Lecture 11 and 12 Acid Base Balance Flashcards

(32 cards)

1
Q

Name primary intracellular buffers

A

Proteins
Organic phosphates
Inorgainc phosphates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

To maintain electrochemical neutrality movement of H+ must be accompanied by what

A

Cl- in red cells
or
Exchanged for a cation K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

An increase of H+ has what effect on K+ levels

A

Increases in H+ in acidosis leads to hyperkalaemia as K+ moves out of cells into plasma to maintain electrochemical neutrality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

For metabolic acid how is H+ buffered

A

Buffered in plasma and cells with HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

For respiratory acid how is H+ buffered

A

Majority occurs within cells

Rest with plasma proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does the kidney regulate HCO3-

A

Reabsorbing filtered HCO3-
Generating new HCO3-
Both dependent on active H+ secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the average GFR in litres per day

A

180

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the net production of urine

A

50-100 mmoles H+ per day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the main buffer in urine

A

dibasic phosphate, HPO4^2-, also uric acid and creatinine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

The process of generation of new HCO3- in the distal tubule is dependent on what

A

PCO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the generation go HCO3- in the distal tubule

A
  1. A Na+ from Na2HPO4 is reabsorbed from the lumen into the tubule cells in exchange for secreted H+
  2. Co2 from the blood combines with H20 to form carbonic acid which dissociates to form H+ and Hco3-
  3. New HCo3- is absorbed into the blood along with Na+
  4. Excreted H+ combines with HPO4^2- to form H2PO4- which is excited
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe ammonium excretion

A
  1. NH3 is produced by deamination of glutamine by renal glutaminase
  2. NH3 moves into tubule and combines with excreted H+, Cl- to from NH4Cl which is excreted
  3. Generation of new HCO3-. CO2 from PT capillaries combines with H2o to form carbonic acid which dissociates
  4. Hco3- is reabsorbed with Na+
  5. H+ is secreted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What effect does intracellular pH fall have on renal glutaminase

A

increase in renal glutaminase activity and more NH4+ produced and excreted to reduce acid load

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How many days does it take for NH4+ production to reach maximum effect

A

4-5 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe respiratory acidosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are causes of respiratory acidosis

A

Acute: Drugs that depress medullary respiratory centres- Barbiturates and Opiates
Chronic: Emphysema, asthma, bronchitis

17
Q

Why is there an increase in NH3 in respiratory acidosis

A

Increase secretion of H+ and HCO3-

18
Q

Describe respiratory alkalosis

A

• 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

19
Q

What are the causes of respiratory alkalosis

A
  • Acute: voluntary hyperventilation, aspirin, first ascent to altitude
  • Chronic: long term residence at altitude,  Po2 to < 60mmHg (8kPa) stimulates peripheral chemoreceptors to increase ventilation.
20
Q

What is the consequence of reduced PCO2 in reparatory alkalosis on H+ secretion and HCO3- reabsorption

A

Less PCO2
Less H+
Less H+ to combine with HCO3- and less is reabsorbed so HCO3- is lost in urine

21
Q

Describe metabolic acidosis

A

Reduced HCO3-

due to increased buffering H+ or direct loss of HCO3-

22
Q

What are the causes of metabolic acidosis

A

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

23
Q

Causes of metabolic alkalosis

A

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-)

24
Q

Between acute and chronic respiratory acidosis an an increase in PCo2 would have a smaller decrease in pH for which one

A

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

25
What is the normal range of anion gap
14-18mmoles/L
26
When is it useful to measure the anion gap
Metabolic acidosis
27
What are the 2 types of metabolic acidosis
In one there is no change from normal and in the other the anion gap increases.
28
If the metabolic acidosis is due for example to a loss of bicarbonate from the gut is there an anion gap? Explain?
then the reduction of bicarbonate is compensated by an increase in chloride and so there is no change in anion gap
29
If the metabolic acidosis is due to lactic or diabetic acidosis is there an anion gap? why?
the reduction in bicarbonate is made up by other anions such as lactate, acetoacetate, -OH butyrate and so the anion gap is increased
30
• pH = 7.32 (low), [HCO-3]= 15 mM (low) , PCO2 = 30mmHg (4kPa) (low) What acid/base disturbance does this patient have
• Metabolic acidosis
31
pH = 7.32 (low), [HCO-3]= 33 mM (high), PCO2 = 60mmHg (8kPa) (high) What acid/base disturbance does this patient have
• Chronic Respiratory Acidosis
32
• pH = 7.45 (high), [HCO-3] = 42 mM (high), PCO2 = 50mmHg (6.7kPa) (high) What acid/base disturbance does this patient have
• Metabolic Alkalosis