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Sita GenitoUrinary System > Lecture 17: Acid Base 2 > Flashcards

Lecture 17: Acid Base 2 Flashcards

1
Q

Three step approach to interpreting acid base data

A
  1. Acidosis or alkalosis
  2. metabolic or respiratory
  3. compensated or not (looking at non/primary component)
    - inappropriate compensation –> hint at mixed disorder
    ..
  4. anion gap (yes = metabolic acidosis)
  5. change in anion gap (yes = co-existing metabolic alkalosis and acidosis)
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2
Q

Base excess BE

A

Calculated measure/parameter (experimental construct = reflects metabolic change) –> pH, pCO2, and Hb haemaglobin
The amount of acid or base needed to restore pH to 7.4
Normal Base excess = 0 (-2 2)
BE = base excess =
1. +ve in alkalosis (too +ve, needs more acid to restore to normal)
2. -ve in acidosis (too -ve pH, needs more base to restore to normal)

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3
Q

Chronic lung disease + ventilator

A
  1. Admitted –> High HCO3- + High BE –> w. Respiratory acidosis + Renal compensation
    Chronic lung disease –> COPD –> obstruction causes decreased CO2 expiration –> admitted as respiratory acidosis
    Renal compensation = +10 BE
  2. –> Ventilator –> increase minute ventilation –> increased CO2 expiration –> respiratory acidosis fixed
    Note: still have BE +10 –> Metabolic alkalosis remains –> POST HYPERCAPNIC ALKALOSIS
    Note 2: Kidneys take a longer time course to begin compensating –> therefore if renal compensation is occurring is a chronic condition –> post hypercapnic (respiratory acidosis) alklaosis
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4
Q

Meaning of Post Hypercapnic Alkalosis

A

COPD:
Post (after) Hypercapnic (High H+ acid from respiratory acidosis) Alkalosis (high BE from renal compensation, which remains after acidosis is fixed by ventilator-increased-minture-ventilation-expiration-of-CO2)

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5
Q

Anion Gap AG

A

AG = difference b/w Cations and anions in blood
(calculated parameter)
Normally reflects unmeasured Protein anions
Normal conditions= cation and anion difference EXCLUDING PROTEINS is equal as reflects ELECTRO NEUTRALITY –> therefore normal range is 14-18 as Protein charge tends to be 16
AG = (cations) - (anions) = (Na + K) - (Cl + HCO3-)
= (140 + 4) - (104 + 24) = 16 = Protein difference = electronuetrality of 0 as Proteins compensate/balance to 0 difference when included in equation
(Na + K) = EQUAL/0 difference = (Cl- + HCO3- + Protein)
Acid in blood –> dissociates in Anion + H+ –> increased difference b/w cations and anion in blood –> increased anion gap
Therefore: out of/above normal AG range = Presence of UNMEASURED ANIONS –> presence of added acid –> Metabolic ACIDOSIS
e.g. Na+ + K+ = Cl- + HCO3- + Protein + Lactate
Note: Lactic acid has dissociated into H+ and a Anion –> therefore contribute to the Anion side of the electroneutrality equation

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6
Q

Why dont you want a change in the Anion Gap?

A

As you want blood to be ELECTRONEUTRAL (want a balance b/w acids and bases in blood) so can have SAME pH

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7
Q

What is the main protein which causes Proteins to have an anion charge of 16

A

Albumin concentration

  • can be a major determinant if protein anion charge changes
  • therefore different reference ranges to compensate for this
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8
Q

What is AG useful for?

A

Metabolic Acidosis
As it is only an increase in metabolic acid forms which increases the concentration acid which dissociates into anions and H+

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9
Q

With the addition of Metabolic acid, what causes the changes in HCO3- and Protein levels?

A

Want to return to 16 balance –> need to decrease anion side of equation –> composed of Cl- and HCO3- and Protein and new metabolic acid –> HCO3- and Protein levels decrease acting as protein buffers –> balances out sides of equation to remain equal = keeps electroneutrality of 0 = keeps pH of 7.4

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10
Q

Electronuetrality equation vs Anion gap equation

A
  1. Anion gap uses the values of Meaurable substances –> forming a value which shows presence of immeasurable substances
    AG = (cations) - (anions) = (Na + K) - (Cl + HCO3-)
    = (140 + 4) - (104 + 24) = 16 = Protein difference
  2. Electroneutrality equation shows the compensation by both the measurable and immeasurable substances
    Electroneutrality of 0 –> illustrates renal compensation by body = (cations) - (anions + proteins + Metabolic acid) = (Na + K) - (Cl + HCO3- + Proteins + Metabolic acid)
    = (140 + 4) - (104 + 24) = 16 = Protein difference
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11
Q

Causes of Acidosis

A
  1. Lactic Acidosis: hypoxia, poor diffusion, drugs
  2. Ketoacidosis: Beta-hydroxbutyrate (ketone body) as main anions (diabetic/alcohol/starvation)
  3. Renal Failure: retention of phosphate and sulphate –> slightly increased AG
    …
  4. Methanol poisoning (formate anion) e.g. moonshine
  5. Ethylene glycol poisoning (glycolate anion, lgyoxylate, oxalate anions) e.g. suicide attempt via antifreeze poisoning
  6. Salicylate (aspirin) overdose –> causes respiratory acidosis
  7. Organic acidurias (children) e.g. methylmalonic aicduria (inheritable)
  8. Pyroglutamic aciduria (adults)
  9. Toxic ED
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12
Q

What is the causative pathway of lactic acid production?

A

Lactic acid is produced due to occurrence of ANAEROBIC METABOLISM
Hypoxia/poor tissue diffusion/drug –> decrease in O2 –> anaerobic metabolism –> Lactic acid production –> dissociates into lactate + H+ –> increase in anion gap (immeasurable protein and metabolic anions) –> greater difference b/w cations Na + K and main measurable anions Cl- and HCO3-

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13
Q

Metabolic acidosis with respiratory compensation vs renal compensation

A

Metabolic acidosis = too much acid = -ve BE
Respiratory compensation = Change in CO2 (decrease) –> Know is primarily Metabolic as has biggest change
Renal compensation = change in HCO3- (decrease due to attempted buffer)

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14
Q

Continued tests on semicomatos, seizuring, metabolic acidosis patient

A

Normal lactic acid (not due to hypoxia/poor tissue diffusion induced anaerobic metabolism)
Normal batehydroxybuturate (not due to diabetic ketoacidosis)
Ethylene glycol poisoning (suicide attempt ia drinking ANTIFreeze
Treatment:
1. Ethanol: inhibits alcohol dehydrogenase metbaolism of ethylene glycol into toxic substances
2. Dyalisis: especially if toxic metabolites are all through the body and need removal

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15
Q

Ethylene glycol

A

Non-toxic shelf substance –> alcohol dehydrogenase –> metabolised to Glycolic and OXALIC acids –> metabolic acidosis –> attempted suicide –> treat with ethanol –> inhibition of alcoholic ehydrogenase –> ethelyene glycol
Good: enzyme alcohol dehydrogenase normally metabolises alcohol –> dont get hangover
Bad: alcohol dehydrogenase metabolises ethylene glycol –> glycolic acid + oxalic acid –> metbaolic acidosis
Note: Ethanol and FOMEPRIZOLE competitively inhibit ethanol dehydrogenase enzyme –> treatment –> toxic products not formed from non-toxic ethylene glycole

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16
Q

Child with Rickets and Failure to thrive (growth delay)

A

Bow legged + Ineffective metabolism (failure to grow/thrive) –> potentially and increase in ENDOGENOUS acid
- normal Na + K
- Increase Cl (HYPERCHLOERMIC) -> not pumped out
- lower acidemic pH
- decreased CO2 (smaller decrease = respiratory compensation)
- biggest decrease bicarbonate (primary metabolic acidosis)
- -ve base excess
Anion gap = 17 (increase in metabolic acid)

17
Q

Causes for relatively Normal Anion Gap + Hyperchloremic acidosis

A
  1. Renal Tubular Acidosis
  2. Aldosterone deficiency or resistance (RTA type 4) (Addison’s disease)
  3. GI bicarbonate loss
  4. Glus/Paint sniffing
18
Q

Renal tubular acidosis

A

Kidney/Renal Defects –> decreased acid excretion

  • increased pH or urine
  • SAME urine AMMONIUM (not increased –> therefore not metabolic acidosis)
  • INCREASED CL- (not pumped out)
  • proximal and distal
  • assoc. with rickets and hyperkalemia
  • potentially also associated with other renal tubular defects such as PT tubular defect in Fanconi sydrome
19
Q

Aldosterone deficiency or resistance (RTA type 4)

A

ADDISONS DISEASE

  1. congenital adrenal hyperplasia syndrome –> enzyme blocking aldosterone production
  2. Renin deficiency –> diabetic neuropathy
  3. Aldosterone resistance (pseudohypoaldosteronism)
20
Q

GI bicarbonate loss

A

Diarrohea/Intestinal/fistula/ileostomy
Acute –> decrease in Na /HCl
Chronic –> decrease in Bicarbonate

21
Q

Glue/paint sniffing

A

Toulene metabolized to hippuric acid –> Hypercalemic acidosis

22
Q

Meaning of Ammonium levels

A

Metabolic acidosis: UAG NEGATIVE –> INCREASED presence of AMMONIUM –> inappropriate acidification
RTA: UAG positive: same NH4 (SAME) –> RTA renal tubular acidosis –> as ammonium not effected –> rickets

23
Q

Normal anion gap acidoses reason for being hyperchloremic

A

Low HCO2- –> Extra Cl- absorbed –> maintained Na balance –> pH/osmolality maintained within 1-2% range

24
Q

Link between potassium and Acid-base. First link via shift of H+ and K+ into and out of cells

A

Relationship b/w H+ ions (move into cells) and K+ ions moving out of cell
Acidosis –> Hyperkalemia (+ increased H+ and decreased pH)
Alkalosis –> Hypokalemia
1: Primary Acidosis –> H+ START moving into cell to try buffer/decreased acid H+ levels –> Causes Secondary Hyperkalemia –> drives an increased K+ movement out of cell
2. Primary Hyperkalemia –> Increased K+ movements out of cell –> Secondary Acidosis –> H+ START moving into cell
3. Primary alkalosis –> H+ START moving out of cell into plasma to buffer/increased alkalotic H+ levels –> causes Secondary hypokalemia –> drives K+ into cell to balance H+ loss inside
4. Primary Hypokalemia –> K+ start moving out of cell to increase plasma K+ concentration –> Causes Secondary Alkalosis –> H+ movement driven into cell to try and balance K+ loss inside cell

25
Q

Link between potassium and acid base: Second link via H+ and K+ competing with each other for secretion

A

When one is slightly high –> the other is preferentially secreted
Na out –> compensated by either H and K in –> relatively more in by the one more out of balance –> Electronuetrality

26
Q

Overall link b/w Potassium and acid base balance

A
  1. Shift of H+ and K+ into and out of cells
  2. Relationship of H+ and K+ pumping opposite way of Na+ –> trying to maintain within 1-2% stable osmolality range –> preferentially secretion which every ion (H+ or K+ is relatively more our of balance) –> maintained electroneutrality and hence pH and hence osmolality
    Exceptions:
  3. Diarrohia (Bicarbonate AND K+ loss)
  4. Renal Tubular Acidosis (DT and PT types –> both associated with Hypokalemia)

Sita GenitoUrinary System (28 decks)

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