Salt and water handling Flashcards

1
Q

Water content in various tissues

A
Kidney
heart
lung
skeletal muscle
brain
skin
liver
skeleton
adipose tissue
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2
Q

Division of TBW

A

60% body weight
1/3 ECF (20%), 2/3 ICF (40%)
ECF: 1/4 plasma (5%), 3/4 ISF (15%)

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3
Q

ISF

A

fluid in lymphatics
crystallized water in bone
CT
transcellular fluid (intraocular, CSF, synovial, peritoneal, pleural, pericardial fluids)

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4
Q

Osmolarity

A

osmol/L water

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5
Q

Osmolality

A

osmol/kg water

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6
Q

ECF solutes

A

Na+

Cl-, HCO3-

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7
Q

ICF solutes

A

K+

proteins, organic phosphates, acids

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8
Q

Plasma water content

A

93%

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9
Q

Normal osmolality

A

280-300 mosmol/kg water

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10
Q

Effective osmoles

A

Na+
cells
plasma proteins

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11
Q

Ineffective osmoles

A

urea

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12
Q

Tonicity

A

effective osmoles /solution

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13
Q

Starling’s forces

A
Jv = Kf ((Pc - Pi) - (pic-pii))
Pc = hydrostatic pressure in capillaries
Pi = hydrostatic pressure in interstitium
pic = oncotic (colloid) pressure in capillaries
pii = oncotic pressure in interstitium

Colloid pressure is key in maintaining intravascular volume

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14
Q

Physiological vasculature fluid movement

A

Hydrostatic - favours movement out of vasculature
Oncotic - favours retention
Net result = slight movement out of vasculature - absorbed by lymphatics and returned to venous circultaion

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15
Q

Causes of edema

A
Increased vascular permeability
Increased hydrostatic pressure in vasculature
Decreased oncotic pressur
Lymphatic obstruction
Increased oncotic pressure in ISF
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16
Q

Glomerulus filtering

A

freely filters Na+ and Cl-

17
Q

PCT

A

65% Na+ and H2O reabsorbed

18
Q

Sodium reabsorption in early PCT

A

Na/K ATPase on basolateral membrane: 3Na out of cell, 2K into cell
Establish a electrical gradient –> allows Na to move down the gradient into the cell

2 mechanisms of Na movement into cells:

1) Na+/H+ exchanger (NHE3):
- H+ generation by dissociation of H2CO3 (generates HCO3-)
- H+ moves into lumen, combines with HCO3- to form H2CO3, which dissociates to CO2 and H2O (carbonic anhydrase)
- CO2 diffuses into cell, gets converted to H2CO3 by carbonic anhydrase
- HCO3- moves into interstitium and is reabsorbed by blood

2) Na+/X- cotransporter
- Na+ moves down concentration gradient along with another solute
- X = amino acids, phosphate, citrate, glucose

Once in the cell, Na/HCO3- move into interstitium via Na/K ATPase and cotransporters
Cl- is not reabsorbed; Cl- concentration rises through this section

19
Q

Sodium reabsorption in late PCT

A

2 mechanisms:

1) coupled Na/H and Cl/HCO3- antiporters
2) Paracellular passive diffusion

Driven by Cl- concentration gradient (high in lumen) established in early PCT

20
Q

Water reabsorption in PCT

A

Movement of Na, Cl, HCO3- into interstitium establishes osmotic gradient for water to move out of lumen –> interstitium and into blood
PCT is highly permeable to water, moves from lumen –> blood via paracellular/transcellular pathways

21
Q

Hormones affecting PCT

A

Angiontensin II: increase water and NaCl reabsorption
Adrenaline/noradrenaline: increase water and NaCl reabsorption
Dopamine: decrease water and NaCl reabsorption

22
Q

Thin descending limb

A

“concentrating segment”
water permeable, solute impermeable
water moves out of filtrate, increasing concentration of filtrate
15% of water reabsorbed here

23
Q

Thick ascending limb

A

“Diluting segment”
water impermeable
25% of Na+, Cl-, K+ reabsorbed here

24
Q

Thick ascending limb transporters

A

NKCC:

  • 2 Cl-, 1 Na+, 1K+ into cell from lumen
  • Na+ moved into interstitium by Na+/K+ ATPase
  • NKCC associated with ROMK: allows K+ to move from cell –> lumen, creates K+ gradient that helps drive NKCC channel
  • also established positive charge in lumen, which drives other cations of urine into blood

Na+/H+ exchanger
Paracellular movement of ions

25
Q

Hormonal effects on Loop of Henle

A

Aldosterone: increase NaCl absorption
Adrenaline: increase NaCl absorption

26
Q

DCT

A

Reabsorbs ~7% of NaCl
secretes variable amounts of K+ and H+
water impermeable, remains a diluting segment

27
Q

Transporters in DCT

A

NaCl cotransporter (NCC)

  • moves 1 Na+ and Cl- into cell from lumen
  • not associated with ROMK, so no electropositivity established in urine to drive other cation diffusion
28
Q

Hormonal regulation of DCT

A

Aldosterone
Adrenaline
ADH: increase water reabsorption

29
Q

Collecting duct

A

makes final decisions about salt and water balance

determination of pH in urine

30
Q

Cell types in CD

A

1) principal cells
- have ENaC (epithelial sodium channels) - moves Na+ into cells from urine
- have ROMK: moves K+ into urine from cell, in response to negative lumen due to sodium movement

2) Intercalated cell
- response for acid-base balance
- determine acid-base balance by secreting/reabsorbing H+ and bicarbonate

31
Q

Hormonal effects in CD

A

Aldosterone: increase chance of ENaC being open - increase water and NaCl reabsorption
Adrenaline
ADH: increase # of ENaC receptors available, increase water reabsorption
ANP: decrease # ENaC receptors available, decrease water/NaCl reabsorption
Urodilatin: decrease water/NaCl reabsorption

32
Q

Urodilatin

A

secreted by DT/CD (not present in systemic circulation)
due to increase in ECFV
acts on CD
decrease NaCl/water reabsorption

33
Q

Dopamine

A

released by dopaminergic nerves in the kidney, also synthesized by cells of PT (oppose action of adrenaline/NA)
Due to increased ECFV
acts on PT to decrease water/NaCl reabsorption

34
Q

Other hormonal regulators

A

PG: PGI2 mainly

  • afferent arteriolar vasodilation + natriuresis
  • low ECFV: PGI2 rises to maintain renal perfusion, despite SNS activation & high AII
  • giving NSAIDs to these patients can reduce PGI2 levels, cause renal failure

Uroguanylin: released in response to salt intake
- inhibits salt reabsorption in kidneys

NO: some diuretic properties

35
Q

ADH

A

2 receptors:
V1 - v/c in arterioles, also found in brain/mesangial cells
V2 - CD cells and cause water resorption

Stimulated by:

  • increasing osmolality in blood
  • volume depletion
  • vomiting/diarrhea
  • pain
  • exercise
  • medications (narcotics, chlorpropamide, carbamapezine)
36
Q

Diluting urine

A

Solute reabsorption without water

  • ascending limb
  • DT and CD in the absence of ADH

1) PT - isoosmotic resorption
2) descending limb - only permeable to water (concentrates urine)
3) thin ascending limb - impermeable to water, NaCl leaves urine, urea enters urine
- more NaCl leaves than urea enters - dilution
4) Thick ascending limb - impermeable to water and urea; active resorption of NaCl, urine leaving segment is hypo-osmotic with regards to plasma
5) DT and cortical CD: active resorption of NaCl, no water resorption in the absence of ADH
6) Medullary CD: active resorption of NaCl, small amount of water resorption in the absence of ADH

  • in the absence of ADH, can get very dilute urine (50 in kids, 100-200 in elderly)
37
Q

Concentrating urine

A

Water is never pumped, only diffuses
Kidney makes a hyperosmotic “sink” in interstitium to pull water out of urine, accomplished by thick ascending limb of LOH

1) PT to thick ascending limb: TAL extremely important in creating hyperosmotic interstitium to pull water out in medullary CD
- action of NKCC and Na/K ATPase
- countercurrent multiplication
2) DT and cortical CD: hypoosmotic filtrate
- ADH presence: presence of aquaporins - water filters out of urine
- can be concentrate to ~290 mosm/ kg water
- composition: less NaCl, more creatinine, urea, ammonia, K+
3) Medullary CD: osmolality of interstitium increases as moves down into medulla
- ADH: makes this permeable to water
- urine can be concentrated to ~1200 mosm/kg

38
Q

Posm equation

A

2[Na+] + glucose + urea