Reg of Body Fluid Osmolarity (Rao) Flashcards

To know: 1. The relationship between total body water and osmolarity 2. The role of osmoreceptors in sensing changes in plasma osmolarity 3. Role of vasopressin/ADH in fluid regulation. 4. How to quantify kidney’s ability to concentrate urine: Osmolar clearance & free water clearance 5. Development and maintenance of medullary hyperosmolarity 6. Impairment in urinary concentrating and diluting ability: Diabetes insipidus

1
Q

size order of output of water

A

urine&raquo_space; breathing ~ skin > feces

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2
Q

size order of input of water

A

Drinking&raquo_space;> food > metabolism

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3
Q

Osmoreceptors (location, effect)

A

hypothalamus, secrete AVP/ADH

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4
Q

Arginine-Vasopressin (AVP)/Antidiuretic Hormone (ADH)

Receptor location & name

A

V1/V2 receptors on apical surface of renal collecting duct epithelium
Also vasoconstricts arterioles, reducing GFR

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5
Q

AVP/ADH cascade

A

Secreted in hypothalamus
act on V1/V2 receptors on CD cells
activates adenylate cyclase -> cAMP synth
Protein kinase A
translocates Aquaporin 2 to luminal surface
takes 10 min

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6
Q

Hyperosmotic plasma response

A

Activation of Osmoreceptors in supraoptic nucleus of hypothalamus
AVP
Excretion of hyperosmotic urine
decrease of plasma osmolarity

Also increases thirst at hypothalamus

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7
Q

Incrase in ECF volume result

A

diuresis

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8
Q

Severe decrease in volume (vomiting/diarrhea) result

A

increase in AVP, retention

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9
Q

Cosm =

osmolar clearance

A

UF x Uosm / Posm

Normal = 1 +/- 0.5 ml/min

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10
Q

Nocturia is a sign of?

A

Decreased ability to concentrate urine

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11
Q

Free Water Clearance =

2 equations & definition

A

Free Water Clearance = UF - Cosm

= UF - UFxUosm/Posm

ability to concentrate urine

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12
Q

Is clearing water or conserving it more efficiently done by the kidney?

A

clearing

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13
Q

Transport in thin descending limb

A

+++++++ water

+ urea

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14
Q

Thin ascending limb transport

A

++ NaCl (permeability)

+ urea

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15
Q

Thick asending limb transport

A

NaCl (active) +++++++++

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16
Q

Distal tubule transport

A

NaCl (active)

water +ADH

17
Q

Collecting duct, cortical transport

A

NaCl (active) +

water +ADH

18
Q

Collecting duct, cortical transport

A

NaCl (active) +
water +ADH
Urea ++++

19
Q

Urea contribution to medullary ISF

A

40%

20
Q

Why is medullary blood flow low?

A

to preserve high osmolarity in the medulla ISF

21
Q

Why does the vasa recta serve as a countercurrent exchanger?

A

to preserve high osmolarity in the medulla ISF

22
Q

3 causes of deficiency in kidney’s ability to concentrate or dilute urine

A

1 defect in AVP secretion
2 inability of CD to respond to AVP
3 failure to form medullary osmolarity gradient

23
Q

Diabetes Insipidus

A

High rates of production of dilute urine

24
Q

Central Diabetes Insipidus

A

pituitary gland fails to produce AVP (rare, congenital)

25
Q

Nephrogenic Diabetes Insipidus

A

CDs don’t respond to AVP
V2 receptor or aquaporin-2 mutation

Drugs: lithium, tetracycline

26
Q

4 causes of medullary hyperosmolarity loss

A

1 diuretics (furosemide, ethacrylic acid)
2 Excessive deliver of fluid into LOH
3 Decreased urea production/filtration
4 Age and renal failure (loss of nephrons)

27
Q

3 causes of deficiency in kidney’s ability to concentrate or dilute urine

A

1 defect in AVP secretion
2 inability of CD to respond to AVP
3 failure to form medullary osmolarity gradient

28
Q

Diabetes Insipidus

A

High rates of production of dilute urine

29
Q

Central Diabetes Insipidus

A

pituitary gland fails to produce AVP (rare, congenital)

30
Q

Nephrogenic Diabetes Insipidus

A

CDs don’t respond to AVP
V2 receptor or aquaporin-2 mutation

Drugs: lithium, tetracycline

31
Q

4 causes of medullary hyperosmolarity loss

A

1 diuretics (furosemide, ethacrylic acid)
2 Excessive deliver of fluid into LOH
3 Decreased urea production/filtration
4 Age and renal failure (loss of nephrons)