Endocrinology Physiology Flashcards
What are the major endocrine organs ? (7)
- Pituitary
- thyroid
- parathyroid
- pancreas
- adrenal
- ovaries
- testes
name the hormone produced from all of these organs
- heart
- liver
- kidney
- GI tract
- blood vessels
- heart (ANP)
- Liver (IGF-1)
- Kidney (erythropoietin)
- GI tract (Gastrin, incretin)
- blood vessels: NO, endothelin
what are the two broad categories of hormones ?
- water soluble
- lipid soluble
describe water soluble hormones ? are they bound to proteins ? where do they bind to receptors ?
give examples
unbound to proteins so bind to surface receptors (can just dissolve in water so don’t need something to help with transport)
- peptides
(stored in vesicles and then released, shorter half life + faster clearance)
describe lipid soluble hormones ? are they bound to proteins ? where do they bind to receptors ?
give examples
bound to proteins so diffuse into cells + bind to receptors
- steroid hormones, thyroid hormones
what is leptin ? where is it released from ? where does it act on ?
eat => increased fat stores => leptin release => bind to receptors in hypothalamus => increase satiety
how do you know when to stop eating after a meal ? what makes you feel full ?
stretching of stomach by X nerve and release of CCK => brain tells you to stop eating (induces satiety)
what effects does CCK have ?
(induces satiety)
- delays gastric emptying
- gall bladder contraction and bile excretion
- insulin release
what is grehlin and what does it cause ?
elicits starvation signal
- grehlin => increase appetite + increase GH release
(vid vagal nerve)
Name the 6 hormones produced by the anterior pituitary ? (6)
- FSH
- LH
- ACTH
- TSH
- GH
- Prolactin
name the 2 hormones produced by the posterior pituitary ?
- oxytocin
- ADH
explain whether AP or PP stores and release hormones. ya know
- AP: produces and releases hormones
- PP: releases hormones produces by hypothalamus (so PP hormone secretion depends on stimulating or inhibiting hormones form hypothalamus)
describe the vasculature of the AP ?
has no arterial blood supply
- receives blood through portal venous circulation form hypothalamus
what is thyroid hormone basic function ?
BMR, growth
what is parathyroid basic function ?
calcium regulation
what is cortisol basic function ?
- stress response
- ## glucose regulation
what is aldosterone basic function ?
- BP
- sodium regulation
what is ANP basic function ?
sodium regulation
what is vit D basic function ?
calcium regulation
what does TRH stimulate release of from pituitary ? what does this hormone then cause ?
TSH release from pituitary
- controls how much energy your body uses (metabolic rate)
what does CRH stimulate release of from pituitary ? what does this hormone then cause ?
ACTH release from pituitary
- regulates glucocorticoid synthesis
- acutely stimulates cortisol release
what does GHRH stimulate release of from pituitary ? what does this hormone then cause ?
GH release from pituitary
- linear growth (children)
- acquisition of bone mass
- stimulates protein synthesis, lipolysis, glucose metabolism
(muscle + bone)
what does GnRH stimulate release of from pituitary ? what does this hormone then cause ?
LH + FSH release from pituitary
- LH: causes estradiol secretion from theca cells (female) and testosterone from leading cells (male)
- FSH: causes inhibit secretion from sertolli cells (male) and granuloma cells (female)
what does dopamine stimulate release of from pituitary ? what does this hormone then cause ?
reduces prolactin release from pituitary
- positive feedback
- milk production => increased prolactin
what are the 2 parts to the adrenal gland ?
- adrenal cortex
- adrenal medulla
what is made in the adrenal cortex ?
corticosteroids
what is made in the adrenal medulla ? from what cells
catecholamines (mainly form chromatin cells)
what are the different sections to the adrenal cortex ?
- zona glomerulosa
- zona fascicolata
- zona reticularis
what does zona glomerulosa produce ? what is the action of this ?
affects GLOMerulus
- mineralocorticoids (aldosterone)
(SALT)
what does zona fasciculata produce ? (type of hormone and example) what is the action of this ?
act Fast (stress, cortisol)
- glucocorticoids (cortisol)
(SUGAR, STRESS)
what does zona reticularis produce ? (type of hormone and example) what is the action of this ?
androgen precursor to be converted to oestrogen + testosterone in gonads
- androgens (DHEA)
(SEX)
what does GH act on ? stimulate secretion of what ?
acts on liver to secrete IGF-1 which acts on bone + other (growth)
in a fasting state, where does glucose come from ? by what process ?
all glucose comes from liver (little bit form kidney) by glycogenolysis
after feeding, describe the glucose and insulin levels ?
high glucose => high insulin => replenish glycogen stores in liver and muscles
describe the actions of insulin (4)
- decrease glycogenolysis
- decrease gluconeogensis
- increase glucose uptake into glucose dependant cells
- decrease lipolysis
- oppose glucagon
what is the action of glucagon ?
- increase hepatic glucose output
- increase peripheral release of gluconeogneic precursors
where does gluconeogenesis take place ? how do the precursors get here ?
in the liver
- precursors transported to the liver to make glucose (FFA from lipids provide energy to drive this process)
what are insulins counter regulatory hormones ?
- Glucagon
- Ad
- cortisol
- GH
what do Alpha, beta and gamma cells of islets of langerhan produce ?
alpha: glucagon
beta: insulin
gamma: somatostatin
how does high glucose lead to insulin release ? on a cellular level
glucose enters beta cells (facilitated diffusion through GLUT 2 glucose transporter) => Ca2+ flood in => insulin release
does the action of insulin at a cellular level
insulin travels to muscle + fat cells => binds to insulin receptor => intracellular signalling cascade => GLUT-4 vesicles travel to + incorporate themselves within membrane => glucose enters cell through GLUT 4 transporter
how is Ad response level affected in diabetes ? what does this then mean ?
Ad defence level is reset at a lower blood glucose level = BAD (glucose level needs to be even lower to elicit response)
- brain doesn’t work properly so doesn’t recognise that glucose levels too low
describe the arterial supply of the thyroid gland ? why is this important ?
- superior thyroid artery (branch of external carotid)
- inferior thyroid artery (branch of thyocervical trunk)
(has rich arterial supply because needs iodine)
describe the venous drainage of the thyroid gland ?
superior, middle and inferior thyroid veins => internal jugular
what are the 2 different forms of thyroid hormone ?
T3, T4
- the thyroid produces mainly T4 and then peripheral conversion to T3 (at target tissue)
- T3 then stimulates cellular oxy consumption and energy generation
patients with which other conditions should get screening for thyroid disease ? (7)
- AF
- hyperlipidaemia
- DM
- patients on amiodarone
- patients with down/turners/addisons
in what 3 forms is calcium present in the body ?
- ionised (most useful to cell/metabolically active)
- protein bound (not metabolically active)
- complexed
what is calcium regulation controlled by ? how does small change in calcium affect this ?
small changes in serum Ca2+ (ionised) => big PTH change
- small range because Ca2+ essential for functioning of nerves and muscles (heart)
how does low calcium affect PTH ? what affects does this then have ?
low Ca2+ => high PTH =>
- Bone: increase bone resorption
- kidneys: increase Ca reabsorption, decrease phosphate reabsorption (when one up the other down)
- Gut: increase active Vit D formation => increase Ca absorption from GI tract
how does PTH affect vit D regulation ?
increase PTH => increase conversion of Vit D to active form in liver => increase Ca2+ + Pi intestinal absorption
what is calcitonin ? secreted from where ? in response to what ?
hormone secreted by C cells in thyroid when Ca is high to lower it
how could low serum albumin affect Ca measurement ?
low serum albumin => low serum calcium but no necessarily low Ca2+ so need to correct
what electrolyte is needed to excrete PTH ? how could this present
if patient presents with low CA and low PTH then could have low Mg because Mg is needed to excrete PTH
vit D deficiency: describe the PTH, Ca2+, Phosphate levels ?
- PTH: high
- Ca: low
- Phosphate: low
(appropriate PTH response)
hypoparathyroidism: describe the PTH, Ca2+, Phosphate levels ?
- PTH: low
- Ca: low
- High: high
(inappropriate PTH response)
pseudohypoparathyroidism: describe the PTH, Ca2+, Phosphate levels ?
- PTH: high
- Ca: low
- Phosphate: high
(appropriate - parathyroid doing what its meant to)
(pseudo…: resistance to PTH - target organs don’t respond)
malignancy: describe the PTH, Ca2+, Phosphate levels ?
- PTH: low
- Ca: high
- Phosphate: varies depending on cancer
(appropriate PTH)
primary hyperparathyroidism: describe the PTH, Ca2+, Phosphate levels ?
- PTH: high
- Ca: high
- Phosphate: low
(inappropriate PTH)
where is phosphate absorbed ?
absorbed in small intestine: passive at high conc, active at low conc (Na dependant)
what is involved in phosphate regulation ? main regulator ?
- PTH
- active Vit D
- FGF-23 (main regulator)
what is FGF-23 ? produced where ? in response to what ?
produced by osteocytes in response to high phosphate (to lower it)
what are the actions of FGF-23 ? (3)
- decreases expression of Na transporter in renal tubule (=> increase renal excretion)
- reduce vit D synthesis
- reduce gut absorption
major extracellular cation ?
anion?
intracellular cation ?
major extracellular cation: Na
anion: Cl
intracellular cation: K
describe how changes in plasma osmolality leads to ADH changes ? and what this causes ?
reduces plasma osmolality => increased cellular hydration => decrease thirst (so reduces water uptake) + reduces Ash (vasopressin) secretion => increase ruine water excretion by kidneys => reduces total body water
where is ADH synthesised ? acts on what ?
synthesised in hypothalamus + acts on collecting duct
- concentrates urine: stops 180L daily filtrate being excreted
how to DPP-4 inhibitors work ? what are they also known as ? give example of one
gliptins (sitagliptin)
- reduce peripheral breakdown of incretins (GLP-1: hormone released by small intestine in response to an oral glucose load)
when are gliptins used ? useful in which patients
used when triple combo of drugs has failed
- useful in patients who are obese
how does metformin work ?
increases peripheral insulin sensitivity and reduces hepatic gluconeogenesis
how do sulfonylureas work ? name one
gliclazide
- augment pancreatic insulin secretion
gliclazide SE ?
(sulphonylurea)
- weight gain (=> increase insulin => increase fat storage)
how do SGLT2 inhibitors work ? name one
dapagliflozin
- lower blood sugar levels by preventing kidneys from reabsorbing glucose
Dapagliflozin SE ? (2)
(SGLT2 inhibitor)
- SE: euglycaemic ketoacidosis
- increased UTI risk
