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55 Cards in this Set

  • Front
  • Back
briefly describe the synthesis of norepi and epi
tyrosine is converted to DOPA via thyrosine hydroxylase

DOPA is decarboxylated to Dopamine

dopamine is hydroxylated to norepi

norepi is methylated to epi
what leads to the activation of tyrosine hydroxylase
preganglionic sympathetic innervation required for catecholamine synthesis
- Ach action at nicotinic cholinergic receptor
under basal conditions what is higher in the plasma norepi or epi
norepi
under certain stimulated states what is higher in the plasma norepi or epi
epi
give an example when epi might be higher than norepi in the plasma?
hypoglycemia
name actions that are produced through the action of mainly alpha-1 adrenergic receptors?
vasoconstriction

relaxation of intestinal SM

pupillary dilation

contraction of internal sphincter of bladder

contraction of uterine SM
name the effects of stimulation of beta 2 adrenergic receptors
vasodilation

bronchodilation

relaxation of uterine SM

increaed glycolysis

decreased glucose utilization
name the effects of stimulation of beta 1 adrenergic receptors
cardioacceleration

positive inotropism

increased lipolysis
name the effects of stimulation of beta 3 adrenergic receptors
increased lypolysis
how are catecholamines cleared?
converted to inactive products
-VMA
-MOPEG
what enzymes are necesary for the conversion of catecholamines so they can be cleared?
MAO - conversion to VMA

COMT - conversion to MOPEG
what is a pheochromocytoma?
excessive production of catecholamines

its a tumor of adrenal chromaffin cells
name some common signs associated with pheocromocytoma
episodic hypertension

severe headache

excessive sweating

palpitations with/without tachycardia
what does the zona glomerulosa produce as a final product
aldosterone
what is the primary substrate for the products of all three zones of the adrenal cortex?
cholesterol
what is a similarity between the three layers of the zona
use CYP11A1 to convert cholesterol to pregnenolone
what is the pregnenolone converted to in both the zona glomerulosa and fasciculata and why can the same thing not happen in reticularis?
progesterone

reticularis is missing the necessary enzyme
what is the product of zona fasciulata
cortisol
what is the product of zona reticularis
DHEA or andronstenedione
what is the rate determining step of steroid synthesis
conversion of cholesterol to pregnenolone
what is the secretogogue of zona glomerulosa
ang II
what is the secretogogue of zona fasciculata
ACTH
was is the secretogogue of zona reticularis
ACTH
how is cortisol found in the bloodstream?
75% bound to CBP

15% albumin

10% free
how is aldosterone transported through the bloodstream
50% albumin
40% is free
10% bound to CBP
how is DHEA-sulfate transported through the bloodstream
98% is bound to albumin

2% is free
describe the mechanism of action of steroid hormones
they are lipid soluble
diffuse across the plasma membrane
through nuclear localizing signal transported to nucleus
have genomic effects
give an example of a glucocorticoid
cortisol
what are some metabolic effects of cortisol
stimulation of gluconeogenesis in the liver
stimulation of glycogenesis in the liver
increased protein catabolism-negative nitrogen balance
increased lipolysis
what are permissive effects of cortisol?
permissive - action of one hormone enables the full effect of another hormone

cortisol enhances action of NE at alpha-adrenergic receptors in VSM
describe the circadian rhythm of ACTH and cortisol
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
describe the regulatoin of glucocorticoid release
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
what is the effect of long term use of exogenous glucocorticoids
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
what would be the effect of removing an individual from long term use of exogenous glucocorticoids?
within a month the ACTH levels recover
cortisol concentrations stay below normal levels for up to six months after stopping the medication
what is addison's disease?
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
describe secondary adrenal insufficiency
inability of AP to produce ACTH

diminished levels of ACTH leads to low levels of cortisol
what are some signs and symptoms of addisons disease
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
what three conditions fall under Cushing's syndrome
cushing's disease

adrenal tumor

ectopic tumor

in all cases there is adrenocortical hyperfunction
what is cushing's disease
hypersecretion of ACTH by AP - excessive production of cortisol
describe how an adrenal tumor would be different when compared to cushing's disease
produces high amounts of cortisol but low levels of ACTH
how is an ectopic tumor different than an adrenal tumor or cushing's disease?
not found in adrenal tissue
pumps out lots of ACTH resulting in elevated levels of cortisol
how could you distinguish between an ectopic tumor vs cushings?
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
what is the most common enzyme deficiency in adrenal steroid biosynthesis and what is the effect?
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
what happens when there is a 11beta-HSD deficiency
this is normally necessary for conversion of cortisol to corticosterone

when its inhibited cortisol levels will rise and stimulate mineralcorticoid receptor
why is eating too much licorice a bad thing?
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
what is the most important mineralcorticoid?
aldosterone
what is the action of aldosterone?
acts on epithelial cells of distal collecting tubules of kidney

promotes reabsorption of Na+ and secretion of K+

stimulates H+ secretion
where else in the body does aldosterone stimulate Na+ reabsorption
salivary glands

sweat glands

colon
what is the affect of aldosterone on the heart?
fibrosis
describe the renin-angiotensin system
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
describe conn syndrome
primary hyperaldoseronism

adrenal glomerulosa tumor---increaed aldosterone production----increase Na reabsorption and increased ECFV-increaed ABP----decreaed JGA renin release
describe secondary hyperaldosteronism
decreased renal perfusion pressure-----increased JGA renin release - - increased aldoseronism---increased Na reabsorption and increaed ECVF---increased ABP
what happens with a defect in 11beta hydroxylase enzyme
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
what is primary hypoaldosteronism
addisons disease

adrenal glomerulosa cell dysfunction---decreased aldosterone---- decreaed Na reabsorption decreaed ECFV---decreaed ABP ----increaed JGA renin release
what is secondary hypoaldosteronism
renal insufficiency------decreaed JGA renin release------decreaed aldosterone releae---- decreased Na+ reabsorption and decreaed ECFV---decreaed ABP