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Endocrine and metabolism > hormones, vadrenal/thyroid > Flashcards

hormones, vadrenal/thyroid Flashcards

1
Q

where are chemical messengers synthesised/released

A

endocrine glands

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2
Q

some facts about hormones

A

hormones diffuse into bloodstream, travels to tissue to give an effect, target tissues have receptors that bind to hormone, receptors can be on membrane or intracellular, slow acting, longer more sustained effects, most hormones metabolised by enzymes in liver, kidney, blood, excreted in urine/faeces

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3
Q

where are hormones metabolised

A

liver, kidney, blood

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4
Q

two categories of the endocrine system

A

primary endocrine organs, secondary endocrine organs

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5
Q

main function of primary endocrine organs

A

secrete hormones

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6
Q

name organs part of the secondary endocrine organs

A

heart, liver, kidney, skin, intestine

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7
Q

what does the neuroendocrine system do

A

balancing/adjusting hormone levels to control normal functions in the body

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8
Q

name the 3 hypothalamic pituitary axis (master regulators)

A

thyroid, adrenal cortex, gonads

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9
Q

name 3 types of functional hormones and describe them

A

releasing hormone- produced by hypothalamus to act on pituitary

tropic/stimulating hormone- produced by pituitary to act on other endocrine glands

non-tropic hormones- produced by endocrine glands to act on target tissue

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10
Q

what are endocrine glands and name 3

A

ductless glands, secrete hormones into interstitial fluid, diffuse into nearby blood vessels

pituitary, adrenal, thyroid glands

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11
Q

what do exocrine glands do and name 2

A

secrete product into associated duct

sweat and salivary gland

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12
Q

name different molecular types of hormones

A

peptide, steroid, amine, eicosanoid

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13
Q

what is autocrine signalling

A

bind receptors on the same cell

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14
Q

what is paracrine signalling

A

targets neighbouring cells

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15
Q

what is endocrine signalling

A

targets distant cells via bloodstream

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16
Q

what is neuroendocrine signalling

A

neuron targets distant cells via bloodstream

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17
Q

what are agonists

A

ligands that bind to a receptor and induce a response, full or partial activity, often conformational changes

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18
Q

what is an antagonist

A

ligands that bind to a receptor but dont induce a response, can compete with agonist to block or reduce activation

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19
Q

what are inverse agonists

A

binds to receptors and induce opposite response

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20
Q

properties of hormones

A

lipophilic- diffuse across membrane to bind to intracellular receptor, eg steroid and thyroid hormones

lipophobic- binds to receptors on cell surface, eg peptides, catecholamines, eicosanoids

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21
Q

how are peptide hormones transported in blood

A

hydrophilic, free/unbound in circulation, half life in serum is minutes

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22
Q

how are steroid and thyroid hormones transported in blood

A

hydrophobic, mostly bound to carrier proteins in blood plasma, protected by carriers, half life is hours/days

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23
Q

synthesis/storage/release of peptide hormones

A

preprohormone–> prohormone–> active hormone–> storage granules–> exocytosis in response to a signal (eg. ca+)

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24
Q

name 2 rhythmic hormones

A

cortisol and melatonin

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25
what can cause hormone levels in blood to fluctuate
food, light, activity, circadian rhythms
26
signals that show endocrine failure/disorder
hormone excess- hypersecretion, hyperfunction hormone deficit- hyposecretion, hypofunction hormone resistant- target cells dont respond to hormone
27
what is a primary endocrine disorder and give example
problem in secreting gland peripheral endocrine glands
28
what is a secondary endocrine disorder and give example
under/over stimulation by tropic hormones pituitary abnormalities
29
etiology/causes of endocrine disorders (hyposecretions/underactivity)
congenital absence or malformation of endocrine tissue, failure of endocrine tissue due to injury/disease, tissue resistant in target cells, loss/faulty receptors, surgical removal of endocrine tissue/other iatrogenic effects
30
what are iatrogenic effects caused by
medical/therapeutic/diagnostic interventions eg. radiation, chemotherapy, surgery, ischaemia, prescription medicines
31
causes of endocrine disorders (hypersecretions/overactivity)
tumour in primary/secondary endocrine tissue affecting hormone production/release, excessive stimulation of gland by tropic hormones, autoimmune disease (antibodies attack endocrine cell and burst and releases hormone into blood stream), autoimmune stimulation (antibodies circulation start behaving like hormones)
32
how can an autoimmune disease cause hypersecretions
antibodies attack endocrine cells, bursts, releases hormones in bloodstream
33
how can an autoimmune stimulation cause hypersecretions
antibodies in circulation start behaving like hormones
34
how to diagnose primary and secondary endocrine disorders
stimulation test- if hyposecretion suspected suppression test- if hypersecretion suspected (too high=suppress it) measure hormone levels in serum/urine/saliva using immunoassays and bioassays
35
treatment for hyperfunction endocrine disorders
remove gland- leads to hypofunction, needs lifelong hormone replacement therapy treat with antihormone therapies- eg. antagonist drugs block synthesis/release of tropic hormone block synthesis of hormone in endocrine gland
36
treatments for hypofunction endocrine disorders
hormone replacement therapy- agonist for hormone receptor treat with prohormone tropic hormone treat to manage physiological symptoms
37
what is thyroid hormone disorder
iodine deficiency, lump in neck, no feedback inhibition of TSH, no T3/4 produced, could be due to diet or geographical location, in foetus causes growth/mental retardation and blindess
38
what is hashimoto's thyroiditis
primary disease that affects thyroid gland, chronic autoimmune disease, autoantibodies produced against thyroglobulin and thyroperoxidase,
39
causes of hashimotos thyroiditis
post partum thyroiditis, radiation therapy, drug induced, viral associated
40
what does hypothyroidism mean
underactive thyroid
41
example of hypothyroidism
hashimotos disease
42
clinical symptoms of hypothyroidism
decreased basal metabolic rate, fatigue, weakness, mild weight gain, bradycardia, cold dry skin, enlarged thyroid, loss of eyebrow, depression, menstrual irregularity
43
2 categories of hyperthyroidism
primary disease- 90% graves disease, chronic autoimmune disease, B cells make autoantibodies against TSH receptors, antibodies activate TSH receptors in follicles to produce T3/4 secondary disease- overproduction of TSH by pituitary due to tumour, adenoma tumour developing from epithelial cells from glandular tissue
44
what is hyperthyroidism
over active thyroid
45
what is TSH
thyroid stimulating hormone
46
clinical symptoms of hyperthyroidism
increased basal metabolic rate, increased appetite, weight loss, insomnia, heat intolerance, palpitations, sweating, tremors, enlarged thyroid, irritability, irregular menstrual, exopthalmos (bulging eyes), diarrhoea, low serum cholesterol and triglycerides
47
what is graves disease/exopthalmos
immune damage to back of eyes, inflammation and swelling, build up of deposits and fluid, protrusion of eyes out of their orbits, double vision
48
come pare a normal thyroid with one with graves disease
normal- TSH binds receptors on follicular cell and T3/4 is released, feedback inhibition of TSH pituitary graves- antibody binds receptors on follicular cell, T3/4 released, feed back inhibition of TSH but antibodies continue to hyperstimulate
49
therapies for hypothyroidism
standard treatment, life long therapy
50
therapies for hyperthyroidism
treat symptoms with beta blockers (tremors/anxiety/palpitations), hormone therapy, radioactive iodide, surgery if lump obstructs breathing/eating
51
name and describe the two layers of the adrenal gland
adrenal cortex- steroid hormones, glucocorticoids, mineralocorticoids, androgens adrenal medulla- L-tyrosine derivatives, epinephrine, dopamine, catecholamines
52
what do mineralocorticoids do
control electrolyte and fluid balance, important in maintaining blood pressure
53
what do glucocorticoids do
immune respones, metabolism, development, anti-inflammatory action
54
what do androgens do
sex hormones, reproduction, sex drive, activates androgen receptor
55
what do catecholamines do
fight or flight, increase heart rate, energy metabolism
56
how do catecholamine hormones create a fight or flight response
CNS neurons innervate the adrenal medulla, alarm signals from hypothalamus causes release of neurotransmitters that activate chromaffin cells, triggers release of epinephrine, cytokines from blood stream can also induce release of neurohormones, epinephrine binds to adrenergic receptors and activates GPCRs
57
fight or flight physiological responses
increased heart rate/breathing, increased blood flow to heart/lungs/large skeletal muscle, reduced blood flow to prefrontal cortex (decision making, rationale thought), increased flow to amygdala, glycogenolysis, lipolysis, thermogenesis in brown adipose tissue and muscle
58
adrenocortical disorders (adrenal cortex)
hypo/hypersecretion of mineralocorticoids- aldosterone regulates salt balance in kidneys hypo/hypersecretion of glucocorticoids- cortisol has opposing action to insulin hypo/hypersecretion of androgens- sex hormone associated with male characteristics
59
adrenal gland disorders
cushing's syndrome- excess cortisol, can result from long term steroid medication, low ACTH high cortisol cushing's disease- pituitary tumour producing ACTH, high cortisol low ACTH, high both in secondary pituitary/ectopic tumour
60
difference between primary and secondary tumour in cushing's disease
primary- produces cortisol and inhibits ACTH secondary- (pituitary and ectopic), produces ACTH and stimulates cortisol
61
symptoms of cushing's syndrome/disease
fat redistribution from limbs to abdomen, frontal balding, acne, menstrual irregularities, protein breakdown, muscle weakness, thin arms and legs, collagen loss, immune suppression, thin skin, bruising, infections, cognitive impairment, depression, sleep disturbance, hypertension, diabetes (trolls bridget body shape type beat)
62
treatments of cushin's disease
scan/locate tumour surgery-radiotherapy chemotherapy
63
what is used to scan and locate each tumour
anterior pituitary- MRI adrenal- MRI/CT ectopic- chest xray
64
effects of low aldosterone
poor regulation of sodium and potassium ions in blood, affects heart, kidneys and circulation
65
what is primary adrenal insufficiency and causes
destruction of gland (addisons disease) causes: autoimmune, infection, hemhorrhage, metastasis
66
secondary adrenal insuffieciency
inadequate CRH production in hypothalamus and inadequate ACTH production in pituitary
66
what is addison's disease
primary hypoadrenalism, hyposecretion of cortisol and aldosterone, chronic autoimmune disease (antibodies destroy adrenal cortex)
67
what does ACTH do
regulate glucocorticoids
67
what does cortisol do
regulate blood pressure/sugar, immune system, response to stress
67
where is cortisol released
adrenal glands
68
treatments for addison's disease
glucocorticoids (hydrocotisone) mineralocorticoids
68
what causes addison's disease
antibodies destroy the adrenal cortex
69
symptoms of addison's disease
fatigue, weight loss, anorexia, postural hypotension, skin pigmentation, frequent urination, thirst, salt cravings, depression, dehydration
70
what happens if addison's disease is left untreated
adrenal crisis, coma, death
71
what is adrenal crisis
adrenal glands dont produce enough cortisol

Endocrine and metabolism (12 decks)

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