Physio2 final pt 1

nibbs06's version from 2015-12-12 04:36


Question Answer
Name a Glucocorticoid & the layer that it’s released fromCortisol, from the Zona Fasiculata
The Zona Reticularis makes which hormones?Aldosterone, from the Zona Glomerulosa
Name a Mineralocorticoid & the layer that it’s released fromThe Androgens
What’s req. to convert NorE à Epi?[Cortisol]x10 in Fasiculata–{Portal Circulation}àPMNT in medulla.
The 5 Steroid Hormones areTestosterone, Estrogen, Aldosterone, Cortisol & Progesterone (“TEA CuP”)
SCC converts cholesterol intoProgesterone
Progesterone turns into a specific hormone based onthe location of progesterone
3 differences in the structure of steroids are# of Carbons (18/19/20), Saturation & Oxidation.
The 3 types of hormones areLipids, Peptides & Tyrosine Derived.
What icosanoid can act as a mediator hormone?Prostaglandin
PL-A2 (icosanoid synth.) is present viahormonal activation via GPCR & lysosomal degradation release.
PL-A2 is inhibited byCortisol
PL-A2 cleaves membrane phospholipids to formArachidonic Acid
The 3 icosanoids areProstaglandins, Leukotrienes & Thromboxanes
What molecule do all of the icosanoids originate from?Arachidonic Acid
Aspirin will inhibitthe COX-pathway(cyclic Endoperoxidase), Prostaglandin & Thromboxane synthesis
Which icosanoid(s) is/are responsible for the inflammatory/allergic response?Leukotrienes
Taking aspirin won’t affect the production ofLeukotrienes since they follow a lipoxygenase pathway
The icosanoid(s) that have an effect on vascular action is/areProstaglandins & Thromboxanes
In prostaglandin synthesis, Arachidonic Acid is made from DG(or phospholipid) via Phospholipase A2 (PLA-2) (analogous to PLC).
Non-Steroid Hormones that have intracellular receptors are(2)Vit. D-R & T3-R
AA seq. of intracellular receptors code for(2)hormone-binding site & the gene that it will regulate.



Question Answer
Oxytocin binds to its GPCR causing (mechanism) GTP binds the G(q)α-subunit that activates PLC to make DG & IP3; DG activates PKC to phosphorylate the -OH of serine & threonine residues of intracellular proteins, & IP3 binds to IP3-R on the ER to release Ca2+ that either ends up activates Ca2+-Calmodulin Kinase or, like DG, activate PKC.
What are the 2 things PKC requires for activation? DG from phosphatidyl-inositol breakdown & Calcium
The kinases of the cAMP differ from the phosphatidyl inositol cycle(PIC), in that the cAMP pathway uses A-Kinase(PKA), which is activated ONLY by cAMP(G(_)type effects [cAMP]); & PIC, has TWO criteria for activation, DAG & calcium
What mechanism does bradykinin use & what mechanism/G-protein does oxytocin use? BradyK uses G(i) & cAMP (lowers cAMP); OxyT uses G(q) & the PIC (req. Calcium)
Peptide & Tyrosine hormone receptors have binding sites that are foundon the E-side.
An example of auto-phosphorylation isInsulin Phosphorylates 6 of its Tyr-sites on the cytosolic side
A Kinase catalyzes putting a phosphate from ATP, onto another protein
What 3 AA’s can be phosphorylated & why?Serine, Threonine & Tyrosine; all have “–OH” groups
What is Tyrosine Kinases function in an Insulin-R?TK is activated, once Insulin binds, & phosphorylates IRS-proteins
TK’s can be apart of (2)the receptor or on protein related to the receptor, called Janus Kinases
Janus Kinases(JAK) are· Intracellular TK-Proteins assoc. w/ the Receptor, but are Non-Receptor TK’s.
TK causes cytokine stimulation when· TK causes cytokine stimulation whenTK is on Janus Kinase Proteins
5 Cytokine Hormones arePRL, GH, Leptin, Ghrelin & EPO [“P.G(H) -L.E.G”]
How many catalytic TK sites doe Janus Kinases have?2
Cytokine Hormone pathH à RèActivates(intra-Protein)èActivates(TK)—[Phosphorylates]àProteins(intra)
G-Proteins are activated whenHormone binds to GPCR, causing GTP to bind to the α-subunit of the G-Protein
4 Hormones that use G-Proteins areFSH, Glucagon, Epinephrine & LH [“F-GEL”]
Which G-Protein Associated Receptor Stimulates Adenylate Cyclase?G(s)
Which G-Protein Associated Receptor Inhibits Adenylate Cyclase?G(i)
Which G-Protein Associated Receptor Stimulates Phospholipase C?G(q)
Epi binds to GPCR, causingGTP to bind to α-subunit of G-Protein, which dissociates from GPCR & attaches itself to Adenylate Cyclase(AC) to activate it. AC will convert ATP to cAMP & the cAMP will activate PKA, which will phosphorylate Proteins/Enzymes
The levels of 5’AMP in a person who drinks an energy drink would below
To increase the amount of cAMP, you couldblock PDE via caffeine & Theophylline
What type (Amino Acids) of Kinase is PKA?Serine-Threonine
How does the G-Protein pathway stimulate glycogenolysis?cAMP binds to PKA, which phosphorylates a protein in the liver to activate it , thus causing it to breakdown glycogen
Which hormone does A-Kinase(PKA) work on?it depends on the area; in liver it stimulates glycogenolysis & on ACTH it will stimulate cortisol production
If BP is high, Atrial Naturetic Hormone(ANH) is released & itincreases Guanylate Cyclase to increase cGMP, in smooth muscle cells, which increases G-Kinase, causing the relaxation of the muscle cells.
For extracellular receptors, Ca2+ willincrease membrane permeability (gradient is 10-2M(o) to 10-7M(i))
IP2 causes Ca2+ release due toCa2+ influx (Calcium-Induced Calcium Release from ER)
Ca2+ is released from ER and thenbinds to Calmodulin to activate Ca2+-Calmodulin Protein Kinase
Inactive NOS is activated byCa2+-Calmodulin
NO-Synthase is inactive & is activated byCalcium-Calmodulin
NO is created byactivation of NO-Synthase that catalyzes the conversion of Arg, in endothelial cells, into NO + Citrulline
What delivery/pathway definition is defined by the release of NO into the cells? Paracrine Pathway
NO goes into the muscle cells and itactivates Guanylate Cyclase to activate cGMP, thus causing phosphorylation of G-Kinase
To increase cGMP you canactivate ANH-R, & through various methods, increase NO-production
The Phosphatidyl Inositol Cycle, oxytocin binds to the GPCR andGTP binds the G(q)α-subunit that activates PLC, which makes (DG & IP3) from the phospholipids. DG(1) will activate PKC, phosphorylating Ser & Threonine residues of intracellular proteins, and IP3(2) stimulates ER Ca2+ release, which either activate Ca2+-Calmodulin Kinase or like DG, stimulate PKC
Insulin binds to I-R, causing tyrosine kinase toautophosphorylate itself and it phosphorylates IRS-proteins which will activate PLC to induce a response & it will activate PI3K to induce a response
Chlorella is a toxin thatincreases cAMP levels by binding an ADP-Ribose group onto the α-subunit of G(s) causing it to be tonically activated and thus raise cAMP levels to cause the symptoms of chlorella, like rapid GI movement.
Bradykinin binds to its receptor, causingGTP to bind to G(i), which will inhibit AC and cause lower [cAMP] & that will lead to reduced phosphorylation of PKA and other mediators in the cell.
Pertussin Toxin works byribosylating the α-subunit of G(i) to inhibit it; the inhibition of this inhibitor-protein causes AC to be activated and thus cause an increase in cAMP, which will cause an increase in the phosphorylation of PKA.
To cause an erecting, drug companies inhibited the GMP-PDE so that cGMP isn’t degraded



Question Answer
POMC produces(5)B-MSH, ACTH, LPH(Lipotropic), Endorphin & Enkephalin(metenkeph.) [“MEEAL”].
The peptide hormones that are glycoproteins are (4)FSH, LH, TSH & hCG
A glycoprotein consists of (3)two peptide chains + 10% carbohydrate
Which chain of the glycoprotein provides “specificity”?Beta-Chain
Which chain of the glycoprotein is interchangeable?Alpha-Chain
Which 1 of the 4 glycoproteins is not secreted from the pituitary?hCG(placenta)
Which peptide hormone stimulates bone growth?PTH + IGF-1, which is stimulated by GH release.
Which of the 2 bone growth stimulating hormones is secreted in a pulsatile fashion?PTH
Which peptide hormone reduces blood pressure?· Atrial Naturetic Hormone.



Question Answer
T3-R’s are dimerized as· Heterodimers [T3(T3-R + Retinoic Acid)]; Retinoic Acid is a T3-R analogue.
What are the 3 primary ways hormones work?They alter the, Transport Process, the Genetic Activity & the Enzyme Activity.
Estrogen(E) Priming is· Eà E-R è—[Nucleus]à mRNA(PgR) —[translation]è Pg-R; à Pg + PgR = mRNA(other)
What does cAMP do to A-Kinase(Akt)?Phosphorylates it
What’s altered when Insulin binds to its R, stimulating glucose uptake?Altered Transport Process


Question Answer
Mineralocorticoids are found in the (layer) Zona Glomerulosa of the cortex
Glucocorticoids are found in the (layer) Zona Fasciculata of the cortex
DHEA & Androsteindione are found in the (layer) Zona Reticularis of the cortex
Pregnenolone is made from cholesterol via (enzyme) Side Chain Cleavage Enzyme
What enzyme is exclusive to the zona glomerulosa? Aldosterone Synthase
Which enzyme isn't found in the Glomerulosa, but found in all the other layers? 17-a-Hydroxylase
What will be the outcome if a patient has a mutation in the enzyme that produces cortisol & aldosterone (21-a-Hydroxylase) Since cortisol regulates all of the hormones being released from the cortex, then if it's missing, it will not be able to feedback & inhibit the androgens (aldosterone is already not being produced), & in females this can cause masculinization.
Besides the androgens, the main regulator of the adrenal cortex hormones is ACTH
Which part of the hypothalamus secretes corticotrophin releasing hormone? Paraventricular Nucleus
What is the main feedback loop for ACTH regulation? Cortisol release goes to the Anterior Pituitary to inhibit ACTH release (Short-Loop)
POMC gets cleaved in the Anterior Pituitary
What is CEH regulated by & what does it do? ACTH binds and activates PKA, which will activate/phosphorylate CEH, located in a lipid droplet, to convert Cholesteryl-Esters into Cholesterol, converting it to Pregnenolone in the mitochondria in the presence of SCC
Cholesterol based hormones differ in release, compared to other hormones in that they are not stored nor are they in vesicles, they just get synthesized and leave
ACTH is released in a _________ fashion Pulsatile
Cortisol dumps glucose into the blood by (3 ways) Gluconeogenesis, increasing appetite and increasing lipolysis
What are the 2 main factors that stimulate aldosterone release? Plasma K+ levels & the Renin-Angiotensin-System (minor stimulation is ACTH)
What are the 3 effects of aldosterone? Decreases Na excretion, Decreases h2o excretion & it increases K+ excretion; (increase plasma [Na], causing h2o to follow & decrease [K] in the plasma)
The feedback to the adrenals for aldosterone is the decreasing [K+] in the plasma
What receptors do steroid hormones use & what's their function and uniqeness? Nuclear Receptors; they change the expression of downstream genes & all of the steroid-receptors work the same.
What's the importance of 11B-Hydroxysteroid Dehydrogenase-2? [Cortisol] is MUCH higher than [aldosterone] & it can bind to aldosterone-receptors. So in areas where aldosterone is absolutely required(kidney), 11B-HSD2 converts cortisol into cortisone(inactive)
Some adipose tissue expand & some contract, in the "remodeling effect" by cortisol, what's the likely reason? Different areas with different ratios of 11B-HSD-1 & 11B-HSD-2
Where are the catecholamines receptors located? Cell Surface
Epinephrine is almost exclusively released only from the Adrenal medulla
The difference between Epi & NorE on their target cells is that Epi is released by adrenal medually & its target cells are far way while NorE is released by Symp. Neuron AT the point of their target cells.
During hypoglycemia, what is released quickly and then inhibited quickly (quick rise & fall)? Epinephrine (some NorE)
The net effect of catecholamines on energy metabolism is similar to (2) Glucagon & Cortisol; dump glucose into the blood
Glycogenolysis in skeletal muscle occurs due to _________ & it will break it down into _________ & _________ Epinephrine breaks glycogen down into lactate & pyruvate, which go to the liver to become glucose
When epinephrine is released, what happens to insulin action and release? Insulin action & release is supressed in the presence of epinephrine
Epi's effects, geographically, are global & they re-adapt the body for emergency situations
Which adrenergic receptor is the only one to use PLC, instead of cAMP? alpha-1 adrenergic
Which adrenergic receptor is responsible for increasing arteriolar dilation(muscle)? Beta
Which adrenergic receptor is responsible for arteriolar vasoconstriction(splanchnic, renal, cutaneous & genital)? Alpha Adrenergic
Which adrenergic receptor does Epinephrine bind to more often? Beta
Which adrenergic receptor does Noepinephrine bind to more often? alpha
alpha-1 adrenergic receptor is responsible for smooth muscle contraction
In the ephinephrine signaling pathway, which molecule is credited to have a global effect on the body? PKA
What's the significance of measuring VMA or Metanephrine? Since Epi has a very short half-life, we cannot measure it, & instead we measure the break-down products (VMA & Metanephrine)
Primary adrenal insufficiency is defined as Primary Addison's, where not enough glucocorticoids are being secreted due to a problem in the adrenal cortex
Secondary adrenal insufficiency is defined as Secondary Addison's, where not enough ACTH is being produced, which causes insufficient release of cortisoll from the adrenals
Primary adrenal insufficiency is defined as Tertiary Addison's, where not enough CRH is being produced, which prevents the release of ACTH & ultimately preventing the release of cortisol
What are the 4 physiological consequences of adrenal insufficiency? Hypoglycemia, Hypotension, Hyperkalemia & Hyperpigmentation
Pheochromocytoma is The over production of catecholamines