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FERGU > Acid/base > Flashcards

Acid/base Flashcards

1
Q

Sources of H+

A 
All from metabolism
Carbonic acid (volatile, H2CO3)
- excreted at lungs
- H+ produced - need CA
-reversed at lungs

Non-carbonic acids (non-volatile, HCl, H2SO4)

  • metabolism of proteins, sulfates, phosphates
  • daily acid load
  • 50-100 mEq/day on normal diet
  • buffered by HCO3-
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2
Q

Buffering systems for H+

A

Intracellular: inorganic phosphates, cystosolic proteins, hemoglobin/RBC
Extracellular: HCO3-/CO2 (primary mechanism), plasma proteins, inorganic phosphates
Bone: important in acidosis, takes up H+, dissolve bone mineral, breaks down carbonate –> bicarb and releases bicarb as buffer

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3
Q

Respiratory compensation for metabolic acidosis

A
  • due to increase in H+ or decrease in bicarb
  • causes decrease in HCO3- concentration
  • increased ventilation –> decrease pCO2, rectifies ([H+] is proportional to pCO2/[HCO3-])
  • H+ ion concentration in plasma determined by pCO2
  • should not be able to completely resolve acidosis

Kusmall breathing: fast, deep –> diabetic ketoacidosis

Rule of thumb: for every decrease in 1 unit of bicarb, should also see 1 unit of decrease in pCO2, otherwise other acid-base issue in play

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4
Q

Respiratory compensation for metabolic alkalosis

A

Decreased ventilation

Not able to fully compensate for alkalosis

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5
Q

Renal compensation for respiratory acidosis

A

decreased ventilation –> increase pCO2
increase renal retention of bicarb
reabsorption of bicarb paired with production & excretion of ammonia

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6
Q

Renal compensation for respiratory alkalosis

A

increased ventilation –> decreased pCO2

increased excretion of bicarbonate

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7
Q

Henderson-Hasselbach

A

pH = 6.1 + log [HCO3-]/0.03(pCO2)

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8
Q

Renal compensation for H+ load

A

regenerates bicarbonate by eliminating H+
for every H+ eliminated, one HCO3- added to ECF
eliminated 50-100 mEq H+ / day

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9
Q

Renal resorption of all filtered bicarbonate

A

Hydrogen ion excretion:

  • not filtered at glomerulus
  • HCO3- filtered at glomerulus
  • H+ secreted by PT and CD into lumen

HCO3- reabsorption

  • all consequence of H+ secretion
  • ~4300 mEq/day filtered
  • almost all reabsorbed - 90% at PT, rest at LOH, CD
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10
Q

Reabsorption of bicarb at PT

A

water –> H+ and OH- in cell
H+ secreted into lumen through Na/H exchanger (gradient by Na/K ATPase)
Lumen: H+ + HCO3- –> H2CO3 –> H2O + CO2
CO2 and H2O passively reabsorbed into cell
Cell: CO2 + OH - –> HCO3- by CA
HCO3- goes to blood by HCO3-/Na+ exchanger

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11
Q

Reabsorption of bicarb at CD

A 
H2O --> OH- and H+ in cell
H+ secreted into lumen via H+ ATPase
H+ + HCO3 --> H2CO3 --> CO2 + H2O (CA)
passively resorbed into cell
CO2 + OH- --> HCO3- by CA
HCO3- moved out of cell into blood via HCO3-/Cl- exchanger
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12
Q

Renal excretion of H+

A

Combination of H+ + titratable acids

Generation of ammonium

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13
Q

Excretion of H+ with titratable acids

A

phosphates
gets used up quickly
once pH < 5.5, all phosphate is in H2PO4- form
PT and CD

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14
Q

Excretion of H+ with phosphate in PT

A

water –> H+ + OH-
H+ secreted through Na+/H+ exchanger
H+ combines with titratable phosphate in lumen –> H2PO4-, excreted
OH- generated in cell combines with CO2 –> HCO3 via CA
HCO3- moves into blood via HCO3-/Na+ exchanger

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15
Q

Excretion of H+ with phosphate in CD

A

water –> OH- + H+ in cell
H+ secreted to lumen via H+ ATPase
OH- + CO2 –> HCO3- via CA in cell
HCO3- moved to blood with HCO3-/Cl- exchanger

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16
Q

Excretion of H+ through ammonium

A

Accounts for ~50% fixed acid load excretion
can increase in response to acid load
NH4+ cant get trapped right away because it isn’t acidic enough
want to avoid losing NH4+ to blood

1) ammonium formation
- hydrolysis of glutamine in PT –> ammonium + alpha-KG
- ammonium excreted into lumen via Na+/NH4+ exchanger
- NH4+ in lumen is in equilibrium with NH3
- AKG –> HCO3- by CA, moved out by HCO3-/Na+ exchanger

2) ammonium reabsorption and recycling
- TAL: ammonium moved into cell in place of K+ through NKCC2
- NH4+ –> NH3 inside cell, NH3 accumulates in interstitium

3) Buffer in CD
- NH3 diffuses from interstitium –> cell –> lumen
- H2O –> OH- + H+
- H+ pumped to lumen via H+ ATPase
- lumen: H+ + NH3 –> NH4+
- NH4+ trapped in urine, excreted
- OH- in cell generates bicarbonate, moved to blood via HCO3-/Cl- exchanger

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17
Q

pH threshold

A

7.4 - above: alkalosis, below: acidosis

18
Q

Bicarbonate threshold

A

Low <12

low pH + low bicarb = metabolic acidosis
high pH + low bicarb = compensation for respiratory alkalosis

19
Q

anion gap

A

Anion gap = [Na+] - [Cl-] - [HCO3-]

Normal add 3 to AG (same threshold)

20
Q

Clinical utility of AG

A

differentiating between different causes of metabolic acidosis

21
Q

Anion-gap metabolic acidosis causes

A 
MUDPILES
Methanol
Uremia
Diabetic ketoacidosis
Paraldehyde/metformin
Iron/isoniazid
Lactic acidosis
Ethylene glycol, ethanol
Salicylates

Presence of acids
Ketoacidosis
Lactic acidosis
- type A: impairment in tissue oxygenation
- type B: no impairment in tissue oxygenation (meds, malignancy, alcoholism, cirrhosis)
renal failure
toxins

22
Q

Non-anion gap metabolic acidosis causes

A

Loss of bicarbonate

GI loss from diarrhea
Renal tubular acidosis
 - impaired reabs at PT
- defective H+ excretion at PT
- aldosterone deficiency/resistance
Dilution acidosis due to rapid ECFV expansion
23
Q

Sx of metabolic alkalosis

A 
Confusion/change in mental status
paresthesias
seizures
muscle cramps/ tetany
Sx related to causes - e.g. vomiting
24
Q

DDx of elevated serum bicarb

A

Metabolic alkalosis
Respiratory acidosis with compensatory metabolic alkalosis

Differentiate with arterial pH:

  • low pH = respiratory acidosis with compensatory metabolic alkalosis
  • high pH = metabolic alkalosis
25
Q

Presentation of metabolic alkalosis

A

increased serum bicarb
increased arterial pH
increased PaCO2 (compensatory respiratory acidosis)
hypokalemia, hypochloremia, hypovolemia also often present

26
Q

Kidney’s role in alkalosis

A

Perpetuates - stimulation of H+ secretion = stimulate bicarb reabsorption, can perpetuate alkalosis

Indirect resorption via H+ secretion/Na+ resorption
- H+ secretion promoted by electronegative lumen
- Na+ resorption promoted by low ECFV, activation of RAAS
New HCO3- generated via glutamine metabolism
CCD: alpha/beta intercalated cells control bicarb resorption
- alpha: H+ secretion
- beta: HCO3- secretion

27
Q

Initiation of metabolic alkalosis

A

1) H+ loss/HCO3- gain
2) Intracellular shift of H+
3) Alkali administration
4) contraction alkalosis

28
Q

Vomiting/nasogastric irritation

A
  • HCl lost
  • parietal cells secrete H+ into stomach, HCO3- into blood
  • loss of neutralization of pancreatic bicarb
  • less Cl- available in urine to exchange with HCO3- in tubular lumen for excretion
  • hypokalemia: alpha-intercalated cell of CCD promotes H+ secretion to take up K+ from lumen, promotes HCO3- return to blood
  • volume depletion: active RAAS promotes hypokalemia - promote Na+ resorption in CCD, increase K+ secretion
  • Na+ resorp –> H+ secretion –> bicarb resorption
  • RAAS also promotes H+ secretion distally, promoting HCO3- resorption
29
Q

renal loss of H, K, Cl

A
  • Diuretics (most common cause of metabolic alkalosis)
  • Primary aldosteronism: hypokalemia, Na+ resorption
  • Bartter’s and Gitelman’s: diuretic-like
  • Posthypercapnic alkalosis: bicarb generated by body due to chronic increase in pCO2 - once pCO2 is corrected, end up with metabolic alkalosis
  • Post-correction alkalosis : give bicarb to treat severe metabolic acidosis –> bicarb load
30
Q

Intracellular shift of H+

A

To compensate for hypokalemia: K+ shifts from ICF –> ECF
to maintain electroneutrality, H+ moves into cell, producing extracellular alkalosis
Causes intracelluar acidosis in PT, promoting HCO3- production, perpetuates metabolic alkalosis

31
Q

Alkali administration

A

Post-correction metabolic alkalosis
Post-hypercapnic metabolic alk
Citrate excess: metabolized to bicarb in liver - massive transfusion

32
Q

Contraction alkalosis/Cl-depletion alkalosis

A

Reduction of ECF with HCO3- staying relatively stable
Also caused by hypochloremia
RAAS

33
Q

Most common initiators of metabolic alkalosis

A

Diuretics
GI loss
Post-hypercapnia
Bicarb administration

34
Q

Maintenance of met alk

A

1) effective circulating vol depletion
2) hypokalemia
3) chloride depletion

35
Q

Effective circulating vol depletion

A

lowered GFR - less HCO3- filtered
RAAS activation
- AngII: upreg of H+ ATPase in PCT and CCD
- aldosterone: ENaC in CCD - electronegative lumen, H+/K+ secretion

36
Q

Hypokalemia - maintenance

A

Leads to intracellular acidosis
increased distal resorption of K+ in CCD
- H/K ATPase
- secretion of H+

37
Q

Chloride depletion - maintenance

A

luminal hypochloremia

  • stimulates RAAS
  • reduced activity of Cl/HCO3- exchanger
38
Q

AII in acid-base

A

activated by low ECFV or reduced NaCl concentration in ultrafiltrate
increase activity of Na/H antiporter in apical PT
increased activity of Na/3HCO3- antiporter in basolateral PT
H+ secretion, HCO3- reabsorption

39
Q

Aldosterone in acid-base

A

increase Na/K ATpase in basolateral side of DT and CD, creating Na+ gradient –> increase Na resorption
electronegative lumen = secrete K+, H+
H+ secretion, HCO3- reabsorption

40
Q

Cortisol in acid-base

A

release stimulated by acidosis

H+ secretion, HCO3- retention

41
Q

PTH in acid-base

A

stimulated by acidosis

increases inorganic phosphate excretion in urine, promoting H+ excretion

FERGU (14 decks)

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