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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
Q

what can cause hormone levels in blood to fluctuate

A

food, light, activity, circadian rhythms

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26
Q

signals that show endocrine failure/disorder

A

hormone excess- hypersecretion, hyperfunction

hormone deficit- hyposecretion, hypofunction

hormone resistant- target cells dont respond to hormone

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27
Q

what is a primary endocrine disorder and give example

A

problem in secreting gland

peripheral endocrine glands

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28
Q

what is a secondary endocrine disorder and give example

A

under/over stimulation by tropic hormones

pituitary abnormalities

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29
Q

etiology/causes of endocrine disorders (hyposecretions/underactivity)

A

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

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30
Q

what are iatrogenic effects caused by

A

medical/therapeutic/diagnostic interventions eg. radiation, chemotherapy, surgery, ischaemia, prescription medicines

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31
Q

causes of endocrine disorders (hypersecretions/overactivity)

A

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
Q

how can an autoimmune disease cause hypersecretions

A

antibodies attack endocrine cells, bursts, releases hormones in bloodstream

33
Q

how can an autoimmune stimulation cause hypersecretions

A

antibodies in circulation start behaving like hormones

34
Q

how to diagnose primary and secondary endocrine disorders

A

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
Q

treatment for hyperfunction endocrine disorders

A

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
Q

treatments for hypofunction endocrine disorders

A

hormone replacement therapy- agonist for hormone receptor

treat with prohormone

tropic hormone

treat to manage physiological symptoms

37
Q

what is thyroid hormone disorder

A

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
Q

what is hashimoto’s thyroiditis

A

primary disease that affects thyroid gland, chronic autoimmune disease, autoantibodies produced against thyroglobulin and thyroperoxidase,

39
Q

causes of hashimotos thyroiditis

A

post partum thyroiditis, radiation therapy, drug induced, viral associated

40
Q

what does hypothyroidism mean

A

underactive thyroid

41
Q

example of hypothyroidism

A

hashimotos disease

42
Q

clinical symptoms of hypothyroidism

A

decreased basal metabolic rate, fatigue, weakness, mild weight gain, bradycardia, cold dry skin, enlarged thyroid, loss of eyebrow, depression, menstrual irregularity

43
Q

2 categories of hyperthyroidism

A

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
Q

what is hyperthyroidism

A

over active thyroid

45
Q

what is TSH

A

thyroid stimulating hormone

46
Q

clinical symptoms of hyperthyroidism

A

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
Q

what is graves disease/exopthalmos

A

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
Q

come pare a normal thyroid with one with graves disease

A

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
Q

therapies for hypothyroidism

A

standard treatment, life long therapy

50
Q

therapies for hyperthyroidism

A

treat symptoms with beta blockers (tremors/anxiety/palpitations), hormone therapy, radioactive iodide, surgery if lump obstructs breathing/eating

51
Q

name and describe the two layers of the adrenal gland

A

adrenal cortex- steroid hormones, glucocorticoids, mineralocorticoids, androgens

adrenal medulla- L-tyrosine derivatives, epinephrine, dopamine, catecholamines

52
Q

what do mineralocorticoids do

A

control electrolyte and fluid balance, important in maintaining blood pressure

53
Q

what do glucocorticoids do

A

immune respones, metabolism, development, anti-inflammatory action

54
Q

what do androgens do

A

sex hormones, reproduction, sex drive, activates androgen receptor

55
Q

what do catecholamines do

A

fight or flight, increase heart rate, energy metabolism

56
Q

how do catecholamine hormones create a fight or flight response

A

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
Q

fight or flight physiological responses

A

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
Q

adrenocortical disorders (adrenal cortex)

A

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
Q

adrenal gland disorders

A

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
Q

difference between primary and secondary tumour in cushing’s disease

A

primary- produces cortisol and inhibits ACTH

secondary- (pituitary and ectopic), produces ACTH and stimulates cortisol

61
Q

symptoms of cushing’s syndrome/disease

A

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
Q

treatments of cushin’s disease

A

scan/locate tumour
surgery-radiotherapy
chemotherapy

63
Q

what is used to scan and locate each tumour

A

anterior pituitary- MRI
adrenal- MRI/CT
ectopic- chest xray

64
Q

effects of low aldosterone

A

poor regulation of sodium and potassium ions in blood, affects heart, kidneys and circulation

65
Q

what is primary adrenal insufficiency and causes

A

destruction of gland (addisons disease) causes: autoimmune, infection, hemhorrhage, metastasis

66
Q

secondary adrenal insuffieciency

A

inadequate CRH production in hypothalamus and inadequate ACTH production in pituitary

66
Q

what is addison’s disease

A

primary hypoadrenalism, hyposecretion of cortisol and aldosterone, chronic autoimmune disease (antibodies destroy adrenal cortex)

67
Q

what does ACTH do

A

regulate glucocorticoids

67
Q

what does cortisol do

A

regulate blood pressure/sugar, immune system, response to stress

67
Q

where is cortisol released

A

adrenal glands

68
Q

treatments for addison’s disease

A

glucocorticoids (hydrocotisone)
mineralocorticoids

68
Q

what causes addison’s disease

A

antibodies destroy the adrenal cortex

69
Q

symptoms of addison’s disease

A

fatigue, weight loss, anorexia, postural hypotension, skin pigmentation, frequent urination, thirst, salt cravings, depression, dehydration

70
Q

what happens if addison’s disease is left untreated

A

adrenal crisis, coma, death

71
Q

what is adrenal crisis

A

adrenal glands dont produce enough cortisol

Endocrine and metabolism (12 decks)

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