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116 Cards in this Set
- Front
- Back
name 7 steroids
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glucocorticoids
estrogen testosterone progesterone aldosterone vitamin D thyroid hormone!! |
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t/f: the alpha subunit of the G protein has the GDP/GTP
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true
(the stimulatory/inhibitory activity of G proteins resides in alpha subunit) if stimulatory--> activates ac-->inc cAMP |
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phosphodiesterase?
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enzyme that degrades cAMP
(inhibited by caffiene) |
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what's the IP3 mechanism?
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hormone binds receptor,
via a G protein, activates phospolipase C phospholipase C liberates DAG and IP3 from membrane lipids IP3 inc Ca DAG + Ca activatesPKC physiologic actions |
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TSH, LH, and FSH have what in common?
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their alpha subunits are identical
their beta ones are different |
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POMC gives rise to.....
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ACTH
MSH (melanocyte stimu hormone) beta-lipotropin beta-endorphin |
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somatomedins=
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IGF
(insulin-growth factor. it's receptor has tyrosine kinase activity...just like insulin!) |
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growth hormone ___glucose uptake
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decreases (GH is diabetogenic)
does it decrease glucose uptake of fat cells and increase of muscle? (check this...) |
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GH ___lipolysis
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GH inc lipolysis
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GH ___protein synthesis
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increases
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GH deficiency can be caused by
(4 things) |
1) dec GHRH (hyp)
2) dec GH (ap) 3) failure to generate IGF in the liver 4)GH receptor deficiency |
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GH excess can be treated by
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octreotride (somatostatin analog)
somatostatatin dec GH GHRH inc GH |
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actions of prolactin
4 functions---on milk, breast, males, GnRH |
-milk production (casien, lactalbumin)
-stimulates, with estrogen, breast development -inhibits GnRH synthesis/release (it's the natural birth control....! its so cool) -inhibits spermatogenesis (by dec GnRH) |
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prolactin excess causes
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1)galactorrhea
2) failure to ovulate and amenorrhea (bc it inhibits GnRH secretion) |
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what stimulates prolactin release?
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TRH (thyrotropin releasing hormone)
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what can treat prolactin excess?
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a dopamine agonist like bromocriptine
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ADH and oxytocin are made where?
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in hyothalamic nuclei, packaged in secretory granules with thier respective neurophysins
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ADH made in which nuclei
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supraoptic nuclei
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actions of ADH on
V1 V2 receptors |
V1--constricition of vascular s muslce
V2--water permeability |
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oxytocin made in...
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paraventricular nuclei
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oxytocin causes...
(2 things) |
ejection of milk from the breast, when stimulated by suckling (via contraction of myoepithelial cells...milk goes from alveoli to ducts to infant)
-contraction of the uterus (oxytocin can be used to induce labor and reduce postpartum bleeding) |
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what increases oxytocin release
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sucking (main)
dilation of the cervix and orgasm |
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thiocyanate & perchlorate anions
inhibit what? |
iodine pump
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5' iodinase _____
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converts T4 to T3 (takes an iodine atom out)
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peroxidase does what?
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basically catalalyzes most of the rxns leading to T4, T3 productions
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what inhibits peroxidase
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propylthiouracil (in follicular cell membrane)
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what's the Wolff-Chaikoff effect?
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high levels of iodine inhibit the iodine pump,--> dec thyroid hormone production
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T/F more t3 is produced, which is the more active form
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more T4 is produced! but yeah, T3 is the more active one
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describe organification of I2
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1) TYROSINE added onto thyroglobulin on the ribosomes of the thryoid follicular cells
2) thryoglobulin is packaged into secretary vescieles on the Golgi apparatus and then goes into the follicular lumen 3) on its way there (at the interface of the cell and the lumen), the tyrosine residues of thyroglobulin react with I2 to form DIT and MIT (monoiodoTYROSINE, and diiodoTRYOSINE) DIT + DIT =T4 DIT + MIT = T3 (they couple, while attached to thyroglobulin) |
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how are thryoid hormones released?
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1) TSH stimulates the cell
2) iodinated thyroglobulin is taken from LUMEN back into CELL 3) in the cell, the lysosomal enzymes digest the thyroglobulin, releasing the T4, T3 into circulation |
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chronic levels of high TSH cause----
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thyroid hypertrophy (goiter)
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what inhibits TSH secretion---> T3 or T4?
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T3 (by downregulating TRH receptors in the ap)
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thyroid hormone affects growth by--------
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thyroid hormones work synergistically with GH and somatomedins (IGF) to inc bone formation
in deficiency: bone age is less then chron age you NEED thryoid hormone to get adult stature |
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thyroid h affects CNS by____
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maturation of CNS absolutely dependent on thyroid hormone during prenatal period...otherwise, there's irreversible mental retardation
(that's why neonatal screening of hypothyroidism is mandatory!!) |
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thyroid h effects on autonomic n system
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has many actions as symp n system bc
1) upregulates B1 adrenergic receptors in the heart ---> inc HR and SV--> in CO |
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thyroid hormone affects BMR:
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increases synthesis of Na, K, ATPase
O2 consumption and BMR are increased by thyroid hormone in all tissues except brain, gonads, and spleen |
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overall of thyroid effect is catabolic
t/f |
true
(inc lipolysis, glycogenolysis, glucose, protein degradation) both protein synthesis and deg are inc but deg is inc more than synthesis |
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where is androstenedione converted to testosterone?
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testes
|
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19 carbon steriods have what kind of activity
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androgenic
(DHEA, androstenedione) (adrenal androgens have a ketone group on C17, an are excreted as 17-ketosteroids in the urine) |
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18 carbon steriods have___
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estrogenic activity!
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oxidation of the A ring (aromatization) to produce estrogens occurs WHERE?
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ovary, placenta
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what's the deal with the dexamethasone suppresion test?
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figures out where exactly the increase of ACTH is coming from
its a synthetic glucocorticoid that's able to inhibit ACTH secretion (just like cortisol does) normal: the dexamethasone inhibits ACTH release (see dec in ACTH) ACTH-secreting tumor: low-dose of dexamethasone doesn't inhibit cortisol release but high-dose does if adrenal corticol tumors: neither low or high dose of dexamethasone does anything |
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cortisol is essential for response to-----
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STRESS
|
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in what ways does cortisol stimulate gluconeogenesis?
(3) |
1) inc protein catabolism
2)dec glucose utilization and insulin sensitivity 3) inc lipolysis..which provides glycerol to the liver for gluconeogenesis |
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antiflammatory effects of cortisol?
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1) inc LIPOCORTIN which inhibits PHOSPHOLIPASE A2, which liberates arachidonate from membrane phospholipids...ARACHIDONATE is the precursor for prostaglandins and leukotrienes which are nec for the inflammatory response
also, cortisol inhibit proliferation of T-CELLS and inhibit production of IL-2 also, cortisol inhibits release of histamine and serotonin from mast cells and platelets |
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cortisol on blood pressure?
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upregulates alpha-1 receptors on arterioles, increasing vasoconstrictor effect of norepinephrine
cortisol excess--> arterial pressure inc |
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primary adrenocortical insufficiency aka
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Addison's disease
primary insufficiency of adrenal cortex (usually, autoimmune destruction of adrenal cortex) |
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secondary adrenocortical insufficiency caused by
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primary deficiency of ACTH
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adrenocortical excess =
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Cushing's disorder!
(there dec ACTH due to neg feedback) (most commonly caused by pharmacologic doses of glucocorticoids) Cushing's disease: when caused by overproduction of ACTH |
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Conn's syndrome is
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hyperaldosteronism
(caused by aldosterone-secreting tumor) |
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21B hydroxylase deficiency
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decreased cortisol and aldosterone
inc adrenal androgens |
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17 -alpha hydroxylase deficiency
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dec cortisol and androgens
inc aldosterone lack of pubic and axillary hair (which depend on adrenal androgens) in women |
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what stimulates glucagon secretion?
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low blood glucose
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where does glucagon act?
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liver + adipose tissue+muscle
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what does glucagon do?
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1) increases glycogenolysis
2) inc gluconeogenesis...by dec production of Fructose 2, 6 biphosphate, decreasing phosphofructokinase activity Increases KETOACID and FATTY ACID conc in blood 1) inc lipolysis 2) the acetyl coA produced from fatty acid degradation -->ketoacids |
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glucagon _____ urea production
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increases
amino acids are used for gluconeogenesis-->and the resulting amino groups are incoporated in urea |
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insulin is packaged along with
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C-peptide
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insulin acts on
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liver, adipose, muscle
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how does insulin decrease blood glucose?
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1) inc glucose uptake (via inc glucose transporters)
2) inc glycogen synthesis (and inhibit glycogenolysis) 3) dec gluconeogenesis (by inc fructose 2, 6 biphosphate...increasing phosphofructokinase activity...substrate diverted from glucose formation) |
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insulin _____blood FA and ketoacid
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decreases!
adipose: stimualates fat deposition, and inhibits lipolysis no ketoacid increase (bc fat is not being degraded...no acetyl CoA....no KA) |
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insulin _____ blood amino acid
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decreases!!
stimulates aa uptake, protein synthesis, |
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insulin is catabolic
t/f |
false! anabolic
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primary vs central hypothyroidism
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primary: TSH high, thyroid hormones low
central: both TSH + thyroid hormone low |
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bone classifications of
1) appearance 2) histogenesis 3) bone tissue/marrow 4) collagen organization |
Appearance:
Long, flat, cuboidal Histogenesis: Endochondral vs. intramembranous ossification Bone tissue/marrow: Compact (cortical) vs. trabecular (cancellous) Collagen organization: Woven (primary) vs.lamellar (secondary) |
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what inhibits RANKL on osteoblasts?
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osteoprotegrin
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Osteoporosis -
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bone resorption exceeds bone formation
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Osteopetrosis –
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defective bone resorption
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Osteomalacia –
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defective mineralization
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Paget’s disease –
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disorganized bone resorption and formation
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common sites of osteoporitic fractures
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vertebrae, hip bone, wrist
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1 alpha hydroxylase is stimulated by_____ , & inhibited by _______
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PTH and hypophosphatemia
1,25 Vitamin D (neg feedback) |
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pathogenesis of osteomalacia
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Vitamin D deficiency-->
dec calcium absorption--> dec serum calcium--> inc PTH--> osteoclastic bone resorption --> release of calcium into circulation--> blood level normalizes--> Loss of bone mineral !! |
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you'll see _____mineralized osteoid in osteomalacia
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dec
|
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Paget's disease
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defective resorption + formation
Disease of osteoclast (overactive) Osteoblast abnormalities Localized areas High bone turnover |
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where is the C-peptide cleaved from proinsulin
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ER
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where does pre-proinsulin--> pro-insulin?
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ER
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how does blood glucose stimulate insulin secretion?
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1) glucose goes through GLUT2
2) inc ATP synthesis 3) ATP-sensitive K+ channels open (Kir6,2) 4) depolarization 5) voltage sensitive Ca+ channels open 6) inc Ca+ in cell 7) exocytosis of insulin |
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t/f both parasymp + symp stimulate glucagon release
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true!
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t/f symp inhibits insulin release and parasymp stimulates insulin release
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true!
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what inhibits both insulin + glucagon?
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somatostatin
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t/f the brain relies on insulin for glucose uptake
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false!
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Normoglycemia
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FPG <110 mg/dL
2-hr PG <140 mg/dL |
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Diabetes, glucose cutoff
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FPG ≥126 mg/dL (fasting)
2-hr PG ≥200 mg/dL |
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Type II diabetes
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Relative insulin deficiency and/or insulin resistance
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what corresponds to the first peak of insulin release after glucose injection?
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the insulin that's in the granules is released
second phase: insulin is being made |
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how do you get dehydration + electrolyte losses in diabetes?
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inc glucose acts as an osmotic diuretic--> loss of hypotonic fluids--> dehydration
osmotic diuretic-->electrolyte depletion |
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Pit-1 gives rise to __________
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thyrotrophs
lactotrophs somatotrophs |
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Russell-Silver Syndrome
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imprinting abnormality:
Intrauterine growth retardation Poor postnatal growth |
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symptoms of GH deficiency
6 |
Marked short stature
Growth failure Hypoglycemia in infancy Central distrubution of body fat Delayed bone age Low serum IGF-1 and IGFBP-3 |
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choose one: intrinsic tallness, advanced growth, accelerated growth
BA= CA normal growth rate |
intrinsic tallness
Familial nl variant Marfans |
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choose one: intrinsic tallness, advanced growth, accelerated growth
BA =HA normal growth rate |
advanced growth
Constitutional normal Obesity Hyperthyroidism Infant giants |
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choose one: intrinsic tallness, advanced growth, accelerated growth
BA > HA increased growth rate |
accelerated growth
(GH excess, sexual precocity) this doesn't seem intuitive...right yiuka? (that BA > HA??)...its right though. i checked on the lecture |
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what are the components of the pituitary gland?
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adenohypophysis (epithelial)
neurohypophysis (neural) |
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any increase in size of pituitary will cause ___________ bc expansion will only happen in 1 direction
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dizziness, vision problems
(will affect optic n) |
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3 types of diabetes insipidus?
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neurogenic (low ADH)
nephrogenic (ADH resistance) psychogenic (compulsive water drinkers) |
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the ap's blood is _________ blood coming from the hypothalamus
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venous
|
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colloid?
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newly synthesized thyroid hormone attached to thyroglobulin
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how do we treat precocious puberty?
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by treating with GnRH (negative feedback)
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cortisol is not absolutely necessary for life as long as ______________ is being produced
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corticosterone
|
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cortisol effect on bone formation?
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dec synthesis of Type 1 collagen
dec osteoblast production dec intestinal calcium absorption overall: dec bone formation! |
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for females, adrenal androgens are the _________ androgens and responsible for __________
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major
pubic and axillary hair and for libido |
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renin is ________ in Conn's syndrome?
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low
(high aldosterone levels--->negative feedback) |
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in 17-alpha hydroxylase insufficiency, is aldosterone high or low?
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low!
why? bc both deoxycorticosterone and corticosterone are high....which have mineralocortical activity....negative feedback-->aldosterone is low! (the renin-angiotensin system controls aldosterone levels) |
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why is oral glucose a more powerful stimulant for insulin secretion than intravenous glucose?
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stimulates secretion of GI hormone, GIP (which has an independent stimulatory effect on glucose)
|
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what's responsible for the insulin resistance of obesity and Type II diabetes?
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downregulation of insulin receptors
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insulin _________ K+ uptake in cells by increasing activity of the ___________
why does it do this? |
increases uptake
Na+K+ ATPase insulin is protecting against an inc in serum K+ (maybe because K+ is released when glucose stimulates insulin secretion in B cells...?) |
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Sertoli cells are to ___________ in female
Leydig cells are to ___________in female |
granulosa cells
theca cells |
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primary spermatocytes become __________ after Meiosis 1 and then become ______________ after Meosis II
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secondary spermatocytes
spermatids primary spermatocytes (diploid 4N) secondary spermatocytes (haploid 2N) spermatids (haploid 1N) spermatozoa (after loss of cytoplasm + flagella) |
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_____________ form tight junctions with each other to form the blood testes barrier
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Sertoli cells
|
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seminiferous tubules-->_________> vas deferens---> urethra
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epididymus
|
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why do seminal vesicles secrete prostaglandins with the sperm?
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1) react with cervical mucosa to make it more penetrable by sperm
2) induce peristaltic contractions in female reproductive tract to propel sperm? |
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primary spermatocytes (______ 4N)
secondary spermatocytes (_____ 2N) spermatids (haploid 1N) spermatozoa (after loss of cytoplasm + flagella) |
diploid
haploid |
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what happens during capacitation?
|
takes 4-6 hrs
--inhibitory factors in the seminal fluid are washed free --cholesterol is withdrawn from the sperm membran --Ca+2 influx into sperm inc motility --acrosomal membrane fuses with the outer sperm membrane |
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what don't Leydig cells have that prevents them from making gluco-and mineralo-corticoids?
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21b and 11b hydroxylase
|
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what do Leydig cells have that allow them to make testosterone from androstenedione?
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17b hydroxysteroid dehydrogenase
|
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98% of testosterone is bound to ________ + ____________
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sex-steroid binding globulin + albumin
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