53 Na+ and K+ homeostasis Flashcards

1
Q

Passage of fluid through the tubules in the absence of ADH (lack of water reabsorption) leads to ___ urine

A

Diluted (aka hypotonic) urine

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2
Q

T/F. In hypotonic urine the osmolarity is less than the plasma osmolarity (CH20<Posm

A

In hypotonic urine the osmolarity is less than the plasma osmolarity (CH20>0), Uosm<Posm

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3
Q

Water is reabsorbed in the presence of ADH leads to ___ urine

A

Concentrated urine

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4
Q

T/F. Uosm = Posm, therefore CH20= 0

A

True

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5
Q

Increases water permeability in DT and collecting tubules

A

Aldosterone

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6
Q

Inserts aquaporin channels into the membranes of the DT and collecting ducts, increasing water reabsorption
 Increases urea permeability by placing a urea channels in the membrane, important for gradient creation
 Stimulates Na+ transport in ascending loop, contributing to the gradient that water needs to move

A

ADH

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7
Q

T/F. High osmolarity of the renal medulla and countercurrent flow of tubular fluid are required for the formation of concentrated urine

A

True

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8
Q

This hormone is released from the posterior pituitary and increases water permeability in the collecting tubules and DT

A

ADH (aka vasopressin)

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9
Q

detect changes in osmolarity and have the ability to stimulate neurons of the hypothalamus that can induce secretion of ADH from the posterior pituitary (into blood).

A

Osmoreceptors

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10
Q
  • Increased plasma osmolarity
  • Decreased blood volume
  • Decreased blood pressure
  • Also, nausea, hypoxia, and certain drugs (morphine, nicotine)
A

Triggers hat stimulate secretion of ADH

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11
Q
  • Decreased plasma osmolarity
  • Increased blood volume
  • Increased blood pressure
  • Alcohol (leads to dehydration)
A

Factors that inhibit ADH secretion

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12
Q

binds to the g-protein coupled receptor V2. This increases cAMP production, which increases aquaporin-2 insertion in the membrane

A

ADH

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13
Q

Failure to produce ADH (deficiency is in the brain –CNS)

A

Central diabetes insipidus

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14
Q

Failure to respond to ADH (deficiency is in the kidneys –i.e. in receptors or in signaling). Salt reabsorption in the loop of henle is impaired. Can be caused by loop diuretics, lithium or analgesics, decreased urea concentration, and kidney disease

A

Nephrogenic diabetes insipidus

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15
Q

In this type of nephron, the glomerulus is in the renal cortex and the tubules are short and mainly in the cortical area

A

Cortical nephron

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16
Q

In this type of nephron, the glomerulus is in the junction b/t the cortex and the medulla, and the loops of henle are very big. These nephrons are responsible for establishing and maintaining the corticomedullary gradient

A

Juxtamedullary nephron

17
Q

This portion of what type of nephron functions as the countercurrent multiplier (creates a concentration gradient)

A

Loops of henle of the juxtamedullary nephrons

18
Q

This portion of what type of nephron functions as the countercurrent exchanger (diffusion occurs)

A

Vasa recta of the juxtamedullary nephrons

19
Q

(so named b/c the thin descending loop and the ascending loop do two different things) creates a hyperosmotic medullary interstitium

A

Countercurrent multiplier mechanism

20
Q

The blood vessels that surround the loop of henle. They ensure that the NaCl that is placed in the interstitial fluid doesn’t diffuse away. Instead it remains there and equilibrates. This is b/c the blood flow through these vessels is very slow, allowing for the time necessary for equilibration (if blood flow was rapid, all of the NaCl that is placed in the interstitium would be lost)

A

Vasa recta

21
Q

T/F. The countercurrent mechanism maintains the corticomedullary gradient (active process), while the vasa recta establishes the gradient (passive process

A

False. The countercurrent mechanism establishes the corticomedullary gradient (active process), while the vasa recta maintains the gradient (passive process)

22
Q

T/F. ADH promotes the insertion of urea channels in the distal collecting duct. Urea leaves and is deposited into the interstitial fluid

A

True

23
Q

T/F. Urea is freely filtered. About 20% is reabsorbed in the PT. After this point, urea is only reabsorbed in the distal collecting tubule

A

False. Urea is freely filtered. About 50% is reabsorbed in the PT. After this point, urea is only reabsorbed in the distal collecting tubule

24
Q

Produced from the ammonia that is produced from the breakdown of proteins

A

Urea

25
Q

T/F. The recirculation of urea helps to trap urea in the renal medulla and contributes to the hyperosmolarity of the renal cortex

A

False. The recirculation of urea helps to trap urea in the renal medulla and contributes to the hyperosmolarity of the renal medulla

26
Q

T/F. High protein degradation is a reason for a high BUN (blood urea nitrogen) value

A

True

27
Q

In the case of ECF volume contraction, which value increases more? Creatinine or BUN?

A

BUN increases more. BUN/creatinine > 20 is a marker for volume contraction

28
Q

These molecules collapse the gradient required for water absorption. They increase filtrate osmolarity by reabsorbing salt in a region in which water cannot follow. This increases water excretion due to increased osmosis

A

Diuretics. In general, diuretics allow for increased excretion of water

29
Q

T/F. The kidney regulates ECF osmolarity by regulating the amount of Na+ that is excreted. This is b/c Na+ is the major determinant of ECF osmolarity

A

False. The kidney controls ECF osmolarity by regulating the amount of water that is excreted: Water is the major determinant of ECF osmolarity (and ADH is the major determinant of water reabsorption)

30
Q

T/F. The physiological control in the PT affect the excretion of sodium and water together, whereas the actions of aldosterone and ADH in the distal nephron regulate sodium and water independently

A

True