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55 Cards in this Set
- Front
- Back
briefly describe the synthesis of norepi and epi
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tyrosine is converted to DOPA via thyrosine hydroxylase
DOPA is decarboxylated to Dopamine dopamine is hydroxylated to norepi norepi is methylated to epi |
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what leads to the activation of tyrosine hydroxylase
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preganglionic sympathetic innervation required for catecholamine synthesis
- Ach action at nicotinic cholinergic receptor |
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under basal conditions what is higher in the plasma norepi or epi
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norepi
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under certain stimulated states what is higher in the plasma norepi or epi
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epi
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give an example when epi might be higher than norepi in the plasma?
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hypoglycemia
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name actions that are produced through the action of mainly alpha-1 adrenergic receptors?
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vasoconstriction
relaxation of intestinal SM pupillary dilation contraction of internal sphincter of bladder contraction of uterine SM |
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name the effects of stimulation of beta 2 adrenergic receptors
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vasodilation
bronchodilation relaxation of uterine SM increaed glycolysis decreased glucose utilization |
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name the effects of stimulation of beta 1 adrenergic receptors
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cardioacceleration
positive inotropism increased lipolysis |
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name the effects of stimulation of beta 3 adrenergic receptors
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increased lypolysis
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how are catecholamines cleared?
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converted to inactive products
-VMA -MOPEG |
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what enzymes are necesary for the conversion of catecholamines so they can be cleared?
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MAO - conversion to VMA
COMT - conversion to MOPEG |
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what is a pheochromocytoma?
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excessive production of catecholamines
its a tumor of adrenal chromaffin cells |
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name some common signs associated with pheocromocytoma
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episodic hypertension
severe headache excessive sweating palpitations with/without tachycardia |
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what does the zona glomerulosa produce as a final product
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aldosterone
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what is the primary substrate for the products of all three zones of the adrenal cortex?
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cholesterol
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what is a similarity between the three layers of the zona
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use CYP11A1 to convert cholesterol to pregnenolone
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what is the pregnenolone converted to in both the zona glomerulosa and fasciculata and why can the same thing not happen in reticularis?
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progesterone
reticularis is missing the necessary enzyme |
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what is the product of zona fasciulata
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cortisol
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what is the product of zona reticularis
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DHEA or andronstenedione
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what is the rate determining step of steroid synthesis
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conversion of cholesterol to pregnenolone
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what is the secretogogue of zona glomerulosa
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ang II
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what is the secretogogue of zona fasciculata
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ACTH
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was is the secretogogue of zona reticularis
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ACTH
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how is cortisol found in the bloodstream?
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75% bound to CBP
15% albumin 10% free |
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how is aldosterone transported through the bloodstream
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50% albumin
40% is free 10% bound to CBP |
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how is DHEA-sulfate transported through the bloodstream
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98% is bound to albumin
2% is free |
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describe the mechanism of action of steroid hormones
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they are lipid soluble
diffuse across the plasma membrane through nuclear localizing signal transported to nucleus have genomic effects |
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give an example of a glucocorticoid
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cortisol
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what are some metabolic effects of cortisol
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stimulation of gluconeogenesis in the liver
stimulation of glycogenesis in the liver increased protein catabolism-negative nitrogen balance increased lipolysis |
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what are permissive effects of cortisol?
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permissive - action of one hormone enables the full effect of another hormone
cortisol enhances action of NE at alpha-adrenergic receptors in VSM |
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describe the circadian rhythm of ACTH and cortisol
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increased ACTH correlates with increased cortisol levels
there are increasing level of these hormones in the early hours- importnant for having systems ready for metabolic activities during the day |
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describe the regulatoin of glucocorticoid release
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ACTH acts at adrenal corticol cells
there s negative feedback of ACTH ath the level of the hypothalamus and anterior pituitary via cortisol ACTH also has a negative feedback at the level of the hypothalamus |
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what is the effect of long term use of exogenous glucocorticoids
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ex: prednisone for arrthritis
suppresses the HPA axis has negative effects at the level of anterior pituitary and hypothalamus which drastically reduces ACTH release the result is reduced cortisol secretion as well as atrophy of adrenal cortex |
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what would be the effect of removing an individual from long term use of exogenous glucocorticoids?
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within a month the ACTH levels recover
cortisol concentrations stay below normal levels for up to six months after stopping the medication |
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what is addison's disease?
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primary adrenal insufficiency
inability of the fasciculata tissue to produce cortisol will see low levels of cortisol but elevated levels of ACTH - feedback normally provided by cortisol is absent |
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describe secondary adrenal insufficiency
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inability of AP to produce ACTH
diminished levels of ACTH leads to low levels of cortisol |
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what are some signs and symptoms of addisons disease
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brain: lethargy, dizziness, depression
muscles: skeletal muscle weakness and fatigue intestines: abdominal pain, constipation skin: increased pigmentation due to increased levels of cortisol blood pressure: postural hypotension |
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what three conditions fall under Cushing's syndrome
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cushing's disease
adrenal tumor ectopic tumor in all cases there is adrenocortical hyperfunction |
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what is cushing's disease
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hypersecretion of ACTH by AP - excessive production of cortisol
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describe how an adrenal tumor would be different when compared to cushing's disease
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produces high amounts of cortisol but low levels of ACTH
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how is an ectopic tumor different than an adrenal tumor or cushing's disease?
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not found in adrenal tissue
pumps out lots of ACTH resulting in elevated levels of cortisol |
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how could you distinguish between an ectopic tumor vs cushings?
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they both produce high levels of ACTH
but if give drug to negatively feedback of ACTH and see modest reduction the problem is in the anterior pituitary if you give the drug and see no reduction - ectopic tumor |
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what is the most common enzyme deficiency in adrenal steroid biosynthesis and what is the effect?
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21alpha - hydroxylase deficiency
you will have excess androgen production from the reticularis and inadequate production of cortisol and aldosterone the enzyme is necessary in the production of aldosterone and cortisol |
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what happens when there is a 11beta-HSD deficiency
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this is normally necessary for conversion of cortisol to corticosterone
when its inhibited cortisol levels will rise and stimulate mineralcorticoid receptor |
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why is eating too much licorice a bad thing?
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contains glycerrhetinic acid which is an inhibitor of 11beta-HSD
excessive amounts of licorice can lead to cortisol stimulation of gene expression in prinicpal cells of the kidneys which can mimic aldosterone actions can lead to volume dependent elevation in blood pressure |
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what is the most important mineralcorticoid?
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aldosterone
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what is the action of aldosterone?
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acts on epithelial cells of distal collecting tubules of kidney
promotes reabsorption of Na+ and secretion of K+ stimulates H+ secretion |
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where else in the body does aldosterone stimulate Na+ reabsorption
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salivary glands
sweat glands colon |
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what is the affect of aldosterone on the heart?
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fibrosis
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describe the renin-angiotensin system
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angiotensiongen produced in the liver is changed by renin from JG cells into angiotenisn I
angI is converted to ang II by ACE AngII causes release of aldosterone which causes increased Na+reabsorption and K secretion |
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describe conn syndrome
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primary hyperaldoseronism
adrenal glomerulosa tumor---increaed aldosterone production----increase Na reabsorption and increased ECFV-increaed ABP----decreaed JGA renin release |
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describe secondary hyperaldosteronism
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decreased renal perfusion pressure-----increased JGA renin release - - increased aldoseronism---increased Na reabsorption and increaed ECVF---increased ABP
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what happens with a defect in 11beta hydroxylase enzyme
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second most common defect in adrenal steroid biosynthesis
aldosterone and cortisol levels greatly decreased there is an excessive production of 11- deoxycorticosterone(DOC) which is an effective mineralcorticoid |
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what is primary hypoaldosteronism
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addisons disease
adrenal glomerulosa cell dysfunction---decreased aldosterone---- decreaed Na reabsorption decreaed ECFV---decreaed ABP ----increaed JGA renin release |
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what is secondary hypoaldosteronism
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renal insufficiency------decreaed JGA renin release------decreaed aldosterone releae---- decreased Na+ reabsorption and decreaed ECFV---decreaed ABP
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