Endo Physiology Review Flashcards by Matt Stanton

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action of estrogen on LH during midcycle

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MSH

melanocyte stimulating hormone

from anterior pituitary

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TRH

thyrotropin releasing hormone

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lipid soluble hormones

steroids
thyroid hormones

receptor intracellular

synthesized as needed

carried on proteins

long half life

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water soluble hormones

peptides
proteins

receptor outer cell surface

stored in vesicles

unbound in plasma

short half life

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plasma analysis

of hormone level

reflect time of sampling

lots of variation

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urine analysis

catecholamines and steroid hormones

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anterior pituitary

has portal system

hypothalamic/hypophysial portal vessels

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posterior pituitary

supraoptic nuclei

paraventricular nuclei

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supraoptic nuclei

produces vasopressin - ADH

posterior pituitary

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paraventricular nuclei

produce vasopressin and oxytocin

posterior pituitary

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actions of ADH

released with increased serum osmolality

acts on principal cells - distal tubule kidney - V2 receptors
-increased expression of aquaporin 2 channels

increase water resorption**

also contraction of vascular smooth m to protect against volume depletion

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oxytocin actions

milk letdown

uterine contraction

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diabetes insipidus

large volume of urine that is hypotonic

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neurogenic DI

hypothalamic/central pathology
-unregulated ADH

low ADH

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nephrogenic DI

unresponsive to ADH

high ADH

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primary polyuria

increase water intake

-pathologic, habitual, psychiatric syndrome

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diagnosis of DI

confirmed by dehydration stimulus followed by inability to concentrate urine

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no change in urine osmolality after dehydration

think diabetes insipidus

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urine osmolality increase after ADH administration

neurogenic diabetes insipidus

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stimulation for GH release

decreased glucose concentration
decreased fatty acid concentration
arginine
fasting/starvation
puberty hormones
exercise
stress
sleep
alpha-adrenergic agonists

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inhibition of GH release

increased glucose concentration
increased fatty acid concentration
obesity
senescence
somatostatin
somatomedins
GH
beta-adrenergic agonists
pregnancy

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actions of GH

diabetogenic effect - insulin resistance

decreased glucose uptake - more in blood
increased lipolysis
increased blood insulin

increased protein synthesis and organ growth - through IGF-1

increased AA uptake
increased DNA, RNA, protein synthesis
increased lean body mass and organ size

increased linear growth - action of IGF-1

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dopamine

inhibit prolactin release

prolactin induces dopamine synthesis

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stimulation of prolactin release

``` pregnancy breast feeding sleep stress TRH dopamine antagonists ```

inhibition of prolactin release

dopamine bromocriptine (dopamine agonist) somatostatin prolactin

slow GnRH pulse

decreased LH | increased FSH**

fast GnRH pulse

decreased FSH | increased LH**

pulsatile GnRH release

prevents downregulation of its receptor

continuous infusion of GnRH

cause decrease in both LH and FSH

thyroglobulin

to T4 and T3

thyroid hormone synthesis

thyroglobulin exocytosis to lumen iodine into cell and oxidized (- by PTU) iodine into MIT and DIT (- by PTU) coupling rxns (- by PTU) DIT and DIT - T4 MIT and DIT - T3 endocytosis of thyroglobulin proteolysis of thyroglobulin - release T3 and T4

TBG

binds T3 and T4 in blood 99% bound in circulation

T4 vs. T3

T4 to T3 ration 10:1 however, T3 is 10x more active at receptor tissue has deiodinase to convert T4 to T3

normal T4 levels

5-12 microgram/dL

normal T3 levels

70-190 nanogram/dL

euthyroid sick syndrome

hypothyroidism pathology - increased deiodinase D3 - forms inactive rT3

stimulation of thyroid hormone release

TSH thyroid stimulating Igs increased TBG

inhibition of thyroid hormone release

``` iodine deficiency deiodinase deficiency excess iodine intake (wolf-chaikoff effect) perchlorate thiocyanate PTU decreased TBG T3 ```

wolf-chaikoff effect

excess iodine causes inhibition of thyroid hormone release

action of thyroid hormones

growth maturation of CNS increased metabolism increased cardiac output

thyrotoxicosis

excess thyroid hormone in body

hot nodule

overproduction of thyroid hormone

granulomatous thyroiditis

painful gland

graves disease

autoimmune disease | -antibodies that activate TSH receptor - increased thyroid hormone release

hashimotos disease

alpha-TPO Abs destruction of thyroid tissue primary hypothyroid

secondary hypothyroid

pituitary insufficiency

zones of adrenal gland

cortex - GFR zona glomerulosa - aldosterone zona reticulata - cortisol zona reticularis - androgens medulla - catecholamines

excess androgens absence of glucocorticoids and mineralocorticoids

21-alpha-hydroxylase deficiency

increased mineralocorticoids and absence of androgens

17-alpha hydroxylase deficiency

stimualtion of cortisol release

``` decreased blood cortisol sleep-wake transition stress - hypoglycemia, surgery, trauma psychiatric disturbance ADH alpha-adrenergic agonist beta-adrenergic antagonist serotonin ```

inhibition of cortisol release

increased blood cortisol levels opiods somatostatin

ACTH

stimulates adrenal cortex to release aldosterone aldosterone also stimulated by ANG II via RAAS system

adrenal steroid hormones

glucocorticoids mineralocorticoids adrenal androgens

glucocoticorticoids

essential for survival during fasting increase protein catabolism decrease protein synthesis increase lipolysis decrease glucose utilization by tissues

metabolic response to stress

to ensure sufficient energy to meet increased demand of body cortisol release, increased E and NE

chronic elevated cortisol

localized obesity muscle wasting/weakness elevated insulin/glucagon ratio

acute elevated cortisol

decreased insulin/glucagon ratio

primary adrenocortical insufficiency

addison disease

``` hypoglycemia anorexia, weight loss, N/V weakness hypotension hyperkalemia metabolic acidosis decreased pubic hair hyperpigmentation ```

addison disease increased ACTH levels -negative feedback of decreased cortisol

primary adrenal hyperplasia

cushing syndrome

excess ACTH

cushing disease

``` hyperglycemia muscle wasting central obesity moon facies buffalo hump osteoporosis striae virilization HTN ```

cushing syndrome decrased ACTH -negative feedback of increased cortisol

aldosterone secreting tumor

conn syndrome

HTN, hypokalemia, metabolic alkalosis, decreased renin

conn syndrome

virilization in females

21-beta hydroxylase deficiency

lack of pubic hair deficient glucocorticoids excess mineralocorticoids

17-alpha hyedroxylase deficiency