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renal > acid-base balance > Flashcards

acid-base balance Flashcards

1
Q

normal pH of aterialised blood

A

7.4

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2
Q

sources of H+

A

respiratory acid

metabolic acid

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3
Q

respiratory acid

A

CO2 + H2O –> carbonic acid –> H+ and bicarbonate

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4
Q

metabolic acid sources

A

a) inorganic acid e.g. S containing amino acid, phosphoric acid from phospholipids
b) organic acids: fatty acids, lactic acids

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5
Q

major source of alkali

A

oxidation of organic anions such as citrate

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6
Q

buffer

A

minimise change in pH when H+ ions are added or removed

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7
Q

normal value and range ph

A
  1. 4

7. 37-7.43

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8
Q

normal value and range bicarbonate

A

24

22-26

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9
Q

what controls elimination of H+ from body

A

kidneys

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

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10
Q

compensatory mechanisms

A

bicarb - renal

CO2 - resp

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11
Q

other buffers in ECF

A

plasma proteins

dibasic phsophate

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12
Q

primary intracellular buffers

A

proteins
organic and inorganic phosphates
haemoglobin (in RBCs)

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13
Q

how does increase in H+ lead to hyperkalaemia

A

buffering H+ by ICF buffers cn cause change in plasma electrolytes need to maintain electrochemical neutrality so must be exchanged for cation K+

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14
Q

how does kidney regulate [HCO3-]

A
  1. reabsorbing filtered bicarb
  2. generating new bicarb

both these processes depend on active H+ secretion from tubule into lumen

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15
Q

mechanism of HCO3- reabsorption

A
  1. active H+ secretion
  2. coupled to passive Na+ reabsorption
  3. filtered HCO3- reacts w H+ –> H2CO3 –> H2O + CO2
  4. CO2 is freely permeable and enters cell
  5. in cell CO2 –> H2CO3 –> H+ and HCO3-
  6. H+ ions are source of secreted H+
  7. HCO3- pass into peritubular capillaries with Na+
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16
Q

where does bulk of bicarb reabsorption take place

A

proximal tubule

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17
Q

is there excretion of H+ ions during HCO3- reabsorption?

A

no

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18
Q

minimum urine pH

A

4.5-5

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19
Q

maximum urine pH

A

8

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20
Q

titratable acidity

A

H+ buffered in urine
several weak acids an bases act as buffers - mostly dibasic phosphate, hydrogen phosphate and also uric acid and creatiine

21
Q

why is urine buffering called titratable acifity

A

because its extent is measured by amount of NaOH needed to titrate urine pH back to 7.4 for a 24hr sample

22
Q

why is tirtatable acifiy important

A

generates new bicarbonate and excretes H+

23
Q

mechanism titratable acidity

A
  1. Na2HPO4 in lumen. One Na+ reabsorbed in exchange for H+. Monobasic phosphate removes H+ from body
  2. new HCO3- is indirectly from CO2 from blood. It enters tubule cell combines w water to form carbonic acid which dissociates to yeild H+ (secreted) and new bicarbonate which passes with Na+ into peritubular capillaries
24
Q

where does titratable acidity predominanly occur

A

distal tubule

25
Q

what is titrtable acidity dependent on

A

PCO2 of blood

26
Q

why is distal tubule site for titratable acidity

A

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

27
Q

ammonium excretion

A

major adaptive response to an acid load

generates new HCO3- and excretes H+

28
Q

differential solubility basis of ammonium secretion

A

NH3 is lipid soluble

NH4+ is not

29
Q

what is NH3 produced by

A

deamination of amino acids, primarily glutamine, by action of renal glutaminase within renal tubule cells

30
Q

mechanism of ammonium excretion

A
  1. NH3 moves out into 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
  2. source of secreted H+ is CO2 from blood
  3. new HCO3- passes with Na+ ions into pertibular capillaries
31
Q

what is activity of renal glutaminase depedent on

A

pH

when intracellular pH falls increase renal glutaminase acitivty and so more NH4+ produced and excreted

32
Q

main adaptive response of kidney to acid loads

A

ability to augment NH4+ production

takes 4-5 days to reach maximal effect as required inc protein synthesis

also takes time to switch off when there is excess alkali

33
Q

what do respiratory disorders effecr

A

PCO2

34
Q

what do renal disorders effect

A

HCO3-

35
Q

respiratory acidosis

A

pH has fallen due to respiratory change, so PCO2 must have increased

results from reduced ventilation and so retention of CO2

36
Q

acute causes of respiratory acidosis

A

drugs which depress medullary resp centres e.g. opiates

obstruction of major airways

37
Q

chronic causes of respiratory acidosis

A

lung disease e.g. bronchitis, emphysema, asthma

38
Q

resp acidosis: response

A

need to protect pH so need to increase [bicarb]

renal compensation protects pH but doesn’t correct original disturbance, only restoration of normal ventilation can remove primary disturbance

39
Q

respiratory alkalosis

A

alkalosis of respiratory origin so must be due to fall in PCO2 and this can only occur through increased ventilation and CO2 blow off

40
Q

acute causes of resp alkalosis

A

voluntary hyperventilation
aspirin
first ascent to altitude

41
Q

chronic causes of resp alkalosis

A

long term resifence at altitide

42
Q

response to resp alkalosis

A

dealt with by HCO3- reabsorptive mechanism

if less PCO2 less H+ available for secretion and so less filtered load of bicarb reabsorbed and is lost in urine

venilation must be normalised to correct disturbace

43
Q

metabolic acidosis

A

acidosis of metabolic origin must be due to decrease in bicarb

increase buffering of H+ or direct loss bicarb

to protect pH, PCO2 must be decreased

44
Q

causes of metabolic acidoss

A
  1. inc H+ production: diabetic ketoacidosis, lactic acidosis
  2. failure excrete normal H+ dietary load (renal failure)
  3. loss bicarb in diarrhoea
45
Q

metabolic acidosis response

A

stimulates ventilation so PCO2 falls

normally kidneys correct disturbance by restoring bicarb and getting rid H+

46
Q

increase mtabolic H+ in body: what occurs

A
  1. immediate buffering in ECF and then ICF
  2. resp compensation within minute
  3. renal correction of disturbance takes longer to develop full response

resp compensation delays renal correction but protects pH

47
Q

metabolic alkalosis

A

inccrease bicarbone

need to increase PCO2 to protect pH

48
Q

causes of metabolic alkalosis

A
  1. inc H+ ion loss - vomiting
  2. inc renal loss H+ - aldosterone excess
  3. excess administration of bicarb if pt has renal impairment
49
Q

response to metabolic alkalosis

A

increase PCO2 protects pH

increased bicarb exceeds level of H+ secretion to reabsorb it, so even in presence PCO2 increaed, excess is lost in urine

renal (29 decks)

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