Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Urinary > Acid base balance > Flashcards

Acid base balance Flashcards

1
Q

what are metabolic reactions sensitive to?

A

ph of the fluid in which they occur

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

what is normal ph of arterialised blood?

A

7.4

freeH+ of 40 x 10-9 moles/l or 40 x 10-6 mmoles/l.

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

what is the only thing that contributes to ph in terms of ions?

A

Only free H+

Other plasma constituents are present in mmoles eg Na+, K+, Cl-, glucose etc. So [H+ ] is one millioneth that of other plasma constituents.

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

what are two sources of H+ in the body?

A

respiratory acid
metbolic acid

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

what is the respiratory acid source of H+?

A

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-

Formation of carbonic acid is not normally a net contributor to ↑ acid because any ↑ in production →↑ in ventilation.

Problems occur if lung function is impaired.

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

what is the metabolic acid source of H+?

A

via metabolism

inorganic acids

organic acids

On a normal diet, there is a net gain to the body of 50-100 mmoles H+ per day.

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

what are examples of inorganic acids?

A

eg S-containing amino acids → H2SO4 and phosphoric acid is produced from phospholipids

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

what are examples of organic acids?

A

fatty acids, lactic acid

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

what is a major source of alkali?

A

Major source of alkali is oxidation of organic anions such as citrate

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

what is the role of a buffer?

A

minimizes changes in ph when H+ ions are added or removed

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

what is henderson hasselbach equation?

A

defines ph in terms of ratio of A- / HA

ph= pK + log ratio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the most important extracellular buffer?

A

bicarbonate buffer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the normal value for pco2?

A

5.3kpa

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

what is the normal range for hco3?

A

24 mmoles/l

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

how can the henderson hasselbach equation be more simply written?

A

ph ∝ [HCO3-]/ PCO2

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

what is a unique importance of the bicarbonate buffer system?

↑H+ + HCO3- ↔ H2CO3 ↔ H2O + CO2

A

Basic mechanism by which it acts as a buffer is evident, an ↑ECF H+ drives the reaction to the right, so that some of the additional ↑H+ ions are removed from solution and ∴a change in pH is reduced.

If this was an ordinary buffer system then as ↑H+ drives the reaction to the right, the ↑ products would begin to push the reaction back to reach a new equilibrium position, where only some of the additional H+ ions are buffered.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

has h+ been eliminated from the body following bicarbonate buffer?

A

H+ has NOT been eliminated from the body. Instead the HCO3- has buffered the H+ and the respiratory compensation has greatly ↑ the buffering capacity so that free H+ions are prevented from contributing to the pH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what organ is elimination of H+ by?

A

kidneys and this excretion is coupled to the regulation of plasma [HCO3-].

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

renal regulation equation?

A

pH ∝ [HCO3-] = renal regulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

respiratory regulation?

A

Pco2 = respiratory regulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are alternate buffers in the ECF?

A

Plasma proteins Pr- + H+ ↔ HPr

Dibasic phosphate HPO42- + H+ ↔ H2PO4- monobasic phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are primary intracellular buffers?

A

proteins, organic and inorganic phosphates and, in the erythrocytes, haemoglobin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what dpes buffering of H+ ions by ICF buffers cause changes in?

A

in plasma electrolytes, since to maintain electrochemical neutrality, movement of H+ must be accompanied by Cl- as in red cells or exchanged for a cation, K+ .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what can movement of K+ out of cells into the plasma cause in acidosis?

A

hyperkalaemia → depolarization of excitable tissues → ventricular fibrillation and death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what carbonate provides an additional store of buffer?

A

bone carbonate

very important in chronic acid loads as in chronic renal failure - wasting of bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how much H+ is aquired from our diet daily?

A

50-100 mmoles H+ per day from diet.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

if H+ was present as free H+ what would the ph be?

A

1.2-2.4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

H+ what percentage is buffered where for metabolic acid?

A

43% buffered in plasma, primarily with HCO3- 57% in cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

H+ what percentage is buffered where for respiratory acid?

A

97% of buffering occurs within cells, Hb particularly important, rest with plasma proteins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

how does the kidney regulate [HCO3-]?

A

Reabsorbing filtered HCO3-

By generating new HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what does kidney regulation of HCO3 depend on?

A

Both of these processes depend on active H+ ion secretion from the tubule cells into the lumen.

32
Q

describe the mechanism for reabsorption of HCO3?

A

Active H+secretion from the tubule cells

coupled to passive Na+ reabsorption

filtered HCO3- reacts with the secreted H+ to form H2CO3. In the presence of carbonic anhydrase on the luminal membrane → CO2 and H2O

CO2 is freely permeable and enters the cell

Within the cell, CO2 → H2CO3 in the presence of carbonic anhydrase (present in all tubule cells) which then dissociates to form H+ and HCO3-

The H+ ions are the source of the secreted H+

The HCO3- ions pass into the peritubular capillaries with Na+

Bulk of HCO3- reabsorption occurs in the proximal tubule >90%

33
Q

what is the importance of HCO3 reabsorption?

A

GFR =180l/day [HCO3- ] = 24mmoles/l = 4320 mmoles HCO3- filtered per day.

Must be reabsorbed, since failure to do so ≡ to adding H+ to the ECF.

34
Q

what is the minimum urine ph in humans?

A

pH = 4.5.-5.0

35
Q

what is the maximum urine ph in humans?

A

8.0

36
Q

several weak acids and bases act as bufers what is this mostly done by?

A

Most is done by dibasic phosphate, HPO42-, also uric acid and creatinine.

37
Q

titratable acidity?

A

its extent is measured by the amount of NaOH needed to titrate urine pH back to 7.4 for a 24hour urine sample.

Importance of the formation of titratable acidity is that it generates new HCO3- AND excretes H+.

Only used for acid loads.

38
Q

describe the mechanism for titratable acidity?

A

Na2HPO4 in the lumen. One Na+ is reabsorbed in exchange for secreted H+. This monobasic phosphate removes H+ from the body.

The source of the new HCO3- is indirectly CO2 from the blood. It enters the tubule cells, combining with H2O to form carbonic acid, in the presence of carbonic anhydrase, which then dissociates to yield H+, used for secretion, and new HCO3- , which passes with Na+ into the peritubular capillaries.

Occurs principally in the distal tubule. This is where, phosphate ions, not reabsorbed by the proximal tubule Tm mechanism, become greatly concentrated because of removal of up to 95% of the initial filtrate.

Process is dependent on Pco2 of the blood.

39
Q

what is the site of formation of titratable acifity?

A

distal tubule

because un-reabsorbed dibasic phosphate becomes highly concentrated by the removal of volume of filtrate.

40
Q

what is ammonium excretion\/

A

Major adaptive response to an acid load, generates new HCO3- AND excretes H+.

41
Q

describe the mechanism for ammonium excretion?

A

Only used for acid loads. . NH3 is lipid soluble, NH4+ is not. This differential solubility is basis for mechanism. NH3 is produced by deamination of amino acids, primarily glutamine, by the action of renal glutaminase within the renal tubule cells. NH3 moves out into the tubule lumen, where it combines with secreted H+ ions to form NH4+ which combines with Cl- ions (from NaCl) to form NH4Cl which is excreted. (Distal tubule mechanism)

  1. The source of the secreted H+ is again CO2 from the blood.
  2. The new HCO3- passes with Na+ ions into the peritubular capillaries.
  3. (In the proximal tubule, there is an NH4+/Na+ exchanger so NH4+ ions formed within the cells pass out into the lumen. Net effect is the same).
42
Q

what is the activity of renal glutaminase dependent on?

A

PH

43
Q

what effect does fall in ph have on renal glutaminase activity?

A

↑ renal glutaminase activity and ∴ more NH4+ produced and excreted.

This ability to augment NH4+ production is the main adaptive response of the kidney to acid loads. It takes 4-5 days to reach maximal effect because of the requirements of ↑ protein synthesis.

Normally only 30-50 mmoles H+ per day are lost as NH4+ , but this can ↑ to 250 mmoles/l in the presence of severe acidosis.
It also takes time to switch off the ability to make NH4+ when there is excess of alkali.

44
Q
A
45
Q

what do respiratory disorders affect?

A

Pco2

46
Q

what do renal disorders affect?

A

HCO3

47
Q

what is repiratory 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.

48
Q

what are acute causes of respiratory acidosis?

A

drugs which depress the medullary respiratory centres, such as barbiturates and opiates.

Obstructions of major airways.

49
Q

what are chronic causes of respiratory acidosis?

A

lung disease eg bronchitis, emphysema, asthma.
Response: Need to protect pH so need to ↑ [HCO3-].

The ↑ Pco2 will → ↑ secretion of H+ and ↑ HCO3- . Acid conditions stimulate renal glutaminase so get more NH3 produced, BUT, it takes time.

So there is ↑ generation of new HCO3- as well as ↑ reabsorption, because having generated more HCO3- , the ↑ Pco2 will also ↑ the ability to reabsorb it.

50
Q

renal compensation to ↑ HCO3- protects the pH, it does not correct the original disturbance, what does?

A

Only restoration of normal ventilation can remove the primary disturbance.

51
Q

in chronic respiratory acidosis such as bronchitis are blood gas values ever normalised?

A

They may be eg pH 7.32, Pco2 65mmHg (8.67 kPa), [ HCO3-] 38 mmoles/l. The underlying disease process prevents the correction of ventilation, but because the kidney maintains high [HCO3-], the pH is protected.

52
Q

what is 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.

53
Q

what are acute causes of respiratory acidosis?

A

voluntary hyperventilation, aspirin, first ascent to altitude

54
Q

what are chronic causes of respiratory acidosis?

A

long term residence at altitude, ↓ Po2 to < 60mmHg (8kPa) stimulates peripheral chemoreceptors to increase ventilation.

To protect pH, [ HCO3-] should ↓

55
Q

what are alkaline conditions dealt by?

A

HCO3- reabsorptive mechanism.

If ↓ Pco2 , less H+ is available for secretion, ∴ less of the filtered load of HCO3- is reabsorbed so HCO3- is lost in the urine.
Again, ventilation must be normalized to correct the disturbance.

56
Q

what is metabolic acidosis?

A

An acidosis of metabolic origin must be due to a ↓ [HCO3-].

So,↓ [HCO3-], either due to ↑ buffering of H+ or direct loss of HCO3-

To protect the pH, Pco2 must be decreased.

57
Q
A
58
Q

what are causes of metabolic acidosis?

A
  1. ↑ H+ production, as in ketoacidosis of a diabetic (acetoacetic acid, β- hydroxybutyric acid) or in lactic acidosis.
  2. Failure to excrete the normal dietary load of H+ as in renal failure.
  3. Loss of HCO3- as in diarrhoea
    ie failure to reabsorb intestinal HCO3-
59
Q

what is the problem with the usual mechanism that would correct metabolic acidosis?

A

The resulting acidosis stimulates ventilation so that Pco2 falls. The ↑ in ventilation is in depth rather than rate, may be very striking, reaching a maximum of 30 l/min cf normal 5-6 l/min when the arterial pH falls to 7.0. This degree of hyperventilation = Kussmaul breathing = an established clinical sign of renal failure or diabetic ketoacidosis. Very serious.

Normally the kidneys correct the disturbance by restoring [HCO3-] and getting rid of H+ ions.

Problem: Source of H+ ions is the carbonic acid from CO2, but the respiratory compensation lowers the Pco2 to protect the pH!!!!!!!!

60
Q

how is metabolic acid compensated?

A

Compensations for A/B disturbances are always in the same direction as the initial disturbance. Remember pH is defined as the ratio of [HCO3-]/ Pco2. However they are never quite to the same extent ie not complete, so pH not restored to 7.4.

Complete compensation would remove the drive to correct the original disturbance. Survival value of this is that if there were no pressure to correct initial disturbance, a further perturbation may push the system so far that compensation can no longer be effective.

Because of the ↓ Pco2, the total amount of H+ secreted by the renal tubule will be less than normal BUT because the plasma [HCO3-] and ∴ filtered load of HCO3- is reduced to an even greater extent , a smaller fraction of total H+ is needed for HCO3- reabsorption and ∴ a greater proportion is available for excretion in the form of titratable acid and NH4+.

↓ H+ secretion = ↓ HCO3- reabsorption + ↑ new HCO3- generated ↓

61
Q

describe how metabolic H+ is increased in the body?

A
  1. Immediate buffering in ECF and then ICF.
  2. Respiratory compensation within minutes.
  3. Renal correction of the disturbance takes longer to develop the full response to ↑ H+ excretion and generate new HCO3- because renal glutaminase takes 4-5 days to reach maximum. As HCO3- starts to ↑, repiratory compensation begins to wear off until eventually get rid of all excess H+ .

So, respiratory compensation delays the renal correction, but protects the pH, much more important.

62
Q

what is metabolic alkalosis?

A

[HCO3-] must have ↑ and Pco2 will ↑ to protect the pH.

63
Q

what are causes of metabolic acidosis?

A
  1. ↑ H+ ion loss- vomiting loss of gastric secretions
  2. ↑ renal H+ loss- aldosterone excess, excess liquorice ingestion
  3. Excess administration of HCO3- is unlikely to produce a metabolic alkalosis in subjects with normal renal function, but may do so if renal function impaired.
  4. Massive blood transfusions can lead to metabolic alkalosis because bank blood contains citrate to prevent coagulation, which is converted to HCO3-, but need at least 8 units to have this effect.
    The greatly ↑ filtered load of HCO3- exceeds the level of H+ secretion to reabsorb it, even in the presence of ↑ Pco2, so the excess is lost in the urine. Again, respiratory compensation delays renal correction, but protects the pH.
64
Q

summarise acid/base disorders?

A
65
Q

what is a decrease in ph (acidosis) caused by? one of two things?

A
66
Q

for a given increase in Pco2, there is a ______ decrease in pH in chronic respiratory acidosis than in acute respiratory acidosis?

A

smaller

67
Q

why is there a smaller decrease in pH in chronic respiratory acidosis than in acute respiratory acidosis?

A

Answer lies in mechanisms used to raise [HCO3-]. NH3 production takes 4-5 days to be fully turned on. So initially can only raise [HCO3-] by titratable acid, so limited. With time, can use NH3 production which has a considerable capacity to raise [HCO3-].

A similar difference is seen between acute and chronic respiratory alkalosis because of the delay in turning off NH3 production. In contrast to renal compensations, which need time to reach completion, respiratory compensations occur in minutes so no differences.

68
Q

onsider a badly controlled diabetic in ketoacidosis = metabolic acidosis (1).
This patient, despite the best advice, has always smoked and has a haemorrhage?

A

has always smoked, = chronic bronchitis = respiratory acidosis (2).
Patient has a haemorrhage = lactic acidosis (3).
ie combined metabolic and respiratory acidosis
blood/gas values: pH = 6.99, Pco2 = 60mmHg (8kPa), [HCO3-] = 13mmoles/l

69
Q

what would you do in the example from the previous flashcard?

A

Insulin (+ glucose if non-diabetic), stimulates cellular uptake of K+.
BUT?????

Also for hyperkalaemia, calcium resonium, either oral or pr (per rectum), exchanges Ca2+ ions for K+ ions (12-24 hours)

Ca gluconate (iv) → ↓ excitability of heart, stabilizes cardiac muscle cell membranes.

70
Q

what should be considered in a bad case of vomiting?

A

loss of NaCl and H2O → hypovolaemia
loss of HCl → metabolic alkalosis

The hypovolaemia will stimulate aldosterone to ↑ distal tubule Na+ reabsorption.

Under conditions of avid Na+ reabsorption, (and due to loss of Cl- ), the main ion exchanged for Na+ is H+.

The respiratory compensation for the metabolic alkalosis ie ↑Pco2 helps drive the H+ secretion and exacerbates the metabolic alkalosis by adding yet more HCO3- to the plasma.

71
Q

what takes precedemce over correction of metabolic alkalosis?

A

restoration of volume

Give NaCl, restore volume, alkalosis will be corrected.
In vomiting and diarrhoea, although lose acid and alkali, become alkalotic because ↓ ECF volume → ↑ aldosterone → “contraction alkalosis”.
Liquorice contains glycyrrhizic acid, which is very similar to aldosterone, so that excess ingestion → metabolic alkalosis.

72
Q

The following blood gas values were seen in a patient. Which simple Acid/Base Disturbance has he got?

pH = 7.32, [HCO-3]= 15 mM, PCO2 = 30mmHg (4kPa)

Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis (acute)
Respiratory Acidosis (chronic)
Respiratory Alkalosis (acute)
Respiratory Alkalosis (chronic)

A
73
Q

The following blood gas values were seen in a patient. Which simple Acid/Base Disturbance has he got?

pH = 7.32, [HCO-3]= 33 mM, PCO2 = 60mmHg (8kPa)

Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis (acute)
Respiratory Acidosis (chronic)
Respiratory Alkalosis (acute)
Respiratory Alkalosis (chronic)

A
74
Q

The following blood gas values were seen in a patient. Which simple Acid/Base Disturbance has he got?

pH = 7.45, [HCO-3] = 42 mM, PCO2 = 50mmHg (6.7kPa)

Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis (acute)
Respiratory Acidosis (chronic)
Respiratory Alkalosis (acute)
Respiratory Alkalosis (chronic)

A
75
Q

The following blood gas values were seen in a patient. Which simple Acid/Base Disturbance has he got?

pH = 7.45, [HCO-3]= 21 mM, PCO2 = 30mmHg (4kPa)

Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis (acute)
Respiratory Acidosis (chronic)
Respiratory Alkalosis (acute)
Respiratory Alkalosis (chronic)

A
76
Q

A 75 year old man has the following blood gas values:
pH = 7.31, PCO2 = 7.7.kPa, (58mmHg), [HCO3-] =36mmoles/l.
1. It is likely that he has renal disease.
2. He may have an acute respiratory infection.
3. It is possible that he may have chronic bronchitis.
4. There will be a decrease in his excretion of ammonium ions.
5. His plasma potassium will be reduced.

A
77
Q

The following acid/base values were obtained:
pH = 7.25, [HCO3-] = 12mmoles/l, PCO2 = 3.3kPa (25mmHg)

They are indicative of a respiratory acidosis
The reduction in Pco2 is a result of under-breathing
The subject has probably been taking bicarbonate of soda
It could be related to impaired renal function
The subject may have been vomiting very badly

A

Urinary (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions