Lect 11 Flashcards

1
Q

What are the three lines of defense against acid/base disturbances

A
  • buffers
    • mainly HCO3-/H2CO3; very fast
  • respiratory compensation
    • adjusts CO2 levels
    • very fast but incomplete
  • renal compensation
    • adjusts HCO3- levels
    • slow but potent
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2
Q

which compensation is always active when primary problem is metabolic

A

respiratory compensation

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3
Q

which compensation will compensate for respiratory problems and metabolic problems if they do not involve the kidney

A

reanl compensation

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4
Q

Problem

  • pH= 7.52
  • HCO3- = 22
  • PCO2 = 28
A
  1. alkalosis
  2. there is a respiratory component: (PCO2 <35)
  3. expected HCO3- = 22 (since PCO2 is 12 mmHg below normal which will depress HCO3- by 2 due to mass action)
  4. actual HCO3- = 22, so there is no renal compensation
  5. this is an uncompensated (pure) respiratory alkalosis
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5
Q

Problem

  • pH = 7.43
  • HCO3- = 18
  • PCO2 = 28
A
  1. normal pH
  2. primary disturbance is respiratory
  3. expect HCO3- = 22, but it = 18; therefore, 4 was removed by kidneys
  4. completely componsated respiratory alkalosis
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6
Q

problem

  • pH=7.25
  • HCO3- = 12
  • PCO2 = 28
A
  • pH = acidosis
  • expected HCO3- = 22, but it =12; therefore must be a primary metabolic acidosis that reduced HCO3- by 10
  • partly compensated metabolic acidosis
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7
Q

Problem

  • pH = 7.30
  • HCO3- = 25
  • PCO2 = 52
A
  1. acidosis
  2. there is a respiratory acidosis
  3. expected HCO3- = 25, which it is
  4. uncompensated (pure) respiratory acidosis
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8
Q

H+ loss or HCO3- gain is consistent with

A

metabolic alkalosis

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9
Q

Hyperaldosteronism and ECF volume contraction can lead to what condition

A
  • metabolic alkalosis
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10
Q

how can ECF volume contraction due to vomiting or extensive use of diuretics maintain metabolic alkalosis?

A
  • increase in renin-angiotensin II-aldosterone system
    • angiotensin II stimulates Na+-H+ antiporter and HCO3- reabsorption
    • aldosterone stimulates secretion of H+ (H+-ATPase) from type A intercalated cells and K+ from principle cells
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11
Q

metabolic alkalsosis is often linked with what

A

hypokalemia

  • volume contraction stimulates aldosterone which intensifies both alkalosis and hypokalemia
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12
Q

hypokalemia has what effect on H+ secretion

A
  • stimulates H+ secretion by type A intercalated cells (H+/K+ ATPase) and can increase NH4+ secretion, both intensify alkalosis
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13
Q

metabolic alkalsos can present with hypochloremia. why?

A
  • due to loss in gastric fluids or urine (diuretics)
  • without Cl- available for co-transport with Na+, the collecting duct lumen develops a more negative potential with respect to the cytoplasms which facilitates the excretion of K+ and H+
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14
Q

how is metabolic alkalosis treated

A
  • repletion of Cl- deficit with saline (NaCl or KCl)
    • corrects saline-responsive forms
    • will adjust the RAAS system
    • Cl- transport with Na+ reduces negativity of CD lumen, H+ and K+ loss reduced
    • result in excretion of bicarbonate
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15
Q

aldosterone excess (secreting tumor) is an example of saline-resistant metabolic alkalosis. What is the treatment

A
  • ECF volume is increased, and [Cl-] is okay
  • administering saline does not help as patient is already volume expanded
  • excess aldosterone increases H+ secretion and Na+ reabsorption
  • treatment: remove tumor or aldosterone antagonist (spironolactone)
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16
Q

a gain of H+ or loss of HCO3- causes

A

metabolic acidosis

17
Q

what are the three types of metabolic acidosis from diminished tubular H+ secretion

A
  1. type I (distal)
    • H+-ATPase activity is reduced
  2. type II (proximal)
    • Na+-H+ antiporter is reduced
  3. type IV
    • reduced formation of NH4+
      • often due to hyperkalemia secondary to aldosterone deficiency
18
Q

what is a anion gap? what is the normal value?

A
  • in the body, the concentration of anions must equal the concentration of cations
    • major anions: Cl = 100; HCO3- = 24; total = 124
    • major cation: Na+ =140
  • anion gap = [Na+] -([Cl-] +[HCO3-])
    • normal gap = 8-16
19
Q

the anion gap often increases in what state? why?

A
  • increases in acidosis where there is an excess of other non-volatile (fixed) acids
    • ​AG is often nml is acidosis due to simple bicarb loss due to Cl- increase
  • fixed acids liberate H+ which is buffered by HCO3- w/o changing Cl- levels, this increases the anion gap
  • **anions associated with these acids (lactate, oxalate) take the place of HCO3-; so Cl- levels do not change
20
Q

name some clinical causes of increased anion gap

A
  • lactic acidosis: due to lactic acid
  • ketoacidosis: acetoacetic acid
  • renal failure: accumulation of phosphoric, sulfuric acid
  • salicylate poisoning
21
Q

high altitude, anxiety, and hypoxemia can cause what state

A
  • respiratory alkalosis
  • due to decrease in PaCO2 via increases alveolar ventilation
22
Q

impairment of central respiratory regulation, chest wall dysfunction, impaired airway mechanisms can cause what state

A
  • respiratory acidosis
  • due to impaired pulmonary excretion of CO2