ChemPath: Acid-Base Handling Flashcards

1
Q

What is the normal range for H+ concentration?

A

35-45 mmol/L in ECF

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2
Q

What equation links H+ concentration to pH?

A

pH = log1/[H+]

inverse log = higher the H+ –> smaller the pH.

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3
Q

What are the three main physiological buffers?

A
  • Bicarbonate (kidneys)
  • Haemoglobin (RBCs)
  • Phosphate (HP04- = H2PO4)

NOTE: also protein and bone

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4
Q

What is the rate of production of H+ ions per day?

Describe where H+ is derived from

A

50 - 100 mmol/day

Metabolism of proteins, carbohydrates and fats produce H+ (alongside: CO2, H2O)

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5
Q

Describe how the kidneys excrete H+ ions.

A
  1. In the filtrate, bicarbonate combines with H+ (which moves from the tubular cell into the filtrate via a Na+/H+ channel) to form carbonic acid.
  2. Carbonic acid is catalysed into H20 and CO2 which diffuse into the tubular cells (as are not polar and can move across the membrane freely)
  3. H20 and CO2 are catalysed back into Carbonic Acid which breaks down into HCO3- and H+
  4. HC03+ is reabsorbed into the blood via Na+/HCO3- or HCO3-/Cl- channels.

Overall kidneys excrete H+ and regenerate HCO3-. (regenerating HCO3- is crucial as in the blood when HC03- buffers H+ it gets used up)

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6
Q

Describe how H+ ions pass through the renal epithelial membrane.

A

H+ ions cannot pass through the membrane itself so a transport system is necessary (Na+/H+ exchange)

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7
Q

What is the rate of production of carbon dioxide per day?

A

20,000-25,000 mmol/day

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8
Q

Describe the respiratory control over carbon dioxide.

A
  • Respiratory is controlled by chemoreceptors in the hypothalamic respiratory centre
  • An increase in CO2 will stimulate an increase in ventilation which then brings down CO2 concentration
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9
Q

Acid-Base Regulation Equation

A
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10
Q

How should you interpret an ABG

A
  1. Look at pH
    Acidic?
    Alkali?
  2. Look at CO2
    Does it fit with the pH?
    Yes! –> its a respiratory cause!
    No! –> its a metabolic cause – if its inverse to what you’d expect = compensation!
  3. Look at HCO3-
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11
Q

What is the primary abnormality in metabolic acidosis? List three causes with examples.

A

Primary abnormality is increased H+ (with decreased bicarbonate as it tried to mop up the excess H+)

Caused by:

  • Increased H+ production (e.g. DKA)
  • Decreased H+ excretion (e.g. renal tubular acidosis)
  • Bicarbonate loss (e.g. intestinal fistula, diarrhoea)
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12
Q

In metabolic acidosis - what can you calculate to help you determine the cause. What are potential causes depending on the calculation result

A

Calculate Anion Gap

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13
Q

What is the primary abnormality in respiratory acidosis? List three causes with examples.

A

Primary abnormality is increased CO2 (therefore, increased H+) and a slight increase in bicarbonate (but not sufficient to buffer H+)

Caused by:
HYPOVENTILATION
* Type 2 respiratory failure (e.g. COPD)
* Opioids
* Sedatives/neuromuscular weakness

NOTE: metabolic compensation is slower than respiratory compensation

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14
Q

What is the primary abnormality in metabolic alkalosis? List three causes.

A

Primary abnormality is decreased H+ (with increased bicarbonate)

Caused by:

  • H+ loss (e.g. pyloric stenosis, vomiting)
  • Hypokalaemia (as main transport agent for H+ in cells due to K+/H+ transporter)
  • Ingestion of bicarbonate (e.g. antacids)
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15
Q

What is the primary abnormality in respiratory alkalosis ? List three causes.

A

Primary abnormality is reduced CO2

Can be caused by hyperventilation due to:
* Stroke
* Meningitins
* Artificial ventilation
* Asthma attack / Anxiety attack (compensation will not occur)

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16
Q

What derangement of acid-base balance would be caused by pyloric stenosis?

A

Metabolic alkalosis due to loss of H+ from profuse vomiting

17
Q

Which condition classically causes a mixed respiratory alkalosis and metabolic acidosis?

A
  • Aspirin overdose
  • Aspirin stimulates ventilation (respiratory alkalosis) and reduces renal excretion of H+ (metabolic acidosis)
18
Q

What are the clinical pictures of the 2 main types of renal tubular acidosis

A