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247 Cards in this Set
- Front
- Back
Where are the 2 adrenal glands,
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on top of each kidney, and NO direct connection between them
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What are 2 endocrine glands of adrenal
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adrenal cortex and adrenal medulla
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Cells of adrenal cortex produce
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steriod hormone--corisol and aldosterol
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Cell of adrenal medulla secretes
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CCAs Epi and norepinerhpine--
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Adrenal cortex has 3 zones that produces specfic STEROID hormones
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Zona glomerulosa
Zona fasiculata Zona reticularis |
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What does Zona glomerulosa (outmost) produce
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aldosterone-mineralocorticoids
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What does Zona fasciculata produce
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cortisol/glucocoticoids
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What does Zona reticularis produce (innermost)
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androgens such as dehyroepianrosterone
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Numerous lipid droplets -that represent stored cholestrol with what zone
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zona fasiculata
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What does Adrenal medulla produce
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CCAs
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What are 3 main STERIODS of Adrenal CORTEX
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aldosterone
cortisol dehydroepindrosterone (DHEA) |
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What steriod is produced in greatest amount
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cortisol
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Androgens are produced in small amounts, and only soure of androgen is in
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females
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If androgens are only in females, they are converted in other tissue cells to
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testorsterole in males---and estrogen in females
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May adrogens be linked to onset of puberty in males and females and menopause
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YES
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All adrenal steriod hormones are dervaties of cholesterol, how do cells acquire and store cholesterol
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cells take up LDL (lioproteins)
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The first step in converting chosterol to specifc steriods is
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conversion of cholestrol to pregenolone
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What is rate-limiting step in steriod hormone biosynthesis
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conversion of cholesterol to pregnenolone
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Are steriod hormones stored, if not why
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NOT stored but synthetsieze and secreted on demand
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Does increased amount of cholesterol inside cells enchane steriod synthesis
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YES
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What are 2 types of stimui for secretion of cortisol (ANTERIOR PITUTIARY
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Circaidm rhythms
OTHER--Stress stimuli |
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What drives the noraml dialy pattern of glucocortidcoid secretion
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ciccadiam rhythm--related to sleep wake cycles RATHER than LIGHT-DARK cycles
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When do cortisol levels reach a peak
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shortly after you awake from sleep
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When do cortisol levels reach a low
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just after you fall asleep
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What can override circadiam rhythm? Which does what
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stress stimuli--can increase cortisol synthetsis and secretion
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Physical and Psych, stress increase cortisol release--what are types of physical stress
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Hypoglycemia--
Trauma Heavy exercise |
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What are types of psyh stress that increase cortisol
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acute anxiety
chronic anxiety |
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Short-term stress response activates
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adrenal medulla--CCAs
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Long-term stress resonse activates
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adrenal cortex (minneral corticoids and glucocorticoids)
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What are effects of ACTH on extraadrenal
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melanocyte stimulation--skin pigmentation
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What can cause skin pigmentation
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excessively high ACTH levels
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What are negative feedback loops of cortisol
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Cortisol feeback inhibition on hypothalmus and anterior pituitary and ACTH does feedback inhibition on HYPOTHALMAUS
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How does cortisol transported in bloodsteam
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boudn to Cortisol Binding globulin
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IS only free coritsol molecules able to interact with receptors 5%
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YES
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Cortisol is steriod hormones so what is MOA
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binds to interacellualr receptors stimulates gene expression and alters protien synsthsis (long DOA_
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What are tissues that Cortisol has an effect on
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Liver, SM, and Adipose Tissue
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What else beside cortisol has an effect on LIVER, SKM< and adipose tissue
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GH
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What are cortisol effect on liver
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Increases gluconeogenesis
Increase glycogen synthesis Increase urea cycle activity |
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How does liver increase glyconeogenesis via
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increase A.A uptake and metabolism
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Why does liver increase area cycle activity
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to remove excess nitrogen from aa metabolism
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Cotisol has an ANABOLIC effect on liver, what effect does it have on SKM and Adipose
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CATABOLIC
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What effect does cortisol have on SM and Adipose
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inhibit glucose uptake,a nd icnrease metabolism of proteins and lipids for gluconeogensis
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Cortisol has addional effect on adipose wihci is altered fat moblization,WHERE
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extemremeites fats depleted
Trunk-fat increases |
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Cortisol is important for what developmental effects
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normal fetal development
contributes to differentiation of cells cortisol to mother--gives infant surfactant |
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Cortisol is important for what type of pschic effect
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emtional stability, and euphoria with high levels
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Permissve effects of thryroid hormone are upregulates beta-adrenegic receptor an enchanes action of epi and norep, what are permissive aciton of cortisol
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increase BV vasoconstriction
cortisol enchances acction of epi on lipid metabolism |
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Does cortisol cause inhibitiron of non-essentail functions such as reproductiona nd growth
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YES
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How is cortisol anti-inflammatory//immunosuppression
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inhibtion of PGs, stabilizae lysoomal membrane preventing release of proteolytic enzymes--immuno suppres growth and immune cells
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What effect do glucorticoids have in high doses (cortisol)
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inhibit inflammaotry resonse
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What are benefits of immunosuppressive actions
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suppress rejection resonse to transplanted organs
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What happens result of chornic use of glucocorticod therapy
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supression of ACTH, results in loss of tropic action on adrenal cortex, so adrenal cortex atrophies
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Can abrupt withdrawl fo glucocorticoid theraphy be life treatening
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YES
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What is benfit of slow withdrawl of glucocorticoid therapy
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allows CRH-ACTH adrenal system to become operational agin, allowing ACTH levels to rise and sumualte adrenal cortex to prodce cortisol
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What is the primary mineralcortoid prodcue by zona glomerulosa
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aldosterone
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What are 2 primary regulators of aldosterone
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K+
Angiotensin II, which is controlled both by kidney |
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What are physiogical actions of aldosterone
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Increase sodium renetion,and water rentention, and increases K+ excretion
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What happens to urinary output from aldosterone
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Urinary sodium decreases, and K+ urinary increases
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Aldosterone is a steriod-bases hormone how does it increase Na+ transport into cell
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increases Na+ channels, and increase Na+K+ ATPase activity
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What is a direct simulatory effect to release aldosterone
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increase K+ or decreased Na+
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What is a indirect effect to release aldosterone
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decreased Blood volume--leads to angiotensive II production with sitmulates aldosterone release
|
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Decrease blood volume/blood pressure triggers kidney
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to release rein, which converts angiotensionoge from liver to angiotnesin I
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Angiotnesiv I is converted to Angio II by
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AcE in ling
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Angiotensin II stimulates
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the zona glomerulosea to produce aldosterone
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Factors that regulate renin rlease from kidneys are
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dedecrease BP and BV
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What are 3 effects of angiotensin II
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vasoconstrtion of BV, stimulates Adernal cortex to increase aldosterone, increases sodium reabsrotion, stiumates brian to increase ADH and increases H20 reabsorption
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What is primary regulator of aldosterone release
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Plassma K+
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Small changes in K+ directly affect what cells
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zona glomeruosa cells, which increase aldosterone secretion
|
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An increase in plama K+ does what
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depolaries excitable membrane results in cardiac arrhythmias
|
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A decrease in plama K+ does what
|
hyperpolarizes cell membrane--leads to cardia arrhytmias and possible death
|
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Is tight control of plsam K+ critical to homoestatis and lfie
|
YES
|
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What is a main disease of primary hypofunction of adrenal cortex
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Addison Diesases
|
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What is cause of Addison Disease or hypofunction
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desturction of adrenal cortical cells--need replacment therapy
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What are clinical mamifestation of Addison's disease of hypofunction
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Hyperpigmentation
Mineralcorticoid deficiency Glucorticoid deficiney |
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What causes hyperpigmentation
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High ACTH levels, b/c cortisol levels lover, and less NEAGIVTE feedback
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What causes mineralcortiocoid defineicy
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increase renal loss of Na+ and increase K+ retention, and decreases ECF/plasma volume and decrease CO
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What is result of glucocorticoid deficinecy
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Hypoglycemia, Ffatigue, weakness,
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What is Andernocrotical hyperfunction disease
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Cushing disease primary or secondy
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What are symptoms of Cushing syndrome
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abnormal fat depoistion, protein metabolism, muscle wasting, and hyperglycemia,
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What are Hypo and Hyper of Throid
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Hypo-Hasimoto's
Hyper--Graves |
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What is hypo /hyper of adernal cortex
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Hypo-addisons
Hyper-Cushing |
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What is site where fetus develops
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uterus
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What is inferios aspect of uterus that extends into vagina
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cervix
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What are 3 layers of uterus
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Perimterium
Myomterium Endoemtrium |
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What wall layers thickness varies during menstual cycle, paritally removed during period, and site for implantation of ovum at start of pregnancy
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endometirum
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What extends laterally from uterus to each ovary, but do NOT contact overay
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Uterine tubes or follopain tubes
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Mature ovulated egg (oocyte) travels from
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ovaeries to fallopain tubes to uterus
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What is distal end of uterine tubues wehre fertilization of oocyte occurs
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ampulla
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What are fimbria
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ends of enterine tubes , that have beating cillia that caputes the ovulated oocyte to carry into uterine tubes
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What is function of ovary
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produces are release mature oocytes
2. produces aer secretes large amount of hormones |
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What is oogenesis
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production of eggs
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What are states of oogensis
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1. Oogogina
2. Primary ooctyes 2. Secondary oocytes |
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When does oogonia occur
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all oogonia are formed within the 1st 3 months of gestation
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What happens during oogonia
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germ cell undero many mitoric divsion, and produce about 4 million ooogonia
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What happens after 3rd month of development
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MITOSSI stops and no new oogniona are ever produced again
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After MITOSIS stops, what happens
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oogonia b/c primary oocyte , then suppround by a single layer of granulosa cells--forming primordial follicule
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What do the primary ooytes do
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BEGIN but do NOT complete a 1st mitotic division
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At birth, what happen
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born with 2 million primoridal follicles
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What is benefit of follocies
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respond to hormonal singals--the oocyte does not
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Orrgoina and Pimary oocytes and primordial follices occur during, where does secondary ooctyes occur
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1st 2 fetus---Secondary occutes is puberty
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By the time puberty is reach, how many primary oocytes remain
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400,000 remain
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Each month what happens
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several follicles or primary oocytes are activate and continue matruation
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What is the dominant follicle
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ONLY one follicle will complete the 1st MEIOTIC division
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THe one folicle that completes the 1st MEIOTIC division will form
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secondary oocyte and a polar body
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What does a secondary oocyte contain
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23 chromosomes and almost all of cytoplasm
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What does polar body contain, and what happen
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nearly devoid of cytoplasm--goes a 2nd meiotic divsions which degenerate
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What happens to secondary oocyte
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START a second meiotic dvision but stops in metaphase II
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When the secondary oocyte is then matrue and ovulated when will it complete 2nd meiotic divsion
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after it is fertilized by a sperm cell--otherwhise deterioes
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Each month only ONE mature oocyte is ovulated, over a normal reproductive life that amounts to how many oocytes
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500
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What are 3 phases of ovarian cycle
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Follicular phase
ovulation luteal phase |
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What cell type does the follicular phase begin with
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primordial follicle
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Several primordial follicles are actived and what happens
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folliclar cells proliferate in number around primary oocyte, adn secrete a glycoprotein rich substance
|
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The follicular cells secrte a glycoprotein rich substance that forms
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the zona pellucia which is bettwen the oocyte and granulosa cell
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Then another outer layer forms around the follice, is
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Theca
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The granulose cel then secrte a fluid which forms
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into an antrum
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Are a number of perantal/early antral follicules always pressent,
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YES
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What marks the REAL begging of the follicular phase
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Dominant follile
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One one of the growing follicles becomes dominant,and continues to grow into a mature follicule, what happens to all other follicules
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atresia
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What happens to dominant follicule
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The primary oocyte inside the follicle completes its 1st meotici division, and b/comes a secondary oocyte, which begins its secondary meotitic division but does not complete it
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What triggers ovulation
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hormonal signals trigger the follicle to secrete enzmes to break down ovrain memrane, and release seoncdary oocyte
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The FOlluclar phase is what
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Development of mature follicle and secondary ooctye
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The luteral phase begins with
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Corpus Luteum
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What composes the corpus luteum
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consits of the granulosa and tecal cells left over after the 2nd oocyte is released from ovary
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The corpus lutem is yellowish in color and increases in size and secretes 3 hormones
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1. Progesterone
2. Estrogen 3. Inhibin |
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What happens if ovum is not fertilized
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corpus luteum degrades in 12-14 days
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What happens if ovum is fertillized
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corpus lutem continues to secrete estrogen and progesteron until placenta can take over (3months
|
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What is the princiap estrogen secrted
|
estradiol
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The ovarian cycle is completely dependent upon
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hypothalamus, anterior pittuairy and ovary interactions
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What are 5 principals hormones of ovarian cycle
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GnRH FSH, LH estrogen and progesterone
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Before puberty, what prevents Follicular phase
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small amounts of estrogen provide negative feedback to hypothalmus to inhibit GnRH secretion
|
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What happens in puberty that starts folliuclar growth
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hypothalamus less senstiive to estrogen, GnRH is rlease an stimulates release of FSH and LH, which start follicle growth
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After a few years of low level actiivty GnRH, FSH adn LH secretion b/c high enough to trigger
|
dominant follicle grwoth and ovulation to start adult ovarian menstural cycle
|
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What days are early folluclar phase
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days 1-6
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What happens in early follicular phase
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GnRH secretes FSH and LH stimulate preantral and antral follcile to growth and devlopment, and estrogen and progesterone very low
|
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What does FSH do
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stimulates granulosa cell to increase in size, and number,and stimulates graulos cells to produce and secrete estrogen
|
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What does LH do
|
sitmulates thecal cells to proliferate and to produce and secrete androgens, which are used by granulosa cells to produce estrogen
|
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LH stimulates Theca cells to
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thecal cells to grow and make androgens, which diffuse to granulosa cells
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What do granulosa cells do with androgens
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covert andogens to estrogen, and FSH helps granulosa cells secrete estrogen
|
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What days mark middle foicilar phase
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6-12
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What happens once follicles cells secrete estrogen
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estrogen rises, and exerts a negative feeback on hypothalmus and anterior pituatiary to decrease GnRH and FSH and LH
|
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How does estrogen act as a postive feeback autocrine mediator
|
it simulates proliferation of granulosa cels and increases stregoen produces
|
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Then one follicle becomes dominant, and other undero atresia, what does dominanst follcile do
|
estrogen levels rise SHARPLY
|
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Does dominant follicle respond to FSH and LH even though their plasam levels are decreasing
|
YES
|
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Increasing inbhibin levels have what effect on anterior pitituary
|
has a negative effect on FSH
|
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What is the late follicular phase
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days 12-14
|
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What happens around days 12-14,
|
estrogen plsama levels peak around days 12-14 due to high output of dominant follicle
|
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What do high estrogen levels stimulate
|
postive feedback effect
|
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What is the postive feedback effect of estrogen
|
estrogen simulates hypothalamus to and anterio pitutary resulting in a LH and FSH surge
|
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When does LH surge occur
|
apporx 18 hours before ovulation
|
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What does the LH surge trigger
|
the primary oocyte to complete its first meiotic division and b/c a secondasry oocyte--dominat follicle is fully matured
|
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What is day 14
|
ovulation
|
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After LH surge causes the development of the matutre follicule (secondary oocyte), what happens
|
mature follicle decrease estrogen production, and begin an increase in progesterone secretion
|
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When does progesteron secretion occur
|
just before ovulation
|
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May one see a rise in body temp during ovulation
|
YES
|
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What is luteal phase
|
days 14-28
|
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What is 1st thing that happens after ovulation
|
formation of corpus luteum
|
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Does LH surge trigger lueinzation
|
YES
|
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What does corpus luteum produce
|
produces and secretes large amount of progestone and estrogen, and inhbin
|
|
Even as LH levels drip does corpus lutem continue to respond to LH for
|
10-12 days
|
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What does progesterone is the presence of estrogen do
|
inhibits the hypothalmus and reduces GnRH secretion leading to decreased LH and FSH secretion
|
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During the luteal phase estrogen concentrations are high gain, what prevents another LH surge
|
progesterone inbhits
|
|
Low FSH and LH levels prevent
|
follicle growth
|
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What does birth control durgs mimic
|
the luteal phase
|
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How do birth control drugs mimic the luteal phase
|
use elveated progesterone and estrogen to suppres LH and FSH and prevent LH surges and ovulation
|
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Corpus lutem if not fertilized degenerates after 10-12 days, and loss of corpus lutem leads to
|
sharp decrease in progesterone and estrogen
|
|
If progesterone and estrogen levels concentrations drop, what happen
|
GnRH and FSH and LH begin to rishe b/c negative feedback inhibhition is gone
|
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What contracts during menstration and during childbirth
|
myometrium
|
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What is the permanant endometrium layer
|
startum basalis
|
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What layer of endometrium undergoes dramituc changes during ovarian/menstural cycle, and site for fertilzied ovum
|
stratum functionalis
|
|
What are phases of UTERINE cycle
|
mentstural phase, proliferative phase, and secretory phase
|
|
What is proliferative phase dependent on
|
estrogen
|
|
The estrogen produced by the maturing follicles sitmulates
|
proliferation of endometerial cell,
growth of myometrium, increases endometrial receptors, and prodcues clear thin mucus in cervix |
|
What is benefit of estrogen producing a clear, thin, mucus in cervix
|
allows easy passage of sperm from vagina into uterus
|
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What is main hormone of secretory phase
|
progesterone
|
|
What happens in secretory phase
|
progesterone from corpus luteum acts on estrogen primed endometium to prepare for uterus implantation
|
|
What does progesterone do n the estrogen primed endometrium
|
futher proliferation of blood vessels and glands
secretion of glycogen and glycoproteins into uterus |
|
Progesterone also stimulates secretion of glycogen and glycoproteins and
|
thick visouc mucus in cervix
|
|
What is the benfit of thick mucus
|
forms a cervical plug to prevent bacterial contamination of uterus
|
|
Does progesteron inhbit smooth muscle activity
|
YES--keeps myometrium from contract and expelling embryo
|
|
If ovum is not fertilized, what happens
|
corpus letuem dengerates and progesterone and estrogen produciton strops
|
|
Without progesteron eand estrogen the straum functionalis is not maintained and degenerates, this is
|
the menstrual phase
|
|
What do events occur in menstural phase, which is mediated by prostaglandins
|
blood vessels constrction depriving endometrium of blood supply leading to degeneration and uterine smooth muscle contracts---expel endometrium
|
|
Can excessive production of prostaglands cause menstrual cramps
|
YES--treat with ibuprofen
|
|
Does blood vessel dialtion occur after intial constrition, what is benefit
|
washes out endometrial debris
|
|
What are sugars, stored as
|
glucose, fructose, stored as carbs
|
|
What are Triglycerids, broken down
|
consists fo fatty acids attached to glycerol, broken down to ketone bodies
|
|
A.A are funciton enzymes, and ca be used as enegy stored as
|
proteins
|
|
Why should we regulate blood glucose
|
is a perferred fuel some for tissue, and at high levels can damage tissues
|
|
Does glucose at high levels cause all problems of diabetes
|
YES
|
|
What are normal fasting levels
|
75-115 mg/100ml
|
|
What are tyical plasma glucose values after a high carb meal
|
>200, and qucily return to fasting level
|
|
Does energy needs conincide with meal times, so what do we need
|
NO--we need more energy when exercise-that why we need storage adn rlease
|
|
How is glucose uptaked inot he cell in presence of high glucose
|
Glucose transports are upregulated, and all passive diffusion of glucose into cell
|
|
What allow passive glucose diffusion into cell
|
conversion of glucose to glycogen once enters cells, allows celluar glucose concentrations below plasma glucose
|
|
How does insulin function to decrease blood glucose
|
by increasing glucose storage
|
|
What is function of glucoagon
|
functions to mobilize glucose from storage
|
|
What are main glucose transporters
|
GLUT2 and GLUT 4
|
|
What is function of GLUT-4
|
reulation by insulin-important drug target for diabetes patients
|
|
What is function of GLUT-2
|
is exresspress in pancretic cells, part of glucose sensing appartatus
|
|
What are 2 functions o f pancrease
|
endocrine--hormone
exocrine-digestive enzymes |
|
What is function of islets of Langerhands
|
secrtes hormones into a portal vein, and transported directly into liver
|
|
What organ sees 2X more insulin, and why
|
LIVER--insulin is released into portal system goes directly to liver
|
|
If 2X of insulin is in liver, is this a main problem of therapetic insulin
|
YES--cant get 2X of drug insulin into liver by injection
|
|
What do alpha cells of islet release
What do beta cells of islet release |
Alpha-glucagon
Beta-insulin |
|
Proinsulin cleaved forms
|
Insulin and C-peptide
|
|
What does C-pepdie levels measure
|
how much insulin your patients is making
|
|
What is most important signal triggering insulin release
|
increase blood glucose
|
|
What are other MAIN factors that trigger insulin rlease
|
Gastric hormones, and parasympathetic nervous
|
|
What are MINOR factors that reulgate insulin secretion
|
GAGE
Glucagon, Amino acid/fatty ction/ Glucocorticoids, and epi |
|
What does epinehirne do to insulin secretion
|
DECREASES
|
|
The insulin is a protein kinase receptor, how does it work
|
phosphorlation leads to activation of enzymes used to store fuel, and inhbit enzymes used to mobilize mobilized fuel
|
|
What is a major symptoms of type 2 diabetes
|
Insulin resistance
|
|
Resistance to insulin effects are coupled to
|
increased insulin production
|
|
Does act of exercise lower blood glucose
|
YES
|
|
What does Foxa2 do
|
activates expression of genes involved in fatty-acid oxidation
|
|
What does Foxo1
|
acctives expres of genes involved in gluconegensis
|
|
Which is more senstive to insulin
|
Foxa2
|
|
Chronic high psla insulin leads to
|
down regulation of receptor number
|
|
What is insulin effect on carbohydrate metabolism
|
glycogen synthesis is simulated in liver and muscle and glucoeneogenesis is inhbitied in liver
|
|
What is major source of glucose for diabetic pts
|
gluconeogensis
|
|
What is insulin effects on lipid metabolism
|
trigylerid storge is activated in adipose tissue
|
|
Direary cholesterol and Triglycerides are transported by chylomicrones, how do triglyceride eneter cell
|
Lipoprotein lipases cleave, and allow enter to enter cell
|
|
What are insulin effects on protein metabolism
|
active protein synthetis especially in muscle
|
|
AA comes from muscle, and is transported to
|
liver
|
|
WHen is muscle tissue senstied to uptake glucose by
|
parasympathetic signal to liver and HISS to muscle
|
|
What are inducers fo glucagon secretion
|
decrease blood glucose and amino acid
|
|
What is most potenet amino acid that induce glucagon secretion
|
arginine
|
|
What happens in high protein diets
|
both insulin and glucagon are secretion
|
|
WHat is benefit of insulin and glucagon BOTH being secreted in high proten diets
|
Glucogaon keeps blood glcucose up, while insulin promotes storage of aa
|
|
Are parasymthpatetic and sympathetic simtuaate inducers of insulin secretion and glucagon secretion
|
YES
|
|
What are inhibitors of glucoagon
|
high blood glucose, and fatty acids
|
|
What effect does glucogon have on carbohydrate metabolism
|
glyocogen breakdown, and stimulates gluconeogenesiss
|
|
What is glucagon effects of lipid metabolism
|
stimulates hormone lipase, which caues breakdown of tryglycerides--fatty acids
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Fatty acids can be used by muscle for energy, ketones boides and then made in liver, and is a source of energy for
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heart adn SKM---
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What is glucagon effect on protein metabolism
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cuases protein degrateion into amino acids used for gluconegensisi
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A product of protein degradion is nitrogen, which builds up as ammonia what happens with glucagon
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stimulates ammonia conversion to urea
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What is function of somatostsin
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inhibts both insulin and glucagon
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Somatostatin may be useful as a therapy to inhibit glucagon secretio in diabetes, why
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need to stop gluconegensis
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IF I/G levels are high what predominates
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insulin predominates--ledags to storgae of fuel
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If I/G levels are low what predominates
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GLUCONG--catabolic state leads to mobilization of fuel
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What role does glucagon play in diabetes (TYPE 1)
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lack of insulin leads to lack of glucose sensing by aplah cells of the islet
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Is insulin require for alpha cell to sense glucose
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YES
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Type 1 Diabetes is caused by combination off TOO little insulin, and too much glucagon
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YES
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Leptin is an adipose tissue secretion that serves to
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inhibit eatin
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Does leptin function as main homeostatic regulator of body weight
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YES
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Leptin levels are quire high in obese people suggseting that obesity may reflect
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leptin resistance
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Increased levels of ciruclating TNF
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insulin resisance
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IS PAl-1 expression a hallmark of obesity
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YES
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