Lecture 11 and 12 Acid Base Balance Flashcards
(32 cards)
Name primary intracellular buffers
Proteins
Organic phosphates
Inorgainc phosphates
To maintain electrochemical neutrality movement of H+ must be accompanied by what
Cl- in red cells
or
Exchanged for a cation K+
An increase of H+ has what effect on K+ levels
Increases in H+ in acidosis leads to hyperkalaemia as K+ moves out of cells into plasma to maintain electrochemical neutrality
For metabolic acid how is H+ buffered
Buffered in plasma and cells with HCO3-
For respiratory acid how is H+ buffered
Majority occurs within cells
Rest with plasma proteins
How does the kidney regulate HCO3-
Reabsorbing filtered HCO3-
Generating new HCO3-
Both dependent on active H+ secretion
What is the average GFR in litres per day
180
What is the net production of urine
50-100 mmoles H+ per day
What is the main buffer in urine
dibasic phosphate, HPO4^2-, also uric acid and creatinine.
The process of generation of new HCO3- in the distal tubule is dependent on what
PCO2
Describe the generation go HCO3- in the distal tubule
- A Na+ from Na2HPO4 is reabsorbed from the lumen into the tubule cells in exchange for secreted H+
- Co2 from the blood combines with H20 to form carbonic acid which dissociates to form H+ and Hco3-
- New HCo3- is absorbed into the blood along with Na+
- Excreted H+ combines with HPO4^2- to form H2PO4- which is excited
Describe ammonium excretion
- NH3 is produced by deamination of glutamine by renal glutaminase
- NH3 moves into tubule and combines with excreted H+, Cl- to from NH4Cl which is excreted
- Generation of new HCO3-. CO2 from PT capillaries combines with H2o to form carbonic acid which dissociates
- Hco3- is reabsorbed with Na+
- H+ is secreted
What effect does intracellular pH fall have on renal glutaminase
increase in renal glutaminase activity and more NH4+ produced and excreted to reduce acid load
How many days does it take for NH4+ production to reach maximum effect
4-5 days
Describe respiratory acidosis
pH has fallen and it is due to a respiratory change, so Pco2 must have increased. Respiratory acidosis results from reduced ventilation and retention of CO2
What are causes of respiratory acidosis
Acute: Drugs that depress medullary respiratory centres- Barbiturates and Opiates
Chronic: Emphysema, asthma, bronchitis
Why is there an increase in NH3 in respiratory acidosis
Increase secretion of H+ and HCO3-
Describe respiratory alkalosis
• Alkalosis of respiratory origin so must be due to a fall in Pco2 and this can only occur through increased ventilation and CO2 blow-off
What are the causes of respiratory alkalosis
- Acute: voluntary hyperventilation, aspirin, first ascent to altitude
- Chronic: long term residence at altitude, Po2 to < 60mmHg (8kPa) stimulates peripheral chemoreceptors to increase ventilation.
What is the consequence of reduced PCO2 in reparatory alkalosis on H+ secretion and HCO3- reabsorption
Less PCO2
Less H+
Less H+ to combine with HCO3- and less is reabsorbed so HCO3- is lost in urine
Describe metabolic acidosis
Reduced HCO3-
due to increased buffering H+ or direct loss of HCO3-
What are the causes of metabolic acidosis
Increase H+ production in ketoacidosis or lactic acidosis
Failure to excrete normal dietary load of H+ due to renal failure
Loss of HCO3- in diarrhoea or reabsorption failure
Causes of metabolic alkalosis
Increase in H+ loss due to vomiting of gastric secretionsIncrease in renal H+ loss- aldosterone excess, excess liquorice
Massive blood transfusion (blood bank contains citrate which is converted to HCO3-)
Between acute and chronic respiratory acidosis an an increase in PCo2 would have a smaller decrease in pH for which one
There is a smaller decrease in pH in chronic respiratory acidosis than in acute respiratory acidosis.
Due to 4-5 days delay of NH3 production