Endocrinology Flashcards
What are the functions of the endocrine system?
- regulate metabolism, water and electrolyte balance
-allow body to cope with stress - regulate growth
- control reproduction
- regulate circulation and red blood cell production
- control digestion and absorption of food
What are the components of the endocrine system?
All hormone-secreting tissues:
- in the brain
- hypothalamus
- pituitary and pineal gland
- periphery in the thyroid, parathyroid and adrenal glands
- gonads
- pancreas
- kidneys
- liver
- thymus
- parts of the intestines, heart and skin
What are peptides?
- a class of hormone
- chains of amino acids, e.g. antidiuretic hormone (vasopressin), growth hormone
- hydrophilic (water soluble)
- stored prior to release
- fast acting
What are amines?
- class of hormones
- derived from amino acid ‘tyrosine’
- all are stored
- some hydrophilic (catecholamines - adrenaline, noradrenaline and dopamine)
- some lipophilic - i.e. fat soluble (thyroid hormones)
What are steroids?
- class of hormone
- derived from cholesterol where appropriate enzymes for conversion are present (e.g. cortisol, testosterone, oestrogens)
- lipophilic
- not stored, made when needed, and released by diffusion
List features of hydrophilic hormones (peptides and catecholamines)
- most transported in blood dissolved in plasma (some also carried on binding proteins)
- can’t pass through cell membrane, therefore binds to specific receptors on surface of target cell
- elicit response either by changing cell permeability (few) or activating ‘second-messenger’ system to alter activity of intracellular proteins (most)
- vulnerable to metabolic inactivation so short-term effects
List features of lipophilic hormones (thyroid hormones and steroids).
- transported in blood mostly bound to plasma proteins
- small unbound amount dissolved - only dissolved portion physiologically active
- free hormone (unbound) easily passes through cell membrane, binds to specific receptor within target cell (mostly in cell nucleus)
- elicit response by activating specific genes within target cell to cause formation of new intracellular proteins
- less vulnerable to metabolic inactivation so effects last longer
Summarise differences between hydrophilic and lipophilic hormones
- hydrophilic likes water, lipophilic hates water
- hydrophilic can’t get through plasma membrane, lipophilic can diffuse across plasma membrane
- hydrophilic have fast onset and are fast acting, whereas lipophilic have slower onset, and are longer acting
What are the five steps involved in the regulation of hormone activity, and what are some considerations at each stage?
- secretion (stimulation, feedback, reflexes, rhythms)
- transport (binding proteins, free/unbound balance)
- metabolism (activation/inactivation, differs for hydrophilic vs lipophilic due to accessibility
- excretion (unregulated - but can be affected by renal/urinary disease)
- target cell responsiveness (receptor expression, amplification, combination with other hormones - ‘permissiveness, synergism and antagonism’
What are the control pathways for secretion in the regulation of hormone activity?
- central regulation
- direct regulation
Discuss features of the central regulation control pathway for secretion.
- controlled by brain
- affected by positive and negative-feedback loops, neuroendocrine reflexes, rhythms (e.g. diurnal)
- can be fast, slow or long term responses
- coordinated by hypothalamus and pituitary gland
What is an example of a rhythm that affects the central regulation of secretion?
Diurnal:
- melatonin (produced by pineal gland - responds to light)
- cortisol
- growth hormone
Discuss features of the direct regulation control pathway for secretion
- endocrine cells respond directly to changes in extra-cellular fluid (especially plasma) levels of substances (e.g. glucose, calcium)
- very rapid response to critical needs
What are two groups of anterior pituitary hormones, when considering actions?
- ‘trophic’ hormones control activity of another endocrine gland (thyroid stimulating hormone, adrenocorticotrophic hormone, luteinising hormone, follicle stimulating hormone)
- hormones which have a direct effect in their own right (prolactin and growth hormone)
How does growth occur and what does it involve?
- primarily through the actions of growth hormone
- involves structural growth of tissues: synthesis or proteins, lengthening of long bones, soft tissue cell size and number increase
What are some other factors that influence the extent of growth?
- genetic determination of height and shape
- dietary impact - especially amino acids
- chronic disease or stressful environment (as cortisol inhibits growth)
- other hormones influencing growth (thyroid hormone, insulin, sex steroids)
Discuss the impacts of the a) anabolic and b) metabolic actions of GH
a) - growth
- increases length and thickness of long bones
- increases size and number of cells in soft tissues
b)
- increases fat breakdown/increases circulating fatty acids
- decreases glucose uptake by muscles
What is the action of growth hormone in muscles?
- (direct via Gh-receptor)
- stimulates amino acid uptake
- decreases glucose uptake
- inhibits protein breakdown
= increase muscle mass
What is the action of growth hormone in adipose tissue?
- (direct via GH-receptor)
- decreases glucose uptake
- increases fat breakdown (lipolysis)
= decrease in fat deposits
What is the action of growth hormone in the liver?
- (direct via GH-receptor)
- increases protein synthesis
- increases gluconeogenesis
= increase metabolism
Provide a one word summary of the action of growth hormone when received directly via GH-receptors.
- primarily metabolic effects
What is the action of growth hormone when indirectly mediated by somatomedins (IGFs)?
IGF-I:
- proliferation of chondrocytes at epiphyseal plates increasing bone length
- stimulates osteoblast activity to produce organic matrix increasing bone thickness
- promotes soft tissue growth through hyperplasia and hypertrophy (increased no. and size of cells respectively)
IGF-II:
- promotes soft tissue and organ growth by increasing protein, RNA and DNA synthesis
What other hormones influence growth hormone’s synthesis and release, and in what ways?
- thyroid hormones: permissive, low TH = low growth
- glucocorticoids: excess inhibits growth
- sex steroids: synergistic, androgens important for pubertal growth spurt, but ultimately promote closure of epiphyses
- insulin: (deficiency = low growth, excess = high growth)
What is a growth abnormality resulting from excess growth hormone in children, and what is a feature of it?
Gigantism
- normal body proportions
What is a growth abnormality in adult resulting from excess growth hormone, and what are some features of it?
Acromegaly
- enlarged extremities
- course/malformed facial features, enlarged tongue, thickened lips, deep voice, sleep apnoea, cadiomegaly, degenerative arthropathy, muscle hypertrophy but weakness
- generally due to pituitary tumour
What is the result of growth hormone deficiency in a) adults and b) children?
a) no major symptoms
b) ‘pituitary dwarfism’
- short stature, normal body proportions, poor muscle development, excess subcutaneous fat
What is the physiological importance of calcium?
- structural component of bones and teeth
- contributes to resting membrane potential
- maintains normal excitability of nerve and muscle cells
- involved in neurotransmitter and hormone release
- muscle contraction (skeletal and cardiac)
- activation of many enzymes
- coagulation of blood
- milk production
How is calcium regulated in the body?
- hormone control - balance maintained between ECF, and GIT, kidney and bone
Compare acute and chronic control of calcium
Acute:
- must maintain constant free Ca2+ concentration in plasma
- mostly by rapid exchange between bone and ECF
Chronic:
- maintain total Ca2+ level in body long-term
- adjust gastrointestinal absorption and urinary excretion
What are the three main hormones that regulate Ca2+ metabolism?
- parathyroid hormone (PTH)
- vitamin D3
- calcitonin
What three types of cells are important for bone formation and resorption?
- osteoblasts - synthesise and secrete collagen and promote deposition of CaPO4 crystals
- osteoclasts - promote resorption of bone
- osteocytes - essential role in exchange of calcium between ECF and bone
List some features of the parathyroid hormone, including its actions and half-life
- parathyroid glands are 4 glands located on posterior surface of thyroid gland
- PTH secreted from chief cells in direct response to changing plasma Ca2+ concentrations
- overall increase calcium, decrease phosphate in plasma
- is a peptide
- half-life in plasma of <20 minutes
- actions on bone, kidneys and GIT
What are the functions on bone of parathyroid hormone?
Short-term:
- stimulates Ca2+ membrane pump in osteocytes, so Ca2+ moves from bone fluid to plasma in central canal
Long-term:
- stimulates osteoclasts
- inhibits osteoblasts
- so Ca2+ and PO4 increase in plasma
What function does parathyroid hormone have on the kidney?
- decreases Ca2+ loss - increased tubular reabsorption of Ca2+ and decreased tubular reabsorption of PO4
What function does parathyroid hormone have on the GIT?
- indirectly increases Ca2+ and PO4 - increases absorption by small intestine by stimulating activation of vitamin D3
What is the function of vitamin D?
- produced either in skin or ingested, and is activated by liver and kidney to vitamin D3
- promotes absorption of Ca2+ from that intestine by increasing its transport across intestinal membrane
- (most ingested Ca2+ is not absorbed by GIT, but lost in faeces)
- promotes absorption of PO4 in intestine
- increases bone reabsorption
- stimulates Ca2+ and PO4 reabsorption in kidneys
Where is calcitonin produced, and what is its function?
- produced in the C cells of the thyroid gland in response to high plasma Ca2+ levels
- decreases bone resorption (effects osteoclasts)
- decreases Ca2+ reabsorption in kidneys, promotes increased excretion
- overall action = decreased Ca2+ and PO4 in plasma
- protects against hypercalcemia
What is hyperparathyroidism, and how is it caused?
- most frequently caused by PTH-secreting adenomas, leads to hypercalcemia
- increased Ca2+ mobilisation from bones causes softening and fractures
- increased Ca2+ excretion through kidneys causes polyuria, polydipsia and nephrocalcinosis
- decreased excitability of nerves and muscles leads to weakness, depression and coma
- hypercalcemia leads to nausea, constipation and increased incidence of peptic ulcers
What is hyperparathyroidism, and what is its cause?
- most frequently caused by PTH-secreting adenomas, leads to hypercalcemia
- increased Ca2+ mobilisation from bones causes softening and fractures
- increased Ca2+ excretion through kidneys causes polyuria, polydipsia and nephrocalcinosis
- decreased excitability of nerves and muscles leads to weakness, depression and coma
- hypercalcemia leads to nausea, constipation and increased incidence of peptic ulcers
What is hypoparathyroidism, and what is its cause?
- most frequently caused by gland destruction, leads to severe hypocalcemia
- hypocalcemia causes increased nerve and muscle excitability
- severe hypocalcemia leads to death by asphyxiation caused by laryngospasm
- mild hypocalcemia causes cramps, twitches and tingles
What are some other causes of hypocalcemia?
- high demand for Ca2+ in pregnancy/lactation (causes tetany or paralysis)
- lack of vitamin D/sunlight
(causes rickets in children, osteomalacia in adults) - change in blood pH
(alkalosis - less free Ca2+) - pancreatitis
What is osteoporosis?
- reduction in the mass (density) of bone and impairment of integrity of spongy bone
- weaker bone = prone to fracture
- progression from osteopenia to osteoporosis
What are risk factors of osteoporosis?
- poor nutrition (particularly low calcium)
- low oestrogen levels, early menopause or loss of normal menstruation
- inadequate sunlight exposure (Vitamin D deficiency)
- smoking, excessive alcohol and caffeine intake
- sedentary lifestyle
- low testosterone
- corticosteroid use
- aortic calcifications
What can be the result of decreased bone mass and structural disruption?
- fractures after minimal trauma
How does oestrogen tie into bone formation/resorption?
- Increased oestrogen -> decreased osteoclast activity and decreased bone resorption
- Less oestrogen (after menopause) -> more bone resorption
What happens when testosterone is converted to oestrogen in bone in males?
Less testosterone -> more bone resorption
How can osteoporosis be prevented?
- good nutrition (Ca2+ and Vitamin D)
- post-menopause (hormone replacement therapy, however side effects include increased risk of cardiovascular disease and cancer)
- maintaining exercise (particularly weight bearing) in older age: reduces bone loss, prevents fractures, and prevents falls
Differentiate the terms ‘genetic sex’, ‘gonadal sex’ and ‘phenotypic sex’.
Genetic sex: sex detemrined by chromosomes
Gonadal sex: if male, gonads differentiate into tests from seventh week of gestation, ovaries form after ninth week
Phenotypic sex: after 8 weeks gestation, testosterone production by testes causes development of Wolffian ducts into male internal reproductive organs, dihydrotestosterone causes masculinisation of external genitalia
What influences the onset of puberty?
- body weight/obesity
- genetics
- health
- melatonin
What does the pre-pubertal increase in pulses of of gonadotrophin-releasing hormone trigger?
- triggers production of gonadotrophins (luteinizing hormone and follicle stimulating hormone) from anterior pituitary, which trigger gonadal activity
What is the result of the production of sex steroids?
- development of secondary sexual characteristics and fertility
How does the hypothalamus control reproduction?
- produces pulses of gonadotrophin-releasing hormone
- stimulates pulsatile release of luteinizing hormone and follicle stimulating hormone
What are two testicular cells and what are their functions?
- Leydig cells:
- produce testosterone and small amounts of other steroids in response to luteinizing hormone
- testosterone: either acts on adjacent Sertoli cells or is released in the blood, actions outside testes - Sertoli cells: (with support from testosterone and follicle stimulating hormone)
- maintain tight junctions (to create seminiferous tubules)
- nourish germ cells and support spermatogenesis
- secrete androgen binding protein (ABP)
- convert testosterone to dihydrotestosterone or oestradiol
What are the actions of the testosterone androgen?
- sex determination in foetus
- at puberty: growth spurt, closure of epiphyses
- development and maintenance of male secondary sexual characteristics - external genitalia, deep voice, hair growth pattern, skin, body shape (lean muscle mass, low body fat)
- development and maintenance of accessory sex organs and libido
- anabolic actions, effects on brain and bone
What is the process of female sexual development, commencing from the ‘awakening’ of the ovary?
- ovary awakened because of LH and FSH release from anterior pituitary: considered the start of follicular development
- developing follicles release oestrogens: development of female secondary characteristics, e.g. fat deposition, growth and maturation of reproductive tract
- growth of auxiliary hair, libido and pubertal growth spurt due to pubertal rise in adrenal androgens
- when sufficient gonadotrophin releasing hormone, LH and FSH to support follicular development to ovulation first ‘period’ - ‘menarche’
- oestrogens cause closure of epiphyses
What are the four stages of the menstrual cycle, and what is the main occurrence at each stage?
- Follicular phase
- follicular and luteal changes in ovary
- oocyte development and follicular growth
- follicle secretes oestrogen (at end) - Ovulation
- LH surge coincides with ovulation
- development of corpus luteum (at end) - Luteal phase
- corpus luteum secretes progesterone and oestrogen
- degeneration of corpus luteum - New follicular phase
What happens to the plasma concentration of oestrogen throughout the different phases of the menstrual cycle?
Follicular phase: very low oestrogen
Ovulation phase: oestrogen level rises, causes thickening of endometrium - oestrogen levels peak (LH surge follows this rise)
Luteal phase: progesterone increases number of blood vessel and secretory glands in endometrium, oestrogen rises again slightly
New follicular phase: returns to low levels
What happens to the plasma concentration of progesterone throughout the different phases of the menstrual cycle?
Follicular phase: very low progesterone
Ovulation phase: progesterone levels rise follow LH surge
Luteal phase: progesterone level peak, and increase in progesterone increases number of blood vessels and secretory glands in endometrium
New follicular phase: returns to low levels
What are the effects of female sex steroids?
- in normal cycle, brief ‘steroid fee period’ followed by sequential exposure to oestrogen then progesterone + oestrogen
- oestrogen stimulates both E-receptor and P-receptor expression
- alone progesterone has very few effects, as its actions require oestrogen priming
- menopause: very low oestrogen and progesterone as menstrual cycles cease, regression of reproductive tract, reversed by treatment with oestrogen
What bodily systems does oestrogen affect, and what are its principle functions?
- oviduct
- uterus
- cervix
- vagina
- breasts (duct growth)
- fat/protein deposition
- brain
- skeleton
- electrolyte balance
- skin
Principle functions: - cellular proliferation
- growth of tissues of sexual organs
- growth/modification of other tissues related to reproduction
True or false: the hormones oestrogen and progesterone cause the mucus of the cervix to be receptive to sperm?
True, and false:
- oestrogen, yes - very receptive to sperm
- progesterone, no - hostile and impermeable to sperm
What bodily systems does progesterone effect, and what are its principle functions?
- oviduct
- uterus (inhibits proliferation and promotes accumulation of secretory products)
- cervix (secretion of hostile mucous)
- vagina
- increase basal body temperature
- breasts (alveolar development)
- brain
Principle functions: - prepares the reproductive tract (and other organs) for pregnancy, modifies or blocks (antagonises) the action of oestrogen
What is the chief difference between progesterone levels in a conception cycle vs. a regular menstrual cycle, and why does this occur?
- progesterone levels do not decline at the end of a conception cycle
- occurs because the corpus luteum does not undergo luteolysis and continues to produce progesterone
What hormone does the foetus produce that triggers birth? Once labour starts, what hormone, produced by the mother, helps the womb contract?
- corticotrophin releasing hormone
- mother’s own oxytocin
Discuss the development of lactation throughout the course of a pregnancy.
- During pregnancy, oestrogen stimulates duct growth, progesterone stimulates alveolar-lobule formation in breasts
- Prolactin and human chorionic somatomammotropin promotes gland development and induces enzymes for milk production
- high levels of oestrogen and progesterone (from placenta) prevent initiation of lactation until after birth
Discuss the hormones involved in birth and the onset of lactation.
Oxytocin: high placental oestrogens in late pregnancy increase number of oxytocin receptors in uterus, oxytocin stimulates rhythmic uterine contractions in labour, through neuroendocrine reflex/positive feedback loop)
Progesterone and oestrogen: decrease after birth, permits lactation to commence
Oxytocin: stimulated by suckling, causes contraction of myoepithelial cells in breast (promotes milk ejection)
Prolactin: suckling stimulus promotes release of prolactin, which acts on alveolar epithelial cells to increase milk secretion (maintains milk production)
Discuss the reproductive disorder of prolactinoma
- prolactinomas are the commonest pituitary adenomas, produce high levels of prolactin, also cause compression of pituitary and optic chiasm
Symptoms: caused either by increased prolactin levels (hyperprolactinemia) or by ‘mass’ effect (due to size of tumour)
Hyperprolactinemia cause: - amenorrhea (no cycles)
- galactorrhoea
- loss of axillary and pubic hair
- hypogonadism, gynecomastia, erectile dysfunction
Mass effects include: - bi-temporal hemianopsia (as optic chiasm compressed)
- vertigo, nausea, vomiting
What is the basal metabolic rate, and what is it primarily determined by?
- energy used at rest
- thyroid hormones
Define follicle.
a fluid-filled sack
What are the follicular cells of the thyroid full of?
- colloid - no connection to rest of body, reason being to make and store thyroid hormone
What are the functions of the thyroid?
- contains follicles, comprised of follicular cells and colloid, that produce the thyroid hormones T3 and T4 from tyrosine and iodine
- thyroid hormones are amines, lipophilic, are transported in plasm bound to carrier proteins, with a balance between bound and free hormone
- most thyroid hormones are secreted as T4 which is converted to T3 in tissues
- virtually every tissue in the body is affected by thyroid hormones
Where is the thyroid gland located?
Lies over the trachea in the neck
What is the effect of thyroid hormone on cells?
- increases metabolism (‘goes faster’) by influencing fuel metabolism (i.e. synthesis and breakdown of protein, fat, and carohydrates)
True or false: T3 is four times more potent than T4
True
Discuss thyroid hormone’s ‘sympathomimetic’ effect
- increases target cell responsiveness to catecholamines (effects cardiac output by increasing heart rate and contractility)
List the four main types of thyroid tumours, as well as their symptoms
- papillary thyroid cancer
- follicular thyroid cancer
- medullary thyroid cancer
- anaplastic thyroid cancer
Symptoms: - nodule in thyroid region; enlarged lymph node; pain in anterior neck, vocal changes
- thyroid hormones can be normal, low or high
List the risk factors and diagnosis & treatment of thyroid tumours
Risk factors:
- radiation exposure, enlarged thyroid
- family history, thyroid disorders
Diagnosis and treatment:
- ultrasound/fine needle aspiration
- surgery, radiation therapy, chemotherapy
List the causes and symptoms of hyperthyroidism
Causes:
- Grave’s disease
- excess thyrotropin-releasing hormone, thyroid stimulating hormone or thyroid hormone production (from tumour in hypothalamus, pituitary, or thyroid gland)
Symptoms:
- increased metabolism, excessive sweating, increased appetite but weight loss, muscle weakness, anxiety, palpitations
- GOITRE (enlargement of thyroid gland)
-exophthalmos (protrusion of eyes)
Discuss Grave’s Disease, mentioning its risk factors, symptoms and treatment
-an autoimmune disease (produces autoantibodies)
- thyroid stimulating immunoglobin
Risk factors:
- family history, other autoimmune diseases, smoking
Symptoms:
- increased metabolism, excessive sweating, increased appetite but weight loss, muscles weakness, anxiety, palpitations, exophthalmos, goitre
Treatment:
- radioiodine therapy, antithyroid medications, thyroid surgery
Discuss the differences between primary and secondary hypothyroidism, as well as in pregnancy.
Primary:
- thyroid gland failure; resection/radiotherapy
- Hashimoto’s thyroiditis
Secondary:
- deficiency of thyrotropin releasing hormone or thyroid stimulating hormone (hypothalamus or pituitary failure)
Pregnancy:
- can cause congenital iodine deficiency syndrome (cretinism) in neonates
Discuss the symptoms, diagnosis, prevention & treatment of hypothyroidism
Symptoms:
- decreased metabolism, poor cold tolerance, excessive weight gain, fatigue; bradycardia, weak pulse, slow reflexes and mental function, myxoedema (puffiness), goitre
Diagnosis:
- blood tests for thyroid stimulating hormone, thyroxine (T4)
Prevention & treatment:
- salt iodisation (where iodine deficient)
- levothyroxine (synthetic TH)
Discuss Hashitomo’s thyroiditis, mentioning its symptoms, diagnosis and treatment.
- Autoimmune disease - autoantibodies attack the thyroid gland
- caused by combination of genetic and environmental factors
- more common in women, family history of autoimmune diseases
Symptoms and treatment: - goitre, decreased metabolism, poor cold tolerance, excessive weight gain, fatigue, etc.
- diagnosis: blood tests for thyroid stimulating hormone, T4 and anti-thyroid antibodies
- levothyroxine
Discuss congenital iodine deficiency syndrome, making specific mention to the signs and symptoms (severe and mild), and prevention & treatment.
Signs and symptoms:
- goitre, poor growth, thick skin, hair loss, enlarged tongue, protruding abdomen, delayed bone maturation and puberty, small adult stature, infertility
- cognitive and neurological impairment (severe, can’t talk, stand or walk; mild, learning disabilities, reduced muscle tone and coordination)
Prevention and treatment:
- iodine supplementation of food, screening pregnant women and neonates
- lifelong administration of thyroid hormone
What are some psychological stressors?
Stimuli which lead to fear, anxiety or frustration
- includes traumatic events such as death, divorce, conflict, abuse, war, and natural disasters
What are some physical stressors?
Stimuli which disrupt normal body function, can be due to internal factors or external environment
- hypoxia, hypoglycaemia, infection, physical strain, injury, starvation, dehydration
- exposure to heat or cold
What is an acute stress response?
- a normal and beneficial adaptive response
- increases alertness and focus, provides energy to respond and cope with stressful situation
- extent of response is dependent on severity of stressor, and on the individual
- mild stress improves mood, creates new memories , encourages creative thinking, promotes neural growth in brain, facilitates problem solving
What can severe stress cause?
- detachment
- reduction in awareness
- derealisation
- depersonalisation
- dissociate amnesia
What is a chronic stress response?
- when stress is prolonged, homeostasis is unable to be maintained
- the body enters an exhausted state, when damage to health can occur, immune suppression, hypertension, gastrointestinal disturbances
- can have detrimental psychological effects - anxiety and mental dysfunction, social withdrawal
What is the ‘General Adaptation Syndrome’ response to stress?
- describes the stages of the bodies response to stress, three phases:
1. alarm - preparing ‘fight-or-flight’
2. resistance - staying alert, but keep on with normal functioning (adaptation), homeostasis maintained
3. exhaustion - resources are depleted, ‘burnout’ sets in, homeostasis cannot be maintained so function impaired
In what ways does the acute stress response ready the body for action?
- increased cardiovascular function - heartrate, contractility, mostly vasoconstriction, with vasodilation to muscles
- increased respiratory function: resting rate and tidal volume, bronchodilation
- liberation of nutrients - increased blood glucose and fatty acids
- skin - paling or flushing, sweating, piloerection
- muscle tension and shaking
- inhibition of gastrointestinal motility, contraction of sphincters
- inhibition of the lacrimal gland and salivation
- relaxation of bladder, inhibition of erection
What is the physiological response to stressors coordinated by?
- the hypothalamus
What is the sympathetic nervous system’s involvement in the physiological response to stress?
- adrenaline (epinephrine) from adrenal medulla
- noradrenaline (norepinephrine) from neurons
- inhibition of parasympathetic nervous system
What is the endocrine’s system’s involvement in the the physiological response to stress?
- cortisol and corticosterone from adrenal cortex
- vasopressin (anti-diuretic hormone) from posterior pituitary
- activation of renin-angiotensin-aldosterone (‘RAAS’, involves liver, kidneys, lungs and adrenal cortex)
- insulin and glucagon from pancreas
Why is aldosterone produced in response to, and what is its function?
- produced in response to changes in ECF volume/blood pressure and stress
- promotes water retention in kidneys by increasing Na+ reabsorption
What are the actions of glucocorticoids (cortisol/corticosterone)?
- allows body to cope with stress by increasing availability of energy and amino acids
- increases vascular reactivity (by largely unknown mechanisms)
- affects mood and behaviour - improving mood, increasing alertness
- stimulates brain function - promotes neural growth in brain which improves memory, creative thinking, problem solving ability
- in chronic stress, may be responsible for immune suppression and other health defects
What is the adrenal medulla and what does it produce?
Part of the sympathetic nervous system
- produce the catecholamines adrenaline and noradrenaline in response to direct stimulation by sympathetic pre-ganglionic neurones from the splanchnic nerve
- hormones are released directly into the bloodstream, and act on distant target tissues including heart, blood vessels, bronchioles, GIT
What do adrenaline and noradrenaline do?
- elicits acute physical reactions of body to prepare for ‘fight or flight’
- increases cardiac and respiratory function, slows digestion/kidney function, tenses muscles, increases sweating
- vasoconstriction to skin and organs (including kidneys), vasodilation to skeletal muscles
- inhibits parasympathetic nervous system
- act on pancreas to reduce insulin secretion, increase glucagon secretion to increase blood glucose
What can chronic stress cause?
- immune suppression through excess glucocorticoid production, increasing risk of infection
- hypertension and cardiovascular disease
- disruption of body weight
- poor growth in children through suppression of growth hormone production
- inhibition of parasympathetic nervous system can result in reproductive failure, poor digestion
- mental disorders
- associated with higher mortality
What is Cushing’s syndrome, and what are the symptoms?
Excess glucocorticoids, due to excess ACTH or adrenal tumour -> excess glucocorticoid secretions (Cushing’s Disease) or excess glucocorticoid administration
Symptoms:
- protein depletion -> muscle weakness
- poor healing, immunodeficiency
- thin skin, prone to damage and hirsutism (hairy)
- obesity and body fat redistribution
- Type II diabetes
What are the symptoms of Addison’s disease?
Chronic failure of adrenal cortex
Symptoms:
- electrolyte imbalance - loss of aldosterone
- dehydration and hypotension
- reduction in stress response (loss of glucocorticoids)
- Addisonian crisis (hypoglycaemia - coma, death)
- loss of vascular reactivity (vasodilation/shock)
- melanin pigmentation (loss of negative feedback causes increased production of ACTH and melanocyte-stimulating hormone
What is adrenogenital syndrome, and what are the symptoms?
Excess levels of androgens due to 21-hydroxylase deficiency or adrenal tumour
Symptoms:
- pre-pubertal females - pseudohermaphroditism
- pre-pubertal males - precocious pseudopuberty
- adult females - virile characteristics, hirusutism, deep voice, increased muscularity, amenorrhea
- adult males - no apparent effect
What is the treatment and management of a) Cushing’s syndrome, and b) Addison’s disease?
Cushing’s: aim to reduce cortisol levels
- surgery, radiotherapy or chemotherapy (if tumour) or medication; diabetes management
