and testosterone
development/maintenance of male/female sexual/reproductive characteristics
91
Mineralocorticoids function
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
example of mineralocorticoids and Glucocorticoids
M: aldosterone G: cortisol
93
describe mineralocorticoid receptors compared to adrenal androgens and Glucocorticoid receptors (cortisol )
G: membrane bound steroid recepors A: low activity of androgens at receptors M: steroid receptors (intracellular) chexck later
94
what is the aldosterone release controlled by
95
aldosterone release: where is the renin released from and what is it stimulated by
from kidney cell decrease blood volume (haemorrhage, dehydration) ▪ increase Na+ levels → detected by specialised sensor cells in kidney
96
aldosterone release: what does the renin release result in
results in angiotensin II production → binds receptors on surface of zona glomerulosa cells → activates biosynthesis of aldosterone
97
3 key Hypercortisolism causes
1.Primary hypercortisolism 2. Secondary hypercortisolism 3. Iatrogenic (physician-caused) hypercortisolism
98
Hypercortisolism causes: Secondary hypercortisolism
excessive ACTH (trophic hormone) production pituitary tumour that secretes ACTH and stimulates too much cortisol
99
Hypercortisolism causes: PRIMARY hypercortisolism
adrenal glands (TUMOUR) produces too much cortisol
100
Hypercortisolism causes: Iatrogenic (physician-caused) hypercortisolism
* occurs following glucocorticoid therapy for other conditions * glucocorticoids are commonly used topical and systemic anti-inflammatory drugs
101
hypercortisolism treatment
surgical removal of tumour * removal of glucocorticoid therapy – must be gradual to allow axis to adapt
102
what happens biologically during Hypercortisolism (Cushing’s syndrome)
diabetagenic (hyperglycemia) → too much glucose in blood * tissue wasting → muscle, fat and bone breakdown (breakdown of proteins/fat
103
key symptoms of hypercortisolism
“plumping” of trunk and “moon face” → redistribution of fat *mood disorder/immunosuppression/impaired inflammatory cascade
104
name 2 key causes of Hypocortisolism
1.primary adrenal insufficiency (at level of adrenal gland 2.Secondary adrenal insufficiency (at level of anterior pituitary trophic hormone)
105
causes of Hypocortisolism: primary adrenal insufficiency
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
causes of Hypocortisolism: secondary adrenal insufficiency
pituitary disease → ACTH deficiency * symptoms less dramatic – aldosterone not affected (not dependent on ACTH)
107
treatment for Hypocortisolism
daily oral administration of glucocorticoids and mineralocorticoids * careful dietary/fluid management * treatment of causative disorder

physiology (10 decks)

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