Endocrine Flashcards
name the 4 main classes of hormones
modified amino acids
steroids
peptides
proteins
what type of hormone is adrenaline
amino acid
what type of hormone is cortisol or testosterone
steroids
what type of hormone is ACTH or ADH
peptides
what type of hormone is insulin
protein
why is the signal transduction cascade that occurs when hormone binds to receptor important
it typically causes an amplification of signal
this amplification is important due to the scarcity of the original signal
what makes the synthesis and release of steroid hormone different from that of amines, peptides and proteins?
steroid is synthesised and secreted upon demand
the others are presynthesised and stored in vesicles
steroid is hydrophobic, the rest are hydrophilic - steroid requires a carrier protein to travel in blood
the others are released via Ca2+ dependant exocytosis
steroid hormones have the shortest 1/2 life and amines have the longest. true?
false - amines have the shortest, steroids have the longest
which hormone receptor is activated by amines
G-protein coupled receptor
which hormone receptor is activated by proteins/peptides
receptor kinases
which receptors are cell surface receptors and have a hydrophilic ligand
GPCR
receptor kinases
which hormone activates class I nuclear receptors
steroid hormones
describe the movement of class I nuclear receptors in presence of activating ligand
in the absence of activating ligand = found in cytoplasm
when activated, they are bound to inhibitory heat shock proteins and move to nucleus
what hormone activates class II nuclear receptors
lipids
what hormones activate hybrid class nuclear receptors
thyroid hormones
which hormone receptors are intracellular with a lipophilic ligand
all the nuclear receptors
does the Gs protein increase or decrease cAMP production. what does this cause
increases production of PKA, causing MORE cellular effects
does the Gi protein increase or decrease cAMP production. what does this cause
decreases production of PKA, causing LESS cellular effects
what does Gq G protein convert. what does this do
INCREASES the conversion of PIP2 –> IP3 by phospholipase C
causes increased calcium release from ER
this causes increased cellular effects
how does glucose enter the B cells and what is it phosphorylated by
through GLUT 2
phosphorylated by glucokinase into glucose - 6 phosphate
what happens to the glucose-6-phosphate
it goes through the TCA cycle and produces 36 ATP
in the process of insulin secretion, what does the increased ATP levels cause
inhibit the ATP-sensitive K+ channel (KATP), causing depolarisation of the cell membrane
this results in opening of the voltage gated Ca2+ channels
an increase in intracellular Ca2+ levels causes fusion of secretory vessels and release of insulin
what are the 2 proteins that make up the KATP channel
KIR6- congenital mutations of this can lead to neonatal diabetes
SUR1
what is the gist of diabetic ketoacidosis
a state of absolute insulin deficiency
if you have no insulin, GLUT2 won’t open, so no glucose can get into cells –> cells are starved of glucose
you get a build up of glucose in the blood, and an increase in production of counter-regulatory hormones
they make more glucose to try and get it into the cells and ketone levels in blood increases
what are the counter regulatory hormones that are produced in DKA and what is their effect
glucagon, cortisol and GH
they cause an increase in gluconeogenesis, glycogenolysis and lipolysis
contributes to the hyperglycaemia and ketone overload in blood
which hormones are released by the anterior pituitary`ry
GH, TSH, ACTH, FSH
which hormones are released by posterior pituitary
ADH and OT - synthesised in the hypothalamus
what does pituitary lie immediately inferior to
the optic chiasm
what is the function of leptin and how is it affected in obesity
it tells your body how full you are
no leptin = brain thinks you’re starving
if you have lots of fat stores, leptin isn’t as effective and causes a flat dose response curve
this means that there is little increase in response over a wide range of doses
what is adaptive thermogenesis
the body perceives weight loss as a threat to survival
as you’re eating less to lose weight, your body will lower metabolic rate, making it harder to lose the weight
where is the thyroid found
on the 5th cervical/1st thoracic vertebrae
in between 2nd and 4th tracheal rings
what gives parasympathetic innervation to the thyroid
the vagus nerve
what gives sympathetic innervation to the thyroid
sympathetic fibres - superior, middle and inferior ganglia of sympathetic trunk
what is the blood supply to the thyroid
superior and inferior thyroid arteries
what does the colloid contain
tyrosine containing thyroglobulin
what cells encapsulate the colloid
follicular cells
what do the parafollicular C cells secrete
calcitonin
what does iodine attach to when it enters the follicular cell and what does this form
attaches to tyrosine residues on thyroglobulin to form MIT and DIT
what is T3 made up of
1x MIT
1x DIT
what is T4 made up of
2xDIT
where are T3 and T4 stored until they are required
the colloid thyroglobulin
are T3 and T4 hyrophobic or phillic
hydrophobic - they need to bind to plasma proteins to be transported
does metabolic rate correlate more closely with free or bound thyroxine
free T3 and T4
what causes an increase in total T4 but not in fT4
pregnancy, newborn state
HEPA, chronic active hepatitis, biliary cirrhosis
acute intermittent porphyria
heroin.
what causes a decrease in total T4 but not in fT4
androgens
loss of glucocorticoids, Cushing’s syndrome
active acromegaly
chronic liver disease, nephrotic syndrome
severe systemic illness
how do thyroid hormones increase responsiveness to adrenaline and noradrenaline
by increasing no of receptors
this is why you need to use B Blocker during initial therapy for hyperthyroidism
what effect does stress have on TRH and TSH release
inhibits their release, causing hypothyroidism
what enzymes are important in the activation/deactivation of thyroid hormones
deiodinase enzymes
D2 activates T4 –> T3
what is the pituitary derived from
rathke’s pouch
what are the 3 zones of the cortex in the adrenal gland and what does each produce
zona glomerulosa - produces aldosterone
zona fasciculata -produces glucocorticoids
zona reticularis - produces adrenal androgens
what does the medulla of the adrenal gland produce
catchecolamines (epinephrine)
what effect does the RAAS system have on ion levels
it causes K+ excretion
increased Na+ absorption (the water follows salt, so you get increased water reabsorption)
what hormone is calcium absorption in small intestine controlled by
parathyroid hormone
what effect does hypocalcemia have on PTH excretion
hypocalcemia causes INCREASED secretion of PTH
what is calcitonin and where is it produced
it opposes the action of PTH (a parathyroid hormone antagonist)
it is produced in the parafollicular cells in thyroid gland
calcitonin is released in response to hypocalcemia? true?
no! calcitonin released in response to Hypercalcemia
it surpasses osteoclast activity
what is bone mostly made up of and what is this compound composed of
hydroxyapatite
made up of calcium phosphate
what enzyme is responsible for the production of hydroxyapatite
alkaline phosphatase
