hormones, vadrenal/thyroid Flashcards
where are chemical messengers synthesised/released
endocrine glands
some facts about hormones
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
where are hormones metabolised
liver, kidney, blood
two categories of the endocrine system
primary endocrine organs, secondary endocrine organs
main function of primary endocrine organs
secrete hormones
name organs part of the secondary endocrine organs
heart, liver, kidney, skin, intestine
what does the neuroendocrine system do
balancing/adjusting hormone levels to control normal functions in the body
name the 3 hypothalamic pituitary axis (master regulators)
thyroid, adrenal cortex, gonads
name 3 types of functional hormones and describe them
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
what are endocrine glands and name 3
ductless glands, secrete hormones into interstitial fluid, diffuse into nearby blood vessels
pituitary, adrenal, thyroid glands
what do exocrine glands do and name 2
secrete product into associated duct
sweat and salivary gland
name different molecular types of hormones
peptide, steroid, amine, eicosanoid
what is autocrine signalling
bind receptors on the same cell
what is paracrine signalling
targets neighbouring cells
what is endocrine signalling
targets distant cells via bloodstream
what is neuroendocrine signalling
neuron targets distant cells via bloodstream
what are agonists
ligands that bind to a receptor and induce a response, full or partial activity, often conformational changes
what is an antagonist
ligands that bind to a receptor but dont induce a response, can compete with agonist to block or reduce activation
what are inverse agonists
binds to receptors and induce opposite response
properties of hormones
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
how are peptide hormones transported in blood
hydrophilic, free/unbound in circulation, half life in serum is minutes
how are steroid and thyroid hormones transported in blood
hydrophobic, mostly bound to carrier proteins in blood plasma, protected by carriers, half life is hours/days
synthesis/storage/release of peptide hormones
preprohormone–> prohormone–> active hormone–> storage granules–> exocytosis in response to a signal (eg. ca+)
name 2 rhythmic hormones
cortisol and melatonin
what can cause hormone levels in blood to fluctuate
food, light, activity, circadian rhythms
signals that show endocrine failure/disorder
hormone excess- hypersecretion, hyperfunction
hormone deficit- hyposecretion, hypofunction
hormone resistant- target cells dont respond to hormone
what is a primary endocrine disorder and give example
problem in secreting gland
peripheral endocrine glands
what is a secondary endocrine disorder and give example
under/over stimulation by tropic hormones
pituitary abnormalities
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
what are iatrogenic effects caused by
medical/therapeutic/diagnostic interventions eg. radiation, chemotherapy, surgery, ischaemia, prescription medicines
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)
how can an autoimmune disease cause hypersecretions
antibodies attack endocrine cells, bursts, releases hormones in bloodstream
how can an autoimmune stimulation cause hypersecretions
antibodies in circulation start behaving like hormones
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
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
treatments for hypofunction endocrine disorders
hormone replacement therapy- agonist for hormone receptor
treat with prohormone
tropic hormone
treat to manage physiological symptoms
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
what is hashimoto’s thyroiditis
primary disease that affects thyroid gland, chronic autoimmune disease, autoantibodies produced against thyroglobulin and thyroperoxidase,
causes of hashimotos thyroiditis
post partum thyroiditis, radiation therapy, drug induced, viral associated
what does hypothyroidism mean
underactive thyroid
example of hypothyroidism
hashimotos disease
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
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
what is hyperthyroidism
over active thyroid
what is TSH
thyroid stimulating hormone
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
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
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
therapies for hypothyroidism
standard treatment, life long therapy
therapies for hyperthyroidism
treat symptoms with beta blockers (tremors/anxiety/palpitations), hormone therapy, radioactive iodide, surgery if lump obstructs breathing/eating
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
what do mineralocorticoids do
control electrolyte and fluid balance, important in maintaining blood pressure
what do glucocorticoids do
immune respones, metabolism, development, anti-inflammatory action
what do androgens do
sex hormones, reproduction, sex drive, activates androgen receptor
what do catecholamines do
fight or flight, increase heart rate, energy metabolism
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
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
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
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
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
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)
treatments of cushin’s disease
scan/locate tumour
surgery-radiotherapy
chemotherapy
what is used to scan and locate each tumour
anterior pituitary- MRI
adrenal- MRI/CT
ectopic- chest xray
effects of low aldosterone
poor regulation of sodium and potassium ions in blood, affects heart, kidneys and circulation
what is primary adrenal insufficiency and causes
destruction of gland (addisons disease) causes: autoimmune, infection, hemhorrhage, metastasis
secondary adrenal insuffieciency
inadequate CRH production in hypothalamus and inadequate ACTH production in pituitary
what is addison’s disease
primary hypoadrenalism, hyposecretion of cortisol and aldosterone, chronic autoimmune disease (antibodies destroy adrenal cortex)
what does ACTH do
regulate glucocorticoids
what does cortisol do
regulate blood pressure/sugar, immune system, response to stress
where is cortisol released
adrenal glands
treatments for addison’s disease
glucocorticoids (hydrocotisone)
mineralocorticoids
what causes addison’s disease
antibodies destroy the adrenal cortex
symptoms of addison’s disease
fatigue, weight loss, anorexia, postural hypotension, skin pigmentation, frequent urination, thirst, salt cravings, depression, dehydration
what happens if addison’s disease is left untreated
adrenal crisis, coma, death
what is adrenal crisis
adrenal glands dont produce enough cortisol
