Lecture 8: Acid-base Balance #1 Flashcards

1
Q

What is pH and why is it so tightly regulated?

A

Measure of [H+] in solution.

Tightly regulated so the proteins/moleules can function.

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2
Q

Acidosis (acidemia) and Alkalosis (alkalemia) ranges

**Acidosis and alkalosis are processes that cause abnormal pH

A

pH 7.4 = normal (7.35-7.45)

if pH <7.35 = acidosis
<7.2 = severe acidosis
<6.9 = incompatible with life

If pH >7.45 = alkalosis
>7.6 = severe alkalosis
>7.9 = incompatible with life

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3
Q

Purpose of a Buffer? Equation

A

A weak acid/base solution that minimises pH change due to +/- of H+

Only removes H+ temporarily

pH = pK + log ([base] / [acid])

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4
Q

pK of a buffer is?

A

pH at which the concentrations of A- (base) and HA (buffer) are equal

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5
Q

What are the 2 main buffers in blood?

A
  1. Bicarbonate
    * H+ (40nmol/L) + HCO3- (24mmol/L) ⇔ H20 + CO2*<u>​​</u>
  2. Proteins: albumi, haemoglobin
    * *H+ + A- ⇔ HA**
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6
Q

Why do we have so much H+ to remove?

A

Body metabolism produces large amounts of CO2 every day (>1500mmol/day), that drives

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7
Q

REspiratory control over pCO2?

A
  • Increased pCO2 → acidosis*
  • decreased pCO2 → alkalosis*

Increased pCO2 → acidosis/ low pH → stimulated increase in ventilation → more expired CO2

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8
Q

What does a blood gas analyser measure?

A

pH, pO2, pCO2

bicarbonate and base excess

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9
Q

Types of Respiratory Disturbances

A

CO2 retention (eg; acute asthma)respiratory acidosis
Low pH and High pCO2

CO2 Expiration (eg; hyperventilation)Respiratory alkalosis
High pH and low CO2

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10
Q

Types of Metabolic Disturbances

A

Metabolic Acidosis: Low pH and low HCO3-

Increased acid production → leads to a low HCO3- as the buffer has been ‘used up’ → eventually renal buffers can also be used up.

Metabolic Alkalosis: High pH and high HCO3-

Either due to an increase of HCO3- injestion or Loss of acid (vomiting)

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11
Q

Main causes of Metabolic Acidosis (low pH and HCO3-)

A
  1. Increased Acid Production
    * *- Lactic Acidosis:** hypoxia, poor tissue perfusion (car accident, MI)
    * *- Diabetic Ketoacidosis (DKA):** increased betahydroxybutyric acids
  2. Decreased Acid Excretion
    * *-Renal Failure
    - Renal Tubular Acidosis**
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12
Q

Role of Kidney Buffers in acid-base balance?

A

Can excrete H+ via Renal buffers (just like bicarbonate). These are generally PO43- and NH3

Maintain urinary pH between 5-8

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13
Q

List a few rarer causes of metabolic acidosis

A

Methanol and ethylene glycol poisoning

Glue/paint sniffing

Alcoholic Ketoacidosis

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14
Q

What is Respiratory compensation in metabolic acidosis

A

Normally M. acidosis is a low pH and low HCO3- .
This low pH stimulates ventilation, “acidotic breathing”, lowering pCO2 and balancing the low bicarbonate change.

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15
Q

3 Roles of Kidney in Acid-base balance?

A
  1. Bicarbonate Reabsorbtion (Proximal Tub.)
  2. New Bicarbonate Generation (Proximal Tub., via carbonic Anhydrase)
  3. H+ secretion (distal Tubule)
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16
Q
  1. Proximal Tubule: Bicarbonate Reabsorbtion
A

Filtered HCO3- is reabsorbed across BL membrane similar to Na+

17
Q
  1. Proximal Tubule: New Bicarbonate generation
A

Acetazolamide= carbonic anhydrase inhibitor that causes metabolic acidosis.

Hypervent. → resp. alkalosis →(acetazolamide) → decreased Carbonic anhydrase activity → decreased HCO3- generation→ metabolic acidosis

18
Q
  1. H+ excretion in the distal Tubule
A

ENaC (Na+ epithelial channel) creates a difference across the membrane by driving Na+ reabsorbtion. THis drives K+ and H+ into the distal lumen for excretion

19
Q

how does renal Compensation counteract Resp. acidosis

A

By increasing HCO3- generation in the proximal tubule, restoring the ratio.