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PHYSIOLOGY IV > LECTURE 14 (Acid-base balance) > Flashcards

LECTURE 14 (Acid-base balance) Flashcards

1
Q

How does the Acid-base balance maintain normal hydrogen ion concentration in body fluids?

A
  • Utilisation of buffers in extracellular and intracellular fluid
  • Respiratory mechanisms that excrete carbon dioxide
  • Renal mechanisms that reabsorb bicarbonate + secrete hydrogen ions
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2
Q

What is the difference between an Acid and a Base?

A

Acid = any compound which forms H+ ions in solution (proton donors)

Base = any compound which combines with H+ ions in solution (proton acceptors)

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3
Q

How is H+ concentration usually expressed as a logarithmic function?

A

pH = -log10[H+]

EXPLANATION:
- minus sign - as H+ concentration increases, pH decreases (vice versa)
- logarithmic relationship, not linear - equal changes in pH do not reflect equal changes in H+ concentration

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4
Q

What is the normal range of arterial pH?

A

7.37 to 7.42

  • pH < 7.37 = acidemia
  • pH > 7.42 = alkalemia
  • pH range compatible with life = 6.8 to 8.0
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5
Q

What are the mechanisms maintaining normal pH?

A
  • Buffering of H+ in ECF and ICF
  • Respiratory compensation
  • Renal compensation
  • Buffering and respiratory compensation occur rapidly (minutes to hours)
  • Renal compensation is slower (hours to days)
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6
Q

What are the two types of acids produced in the body?

A
  • Volatile acid
    [CO2 produced from aerobic metabolism of cells; combines with H2O to form H2CO3 “CARBONIC ACID”, which dissociates into H+ and HCO3- “BICARBONATE ION” (a reversible reaction catalysed by CARBONIC ANHYDRASE)]
  • Non-volatile acid/”fixed acids”
    [e.g sulphuric acid, ketoacids, lactic acid, salicylic acid - produced from catabolism of proteins and phospholipids]
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7
Q

What is the difference in transport and excretion between Volatile acids and Non-volatile acids?

A

Volatile acids = CO2 produced by cells is added to venous blood, converted to H+ and HCO3- in red blood cells and carried to lungs where CO2 is regenerated and expired

Non-volatile acids = Buffered in body fluids until excreted by kidneys

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8
Q

How are Ketoacids, Lactic acid and Ingested acids produced?

A
  • Ketoacids = B-hydroxybutyric acid and Acetoacetic acid in untreated diabetes mellitus
  • Lactic acid = Generated during strenuous exercise or hypoxia
  • Ingested acids = Salicylic acid from aspirin overdose, Formic acid from methanol ingestion and Glycolic & Oxalic acids from ethylene glycol ingestion

ADDITIONAL INFO: Overproduction or ingestion of fixed acids leads to metabolic acidosis

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9
Q

What is a buffer?

A

A mixture of a weak acid and its conjugate base or a weak base and its conjugate acid that prevents a change in pH when H+ ions are added to or removed from a solution

ADDITIONAL INFO: In Bronsted-Lowry, a weak acid is “HA” and is the H+ donor, base is A-. A weak base B and BH+ is the H+ donor.

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10
Q

What is the function of a buffered solution?

A

To resist a change in pH
[H+ can be added to or removed from a buffered solution but the pH will change only minimally]

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11
Q

What is the Henderson-Hasselbach equation to calculate pH?

A

pH = pK + log [A-]/[HA]

  • A- is the base of the buffer (H+ acceptor)
  • HA is the acid of the buffer (H+ donor)
  • When the concentrations of A- and HA are equal, the pH of the solution equals pK of the buffer
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12
Q

What is pK and what determines it?

A

Equilibrium constant is the ratio of the rate constant of the forward reaction divided by the rate constant of the reverse reaction

WHAT DETERMINES IT?
- Strong acids are more dissociated into H+ and A- -> high equilibrium constants -> low pKs
- Weak acids are less dissociated -> low equilibrium constants -> high pKs

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13
Q

Describe what a titration curve shows

A
  • As H+ ions are added to solution, the HA form is produced; as H+ ions are removed, the A- form is produced
  • A buffer is most effective in the linear portion of the titration curve
    [where addition or removal of H+ causes little change in pH]
  • When the pH of solution equals the pK, the concentrations of HA and A- are equal (Henderson-Hasselbach equation)
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14
Q

What are the different extracellular buffers?

A
  • HCO3- produced from CO2 and H2O (major extracellular buffer)
    [pK of CO2/HCO3- buffer pair is 6.1]
  • Phosphate (a urinary buffer; excretion of H+ as H2PO4- is “titratable acid”)
    [pK of H2PO4-/HPO42- is 6.8]
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15
Q

What are the different intracellular buffers?

A
  • Organic phosphates
  • Proteins
    (haemoglobin is a major intracellular buffer; in physiologic pH range, deoxyhaemoglobin is a better buffer than oxyhemoglobin)
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16
Q

What are the properties of the Carbonic acid-Bicarbonate buffer system?

A
  • Prevents changes in pH caused by organic acids and fixed acids in ECF
  • Cannot protect ECF from changes in pH that result from elevated or depressed levels of CO2
  • Functions only when respiratory system and respiratory control centers are working normally
  • Ability to buffer acids is limited by availability of bicarbonate ions
17
Q

What are the properties of the haemoglobin buffer system?

A
  • Helps prevents major changes in pH when plasma PCO2 is rising or falling
  • The only intracellular buffer system with an immediate effect on ECF pH

MOA:
1) CO2 diffuses across RBC membrane (no transport required)
2) Carbonic acid dissociates + bicarbonate ions diffuse into plasma in exchange for chloride ions “CHLORIDE SHIFT”

18
Q

What are the properties of the Phosphate buffer system?

A
  • Consists of anion H2PO4- (a weak acid) + works like the carbonic acid-bicarbonate buffer system
  • Important in buffering pH of ICF

LIMITATIONS:
- Provide only a temporary solution to acid-base imbalance
- Do not eliminate H+ ions
- Supply of buffer molecules is limited

19
Q

What are the properties of the Respiratory acid-base control mechanisms?

A
  • When chemical buffers cannot prevent changes in blood pH -> respiratory system is the SECOND LINE of defence against changes
  • Eliminate or retain CO2
  • Change in pH are RAPID
  • Occur within minutes
20
Q

What are the properties of the Renal acid-base control mechanisms?

A
  • THIRD LINE of defence against changed in body fluid pH
  • Long term regulator of ACID-BASE balance
  • May take hours to days for correction

MOA:
- movement of bicarbonate
- retention/excretion of acids
- generating additional buffers

21
Q

What are the roles of kidneys in Acid-base balance?

A
  • Reabsorption of HCO3- (bicarbonate ions)
  • Excretion of H+
    [excretion of H+ as titratable acid (buffered by urinary phosphate), excretion of H+ as NH4+ (accompanied by synthesis + reabsorption of new HCO3-)]
22
Q

Describe the reabsorption of filtered HCO3-

A
  • Almost 99.9% of filtered HCO3- is reabsorbed (ensures conservation of major extracellular buffer)
  • Reabsorption primarily occurs in PROXIMAL TUBULE
  • Minimal reabsorption in loop of Henle, distal tubule and collecting duct

MOA:
1) Na+-H+ exchanger in luminal membrane
[Na+ moves into cell down its electrochemical gradient + H+ moves into lumen against electrochemical gradient]
2) Catalysed by CARBONIC ANHYDRASE on brush border, H+ combines with HCO3- to form H2CO3 -> H2CO3 decomposes into CO2 and H2O which enter the cell
3) Inside the cell, CO2 and H2O recombine to form H2CO3 catalysed by intracellular CARBONIC ANHYDRASE -> H2CO3 decomposes into H+ and HCO3- -> H+ is secreted by Na+-H+ exchanger to aid in reabsorption of another filtered HCO3- -> HCO3- is transported into the blood via Na+-HCO3- cotransport and Cl- HCO3- exchange

23
Q

What are the special features of HCO3- reabsorption?

A
  • Net reabsorption of Na+ and HCO3-
  • No net secretion of H+
  • Little change in tubular fluid pH
24
Q

What are the factors affecting HCO3- reabsorption?

A
  • Filtered load of HCO3-
    [when plasma HCO3 reabsorption mechanism is saturated, excess HCO3 is excreted]
  • Extracellular fluid (ECF) volume
    [ECF volume EXPANSION inhibits isosmotic and HCO3 reabsorption + ECF volume CONTRACTION stimulates isosmotic and HCO3 reabsorption + Involves angiotensin II stimulating Na+-H+ exchange + Explains contraction alkalosis]
  • Effect of PCO2
    [Increased PCO2 increases HCO3- reabsorption (respiratory acidosis compensation) + Decreased PCO2 decreases HCO3- reabsorption (respiratory alkalosis compensation)]
25
Q

What is the mechanism of excretion of Titratable acid?

A

Located primarily in the a-intercalated cells of the LATE DISTAL TUBULE and COLLECTING DUCTS

MOA:
1) H+ secretion (active transport by H+ ATPase [stimulated by aldosterone] and H+-K+ ATPase [responsible for K+ reabsorption] -> secreted H+ combines with HPO42- to form H2PO4-
2) Production of H+
[H+ produced from CO2 and H2O forms H2CO3 with CARBONIC ANHYDRASE which dissociates into H+ and HCO3- (reabsorbed into the blood via Cl- HCO3- exchange)
3) Synthesis and reabsorption of HCO3-
[for each H+ excreted, one new HCO3- is synthesised and reabsorbed]

26
Q

What is the mechanism of excretion of H+ as NH4+?

A

LOCATION:
- proximal tubule
- thick ascending limb (of loop of Henle)
- a-intercalated cells of the collecting ducts

MOA:
PROXIMAL TUBULE
1) Glutamate is metabolised to a-ketoglutarate, then to CO2 and H2O forming HCO3- -> HCO3- reabsorbed into blood via Na+-HCO3- co-transport
2) NH3 diffuses from cell to lumen -> H+ secreted into lumen on Na+-H+ exchanger -> NH3 and H+ recombine to form NH4+
3) Some NH4+ is excreted into urine, some is reabsorbed by thick ascending limb to be secreted in collecting ducts for final excretion

THICK ASCENDING LIMB
NH4+ reabsorbed by substituting for K+ on Na+-K+-2Cl- co-transporter -> concentrated in interstitial fluid of inner medulla and papilla

COLLECTING DUCT
NH3 diffuses from medullary interstitial fluid into lumen + combines with secreted H+ to form NH4+ which is trapped in tubular fluid and excreted
[H+ is from H2CO3 that dissociates into H+ and HCO3-]

27
Q

What is the effect of urinary pH on NH4+ excretion?

A
  • Lower urinary pH increases NH4+ excretion
  • Acidosis leads to increased H+ excretion
  • Lower pH favours NH3 diffusion from medullary interstitial fluid into tubular fluid
28
Q

What is the effect of acidosis on NH3 synthesis?

A
  • Chronic acidosis increases NH3 synthesis
  • Decrease in intracellular pH induces synthesis of glutamine metabolism enzymes
  • More H+ excreted as NH4+, more new HCO3- reabsorbed
29
Q

What is the effect of Hyperkalemia on NH3 synthesis?

A
  • Inhibits NH3 synthesis
  • Reduces H+ excretion as NH4+
  • Causes type 4 renal tubular acidosis (RTA)

MECHANISM:
K+ enters renal cells, H+ leaves, increases intracellular pH and inhibits NH3 synthesis

30
Q

What is the effect of Hypokalaemia on NH3 synthesis?

A
  • Stimulates NH3 synthesis
  • Increases H+ excretion as NH4+

MECHANISM:
K+ leaves renal cells, H+ enters, decreases intracellular pH, stimulates NH3 synthesis

31
Q

What is the difference between Acidemia and Alkalemia?

A

Acidemia = an increase in H+ concentration in blood (decrease in pH) caused by acidosis

Alkalemia = A decrease in H+ concentration in blood (increase in pH) caused by alkalosis

32
Q

What is the difference between respiratory acidosis and alkalosis?

A

Respiratory acidosis = caused by hypoventilation which results in CO2 retention, increased PCO2 and decreased pH

Respiratory alkalosis = caused by hyperventilation which results in CO2 loss, decreased PCO2 and increased pH

33
Q

What are the four basic types of imbalance?

A
  • Metabolic acidosis
  • Metabolic alkalosis
  • Respiratory acidosis
  • Respiratory alkalosis
34
Q

Describe metabolic acidosis

A

Overproduction or ingestion of fixed acid or loss of base produces a decrease in arterial [HCO3-]

COMPENSATION:
- hyperventilation (Kussmaul breathing)
- increased excretion of excess fixed H+ as titratable acid and NH4+ and increased reabsorption of HCO3-
- In chronic metabolic acidosis, increase in NH3 synthesis increases excretion of excess H+

35
Q

Describe metabolic alkalosis

A

Loss of fixed H+ or gain of base produces an increase in arterial [HCO3-]

COMPENSATION:
- Hypoventilation
- Excretion of HCO3-

ADDITIONAL INFO:
If metabolic alkalosis is accompanied by ECF VOLUME CONTRACTION, the reabsorption of HCO3- increases, worsening the metabolic alkalosis

36
Q

Describe Respiratory acidosis

A

Caused by decreased alveolar ventilation and retention of CO2 causes an increase in [H+] and [HCO3-]

COMPENSATION:
- no respiratory compensation
- renal compensation (occurs in CHRONIC respiratory acidosis, not acute) consists of increased excretion of H+ as titratable acid and NH4+ and increased reabsorption of HCO3-
[H+ is aided by increased PCO2]

37
Q

Describe Respiratory alkalosis

A

Caused by increased alveolar ventilation and loss of CO2 which causes a decrease in [H+] and [HCO3-] by mass action

COMPENSATION:
- no respiratory compensation
- renal compensation (only occurs in CHRONIC respiratory alkalosis) consists of decreased excretion of H+ as a titratable acid and NH4+ and decreased reabsorption of HCO3-
[process aided by decreased PCo2]

PHYSIOLOGY IV (14 decks)

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