11 + 12 - Acid and Base Flashcards

1
Q

What is a buffer

A

solution that can resist pH change upon the addition of an acid or a base. Able to neutralize small amounts of added acid or base, thus maintaining the pH of the solution relatively stable.

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2
Q

What makes up a buffer

A

Consist of a weak acid and the salt of that acid functioning as a weak base

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3
Q

Where is HCO3- reabsorbed mainly

A

PCT

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4
Q

What do alpha intercalated cells excrete (DT)

A

secretes acid, absorbs bicarb

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5
Q

What do beta intercalated cells excrete and absorb

A

Secrete bicarb

absorb acid

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6
Q

What is the cause of metabolic alkalosis

A

Increased bicarb production/reduced excretion

Decreased production of H+ or excretion of H

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7
Q

Causes of H+ loss

A

Low chloride - Diuretics which inhibit chloride resorption
= Volume depletion results in secondary hyperaldosteronism as a result there is increased exchange of sodium for K and H, K depletion further promotes H excretion
Low K+
= Hyperaldosterone
= Liquorice
= Barters, liddles, gitelmans

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8
Q

Causes of alkali intake

A

Milk/alkali syndrome

Bicarb therapy

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9
Q

Cause of metabolic acidosis

A

an excess of hydrogen ions, can result either from an excess production of hydrogen ions, a loss of bicarbonate/ failure to regenerate bicarbonate in the kidney.
o ‘metabolic acidosis’.

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10
Q

Normal anion gap

A

12-16

12 if K+ excluded

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11
Q

Raised anion gap acidosis

A

o Bicarbonate goes down

o Increase in unmeasured anion

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12
Q

Causes of increased anion gap

A
o	Methanol intoxication
o	Uremia
o	Isoniazid or Iron overdose
o	Salicylate intoxication	
o	Ketoacidosis		
o	Methanol
o	Aldehyde (paraldehyde)
o	Lactate
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13
Q

Normal anion gap acidosis

A

o Chloride increases but bicarb decreases because chloride is swapped for bicarb via an antiport

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14
Q

Renal causes of normal gap acidosis

A

 Renal Tubular Acidosis (cannot excrete H+)

 Carbonic anhydrase inhibitors

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15
Q

GI causes of normal anion acidosis

A

 Severe diarrhoea (loss of bicarb)
 Uretero-enterostomy or Obstructed ileal conduit
 Small bowel fistula

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16
Q

Other causes of normal anion gap acidosi

A

 Losses via NG tube
 Villous adenoma
 Recovery from DKA
• Ketone anions secreted as potassium/sodium salts
• Chloride ions retained to maintain electrical neutrality

17
Q

Low gap acidosis

A

 Decrease in Unmeasured anion (e.g. loss of albumin)
• Haemorrhage
• Liver cirrhosis
• Nephrotic syndrome.

18
Q

In PCT

CA and bicarb ting (draw it out)

A
  • In the lumen, CA converts H+ and bicarbonate into carbonic acid, the pumping out of the hydrogen atoms via Na/H pump pushes the equation to the left producing H2O and CO2.
  • Water and carbon dioxide diffuses into the cell where the equation to the right is favoured as the H+ is constantly being pumped out
  • The water and carbon dioxide form carbonic acid which then breaks down into bicarb and acid. The bicarb cannot leave through the lumen so it is pumped into the interstitium via the Na+/HCO3¬¬¬-
19
Q

Normal pH

A

7.35 to 7.45

20
Q
  • Formation of H+ from cellular metabolism
A

o Acids produced during the breakdown of foods (esp. proteins)- 60 mmol/d
o CO2 metabolically produced and form carbonic acid with H2O- 15 mol/d,
o Acids resulting from other metabolic activity e.g. lactic acid in exercise- 1.5 mol/d
o In disease state, even more ketoacids

21
Q

Methanol poisoning forms what acid

A

formic acid

22
Q

Ethylene glycol forms what acid

A

Glycolic acid + oxalic acid

23
Q

CO poisoning, drugs form what acid

A

Lactic acid

24
Q

How does acidaemia lead to hyperkalaemia

A

tissues release K+ from within the cells
o Potassium swapped and replaced by the H+ and in order to maintain electroneutrality.
 H+ taken up by cells to reduce serum H+.