Endocrine Flashcards
what 3 kinds of chemical messengers are used for signalling?
paracrine- hormones sent to neighboring target cells, NT and hormones (endocrine)
what are the major functions of the endocrine system?
-Metabolism
-Growth and development
-Reproduction
-Stress response
-Water and electrolyte balance
what is the difference between primary and secondary endocrine organs?
primary- make and secrete hormones
secondary- involved in a variety of biological processes in addition to hormone secretion
what factors regulate hormone secretion?
NT, other hormones, metabolites and ions
is diabetes an endocrine disorder?
yes
what are the 2 classes of hormones?
Hydrophobic and Hydrophilic
what kinds of hormones are hydrophobic? what are characteristics of hydrophobic hormones?
steroids and thyroid hormones
-poor solubility
-travel in blood bound to carrier proteins
-can cross the lipid bi-layer
-receptor found inside the cytosol or nucleus
what kinds of hormones are hydrophilic? what are characteristics of hydrophilic hormones?
peptides and catecholamines
-water soluble
-travel freely in the blood
-cannot cross the lipid bilayer
-receptor found ON membrane
how are signals sent for hydrophobic hormones?
hydrophobic hormones bind to a receptor to create a complex that is able to diffuse across the membrane
https://youtu.be/RnERznH4Gz8?si=uZ6sSIdhNiVImRuB
5, 2, 1, 4, 3
how are signals sent for hydrophilic hormones?
messenger binds to receptor outside of the cell which activates G-coupled receptor
-receptor converts GDP to GTP and cAMP is made
-Protein kinase A is then activated and cellular proteins are phosphorylated
https://youtu.be/RnERznH4Gz8?si=uZ6sSIdhNiVImRuB
2, 1 ,6, 5, 4, 3
how does caffeine affect hydrophilic messenger activity?
Inhibits phosphodiesterase’s which typically turn off cAMP signal. Inhibition of cAMP will leave signal on for longer which decreases adrenaline effects-
inhibits supressing effects
https://youtu.be/jOfquPE1cnU?si=fd7CY6xebkoWJfGU&t=200
where is the pituitary located in relation to the hypothalamus?
the pituitary lies outside of the brain and is conncted under the hypothalamus
what are the paraventricular nuclei?
located in the hypothalamus and extending to the posterior pituitary; they make and secrete ADH and oxytocin
what are the nuceli sending axons to median eminence?
neurons that origin in the hypothalamus and feed into the median emimence
what kind of blood circulation is there in the anterior and posterior pituitary?
portal circulation- blood goes against conventional flow of blood
is the anterior pituitary located in front or behind the posterior pituitary?
in front
what is the main function of the posterior pituitary?
make and secrete ADH and oxytocin
what is the major role of ADH (vasopressin)?
conservation of body water and blood volume
-increases water reabsorption in the kidneys
-increases blood pressure through vasoconstriction
explain step-wise how ADH affects the kidneys?
- ADH Release: Stimulated by high blood osmolarity or low blood volume.
- Receptor Binding: ADH binds to vasopressin receptors (V2) in renal collecting ducts.
- Second Messenger Activation: ADH activates adenylate cyclase, forming cAMP.
- Aquaporin Insertion: cAMP triggers insertion of aquaporin-2 channels.
- Water Reabsorption: Aquaporin channels allow water reabsorption.
- Urine Concentration: Increases water reabsorption, leading to concentrated urine.
what detects osomolarity in order to regulate ADH release?
-reduced stretch of walls due to high osmolarity (low blood volume)
fill in this chart
what system do hormones travel through to get to the capillaries?
the portal system
what kinds of hormones regulate the release of hormones produced in the anterior pituitary?
hypothalimic hormones
explain the general negative feedback system for hormones
there are 2 feedback systems to ensure proper regulation
1) increases in hormone 3 will supress releasing hormone from hypothalamus
2) increases in hormone 3 will inhibit stimulating hormone from the anterior pituitary
explain the feedback system for cortisol release
1) increased cortisol levels will work on the hypothalamus to inhibit release of corticotropin releasing hormone (CRH)
2) increased levels of cortisol will work on the anterior pituitary to inhibit release of adrenocorticotropic hormone (ACTH)
what hormones are released from the hypothalamus?
1) GHRH- growth hormone releasing hormone
2) GnRH- gonadotropin-releasing hormone
3) SST- somatostatin
4) TRH- thyrotrophin-releasing hormone
5) DA- Dopamine
6) CRH- corticotropin-releasing hormone
what hormones are released by the anterior pituitary?
growth hormone, thyroid stimulating hormone, prolactin, ACTH, FSH and LH
what affect does GHRH have on growth hormone?
increases GH release
what affect does SST have on growth hormone?
inhibits it
what affect does TRH have on TSH?
increases it
what affect does DA have on prolactin?
inhibits it
what affect does CRH have on ACTH?
increases it
what affect does ACTH secretion have?
cortisol release
what affect does prolactin secretion have?
breast development and milk production
what affect does TSH secretion have?
secretes thyroxine and triiodothyonine hormones (T4/T3)
what does growth hormone stimulate the release of? what affect does this have on metabolism?
secretion of IGF-1, protein synthesis and carb/lipid metabolism
what affect does FSH and LH secretion have?
improvement in reproductive development/ maturation
Around what age ie brain growth rapid?
4-8 years old
what ages are most common for growth spirts in humans?
postnatal growth spirt and puberty growth spirt
what is the epiphyseal plate?
site of bone growth
-cartilage between epiphysis and diaphysis
where are taget cells for GH and IGF-1 located?
in the epiphyseal plate
what are osteoblasts?
site of bone production
-provides collagen and proteoglycans
what are osteoclasts?
cells responsible for resorption or breakdown of the bone
-secretes acid to breakdown minerals
what are osteocytes?
osteoblasts that have become mineralized
-bone maintainers
what happens to bones without minerals?
they become very flexible and have little structure
what hapoens to bones that don’t have collagen?
They have no flexibility and may easily break
how does bone growth occur?
chondrocytes (bone cells) grow in size and become trapped by osteoblasts in order to be calcified and die
what are the steps in bone growth? what causes growth plate closure?
explain the steps in bone reparation?
1) blood escapes from bone making a hematoma
2) Tissue repair begins with fibrocartilaginous callus (compact bone)
3) osteobalsts produce spongy bone and to convert fibrocartilage to a bony callus, joining broken bones
4) osteoblasts build new compact bone and osteoclasts absorb spongy bone
what factors influence growth?
explain the GH feeback system
increased GH stimulates increased IGF-1 which:
1) ihibits GH at the anterior pituitary
2) inhibits GHRH at the hypothalamus
3) stimulates the release of SST (GH inhibitor)
what factors stimulate GH?
-sleep
-exercise
-stress
-low blood glucose
how does GH/ IGF-1 affect growth?
increased cell size- hypertrophy
increased cell number- hyperplasia
how does GH/ IGF-1 affect metabolic actions?
what is acromegaly?
excessive GH when growth plates are not open or responsive to it; past adolescence- GH gets triggered in other places high in cartilage (face)
what is gigantism?
excessive GH while growth plates are open and responsive to it
what are the effects of growth hormone-secreting hormone?
what important functions does Ca+ have?
-bone / teeth health
-muscle contraction
-heart contractions
-vesicle release
-blood clotting
where is the storage site for Ca+?
The bones
how do osteoblasts work with Ca+?
responsible for bone deposition and addition of Ca+ to the bone
how do osteoclasts work with Ca+?
responsible for bone resorption and release of Ca+ from the bone into the blood
what 3 hormones control plasma Ca+ levels?
1) parathyroid hormone (PTH)
2) Calcitriol (1,25-dihydroxycholecalciferol)
3) calcitonin
what are the three main target sites for hormones that control plasma Ca+ levels?
1) bones
2) kidneys
3) digestive tract
what stimulates PTH release?
low plasma [Ca+]
what does PTH release do to the bones?
stimulates bone resorption
what affect does PTH have on the kidneys?
-increases Ca+ reabsorption
-decreases phosphate reabsorption
-stimulates sythesis of calcitriol—> increases Ca+ absorption in the digestive tract
what is the overall effect of PTH?
increases plasma [Ca+ ]
what is hyperparathyroidism?
excess secretion of PTH = high blood [Ca+] levels
-tumours/hyperfunction of the parathyroid glands
-Vit D3 deficiency or chronic kidney disease
what is hypoparathyroidism?
inadequate secretion of PTH = low blood Ca+
-trauma to parathyroid glands
autoimmune damage to parathyroid glands
-congenital malformation
-PTH resistance if low blood [Ca+] but high [PTH}
what are symptoms of Hyperparathyroidism?
what are symptoms of Hypoparathyroidism?
how is calcitriol synthesized?
1) Vit D (7-dehydrocholesterol) is absobed by the skin and [Vit D] increase
2) in the liver, vit D is converted into 25-OH D3 by 25-hydroxylase which incerases the [ ] in blood
3) in the kidneys PTH stimulates the conversion of 25-OH D3 into Calcitriol by 1-hydroxylase
4) calcitriol levels increase which causes and increase in Ca+ absorption
what does Vit D defieciency cause?
rickets
-softening of bones due to mineral deficiency
-increases cancer risks and autoimmune diseases
where is calcitonin secreted from?
C cells in the thyroid gland
what is osteoporosis?
“porous bone”
-decreased bone mass leading to bone fragility and. increased fracture risk
what are risk factors of osteoporosis?
what can prevent osteoporosis?
what are treatments for osteoporosis?
how is TH regulated?
stimulation - cold
inhibition - stress and warmth
what is the function of the colloid in the thyroid?
contains thyroglubulin protein which is a precursor for thyroid hormones
-also contains enzymes and iodine
how are thyroid hormones synthesized?
1) Iodide Uptake: Active transport of iodide into thyroid follicular cells.
2) Thyroglobulin Synthesis: Production and secretion of thyroglobulin into the follicular lumen.
3) Iodide Oxidation:Conversion of iodide to iodine within the follicular lumen.
4)Iodination of Tyrosine: Attachment of iodine to tyrosine residues on thyroglobulin.
5)Coupling of Iodotyrosine: Formation of T4 and T3 by coupling iodotyrosine residues.
6)Endocytosis of Thyroglobulin: Internalization of thyroglobulin-T4/T3 complexes into follicular cells.
7)Lysosomal Proteolysis: Breakdown of thyroglobulin, releasing T4 and T3.
8)Release of T4 and T3: Diffusion of T4 and T3 into bloodstream for transport
what are symptoms of hyperthyroidism?
goiter (can occur withy hyper/hypothyroidism), proptosis, nervousness, insomnia, increased HR, eye disease, weight loss and anxiety
what is graves disease?
an autoimmune disease where the body has antibodies against the TSH receptor
what is cretinism?
dwarfism and an under-development of the brain resulting from hypothyroidism
what is myxedema?
hypothyroisim disease where the body retains excess water causes pufiness in the face
what is the precursor for adrenal cortex hormones?
cholesterol
what does dehydroepiandrosterone differentiate into?
androstenedione
what does progesterone differentiate into?
corticosterone —> aldosterone
what is the precursor to cortisol?
17-Hydroxyprogesterone
what part of the adrenal cortex is aldosterone secreted from?
zona glomerulosa
what part of the adrenal cortex is cortisol secreted from?
zonae fasciculata and reticularis
what part of the adrenal cortex are sex hormones secreted from?
zonae fasciculata and reticularis
what is the mechanism of aldosterone secretion?
-aldosterone diffuses towards target call
-receptor-ligand complex causes transcription events
-creates and inserts channels on the apical membrane of the target cell
-increases synthesis and insertion of K+ cells which leads to increased Na+ absorption
-K+ circulation increases
-Na+ is retained and K+ is excreted
what stimulates aldosterone secretion?
-high plasma [K+]
-angiotensin II
how is cortsol regulated? explain the feedback
what are metabolic effects of cortisol?
gluconeogenisis, protein catabolism and lipolysis
what occurs from hyper secretion of glucocorticoids?
what is Cushing’s syndrome?
excess cortisol secretion leading to many symptoms:
-buffalo hump
-hypertension
-thin skin, arms and legs
-red cheeks
-increased visceral fat storage
what hormones are categorized as catecholamines?
epinephrine and norepinephrine
what are the actions of epinephrine?
How are carbs dealt with in the absorptive state?
Glucose = primary fuel
-glycogen synthesis and storage
-conversion of excess glucose to triglycerides and storage in fat
How are carbs dealt with in the post-absorptive state?
glycogen breakdown and glucose synthesis
how are proteins dealt with in the post-absorptive state?
-protein breakdown
-AA used for gluconeogenisis by liver
how are lipids dealt with in the absorptive state?
-triglyceride synthesis and storage (lipogenesis)
how are lipids dealt with in the post-absorptive state?
-triglyceride breakdown
-FA primary fuel
-glycerol conversion to glucose
-FA conversion to ketones
summary of transition between apsorptive and post-absorptive:
explain how blood glucose levels are regulated by insulin
explain the steps in insulin signalling
Insulin binds to receptor
-glucose receptors are added to membrane
-glucose uptake increases
what are targets of insulin action?
muscle, adipocytes and the liver
what effect does increases in plasma insulin have on muscles?
increases glucose uptake and utilization
-glycogen synthesis
-AA uptake
-protein synthesis
what effect does increases in plasma insulin have on adipocytes?
increases glucose uptake and utilization
-triglyceride synthesis
what effect does increases in plasma insulin have on the liver?
decreases gluconeogenisis
-glycogen synthesis
-triglyceride synthesis
-no ketone synthesis
what effect does decreases in plasma insulin have on muscles?
decreased glucose uptake / utilization
-glycogen catabolism
-protein catabolism
-AA release
-FA uptake and utilization
what effect does decreases in plasma insulin have on adipocytes?
decreased glucose uptake/utilization
-triglyceride catabolism and release of glycerol / FA
what effect does decreases in plasma insulin have on the liver?
increased glucose release due to removal of inhibitory effects on glycogen catabolism and gluconeogenisis
-increased ketone synthesis / release
how does glucagon regulate glucose levels?
as plasma glucose levels decrease, plasma glucagon increases which stimulates glycogenolysis, gluconeogenesis and ketone synthesis
what actions does glucagon release to the liver cause?
increased:
-glycogenolysis
-gluconeogenesis
-ketone synthesis
-protein breakdown
decreased:
-glycogen synthesis
-protein synthesis
what actions does glucagon release to the adipose tissue cause?
-increased lipolysis
-decreased triglyceride synthesis
does GLUT2 in the liver cells respond to insulin?
no, glucose uptake in the liver cells is not insulin dependent
what is the biochemical response to insulin on muscle cells?
increased:
-GLUT 4 translocation
-enzymes for glycogen synthesis
-AA uptake
-protien synthesis
decreased:
-enzymes for glycogenolysis
what is the biochemical response to insulin on adipocytes?
increased:
-GLUT 4 translocation
-Lipoprotein lipase
-enzymes for FA synthesis
-enzymes for triglyceride synthesis
what is the biochemical response to insulin on liver cells?
*glucose uptake not insulin dependent
increased:
-enzymes to keep glucose in cells
-enzymes for glycogen synthesis
-enzymes to make pyruvate
-enzymes for lipogenesis
decreased:
-enzymes for gluconeogenesis
-enzymes for gluconeogenesis
what is diabetic ketoacidosis?
condition where ketones are acidic, causes blood pH to lower
-results from insulin deficiency
what are characteristics of diebetic ketoacidosis?
-urinary excretion of glucose and ketones
-osmotic diuresis
-plasma acidosis
how is food intake regulated?
leptin - supresses hunger
ghrelin- stimulates hunger
how does leptin work to control energy stores?
food intake > energy expenditure —> increased fat deposition resulting in leptin secretion —-> works on the hypothalamus to decrease food intake and incerase metabolim
-negative feedback
what is hypoglycaemia?
most serious acute complications in intensively treated diabtes
-a condition in which your blood sugar level is lower than the standard range
what is the sympathetic response to low plasma glucose?
adrenal medulla releases epinephrine to work on skeletal muscle, liver and adipose tissue
-glycogenolysis, gluconeogenesis and lipolysis are stimulated to increase plasma glucose
what are long term complications of diabetes mellitus?
