Acid Base Balance

Question 0

Describe the clinical effects of acidaemia and alkalaemia

Answer 0

Acidaemia - increased K+ –> decreased cardiac and skeletal muscle contractility (arrhythmias, heart stops, decreased glycolysis, decreased hepatic functioning
Alkalaemia - decreased free Ca2+ –> increased excitability of nerves (paraesthesia, tetany)

Question 1

Be able to state the normal range of plasma pH

Answer 1

7.38-7.42

Question 2

Describe the carbon dioxide/hydrogen carbonate buffer system and the factors influencing pCO2 and [HCO3-]

Answer 2

H2O + CO2 HCO3- + H+
pCO2 influenced by respiration, chemoreceptors
[HCO3-] influenced by kidney, reactions in RBC

Question 3

Be able to identify from values, respiratory acidaemia (acidosis) and alkalaemia (alkalosis), and metabolic acidosis and alkalosis

Answer 3

Respiratory acidosis - due to hypoventilation –> hypercapnia –> high H+ –> low pH
Respiratory alkalosis - due to hyperventilation –> hypocapnia –> low H+ –> high pH (also low calcium)
Metabolic acidosis - increased H+ or inability to form bicarbonate in kidney, increased anion gap
Metabolic alkalosis - due to persistent vomiting –> acid doesn’t enter duodenum –> HCO3- not removed from blood, decreased H+ or increased bicarbonate

Question 4

Describe cellular mechanisms of reabsorption of HCO3- in the proximal tubule

Answer 4

Na+/K+ATPase on basolateral membrane
NHE on apical membrane 
H+ + HCO3- --> H2O + CO2 
CO2 enters on apical membrane 
CO2 + H20 --> H+ + HCO3-
HCO3- leaves on basolateral membrane

Question 5

Describe cellular mechanisms of H+ excretion in the distal tubule

Answer 5

?

Question 6

Describe the mechanism of buffering H+ in urine, and explain the concept of titratable acid, and the role of NH4+

Answer 6

?
In distal tubule:
Titratable acid - some acid buffered by phosphate

Question 7

Describe interactions between acid base status and plasma K+

Answer 7

K+ moves out of cells
Increased reabsorption in distal nephron
Increased K+ = acidaemia

Question 8

Describe the common causes of metabolic acidosis, in particular the effects of persistent vomiting

Answer 8

Causes - lactic acidosis, ketoacidosis, chronic renal failure, longstanding diarrhoea (bicarbonate loss)
Persistent vomiting –> removal of H+ from body (acid doesn’t enter duodenum) –> HCO3- not removed from blood
Inability to lose HCO3- if dehydrated

Question 9

Describe the main classes of metabolic acidosis and the role of anion-gap measurements in distinguishing between them

Answer 9

Low levels of cations = increased anion gap:
Increased in lactic acid/ketoacids, kidney failure, ingesting methanol, aspirin overdose
Increased production of chloride/increased excretion of bicarbonate = normal anion gap:
Diarrhoea, carbonic anhydrase inhibitors, renal tubular acidosis, spironolactone

Question 10

Describe compensation and correction

Answer 10

Compensation:
Changes in [HCO3-] (kidneys)
Changes in ventilation (lungs)
Correction:
Alter [HCO3-] (kidneys) 
Variable - excretion/creation

Question 11

Describe the creation and sexcretion of HCO3-

Answer 11

Creation:
Glutamine –> a-ketoglutarate –> HCO3- (to ECF) + NH4+ (to lumen)
Excretion:
Proximal tubule/thick ascending limb of LoH

Question 12

Explain the anion gap

Answer 12

([Na+] + [K+]) - ([Cl-] + [HCO3-]) = 10-15 mmol/L
Increased gap - anions replace plasma HCO3-
Same gap - HCO3- replaced with Cl-