2A : *Hormones
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shell formation in bird eggs: How quickly is Ca 2+ deposited to make eggs? Source of ca is ______
-A chicken egg shell contains ~2gm of Ca++ (as CaCO3), and is laid down in ~16hrs. Therefore Ca++ is deposited at a rate of ~125mg/hr. (-Total circulating blood Ca++ is ~25mg. Therefore every 12 minutes *for 16 hrs an amount of Ca++ equal to the total circulating Ca++ is laid down in the shell by the shell gland.* ) source: Diet and *medullary bone (only found in "laying" females, formation stimulated by 🔹estrogens and 🔹androgens).* How? Remember, abnormal blood (Ca++) is quickly lethal. So, mobilization of medullary bone (getting Ca from braking down specially-reserved bone) is under the exquisite control of PTH.
1 How sensitive is blood Ca+ controlled? 2 What hormones control Ca+ i the blood?
1 🎈Calcium levels in the blood MUST be regulated within a NARROW range AS SIGNAL TRANSDUCTION PATHWAY. TINY changes in blood calcium levels have SERIOUS effects!!! (Calcium= western bridle) 2🎈Three hormones control (Ca++) in blood: *calcitonin (by thyroid) parathyroid hormone vitamin D.*
Where is most calcium in the body?
99% IN bones ~1% IN cells 0.1% IN extracellular fluids.
importance of enough Ca source in cows:
Common that dairy corws had calf, fed calf and not uncommon for farmer to see cow looking like almost dead, then realized that was a lactating mother who was losing lots of Ca as she gave away lots to baby Gave iv with calcium and like resurrection Ex of what happens when controls get out of wack
raise glucose by glycogenolysis
epinephrine glucagon cortisol by gluconeogenesis, not glycogenolsysi tho grwoth hormone by inbhiting glucose uptake and by glycogeneolsys too i think
why you don't need thyroid but need parathyorid
example of how imp calcium control is calciferol is activated vitamin d drug that works similar but not as well
alpha cell is _____ beta cell is ____
glucagon insulin
glucose and blood hormone
growth hormone inbhitis glucose uptake so more is present in blood, sim to glucagon, more aa uptake and protein synthesis the opposite is done by insulin, which is antagonistic to growth hormone
the posterior pituitary
part of the hypothalamus a stock that runs down connects it
Vitamin D & ___ are synergistic but antagonistic for ______.
synergistic role with parathyroid hormone (PTH) in stimulating osteoclast proliferation and bone resorption. BASICALLY, THE VITAMIN D AND PTH NET: INC BLOOD CALCIUM, ALTHOUGH THE VITAMIN D IS REABS SOME CA INTO BONES, BUT THIS is kind of like buying ingredients for a bakery and then selling: get net, altho some is needed to input.
How is vitamin D activated? What does active form do???
🍵Vitamin D itself is not very active, but in the liver it receives an -OH group and in the kidneys another -OH to become the active form. PTH stimulates the final step in the kidneys. *The active form binds to cytoplasmic receptors and forms transcription factors. * wants to inc uptake of Calcium! grab that ca up! -to increase synthesis of calcium pumps, calcium channels, and calcium-binding proteins = promoting uptake of calcium.
hormonal regulation of Ca: relationship of vitamin d with PTH
🍵imbalance: see pic!
What processes regulate blood calcium?
* DEPOSITION, EXCRETION, ABSORPTION* - ➠Deposition and absorption of bone (a calcium phosphate mineral) -➠Excretion of calcium by the kidneys -➠Absorption of calcium from the digestive tract
effects of diabetes mellitus:
-Excessive urine production. BECAUSE: High glucose levels in the blood result in such➠➠high (glucose) in the kidney tubules that significant amounts of ➠➠glucose are NOT reabsorbed, ➠➠➠resulting in an increased osmotic PRESSURE in the tubules that in turn ➠➠➠➠INHIBITS WATER reabsorption and ➠➠➠➠➠causes EXCESSIVE urine volume. The term "diabetes" refers to this high urine output which in untreated individuals results in dehydration.
Starvation in the midst of plenty:
=Cells not taking up glucose, use fat and protein for fuel, resulting in the body's wasting away and tissue and organ damage. Diabetes militus^ *Other prob: nerve cells don't need insulin to take up glucose, so nerve cells take in TOOOO much glucose, causes osmotic prob for cells that favors influx of water, SOO NERVE cells can swell up and get damage :((((* Over time, ind may get neuro prob = numbness in fingers, difficulties, blindness as nerve cells in retina
other type of diabetes
Diabetes insipidius: is caused by* hypo-secretion of antidiuretc hormone ADH *.(ANOTHER TYPE OF DIABETES COMPLELETEY than diabetes mellitus, Diabetes insipidus (DI) is a rare disease that causes frequent urination. The large volume of urine is diluted, mostly water. To make up for lost water, a person with DI may feel the need to drink large amounts and is likely to urinate frequently,
Type I and II diabetes mellitus
Diabetes mellitus is a disease caused by a *lack of the protein hormone INSULIN Type I juvenile diabetes or a lack of insulin RECEPTORS on target cells (Type II).* (normal insulin, but rec don't turn no and func well) maturing onset Insulin binds to RECEPTORS, this stim glucose transporters to take up glucagen * without insulin stimulation, the cells don't take it up! (except for nerve cells) 🔶Nerve cells don't need insulin to take up glucose🔶 : If high glucose conc, nerve cells take up more; if low conc, take up less
how does glucose and other absorption work in the kidneys?
Filtration, reabs, secretion Filtration, reabs, secretion Filtration, reabs, secretion!!!!! ✰All the blood gets filtered into kidney tubules, nonselective, constantly, into proximal tubule to loop of henle then ascending to distal convoluted tublule -Osmotic conc from cortex of kidney (normal, like in blood) to outer then inner medulla and center of body increases Stuff nonselectively filtered out of blood; form lotsof initial urine, then things get reabs a lot in PROXIMAL TUBULE. The glucose gets reabs If you did urine test, have no glucose in urine despite eating tons of doughnuts if you have normal sys
roles of insulin how does insulin do it's job? what's does the stuff it affects then do? if there were not insulin or receptors... insulin also inhibits _______ and stimulates _______
REQ FOR glucose uptake by most cells, but NOT nerve cells. -Insulin binds to receptors on the cell membrane and this stimulates glucose uptake. -This glucose is then used as an energy source, stored as glycogen or converted to fat. Without insulin or the receptors, glucose accumulates to very high levels in the blood, and is lost in urine. (1) inhibits lipid breakdown via lipase in adipose tissue, and (2) stimulates amino acid uptake by cells (while limiting aa release from ___ to not waste)
When cells stim to take up gluocse by ______, most is funneled down for _______ for_________; but, when extra, get _______ and ______
When cells stim to take up gluocse by 🔹insulin, most is funneled donw 🔹glycolysis for 🔹energy prod; but, when extra, 🔹get lipid synthesis and sometiems 🔹glycogen Muscle cells put extra glucose into glycogen Fat syn is common mechanisms to store away extra glucose
what happens for kidney filtration if you lack insulin or receptors?
___If lack insulin or lack receptors, you have overwhelmed proximal tubule and some of glucose gets past proximal tubules, the glucose conc is still small compared to other solutes—most is Na and Cl (less than 1% is glucose) 🔸Look where water being reabs as osmotic conc inc relative to extracellular, so water moves out from lumen to extracell conc across cells; bigger gradient = more water that moves out and gets reabsorbed; (this is bec of reabs but the gradient makes more/less water move out, bec I thought less would leave ?) 🔸But, as you go along, the low conc of glucose (which normally is 0 glucose at that point, bec of reabs) is magnified since water is getting reabs so by end, glucose conc is pretty high, so because of higher conc you get more water in urine, therefore more urine is produced overall!
somatostain
acts to decrease growth hormone so w negative feedback inh growth hormone, insulin, and glucagon main control on insulin and glucagon and cells that prod those hormones are monitoring
temperature compensation on evo and seasonal time scales
allows fish to have same mr in winter vs summer temps slow acclimazation compensates for seasonal temp changes winter vs summer enz that work at diff temp in toehr animals, don't ave both kinds, ex: tropical or polar fish (don't need cold or hot enz, respectively)) __lots of times where evolve better enz for certain temps plat fish have higher MR than expect if you inc catalyst, inc rate of rxn and metabolism
What goes on with bones, and how often?
always being worked: broken down, reformed
concentrating the urine
ca is reabs wel in proximan convoluted region -Urine usually has high phsophate conc and super common in most plants so you are eating lots of phosphate anyway -The body neeeds to get rid of phosphate, filters in to kidney tubules that let it basically pass thru and not reabs much -Phosphate is secreted actively into urine at distal convulted tubule and practically body puts more phosphate into urine to get rid of it!
hunting response
cool day, core temp is struggling so vasoconstriction to periphery. includes the hands. hands get cold, which is ok as long as not too cold, bec want to keep core temp. once in while, vasodilation to hand and hand warms up, then return to vasoconstriction. sys hunting for control sys by vasoconstriction and if possible will return heat to hand occasionally
stomach
has endocrine and exocrine functions produces hormones like gastrine (endocrine) secrete enzymes like HCL and releasing pepsin
half life
how long it lasts in system before it's half gone protein, larger hormones take longer to be filtered out smaller hormone filtered as passes through kidney tubule, so lots of hormones are spec carrier proteins that move around and release and help them stay and not be excreted CARRIER PROT INC HALF LIFE, DEC LOSS ACROSS KIDNEYS so, if removed all steroid carrier prot, would have shorter half life
inc metamorphosis
insects w less elaborate development where young insect looks like adult
days 12 to 14 estrogen increase
it occurs to stimulate ovulation, why LH surge why it goes from neg to positive feedback is turning up or down of trash factors estrogen is feeding back to get more LH and inc estrogen and progesterone to stim the endometrium
how does ADH (ANTIDIURETIC HORMONE) (vasopressin) inc blood pressure?
it opens aquaporins in kidneys, raises blood volume and pressure, cause more reabs of water, and stim constriction vasopressin: vasoconstriction is caused to vascular sys
neurohormone
just hormones wing released from nerve cel like adrenal medulla any hormone released by nerve cell are neurohormones
In ____, vit D acts with _____ to __________. In ____, vit D acts like _____ to ______. vitamin D also acts _______ to _______ in ____>
kideys with PTH decrease ca loss in urine ---bone like PTH stim bone turnover and liberate ca in negative feedback loop to inhibit transc of PTH gene in parathyroid glands vitamin D loves Calcium! clap clap clap clap clap
which cells store glycogen? what do they do with glycogen when they brk it down?
liver and skeletal cells when skel. cells brk it down into glucose they use it when liver brks glycogen down, it releases glucose into blood
glucagon
main effect on glucose and stim glycogenolysis (MAKING OF GLUCOSE)
neuroepinephrine
mostly epi released by mammals opens up uncoupling protein in brown fat, restricting ATP from being made into energy and instead into heat, but cell still needs atp also exists to make sure brain gets energy, so released as hormone
neuroepineprine as hormone
most mammals produce more epi than neuro but, nerve cells release more neuroepinephrine pacemakers in heart release neuroepinephrine as hormone, epi raises heart rate and what hormone does aplha and beas bind both, there's just a preference for one over other the receptors are the difference
neg vs pos feedback
neg: downregulates ex: estrogren most of time dec the releasing factors, LH and FSH that's made by anterior pituitary estrogen feeds back and dec factors that will affect the parameter estogren is steroid: stim transc that stim or inhibits the receptors: estrogen feeds back, binds to receptor in cells and tunes down transcription. pos: it up regulates ex: estrogen right before ovulation, stim release & surge of LH and FSH has diff receptor vs in neg feedback.
does inc aa uptake correlate to inc blood glucose?
not necessarily in cortisol, it does in grwoth hormone case that stim muscle to take up aa for protein synthesis.
Vitamin D what is it? It's made in _____ cells from _________ via stimulation of ___________. What does it do?
not true vitamin; it's a hormone. ➠ we make it in skin cells from cholesterol, stimulated by ultraviolet light ➠circulates in the blood, and acts on distant target cells; therefore it is a hormone.
diagram
pacnreas and blood glucose pancreas stim to produce insuiln; that insulin dec paslma glucose; hypoglycemia stim GRH and then that does toehr things, like inn glucose uptake, fatty acid mobilization, and ketone body synthesis
how to dec evaporative heat loss?
panting or sweating sweat glands: dec the sweating a tiny bit bec not much sweating when you aren't that hot if metabolic rate is up, you lose more heat across respiratory surface in winter than summer bec respiratory rate also increases so, you'd want to slow breathing, but can't bec you need high metabolism that's generating your heat although chipmunk does slow breathing & MR
in mother cat 2 days after birth, which is higher than normal in blood when feeding litter?
prolactin oxytocin parathyroid hormone (raises calcium) glucagon (raises glucose) E) all of the above! yes
epinephrine
released as neurotransmitter (local effect) relesaed as hormone (slower effect but faster than cortisol)
How do the 3 hormones controlling blood calcium work?
remember: calcitonin, parathyroid, vitamin D 🔻Calcitonin, released by thyroid gland, LOWERS blood calcium levels. by: DECREASING osteoclast activity and stimulating osteoblasts to take Ca from blood for bone growth. 🔻Bone is constantly remodeled by absorption of old bone and production of new bone. 🔻OsteoClasts BREAKS down bone and release calcium to the blood. 🔻OsteoBlasts secrete collage in the protein matrix and use circulating calcium to BUILD new bone. As the bone is laid down the osteoblasts are surrounded and develop into osteocytes. WOAH! alter ego much!
why is aldosterone associated w inner cortex?
renin is from kidney and stimulates the adrenal cortex to make mineral corticoid
bumblebees
shiver flight muscles have natural heat exchanger bet thorax and abdomen honeybees: unique in keeping hive warm entire winter, which bumblebees do not do bec they are enclosed, large number, food they've made, so endothermic thru winter. bumblebees don't make honey. males inseminate new queens which leave and hibernator by themselves, and don't feed in spring, she starts new colony and feeds; collect nectar, lays eggs, feeds on nectar (not honey), shivers wings, warms new eggs with heat from abdomen until hatch, then when workers come out, they do all the work bumblebees like other insects, survive w suppressed metabolism
egg shell formation
significance: ex of female bird mobilizing calcium that is still controlled by fine set point, by using hormones that mobilize certain types of bone parathyroid is suepr imp and activated vitamin d
snout length and evaporation
started w heat storage, camel raises core temp to higher setpoint w/out brain damage when you inhale air, it's down in lungs and at core temp bec has moved through membranes when exhale, it's warm and water saturated, so that air cooled off bec when we cool the saturated air, get condensation and heat back in snout, the longer snout of longer respiarotyr passages allows for more of this process to recover air and humidity bec long and narrow (high surface area) so also the cooled arterial blood to brain is now cooler as well
What stim estrogen at beginning of cycle?
stim by LH (luteinzing hormone) of course, about the receptors! follices inc in size so more tissue can produce more estrogen
L aldosterone
stim uptake of sodium reasb more sodium so reabs more water, can be could w ADH hormone and in turn has effect on water if adh can open up aquaporins
What does blood calcium decrease trigger?
triggers the release of *parathyroid hormone (PTH)*. PTH causes an increase in blood Ca++ by: -causing osteoClasts 2 dissolve bond = release Ca -promote Ca reabs. by kidney (so less lost in urine) -promote vitamin D activation (=stim gut to abs Ca from food)
why do pancreas cells made somatostain if it lowers glucagon and insulin prod?
tune down or up whole system not imp tho
free convection
when there's no wind force convection: there's wind explains why winds chill factor, which instills boundary layer near skin; as heat leaves, it heats boundary layer of air that rises and is replaced by cooler air; winds destroys boundary layer and keeps gradient up
is lizard an ectotherm? insects?
yes, gets heat from environment if nonactive insect, it's ectotherm if active insect, it's endotherm (at least thorax, and some of rest of body) ex of terminology not always fitting so it's a temporal (depends on what it's doing) and spatial (thorax vs rest of body) ectotherm lizard as ectotherm but animal can be ecothermic homeotherm too
✨So, which two hormones act antagonistically for blood ca levels?
✨Parathyroid hormone and calcitonin act antagonistically to regulate blood calcium levels. -parathyroid hormone (PTH) INC BLOOD CA (by inc osteoclast act, etc.) VS -calcitonin DECREASES BLOOD CA (by dec osteoclast act)
growth of long bones: How does it work? How does it end????
➠Growth Hormone (via insulin like growth factors) stimulates long bone growth (cartilage), increasing thickness of the epiphyseal plate. ➠Testosterone eventually closes the epiphyseal plate, stopping long bone growth. ➠Stimulate liver to make growth factors that stim prod of long bone (cartilage) More ossification (process in which cartilage is transformed into bone) as you see the bones devleop At ends of long bonds there are seocnardy ostification regions osteoblasts as child grows laying down hard bone in side and on the ends Cartilage is laid down by growth at ends of horomone Epiphyseal cartilage/plate: more ostification and epiphyseal plate remains open; late in adolescense gets closed off, long bones cannot grow anymore and testosterone causes realization of epiphyseal plate (in males and females (make more energins) The tall ones in middle school who made testosterone early on were Producing lots of testoterone and by time graduated, they weren't the tallest ones in group and other people had coninued to grow
endocrine pancreas: _____ & _____ are produced in pancreas in _______ called __________. These ^ have several cell types: *___ cells *___ cells *___ cells The rest of pancreas is what with what functions?
➠Insulin and glucagon are produced in the pancreas in cell clusters called islets of Langerhans. Several cell types have been identified in the islets: 🔹Alpha (a) cells produce and secrete GLUCAGON (RAISIN da roof: inc blood glucose, no lbs in dis house) (antagonist of insulin). 🔹Beta (b) cells produce and secrete INSULIN (boring, lower glucose levels) 🔹Delta (d) cells produce somatostatin (inhibits insulin and glucagon secretion) The remainder of the pancreas acts as an exocrine gland (sec enzymes) with digestive functions.
What's Ca homeostasis?
🍵SEEKING homeostasis of 9-11 mg/100mL
What does the medication calcitriol/calciferol do? vs what thyroid does?
🍵mimics activated vit D if parathyroids secrete PTH, EITHER: A) goes to vitamin D, which makes cacitriol and increases Ca abs in kidneys & gut, = 🎈blood ca RISES OR B) inc bone turnover via act of osteoblasts and coasts; shifts ca from bone to blood; stim ca retention by kidneys; 🎈blood ca2+ RISESS 🍵vs Thyroid: secretes calcitonin that inhibits osteoclasts, shifts Ca uptake by osteoblasts that make new bones w Ca in blood, BLOOD CA LEVEL FALLS
You can live without your ____ but NOT without your _____?
🎈no se necesita thyroid glands (control metabolism), pero 🎈NOSOTROS NECESITAMOS PARATHYROIDS! bec they make PTH! they ONLY REGULATE ca levels, that's their sole job, and remember how the PTH regulates CA like a western bridle?......
Describe what happens after a meal with blood glucose.
🔶blood glucose levels rise; = stimulate the b cells to release insulin. (remember: booooring, lower dat blood glucose) then, Insulin (indirectly) stimulates cells to metabolize glucose and/or to convert it to glycogen and fat. Later, When blood glucose levels FALL, the pancreas DEC the RELEASE of insulin, and cells switch to USING GLYCOGEN and fat for ENERGY. If blood glucose falls too low, the a cells release glucagon which stimulates the liver to convert glycogen back to glucose (glycogenolysis). 🔸 🔶 🔸
blood sugar and effects diagram
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if inc in blood glucose, then.... dec in blood glucose...
🔹inc in blood glucose: -stim pancreas to secrete insulin -insulin inc uptake of glucose by cells -metabolic E produced, fat made, glycogen made 🔹dec in blood glucose: -when LBS, stim pancreas to secrete glucagon ; inc breakdown of glycogen in liver; release glucose to blood *glucoNEOgenesis: making glucose glycolysis: brking down glucose into ATP
releasing ca from bone also ___ this is a problem because ...
🔹releases phosphate from bone! 🔹^^Normal levels of calcium and phosphate in the blood are close to the concentration that could cause them to precipitate as calcium phosphate salts. 🔹imp bec Calcium phosphate salts are involved in the formation of kidney stones and hardening of artery walls. 🔹PTH acts on the kidneys to increase the elimination of phosphate to reduce the possibility of calcium phosphate salt precipitation. this is a potential problem bec ______