Acid Base Balance Flashcards

1
Q

State the normal range plasma pH

A

7.35 - 7.45

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2
Q

Explain the effects of alkalaemia

A
  • pH > 7.45
  • Lowers free calcium by causing Ca2+ ions to come out of solution
    • Binds proteins
    • Increases neuronal excitability (calcium makes membrane less excitable)
  • More serious than acidaemia
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3
Q

Explain the effects of acidaemia

A
  • pH < 7.35
  • Increases plasma potassium ion concentration - hyperkalaemia
    • Affects excitability - particularly cardiac muscle
    • Arrhythmia
  • Increasing [H+] denatures enzymes
    - Affects muscle contractility, glycolysis, hepatic function
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4
Q

Interpret uncomplicated blood gas abnormalities and recognise respiratory acidosis, respiratory alkalosis, metabolic acidosis and metabolic alkalosis

A
  1. Look whether pH has increased or decreased
  2. Loos at pCO2 and [HCO3] and see if increased or decreased
  3. If pH change and pCO2 change are in the opposite direction, then respiratory cause
  4. If pH change and [HCO3] change are in the same direction, then metabolic cause
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5
Q

How do the kidneys compensate for respiratory acidosis/alkalosis

A
  • Kidneys increase [HCO3] to compensate for respiratory acidosis
  • Kidneys decrease [HCO3] to compensate for respiratory alkalosis
  • Takes time, 2-3 days
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6
Q

Describe how reabsorption of HCO3 in proximal tubule works

A
  • HCO3 filtered at the glomerulus and most recovered in PCT
  • Basolateral membrane has Na/K ATPase pumping sodium out of the cell
  • Na/H exchanger allows Na entry into the cell which drives H+ secretion into the nephron lumen
  • H+ reacts with HCO3- in the lumen to form CO2 which enters cell freely
  • Converted back to HCO3, which enters ECF through Na/HCO3 cotransporter
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7
Q

Outline how HCO3 creation occurs in proximal tubule

A
  • Glutamine is converted to α-ketoglutarate and NH4
  • NH4 dissociates into NH3 and H+
  • NH3 uncharged so can cross membrane and enter lumen where it forms NH4 which exits through urine
  • α-ketoglutarate forms 2 HCO3 which enters ECF
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8
Q

Define titratable acid

A

Any acid that has the ability to lose a proton in an acid base reaction

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9
Q

Outline the role of NH4 in buffering H+

A
  • Ammonium generation from glutamine in proximal tubule can be increased in response to low pH
  • NH4+ -> NH3 + H+
  • NH3 freely moves into lumen and through interstitium
    • Able to move from PCT (where it is formed) to the DCT and CT to buffer H+
  • H+ actively pumped into lumen in DCT and CT
  • H+ combines with NH3 to form NH4+
    • Trapped in lumen and excreted in urine
  • NH4+ can also be taken up in ascending limb and transported to interstitium and dissociates to H+ and NH3
    - NH3 then enters lumen of collecting duct
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10
Q

What titratable acids can buffer H+

A

NH4, H2PO4

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11
Q

Explain the effect of H+ levels on K+ concentration

A
  • Acidosis leads to hyperkalaemia
    • H+ moves into cells as high concentration of [H+] out of cell
    • Causes potassium ions to move out of cells
    • Decreased potassium excretion in distal nephron
  • Alkalosis leads to hypokalaemia
    • H+ moves out of cells
    • Potassium ions move into cells
    • Enhanced excretion of potassium in distal nephron
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12
Q

State some causes of respiratory acidosis

A
  • Type 2 respiratory failure
    • Low pO2 and high pCO2
    • Alveoli cannot be properly ventilated
    • Severe COPD, severe asthma, drug overdose, neuromuscular disease
  • Can be compensated for by increase in [HCO3]
  • Chronic conditions can be well compensated such that pH near normal
    - However, higher level of ‘normal’ pCO2 will be established
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13
Q

State some causes of respiratory alkalosis

A
  • Hyperventilation
    • Anxiety/panic attacks - acute setting
    • High altitude
    • Low pCO2, rise in pH
  • Hyperventilation in response to long-term hypoxia - type 1 respiratory failure
    • Low pCO2 with initial rise in pH
    • Chronic hyperventilation can be compensated for by fall in [HCO3]
      • Can restore pH to near normal
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14
Q

Describe the common causes of metabolic alkalosis

A
  • Stomach is a major site of HCO3 production
    • By-product of H+ secretion
    • Severe prolonged vomiting - loss of H+
    • Mechanical drainage of stomach
  • Hypokalaemia makes the intracellular pH of tubular cells more acidic
    • H+ ions move into tubular cells as K+ exits cells
    • Favours H+ excretion and HCO3 recovery
    • Metabolic alkalosis
  • Certain diuretics - loops and thiazide
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15
Q

How can metabolic acidosis occur

A
  • If the tissues produce acid, this reacts with and removes HCO3
  • Leads to a fall in [HCO3] and fall in pH
  • Extra CO2 produced is breathed off at the lungs so there is no increase in arterial pCO2
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16
Q

Describe the anion gap

A
  • Difference between measured cations and anions

- ([Na] + [K]) - ([Cl] + [HCO3])

17
Q

How can anion gap change

A
  • Gap is increased if HCO3 is replaced by other anions
    • If a metabolic acid (such as lactic acid) reacts with HCO3, the anion of the acid replaces HCO3
  • In renal causes of acidosis anion gap will be unchanged
    - Not making enough HCO3, but this is replaced by Cl
18
Q

Give examples of metabolic acids which can increase anion gap

A
  • Keto acidosis - diabetes
  • Lactic acidosis
  • Uraemic acidosis - advanced renal failure
19
Q

Gives examples when anion gap has not changed in metabolic acidosis

A
  • Renal tubular acidosis (RTA) - rare
    • Problems with transport mechanisms in the tubules
    • Type 1 (distal) RTA - inability to pump out H+
    • Type 2 (proximal) RTA - problems with HCO3 reabsorption
  • Severe persistent diarrhoea
    - Loss of HCO3 replaced by Cl