Lectures 22 & 23 (endocrine intro + pituitary) Flashcards
how endocrine hormonal messages function vs neural messages
- hormones circulate through the entire body whereas neurons only deliver signals to specific areas
- they last from minutes to days whereas neural is less than a second to minutes
- slow to begin signalling (s to m) whereas neural is milliseconds
- blood borne
- many are also neurotransmitters
Endocrine glands
- hypothalamus
- pineal gland
- pituitary gland
- thyroid gland
- parathyroid glands
- adrenal glands
- pancreas
- testes or ovaries
**placenta (temporary, only during pregnancy)
Pathology associated with endocrine system
- gigantism or acromegaly (excess growth hormone)
- hyper/hypothyroidism (excess/defficient thyroid hormone)
- hyper/hypoprolactinaemia (excess/deficient prolactin)
- diabetes (low/insensitivity to insulin)
- adissons disease (deficient cortisol or ACTH)
- cushing’s syndrome (excess cortisol)
Hunger hormone communication
- fat cells make leptin when ‘full’ to signal the hypothalamus –> stop eating
(leptin deficiency can cause individual to overeat) - empty stomach produces ghrelin to signal the hypothalamus –> start eating
Endocrine cell hormone communication (pathway + types)
- hormones made in endocrine cell, travels through blood, captured by receptor on distant cell, trigger hormone effect, hormone detaches, effects dissipate
- hydrophillic (most common) and lipophillic
Paracrine cell hormone communication
- hormones made in paracrine cell only effect nearby cells
(eg: prostaglandins and nitric oxide)
Autocrine cell hormone communication
- hormones made in autocrine cell only effect the cell itself
(eg: IGF1 - growth factors work as autocrine at times)
hydrophillic circulating hormones
- water soluble, travel through blood
- bind to extracellular receptors
- message must be transduced to effect the cell
- often leads to production of second messengers (eg. cAMP, IP3)
- second messengers alter cellular function (one H hormone can cause many SM)
- SM concentration fluctuates depending on H hormone receptor binding
*some hormones (eg: insulin) do not need second messengers
lipophilic endocrine hormones
- travel through blood
- pass through phospholipid bilayer (intracellular or even intranuclear)
- bind to intracellular receptors
- hormone-receptor complex binds to DNA
(steroid hormones)
Controlling hormone secretion (loop)
all hormones work with negative feedback
(stimulus –> increased hormones –> signal decreased stimulus –> decreased hormones)
eg:
- chemical alteration in blood (exercise)
- nervous stimulation (fear response)
- other hormones can signal hormone production
Posterior pituitary gland hormone circulation
- hormones made by neurosecretory cells in hypothalamus
- hormones travel in axons to the PPG
- enter bloodstream through hypophyseal veins and arteries
Anterior pituitary gland hormone circulation
- releasing hormones made by neurosecretory cells in hypothalamus
- travel in axons to hypophyseal portal system
- travel through blood to APG
- triggers stimulating/tropic or non-tropic/direct hormone production in APG release into blood
- stim. h. goes to target area (may produce another direct/non-tropic hormone)
- hormones travel back to hypothalamus and APG, inhibiting hormone production
(fluctuating cycle of hormones)
Thyroid hormone regulation
- hypothalamus: thyrotropin releasing hormone (TRH)
- anterior pituitary: thyroid stimulating hormone (TSH)
- thyroid gland: thyroid hormone
- triggers increased metabolic rate, protein synthesis and fat breakdown
Inhibiting hormones
- inhibits production of stimulating hormone
(eg: growth hormone inhibiting hormone GHIH inhibits GH and TSH)
(prolactin is almost completely regulated by its inhibiting hormone PIH (dopamine), little bit by releasing hormone TRH)
Pituitary gland development
anterior: outgrowth of the ectoderm of the roof of the mouth (pars distalis)
posterior: outgrowth of the ectoderm at the base of the hypothalamus (pars nervosa)
pars intermedia: seperates ant. and post.
(develops at 5 - 16 weeks of pregnancy, W13, the pituitary, 3:00)
alternate names for posterior and anterior pituitary
anterior: adenohypophysis
posterior: neurohypophysis
pituitary: hypophysis
bone of the skull where the pituitary is located
Sphenoid –> hypophyseal fossa
structures that form turk’s saddle/sella turcica
tuberculum (front), hypophyseal fossa, dorsal (back) sellae
(part of sphenoid)
Pituitary tumour
pituitary adenoma –> can cause a depression in the hypothalamus (called mass effect)
symptoms: visual defects (optic chiasm, bitemporal hemianopia) and headaches
removal: transsphenoidal hypophysectomy, remove tumour through sphenoid sinus (up nose), replace with fat and seal in with cartilage and glue
Pituitary blood supply
- Ant: superior hypophyseal artery –> hypophyseal portal veins –> ant. hypo. v.
- Post: inferior hypophyseal artery –> post. hypophyseal veins
issues: BP extremely low in AHV, if BP drops in body (eg: extreme blood loss) it’s easy for blood flow to stop here, APG can die –> panhypopituitarism
Main hormones in Anterior pituitary
Tropic (stimulating):
- FSH: follicle stimulating hormone - promotes follicle and sperm development
- LH: luteinizing hormone - promotes ovulation, sex steroid production
- ACTH: adrenocorticotropic hormone - promote production of glucocorticoids
- TSH: thyroid stimulating hormone - stims thyroxin release
Non-tropic (direct):
- PRL: prolactin: stimulates milk production in F
- hGH: human growth hormone - promote protein synthesis + bone growth + glycogen –> glucose
- MSH: melanocyte stimulating hormone - increase pigmentation (pars intermedia)
(FLAT PeG M)
Main hormones in Posterior pituitary
**produced in hypothalamus, just travel through PPG
- Oxytocin: increase uterine contraction + ejection of milk
- ADH: Antidiuretic hormone (vasopressin) causes water re-uptake in kidneys (suppresses urination) - triggered by high Na in blood
Hormones produced in Hypothalamus
- TRH –> produce TSH
- CRH –> produce ACTH
- GnRH –> produce FSH and LH
- GHRH –> produce hGH
- GHIH –> inhibit hGH
- PIH –> inhibit PRL
stimuli that regulate growth hormones
hypoglycemia (low blood glucose) –> release GHRH (promote (hGH)
hyperglycemia (high BG) –> release GHIH (inhibit hGH)
- normal BG is about 90mg/mL
growth of long bones stimulus
- hGH stimulates formation of new cartilage at epiphyseal line
- growth plate is ‘closed’ by testosterone and estrogen
hGH secreting tumors
before growth plate closes: gigantism (very tall)
after growth plate closes: acromegaly (thick skin, broad nose…)
both diabetic due to high BG
Main sex steroids
progesterone, estrogens, androgens (testosterone, DHEA)
*act as inhibitors for GnRH
Prolactin regulation
TRH promotes PRL
PIH inhibits PRL
suckling inhibits PIH
- domperidone (dopamine receptor blocker) inhibits PIH since it is dopamine
excess/deficient prolactin issues
hyperprolactinaemia (excess)
- galactorrhea (large amount of milk/milk outside pregnancy)
- amnenorrhea (lack of menstrual cycles)
- infertility
- impotence (inability to get erect - males)
hypoprolactinaemia (deficient)
- sub/infertility in both men and women (cause unclear)
development of lactating (active) mammary glands
high levels of estrogen and progesterone trigger activation
- that’s why breaks are needed from hormonal birth control pills
