Lecture 12: Renal Endocrinology Flashcards

1
Q

ADH is critical for which function?

A

Water reabsorption

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2
Q

What is the pathway of ADH release?

A

paraventricular/supraoptic nuclei synthesizes ADH > travels though the hypothalamic hypophyseal tract > released as vesicles by the posterior pituitary > targets kidneys and arterioles

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3
Q

What is the pathway of ADH synthesis?

A

Prepropressophysin cleaved to propressophysin in hypothalamus
Travel to posterior lobe where it is cleaved to ADH > released

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4
Q

Very simply, what is osmolarity and how does ADH relate to it?
What is blood volume and how does ADH relate to it?

A
  • How concentrated the ECF is. ADH wants to “dilute” concentrated blood
  • How much fluid is in the ECF. Directly proportional to BP. ADH reabsorbs water to add to the blood volume if it is low
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5
Q

How does the hypothalamus detect body osmolarity?

How does the hypothalamus detect blood pressure?

A

Osmoreceptors (relays info to PVN and SON

Baroreceptors (relays info to PVN and SON via CN Ix/x

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6
Q

____ blood pressure, _____ arterial stretch, ______ osmolarity trigger ADH release

A

Low; low (due to blood volume), high

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7
Q

ADH secretion is most sensitive to _______ changes

A

Plasma osmolality (small changes affects regulation a lot compared to other variables)

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8
Q

What receptors does ADH bind in the arterioles?

In the kidneys?

A

V1

V2

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9
Q

What does ADH specifically do in the collecting duct that allows water reabsorption?

A

Increase in aq2 expression on the luminal side to let more water through

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10
Q

During dehydration/hyperosmolarity, what happens to …
BV
Osmolarity
Urine

A

Low
High, can lead to hypernatremia
Low volume and more concentrated urine (body attempts to keep as much water in)

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11
Q

During hypervolemia/hypoosmolarity, what happens to …
BV
Osmolarity
Urine

A

High
Low
High volume, diluted (body gets rid of excess water)

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12
Q

What is the characterizing symptom of diabetes insipidus?

A

Losing water/low water (polyuria, polydipsia)

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13
Q

Central DI vs Nephrogenic DI (causes, treatments)

A
  • Central: no ADH so you can’t keep the water. Damage to pituitary or hypothalamus. Tx with desmopressin which inhibits water excretion
  • Nephrogenic: kidney not responding to ADH so you can’t keep water. Kidney disease/damage.
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14
Q

How does the water deprivation test for DI work?

A

Patient stops drinking water but still makes high urine volume/diluted urine.

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15
Q

Syndrome of inappropriate ADH secretion (SIADH)
Cause
What disease is this associated with usually?

A

High ADH secretion leading to water retention and diluted blood
Small lung cell carcinoma

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16
Q

What is the main purpose of aldosterone?

A
Na+ reabsorption and K+ excretion (direct)
Water reabsorption (indirect, water follows the salt)
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17
Q

What does aldosterone specifically control at the nephron tubule?

A

Increases expression of ATPases/channels that change the passage of K+ and Na+

18
Q

What is the RAAS?

A

Renin-angiotensin-II-aldosterone system

Activated during conditions of low BP and BV > Na+ resorption

19
Q

What does primary adrenal gland insufficiency mean?

What does secondary or tertiary adrenal gland insufficiency mean?

A
  • Defect at Adrenal cortex leading to low aldosterone and cortisol
  • Defect at pituitary or hypothalamus leading to low cortisol (area responsible for aldosterone not affected)
20
Q

Myocytes produce ______ which _________

A

ANP and BNP; reduce workload on the heart by decreasing blood volume

21
Q

What is urodilatin?

A

Released by the kidney at the distal tubule and collecting duct. Similar functions to ANP and BNP by inhibiting resorption at the nephron > decrease blood volume

22
Q

How do natriuretic peptides regulate renal vasculature?

A

Goal is to excrete Na+ so increases GFR by vasodilation of afferent arterioles and vasoconstriction of efferent arterioles

23
Q

What other processes control salt and water regulation?

A

SNS > renin > promote resorption

24
Q

What effect does sodium intake have on the body?

A

More sodium intake = water is reabsorbed as it follows it = increases blood volume

And vice versa

25
Q

What is the major regulator of K+ concentration in cells and ECF?

A

Insulin - keeps K+ in the cell by stimulating the Na/K ATPase
Deficiency in insulin causes hyperkalemia, since K+ accumulates in the ECF

26
Q

What is the aldosterone paradox?

A

There is negative feedback between K+excretion and aldosterone release that stops its actions when body is losing too much K+

27
Q

What are some major causes of hypokalemia?

A
E-Nac increase 
Decreased B-hydroxysteroid dehydrogenase
Adrenal tumor/hyperplasia
Congenital renal hyperplasia
Renin secreting tumor
28
Q

_______ prevents mineralocorticoid receptor activation by cortisol

A

Enzyme 11B-HSD2

29
Q

17a hydroxylase deficiency leads to…
21B hydroxylase deficiency leads to …
11B hydroxylase deficiency leads to…

A

Low cortisol
Low mineralocorticoids and cortisol
Low mineralocorticoids and cortisol

30
Q

What are some major causes of hyperkalemia?

A

Decrease E-Nac
Hypoaldesteronism
Insulin deficiency

31
Q

What are the major symptoms of hypocalcemia and why is this so?

A

Too much muscle activity. Due to increased ICF Ca2+ that increases AP threshold = easier AP’s = more frequent muscle activity

32
Q

Chvostek and Trousseau signs are indicative of….

A

hypocalcemia

33
Q

What are the major symptoms of hypercalcemia and why is this so?

A

Less muscle activity. Due to increased Ca2+ in the ECF, keeping membrane potential more negative = harder to make AP’s = harder to generate muscle activity

34
Q

How can you change plasma Ca2+ concentration?

A
  1. Change protein bound calcium directly (proportional)

2. Increase anions for Ca2+ to pair with so that there’s less Ca2+ floating in the blood (Inverse)

35
Q

Acidemia leads to _______. Why?

Alkalemia leads to _______. Why?

A

Hypercalcemia. More H+ bound to albumin, leaving more Ca2+ in blood
Hypocalcemia. Less H+ bond to albumin, allowing Ca2+ to bind and escape from the blood

36
Q

Vitamin D leads to …
PTH leads to ….
Calcitonin leads to…

A
  • Ca2+ absorption at intestines (active at low Ca2+)
  • bone resorption/Vitamin D activation/Ca2+ increase (secreted at low Ca2+)
  • bone deposition/Ca2+ decrease
37
Q

The concentration of phosphate in the blood is _______ proportional to Ca2+ concentration

A

inversely

38
Q

How does PTH act on the kidneys?

A

PTH binds to receptor at thick ascending, PCT and DCT > AMP to cAMP > Protein kinase activation > Ca2+ channel upregulation and NPT2 (phosphate transporter) inhibition

39
Q

How is PTH regulated?

A

CasR senses Ca2+ levels and inhibits more PTH production

Vice versa if Ca2+ is low

40
Q

What enzyme produces the active vitamin D (1,25, dihydroxycholecalciferol and where does this happen?

A

1a hydroxylase in the PCT

41
Q

How is the 1a hydroxylase enzyme regulated on the transcriptional level?

A

CYP12 gene (transcribed when Vit. D is low)

42
Q

Familial hypocalciuric hypercalcemia (FHH)

A

Autosomal dominant. CasR is inactivated so cell cannot sense Ca2+ levels accurately. Ca2+ is not regulated and concentration in blood is high.