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CPR 2 > Acid Base Balance 2 > Flashcards

Acid Base Balance 2 Flashcards

1
Q

What is the role of kidney in acid-base balance?

A
  • Kidneys regulate plasma [HCO3-]
  • Urine pH is 5.8-6 (acidic relative to plasma pH)
  • Filtered HCO3^- completely reabsorbed
    • HCO3^- freely filtered at glomerulus
  • Kidneys secrete H+
    • Protons accepted by urinary buffers (phosphate and ammonia)
  • HCO3- can also be newly formed in renal tubules
    • Replenish HCO3^- lost by buffering nonvolatile acids (sulfate or lactic acid)

-Excrete sulfate and phosphate (non-volatile acids)

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2
Q

Give an overview of a nephron and Reabsorption of bicarbonate

A

For every bicarbonate reabsorbed, one H+ must be secreted unto t7bukar lumen

Bucarbonate Reabsorption in various parts of renal tubule

All filtered HCO3^- is reabsorbed (No HCO3^- in urine)

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3
Q

Explain Reabsorption of filtered bicarbonate

A
  1. Formation of carbonic acid (H2CO3) by carbonic anhydrase in tubular cell
  2. Dissociation of carbonic acid (weak acid) to bicarbonate and proton
  3. Secretion of proton into tubular lumen (via Na+ -H+ exchanger)
  4. To maintain electrical neutrality, bicarbonate enters blood (for every proton secreted into lumen, one bicarbonate enters blood)
  5. Secreted portion associated with filtered bicarbonate in tubular lumen to form carbonic acid
  6. Carbonic anhydrase in brush border of tubular cells converts Carbonic acid to CO2 (which may diffuse into tubular cell to be reused)
  7. 85% of filtered bicarbonate is reabsorbed in proximal tubule; rest in distal tubule

When secreted proton buffered by bicarbonate buffer in tubular lumen= Reabsorptionof filtered bicarbonate

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4
Q

Summarize the formation of ‘NEW’ bicarbonate

A

When H+ ions (metabolism) added, HCO3- used to buffer H+
HCO3- levels fall

50-100 mEq non-volatile acid/day

If kidney does NOT form new bicarbonate, serum HCO3^- levels decrease

Two mechanisms form NEW bicarbonate (non-bicarbonate buffers)-very active in collecting duct

  • phosphate buffer system
  • ammonia buffer system
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5
Q

What is the secretion of protons in the fold of phosphate buffer/ formation of ‘NEW’ bicarbonate?

A
  1. Formation of carbonic acid (H2CO3) by carbonic anhydrase in tubular cell
  2. Dissociation of carbonic acid (weak acid) to bicarbonate and proton
  3. Secretion of H+ into tubular lumen
  4. To maintain electrical neutrality, a bicarbonate enters blood (For every proton secreted into lumen, a bicarbonate enters the blood)
  5. Proton associates with filtered phosphate to form acid phosphate (alpha-intercalated cells in distal tubule)
  6. Acid phosphate excreted in urine and contributes to titratable acidity in urine.

When secret3d proton buffered by a non-bicarbonate buffer (phosphate/ammonia) in t7bukar lumen= formation of NEW bicarbonate

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6
Q

Explain the role of ammonia in formation of new bicarbonate

A
  1. Formation of carbonic acid (H2CO3) by carbonic anhydrase in tubular cell
  2. Dissociation of carbonic acid (weak acid) to bicarbonate and proton
  3. Secretion of H+ into tubular lumen
  4. To maintain electrical neutrality, a bicarbonate enters blood (For every proton secreted into lumen, a bicarbonate enters blood)
  5. Hydrolysis of glutamine by glutaminase forms ammonia in renal tubule
    - NH3 is lipid soluble and diffuses into tubular lumen
  6. NH3 binds to secreted proton in tubular lumen to form ammonium ion(NH4-)(pk=9.2)—>. Trapped in lumen (distal tubule and collecting duct)
  7. NH4^+ excreted as ammonium chloride in urine
  8. Tubular capacity to excrete ammonium is unlimited and highly stimulated in prolonged acidosis.

When secreted proton buffered by a non-bicarbonate (phosphate/ammonia) in tubular lumen = formation of NEW bicarbonate

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7
Q

Describe H+ secretion in collecting duct

A

H+ ATPase

K+ H+ ATPase

Secreted protons buffered by:

  • HPO4^- to form acid phosphate (NaH2PO4^-)
  • NH3 to form NH4+Cl (urinary ammonium chloride/sulfate)
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8
Q

Describe bicarbonate secretion in urine

A

Beta-intercalated cells (collecting duct)

  • Secrete HCO3- in urine
  • Reabsorb H+
  • Makes urine alkaline
  • Active in chronic alkalosis
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9
Q

How can we quantify urinary acid loss?

A

H+ in urine = acid phosphate (titratable acidity) + ammonium- urinary bicarbonate

Chronic acidosis —> increased H+ secretion in tubules and increased urinary acid phosphate and ammonium excretion

Chronic alkalosis—> decreased H+ secretion in tubules and decreased urinary acid phosphate and ammonium. Tubules secrete bucarbonate which is lost in urine

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10
Q

What are the factors that increase H+ secretion in renal tubules ?

A
  • Increased PCO2 (respiratory acidosis)
  • Decreased pH (acidosis)
  • hypokalemia
  • Increased aldosterone
  • Decreased ECF volume
  • Diuretics (increase sodium load in renal tubules)
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11
Q

Describe H+ and K+. Interrelations

A

K+ (major intracellular cation)

K+ and H+ are closely related

Diabetes mellitus: insulin deficiency and hyperglycemia (hyper osmolarity)—> K+ shift from ICF to ECF (hyperkalemia)

Changes in pH affect serum (ECF) K+ levels

  • metabolic acidosis- hyperkalemia
  • metabolic alkalosis- hypokalemia

Also, changes in serum K+ affects pH

  • Hyperkalemia- acidosis
  • Hypokalemua- alkalosis
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12
Q

What is the relevance of potassium in metabolic acid-base disturbance ?

A
  • In metabolic acidosis, excess H+ from ECF enters into ICF
  • Intracellular K+ moves to ECF (hyperkalemia)
  • Metabolic acidosis usually accompanied by hyperkalemia

Metabolic alkalosis associated with shift of K+ into ICF (hypokalemia)

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13
Q

What is the effect of hypokalemia effect alkalosis?

A

-Low serum K+ levels facilitates entry of H+ into cells (ECF alkalosis)

  • Effect of Hypokalemia on renal tubules
    • stimulates H+ secretion into lumen
    • Stimulates ammonia formation
    • stimulates formation of new HCO3 and increases serum HCO3 (alkalosis)

Hypokalemia maintains and worsens alkalosis

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14
Q

Whaat is primary hyperaldosteronism(Conn’s syndrome)?

A
  • Aldosterone stimulates Reabsorption of Na+ (increases serum Na+ levels and blood volume- hypertension )
  • stimulates K+ excretion in urine(hypokalemia)
  • stimulates renal tubular H+ ATP?ase(alkalosis)
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15
Q

How does decreased ECF (volume contraction) effect RAAS?

A

Stimulates RAAS secretion

Angiotensin II increases Na-H anti porter to increase Na Reabsorption (H+ secreted —> increased Reabsorption of HCO3)

  • Aldosterone increases sodium Reabsorption + CL- and H2Oreabsorption
  • Stimulates H+ secretion (ENaC reabsorbs Na and lumen becomes negative- So, H+ is secreted by A-intercalated cell)
  • Volume contraction and metabolic alkalosis, there is increased Na+ Reabsorption (to increase blood volume) and H+ secretion in urine (paradoxical aciduria)
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16
Q

Contrast loop and thiazide diuretics

A

Loop diuretics-decrease Na+ Reabsorption in loop of henle
-result = decreased Na+ Reabsorption- -> increased Na+ delivery to the distal tubule

Thiazides- decrease Na+ Reabsorption in distal convuluted tubule
-result= decreased NaCl Reabsorption

17
Q

What are the similarities of loop diuretics and thiazide diuretics ?

A

Both cause ECF volume contraction —> secretion of aldosterone and angiotensin II

Decreased Na+ Reabsorption in tubules leads to increased Na+ delivery to distal tubule leads to K+ secretion and increased proton secretion leading to metabolic alkalosis and hypokalemia

18
Q

What are the factors affecting tubular H+ secretion?

A
  • Decreased intracellular pH (acidosis)
  • Increased PCO2 (respiratory acidosis)
  • Increased plasma aldosterone
  • Hypokalemia
  • Increased Na+ Reabsorption (volume contraction)
  • Inhibition of carbonic anhydrase (Acetazolamide)- decreases H+ secretion
19
Q

Describe renal compensation in respiratory/metabolic acidosis

A

Chronic acidosis (if kidney normal)

  • increased H+ secretion by tubule
  • Filtered bicarbonate is reabsorbed
  • Urinary Acid phosphate (titratable acidity) is increased
  • Ammonium in urine is increased
  • Urine pH becomes acidic

Increased phosphate and ammonium excretion in urine

20
Q

Describe renal compensation in respiratory/metabolic alkalosis

A
  • Alkalosis (if kidney normal and fluid volume normal)
  • Decreased H+ secretion by tubule
  • Filtered bicarbonate NOT reabsorbed.
  • Urinary bicarbonate loss increases
  • Acid phosphate and ammonium in urine decreases
  • Bicarbonate also secreted by tubular cells
  • Urine pH b3comes alkaline
21
Q

What are the mechanisms to maintain acid base homeostasis?

A 
Buffers- ECF and ICF buffers are the first line of defense
 Bicarbonate (ECF)
 Phosphate(ICF and urine)
 Proteins(RBC and ICF)
 Ammonia (urine)

Respiratory system (responds in minutes)
Removal of CO2
Rate of respiration regulates PCO2

Renal system (responds in hours-days)
Reabsorption of HCO3^-
Maintenance of serum HCO3^- levels (form NEW HCO3^-)
Excretion of H+
Excretion of non-volatile acids (sulfate, phosphate, lactate)

22
Q

Contrast acidosis disorders

A

Respiratory acidosis -pH less than 7.4
PCO2: increased

Metabolic acidosis- pH less than 7.4
HCO3: decreased

23
Q

Contrast alkalosis disorders

A

Respiratory alkalosis: pH: increased 7.4
PCO2: decreased

Metabolic alkalosis: pH above 7.4

HCO3: increased

CPR 2 (32 decks)

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