endocrine system Flashcards
compare the differences between endocrine system and nervous system
endocrine system - slow, releases hormones, regulate activities that require duration rather than speed like growth and reproduction, maintains homeostasis, long distance signalling where the hormone travels in the bloodstream to target cells
nervous system - fast, releases neurotransmitters, regulate activities of muscles and glands, local signalling through paracrine and synapse signalling
what is paracrine signalling
secreting cells act on nearby target cell by discharging molecules from a local regulator into ecf
what is synapse signalling
nerve cells release neurotransmitter molecules into a synapse, stimulating the target cell
what is hormonal signalling
specialised endocrine cells that secrete hormones into body fluids
what is a hormone
substances released by endocrine glands that travel in the bloodstream to target tissues where they act to regulate specific functions by binding to hormone receptors on target cells
how do you classify hormones
central and peripheral
what are examples of central glands
pineal, hypothalamus, pituitary
what are examples of peripheral glands
thyroid, parathyroid, thymus, adrenal, pancreas, ovary/testis
what hormone does hypothalamus secrete
releasing and inhibiting hormones
what hormone does thyroid gland secrete
T4, T3, calcitonin
what hormone does parathyroid gland secrete
PTH
what does adrenal gland secrete
cortex - aldosterone, cortisol, androgens
medulla - epinephrine, norepinephrine
what does the gonads secrete
testis - testosterone, estradiol, inhibin, mullerian-inhibiting hormone (MIH)
ovary - progesterone, estradiol, inhibin
what does the placenta secrete
human chorionic gonadotropin (hCG), progesterone, estrogen
what does the pancreas secrete
insulin, glucagon, somatostatin
what does the pineal secrete
melatonin
what does the kidney secrete
calcitriol (vitD)
which of the hormones are proteins and peptides
LH, FSH, GH, ACTH, PTH, inhibin, calcitonin, ADH, vasopressin oxytocin, hCG, insulin, glucagon
which of the hormones are amines
T4, T3, epinephrine, norepinephrine, melatonin
which of the hormones are steroids
cortisol, aldosterone, testosterone, progesterone, estradiol, estrogen, calcitriol
compare the difference between an endocrine gland and an exocrine gland
endocrine glands produce hormones and are ductless glands that releases hormones into surrounding tissue fluid
exocrine glands produce nonhormonal substances and have ducts that carry substances to a membrane surface
what hormones does the pituitary secrete
anterior - LH, FSH, GH, adrenocorticotropin (ACTH), TSH, prolactin (PRL)
posterior - antidiuretic hormone (ADH), vasopressin oxytocin
are protein and peptide hormones hydrophilic or lipophillic
all hydrophilic
are steroid hormones hydrophilic or lipophilic
all lipophilic
are amine hormones hydrophilic or lipophilic
hydrophilic - T3, T4
lipophilic - NE, E
what does it mean for a hormone to be hydrophilic
dissolved and transported freely in blood
what does it mean for a hormone to be lipophilic
bound to plasma protein, bind to intracellular receptors
what is the moa of hormones
signal amplification and alteration of functional and structural proteins, enzyme activation and transcription
what happens during signal amplification
hormones bind to receptor which activate G proteins (guanine), subsequently activate adenylyl cyclase to trigger formation of cAMP
what happens during alteration
alteration occurs in channel permeability by acting on pre existing channel forming proteins, second messenger systems to alter activity of pre existing proteins and activate specific genes to form new proteins
how to measure hormone levels
radio immunoassays (RIA), enzyme linked immunosorbent assays (ELISA), measurement sites (blood, urine, saliva, tissue)
what are the two types of hormone receptors
cell membrane receptors and intracellular receptors
what type of hormones are cell membrane receptors for
lipophilic
what type of hormones are intracellular receptors for
hydrophilic
what AA is amine hormones
tyrosine derivatives
where is the thyroid located
in the neck, anterior surface of trachea, immediately below the larynx
what are some characteristics of the thyroid
two lobes connected by isthmus, extensive blood supply for hormones produced to go into circulation
what are the components of the thyroid
follicular cells, thyroid follicles, colloid, parafollicular/ C cells
what is the function of the follicular cells
generate a globular protein called thyroglobulin and secrete into colloid of thyroid follicles
what is the function of the thyroid follicle
functional unit for thyroid hormone production
what is the function of the colloid
extracellular space where storage of thyroglobulin that is attached with iodine atoms
what is the function of the parafollicular cells
cells in between the follicles that secrete calcitonin to regulate Ca homeostasis
how is thyroid hormone synthesised
thyroglobulin produced by ER/ golgi complex in the follicular cells and Tyr is attached during its production which is then exported in vesicles from follicular cells into colloid by exocytosis
I- is picked up by thyroid from blood stream and is transferred into the colloid by Na/K pump whre Na+ enters the cell down its concentration gradient and I- enters the cell against its concentration gradient
I- oxidised to active iodine by thyroperoxidase (TPO) which is a membrane bound enzyme and active iodide enters the colloid through a channel
TPO attaches the active iodide to Tyr within the Tg molecule to produce mono-iodotyrosine (MIT) and di-iodotyrosine (DIT)
coupling of MIT and DIT produces tri-iodothyronine and coupling of DIT and DIT produces tetraiodothyronine/ thyroxine
when there is stimulation of production of TH, the follicular cells internalises a part of the Tg-hormone complex by phagocytosing a part of the colloid such that it shuttles the colloid into the follicular cells
lysosomes attack engulfed vesicles and split the iodinated products from Tg
lipophilic T3 and T4 diffuse freely through the outer membranes of the follicular cells into the blood
iodinase enzymes in follicular cells removes iodide frm MIT and DIT since it is of no endocrine value such that it allows freed iodide to be recycled for hormone synthesis
when T3 and T4 enters the blood, since it is lipophilic it will quickly bind to plasma proteins
how is T3 and T4 metabolised and excreted
they are metabolised by conjugation with glucoronic acid in the liver which is then secreted in the bile and largely eliminated in the feces with small amounts in the urine
is T3 or T4 the active form
T3, primarily makes T4 first then 80% of T3 derived from secreted T4
how is T3 and T4 released
hypothalamus uses precursor thyrotropin releasing hormone (TRH) to stimulate the anterior pituitary to release TSH which stimulates thyroid glands to release T3 and T4
how is the level of TH managed
by negative feedback
if there is sufficient T3, negative feedback to anterior pituitary to stop releasing TSH and hence causes hypothalamus to stop releasing TRH
if insufficient T3, positive feedback to hypothalamus to make TRH and to pituitary to release TSH, TSH will form peptide bonds with TSH receptors to cause signal amplification which causes release of T3 and T4
what are the physiological effects of T3 and T4
increases BMR
sympathomimetic effects
cvs effect
essential for normal bone growth and development
for cns development
increase synthesis and metabolism of protein, lipids and carbs
which tissues does not have BMR
brain, skin, spleen, gonads, thymus
how does T3 and T4 increase BMR
increase in number and size of mitochondria and increase in enzymes that regulate oxidative phosphorylation thus resulting in increase in O2 consumption and energy use under resting condition
what happens when there is increase in BMR
heat production
how does T3 and T4 cause sympathomimetic effects
TH increases proliferation of catecholamines target cell receptors hence increases target cell responsiveness to catecholamines
what happens when there is sympathomimetic effects
increase heart responsiveness to cathecolamines which increases HR and force of contraction and thus increase CO
why is TH essential for bone growth
TH stimulates secretion of GH and increases IGF-1 production by liver and promote effects of GH and IGF-1 on synthesis of new structural proteins on skeletal growth
what are the causes of hypothyroidism
primary failure of thyroid gland itself, cannot make TH
secondary to deficiency of TRH, TSH/ both
inadequate supply of iodine
what are the clinical symptoms of hypothyroidism
dull blank expression, extreme fatigue, brittle hair and nails, constipation, intolerance to cold
what are the late manifestations of hypothyroidism
subnormal temperature, bradycardia, weight gain, cardiac complications, thickened skin
what are the causes of hyperthyroidism
production of TSI (an immunoglobulin)
secondary to excess TSH, TRH or both
hypersecreting thyroid tumor which causes excess secretion of TH
what are the clinical symptoms of hyperthyroidism
bulging eyes, intolerance to heat, diarrhoea, weight loss, increase systolic BP, enlarged thyroid, muscle wasting, fatigue, restlessness, oligomenorrhea and amenorrhea, irritability, sweating
what are the treatment options for hyperthyroidism
antithyroid drugs that interfere with TH synthesis by either blocking uptake of I- or inhibition of TPO, surgical removal of hypersecreting thyroid gland, administration of radioactive iodine to destroy thyroid glands
what is grave’s disease
an autoimmune disease that leads to hyperthyroidism
what is the cause of grave’s disease
production of TSI which is an Ab that competes with TSH for binding to TSH receptors and is not susceptible to negative feedback thus leading to hypersecretion and growth of the thyroid
what is goiter
enlarged thyroid gland and develops when thyroid gland is overstimulated by increase in TSH or increase in TSI
how does hypothyroidism cause goiter
due to inability to make TH, there is increase in TSH production by anterior pituitary
if there is lack of iodine, there is also low TH which causes negative feedback and cause high TSH
how does hyperthyroidism cause goiter
excessive TSI-TSH receptor activation
how does growth of thyroid tissue occur
increase follicle formation, increase number and size of cells, increase DNA, RNA, protein and phospholipid synthesis
where is the pancreas located
in the abdomen, behind the stomach
what are the two parts of the pancreas
exocrine portion and endocrine portion
what are the components in the exocrine portion
acinar and duct cells
what are the components in the endocrine portion
islets of langerhans
what do acinar and duct cells secrete
acinar cells secrete digestive enzymes, duct cells secrete NaHCO3 solution
what do islets of langerhans secrete
hormones into blood stream
what are the cell types in islets of langerhans
beta cell, alpha cell, D cell, capillaries
what do beta, alpha and D cell secrete
beta cells secrete insulin and amylin, alpha cell secrete glucagon, D cell secrete somatostatin
what is the importance of insulin and glucagon
to regulate fuel metabolism
how is insulin produced
result from excitation-secretion coupling
foods rich in carbohydrates causes beta cell to uptake glucose via transporter GLUT2
glucose undergoes phosphorylation to form glucose-6-phosphate which feeds into the Krebs cycle in the mitochondria
G-6-P undergoes oxidation which releases ATP as a product and acts on ATP sensitive K channel which causes depolarisation such that there is more K+ in the cell as less leaves
this causes increase in Ca2+ entering the beta cell through the voltage gated Ca channel and thus beta cell produces and releases insulin from the insulin vesicle
what is glucose phosphorylation
trapping of glucose inside the cell and keep plain glucose levels low to maintain diffusion gradient
what are the actions of insulin
glucose uptake through GLUT4 and increase glycogenesis, lipogenesis and proteogenesis
where are the different GLUT transporters located
GLUT1 - endothelial cells in bbb
GLUT2 - kidney, liver, beta cells in pancreas
GLUT3 - neurons
GLUT4 - insulin sensitive in adipose and muscle tissues
what is the process of glycogenesis
carbohydrates (metabolic fuel) -> glucose (circulating) -> glycogen (stored form)
what is the process of lipogenesis
fats -> FFA -> TGL in adipose tissues
what is the process of proteogenesis
protein -> AA -> protein in muscles
how is blood glucose regulated
by uptake for cellular and brain function, storage of excess glucose for later use (in liver and muscles as glycogen and as TGL in adipose tissues)
what is the function of glucagon
mobilise energy rich molecules from their stores, opposes action of insulin and overall increases blood glucose levels
what is the difference between type 1 and type 2 DM
type 1 diabetes occurs as a result of an autoimmune process where the beta cells in pancreas is destroyed and thus insulin cannot be produced, is affected by genetic and/or environmental factors
type 2 diabetes occurs as the insulin produced is insufficient or not well utilised due to insulin resistance, is affected by lifestyle and genetics
what is insulin resistance
cells with receptors cannot be activated by insulin for gate to open and uptake
what is glucogenesis
glucose formation from non carb sources (eg. from protein)
draw flow chart of effects of insulin deficiency
carbs metabolism (increased hepatic output, decreased uptake by cells)
fat metabolism (decrease TG synthesis, increased lipolysis)
protein metabolism (decrease AA uptake by cells, increased protein degradation)
what are the chronic complications of DM
microvascular (nerve damage, retinopathy due to damage to eye blood vessels, kidney failure)
macrovascular (stroke due to damage of blood vessels in brain, heart attack due to damage and blockage of heart blood vessels, reduced blood circulation)
what is the balance equation for ketosis
H2O + CO2 -> H2CO3 -> H+ + CO3-
