Endocrine Lecture Flashcards

1
Q

Familial Hypocalciuric Hypercalcemia

(again)

PTH

Serum Ca

Urine Ca

Pi

Vit. D

A

PTH normal to high

Serum Ca high

Urine Ca low

Pi normal

Vit. D normal

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2
Q

What enzyme makes Vit. D into the active form and what is the name of the active form?

A

CYP1a (a-hydroxylase) makes it the active form

1, 25 OH2 cholecalciferol is the active form

occurs in the kidney (PCT)

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3
Q

What is the effect of PTH on the kidney (DCT)

Inhibition of the Na/Pi channel causes what?

A

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

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4
Q

Is free ionized Ca high or low during acidemia?

Is free ionized Ca high or low during alkalemia?

A

high because less Ca is bound to albumin

low because more Ca is bound to albumin, often accompanied by hypocalcemia

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5
Q

Hyperkalemia due to Decreased ENaC

Renin (high or low)

Aldosterone (high or low)

BV and BP (high or low)

A

Renin-high

aldosterone-high

BV/BP-low or normal

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6
Q

Hyperkalemia due to hypoaldosteronism (adrenal insuffieciency)

Renin (high or low)

Aldosterone (high or low)

BV and BP (high or low)

A

Renin-high

Aldosterone-low

Bv/BP-low

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7
Q

Hyperkalemia due to hyporenin-hypoaldosteronism (b-blockers, autonomic neuropathy)

Renin (high or low)

Aldosterone (high or low)

BV/BP (high or low)

A

Renin-low

aldosterone-low

BV/BP-low

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8
Q

Adrenal Hyperplasia: 17a deficiency

Sx

mineralcorticoids

cortisol

sex hormones

BP

K

labs

A

undescended testes, lack of 2’ sex development

mineralcorticoids: high
cortisol: low

sex hormones: low

BP: high

K: low

Labs: low androstenedione

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9
Q

Adrenal Hyperplasia: 21B deficiency

Sx:

Mineralcorticoids:

Cortisol:

Sex Hormones:

BP:

K:

Labs:

A

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

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10
Q

Adrenal Hyperplasia: 11B deficiency

Sx:

Mineralcorticoids:

Cortisol:

Sex Hormones:

BP:

K:

Labs:

A

Virilization

Mineralcorticoids: low aldosterone, high DOC

Cortisol: low

Sex Hormones: high

BP: high

K: low

Labs: low renin

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11
Q

Hypokalemia due to increased ENaC

Renin

Aldosterone

BV/BP

A

Renin: low

Aldosteorne: low

BV/BP: high

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12
Q

Hypokalemia due to decreased B-hydroxysteroid (caused by mineralcorticoid excess or licorice?)

Renin

Aldosterone

BV/BP

A

Renin: low

Aldosteorne: low

BV/BP: high

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13
Q

Hypokalemia due to adrenal tumor or hyperplasia

renin

Aldosterone

Bv/BP

A

renin: low
aldosterone: high

BV/BP: high

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14
Q

Hypokalemia due to congenital adrenal hyperplasia (caused by 17 hydroxylase deficiency)

Renin:

Aldosterone:

BV/BP:

A

Renin: low

Aldosterone: high

BV/BP: high

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15
Q

Hypokalemia due to renin secreting tumor

Renin

Aldosterone

Bv/BP

A

Renin: high

Aldosterone: high

BV/BP: high

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16
Q

What is the effect of insulin on K balance?

A

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

17
Q

Causes of K to shift out of cells and cause Hyperkalemia

A

insulin deficiency

B2 adrenergic antagonists

A-adrenergic agonists

acidosis

hyperosmolarity

cell lysis

exercise

18
Q

causes of K to shift into cells and cause hypokalemia

A

insulin

B2 adrenergic agonists

a-adrenergic antagonists

alkalosis

hyposmolarity

19
Q

What is the overall effect of increased Na intake?

A

Increased ECF and BV

Decreased SNS

Increased ANP

Decreased pic

Decreased RAAS

Increased Na Excretion

20
Q

What is the response to decreased Na intake?

A

Increased SNS

Decreased ANP

Increased Pic

Increased RAAS

Decreased excretion of Na

21
Q

What is the effect of Renal Sympathetic Nerves

A

Increase nerve activity, decrease NaCl excretion

Decrease GFR

Increase Renin secretion

Increase Na reabsorption along nephron

22
Q

What is the result of the RAAS

A

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)

23
Q

What is the result of ANP/BNP, Urodilatin?

A

increased secretion of ANP/BNP/Urodilatin: increased NaCl excretion

increased GFR

decreased renin, aldosterone, ADH and NaCl reabsorption

24
Q

What is the result of ADH?

A

increased secretion of ADH: decreased Water excretion

Water reabs. by DCT and CD

25
Q

What is SIADH?

A

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

26
Q

Central Diabetes Insipidus Results from Water Deprivation Test

Plasma Osm:

Urine Osm:

Plasma ADH:

Urine Osm. post-desmopressin

A

Plasma Osm: 342 (increased from normal)

Urine Osm: 102 (decrease from normal)

Plasma ADH: low

Urine osm post desmopressin: 622 (decrease from normal)

27
Q

Neprhogenic Diabetes Insipidus results from Water Deprivation Test

Plasma Osm:

Urine Osm:

Plasma ADH:

Urine Osm post-desmopressin:

A

Plasma Osm: 327 (increased from normal)

Urine Osm: 106 (decreased from normal)

PLasma ADH: high

URine Osm post-desmopressin: 118 (way decreased from normal)

28
Q

Key difference between central and nephrogenic DI?

A

Central: Lack ADH, damage to pit. or hypothalamus, tx with desmopressin

Nephrogenic: High ADH, lithium damage or chronic dz. Can’t treat with desmopressin

29
Q

ADH secretion is triggered by

A

High Plasma Osm

Low BP or Low BV

Ang II

SNS

Dehydration

30
Q

ADH does what in response to low BP/BV or high osm?

A

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.*