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HST.110 Renal Pathophysiology > 6_HST110 Osmoregulation and Disorders of Water Balance 2017 > Flashcards

6_HST110 Osmoregulation and Disorders of Water Balance 2017 Flashcards

1
Q

What percentage of the total body weight is water in healthy adults?

A

60%

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2
Q

Positive water balance is when there is more (X) than (Y). Negative is the opposite

A 
X = input
Y = output
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3
Q

What percentage of TBW is extracellular, plasma, and arterial (effective), in order of decreasing quantities

A

Extracellular: 1/3
Plasma: 1/12
Arterial: 1/60

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4
Q

Plasma and interstitial Na+ concentration is (X) than inside the cell, where (Y) dominates

A 
X = higher
Y = K+
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5
Q

(X) determines the distribution of body water between the different fluid compartments. Water moves from low (Y) to high (Y)

A 
X = Osmotic pressure
Y = osmolality
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6
Q

(X) determine movement of water between plasma and interstitial compartments across a capillary wall.

A

X = Starling forces

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7
Q

Changes in plasma osmolality or plasma (X) reflect changes in water balance

A

X = [Na+]

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8
Q

(X) of all fluid compartments is essentially equal, so we can use plasma (X) to estimate (X) of the total body water

This is the parameter that is sensed and tightly regulated to maintain water balance

What is its normal range?

A

X = Osmolality

Normal range is 275-290 mOsm/kg

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9
Q

What is the expression for plasma osmolality (mOsm/kg)

A

P_osm ~ 2* Na+ (major component)

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10
Q

What is the human form of ADH?

A

Arginine Vasopressin (AVP)

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11
Q

ADH is produced by neuroendocrine cells in supraoptic and paraventricular nuclei of the (X). It is packaged in granules, transported down axons, and stored in nerve terminals located in the (Y). Acts on collecting ducts to regulate (Z)

A 
X = hypothalamus
Y = posterior pituitary
Z = water reabsorption
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12
Q

The absence or presence of (X) is the major physiologic determinant of urinary water excretion or retention

A

X = ADH

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13
Q

What are the actions of ADH in the kidney (V2 receptors)

A

Increases permeability of the collecting ducts to water (AQP)

Increases permeability of the medullary collecting ducts to urea

Stimulates reabsorption of NaCl by the thick ascending limb, distal tubule, and collecting duct

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14
Q

What are the actions of ADH on the vasculature (V1 receptors)

A

Vasoconstriction

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15
Q

What are the 2 major stilmuli that regulates ADH release?

A

Plasma osmolality (Changes in plasma osmolality play the MOST important role in regulating ADH secretion)

Volume depletion

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16
Q

Osmolality is sensed by (X) in the anterior hypothalamus, which shrink or swell in response to changes in osmolality

A

X = osmoreceptors

Increase in Posm -> osmoreceptors shrink -> stimulates ADH secretion

opposite effect for decrease in Posm

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17
Q

Volume is sensed by baroreceptors
Carotid sinus, aortic arch, atria, afferent arteriole.

Over the physiologic range of effective circulating volume, ADH levels are determined almost entirely by plasma osmolality

However, volume depletion of (X) or greater significantly influences ADH levels (shifts ADH-osmolality curve to the left, resetting osmostat)

A

X = 10%

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18
Q

Name a few other stimuli for ADH release

A 
Nausea
Stress (pain, emotion, exercise)
Drinking
Acute hypoglycemia (>20% decrease)
Drugs (Nicotine, Narcotics, Cyclophosphamide, Tricyclic antidepressants, Phenothiazine antipsychotic agents
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19
Q

Increase in plasma osmolality or decrease in volume stimulates (X). Osmotic threshold for triggering (X) is higher than that for ADH secretion (295 vs 285 mOsm/kg)

A

X = thirst

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20
Q

The differences between descending and ascending limbs of the (X) are essential to the process of concentrating or diluting the urine to conserve or remove water

A

X = LOH

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21
Q

Countercurrent Exchange occurs primarily in the juxtamedullary nephrons with (X) loops of Henle

A

X = long

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22
Q

What is the goal of the countercurrent exchange mechanism?

A

To establish a hyperosmotic medullary interstitium that will promote the reabsorption of water in the collecting duct

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23
Q

What are the 3 components of the countercurrent exchange mechanism?

A

Active NaCl transport by TAL (loop of Henle)

Medullary vasa recta

Urea recycling

24
Q

Countercurrent exchange mechanism: Active NaCl transport occurs at thick ascending limb of the loop of Henle. Mediated by (X) and removes solute without water, diluting tubular fluid and Establishes interstitial (Y)

A 
X = Na+-K+-2Cl- symporter
Y = osmotic gradient
25
Q

At the tip of the LOH, what is the osmolality? What is this due to?

A

1200 mOsm/kg

Countercurrent multiplier

26
Q

Tubular fluid leaving the ascending limb and entering the CCD is hypoosmotic to plasma (usually (X) mOsm/kg). With No ADH, dilute urine. With ADH, concentrated urine

A

X = 100

27
Q

Final osmolality and volume of the urine is determined by water permeability in the (X), not by the events in the loop of Henle

A

X = collecting ducts

28
Q

Countercurrent exchange mechanism: Descending and ascending vasa recta run near each other in parallel but in opposite directions. They return NaCl and water reabsorbed in LOH and MCD to systemic circulation
What is this called?

A

Countercurrent

29
Q

Countercurrent exchange mechanism: Vasa Recta maintains the hyperosmotic interstitial gradient. Vasa recta exchanges water and solutes with surrounding interstitium and equilibrates osmotically with the surrounding interstitium. (X) permits solutes to accumulate in the medullary interstitium.

A

X = low blood flow

30
Q

Countercurrent exchange mechanism: Urea recycling. Urea is (X) filtered. (Y)% is reabsorbed in the PCT and 50% secreted into LOH. It is “trapped” in tubule from distal tubule to OMCD and then reabsorbed in (Z)

A 
X = freely
Y = 50
Z = IMCD (Intermedullary collecting duct)
31
Q

In the presence of ADH:
Urea concentration in the collecting duct rises

Permeability of IMCD to urea is (X)

This favors urea reabsorption into the interstitium (via UT1)

Contributes ~50% to the hyperosmostic interstitial gradient at the (Y) tip

A 
X = increased
Y = papillary
32
Q

Urine osmolality can range from (X) (maximally dilute) to (Y) mOsm/kg (maximally concentrated)

A 
X = 50
Y = 1200
33
Q

Urine volume can range from (X) to as low as (Y) L/day

A 
X = 18
Y = 0.5
34
Q

Disorders of water balance are detected on the basis of abnormally low or high (X) concentration in the blood. These are disorders of WATER, not sodium

A

X = Na+

35
Q

What is the formula for plasma osmolality?

A

(2Na+ + 2K+)/TBW

36
Q

What is the formula for plasma sodium concentration?

A

(Na+ + K+)/TBW

37
Q

What is the threshhold for hyponatremia?

A

Plasma [Na+] < 135 mEq/L (normal 136-145)

Usually associated with hypoosmolality

38
Q

Theoretically hyponatremia can result from either of two situations. What are they?

A

Loss of Na+ and K+

Increase in total body water (retention of ingested or infused water)

39
Q

Nearly all causes of hyponatremia are due to excessive (X). This generally only occurs if there is a defect in renal water excretion, specifically the inability to suppress ADH secretion, which can be appropriate or inappropriate.

A

X = water retention relative to solute

40
Q

Name the 3 categories of decreased plasma osmolality (hyposmolar hyponatremia) categorized based on the patient’s total body volume status

A

Hypovolemic (Diarrhea, vomiting, diuretics)

Euvolemic (Adrenal insufficiency, SIADH)

Hypervolemic (Congestive heart failure, cirrhosis, nephrotic syndrome)

41
Q

In the setting of volume depletion: Since most fluid losses are isoosmotic, (X) does not typically occur unless you replace those lost fluids with ingested water (hypotonic)

A

X = hyponatremia

42
Q

Treatment for volume depletion hyponatremia: Treatment involves correcting the volume depletion with (X) fluids (e.g. (X) saline)

Correction of the volume deficit will also suppress the stimulus for (Y) release and prevent further water retention

A 
X = isotonic
Y = ADH
43
Q

In patients with SIADH (Syndrome of (X) antidiuretic hormone), there is (X), non-osmotic secretion of ADH, which stimulates renal water retention

A

X = inappropriate

44
Q

What is the treatment for SIADH?

A

Restrict free water intake to minimize further water retention
If possible, remove the stimulus for ADH secretion
-Stop causative medications
-Treat nausea and/or pain
-Treat pulmonary or CNS diseases

45
Q

What is the threshhold for hypernatremia?

A

Plasma [Na+] > 146 mEq/L (normal 136-145)

Associated with hyperosmolality

46
Q

Theoretically hypernatremia can result from either of two situations. What are they?

A

Administration/ingestion of hypertonic fluids (too much sodium)
Increased water losses (more likely/common)

47
Q

Normally, an increase in plasma osmolality activates ADH secretion and thirst mechanisms, which promote (X) and increase water intake

Therefore, in order for hypernatremia to occur, (Y) function or thirst must be impaired

A 
X = water retention
Y = ADH
48
Q

Name common causes of Hypernatremia from water loss

A

Renal Loss: Diabetes insipidus (central, nephrogenic) and osmotic diuresis)

Non-renal loss: Insensible losses (sweating, burns, respiratory infections), GI losses, etc.

49
Q

Name common causes of Hypernatremia from increased sodium

A

Administration of hypertonic NaCl or NaHCO3

Ingestion of sodium

50
Q

Diabetes Insipidus: Complete or partial failure in either:
ADH secretion ((X) DI)
Renal response to ADH ((Y) DI)

Impaired renal water reabsorption results in excretion of (Z) urine (3-20 L/day)

A 
X = central
Y = nephrogenic
Z = dilute
A = polyuria and polydipsia
51
Q

Diabetes insipidus (hypernatremia) presents with (X). Does not cause hypernatremia as long as (Y) mechanism is intact

A 
X = polyuria and polydipsia
Y = thirst
52
Q

What is Central Diabetes Insipidus characterized by?

A

Inability to produce or secrete ADH

75% of cases are due to:
Idiopathic DI
Autoimmune
Familial
Neurosurgery
Head trauma
Neoplasm
Infiltrative diseases
Histiocytosis X
Sarcoidosis
53
Q

What is Nephrogenic Diabetes Insipidus characterized by?

A

Impaired renal response to ADH

ADH production is normal

Causes:
Congenital
V2 receptor mutations
AQP2 mutations

Acquired
Drugs (eg, lithium)
Hypercalcemia
Osmotic diuresis

54
Q

Treatment of Hypernatremia

A

Replace water losses
(Oral, Intravenous (as 5% dextrose in water))

Replace both the existing water deficit and any ongoing water losses

In patients with DI:

  • Exogenous ADH (if central DI)
  • Induce mild volume depletion (thiazide, low-salt diet)
55
Q

What is “Free Water?”

A

Solute-free (e.g. Na+ free) water, created when Na+ is separated from water

Occurs in the diluting segments of the nephron (TAL, DCT) that are impermeable to water but carry out active Na+ reabsorption

56
Q

What is the equation for free water clearance?

A

C_H2O = V’ - (U_osm/P_osm)*V’

HST.110 Renal Pathophysiology (17 decks)

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