10. Endocrinology Integrative Session Flashcards by Priyanka Barad

how are the hypothal & post pit connected

hypothal (supraoptic nucleus & paracentricular nucleus)

–> send axons (hypothalamic-hypophyseal tract)

to post pit - release ADH

connection = neural

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where are most of the ADH cell bodies located

supraoptic nucleus (SON)

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what triggers ADH secretion

decreased BP - (sensed by cardiac & aortic baroreceptors)

decreased arterial stretch due to low BV - (sensed by artial stretch)

increased osmolality - (sensed by hypothalamic osmoreceoptors) *MOST SENSITIVE*

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carotid sinus and aortic arch uses which nerves to signal the medulla oblangata

vagus N & glossopharyngeal N

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what is the response generated by ADH

vasoconstrict blood vessels (V₁ receptors)

increase reabs in kidneys (V₂ receptors)

==> increase BP & blood vol

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what happens during hyperosmolarity (dehydration)

decreased h2o & hypernatremia –>

stimulate osmoreceptor in ant. hypothalmus –>

increase thirst & post pit release ADH –>

increase h2o permeability of principal cells in distal tubule & collecting duct –>

increase h2o reabs –>

–> kidneys removed LESS h2o from blood –> increase [urine]

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what is the response to hypoosmolarity (hypervolemia)

inhibit osmoreceptors in ant hypo –>

decrease thirst & ADH secretion from post pit –>

decrease h2o permeability of principal cells –>

decrease h2o reabs

–>kidneys remove MORE h2o from blood = urine more dilute

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what is caused by decreased levels or effects of ADH on renal collecting duct

diabetes insipidus (DI)

freq urination & polydyspia

large vol urine & its diluted

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how do you get central DI

lack of plasma ADH bc..

damage to pituitary or destruction of hypothal

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what is desmopressin

drug that prevents h2o excretion

use for central DI

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how does nephrogenic DI happen

kidney is unable to respond to ADH (increased plasma ADH levels) bc..

drugs like lithium or chronic disorders (polycystic KD, sickle cell anemia)

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what is the h2o deprivation test for DI

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how do you differentiate btn central & nephrogenic DI

both - increase plasma Osm & decrease urine Osm

central: decreased ADH & respond to desmopressin (increase urine Osm)
nephrogenic: increased ADH & NO response from drug

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what is syndrome of inappropriate ADH secretion (SIADH)

excess secretion of ADH –> excess h2o retention, HYPOnatremia, plasma Osm decrease & urine Osm increased

bc : (adrenal insufficiency: drugs, trauma, CNS disorders)

ectopic : small cell lung carcinoma

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when is aldosterone stimulated

decreased Na/increased K in blood

decreased BV & BP

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what does angiotensin II stimulate

aldosterone –> increase Na reabs - increase ECF vol
increase Na-H exchange –> (result above)
increase thirst
vasoconstriction –> increase TPR

all together increase P_a

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what is primary adrenal insufficiency

adrenal cortex not working

both cortisol & aldosterone decrease

ACTH & CRH increase

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what is the cause of secondary adrenal insufficiency

ant pit affected -> decrease cortisol

but normal aldosterone bc RAAS stil fxning

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what is ANP & BNP

when is its released

atria distend –> release ANP

ventricle release BNP

–> reduce BP (decrease TPR) and increase excretion of NaCl and h2o by kidneys (collecting ducts)

what is urodilatin

secreted by distal tubule & collecting duct

stimulated by increased BP & increase ECF vol

inhibit NaCl and h2o reabs in medullary collecting duct

(like ANP but only fxn of kidneys)

how do the natriuretic peptides control NaCl excretion

vasodil afferent & vasocon efferent arterioles ==> increase GFR

inhibit renin, aldosterone, ADH secretion

inhibit NaClo reabs by collecting ducts

how does sym N contribute to NaCl and h2o reabs

catecholamines stimulate NaCl & h2o reabs by PCT, thick ascending limb, DST and collecting tube

what happens if there is increased Na intake

what happens if there is decreased Na intake

what can cause hyperkalemia

insulin deficiency beta2- antagonists alpha agonists acidosis hyperosmolarity cell lysis exercise

what can cause hypokalemia

insulin beta2 agonists alpha antagonists alkalosis hyposmolarity

what does insulin do to K+

stimulates K+ uptake into cell by increasing Na/K ATPase (deficiency leads to hyperkalemia)

what happens with decreased beta-hydroxysteroid dehydrogenase, apparent mineralocorticoid excess, licorice

renin & aldosterone: low extracell vol or BP: high -hypokalemia

what would a adrenal tumor or hyperplasia lead to

renin: low aldosterone, extracell vol or BP: high -hypokalemia

what would congenital adrenal hyperplasia (17-hydroxylase deficiency)

renin: low aldosterone, extracell vol, blood pressure: high -hypokalemia

what would a renin-secreting tumor lead to

high renin, aldosterone, extracell vol &/or BP hypokalemia

what would a 17-alpha enzyme deficiency lead to

increased: mineralocorticoids, BP decreased: cortisol, sex hormones, [K+], androstenedione male: undescended testes female: lack secondary sexual development

what does 21-beta enxyme deficiency lead to

increased: sex hormone, [K+}, renin activity, 17 hydroxy-progesterone decreased: mineralocorticoids, cortisol, BP infants: salt wasting precocious puberty virulation

what would a 11-beta enzyme defiency lead to

increased: DOC, BP, sex hormone decreased: aldosterone, cortisol,[K+}, renin activity virilization

what occurs with hypoaldosteronism (adrenal insufficiency)

high: renin low: aldosterone, extracel vol or BP =hyperkalemia

what is present when renin, aldosterone, extracel vol &/or BP are low (hyperkalemia)

hyporenin-hypoaldosteronism: beta-blockers, autonomic neuropathy

what are symptoms present with hypocalcemia

hyperreflexia, spontaneous twitching, M cramps, tingling & numbness chvostek sign: twitch face when tapping facial N trousseau sign: carpopedal spasm up inflation of BP cuff

what are the symptoms of hypercalcemia

decreased QT interval constipation, polyuria, polydispia lack of appetite M weakness, lethargy hyporeflexia coma

how can you change Ca in the plasma

change in plasma protein concentration (proportional) change in [anion] (increase phosphate -\> increase Ca) acid-base abnormalities (change amount of Ca bound to albumin)

what happens to Ca in acidemia

increase free [Ca] bc less bound to albumin

what happens to Ca in alkalemia

decrease free [Ca] bc more bound to albumin -associated with hypocalcemia

what happens in the bone, kidneys and intestine w/ decreased plasma Ca

increase PTH 1. bone: increase resorption 2. kidney: decrease Pi reabsorption, increase Ca reabs & urinary cAMP 3. intestine: increase Ca abs (indirect via vit D)

what is the action of PTH on kidneys

inhibit NPT2 receptor --\> decrease Pi reabs cAMP made in cells of proximal tubule is excreted in urine (increase urinary cAMP) stimulates Ca reabs by TAL and distal tubule (overall: increase Ca reabd and reduce excretion)

what is the regulation of vit D synthesis

how is kidney 1alpha-hydroxylase enzyme regulated

transcriptonal level Ca and Vit D inhibits the CYP1alpha gene PTH stimulates CYP1alpha gene --\> make more 1alpha-hydroxylase

what is familial hypocalciuric hypercalcemia

auto dont cause mutations that inactivate CaSR in parathyroid glands & parallel Ca receptors in ascending limb of the kidney ==\> decreased urinary Ca excretion (hypercalcemia)

what is prepropressophysin

peptide precursor for ADH cleave into propressophysin & then packages in vesicles to travel down hypothalamic-hypophyseal tract (en route- they're cleaved into ADH)