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Organisation of the Body

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Function of the pituitary   To produce and secrete eight peptide/glycoprotein hormones and in turn these hormones exert many functions important for health E.g. PRL, ACTH, TSH, GH, LH, FSH, ADH and Oxytocin  
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Location of the pituitary   Hypothalamus is superior Optic chiasma is directly in front (where optic nerves cross) At the base of the brain behind the nasal cavity  
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Pituitary fossa   The pituitary gland sits at the base of the skull in a recess of the sphenoid bone called the sella turcica This is a bony cavity in which the pituitary sits Relatively protected from trauma except the stalk Tumours cannot expand within the fossa  
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Anterior pituitary tumours   Hormonal effects - hormone secreting tumours effects depend on cell type - present as over excretion of the hormone Mechanical effects - affect vision as tumour presses on optic chiasm - affects peripheral vision field leading to tunnel vision  
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Development of the pituitary   Downgrowth from developing hypothalamus - neural ectoderm - posterior pituitary Upgrowth of oral ectoderm from roof of mouth - anterior pituitary Development directed by different transcription factors for each section  
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Posterior pituitary   Axons and nerve endings - direct extension of the brain Neurons originate in the brain Hormones are stored and released from nerve endings Responsible for neurosecretion  
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Anterior pituitary   No neural innervation - controlled by hormones from the posterior Capillaries are fenestrated to allow each diffusion of hormones into blood - enters jugular vein Rabbits perfused with ink allows view of blood vessels - shows hormonal control  
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What hormones does the pituitary release   Anterior - TSH, ACTH, LH, FSH, GH, prolactin Posterior - Oxytocin and vasopressin (ADH)  
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Anterior pituitary histology   Five endocrine cell types each secrete different trophic hormones Cell types can be differentiated by antibody labelling and cell structure of tumours Non-secretory supporting call types = Folliculo-stellates These support the cells  
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Anterior pituitary vasculature   Prominent vessels in the pituitary stalk Gonadotrophs directly adjacent to capillaries - allows rapid diffusion into bloodstream Pituitary can adapt to demands e.g. during pregnancy, lactation, menopause, stress, seasons, fetal stress and puberty  
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Ultrastructure of anterior pituitary   Lots of mitochondria Euchromatin - high transcription rate Hormones stored in secretory granules RER Majority of exocytosis occurs at boundary with capillaries - directed  
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Feedback loops   Short feed back loop - anterior pituitary inhibits hypothalamus e.g. GH and PRL Long feedback loop - endocrine gland inhibits both anterior pituitary and hypothalamus e.g. cortisol, IGF and testosterone  
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Posterior pituitary histology   Formed by axons and terminals of hypothalamic neurosecretory neurons Secretes peptide hormones ADH (vasopressin) and oxytocin Nuclei present are of glia cells - control nutrient environment  
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Hypothalamic-pituitary-thyroid axis   Stimulus e.g. cold triggers hypothalamus to produce thyrotrophin releasing hormone Anterior pituitary thyrotroph cells then secrete thyroid stimulating hormone Thyroid then secretes T3 and T4 Long feedback loop Pathology of TSH secretion is rare  
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ACTH   A polypeptide hormone from POMC precursor - secreted by corticotroph cells GPCR coupled to cAMP Stimulates secretion of cortisol from adrenal cortex in stress Stimulates growth of adrenal cortex  
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Hypothalamo-pituitary-adrenal axis   Stress e.g. infection, pain etc stimulates hypothalamus to secrete corticotrophin releasing hormone Anterior pituitary corticotroph cells release ACTH Adrenal cortex secretes cortisol Long feedback loop  
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Diurnal rhythm of plasma ACTH and cortisol   Released in pulses - increase in ACTH followed by increase in cortisol Peaks at 7am to prepare the body for waking Disruption of this leads to increased risk of CVD, T2 diabetes and depression Best health outcomes when hormones given by this rhythm  
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ACTH pathology   Excess ACTH from adenoma and in turn excess cortisol - Cushing's syndrome Deficiency of ACTH in turn cortisol deficient - adrenal insufficiency - treat with replacement cortisol  
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Gonadotrophins - LH and FSH   Used for reproduction Women - act in ovary via GPCR - FSH for follicle development and LH for ovulation and progesterone production Male - act in testes - LH for testosterone production and FSH for sperm production  
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Pathology of Gonadotrophins   Deficit - infertility in adult life - lack of sexual maturation Excess - precocious puberty at age 4/5  
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Hypothalamo-pituitary-gonadal axis   Hypothalamus secretes gonadotrophin releasing hormone Anterior pituitary gonadotroph cells release LH and FSH Ovary - oestrogen and progesterone Testes - testosterone Released in pulses every 90 mins Cyclical release in menstrual cycle  
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Control of prolactin release   Suckling inhibits dopamine release from hypothalamus Dopamine usually inhibits prolactin release, so this allows anterior pituitary lactotroph cells to release prolactin This triggers breast growth and milk production as well as causing infertility  
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Differences in prolactin release   Only pituitary hormone whose principle control is inhibitory PRL production is stimulated by estrogen during pregnancy Dopamine agonists e.g. bromocryptine suppress lactation Pathology - prolactinomas hyper secrete PRL - cause infertility  
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Control of growth hormone   Metabolites, sleep, stress and exercise trigger hypothalamus to secrete growth hormone releasing hormone Anterior pituitary somatotroph cells release growth hormone Short feedback loop GH acts directly + via liver IGFs to induce bone and muscle growth  
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GH pathology   Inactivating mutation in GHRH receptor - dwarfism No response to GHRH due to a single AA change in the GPCR Gigantism due to excess GH secretion Short stature if lack GH Only if occurs before epiphyseal plate fusion  
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Acromegaly   Due to excess GH secretion after epiphyseal plates have fused Enlargement of hands and feet Coarsening of facial features - largening of nose Weight gain  
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Stimulation of posterior pituitary hormone release   Neural stimulus depolarises neuron AP down axon Ca influx Exocytosis E.g. osmoreceptor cells outside BBB sense increased osmolarity and depolarise ADH neurons  
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Action of ADH   Increases water reabsorption in collecting ducts of kidney Triggered by increased osmolarity or volume of blood  
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Diabetes insipidus   Disorder of insufficient ADH production Hypothalamic - lack of ADH production by posterior pituitary Renal - Kidney fails to respond to ADH Characterised by production of large amounts of very dilute urine resulting in dehydration and polydipsia  
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Actions of oxytocin   Contraction of uterine muscle in childbirth Milk ejection by contraction of breast myoepithelium Role in social behaviours and parental behaviours due to release in brain Trust hormone  
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Control of oxytocin release   Stretch of cervix/vagina at parturition Sucking - nipple stimulation causes milk ejection reflex  
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Pathology of oxytocin   Deficit may cause prolonged labour Knockout mice labour normally but no milk ejection and impaired social recognition  
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Endocrine disrupting chemicals   Several reports of altered hypothalamic and pituitary hormone secretion, clinical disruption of circadian secretion and delayed puberty Molecules in the environment can disrupt pituitary function  
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