Pathophysiology of Sodium Handling Flashcards Preview

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Flashcards in Pathophysiology of Sodium Handling Deck (22)
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1

Effective arterial blood volume definition

  • =volume of blood detected by volume sensors @ arteries
  • arterial blood volume required to "fill" the capacity of arterial circulation

2

Types of volume sensors

  • low-pressure baroreceptors
  • high-pressure baroreceptors
  • intrarenal sensors
  • hepatic and CNS sensor

3

Characteristics of low-pressure baroreceptors 

  • include: cardiac atria receptors, left ventricular receptors, pulmonary vascular bed receptors
  • located @ venous side of circulation
  • protect against ECF volume expansion/contraction
  • expansion stimulation ==> decreased renal sympathetic nerve activity ==> net loss of sodium and water

4

Characteristics of high-pressure baroreceptors

  • carotid sinus body @ bifurcation of carotid
  • aortic body @ aortic arch
  • located @ arterial side + protect against volume contraction and expansion
  • maintain MAP and protect vital organs from fluctuations
  • volume contraction ==> increased renal sympathetic nerve activity ==> anti-natriuresis + anti-diuresis

5

Characteristics of intrarenal volumes sensors

  • formed by renal JGA (<== releases renin)
  • renin release influenced by:
    • changes in renal perfusion pressure
    • NaCl delivery to JGA
    • renal sympathetic nerves

6

Kidney effectors of fluid volume homeostasis

  • glomerular filtration
  • physical forces @ proximal tubule
  • humoral effectors
    • AgII, aldosterone, catechlamines ==> salt retention
    • Pgs, bradykinin, ANP ==> natriuresis
  • renal sympathetic nerves
    • innervate afferent & efferent arterioles
    • stimulated in volume contract ==> sodium conservation
    • enha

7

Regulatory mechanisms of glomerular filtration


  • renal autoregulation 



  • tubuloglomerular feedback (TGF) = NaCl ==> macula densa ==> increased afferent arteriolar tone 





  • glomerulo-tubular balance = GFR changes ==> proportional change in rate of proximal tubular sodium reabsorption
     

8

Major sodium transport channel/mechanism @ proximal tubule, TALH, Distal tubule, collecting duct

  • proximal tubule = Na/K ATPase, Na/H Antiporter, Carbonic anhydrase
  • TALH = Na/K/2Cl cotransporter
  • Distal tubule = Na channels, Na/Cl co-transporter, Na/H antiport
  • collecting duct = @ principal cells: via Na channels in exchange for K

9

Renal response to extracellular volume contraction

  • Decreased GFR resulting in a smaller filtered load of sodium.
  • Activation of the renal sympathetic nerves ==> vasoconstriction of the afferent arteriole (decreases GFR) + increased tubular re-absorption of sodium.
  • Decreased hydrostatic pressure and increased oncotic pressure in the peritubular capillaries = enhance fluid reabsorption into the peritubular capillaries.
  • Stimulation of renin-angiotensin-aldosterone system.
  • Increased secretion of ADH ==> increased water reabsorption @ collecting duct
  • Inhibited secretion of atrial natriuretic peptide (ANP) from the atrial myocytes. 

10

Common signs/sx of volume contraction

  • thirst, postural dizziness, weakness
  • confusion, decreased urine output
  • weight changes
  • orthostatic hypotension**
  • tachycardia
  • decreased CVP, RA pressure, PCWP, CO + increased systemic vascular resistance

11

Serum indication of volemic contraction

  • Increased BUN (comes w/Na reabsorb)
  • Metabolic alkalosis = upper GI loss of fluid
  • Metabolic acidosis = lower GI loss of fluid
  • increased heatocrit + albumin

12

Tx of extracellular volume contraction

  • acute hemorrhage = give blood or plasma volume expanders e.g. albumin or dextran ==> preferentially expand intravascular volume
  • Isotonic normal saline (0.9% NaCl) ==> prefentially expands ECF (also expands IV volume)
  • D5W ==> expands intracell and extracell fluids

13

Main types of pathophysiology ==> extravascular volume expansion

  1. distrubed starling forces ==> reduced effective arterial volume
    1. CHF
    2. nephrotic syndrome
    3. cirrhosis
  2. primary hormone excess
    1. primary hyperaldosteronism
    2. cushing's syndrome
    3. SIADH
  3. primary renal sodium retention
    1. acute glomerulonephritis

14

Formation/maintenance of edema

  • decrease in capillary oncotic pressure and/or
  • increase in capillary hydrostatic pressure ==.
  • edema from fluid flowing out of capillaries and into ECF
  • baroreceptors maintain edema via perceived reduced effective arterial circulating volume
  • arterial underfilling ==> stimulates kidney to retain sodium + water

15

Pathogenesis of CHF

  • edema due to increased filling pressures + reduced CO ==> decreased flow to arterial sensors

16

Pathogenesis of Nephrotic Syndrome

  • hypoalbuminemia ==> fall in capillary oncotic pressure
  • ==> edema + fall in effective arterial blood volume
    • commonly leg and face swelling or diffuse

17

Pathogenesis of cirrhosis

  • intrahepatic hypertension + portal hypertension + splachnic vasodilation + hypoalbuminemia ==> decreased effective arterial pressure

18

Tx of extracell volume expansion

  • treat underlying condition
  • salt restriction
  • diuretics

19

Common diuretics @ proximal tubule

  • acetazolamide ==> blocks carbonic anhydrase ==> wastage of bicarbonate in urine
  • weak diuretic
  • tx: metabolic alkalosis w/volume overload

20

Common diuretics @ LOH

  • furosemide, bumetanide, torsemide
  • inhibit Na/K/2Cl transport @ apical membrane
  • potent diuretic
  • side effects: met alkalosis, hypokalemia, hypocalcemia, hypomagnesemia

21

Common diuretics @ distal tubule

  • thiazide diuretics
  • inhibit NaCl transporter @ apical membrane
  • side effects: met alk, hypokalemia, hypomagnesemia

22

Common diuretics @ collecting duct

  • tramterene, amiloride
  • spironoactone = competitive inhibitor of aldosterone
  • potassium-sparing diuretics (help prevent hypokalemia)