Chapter 29: Renal Regulation of K+, Ca++, Na+/Fluid Volume (Discussion 3) Flashcards

1
Q

Location of K+ in the body

A

Primarily in cells (4.2 mEq/L ECF vs. 140 mEq/L ICF) High ECF [K+] can cause cardiac arrhythmias/death

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2
Q

Hypokalemia

A

Low plasma [K+]

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3
Q

Hyperkalemia

A

High plasma [K+]

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4
Q

Factors that shift K+ into cell

A

Aldosterone (excess = Conn’s syndrome) Insulin B-adrenergic stimulation Alkalosis

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5
Q

Factors that shift K+ out of cell

A

Deficient Aldosterone (Addison’s disease) Diabetes mellitus B-adrenergic blockade Acidosis (H+ inhibits Na-K pump) Cell lysis Strenuous exercise ↑ECF osmolarity

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6
Q

Excretion/Renal Regulation of K+

A

65% reabsorbed in proximal tubule

25-30% reabsorbed in loop of Henle (relatively constant; Na/2Cl/K pump action in thick ascending limb)

Reabsorb (minimally) by intercalated cells (H/K ATPase)

Secrete by principal cells (diffusion)

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7
Q

Factors that control excretion/renal regulation of K+

A
  1. ECF [K+]: Increase in ECF concentration will:
    1. Stimulate Na-K pump
    2. Reduce back-leakage
    3. Stimulate aldosterone
  2. Aldosterone: Increase in aldosterone will:
    1. Stimulate Na-K pump
    2. Increase in the # of luminal K+ channels
  3. Tubular flow rate: increase in flow rate
    1. “Washdown” of K+ –> Increase in diffusion
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8
Q

Location of Ca++ in the body

A
  • Higher concentrations in ECF but much lower quantities than Na+
  • Most ECF Calcium bound to plasma proteins/non-ionized –> 2.4 mEq/L active Ca++
    • Binding affected by pH (acidosis –> decreased binding)
    • Only free Ca++ filtered into nephron (~50%)
      • 99% reabsorbed (~65% at proximal tubule)
  • ~99% stored in bone (acts as Ca reservoir)
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9
Q

Hypocalcemia

A

Decrease [Ca++] ECF

Cause nerve/muscle hyperexcitability –> tetany

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10
Q

Hypercalcemia

A

Increase [Ca++] ECF

Depress neuromuscular excitability –> arrhythmias

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11
Q

Parathyroid Hormone (PTH)

A

Stimulated by low ECF [Ca++] or high [PO43-]

Regulate [Ca++]

  • Increase bone resorption (release Ca++)
  • Increase reabsorption of Ca++ in kidneys (acts at thick ascending loop/distal tubule)
  • Activate vitamin D –> increase intestinal reabsorption of Ca++

Regulate PO43-

  • Increase bone resorption (release PO43-)
  • Decrease PO43- reabsorption in renal tubules
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12
Q

Na+/Volume Regulation

A

Major regulator is pressure natriuresis & diuresis (more powerful in chronic hypertension)

  1. slight increase in GFR
  2. High peritubular capillary hydrostatic pressure –> decrease reabsorption of Na/H2O
  3. High arterial pressure –> decrease angiotensin II/aldosterone formation –> decrease reabsorption of Na/H2O
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13
Q

Sympathetic Nervous Control of Excretion

A

Baroreceptors sense low BP –> sympathetic stimulation

–> constrict renal arterioles –> decrease GFR –> increase reabsorption of water/salts –> increase renin/angiotensin II/aldosterone –> increase tubular reabsorption

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14
Q

Angiotensin II

A

Increase NaCl/H2O reabsorption

Amplify pressure natri/diuresis (thus important for controlling NaCl/H2O reabsorption)

ACE inhibitors/angiotensin II receptor antagonists block its effects and shift excretion curve to lower pressures

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15
Q

Aldosterone

A

Increase Na+/H2O reabsorption and K+ secretion

During over-secretion of aldosterone, rise in BP will be minimized by pressure natriuresis

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16
Q

ADH

A

Increase water reabsorption

Excessive ADH only slightly increases ECF volume and BP because of pressure diuresis –> significant decrease in [Na+] ECF

17
Q

ANP

A

Increase GFR and decrease Na+/H2O reabsorption

18
Q

Response to adjust volume/Na+ output

A

Output lags behind input –> rise in ECF –> response

  • Inhibition of pressure receptors –> inhibit sympathetic stimulation
  • Pressure natriuresis
  • Suppression of Ang II –> decrease water/Na+ reabsorption and aldosterone release
  • Stimulate of ANP
19
Q

Conditions that increase ECF volume - Cardiovascular Failure

A

Increase Na/H2O retention

  • Valvular disorders (less effective pumping/pressure)
  • Congenital heart defects
  • Increased circulatory capacity
    • Vascular dilation
    • Pregnancy
    • Varicose veins
20
Q

Conditions that increase ECF volume - Nephrotic Syndrome

A

Loss of proteins into urine

  • Caused by tubule protein failure (could have lost negative charge, membranes became porous, etc)
  • Normal blood volume but large ↑ECF volume
  • Glomerulus fills large # of proteins into tubules –> ↓ in capillary osmotic pressure
    • capillaries filter large amounts of fluid into interstitial spaces –> extracellular edema
  • –> ↓blood volume triggers water/Na retention
21
Q

Conditions that increase ECF volume - Liver Cirrhosis

A

Fibrous tissue in liver w/o protein production capabilities

  • –> decrease in plasma proteins
  • Fibrotic tissue obstructs portal vein –> increase in Pc (abdominal) –> edema (ascites)