EK B2 Ch3 Endocrine

Question 1

endocrine system 1

Answer 1

glands that produce and secrete hormones, not by way of ducts, they secrete hormones directly into blood! means hormones get moved around by circualtory system adn can effect very distant targets, hormone once gets into blood can bind to something far away -often works with nervous system but nervous system obviously works much faster -endocrine control usually slower but long lasting

Question 2

endocrine v exocrine

Answer 2

exocrine release secretions into ducts so like pancreas has an exocrine function it releases all of its digestive enzymes through ducts, travel through duct system to get to ducts -other similar things/terms endocrine

Question 3

endocrine regulation

Answer 3

hormone goes into blood, criculates all over body, bind to receptors far away, two other types of regualted autocrine adn paracrine

Question 4

autocrine regulation

Answer 4

released by cell turns around and binds to cell, regulating it in some way

Question 5

paracrine regulation

Answer 5

• secreted locally, doesn’t secrete all over the body just binds to nearby cells
• so also a lot of growth factors taht work this way and they are considered paracrine regualtors, in cluster of cells one cell will release a growth factor and make one cell in region grow more!

Question 6

tyrosine derivatives

Answer 6

epinephrine, norephinephrine, thyroid hormones

Question 7

hormones binding

Answer 7

can bind inside or outside cell depending if hormone is lipid soluble, if lipid soluble hromone can go through membrane and bind to receptor inside the cell! then cell and receptor usually go ot nuc and act as transcription factor and alter DNA expression

Question 8

peptide hormones

Answer 8

can’t cross cell membrane, so binds to g protien coupled receptor or other receptor on cell surface, and then send the message deeper into the cell using signal transduction pathway*

• bind extracellular receptors like g protein coupled receptor, called that because coupled to a g protein that then activates a second messenger like cAMP or one of the other ones

Question 9

hormones can’t cross membrane…

Answer 9

need to meet receptor on extracellular surface on membrane - so first way this can happen is through adenyl cyclase pathway, inactive g protein receptor with nothing bound to it, and then next to that have G protein holding a GDP molecule so that is a sign that the G protein is not active! b/c it is bound to gdp, so can see nearby enzyme adenylul cyclase but whole pathway is off right now and enzyme is just sitting there

Question 10

g protein

Answer 10

• gamma, beta and alpha subunits, alpha subunit binds GDP when inactive

Question 11

active adenyl cyclase pathway

Answer 11

• when active hormone swipes out GDP with GTP, sign that this protein is on and G protein is active
• then what protein does is activate adenyl cyclase, which is enzyme that converts ATP to cyclic AMP first example of second messenger, structure of cAMP in notes, this is very much like atp except only one phosphate group and weirdly looping around on itself which makes cyclic amp cyclic phospahte group doing some stunt looping around to 3’ O, that is what makes it cyclic, cyclic amp in turn activates protein kinase A
• protein kinase A as a kinase is responsible for phosphorlating other enzymes in the cell, so when we talk about this mention activation cascades, one thing phosphoraltes another molecule which phosphorlates another moelcule etc all which originates with hormone binding to cell, like game of telephone inside cell, also as part of that get amplification of signal, one protein kinase A can activate 10 other enzymes which can also activate 10 other enzymes, benefit of having signal transduction cascade, a lot of bang for your buck small number of hormones binding to receptors can get a pretty loud message inside of the cell

Question 12

Adenyl cyclase pathway 1

Answer 12

-turned off cAMP deactivated by enzyme called phosphodiesterase, cleave ring part of cyclic AMP and turn it back into regular amp -other thing happens to turn off this pathway, GTP being held by G protein gets hydrolyzed to GDP** so G proteins have this built in GTPase activity and once we are back to GDP we consider the G protein not active anymore

Question 13

phospholipase C pathway 1

Answer 13

another ex of where there is a receptor binds a hormone that activates a G protein, here it is shown in active form with GTP bound

-enzyme nearby is phospholipase C- which cleaves PIP2 into IP3 and DAG, PIP2 in membrane and DAG remains in membrane

IP3 floats off into cytoplasm, dag and ip3 are both considered second messengers!

Question 14

IP3

Answer 14

=inositol triphosphate

-second messenger, binds to ER membrane and opens up Calcium channels, Ca2+ does signaling alone or with Calmodulin

-calcium concentrations kept very low in cytoplasm of cells, when open up calcium channel in membrane of ER, calcium will passively flow out of ER and into cytoplasm, other ex of when open Ca2+ channel in membrane, and ca2+ will come rushing into cell because in cytoplasm concentrations are really low

-here allows Ca2+ to rush out of ER and also considered a second messenger, involved in further downstream signaling and sometimes it partners with protein called Calmodulin, a calcium binding protein, and two of them hand and hand run around and activate some things, other things calcium ions activate by themselves but a lot of different downstream options depending on what kind of cell we are in

Question 15

PIP2

Answer 15

Phosphatidylinositol bisphosphate

Question 16

DAG

Answer 16

diacylglycerol -activates protein kinase C together with Calcium, so basically if in a cAMP system protein kinase A is the big work horse, and if in phospholipase C pathway then its doing heavy lifting of running around and phosphorylating enzymes

Question 17

3rd signal transduction pathway = receptor tyrosine kinase

Answer 17

receptor itself acts as enzyme, a kinase! - so on extracellular side looking at structure, this is an example involving insulin, receptor is a dimer, two parts and then on the bottom intracellular side whole bunch of tyr side chains coming off of receptor, when hormone binds for ex when insulin binds to receptor, going down to bottom picture, hormone binds to each subunit, receptor dimerizes meaning two parts come together, and then tyrosines on intracellular side pick up phosphate groups from ATP, and then phosphate groups transferred to other enzymes ex of receptor on intracellular side acting as kinase, picks up phosphates from ATP then moves them onto other enzymes so phosphorylating other stuff

tyrosine kinase- two subunits, intraecellular side whole bunch of tyrosine part of proteins structure important but right now just sticking out into cytoplasm, in lower picture active hormone insulin will bind to each subunit and then the receptor will dimerize and two subunits will come together and form a dimer, triggering tyrosine on intracellular side to pick up phosphate groups* getting phosphate groups from atp* and then other enzymes can be phosphorylated in other words they can come by and pick up phosphate group, that phosphate group can be transferred to other enzymes** so the whole receptor especially the intresellar side can be considered a kinase becuase phsophorlated*

whatever needs to be phoisphorlated comes over because it is stuck in the membrane= whole names receptor tyrosine kinase

Question 18

NOT LIPID SOLUBLE

Answer 18

probably proteins, if is lipid soluble slides through membrane and meets receptors inside cell, ex steroid like cholesterol glide through membrane easily, plenty of peptides or proteins that need to do this to meet receptors on surface of cell, tyrosine derivatives split difference -epinephrine is an ex of tyrosine derivative that uses an extracellular receptor, thyroid hormone ex of tyrosine derivative that is lipid soluble and able to use an INTRACELLULAR receptor! only two things in category that split difference in terms of whether lipid soluble or not and if they combine with receptors

Question 19

Hypothalamus

Answer 19

• referred to as master gland, same with pituitary gland, two competing masters -everything it produces is a protein! 2 roles: 1. interaction with posterior pitutiary and other 2. with anterior pituitary - in brain hypothalamus is above pitutiary gland, which dangles down has two parts posterior pituitary and anterior pitutiary, each one interacts with hypothamlus but each does it in slightly different ways

Question 20

posterior and hypothalamus connection is….

Answer 20

neuron connection

hypothalamus sends signal to posterior pitutiary

hormones ADH and oxytocin are made in hypothalamus travel down these axons and released from posterior pitutiary into blood stream

posteior pituitary doesn’t make any of its own hormones it release ADH and oxytocin made in hypothalamus! remember hypothalamus doesn’t release oxytocin! sythensies it but posterior pituitary releases it!

Question 21

ADH

Answer 21

targets kidney collecting duct, antidieretic hormone, makes you pee less, dieretic would make you pee more does opposite

-if retain water blood volume goes up and blood pressure goes up because of increased water! so ADH has bottom line effect or raising blood pressure

Question 22

oxytocin

Answer 22

• responsible for contractions when women go into labor, targeted mammary glands, uterine muscles
• prosocial, military studies

Question 23

anterior pituitary

Answer 23

-connection btw hypothalamus and other part of pituitary, blood connection not neuronal, portal vessels NOT NEURONS, neurons are yellow portal blood vessels shown in pink, hypothalamus talking to anterior pituitary and then anterior sends out a ton of different hormones, FSH, TSH, Prolactin, MSH (ignore), GH and targets else where in the body

Question 24

TRH

Answer 24

hypothalamus has a hormone called TRH, goes to anterior pit. and tlels anterior to send out TSH which stands for thyroid stimulating hormone, then TSH relay race goes to thyroid gland and then causes thyroid gland to release thyroid hormone

Question 25

ACTH

Answer 25

another pathway where there is something from hypothalamus tells ant. pitutiary to release ACTH -releases coritsol, stress pathway -prolactan, releases milk

(Adrenocorticotropic hormone) causes secretion of cortisol from adrenal cortex ACTH secretion is triggered by stress

Question 26

growth hormone

Answer 26

released by anterior, goes all over body

Question 27

FSH

Answer 27

causes maturation of ovarian follicles in females, sperm production in males

goes to testes or ovaries

Question 28

anterior pituitary hormones

Answer 28

ALL MADE and released by anteiror pituriary

Question 29

GHRH

Answer 29

• hypothalamus releases GHRH promotes GH secretion and is released by anteiror pituitary
• actual signaling molecule or hormone goes through hypothalamus to anterior pitutiary and then the anterior produces and releases another hormone in response, so that interaction is different than what we saw with hypothalamus and posterior pitutiary which has a connection of neuron stretching down to posteiror pituitary
• hypothalamus sends these signals to anterior pituitary, where it is made and then released

Question 30

common pituitary gland defects ex. too little GH in childhood

Answer 30

• do not grow to full stature, traditionally called dwarf

too much GH people can grow too much/ gigantism

too much GH in adulthood: as a result of tumor, anterior pituiary tumors causes anterior pitutiary to start massively pumping out some hormone, if start over producing growth hormone as result, don’t get taller but get acromegaly where bones, face, head and hands start really thickening, like lincoln ppl though he had that

Question 31

thyroid

Answer 31

2 roles: one mediated by TH and other calcitonin, protein, focusing on thyroid hormone -it controls our baseline metabolic rate, people say TH or thyroid hromone when biologists when crazy with naming, but it encompasses T3 or T4, two different variations on moelcule -T3, T4 or TH or trioxy are the same thing, T3 has 3 iodines on it, and T4 has 4 iodines on it, doesnt make a different in terms of function -thyroid hormone tyrosine derivative lipid soluble, binds to receptor inside the cell, but together with repcetor acts as transcription factor inside nucleus to bind to DNA, impact on metabolism

Question 32

negative feedback thyroid

Answer 32

• T3/T4 does negative feedback on anterior pituitary and hypothalamus, look page 90
• high levels of Thyroid hormone puts breaks on hypothalamus, less TRH and less TSH because breaks on anterior pituiary, so means thyroid simulated less so should bring down the levels of t3 and t4, idea of negative feedback able to keep the concentration of something within a narrow range

Question 33

thyroid defects childhood hypothyroidism

Answer 33

-kid born with low levels of hypothyroidism, historically one of the major causes of mental retardation, now testing thyroid hromone cocnentraiton in babies is routine very easy to give someone thyroid hromoen supplements if miss it tragic to miss it and compromsie someone’s brain development, HUGE DEAL hypothyroidsim= hypo means too little thryoid hromone, hyper means too much, those prefixes will aply to hypergylcemia or hypoglycemia

Question 34

adult hypothyroidism

Answer 34

low baseline metabolic rate, cold, sluggish, depresed, ppl present with depression considered good practie to test thyroid hormone concentration because can actually cause depression

Question 35

hyperthyroidism

Answer 35

very hot, lose weight, people are really strung out, jittery, anxious, like on amphetimnes, effects of metabolism cranked up too high

high metabolism taken to a very abnormal extreme is hyperthyroidism

Question 36

Graves Disease

Answer 36

autoimmune disease in which antibody activates TSH receptor so remember TSH is released by the anterior pituiary and it binds to a receptor located on the thyroid, TSH thryoid stimulating hormone is suppose to stimulate thryoid to release, but if have antibody binding to that receptor would over stimulate thyroid becuase no negatvie feedback control and antibody telling feedback to go go go one way to get hyperthryodism, not brought down by usual feedback loops

remember it- think graves disease, grave site has all those tomb stones think antibody on tsh rceptor on the thyroid (tomb stone on tsh receptor blocking)

Question 37

Goiter

Answer 37

-when thyroid is massively overstimulated and produces too much, called goiter big growth in neck -can happen with hypothyroidism or hyperthyroidism, very dramatic mass develops from an enlarged thyroid, do not see it much in US -another cause of goiter is iodine deficiency, can think about feedback loop, iodine part of molecule of thyroid hormone, variants that contained 3 or 4 iodines, if have an iodine deficiency meaning cannot literally make thyroid hormone to complete molecule another cause of hypothyroidism which causes adults to feel sluggish or depressed but can also potentially cause goiter in following way= if you are not able to make thyroid hormone, if cannot make T3 or T4, if no thyroid hormone, anterior pituitary secretes more trh and tsh means these hormones are shouting at thyroid to produce and produce but thyroid cannot because no iodine which can also result in thyroid becoming overgrown and causing goiter

Question 38

thyroid also involved in regulating blood concentrations of calcium

Answer 38

-calcitonin=lowers blood Ca2+ -body wants to keep concentration of ca in blood in narrow range, Calcitonin TONES DOWN Ca in blood, if goes too high thyroid releases calcitonin, which has a net result to reduce blood calcium concentration -causes less Ca2+ to be released from bone and keep more in bone, have less calcium reabsorption in the kidney, meaning let body pee out more Ca to get rid of it -third way is absorb less Ca from food, just not take it in first place from food, targeting digestive tract

Question 39

parathyroid gland

Answer 39

-right besides thryoid, few little glands secrete parathyrid hormone another protein that does the exact opposite of what Calcitonin does -if Ca dips too low, pth is secerted by parathrypid galnd and do a few things that raise Ca concentration in the blood! which to break down bone to release ca, to cause more calcium to be reabsorbed in kidney, and more to be taken up through food through walls of small intestine!

Question 40

pancreas

Answer 40

-talked a bunch for digestive system, now in endocrine chapter focus on endocrine part of pancreas, secretes 2 hormones insulin and glucagon, both proteins, they are secreted from an area of the pancreas called islets of Langerhans, beta cells produce insulin and alpha cells produce glucagon, important because there are so many passages on diabetes, beta cells cells that produce insulin!

Question 41

insulin and glucagon

Answer 41

-released in respone to changes in blood glucose concentration, action of insulin is to decrease blood glucose, secrete insulin in fed state, after just eaten and do all the digestion processes and asborption, blood sugar is high because all nutrients have been absorbed in blood, when pancreas will release insulin! -turns of how insulin decreases blood glucose, allows cells to take up glucose from blood, and specifically causes blood to insert glut4 transporterr into membranes -insulin has these muscle and fat cells, transporters in memrbane allow glucose to come passively into cell, glucose will come in if door is there, and insulin causes door to be put into the wall

Question 42

insulin 2

Answer 42

most famous for allowing glcose to be taken up by cells, also true because insulin working at a moment where body well fed, nutrients high, promotes fat storage and protein syntehsis, acts in that context when there is a lot of available nutrients that has to be dealt with

Question 43

glucagon

Answer 43

-glucagon works oppositely to insulin, meaning it raises blood glucose levels, where insulin would lower blood glucose levels! -if raise blood glucose levels that could involve breakdown of glycogen in liver, could involve gluconeogenesis in liver probably biggest ways we have to raise blood glucose concentrations -both insulin and glucagon respond directly to blood level of glucose, negative feedback situation under normal situations blood can keep glucose concentrations in tight range, if too high release insulin if too low release glucagon, so able to regulate blood glucose concentrations tightly

Question 44

diabetes

Answer 44

type I- body doesnt produce insulin otherwise no way of bringing down blood sugar after they eat type II- usually occurs in adults where ppl do produce insulin but receptors like on muscle cells receptors not sensitive enough so blood sugar remains too high -usually because body not using glucose effectively, ppl with diabetes will metabolize fats more, do more beta oxidation get more ketone bodies, because mobilziing fats soo much get fatty deposits in arteires, get clogging of arteries from cholesterol, most common cause of death from diabetes is cardiovascular incidents like heart attacks

Question 45

adrenal glands

Answer 45

sit on top of kidneys, kidneys on small of your back, right there on top are adrenal glands, two parts an inner area called adrenal medulla, and outer area called adrenal cortex

Adrenal cortex is outside, adrenal medulla is inside

Question 46

cortex

Answer 46

outer

Question 47

medulla

Answer 47

inner area

Question 48

adrenal medulla 2

Answer 48

• secretes epinephrine and norepinephrine
• BOTH are tyrosine derivatives bind to extracellular receptors! -do a fight or flight response -neuro endocrine gland, works v closely with sympathetic nervous system that does fight or flight response
  *

Question 49

adrenal cortex

Answer 49

secretes 2 hormones, both are steroids 1. aldoesterone= acts on kidney, inc water reabsorption, water going back to blood and therefore raises blood pressure! 2. cortisol= part of a class of hormones called glucocorticoids, cortisol is the most famous ones, all inc blood sugar and cause greater break down of fats, mobilizing resources

Question 50

adrenal defects

Answer 50

Addison’s disease= too little cortisol causes problems to poor glucose regulation, abnormal response to stress Cushing’s disease= condition with too much cortiosl, fat deposited because is too high

Cushing’s disease founded by babe paley’s father

Question 51

Stress pathway

Answer 51

Hypothalamus- releases CRF goes to Anterior Pituitary- releases ACTH goes to adrenal gland, specifically adrenal cortex, which releases glucoroticoids, incl. cortisol, WHICH RAISES BLOOD GLUCOSE*** so if have high CRF high ACTH high glucocorticoid, amped up signal all the way down through pathway

Question 52

Higher than normal blood calcium levels would most likely cause:

Answer 52

• calcintonin is released by thyroid not parathyroid! =decreased uptake of calcium along the GI tract, if blood calcium is too high, want blood calcium concentration to be within a tight narrow range, if blood calcium is too high, release calcitonin, causes more uptake of calcium by bone, do anything it can to get calcium out of blood, more uptake of calcium by the bone, less absorption of calcium from food, if blood calcium is already too high calcitonin reacts by causing less calcium to be absorbed from dietary sources along the digestive tract! 3. third way has to do with kidney, in terms of reabsorption of calcium, if blood levels of calcium are already too high calcintonin will act to cause less to be reabsorbed, peeing out less calcium in that case

Question 53

g- protein question

Answer 53

-the alpha subunit holds GTP

Question 54

endocrine system 3

Answer 54

-Endocrine glands produce and secrete hormones

• Endocrine glands have NO ducts
• Hormones secreted directly into blood or interstitial fluid
• Transported by circulatory system to target organs (can be distant)
• Some organs have both endocrine and exocrine secretions (e.g., pancreas)
• Links exist between nervous and endocrine systems
• Nervous system control is faster
• Endocrine system control is slower and longer lasting
• Hallmark of endocrine system is negative feedback control

Criteria using here are how far hormone travels, actually locally or all over the place, endocrine is all over the place

Nervous system electrical signaling very fast, molecules traveling through cirualtory system which tends ot be slower*

Question 55

exocrine glands 2

Answer 55

-Exocrine glands release secretions into ducts • Sweat, saliva, mucus, milk, digestive juices are exocrine secretions

Question 56

paracrine regulation 2

Answer 56

hormone acts locally on nearby cells

Question 57

Autocrine regulation 2

Answer 57

a hormone acts on the same cells that secreted it

Question 58

Endocrine regulation

Answer 58

hormone is carried by blood and acts on a distant target

Question 59

Classes of hormones

Answer 59

Four classes of hormones:

Steroids: cholesterol-derived (e.g., estrogen, testosterone, progesterone, cortisol)

Tyrosine derivatives (e.g., epinephrine, norepinephrine, thyroid hormones)

Peptides & proteins (everything else)

Fatty acids derivatives (e.g., prostaglandins, leukotrienes)

Question 60

intracellular and extracellular hormones

Answer 60

Hormones bind receptors inside or outside of target cells

Lipid soluble hormones cross the membrane and bind intracellular receptors

Lipid soluble: steroids and thyroid hormone

Peptide/protein hormones can’t cross the membrane and bind extracellular receptors

Non-lipid soluble: everything else

Question 61

Lipid soluble hormones bind intracellular receptors

Answer 61

Steroids and thyroid hormones are lipid-soluble-

1. Steroid hormone plus receptor will directly go into nucelus and change gene expression and act as a transcription factor, goes into intracellular receptors or nucelar receptors b/c its lipid soluble

Lipid soluble hormones cross the cell membrane and enter the nucleus

In the nucleus steroids/thyroid hormone bind to a nuclear hormone receptor

Nuclear hormone receptor is a transcription factor

Hormone binding to nuclear receptor causes a conformational change = ON/OFF

Conformational change may cause the nuclear receptor to (1) move from cytoplasm to nucleus, (2) bind DNA, and (3) turn gene transcription ON/OFF

Change in gene expression mediates hormonal effects

Question 62

peptide hormones bind extracellular receptors

Answer 62

• Peptides and protein hormones cannot cross the cell membrane

Peptide/protein hormones bind a receptor on the plasma membrane

Receptor initiates a signal transduction cascade, information flows to interior of cell

Receptor may initiate signal transduction by two mechanisms:

Receptor has enzymatic activity (e.g., receptor tyrosine kinase)

Receptor is G protein-coupled

End-point for signal transduction is change in gene expression

Question 63

receptors can be enzymes

Answer 63

Some receptors have enzymatic activity in their intracellular domains (e.g., kinase)

Hormone binding switches activity ON/OFF

Example: insulin → binds to insulin receptor kinase → two receptor monomers form a dimer → tyrosine kinase regions on intracellular side become phosphorylated → other proteins bind and become activated → cellular responses

Question 64

g-protein coupled receptors (g proteins 2)

Answer 64

Some hormone receptors act through G-proteins

G-protein forms complex with intracellular portion of receptor

G protein can bind GDP or GTP

Hormone binding → receptor conformational change → receptor activates G-protein

G-protein releases GDP and binds GTP

GDP bound = OFF

GTP bound = ON

Active G-protein then activates other targets

Hormone binding can EITHER switch G-protein ON or OFF

Question 65

cAMP

Answer 65

A common second messenger is cAMP (cyclic AMP)

G-protein turns adenyl cyclase ON at the membrane (ATP → cAMP)

cAMP activates protein kinases

Protein kinases phosphorylate targets, altering their function

Phosphodiesterases hydrolyze cAMP → AMP, turning cAMP pathway OFF

Question 66

Calcium 2+ (2)

Answer 66

Ca2+ also a second messenger

Hormone → hormone receptors → G-protein → Ca2+ ion channel

Ca2+ ion channel opening allows Ca2+ influx to cell

Alternatively, Ca2+ is released from ER

Ca2+ binds calmodulin → conformational change → Ca2+-calmodulin is “ON”

Ca2+-calmodulin complex activates enzymes such as kinases

Question 67

phospholipids

Answer 67

Phospholipids are also second messengers

G protein can activate phospholipase C

Phospholipase C breaks membrane bound PIP2 (phosphotidylinositol 4,5 bisphosphate) into inositol triphosphate (IP3) and diacylglycerol (DAG)

IP3 and DAG act as second messengers

IP3 causes Ca2+ release from ER, activating calmodulin

Activated Ca2+-calmodulin and DAG together activate protein kinase C (PKC)

PKC phosphorylates targets

Question 68

amplification

Answer 68

Hormones can act at low concentrations because of enzymatic amplification

A single receptor binding event → activation of many molecules

1 receptor → G-protein → 100 cAMP → active kinases → 1000s of substrates

Question 69

kinases in endocrine

Answer 69

Kinases transfer P to hydroxyl (-OH) group of: serine, threonine, tyrosine

PHOSPHORYLATION

Question 70

phosphatases

Answer 70

Phosphatases remove P by hydrolysis again work on amino acids with OH

Question 71

HYpothalamus 2

Answer 71

Secretes inhibiting and releasing hormones that control other endocrine glands

Physically connected to pituitary

Produces PROTEIN hormones

GHRH (Growth hormone releasing hormone) promotes GH secretion from pituitary

GHIH (Growth hormone inhibiting hormone) inhibits GH secretion from pituitary

GnRH promotes release of LH and FSH from pituitary

CRF (Corticotropin releasing factor) promotes ACTH secretion from pituitary

TRH (TSH releasing factor) promotes TSH release from pituitary

Question 72

GHRH

Answer 72

(Growth hormone releasing hormone) promotes GH secretion from pituitary

Question 73

GHIH

Answer 73

(Growth hormone inhibiting hormone) inhibits GH secretion from pituitary

Question 74

GnRH

Answer 74

GnRH promotes release of LH and FSH from pituitary

Question 75

CRF (Corticotropin releasing factor)

Answer 75

CRF (Corticotropin releasing factor) promotes ACTH secretion from pituitary

CRF from hypothalamus tells anterior pituitary to release ACTH, stress goes to adrenal cortex** target will be endocrine gland to release next hormone in pathway*

Adrenocorticotropic hormone (ACTH) is a tropic hormone produced by the anterior pituitary

ACTH binds to receptors on the membrane of the adrenal cortex releasing cortisol, stress shuts down immune system research shows our immune systems are stopping so many precancerous events constantly having these slipups if completely unchecked and bad luck turn into cancer, so by compromising immune system gives tehse abnormalities much more opportunity to turn into something bad

Question 76

TRH (TSH releasing factor)

Answer 76

TRH (TSH releasing factor) promotes TSH release from pituitary

Question 77

Pituitary gland 2

Answer 77

Pituitary is a “master gland”

Produces PROTEIN hormones

Posterior pituitary RELEASES oxytocin and ADH

Anterior pituitary secretes GH, prolactin, TSH, ACTH, FSH, LH

Question 78

Posterior pituitary

Answer 78

• Posterior pituitary RELEASES oxytocin and ADH
• Hypothalmus PRODUCES oxytocin and ADH
• Oxytocin and ADH travel to posterior pituitary via axons of hypothalamic neurons
• Oxytocin and ADH enter blood only after leaving posterior pituitary

Question 79

ADH/vasopressin

Answer 79

ADH/vasopressin: increases water reabsorption in kidney collecting duct

Increases water reabsorption, blood pressure, decreases urine output

Secreted when plasma osmolarity is high, when blood pressure is low

Question 80

oxytocin 2

Answer 80

Oxytocin: promotes uterine contractions and ejection of milk from milk glands

Involved in mother-child bonding and pro-social behavior

Secreted during suckling, childbirth

Question 81

anterior pituitary 2

Answer 81

Anterior pituitary secretes GH, prolactin, TSH, ACTH, FSH, LH

Secretion controlled by hormones from hypothalamus (see above)

Blood connection between hypothalamus and anterior pituitary (portal system)

Question 82

thyroid gland 2

Answer 82

Secretes TH (TYROSINE DERIVATIVE) and calcitonin (PROTEIN)

TH controls metabolic rate

Basal metabolic rate decreases with age

TH = triiodothyronine (T3, three iodine) and thyroxine (T4, four iodine)

Thyroid hormones are lipid soluble and bind nuclear receptors

TRH → TSH → thyroid secretes TH

TH regulated by negative feedback loop

High TH inhibits TRH and TSH secretion

Question 83

Prolactin

Answer 83

stimulates milk production in milk glands, secretion is stimulated by suckling

prolactin goes to mammory glands, involved in milk secretion

Question 84

TSH

Answer 84

TSH (Thyroid stimulating hormone): causes thyroid hormone secretion, thyroid growth

Question 85

LH

Answer 85

LH: causes ovulation in females, testosterone synthesis in males

Question 86

common pituitary gland defects

Too little GH in childhood

Answer 86

= dwarfism or pituitary dwarf (miniature person)

Question 87

common pituitary gland defects

Too much GH in childhood

Answer 87

gigantism

Question 88

common pituitary gland defects

Too much GH in adulthood

Answer 88

acromegaly (thicker bones in face, head, hands, feet)

Question 89

thyroid gland pathway

Answer 89

TRH → TSH → thyroid secretes TH

TH regulated by negative feedback loop

High TH inhibits TRH and TSH secretion

Calcitonin lowers blood Ca2+

Decreases Ca2+ release from bone and Ca2+ reabsorption in kidney

Feedback regulation by Ca2+

Works oppositely to parathyroid hormone (see below)

Question 90

Thyroid defects

Answer 90

Childhood hypothyroidism can cause cretinism (physical/mental retardation)

Adult hypothyroidism → reduced metabolism, feeling cold, low physical/mental activity

Hyperthyroidism → increased metabolism, feeling hot, weight loss

Question 91

thyroid defects 2

Goiter

Answer 91

Goiter is abnormally large thyroid gland, can reflect TH hypo- or hypersecretion

Hypersecretion of TSH causes thyroid growth

Question 92

Iodine deficiency (thyroid defects)

Answer 92

Iodine deficiency: no T3/T4 synthesis → low TH → increased TSH → thyroid growth

Question 93

parathyroid gland 2

Answer 93

Located next to thyroid gland

Secretes PTH (parathyroid hormone), a PROTEIN

PTH increases Ca2+ levels in blood and interstitial fluid

PTH increases Ca2+ release from bone, reabsorption in kidney, and uptake in intestine

High blood Ca2+ inhibits PTH secretion (negative feedback)

Calcitonin works oppositely to PTH

Question 94

pancreas 2

Answer 94

Pancreas secretes insulin and glucagon, both PROTEINS

Insulin and glucagon are secreted by the islets of Langerhans in the pancreas

Beta cells produce insulin, alpha cells produce glucagon

Insulin decreases blood glucose

Glucagon works oppositely to glucose

Both insulin and glucagon are regulated by negative feedback

After a meal, high blood glucose → insulin secretion

Insulin secretion → glucose uptake from blood → decrease in blood glucose

Fasting → low blood glucose → glucagon secretion → rise in blood glucose

Question 95

insulin 2

Answer 95

Insulin decreases blood glucose

In response to insulin, cells take up glucose from blood

Fat and muscle cells insert GLUT4 transporters into their membranes, which allow glucose to enter passively

Insulin promotes fat storage, protein synthesis

Question 96

glucagon 2

Answer 96

Glucagon works oppositely to glucose

Glucagon raises blood glucose levels

Promotes glycogen → glucose breakdown in liver (glycogenolysis)

Promotes glucose production through gluconeogenesis

Liver cells can release glucose into blood (muscle cells cannot)

Question 97

insulin defects and diabetes

Answer 97

Loss of insulin pathway function can cause diabetes mellitus

Diabetes causes hyperglycemia = high blood glucose (can appear in urine)

Diabetes causes increased metabolism of fats, high blood lipids, atherosclerosis

Question 98

insulin defects and diabetes (hypoglycemia)

Answer 98

Hypoglycemia = low blood glucose

Hypoglycemia may cause loss of consciousness due to lack of brain glucose

Can result from insulin overdose

Question 99

Diabetes causes hyperglycemia =

Answer 99

high blood glucose (can appear in urine)

Question 100

type 1 diabetes

Answer 100

Type 1 diabetes – beta cell loss, causes insulin deficiency

Type 1 is typically childhood onset, can treat with insulin injection

Question 101

type 2 diabetes

Answer 101

Type 2 diabetes – insulin resistance, insulin receptor is unresponsive

Type 2 is typically adult onset

Question 102

aldosterone

Answer 102

• Aldosterone causes Na+ reabsorption and K+ excretion in kidney distal tubule
• Increases water reabsorption, blood pressure, decreases urine output
• Secreted when plasma osmolarity is high, when blood pressure is low

Question 103

Cortisol

Answer 103

• Cortisol increases blood glucose via gluconeogenesis in liver, breakdown of fat
• Cortisol is anti-inflammatory and immunosuppressive
• ADRENAL GLANDS

Question 104

Stress feedback loop 2

Answer 104

Stress promotes CRF (hypothalamus) → ACTH (anterior pituitary) → cortisol

Question 105

Addison’s disease

Answer 105

• Addison’s disease is hypoadrenocorticism = low cortisol
• Many problems, poor glucose regulation, response to stress
• ADRENAL DEFECT 1

Question 106

Cushing’s disease

Answer 106

• Cushing’s disease is hyperadrenocorticism = high cortisol
• Many problems, glucose too high, fat deposited in trunk of body

ADRENAL DEFECT 2

Question 107

Question from QBank

“Bacterial endotoxins may also cause Waterhouse-Friderichsen syndrome, in which acute adrenal failure leads to septic shock. An individual suffering from WF syndrome would NOT be expected to exhibit which symptom?”

Answer 107

Answer= Decreased circulating potassium concentration

WF syndrome is characterized by failure of the adrenal gland following systemic hemorrhage due to infection. As a result of adrenal gland failure, there is no response to ACTH stimulation, and circulating mineralocorticoid and glucocorticoid levels drop precipitously. Deficiency of the glucocorticoids results in hypoglycemia (low blood sugar), and lack of the mineralocorticoids —specifically aldosterone—causes hypotension (low blood pressure and both hyponatremia (low blood Na+ concentrations) and hyperkalemia (elevated blood K+ concentration).

So it is not: low blood sugar, low blood pressure and decreased circulating sodium concentration

Aldosterone’s function is to act on the principal cells of the distal tubule and the collecting duct of the nephron, to upregulate and activate the basolateral Na⁺/K⁺ pumps, which pump three sodium ions out of the cell into the interstitial fluid, and two potassium ions into the cell from the interstitial fluid. This creates a concentration gradient which results in reabsorption of Na⁺ and water into the blood, and the secretion of K⁺ into the lumen of collecting duct and eventually the urine. If the activity of aldosterone is impaired, each of these symptoms could be seen in a patient suffering from WF syndrome.

Question 108

Proteins/fatty acids signal transduction pathway*

Answer 108

1. Proteins/fatty acids signal transduction pathway* have to meet extracellular receptor, three scenarios allow message to be conveyed deep into cell: 1. g protein coupled pathway involving cyclic AMP as second messenger. 2. gprotein receptor pathway lots of details second messengers were dag and IP3 and calcium is always downstream of IP3. 3. signal transduction pathway* didn’t involve g protein receptors exactly but receptor tyrosine kinase pathway, just another way for message for hormone carrying to be transduced or conveyed into the cell even when hormone isn’t entering the cell itself
   
   1. Big example for that one is insulin*

Question 109

Tyrosine derivatives

Answer 109

The name tyrosine derivative means body makes these hromones from tyrosine

Tyrosine= thyroid hormone is lipid soluble and ephinephrine isn’t lipid soluble meets receptor on surface of cell

Question 110

ADH 3

Answer 110

Inc reabsorption of water ADH causes higher blood volume and pressure*

if inc volume also inc the pressure***

Difference btw gases when inc volume of gas what you mean is inc the volume of container because gas molecules spread out to fill the container, taking same number of molecules, giving them more space so they are under less pressure* that is the gas law, inc volume means making container bigger, when talking about blood what we mean by inc volume means more water so more stuff*** the volume of blood vessels is not changing so putting more fluid into the same size vessel so more pressure inside the vessel

Question 111

If inject too much insulin…..

Answer 111

Injecting too much insulin then going to sleep from hypoglycermia/ from an insulin overdose lose consciousness and they die in their sleep*

idea that insulin is hard for people to get and so incredibly expensive, how difficult and high stakes it is to get insulin dosing right even when have perfect access to it incredible stressing out there to ration insulin* for people who cannot afford insulin* huge healthcare access issue, lots of those cases are people not having enough insulin send people to emergency room on that side its ketoacidosis*

Question 112

FLAT PIG

Answer 112

FLAT PIG= FSH, LH, ACTH, TSH, Prolactin, I= ignore, G growth hormone****

1. Not break down more bone in perfect world store more calcium in bone harder in older people, bone is a repository of calcium, and if want not reabsorb it as much at kidney, absorption is process in small intestine* if don’t want it soo much in blood, peeing it out and pooping out let it go
2. FLAT PIG= FSH, LH, ACTH, TSH, Prolactin, I= ignore, G growth hormone**** CRF from hypothalamus tells anterior pituitary to release ACTH, stress goes to adrenal cortex** target will be endocrine gland to release next hormone in pathway* ACTH binds to receptors on the membrane of the adrenal cortex releasing cortisol, stress shuts down immune system research shows our immune systems are stopping so many precancerous events constantly having these slipups if completely unchecked and bad luck turn into cancer, so by compromising immune system gives tehse abnormalkities much more opportunity to turn into something bad
3. People are really strung out jittery, sweaty lose weight amphetimes, high metabolism taken to a very abnormal extreme is hyperthyroidism**
4. Not break down more bone in perfect world store more calcium in bone harder in older people, bone is a repository of calcium, and if want not reabsorb it as much at kidney, absorption is process in small intestine* if don’t want it soo much in blood, peeing it out and pooping out let it go

Question 113

Growth hormone would promote ……

Answer 113

Growth hormone would promote process cartilage cells in metaphasis of the long bones*** promotes conversion of cartilage to bone* in the metapheses of long bones*

Question 114

Both parts of adrenal are….

Answer 114

Both parts of adrenals are involved with stress response, coristol secreted right next to epinephrine

coristol is chronic stress, pathways where those two talk to eachother and boost eachother as well

Question 115

The reason if we inc blood volume we inc pressure different than gas laws is because…..

Answer 115

When inc blood volume you can’t inc volume of container because its in an artery, whereas gas is like a balloon so therefore increase can increase volume of it and dec pressure

Question 116

2. Receptors located at the cell-surface are least likely to bind:
   a. glucagon
   b. thyroxine
   c. insulin
   d. epinephrine

Answer 116

b. thyroxine

so will either bind to receptor on surface of cell or inside cell

proteins bind to extracellular sites; so everything else protien peptide binds extrarcelluarly*

steroids bind intracellularly to their receptors* aldosteorne, cortiosl, protegerstone, estrogen

least likely= one that is most liekly to slide into the cell to receptor, thyroxine/thryoid hormone binds to its receptor inside of the cell* this is a tryosine derviative.

Thyroid hormone lipid soluble slides in meets receptor inside cell

other one is epin. not lipid soluble and binds to receptors on cell surface*

Question 117

3. iodine deficiency would be LEAST likely to cause:
   a. goiter
   b. high levels of TSH
   c. high levels of T4
   d. high levels of TRH
   e. slowed metabolism

Answer 117

c. high levels of T4, cannot make t4 then obviously will not have high levels of it*

iodiine is necessary as part of t3 adn t4 molecule, those numbers actually refer to how many are on the moelcules they are the thyroid hormone being released by thyroid itself and influencing metabolism*

if do not have enough iodine cannot build a molecule of t3 or t4** VERY VERY VERY IMPORTANT that would be deficient**

if look at chemical structure of T3 and T4 that moelcule has iodine in it! literally cannot have fully made and functional moelcules of T3 adn T4 if you do not have enough iodine its an ingreident in the thyroid hormone**

Question 118

6. The posterior pituitary:
   a. synthesizes a hormone that increases milk secretion in breast-feeding women.

synthesizes a hormone that acts on the kidney

c. synthesizes a hormone that acts to increase blood volume
d. synthesizes a hormone that promotes uterine contractions during childbirth
e. none of the above

Answer 118

answer is e. none of the above

Reason these are wrong is because of word syntheses!*****

poster pituitary doesnt synthesize any of these things** just releases them, for example ADH is created by hypothalamus* and secreted by posterior pituitary

Posteiror pitutiary RELEASES ADH and oxytocin

Question 119

Q. 11 Which of the following would likely be true of the patients(s) priors to treatment?

Background- patien A was diagnosed with IDDM (diabiets type I) body is generally unable to produce insulin beacuse of destruction of pancreatic beta cells. Patient B was diagnosed with NIDDM at the age of 50. Her beta cells can produce insulin, but she has been foudn to have insulin resistance.

a. neither patient would have measurable blood insulin levels
b. patient A would exhibit hyperglycemia (high blood sugar) whereas patient B would not
c. Patient B wold exhibit hyperglycemia whereas patient A would not
d. Patient B might have elevated blood insulin levels
e. none of the above

Answer 119

A. is wrong because patient B IS producing insulin would definitely be able to detect insulin, but the cells are not responding to the insulin - so it is wrong to assume neither pt would have measurable blood insulin levels

d. is right because patient B might have even high elevad blood insulin levels, cells aren’t responding so may be the case that pancreas pumping out more and more but receptors are not sensitive to it*** that is the issue with type 2 diabetes*

Question 120

13. the receptor for insulin is:
    a. located within the nucleus
    b. translated on free ribosomes
    c. present at the cell surface
    d. made in the nucleolus
    e. none of the above

Answer 120

c. present at the cell surface** FOR INSULIN tyrosine kinase receptor

TRANSMEMBRANE RECEPTOR

so made and then inserted into plasma membrane so that is bound ribosomes on ER**

so b is wrong, translated on ribosomes in ER. it is not located within the nucleus, and it is not made in the nucleolus

Question 121

16. Intracellular receptors are least likely to bind:
    a. estrogen
    b. testosterone
    c. thyroxine
    d. growth hormone

Answer 121

the answer is d= growth hormone

Growth hormone is a protein, so will defintely bind to a receptor on the cell’s surface*

thryoxine- inside** special tyrosine derivative*

estrogen and testosterone are steroids

Question 122

19. Which of the following is a second messenger?
    a. Diacylglycerol
    b. Protein Kinase A
    c. Protein Kinase C
    d. Calmodulin

Answer 122

answer is a

downstream of second messengers, not called second messengers

can be part of the same pathways but they are not, come after second messenger stage*

second messengers are: cAMP, IP3, Calcium, or Diacycylgylcerol (aka DAG)

Question 123

adenyl cyclase pathway summary 3

Answer 123

hormone first messenger and binds to receptor, activating g protein

gprotein now in active form, know that because holding GTP

activated GTP protein in turn activates adendyl cyclase- which converts ATP to cyclic AMP***

cyclic part where basically phosphate group is forming this really really weird looking ring, very strange molecule and cyclic amp activates protein kinase A and other things happen in cell but eventually this enzyme phosphodiesterase will turn off cAMP***

phosphodiesterase breaks a phosphodiester bond**** product is 5’ AMP

Question 124

drawing of phosphodiesterase breaking the phosphodiester bond

Answer 124

phosphodiesterase breaks a phosphodiester bond**** product is 5’ AMP

Question 125

Phospholipase C pathway Review

Answer 125

Dag stays in membrane

IP3 moves into cell BOTH ARE SECOND MESSENGERS

IP3 first move is to remove calcium from endoplasmic reticulum, example of a ligate gated calcium channel

calcium then moves into cytoplasm, sometimes does signally alone sometimes it teams up with calmodulin hanging around

calcium also considered a second messenger

calcium can also go and activate DAG and then Ca and Dag together will be activated and in turn activate protein kinase C

Question 126

What does 5’ AMP look like?

Answer 126

Question 127

Which of the following is also a second messenger?

a. ATP
b. Protein Phosphatase
c. Inositol 1,4,5-triphosphate
d. Adenylate cylcase

Answer 127

c. Inositol 1,4,5-triphosphate

wrong-d. obviously enzyme with that last phrase “ase” enzyme that forms, proteins/enzymes are not second messengers!

Question 128

22. cAMP is hydrolyzed to form:
    a. ATO
    b. 5’ ADP
    c. adenylate cyclase
    d. 5’AMP

Answer 128

d. 5’AMP

Question 129

7. Higher than normal calcium levels would most liekly casue:
   a. release of calcitonin by the parathyroid
   b. decreased uptake of calcium along the GI tract
   c. increased release of calcium from intracellular stores
   d. increased reabsorption of calcium in the kidneys
   e. release of parathyroid hormone

Answer 129

7. answer is b=
   b. decreased uptake of calcium along the GI tract

If already have a lot of calcium in blood, you want a mechanism that would reduce calcium in blood bring it back down! conservation of calcium in blood is a homeostatic variable liek glucose cannot let it go too high or too low, if too high abnormally high, first of all secrete calcitonin but then looking further downstream in terms of what calcitonin would do is cause you to absorb less calcium from food* to bring down amount of calcium in blood and make it not go higher* why B is correct!!!

d- wrong becuase means calcium in filtrate leaving body gotten rid of would instead be reabsorption in kidneys and go back into blood, so reABSORBED means on the way out you get more in the kidney, already have too much calcium in the blood you do not want to reabsorb calcium from the filtrate—want to pee out how much is going into filtratre/ pee it out and get rid of it through excretion**

notice this is not resoprtion/breaking done bone, this is REABSORPTION** taking place in kidney* Bone resorption is resorption of bone tissue, that is, the process by which osteoclasts break down the tissue in bones and release the minerals, resulting in a transfer of calcium from bone tissue to the blood.

Question 130

Is calmodulin a second messenger?

Answer 130

NO

Calmodulin is a protein that just hangs out in cytoplasm and it doesn’t really do very much unless Ca is there* just a protein and sometimes as part of the system Ca will act with calmodulin if calcium spikes can cause things to happen just by itself, sometimes hte calcium has to work together with calmodulin but calmodulin by itself is just sitting there* it is not by itself created a second messenger* sometimes referred to as calcium binding protein*