Regulation of Water Balance Flashcards

1
Q

What concentration difference can the thick ascending loop of henle maintain?

A

200 mOsmol/kg H2O btw tubular fluid and interstitium

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2
Q

About what osmolality is the tubular fluid leaving the ascending LoH?

A

100 mOsm/L

hypotonic and less concentrated than the fluid entering the LoH

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3
Q

What is the fluid entering the descending LoH like?

A

isotonic = 300 mOsm/L

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4
Q

What limb of the LoH is the interstitial fluid in equilibrium with?

A

the descending limb

their osmolalities are equal

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5
Q

What does the vasa recta do?

A

supplies blood to the medulla

highly permeable to solute and water = remove stuff that is removed from tubular fluid and put into the IF

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6
Q

How is the vasa recta’s ability to maintain medullary interstitial gradient regulated?

A

flow dependent
increased blood flow –> decreases salt and solute transport by nephron segments in the medulla –> reduced ability to concentrate urine

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7
Q

How does urea recycling work?

A

50% urea reabsorbed in PCT –> very little reabsorbed until the medullary collecting duct –> UT-A1 and UT-A3 transporters reabsorb urea into medullary interstitium –> some of the urea eventually diffuses back into thin LoH and goes again back to collecting duct

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8
Q

Without ADH, what is the collecting duct like?

A

impermeable to water (will maintain low osmolality urine)

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9
Q

What is the thin descending limb membrane like?

A

combo of aquaporins and no tight junctions –> water can flow freely w/out solutes

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10
Q

What are the 2 nuclei in the pituitary that synthesize ADH?

A

supraoptic nucleus

paraventricular nucleus

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11
Q

What part of the pituitary gland produces ADH?

A

posterior pit

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12
Q

How is the pituitary stimulated to release ADH?

A

increased osmolarity or other factors –> supraoptic and paraventricular nuclei stimulated –> Ca entry –> stored ADH is released

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13
Q

If osmoreceptors sense changed is osmolality, what does it signal the body to do?

A

first activated ADH pathway

thirst pathway activated later

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14
Q

What cell type does ADH work on?

How does it affect these cells?

A

principal cells in late DCT and collecting duct

directs the insertion of aquaporin 2 channels –> H2O permeability is increased

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15
Q

In general, what do principal cells do?

A

reabsorb Na+, Cl-, and secrete K+

acted on by ADH

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16
Q

In general, what do intercalated cells do?

A

reabsorb K+ and secrete H+

Target of aldosterone

17
Q

How does aldosterone work?

A

In response to high plasma K levels or Angiotensin II:
increases ENaC channels, which pull in Na from the tubular lumen
Na is then transported into the IF via the Na/K ATPase pump = increased Na reabsorption and K secretion

18
Q

What side of a tubule cell is an aquaporin-2 channel inserted in response to ADH?

A

apical membrane

19
Q

What is the major difference btw the cortical and medullary collecting ducts?

A

cortical are always permeable to water

medullary H2O permeability is determined by ADH

20
Q

What is type I/central Diabetes Insipidus?

A

failure to produce or release ADH from the posterior pituitary (after head injuries or congenital)
see large volumes of dilute urine
if water intake is restricted –> severe dehydration
treatment = desmopressin

21
Q

What is type 2/ nephrogenic diabetes insipidus?

A

inability of the kidneys to respond to ADH
normal or elevated levels of ADH
result of failure of countercurrent or failure of distal and collecting tubules to respond to ADH
still see large volumes of dilute urine
loop diuretics, lithium, and tetracyclines can cause this

22
Q

What can treat type 2/ nephrogenic DI?

A

low sodium diet and treatment with thiazide diuretics can help hypernatremia

23
Q

What occurs in SIADH?

A

too much ADH –> hypotonic volume expansion –> cells swell
major cause of low sodium levels
low urine output
still have excessive thirst

24
Q

What is the most common electrolyte disterbance?

A

hyponatremia

present in 15-30% of hospitalized patients

25
Q

What are the most common causes of hyponatremia?

A

drugs, pain, nausea, decreased effective arterial volume, strenuous exercise
(NOT usually bc of consuming little solute or polydipsia)

26
Q

What defines hypernatremia?

A

deficit of free water relative to solute
inadequate free water intake
most ppl also have concurrent volume depletion
(see it in DI and osmotic diuresis)

27
Q

What defines polyuria?

What 4 mechanisms can cause it?

A

> 2.5 L/day
caused by:
1. increased intake of fluids
2. increased GFR as in hyperthyroidism, fever, hypermetabolic states
3. increased output of solutes (DM, hyperthyroidism, hyperpara, diuretics)
4. inability of the kidney to reabsorb water in DCT

28
Q

What is oliguria?

A

output below the minimum volume
300-500 ml/day
dehydration, blood loss, etc

29
Q

What is anuria?

A

virtual absence of urine production

< 50 mL/day

30
Q

What is water diuresis?

A

increased water excretion without corresponding increase in salt excretion

31
Q

What is solute diuresis?

A

increased water excretion concurrent w/ increased salt excretion

32
Q

What is obligatory urine volume?

A

minimal amount of solutes that a bedridden person must excrete in a day
about 700 mOsm
1000 mOsm/day for an active person

33
Q

What is maximal urine concentrating ability?

A

1200 mOsm/L

34
Q

What does it mean if free-water clearance is positive?

A

excess water is being excreted by the kidneys

35
Q

What does it mean if free-water clearance is negative?

A

excess solutes are being removed from the blood by the kidneys and water is being conserved
when urine osmolarity > plasma osmolarity

36
Q

What is the equation for free-water clearance?

A

CH2O = V-Cosm = V - (Uosm * V)/(Posm)

37
Q

What is responsible for the countercurrent exchange that sets up the medullary osmotic gradient?

A

the vasa recta