Endocrinology Flashcards
endocrine glands
cells that synthesise and secrete hormones into blood
hormone
chemical secreted into blood, acts on specific target cells to regulate cellular function
3 chemical classifications of hormones
peptides/ proteins - from DNA transcription and mRNA translation on RER - exocytosis (hydrophilic) steroids - from cholesterol - diffusion (lipophilic) biogenic amines - from tyrosine (aa) - diffusion (lipophilic), exocytosis (hydrophilic)
mechanism of action of hydrophobic hormones
e.g. steroid, biogenic amines (thyroid) hormones
bind to intracellular receptors
alters transcription, more/ less protein produced
mechanism of action of hydrophilic hormones
e.g. peptides, biogenic amines
binds and activates cell surface receptors
stimulates secondary messenger
two types of endocrine control
homeostatic response - homeostatic function e.g. ADH, PTH
adaptive response - adapt to specific stimulus e.g. insulin
regulating simple hormone response
involves one endocrine gland
regulated by circular response
e.g. ⬆ blood glucose, ⬆ pancreas insulin, glucose taken up by target cell, ⬇ blood glucose, pancreas stops releasing insulin
regulating complex hormone response
involves action of two or more endocrine glands
regulated by
- long, indirect feedback loop - final hormone affects first endocrine secretion
- long, direct feedback loop - final hormone affects second endocrine secretion
- short feedback loop - second hormone affects first endocrine secretion
- negative feedback - hormone output reverses stimulus
- positive feedback - hormone output encourages stimulus
anterior lobe of pituitary connection with hypothalamus
portal vessels transport hormones down pituitary stalk from hypothalamus to stimulate synthesis and secretion of hormones from anterior lobe
anterior pituitary hormones
synthesised in anterior lobe
tropic hormones - target cell is another endocrine cell
- gonadotrophs e.g. FSH (gametogenesis), LH (steroidogenesis)
- thyrotrophs e.g. TSH (thyroid secretion)
- corticotrophs e.g. ACTH (adrenal cortex secretes cortisol and aldosterone)
non-tropic hormones - directly affect target cell
- somatotrophs e.g. GH (increase glucagon and insulin)
- lactotrophs e.g. PRL (mammary glands, Na+ kidney reabsorption)
all are trophic hormones - induce cell growth in target cell
regulation of hormones from hypothalamus to anterior pituitary
controlled by tropic neurohormones of hypothalamus
posterior lobe of pituitary connection with hypothalamus
neurosecretory neurons connect posterior lobe of pituitary to hypothalamus
posterior pituitary hormones
synthesised in hypothalamus, stored and secreted in posterior lobe
magnocellular neurones synthesise
- ADH (water reabsorptionin kidney)
- oxytocin (uterine contractions)
three ways of hormone excess
primary hypersecretion from final endocrine gland
secondary hypersecretion from middle endocrine gland
secondary hypersecretion from first endocrine gland
functions of calcium (6)
calcium salt (calcium hyroxyapatite) in bone and enamel
trigger neurotransmitter release (exocytosis)
trigger hormonal secretion (exocytosis)
blood coagulation (cofactor)
enzymatic regulation (cofactor)
muscle contraction
calcium homeostasis in intestine (absorption and secretion)
paracellular pathway - Ca2+ passively between epithelial cells of ileum
transcellular pathway - taken up into epithelual cell and actively released into blood in dueodenum and jejunum
calcium homeostasis in kidney (filtration and reabsorption)
60% actively transported out of proximal tubule
30% diffuse out of loop of henle
9% actively transported out of distal tubule (PTH)
1% urine
calcium homeostasis in bone (formation and resorption)
remodelling - bone is always formed and resorbed in trabecullar bone to ECF
osteoclast secrete enzymes to resorb bone, Ca2+ into blood regulated by PTH (activate) and calcitonin (inhibit)
three primary cell types of trabecullar part of bone
osteoblast - form cells, secrete organic bone matrix (collagen, caclium hydroxyapatite)
osteocyte - mature bone cells
oestoclast - release hydrolytic enzymes to resorb bone, release Ca2+ into blood
preprohormone
preprohormone -> prohormone -> peptide hormone
PTH function (3 ways it does its function)
increase plasma [Ca2+] (stimulated by low [Ca2+])
stimulates Ca2+ reabsorption in kidney distal tubule
stimulates Ca2+ resorption in bone
stimulates 1-α-hydroxylase which catalyses 1,25 DHCC formation increases Ca2+ reabsorption in small intestine
1,25 DHCC formation
metabolite of vitamin D3 formed in skin by UV radiation or from diet
PTH triggers 1-α-hydroxylase to form 1,25 DHCC
1,25 DHCC function (3 ways it does its function)
increase plasma [Ca2+] (stimulated by low [Ca2+])
stimulates Ca2+ reasborption in kidney
stimulates PTH to bone resorb (but inhibits PTH gene expression so not out of control positive feedback)
stimulate Ca2+ absorption in intestine (stimulated by PTH)
calcitonin formation
in thyroid glands
calcitonin function (2 ways it does its function)
decrease plasma [Ca2+] (stimulated by high [Ca2+])
inhibits Ca2+ in bone resorption
decreases Ca2+ reasborption in kidney
osteoperosis
reduced bone density by bone resorption exceeding bone formation
osteomalacia/ rickets
inadequate mineralisation of bone by vitamin D activity deficiency
hypocalcaemia
insufficient Ca2+ by deficiency/ resistance to PTH
pancreas endocrine/ exocrine
exocrine 98% - synthesise and secrete digestive hormones into central duct
endocrine 2% - 3 cell types
- α-cell secrete glucagon
- β-cell secrete insulin
- D-cell secrete somatostatin (aka GIH inhibit glucagon and insulin secretion)
glucose taken into target cells when in fed state
muscle - glycogen
liver - glycogen, triglyceride
adipose cells - triglyceride
every cell in body is target to insulin except liver and brain (able to take up glucose without insulin)
insulin dependent diabetes mellitus (type 1)
insulin deficiency due to β-cell destruction
insulin independent diabetes mellitus (type 2)
abnormal target cell response to insulin
Cushing’s syndrome
hypercortisolism (excess cortisol produced in zona fasciculata in adrenal glands)
excess lipolysis (fat redistribution to face) excess protein breakdown/ tissue wasting (weak, thin arms and legs) excess gluconeogenesis (diabetes) surpressed immune response
Grave’s disease
hyperthyroidism (excess thyroxine) primary hypersecretion
edema causes exophthalmos (wide staring gaze, bulging eyes)
