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Renal System > Regulation of Body Fluid Osmolarity > Flashcards

Regulation of Body Fluid Osmolarity Flashcards

1
Q

What is a good indicator of total body water? How is it calculated?

A

Plasma osmolarity

= 2x plasma [Na] + [glucose]/18 + [BUN]/2.8

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2
Q

What senses changes in body osmolarity? Where is this located?
What stimulates it?

A

Osmoreceptors
- located on supraoptic and paraventricular nuclei of the hypothalamus

  • stimulated by an increase in body fluid osmolarity. (i.e. cell shrinkage)
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3
Q

How do the sensors of osmolarity regulate?

A
  1. Activation at the cell body of supraoptic nerves transmits signal to the nerve ending that is located in the posterior pituitary gland.
  2. The final cellular signal in the nerve ending is increase in intracellular calcium.
  3. Elevated intracellular calcium stimulates membrane fusion of ADH containing vesicles resulting in exocytosis of ADH into ECF.
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4
Q

Where does ADH work?

A

Collecting duct epithelial cells

-specifically on receptors of the basolateral membrane

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5
Q

How does ADH work?

A

increases water reabsorption

  • by increasing water permeability in the CD causing reduced urinary excretion of water
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6
Q

Besides secretion of ADH, how else do the osmoreceptors attempt to regulate increased osmolarity?

A

Stimulates thirst centers in the hypothalamus

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7
Q

Other name for ADH?

A
  • Vasopressin

- Arginine-vasopressin

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8
Q

Describe the intracellular activity once ADH binds to its receptor

A
  1. Activates the adenylate cyclase that converts ATP into cAMP
  2. cAMP activates protein kinase A which phosphorylates vesicles containing aquaporin-2 in their membranes
  3. AQP-2s fuse to plasma membrane on the luminal side

=> increases water permeability of the cells.

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9
Q

What is the name of the receptor that ADH binds to?

A

V2

  • coupled to adenylate cyclase
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10
Q

T or F: ADH activity is rapid, taking less than 10 minutes

A

T

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11
Q

Where is ADH degraded after its use?

A

In the proximal tubule and liver

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12
Q

ADH levels during dehydration?

A

HIGH

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13
Q

ADH levels when hydrated

A

Low

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14
Q

Normal range of AVP/ADH level?

A

.5 - 1.8 pM

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15
Q

ADH level at 270 mOsM?

A

about .5 pM

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16
Q

Describe the trend of plasma [ADH] as a function of osmolarity

A
  • increases linearly w/ increasing osmolarity untill it reaches a maximum of about 18pM
  • plasma [ADH] levels off at an osmolarity of 290 pM and greater
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17
Q

When is the thirst response stimulated?

A

Only at high levels of osmolarity

  • so small changes in osmolarity is mainly corrected by ADH
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18
Q

What is the effect of ECF volume on ADH?

A

inversely proportional

19
Q

What has a more dominant effect on ADH levels,

ECF volume or osmolarity?

A

Under condition of severe loss of ECFV its effect overrides osmolarity’s

In other words, it does not matter what the osmolarity is at low ECFV, the AVP level rises high.

20
Q

Describe how ECF volume’s effects on ADH are “disconnected” from those of osmolarity?

A
  • plasma ADH is increased proportionally with 1-7% increase in plasma osmolarity
  • Plasma ADH level increased only when the ECFV reduced by greater than 10%
21
Q

How does Diarrhea and Vommiting result in hyponatremia

A

Both cause large drop in isotonic fluid from the body
- dec ECFV => ADH secretion => increased water reabsorption

-inc water w/ low levels of Na => hyponatremia

22
Q

Clinical signs of hyponatremia?

A
  • Lethargy
  • hyporeflexia
  • mental confusion
23
Q

Tx of hyponatremia?

A

Isotonic saline

infuse slowly!

24
Q

Conditions associated with hyponatremia to consider in DDx?

A
  1. Heart Failure
    - where low BP stimulate secretion of hypovolemic hormones
  2. Liver Failure
    - reduced Plasma Volume due to fluid redistribution into ISF driven by low plasma oncotic pressure. Reduced plasma volume stimulates hypovolemic hormone secretion
25
Q

Factors affecting plasma [ADH]?

A
  1. Osmolarity

2. ECF volume

26
Q

What is nocturia?

A

Frequent urination during night

  • A common symptom of decreased ability of the kidneys to concentrate urine
27
Q

Terminology card:

  • Concentrate urine = less urination
  • Dilute urine = more urination
A

Terminology card:

  • Concentrate urine = less urination
  • Dilute urine = more urination
28
Q

How does one assess the ability of the kidneys to concentrate or dilute urine?

A

Quantify Osmolar clearance

  • the rate at which solute is removed from plasma and excreted in urine
  • (Urinary flow) x (urine osmolarity) / (plasma osmolarity)
29
Q

Normal osmolar clearance?

A

2 ml/min

30
Q

Factors that effect the kidney’s ability to concentrate urine?

A
  1. Age
  2. Renal Failure
  3. Infection
  4. Prostatic hypertrophy
31
Q

What is Free Water Clearance? Equation?

A

The difference between osmolar clearance and water clearance

= Urinary flow x [1 - Urine osm/plasma osm]

32
Q

CL(os) = CL(w)
Free water clearance = 0

What does this tell you?

A

Kidney is producing urine iso-osmotic with respect to the plasma

33
Q

CL(os)

A

Free water clearance > 0 (positive)

Kidney is producing dilute urine through the excretion of solute-free water

34
Q

CL(os) > CL(w)

What does this tell you?

A

Free water clearance

35
Q

Where is urea permeable?

A
  1. Inner medullary CD (High permeability)

2. Thin limb of LOH (slightly permeable)

36
Q

How is urea absorbed into the ISF of the inner medulla?

A

Passively

  • due to the large gradient created by its concentration as it flows through the tubule
37
Q

How does urea contribute to the hyperosmolarity of the inner medulla?

A
  • due its high permeability of Inner medullary CD AND due its low permeability in the Thin Limbs of the LOH
38
Q

What special features prevent the medullary capillaries from washing out the medullary hyperosmolarity?

A
  1. medullary blood flow is low

2. Vasa recta serves as a counter current exchange due to its loop structure

39
Q

Causes of a deficiency in Kidney’s ability to concentrate urine?

A
  1. Defect in production or regulation of AVP secretion.
  2. Inability of collecting ducts to respond to AVP
  3. Failure to form medullary osmolarity gradient
40
Q

What is Diabetes Insipidus? What are the two types?

A

Disease characterized by high rates of dilute urine production

  1. Central diabetes insipidus
  2. Nephrogenic diabetes insipidus
41
Q

Causes of Nephrogenic diabetes insipidus?

A
  1. Collecting ducts do not respond to AVP
  2. V2 receptor mutation
  3. Aquaporin-2 mutation
  4. Drugs: lithium, tetracycline
42
Q

Cause(s) of Central diabetes insipidus?

A
  • Pituitary gland fails to release AVP

rare congenital disease
Patients get dehydrated very quickly

43
Q

What is Polydipsia? complications?

A

Psychiatric condition characterized by obsession of water drinking

  • hyponatraemia (water intoxication); coma and death.
44
Q

What could cause a loss of medullary hyperosolarity?

A
  1. Diuretics - furosemide, ethacrylic acid inhibits Na+ transport
  2. Excessive delivery of fluid into LOH
  3. Decreased urea production - decreased filtered load of urea
  4. Age and renal failure - reduced number of functional nephrons

Renal System (19 decks)

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