Endocrine Lecture Flashcards
Familial Hypocalciuric Hypercalcemia
(again)
PTH
Serum Ca
Urine Ca
Pi
Vit. D
PTH normal to high
Serum Ca high
Urine Ca low
Pi normal
Vit. D normal
What enzyme makes Vit. D into the active form and what is the name of the active form?
CYP1a (a-hydroxylase) makes it the active form
1, 25 OH2 cholecalciferol is the active form
occurs in the kidney (PCT)
What is the effect of PTH on the kidney (DCT)
Inhibition of the Na/Pi channel causes what?
Triggers second messenger system via GPCR and makes Ca channels to suck Ca in from the lumen and then into the blood via Na/Ca exchange and Ca/H exhange
Inhibition of the Na/Pi channel causes phophaturia
Is free ionized Ca high or low during acidemia?
Is free ionized Ca high or low during alkalemia?
high because less Ca is bound to albumin
low because more Ca is bound to albumin, often accompanied by hypocalcemia
Hyperkalemia due to Decreased ENaC
Renin (high or low)
Aldosterone (high or low)
BV and BP (high or low)
Renin-high
aldosterone-high
BV/BP-low or normal
Hyperkalemia due to hypoaldosteronism (adrenal insuffieciency)
Renin (high or low)
Aldosterone (high or low)
BV and BP (high or low)
Renin-high
Aldosterone-low
Bv/BP-low
Hyperkalemia due to hyporenin-hypoaldosteronism (b-blockers, autonomic neuropathy)
Renin (high or low)
Aldosterone (high or low)
BV/BP (high or low)
Renin-low
aldosterone-low
BV/BP-low
Adrenal Hyperplasia: 17a deficiency
Sx
mineralcorticoids
cortisol
sex hormones
BP
K
labs
undescended testes, lack of 2’ sex development
mineralcorticoids: high
cortisol: low
sex hormones: low
BP: high
K: low
Labs: low androstenedione
Adrenal Hyperplasia: 21B deficiency
Sx:
Mineralcorticoids:
Cortisol:
Sex Hormones:
BP:
K:
Labs:
salt wasting in infancy, precocious puberty, virilization
Mineralcorticoids: low
Cortisol: low
Sex hormones: high (enlarged clitoris)
BP: low
K: high
Labs: renin high, 17 hydroxyprogesterone high
Adrenal Hyperplasia: 11B deficiency
Sx:
Mineralcorticoids:
Cortisol:
Sex Hormones:
BP:
K:
Labs:
Virilization
Mineralcorticoids: low aldosterone, high DOC
Cortisol: low
Sex Hormones: high
BP: high
K: low
Labs: low renin
Hypokalemia due to increased ENaC
Renin
Aldosterone
BV/BP
Renin: low
Aldosteorne: low
BV/BP: high
Hypokalemia due to decreased B-hydroxysteroid (caused by mineralcorticoid excess or licorice?)
Renin
Aldosterone
BV/BP
Renin: low
Aldosteorne: low
BV/BP: high
Hypokalemia due to adrenal tumor or hyperplasia
renin
Aldosterone
Bv/BP
renin: low
aldosterone: high
BV/BP: high
Hypokalemia due to congenital adrenal hyperplasia (caused by 17 hydroxylase deficiency)
Renin:
Aldosterone:
BV/BP:
Renin: low
Aldosterone: high
BV/BP: high
Hypokalemia due to renin secreting tumor
Renin
Aldosterone
Bv/BP
Renin: high
Aldosterone: high
BV/BP: high
What is the effect of insulin on K balance?
insulin stimulates uptake of K into cells by acting on Na/K ATPase
Low insulin levels result in decreased uptake of K and hyperkalemia
high levels of insulin lead to hypokalemia
Causes of K to shift out of cells and cause Hyperkalemia
insulin deficiency
B2 adrenergic antagonists
A-adrenergic agonists
acidosis
hyperosmolarity
cell lysis
exercise
causes of K to shift into cells and cause hypokalemia
insulin
B2 adrenergic agonists
a-adrenergic antagonists
alkalosis
hyposmolarity
What is the overall effect of increased Na intake?
Increased ECF and BV
Decreased SNS
Increased ANP
Decreased pic
Decreased RAAS
Increased Na Excretion
What is the response to decreased Na intake?
Increased SNS
Decreased ANP
Increased Pic
Increased RAAS
Decreased excretion of Na
What is the effect of Renal Sympathetic Nerves
Increase nerve activity, decrease NaCl excretion
Decrease GFR
Increase Renin secretion
Increase Na reabsorption along nephron
What is the result of the RAAS
increased RAAS: decreased NaCl excretion
increase Ang. II stimulates Na reabsorption along nephron
increased aldosterone stimulates Na reabsorption along asc. limb of LOH, DCT, and CD
increased Ang. III stimulates ADH secretion (water reabs. via AQ2)
What is the result of ANP/BNP, Urodilatin?
increased secretion of ANP/BNP/Urodilatin: increased NaCl excretion
increased GFR
decreased renin, aldosterone, ADH and NaCl reabsorption
What is the result of ADH?
increased secretion of ADH: decreased Water excretion
Water reabs. by DCT and CD
What is SIADH?
Syndrome of inappropriate ADH secretion
excessive secretion of ADH
Excessive water retention
hyposmolality fails to inhibit ADH release
can cause anorexia, N/V, confusion, lethargy, coma
Central Diabetes Insipidus Results from Water Deprivation Test
Plasma Osm:
Urine Osm:
Plasma ADH:
Urine Osm. post-desmopressin
Plasma Osm: 342 (increased from normal)
Urine Osm: 102 (decrease from normal)
Plasma ADH: low
Urine osm post desmopressin: 622 (decrease from normal)
Neprhogenic Diabetes Insipidus results from Water Deprivation Test
Plasma Osm:
Urine Osm:
Plasma ADH:
Urine Osm post-desmopressin:
Plasma Osm: 327 (increased from normal)
Urine Osm: 106 (decreased from normal)
PLasma ADH: high
URine Osm post-desmopressin: 118 (way decreased from normal)
Key difference between central and nephrogenic DI?
Central: Lack ADH, damage to pit. or hypothalamus, tx with desmopressin
Nephrogenic: High ADH, lithium damage or chronic dz. Can’t treat with desmopressin
ADH secretion is triggered by
High Plasma Osm
Low BP or Low BV
Ang II
SNS
Dehydration
ADH does what in response to low BP/BV or high osm?
Acts on V2 receptors in kidney to reabsorb water
V1 receptors on Blood vessels to vasoconstrict
all in effort to restore BV (and osm) and BP
*most triggered by high osm.*
