Endocrine system Flashcards
What are the main endocrine organs
pineal, hypothalamus, pituitary, thyroid, PTH, thymus, pancreas and ovary/testis
What are hormones
chemicals that are released by 1 part of a cell and affect cells in a different body area
——- secreted
Difference between endocrine and Neuroendocrine
Endocrine: secreted into BS
Neuroendocrine: made by neurons + secreted into BS
What does exocrine mean
secreted into a duct which then goes into the BS
- not direct secretion into the BS
T or F: autocrine and paracrine chemicals are hormones
F- work locally not in a different part of body
What is autocrine
chemical that effect the same cell (or type of cell) that secretes it
What is a paracrine chemical
chemical that affect nearby cells; responses to allergens, tissue repair, and blood clotting
T or F: a chemical can be autocrine and paracrine
True
How do hormones work (general)
bind to target cell receptor and alter its activity by…
1) activating secondary messengers
2) direct gene activation (ex// steroid) —- go into cell directly
Effects of hormones on cells (general)
increase PM permeability, change protein synthesis, change enzyme states, stimulate mitosis
Where does hormone specificity come from
come from receptor binding; hormone binds to a specific receptors
- receptors can be found on only 1 cell type or can be on multiple tissues
What impacts receptor and hormone binding/activation
blood hormone levels, number of receptors on target, and affinity of hormone for receptor
—- can upregulate or downregulate receptor amount on target cell in response to hormone-receptor binding
T or F: hydrophobic hormones freely circulate in blood
F —- hydrophobic hormones need to be bound to protein
hydrophilic —- freely circulate
What controls hormone level in the blood
controlled by negative feedback loops
- vary within desired range
- concentration represents the rate of release, speed of inactivation and removal of hormone from the body
What stimulates hormone synthesis/release
1) humoral: ion/nutrient stimulated release; released based on changes in levels (Ex/// Calcium and PTH)
2) Neural: nerve fibers stimulate release (Adrenal medulla — NE + E)
3) Hormonal: release in response to different hormones (tropic — hormones that cause the release/effect other hormones)
Types of interactions of hormones with target cells
1) Permissiveness: 1 hormone doesn’t work without the others (allow each other to work)
2) Synergism: 2 hormones have the same effect
3) Antagonism: work against each other
T or F: The NS can override and take control of the endocrine system (ex// release of hormones —— go outside of normal range)
T
- NS can modify the stimulation of the endocrine glands and their negative feedback loops
—- if we really need something (ex// need more glucose due to stress) : NS can kick in and increase glucose amounts outside of the normal range set by the endocrine organs
T or F: Eicosanoids are true hormones
F - they are autocrine and paracrine
Types of Eicosanoids (general classes)
prostaglandins - inflammation , fever, induce labour, prevent BC
thromboxane - promote BC
leukotrienes - allergic rxn
T or F: Eicosanoids are derived from AA
true —- from AA in PM
- AA produced from alpha-linolenic acid (omega 3) and linoleic acid (omega 6)——— don’t make these
T or F: AA is converted into prostaglandins by LOX enzyme
F - Membrane PL —— AA (by phospholipase) —- PGH2 (COX) —— prostaglandins + thromboxanes
AA——- Leuokotrienes by LOX
What inhibits the COX enzyme
NSAIDS
What specifically inhibits COX2
VIOX — increase CVD risk
Different eicosanoids produced in the prostanoid path and their effects
Prostaglandins- induce labour, vasodilator, pain , pyretic
prostacyclins- inhibit BC, vasodilation
thromboxane - promote BC, vasoconstrictor
What are the AA hormones
amines, thyroxines, peptides, protein hormones
What does Gs do when activated
activated adenylate cyclase —— converts ATP to cAMP —- activate PKA
What does Gi do
inhibits adenylate cyclase —- decrease cAMP and PKA activation
What is the PIP2 path
hormone + receptor —- activate Gq —- activate PC
PC- cleaves membrane bound PIP2 into IP3 (free) and DAG
— IP3: causes release of Ca from ER—- Ca interact with calmodulin
— DAG: activate PKC
** together trigger cell response
T or F: cAMP, DAg and IP3 are synergistic
T- cause insulin release from cell
T or F: steroid hormones are hydrophobic and can just move into the cell and through the PM and NM
T-just move into the nucleus and interact with receptor/chaperone complex
—— this complex (minus chaperone - leaves once hormone binds) binds to DNA and causes changes in gene expression
—— need 2 hormone+receptor complexes to bind to DNA to get effect
T or F: steroid hormones and AA hormones cause immediate cell response
F — steroid takes longer because cause changes in gene expression —- change proteins etc
E2 and Breast cancer
- E2 levels are higher in BC — drugs look to modulate and target this pathway
- block the interaction bw the 2 receptors
How do Tamoxifen and Raloxifiene work - BC
block the e2 binding by changing receptor shape
How does herceptin work
AB used to treat BC with HER2 (found in more metastatic BC)
— prevents dimerization of HER2 + targets cell for destruction
T or F: Neurohypophysis is found in the anterior lobe
F
Neurohypophysis : posterior lobe, neural tissue — extension of hypothalamus into PG ( cell body in hypo and axons release hormones here
—- fxn to receive, store and release hypothalamus hormones
Adenohypophysis: anterior lobe, glandular tissue that make and secrete their own hormones
What connects the PG and the hypothalamus
infundibulum
Posterior Lobe pathway
cell bodies in PVN and SON (hypothalamus )- axons pass through infundulum
—- hypothalamic - hypophyseal tract
—— synapse in Posterior lobe
Anterior lobe pathway
cell body in VH of hypothalamus —- secrete hormones into the blood via hypophyseal portal system (how Anterior lobe and hypo connected)
—- primary capillary plexus —- hormone travels along hypophyseal portal veins to anterior pituitary glands where stimulates or inhibits hormone release from anterior lobe— anterior lobe releases hormones in the 2nd capillary plexus
What connects the hypothalamus and anterior lobe
vascular connection vis hypophyseal portal system
What hormones are released from Anterior lobe of pituitary
TSH
FSH
LH
ACTH
GH
PRL
Tropic anterior lobe hormones
TSH, ACTH, FSH, LH, GH,
What does hypothalamus CRH stimulate release of in AL
corticotroph cells release ACTH
What does hypothalamus TRH stimulate release of in AL
stimulate TSH (Thryotroph) and PRL (Lactotroph) secretion
What does hypothalamus GHRH stimulate release of in AL
stimulate GH release by somatroph
What does hypothalamus GHIH stimulate release of in AL
inhibits release of GH by somatotroph cells
What does hypothalamus GRH stimulate release of in AL
release of LH and FSH by gonadotroph cells
What does hypothalamus prolactin releasing hormone stimulate release of in AL
stimulate PRL release (along with TRH) by lactotroph
What does hypothalamus dopamine stimulate release of in AL
inhibit release of PRL by lactotroph
Growth hormone function
anabolic tissue building —- increase size, division and metabolic activity
targets- liver (primary target) bone and skeletal muscle
Directly - affects the metabolic activity, fat breakdown and carb metabolism in liver, SM and bone
Indirectly - stimulate release of IGF-1 by liver: IGF-1 stimulates cartilage growth and extra skeletal protein synthesis and division
Affect of IGF-1 on GH release
negative feedback loop—- inhibits GHRH release by hypothalamus and increase release of GHIH by hypo
What is Acromegaly
when make too much GH; occurs after puberty (epiphyseal plates fused)
—- tissue swelling, changes in pigment and skull expansion
Gigantism
excess GH secretion that occurs before puberty —- bone elongation and tissue swelling
Impact of ACTH
released by corticotropin cells in anterior lobe
—- stimulated by internal and external stressors
— target the adrenal gland
*stimulate release of cortisol by cortex (long term stress)
*Medulla: not regulated by NE and E
What do FSH and LH do
regulate function of ovaries and testes
- FSH is not released until puberty
FSH - stimulate gamete production
FSH and LH: females
cause maturation of ovarian follicle
LH: trigger ovulation on its own , mediate synthesis and release of estrogen and progesterone
FSH and LH: males
make and mature sperm
What does Prolactin do
stimulate milk production in females (release triggered by PRH and inhibited by PIH)
—- levels increase near end of pregnancy
— sucking stimulate release of PRH —- increase PRL and milk production
What hormones are released at posterior lobe
oxytocin and ADH
- made in PVN and SON of hypothalamus — travel along axons via hypothalamic and hypophyseal tract —— released from posterior lobe when stimulated
—- released directly into blood (axons synapse with BS)
T or F: Oxytocin is regulated by a negative feedback loop
F - positive feedback loop
—- leads to increased intensity of uterine contractions during birth
—- used to induce labour + trigger milk ejection (let down reflex)
Roles of oxytocin
increase intensity of uterine contractions
let down reflex : increase in levels cause milk to spit out : cause mammary lobes to contract and eject milk (will keep going till no more sucking)
role in sexual arousal in M+ F
Role of ADH : posterior lobe hormone
helps maintain plasma osmolarity
— osmoreceptors in hypo
—-High solute: ADH release —— increase water preserved (increase uptake at kidney, decrease )
— Low solute: inhibit ADH release
T or F : alcohol inhibits ADH release
T
Cells that make up the thyroid gland and their roles
Follicle cells - produce glycoprotein thyroglobulin (thyroid hormone precursor)
Parafollicular cells : fill space bw follicle and colloid
colloid : fluid filled space
What does thyroid hormone do
targets a lot of cells
- concerned with glucose oxidation , increase metabolic rate, heat production
- maintain BP, regulate tissue growth, develop skeletal and NS (not adult brain)
**elevated and maintain normal body fxn
What tissues does thyroid hormone not affect
USTAT
- uterus, spleen, thyroid gland, adult brain, and testes
T or F: there are two types of TH iodine compounds
T
T4 : thyroxine , 2 tyrosine + 4 iodine (less active)
T3: Triiodothyronine: 2 tyrosines + 3 iodines ( more active)
Steps to TH synthesis
- thyroglobulin (134 tyrosine) synthesized in follicle and discharged into the lumen —- sent to the colloid via exocytosis
- Iodides (I-): actively taken into the cell, oxidized into I2 + release into lumen (colloid)
- Thyroid peroxidase (made by follicle) : sent into colloid, attaches iodine to tyrosine —- T1 and T2 in lumen
- Link them together to make T3 and T4 in colloid
- Endocytosis of T3 and T4: cleaved in follicle cell lysosome; diffuse into BS (taken up by carrier protein)
Who makes the thyroid binding protein
liver ; binds to T3 and T4
- binds to t3 better
T or F: peripheral tissue can convert T4 to T3 if need more TH
T
Mechanism of TH activity
steroid like
- bind to receptor in cytosol or nucleus —- bind to DNA
Hypothyroidism
- low levels of T4 (and T3) —- increased release of TSH by pituitary
—- stimulating thyroid to make shit but not enough iodine to make TH
—- stimulating formation but not making cuz cant
Effects: decrease metabolic rate, lethargy, goiter (enlarged gland)
Infants —- Cretinism
Graves’ disease
autoimmune
AB mimics TSH : so keeps stimulating TH release
—- symptoms caused by high levels of T4 and T3
Symptoms: high heart rate, muscle weakness, disturbed sleep, goiter exophthalmos
What is Calcitonin
peptide hormone produced by parafollicular cells
- helps decrease blood Ca levels in children
- inhibit osteoclasts activity and stimulating Ca incorporation in bone matrix
T or F: PTH oxyphil cells release PTH
F. chief cells secrete it
Function of PTH
regulate Ca levels in the blood : increases Ca levels in the blood
- works against calcitonin
- stimulating osteoclasts, enhancing reabsorption of Ca + increase P secretion by kidneys; promotes Vit D activation to calcitriol
—- negative feedback loop: inhibits its own release as Ca levels rise
T or F: the adrenal medulla is the external neural tissue part of the adrenal gland and the adrenal cortex is the endocrine tissue on the inside of the gland
F
medulla: internal and neural tissue; part of the SNS (release NE +E)
cortex: external and release steroid hormones — corticosteroids
Layers of the adrenal cortex
Zona glomerulosa: top, release mineralocorticoid
Zona Fasciculata: release glucocorticoids
Zona reticularis: bottom , release gonadocorticoids
What are the classes of hormones released by the adrenal cortex? what is the precursor
precursor: cholesterol
classes;
progesterone
Glucocorticoid: cortisol, and corticosterone (long term stress)
Androgens: Testosterone + DHEA, DHT
Estrogens: E1-3
Mineralocorticoids: aldosterone
Connections between the different classes of adrenal cortex hormones
cholesterol ——- progesterones ——- glucocorticoids — mineralocorticoid
progesterones —— androgens —— estrogens
Fxn of Aldosterone
regulate Na levels: maintain levels by decreasing excretion + stimulating resorption by kidneys
4 regulators
1) Renin angiotensin : decrease in BV/BP — causes renin release by kidneys —- angiotensin II release — stimulate aldosterone
2) increase K- influence zona g. cells
3) ACTH: released by Anterior PG due to stress to increase
4) ANP - inhibit release (made by heart; detect increase in BP/BV)
Functions of glucocorticoids (cortisol, cortisone and corticosterone)
help body resist long term stress
- help keep glucose levels constant + BV constant; prevent water shift to tissue
- provoke gluconeogeneis : increase glucose, AA and FA —— energy motivator
=if high for a long time : negative impacts (decrease bone formation , inhibit inflammation and immune)
Fxn of Gonadocorticoids
Mostly androgens (test)
- contribute to start of puberty, appearance of 2nd sex traits + female sex drive
androgens convert to estrogen after menopause
What cells release hormones in adrenal medulla
chromaffin cells — release the catecholamines (NE, E and dopamine)
— strong term stress
NE fxn
peripheral vasoconstriction and increase BP
E fxn
increase HR, dilate bronchioles, increase BF to skeletal muscle, brain and heart
- liver breaking down glycogen —- glucose
What has a more rapid onset: cortex or medulla
Medulla —- nervous system
cortex —— hypothalamus —- CRH —— ACTH —- cause release of hormones at cortex
Paracreas : cell types
exocrine : produce enzymes and buffers for digestion
endocrine ; form islets which release hormones (islets made from alpha cells, beta and delta cells
What does the pancreas alpha cells make and what does it do
glucagon made by alpha cells (exterior of pancreatic islets)
- hyperglycemic agent
- released in response to low glucose: causes increase in glucagon breakdown, glucose synthesis
- glucagon inhibits B cells
- negative feedback
**Long term hypoglycemia — liver produces ketones from FA as energy source to use in place of glucose *
What does B cells secrete and its function
insulin + amylin secreted by internal B cells
insulin: made from proinsulin (contains A,B.C peptides: cleave off C; so 2 AA chains with disulfide bonds
- function : increase glucose transport in cells/ decrease blood glucose levels
- release when glucose is high: causes liver to increase making/storing glucose as glycogen )
- inhibit alpha cells
differences between Type 1 and Type 2 diabetes
Type 1: early onset, more severe — autoimmune so attack and kill B cells (can’t make insulin) , eating —- but wasting away
Type 2: adult onset, cells don’t respond right to insulin (disregulation of insulin secretion , increase or decrease release); diet and exercise help
Cardinal symptoms of Type 1 diabetes
polyuria, polydipsia and polyphagia
Main targets of insulin
liver, skeletal muscle and adipocytes
Impacts of low insulin: diabetes
Liver (break down glycogen) + SM (breakdown protein) —- increase in blood glucose levels —- increase in glucose in urine which pulls more water out of the body
—— causes polyuria and polydipsia
adipocytes; increase breakdown of fat + SM break down protein —- polyphagia
—- increase fat breakdown also converted into ketone bodies in liver, decrease blood pH=== more ketones in blood which pulls more ions with it
**increase in glucose and ketones in urine —- pulls water and ions in urine —— give symptoms
What do ovaries produce and what does it do?
produce estrogen and progesterone — help maturation reproductive organs,2nd sex traits, breast development and cyclic changes
— cyclic release of FSH and LH which impacts estrogen and progesterone
-increase in estrogen during follicular phase
luteal —- high progesterone
What do the testes produce and what does it do
produce testosterone —- starts maturation of reproductive organs, sex drive, 2nd sex traits and sperm production
What does the pineal gland produce and how is its release controlled?
produces melatonin- helps with rhythmic control of body temp, appetite and day/night cycles
- has neural projections from SCN: gets light signals
- melatonin helps SCN sense length of night
- circadian pacemaker — SCN (regulates melatonin release to ensure right levels at right time
What does the thymus produce and its function
thymopoietins and thymsins - T cell maturation
Adipose produces..
leptin, resisted, adiponectin
GI produces…
gastric, intestinal gastric, secretin, CCK and incretins
Heart produces
atrial natriuretic peptide
kidney produces..
EPO and Renin
skeleton produces..
osteocalcin
skin produces…
cholecalciferol
