hormones Flashcards
What are organs that secrete a hormone into the blood called?
endocrine glands
What are the three types of hormone?
steroid hormones, peptide hormones, amino acid derived hormones
What is the mechanism of action of steroid hormones?
bind DNA/modify transcription
What is the mechanism of action of peptide hormones?
second messengers
What is the mechanism of action of peptide hormones?
second messengers
Where is the pituitary gland?
at the base of the brain, below the hypothalamus with the optic chiasm between
What are the two parts of the pituitary gland?
anterior lobe (pars distalis) and posterior lobe (pars nervosa)
What hormones does the posterior pituitary release?
oxytocin and vasopressin
What does oxytocin do?
controls milk release from lactating breast and controls uterine contractions at onset of labour
What does vasopressin do?
acts on kidney to reabsorb water
What does the interaction of oxytocin with its receptors do?
raises the level of intracellular calcium in the myoepithelial cells of the mammary gland
How many hormones does the anterior pituitary secrete?
six
Which hormones does the anterior pituitary secrete?
growth hormone, prolactin, ACTH, TSH, FSH, LH
What vessels are in the anterior pituitary?
portal vessels
What are the five different cell types for the hormones?
somatotrophs (growth hormone), lactotrophs (prolactin), corticotrops (ACTH), gonadotrophs (FSH, LH), thyrotrophs (TSH)
What controls the secretory activity of the anterior pituitary?
the hypothalamus
Where is growth hormone synthesised and stored?
somatotrophs
What are the principle targets of growth hormone?
targets bone and skeletal muscle
What does growth hormone do in children and adults?
stimulates growth in children and adolescents but continues to exert important effects throughout adult life
What are direct effects of growth hormone on muscle?
decreases glucose uptake, stimulates amino acid uptake/protein synthesis, inhibits protein breakdown = increased muscle mass
What are the direct effects of growth hormone on adipose tissue?
decreases glucose uptake, increases lipolysis = decrease in fat deposits
What are the direct effects of growth hormone on liver?
increases gluconeogenesis, increases protein synthesis = stimulates IGF (insulin-like growth factor) production
What does insulin-like growth factor do?
skeletal growth - cartilage formation, bone deposition. soft tissue growth - protein synthesis and cell proliferation
What is somatopause?
decrease in lean body mass, decline in bone mineral density, increase in body fat
What is gigantism?
abnormally high linear growth due to excess action of IGF while the epiphyseal growth plates are open (children). they have normal body proportions due to soft tissue also being affected
What is acromegaly?
increased growth hormone later in life after fusion of growth plates
What are features of someone with acromegaly?
course facial features, enlarged hands and feet, protruding jaw, enlarged tongue, deep voice, diabetes
What is pituitary dwarfism?
GH insufficiency in children, growth rate below third centile on age/height, normal body proportions, poor muscle development
What does GH insufficiency in adults?
no major symptoms
Where is the thyroid gland?
discrete organ, adheres to the trachea - 2 large flat lobes connected by isthmus
When is the thyroid gland fully developed?
by week 12 of gestation - responsive to TSH at 22 weeks - capable of producing T3/T4 by 14 weeks
What is the functional unit of the thyroid gland?
follicles (200-300 um in diameter) - 1000’s in each gland
What are the thyroid hormones?
triiodothyronine (T3) and thyroxine (T4)
How much of each is secreted by day?
80-100 ug of T4, 5 ug of T3
Which thyroid hormone has the greatest biological activity?
T3
In what hormone class is thyroid hormones?
amino acid derived, tyrosine & iodinated
In plasma, what are T3 and T4 bound to?
thyroxine-binding globulin, albumin
What does synthesis of thyroid hormones require?
tyrosines - provided by thyroglobin and secreted by follicle cells into lumen as colloid. iodine - essential requirement, pumped into follicular cells against concentration gradient
How is monoiodotyrosine (MIT) and diiodotyrosine (DIT) formed?
when iodine is attached to tyrosine in the colloid it forms MIT and DIT
How is T3 and T3 formed?
by MITs and DITs linking together
What is the advantage of the thyroid system?
it is capable of storing many weeks worth of thyroid hormone - if no iodine is available for this period, thyroid hormone secretion will be maintained
What are the effects of thyroid hormones?
they bind to intracellular receptors. form a complex with thyroid response elements (TRE) that bind to DNA and influence gene expression. enzymatic conversion of T4 into T3 in peripheral tissue
What do the transcribed proteins do? (after thyroid hormones increase gene expression & transcription)
increased: cellular metabolism, oxygen consumption, cellular glucose, circulation and respiration
What are cardiovascular thyroid hormone effects?
increased cardiac output, increased heart rate and contractility
What are the thyroid hormone effects of growth and maturation?
bone growth, synergy with growth hormone, CNS development and function
What does TSH stimulate?
promotes the release of thyroid hormones into the blood, increasing the activity of the iodide pump and iodination of tyrosine
What is hypothyroid?
underactive thyroid. in general metabolic rate increases weigh gain
What is hyperthyroid?
overactive thyroid, in general metabolic rate increases weight loss
What are symptoms of hypothyroidism?
dry, cold skin, weight gain but loss of appetite, impaired memory, mental dullness, lethargy
What are the levels of T3 and T4 with hypothyroidism?
low plasma levels of ‘free’ T3 and T4
How do you treat hypothyroidism?
thyroxine, dose determined by TSH monitoring
What does iodine deficiency cause?
endemic goitre
What causes endemic goitre?
insufficient dietary iodine, insufficient T3 & T4, abnormally high TSH
What is endemic goitre?
abnormal growth of the thyroid due to the trophic effects of TSH
What is Hashimoto’s disease?
leads to destruction of thyroid gland, interferes with thyroid hormone synthesis, antibodies against TSH receptor, prevents stimulation of T3 and T4 release
What is congenital hypothyroidism?
lack of gland or incorrect hormone biosynthesis. intellectual disability if treatment later than 3 months
What are the symptoms of congenital hypothyroidism?
short disproportionate body, thick tongue and neck
What are the symptoms of hyperthyroidism?
loss of weight, excessive sweating, palpitations and an irregular heartbeat, anxiety and nervousness, exopthalamus (bulging eyeballs)
What can be seen in a clinical exam of someone with hyperthyroidism?
raised metabolic rate & oxygen consumption, increased heart rate, hypertension
What is the treatment for hyperthyroidism?
surgical removal of all or part of the thyroid, ingestion of radioactive iodine that selectively destroys the most active thyroid cells, drugs that interfere with the gland’s ability to make T3/T4
What is graves disease?
abnormal antibodies that mimic TSH - activates TSH receptor inducing T3/T4 release
What are symptoms of graves disease?
goitre, exopthalamus, lid retraction, muscle weakness, heart palpitations, irritability
Where are the adrenal glands?
a pair - lie above the kidney. each gland is enclosed in a fibrous capsule surrounded by fat and each gland is equivalent to 2 endocrine glands
What is the inner layer of the adrenal glands?
adrenal medulla
What is the outer layer of the adrenal glands?
adrenal cortex
What is the blood supply of the adrenal glands like?
rich blood supply - adrenal arteries arise directly from the aorta. blood flows through the cortex and drains into the medulla
What is the adrenal medulla a modified part of?
the sympathetic nervous system
What catecholamine hormones does the adrenal medulla secrete?
adrenaline (80% of secretions) and noradrenaline (20% of secretions)
Is the adrenal medulla a true endocrine gland?
no! but the adrenal cortex is
What is the adrenal medulla composed of?
chromaffin cells
What response is adrenaline and noradrenaline important for?
fight or flight
What are the cardiovascular effects of adrenaline?
increases heart rate and stroke volume, increases blood pressure, vasodilation of coronary and skeletal muscle blood vessels but vasoconstriction of others
What are the metabolic effects of adrenaline?
increases the amount of energy for immediate use, liver converts glycogen to glucose, metabolic rate increases, blood flow changes, reducing digestive system activity and urine output
What part of the adrenal glands is involved in long-term stress?
adrenal cortex
What part of the adrenal glands is involved in short-term stress?
adrenal medulla
What are the three distinct zones of the adrenal cortex?
zona glomerulosa - mineralocorticoids (salt), zona fascilculata - glucocorticoids (sugar) - cortisol, zona reticularis - gondocorticoids (sex)
What does high circulating testosterone lead to in fetuses?
masculinisation of fetal external gentialia to variable degrees
What are androgens?
thought of as male hormones but the female body naturally produces a small amount of androgens too
What do adrenal glands produce in relation to androgens?
dehydroepiandosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S) and androstenedione. they are testosterone and oestrogen precursors
Where are DHEA, DHEA-S and androstenedione converted to testosterone?
in peripheral tissues
What controls adrenal androgens?
anterior pituitary
What is the effect in males of adrenal androgens?
the contribution of testosterone derived from adrenal glands pales in comparison to the normal output of testosterone, however, in young boys its though to cause aggression and male secondary characteristics
What are the effects of adrenal androgens in females?
responsible for growth of pubic and axillary hair and sex drive. kick starts puberty, maintains muscle and bone mass
What can occur with excessive production of adrenal androgen?
overproduction of ACTH, adrenal tumour, Cushing’s syndrome. masculinisation of females, acne, irregular periods, breast shrinkage. plays a role is PCOS
What is the most abundant circulating hormone in young adults?
DHEA-S
What is aldosterone regulated by?
the plasma levels of sodium and potassium via the renin-angiotensin system
Do we need aldosterone?
yes! it is essential to life - absence leads to circulatory failures and death within a few days
What are the principle actions of aldosterone?
control ECF volume, conserve body sodium, stimulates reabsorption of sodium in renal distal convoluted tubules in exchange for potassium
What stimulates cortisol production?
stress = physical trauma, intense heat or cold, infection, mental or emotional trauma
What does cortisol do?
metabolic effects, increases plasma glucose and free fatty acid (FFA) concentration, provides energy substrates to body tissues for their response to the stressful event. may contribute to emotional instability, anti-inflammatory, immunosuppressive
What else does cortisol do?
increased catabolism, increased lipolysis, increased intake
What is Cushing’s syndrome?
overproduction of cortisol as a result of an adrenal or pituitary tumour
What are symptoms of Cushing’s syndrome?
redistribution of body fat, muscle wastage, thin skin, bruising, hyperglycaemia, hypertension
What is the treatment of Cushing’s syndrome?
surgery, radiation, medication
What is Conns disease?
mineralocorticoid excess
What happens during Conns disease?
overproduction of aldosterone, retention of sodium, loss of potassium and alkalosis
What is Addison’s disease?
adrenal cortex hypofunction
What does Addison’s disease do?
damage to adrenal glands, autoimmune disease or pituitary damage, deficits in glucocorticoids and mineralocorticoids, progressive weakness, weight loss
What is calcium important in doing?
structural component of bones and teeth, maintains normal excitability of nerve and muscle cells, involved in neurotransmitter release
Does calcium exist naturally in nature and the body?
no in nature but yes in the body
What are plasma calcium concentration levels?
2.2-2.6 mM
What is hypocalcaemia?
too low calcium - involuntary muscle contraction. neuronal hyper-excitability (tetany)
What is hypercalcemia?
too high calcium - depression & kidney damage/stones. neurones less excitable
What are control points for calcium?
absorption (intestines), excretion (kidney/urine), temporary storage (bones)
What do osteoblasts do?
synthesise and secrete collagen and promote deposition of calcium phosphate crystals
What do osteocytes do?
essential role in exchange of calcium between ECF and bone
How is acute control of calcium done?
rapid exchange between bone and ECF
How is chronic control of calcium done?
GIT absorption and urinary excretion
What is plasma Ca2+ concentration determined by?
net absorption of Ca2+ from the GIT, net excretion of Ca2+ in urine, exchange of Ca2+ with bone
What three hormones is plasma calcium controlled by?
parathyroid hormone, 1,25-dihydroxycholecalciferol (calcitriol) , calcitonin
What does the parathyroid hormone (PTH) gland monitor?
the concentration of calcium in the blood perfusing the glands
What type of hormone is PTH?
peptide
Where is PTH stored?
chief cells
What is PTH released in response to?
low blood calcium - exerts its effect on bone, gut and kidneys
What is the main target tissue of PTH?
kidney and bone - increased resorption of calcium from the urine. decreased urinary calcium in minutes
What enzyme does PTH increase the expression of?
1 alpha-hydroxylase (activates vitamin D)
What does PTH do in bone?
increases osteoclast activity which causes a increase in bone resorption
What types of vitamin D are there?
D2 = plant sources. D3 = obtained from diet, food supplements and synthesised in the skin in the presence of sunlight
Are D2 and D3 inactive or active?
relatively inactive
What are D2 and D3 converted to?
1, 25 dihydroxycholecalciferol aka calcitriol
Is vitamin D a true vitamin?
no
What are the actions of calcitriol?
acts on cells on the GIT to increase production of calcium transport proteins so there is an increase in calcium uptake from GIT, increases calcium stores, increases rate of bone resorption, minor effect in decreasing urinary loss of calcium
How does calcitriol work?
by increasing how much calcium we can absorb from food
What is calcitonin secreted by?
C-cells (parafollicular cells) of the thyroid
What does calcitonin do?
lowers the level of free plasma calcium. inhibits osteoclast activity - bone resorption reduced. increases excretion of calcium and phosphate by the kidneys
What other hormones are involved in the regulation of plasma calcium?
growth hormone, adrenal glucocorticoids, thyroid hormones, oestrogen, androgens
What happens in hyperparathyroidism?
inappropriate secretion of PTH, resulting in hypercalcaemia. elevated PTH and raised serum calcium. increased bone resorption, increased GIT absorption and decreased renal secretion
What are most cases of hyperparathyroidism caused by?
85% of cases cause by a single parathyroid adenoma
What are symptoms of hyperparathyroidism?
kidney stones, increased thirst, increased urination, loss of appetite, nausea, vomiting. bones, stone, abdominal groans and psychic moans
What is rickets caused by?
hypocalcaemia - vitamin D deficiency
Why does rickets happen?
bone remodeling impaired, failure of calcification
What are causes vitamin D deficiency?
poor diet, malabsorption, decreased sunlight, liver or kidney disease
What happens in osteomalacia?
softening and weakening of bones, pain in lower back and hips
