Physiology Exam 3

what do endocrine glands do

release hormones into the blood that act on target cells (has receptor for the hormone)

neurohormones

secreted by specialized cells of the hypothalamus

what do hormones regulate

body metabolism, growth, and reproduction

what are the 4 different chemical classifications?

1. amines
2. polypeptide and proteins
3. glycoprotein
4. steroids

amines

comes from amino acids tyrosine and tryptophan

* E and NE (adrenal medulla made) and thyroid hormone

polypeptides …

less than 100 amino acids long (ADH)

protein

insulin and growth hormones

glycoprotein

luteinizing hormones and follicle stimulation hormones

steroids

produced my cholesterol

sex steroids

testosterone and estrogen

* produced by gonads

corticosteroids

produced by the adrenal cortex

lipophilic

* non polar and hydrophobic
* steroid hormones, thyroid hormones and melatonin
* moves through membrane → receptors in the cell/in nucleus (sometimes)
* taken orally and absorbed quickly

what is the genomic action of lipophilic

turns genes on or off, altering gene activity

polar, water-soluble hormones

* can’t be taken orally (ex: insulin)
* can’t pass plasma membrane
* receptor is on/in membrane
* uses secondary messengers that cause the effect on the target cells
* no genomic action generally
* open/close ion channels and turn enzymes off/on

prehormones

molecule produces by endocrine gland that is inactive until altered by the target cell

* EX: T4 (thyroxine)→ concerted to T3

prohormones

molecule produced by the endocrine gland that isn’t active and must be cut/sliced together within the gland

* EX: proinsulin → pancreas

how are Neural and Endocrine regulation similar? (5 things)

1. both NTs and hormones interact with specific receptors
2. bind to a receptor→ change in target cells
3. mechanisms to turn it off
4. NTs and hormones are similar chemically/structurally
5. some hormones that are also NTs (EX: NE)

receptors

unclear hormone receptors

* located in the cytoplasm or in the nucleus

transcription factors

bond with promoter genes and turn it on or off (typically on)

2 major domains

1. ligand binding domain: hormones bind here
2. DNA binding domain: bind to hormone response element ( composed of 2 half sites with a spacer)

dimerize

combos join together and creates homodimer

9-cis-retinoic acid

comes from vitamin A

calcitonin

comes from vitamin D

what comes from tyrosine

T3 (triiodothyronine) and T4 (tetraiodothyronine/thyroxine AND most abundant AND prehormone)

what are the 3 ways the steroid and thyroid mechanism differ?

1. homodimer vs. heterodimer
2. prehormone
3. steroid → cytoplasm or nucleus (thyroid = only nucleus)

Lipophobic/hydrophobic

* Catecholamines, polypeptides, proteins, glycoproteins
* Receptors must be on/in the membrane
* Uses secondary messenger system

Adenylate cyclase/cAMP system

* mainly used by monoamines (E and NE) and beta adrenergic receptors
* many polypeptides and glycoproteins use

steps of Adenylate cyclase/cAMP system

1. hormone binds to receptor
2. g-proteins so their thing
3. g-proteins turn into adenylate cyclase
4. adenylate cyclase makes cAMP
5. cAMP inadvertently activated protein kinase by binding to regulatory subunit
6. protein kinase can phosphorylate things (enzymes and ion channels)

how to turn off Adenylate cyclase/cAMP system

1. protein phosphatase → opposes protein kinase
2. PDA destroys cAMP
3. g-proteins turn themselves off

steps of Phospholipase C/Ca2+ System on A1 adrenergic receptor

1. hormones binds to receptors
2. g-proteins
3. turns into phospholipase C
4. phospholipase C takes a membrane phospholipid → inositol triphosphate (IP3) and diacylglycerol (DAG)
5. IP3 binds to calcium voltage gated channel on ER
6. calcium channels open and moves into cell
7. calcium binds calmodulin
8. calcium/calmodulin turns on protein kinase
9. protein kinase phosphorylates

* A1= EPSP in smooth muscles on skin and digestive organs→ vasoconstriction

how to turn off Phospholipase C/Ca2+ System

1. IP3 phosphatase destroys IP3
2. calcium pumps in the membrane of ER
3. g-proteins turn themselves off
4. protein phosphatase

tyrosine kinase system

* ligands of this system are growth factors → cell division
* issues: cancer

tyrosine kinase receptors

* 2 inactive monomers
* outer surface: ligand binding domain
* inter cell: catalytic domain (enzymatic)

steps of tyrosine kinase system

1. 2 molecules of growth molecules bind to ligand binding domain
2. dimerize (join)
3. autophosphorylation
4. conformation change of the catalytic domain and turn on enzymatic activity
5. catalytic domain phosphorylates tyrosine residues of signal protein
6. signal protein activates a metabolic path

how to turn off tyrosine kinase system

protein tyrosine phosphates (PTPs): dephosporylates catalytic domain that turns the whole system off

what is dangling from the diencephalon

hypothalamus (hypo)

what is infundibulum

structure that attaches the neurophypophysis/postsrior pituitary (NH/PP) to hypo

adenohypophysis/anterior pituitary (AH/AP)

* Notochord produces growth factors


* tip: development of pituitary of NH/PP from floor of Di (hypo)
* downward ventral evagination


* mouth region of embryo (stomodeum)
* Rathkes pouch→ loses connection to stomodeum
* AH/PP

what are ^^ALL ^^of the adenohypophyseal (AHPP) hormones?

* growth hormones (GH) or somatotropin
* thyroid stimulating hormones (TSH) or thyrotropin
* adrenocorticotropic hormone (ACTH) or corticotropin
* follicle stimulating hormone (FSH) or folliculatropin
* luteinizing hormone (LH)
* protection (PRL) luteotropic hormone (LTH) aka luteotropin or lactotropin

growth hormones (GH) or somatotropin

* controls tissue and organ growth
* stimulates target cells to take in AAs and turn them into proteins

thyroid stimulating hormones (TSH) or thyrotropin

* thyroid gland- secrete the thyroid hormones (T3 and T4, calcitonin, and 9-cis-retnoic acid)

adrenocorticotropic hormone (ACTH) or corticotropin

* adrenal cortex→ secretes corticosteroids

follicle stimulating hormone (FSH) or folliculatropin

* females
* stimulate development of follicles of ovary
* produces eggs and estrogen
* males
* testes→ produce sperm

luteinizing hormone (LH)

* females
* triggers ovulation and the release of egg from ovary
* development of corpus luteum
* males
* testes→ interstitial cells → produces testosterone

protection (PRL) luteotropic hormone (LTH) aka luteotropin or lactotropin

* serves a supporting role in males
* stimulates milk after birth

Neurohypophyseal (NHPP) hormones

\*\* **secretes/releases 2 hormones (DOES NOT MAKE ANYTHING, JUST RELEASES)**\*\*

* produced in the supraoptic nucleus (CNS) and paraventricular nucleus (both found in hypo)
* the hormones travel down axon to NHPP and releases 2 hormones into blood stream when stimulated
* infundibulum connects hypo to the NHPP (hypothalamic neurohypophyseal tract)
* antidiuretic hormone (ADH) and oxytocin hormone involved with NHPP

antidiuretic hormone (ADH)

* kidney consumes water (small volume with bright yellow urine)
* hypo→ osmoreceptors→ osmotic pressure of the blood increase and triggers secretion of ADH→ neurons generate APs causing NHPP to release ADH→ kidney→ conserve water to dilute the blood
* inhibited by stretch receptors in atrium of heart → stretched too much (increase blood volume)→ inhibition of ADH→ kidneys secrete more water
* large volume, pale color
* alcohol consumption: inhibition of ADH→ pee more fluid while drinking
* vasopressin= high doses can cause vasoconstriction→ increase blood pressure

oxytocin (hormone)

* females: contracts uterus during birth
* neuroendocrine reflex: sensory input followed by motor response
* milk ejection reflex: lactating females
* Child sucking at nipple → hypothalamus → neurons generate Aps → release of oxytocin → acts on smooth muscle of mammary glands and causes contraction → force milk to nipple

adrenal cortex has…

no innervation

ACTH from HA/AP which stimulates, produced and secretes what?

its hormones (corticosteroids aka corticoids) from cholesterol

zona glomerulosa

responsible for ==mineralocorticoids== → regulating electrolytes concentration in blood

aldosterone

acts on the kidneys and tells it to reabsorb salt and water from the filtrate= increase blood volume and increase blood pressure

hyper kalemia

increase K+ in blood

* Dr. Kevortian: inject patients with K+ Cl- = too much k+ depolarizes the cell and doesn’t give Aps (heart and diaphragm) and stop working (assisted suicide)

renin angiotensin aldosterone mechanism

look blood volume and low blood pressure→ kidneys respond and produce hormone called renin which triggers production of angiotensin (hormone) = vasoconstrictor= increase blood pressure

* andiotension also acts on the angiocortex, and releases aldosterone→ salt and water reabsorb - increase blood volume and blood pressure

zona fasciculata

produce ==glucocorticoids== = metabolism of glucose

* trigger is ACTH
* __cortisol aka hydrocortisone__
* conserve glucose


1. restrict entry of glucose in the cells
2. cause lipolysis: breakdown of fats → use these as a source of energy (rather than glucose)
3. cause gluconeogenesis= make glucose from novel sources (amino acids)

* cause immune supression
* good for inflammatory issues

zona reticularis

sex steroids= weak androgens→ step in producing other sex steroids

* pre hormones

Cushing’s syndorme

hyper secretion of corticoid steroid

* too much ACTH
* tumor on adrenal cortex
* causes hyperglycemia (elevated glucose in blood)
* causes hypertension (high blood pressure)
* causes muscle weakness
* normally appears with a puffy appearance (moon shaped face)

addisions disease

hyposecretion of corticoid steroid

* causes hypoglycemia
* causes generalized weakness (no energy)
* sodium and potassium imbalances
* rapid weight loss
* fatal condition if not treated
* treated with corticoid steroids (supplements)

adrenal medulla

hormones: E and NE= same effects as sympathetic division → longer lasting

* metabolic effects
* binding to B2 receptors located on liver cells
* A1 receptors on liver cells


* stress
* adrenal medulla= more for immediate emergency
* cortex: more for long term stress
* increase ATCH→ cause increase in glucocorticoids= immune system suppression (more sick more often)

binding to B2 receptors located on liver cells

* use adenylate cyclase/cyclic AMP
* protein kinases→ causes glycogenolysis= breakdown glycogen into glucose (important in fight or flight)

A1 receptors on liver cells

* use phospholipase C/Ca2_ system
* activates protein kinases→ trigger glycogenolysis
* stimulate glycoside which give you more energy during fight or flight

thyroid glands

* largest, pure endocrine gland
* composed of thyroid follicles

T3 triiodothyronines

genomic action (turns genes on and off)

* forms heterodimer with 9-cis-retinoic acid

TSH

release of T3 and T4 into the blood

cells of thyroid follicle remove iodide from the blood

enzymes that combine the iodine with tyrosine residues of the protein called thyroglobulin

= MIT

monoiodotyrosine

= DIT

diiodotyrosine

combine MIT and DIT

T3/thyroglobulin

combine DIT and DIT

T4/ thyroglobulin

genomic action of T3 and T4

protein synthesis, thyroid hormone promotes maturation of the nervous system, and increase in basal metabolic rate (BMR)

hyperthyroidism info

* hot
* increase activity, decrease sleep
* manic, panicky
* rapid heart rate
* frequent bowl movements
* increase appetite
* weight loss

hypothyroidism info

* cold
* tired, increase sleep
* depressed
* slow heart rate
* slow reflexes
* constipation
* decreases appetite
* weight gain

goiter

enlarged thyroid gland

hypertrophy

too much AH/AP hormone

endemic/iodine deficient

not enough iodine in diet= thyroid gland can’t make T3/T4= no negative feedback to hypo (increased TRH)/AHAP→ increased TSH= thyroid gland enlarges

* used to be an issue in the US (started putting iodine in salt)

WIS= wonderful iodine state

1920s→ fruit and veggies grown here; milk produced here= increased iodine level

* salt contents

graves disease (thyrotoxicosis/hyperthyroid)

* thyroid gland is enlarged (hyperthyroid)
* autoimmune disease

cretinism

* seen in infants/children, not having enough thyroid hormone
* severe mental and physical retardation

parathyroid galnds

* embedded in back of thyroid
* 4 small, yellow colored, masses of tissue
* produces parathyroid hormone (PTH)

parathyroid hormone (PTH)

trigger and increase amount of Ca2+ in blood

parathyroid glands antagonistic to calcitonin

* kidney: excrete less Ca2+ into urine→ absorb Ca2+ from filtrate
* osteoclasts (Bone): increase in activity, dissolving bone= increase in Ca2+ in blood

pancreas

* spongy, airy organ
* located in the loop of duodenum (small intestine)
* has both endocrine and exocrine glands→ released by pancreatic duct

pancreas: exocrine portion

pancreatic juice= contains enzymes that breakdown all major organic molecules

pancreas: endocrine portion

islets of langerhans

* alpha cells: produce glucagon
* beta cells: produce insulin
* delta cells: produce somatostatin→ inhibits the activity of the alimentary canal

main function of pancreas: endocrine portion

regulate the amount of glucose in blood

glucagon

increase amount of glucose in blood

insulin

decrease amount of glucose in blood

decrease in blood glucose does what?

alpha cells produce glucagon

glycogenolysis

breakdown of glycogen into glucose (in liver)

lipolysis

breakdown of lipids= energy substrates during fasting

gluconeogenesis

make glucose from novel sources

increase in blood glucose

beta cells produce insulin

* promotes entry of glucose into cells (GLUT 4)
* ==lipogenesis:== glucose→lipids
* ==glucogengenesis:== glucose → glycogen

pineal gland

found in epithalamus (Di roof), looked like a pinecone, sensitive to light

* pineal eye: 3rd eye in early reptiles and amphibians
* retina relays a lone pathway to the pineal gland
* current day mammals and others have no pineal eye

melatonin hormone

* synthesized by tryptophan
* enzymatically converts serotonin to melatonin
* light inhibits melatonin secretion → melatonin gets secreted at night because there is no light to get to the pineal gland

entrain circadian rhythms

* about 24 hours in length
* most animals active during the day and sleep at night
* isolation from light/dark cycle= still have circadian rhythms but it looses a few minutes everyday
* melatonin resets circadian rhythm daily

photoperiodism

doesn’t seem to be important in humans compared to other animals/plants

* response to change in day length
* melatonin is antigonadotrophic (FSH and LH stimulate gonads)
* melatonin inhibits gonads
* stops production of gametes and sex hormones
* also helps with sleep and getting over jet lag

less melatonin in animals

bread in the spring in SC

why do deciduous trees shed their leaves in the fall

decreasing periods of daylight

gonads

* produce gametes (exocrine)
* produce sex hormones (estrogen and testosterone)

male gonads: testes

seminiferous tubules→ hallow organ

* lined with germinal epithelium= produce sperm
* undergoes meiosis resulting in sperm cells