A&P Endocrine

hormones definition

chemical signaling molecules that are secreted by ductless glands

how to hormomes get to tissue

they exit the gland, diffuse into interstitial space, and transport into blood to get to tissue

"main ""job"" of hormones"

binds to target tissue with specific hormone receptors to trigger a cellular response to fix an issue

examples of hormone homeostasis maintanance 

body temp, blood pressure, metabolism

hormonal stimulation

a gland cell releases its hormone in response to another hormone binding to it

hormonal stimulation example

anterior pituitary releases TSH, TSH stimulates thyroid gland to release TH, which then goes into bloodstream

humoral stimulation

"a hormone released in response to changes in blood levels of nutrient or ion ""problem to be fixed"""

humoral stimulation example

blood glucose levels increase, it stimulates pancreas to release insulin, and the insulin goes into blood

nervous stimulation

"a hormone is release in response to direct nervous stimulation ""smth scares you, inc heart rate"""

nervous stimulation example

sympathetic division is activated, sympathetic preganglionic axons stimulate adrenal medulla to release epi and norepi

biogenic amines

FAST ACTING bc derived from modified amino acids, and water soluble except TH.

biogenic amines examples

epinephrine, norepinephrine, dopamine, serotonin, melatonin

what is serotonin deprived from

tryptophan

what is histamine deprived from

histodine

peptides/proteins

PRETTY FAST ACTING, sometimes needs receptor. not always active so it can be stored. composed of aa chains, water-soluble

peptides/proteins examples

vasopressin, growth hormone, insulin, glucagon

steroid

SLOWEST ACTING, no receptor needed bc it goes thru cell membr., derivative of cholesterol, lipid-soluble. job is to maintain fluid/chemical balances

steroid examples

sex hormones (testosterone, estrogen, progesterone), cortisol, aldosterone

cortisol what is it

stress hormone, hard to come down from (slow to act, but stays)

lipid-soluble hormones steps

1. hormone crosses plasma membrane binding intracellular hormone receptor
   2. hormone receptor complex interacts with hormone-response element on DNA
   3. initiates transcription of specific genes (mRNA synthesis)
   4. mRNA goes to ribosomes to convert to aa chains

water-soluble hormones steps

"travels ""free"" dissolved in plasma, first messanger binds membrane bound receptors, depends on intracellular second messangers to cause its effect"

signal transduction pathways

1. hormone binding of the plasma membrane receptor activates G-protein
   2. G-protein travels inside of membrane activating/inhibiting other intracellular enzymatic cascades

adenylate cyclase pathway (AC)

1. activated G protein activates plasma membrane enzyme (AC) and uses ATP to generate cAMP
   2. cAMP is a second messenger, activates protein kinase A enzyme
   3. protein kinase A is a phosphorylating enzyme that adds a phosphate to other molecules to inhibit/activate them

phosphorylase job vs protein kinase A job

phosphorylase group: removes phosphate group
protein kinase A: adds phosphate group to a molecule to activate it

phospholipase C pathway 

1. phospholipase C splits PIP2 into second messangers
   2. DAG activates protein kinase C (phosphorylating enzyme)
   2. IP3 leaves the membrane and causes an increase in Ca2+ levels in cytosol

up-regulation

"increases # of receptors
increases sensitivity to hormone"

when would up-regulation occur

• when blood levels of hormone are low
  - when development, cell cycle/activity changes
  ex) blood glucose raises from too much sugary foods, need to upregulate

down-regulation

decreases number of receptors
decreases sensitivity to hormone

down-regulation when does it occur

• when blood levels of hormone are high
  - with changes in development cycle/activity
  ex) insulin: not enough food, need to downregulate

synergistic

"estrogen and progesterone effects on a target cell
""works tg"" = greater effect"

antagonistic

"glucagon increases blood glucose while insulin lowers it
""against eachother"" = less effect"

permissive

oxytocin's milk ejection effect requires prolactin's milk generating effect
(one hormone needs another to be there first to work)

ADH and oxytocin

1. neurosecretory cells in hypothalamus make ADH and oxytocin
   2. they transporrt to posterior pituitary gland thru axons
   3. they are stored and released from axon terminal

oxytocin functions 

female: uterine contraction, milk ejection, emotional bonding
male: present in low levels, but function uncertain

ADH (antidiuretic hormone/vasopressin) function

decrease urine production, retain fluid in body, maintain blood volume, stimulate thrist, constrict blood vessels to increase BP

anterior pituitary hormones

• thyroid stimulating hormone (TSH)
  - prolactin (PRL)
  - follicle stimulating hormone (FSH)
  - luteinizing hormone (LH)
  - growth hormone (GH)
  - adrenocorticotropic hormone (ACTH)

GnRH 3 step sequence

1. GnRH 
   2. releases FSH and LH
   3. triggers Gonads to create sperm/eggs (FSH) or make estradiol/progesterone/testosterone (LH)

GHRH SS 3 step sequence 

1. GHRH (triggers) and SS (inhibits)
   2. release/inhibit Growth Hormone
   3. go to a bunch of organs/tissues 

TRH 3 step sequence

1. TRH releases
   2. triggers TSH 
   3. triggers Thyroid to secrete TH

high vs low TH effects

high: underweight, high energy, heat, heart rate, BP
low: opposite symptoms

DA 3 step sequence

1. DA releases and inhibits prolactin
   2. inhibited prolactin triggers breasts
   3. breast develop and milk produce

CRH 3 step sequence

1. CRH releases and triggers ACTH
   2. ACTH gets activated and triggers adrenal cortex
   3. adrenal cortex secretes cortisol

organ 3 in 3 step process is always…

primary organ

thyroid location

straddles esophagus, just below the larynx in the neck

what causes TRH release

cold temp, pregnancy, high altitiude, hypoglycemia, low TH

how do TH (T3 and T4) get released

TSH binds to receptors of follicular cells and triggers TH release

how do TH get transported

they get carried through blood by carrier molecules

what type of feedback with TH

negative feedback relationship with hypothalamic/pituitary hormones that influence TH synthesis

Thyroid gland parts

follicles (follicular cells and follicular lumen) and C cells

follicular cells 

produce/release TH
makes more T4 than T3, and target cells convert T4 to T3

what is T4 vs T3

T3 is the active form of T4, and T3 has 3 iodine while T4 has 4

follicular lumen

has liquid mixture (colloid) with enzymes that help produce TH

C cells (parafollicular cells)

secretes calcitonin to maintain blood calcium levels, and its free floating

TH formation steps - follicular cell

1. iodide ion transported from cell to colloid at follicular lumen
   2a. iodine molecule forms at follicular cell membrane near lumen
   2b. thyroglobulin protein synthesis occurs inside the follicular cells and released into colloid by exocytosis

TH formation steps - colloid

3. I_2 is enzymatically attached to thyroglobulin, one I_2 added to form MIT/T_1, or two I_2 are added to form DIT/T2
   4. enzymes in colloid facilitate MIT and DIT joining. this forms T3, and two DIT form T4
   5. thyroglobulin with attached T3 and T4 is transported to a follicular cell

TH formation steps - follicular cell 2

6. a vesicle with thyroglublin and T3+T4 fuses with a lysosome and enzymes cleave T3 and T4 from thyroglobulin
   7. T3 and higher levels of T4 move from follicular cell into the blood

TH action - general

TH increases metabolic rate and protein synthesis in target cells (generates heat, raises body temp)

TH action in liver

increases blood glucose by increasing glycogenolysis and gluconeogenesis and decreasing glycogenesis

TH action - adipose tissue

saves glucose for brain (glucose sparing effect) by increases lipolysis and decreasing lipogenesis

TH action - lungs

increased breathing rate to meet O2 demand for aerobic cellular respiration

TH action - heart

increased heart rate
increased force of action (every beat sends more blood)

goiter

enlargened thyroid gland due to low TH levels
goiter will not shrink despite being given iodine pills

trophic hormones

hormones that encourage growth
always hormones coming from anterior pituitary

causes of hypothyroidism

low iodine
issues in hypothalamus/anterior pituitary (secondary)

graves disease

autoimmune disease where immune cells attack normal tissue
thryoid stimulating immunoglobulins (antibodies) bind to TSH, makes thyroid think it needs to secrete T3/T4

GH (somatotropin) regulation

negative feedback
more GH and IGF inhibits GHRH release from hypothalamus
more GH also inhibits the release of GH from anterior pituitary

GH release steps

1. hypothalamus releases GH, releasing GHRH into hypothalamo-hypophyseal portal system
   2. anterior pituitary releases GH in response to GHRH
   3. GH stimulates hepotocytes to release insulin-like growth factor (IGFs) into blood

GH high levels and growth plates

sealed growth plates: you will see excess growth in soft tissues like hands/face
open growth plates: allows for proportionate, normal bone growth

what is required for normal production of GH

TH

what does GH cause liver to secrete

insulin-like growth factors (IGF-1)

which body cells have receptors for GH/IGF

all body cells

what does GH cause in cells

more cell division, cell differentiation, and amino acid uptake/protein synthesis

what parts of body as especially responsive to GH

bones and muscle (bones elongate and muscles have hypertrophy)

GH effect in liver

increase in glycogenolysis and gluconeogenesis, and decreased glycogenesis

GH effect in adipose

increase lipolysis (breaking down fat for ATP) and decrease lipogenesis to release nutrients

what factors affect circulating GH levels

age (lowers with age), time of day (highest before sleep), stress/trauma (affects differently for diff ppl)

kidneys location

in back of body in lower back

adrenal medulla hormone release

sympathetic axons cause release of epinephrine and norepinephrine and small amt of dopamine

adrenal medulla - why it activates

in response to decreased blood pressure, pain, injury, emotional upset, hypoglycemia

adrenal medulla effect

increased heart rate, anxiety, increased perspiration, increased blood glucose

what does adrenal cortex secrete

aldosterone, cortisol, DHEA and androgens

aldosterone effect

Na+ and water retention, and K+ and H+ secretion

cortisol regulation steps

1. hypothalamus releases CRH into hypthalamo-hypophyseal portal system

2. after CRH the anterior pituitary releases ACTH

3. ACTH stimulates adrenal cortex to release glucocorticoids into the blood

4. cortisol stimulates target cells (effectors)

what type of feedback is cortisol regulation and why

negative feedback bc higher cortisol inhibits the release of CRH and ACTH

cortisol effects

increases nutrient storage in blood to better handle injured tissue

causes cells to decrease glucose uptake to save it for the brain

acts as anti-immune function

cortisol effect on kidneys

increased glycogenolysis and glunconeogenesis

decreased glycogenesis

cortisol effect on adipose tissue

decreased lipogenesis

cortisol effect on all cells

stimulation of protein catabolism

decreased glucose uptake

pancreatic hormones job

maintains blood glucose levels in normal range

high blood glucose effects

damages blood vessels and kidneys

low blood glucose effects

lethargy, mental/physical impairment, death

pancreatic hormones

glucagon and insulin

alpha cell what does it secrete and why

it secretes glucagon due to low blood glucose

beta cell what does it secrete and why

it secretes insulin due to high blood glucose (tells cells to take up glucose)

what signal to beta cells of pancreatic islet inhibits insulin secretion

sympathetic activity (epinephrine)

what signals to beta cells of pancreatic islet increase insulin secretion

high plasma glucose and amino acids, and high parasympathetic activity

why does parasympathetic activity increase insulin secretion

because parasympathetic (rest and digest) excepts sugar to come into the body, so it prepares by giving out insulin

extreme insulin problem: impaired/failure to secrete insulin does what?

The body switches from primarily using glucose to using fat, which causes the liver to produce ketones that can make the blood acidic.

extreme insulin problem: hyperglycemia-induced diuresis does what?

reduces blood volume to the point of hypotension and inadequate blood delivery to the brain

what causes less hunger signal in brain

insulin, glucagon, GI hormones, leptin, body temp, and stretch/chemoreceptors in stomach being high causes less hunger