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acid regulation Flashcards

1
Q

what is the importance of ph on the body?

A
  • pH has an effect on the 3D structure of proteins
  • Controls the speed of enzyme activity
  • Controls the speed of electrical reactions – synaptic function depends on intra + extracellular pH gradients
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2
Q

what is an acid?

A

proton donor

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3
Q

what is a base?

A

proton acceptor

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4
Q

what is the pH of gastric juice?

A

pH 2

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5
Q

what is the pH of urine and saliva?

A

pH 6

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6
Q

what is the pH of pure water, human blood, tears?

A

pH 7

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7
Q

what is the pH of the small intestines?

A

pH 8

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8
Q

what should the pH of normal blood be?

A

7.35 to 7.45

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9
Q

what is the pH of venous blood and why?

A

Venous blood is slightly acidic bc it picks up the CO2 made by the tissues –> converted to carbonic acid

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10
Q

when does acidemia occur?

A

when the pH is below 7.35

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11
Q

when does alkalemia occur?

A

when the pH is above 7.45

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12
Q

in what pH range can death occur?

A

below 6.8

above 8.0

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13
Q

what diets produce more acids than bases?

A

diets high in proteins

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14
Q

what processes form acid in the human body? what acids are formed?

A

o Produced from breakdown of foods (e.g. proteins)
 Oxidation of sulfur-containing amino acids  sulfuric acid
 Acid in diet produces about 60mmol/day
o CO2 + H2O  carbonic acid
 15 mol/day of CO2 leads to carbonic acid production
o Anaerobic respiration of glucose –> lactic acid
o Incomplete oxidation of fatty acids –> acidic ketone bodies
o Hydrolysis or phosphoproteins and nucleic acids –> phosphoric acids

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15
Q

which diseases can produce more acid and what acid do they produce?

A

o Uncontrolled diabetes, starvation –> acetoacetate B-hydroxybutyrate
o Liver disease –> impaired lactate clearance –> lactic acid

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16
Q

what mechanisms regulate concentrations of H+?

A
  • Chemical buffer systems in blood and ICF (immediate action)
  • Respiratory centre in the brainstem (acts within 1-3 mins)
  • Renal mechanisms (requires hours to days to affect pH changes)
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17
Q

what is a buffer?

A

can resist changes in pH when small amounts of acid or base are added.
• Acts quickly (but temporarily) to bind/release H+
• Consists of a weak acid + salt of that acid (acts as a weak base)

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18
Q

what are the 3 major chemical buffer systems in the body?

A 
o Bicarbonate (HCO3-) buffer system (main)
o Proteins (hemoglobin & albumin) buffer system 
o Phosphate (P043-) buffer system
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19
Q

what effect does acidaemia have on potassium?

A

Acidemia leads to hyperkalemia (tissues release K+)

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20
Q

what effect does alkalaemia have on potassium?

A

Alkalaemia leads to hypokalaemia (tissues take up K+)

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21
Q

what are cations?

A

+ve ions

22
Q

what are anions?

A

-ve ions

23
Q

name unmeasured cations

A

calcium
magnesium
proteins

24
Q

name unmeasured anions

A

phosphates
sulfate
proteins

25
Q

what does the anion gap calculate?

A

measures how many ions aren’t accounted for – unmeasured ions are mainly anions (hence why it’s called the anion gap)

26
Q

how do you calculate the anion gap? what should it normally be?

A

(Na+) – ([Cl-] + [HCO3-]) = 8 to 12 mEq/L

27
Q

why is the anion gap measured without potassium?

A

so small it’s irrelevant

28
Q

how does normal gap metabolic acidosis occur?

A
  • Big drop in HCO3- and an increase in Cl- –> anion gap doesn’t show a change
  • Cl- is exchanged for a HCO3- to maintain the electroneutrality of the body
  • HCO3- bc it’s being used to buffer the acid
29
Q

name causes of normal gap metabolic acidosis

A

severe diarrhoea, type 1 and 4 renal tubular acidosis and chronic laxative abuse

Also; villous adenoma, external drainage of pancreatic/biliary secretions; losses via NG tubes; administration of acidifying salts; urinary diversions

30
Q

what is normal gap metabolic acidosis seen in?

A

loss of bicarbonate

reduced kidney H+ excretion

31
Q

how does elevated gap acidosis occur?

A
  • drop in HCO3-
  • isnt compensated for by the surge of Cl-
  • isnt compensated for bc there’s either a pathological amount of H+ or not enough HCO3-
32
Q

why is there a high anion gap in elevated gap acidosis?

A
  • no surge in Cl- to compensate for the decrease in HCO3-
  • low levels of Na+ and K+
  • unmeasured anions increase
33
Q

what causes elevated gap acidosis?

A

ketoacidosis, lactic acidosis, renal failure, toxic ingestions

34
Q

what is the major unmeasured anion?

A

albumin

35
Q

what is low gap acidosis linked to?

A

hypoalbuminaemia

causes a surge in HCO3- and Cl-

36
Q

what are the causes of low gap acidosis?

A

haemorrhage, nephrotic syndrome, intestinal obstruction and liver cirrhosis

37
Q

how does haemorrhage lead to low gap acidosis?

A

Haemorrhage leads to acidosis bc you lose blood –> less O2 –> anaerobic respiration –> lactic acid –> acidosis

38
Q

what can cause metabolic acidosis?

A

vomiting or diuretic use

39
Q

how does the serum anion gap change in metabolic acidosis?

A

small increase in the serum anion gap - approx 4-6 mEq/L

40
Q

how does the serum anion gap change in respiratory alkalosis?

A

doesnt change notably

41
Q

what are the 2 main roles of the kidneys in metabolic acidosis?

A

o Reabsorption of all filtered bicarbonate

o Excrete the daily acid load

42
Q

how does the kidney get rid of metabolic acids?

A

o Hydrogen secretion
o Bicarbonate reabsorption
o Excretion of H+ ions with urinary buffers

43
Q

where is bicarbonate reabsorbed and how?

A

reabsorbed by the PCT via carbonic anhydrase (converts CO2 and H2O to bicarbonate)

44
Q

how is H+ excreted in the distal kidney?

A

o Via ATP pump (main way)
o Swapped for Na+
o Proton-potassium pump – hence why hyer/hypokalaemia is linked to acidosis

45
Q

what do a-intercalated cells do and how?

A
  • Secretes acid as H+ ions (via an apical H+-ATPase and H+/K+ exchanger)
  • Reabsorbs bicarbonate (via band 3, a basolateral Cl-/HCO3- exchanger)
46
Q

what do b-intercalated cells do and how?

A
  • Secretes bicarbonate (via pendrin – specialised apical Cl-/HCO3-)
  • Reabsorbs acid (via a basal H+-ATPase)
47
Q

how is bicarbonate produced?

A
  • Glutamine is broken down in tubule cells to alpha-ketoglutarate
  • A-ketoglutarate –> NH4+ + glucose + HCO3-
48
Q

in acidosis, how is acid removed?

A
  • In acidosis, the kidney needs to reclaim the carbon to make bicarbonate
  • Releases bicarbonate back into the system
  • H+ can be exchanged for Na+ to pump it out
  • H+ needs to stay out, so it’s titrated either by an ammonium or phosphate buffer
49
Q

in alkalosis, how is H+ retained?

A
  • In alkalosis, tubular cells secrete HCO3- and reabsorb H+ to acidify the blood
  • Uses separate ATPases
  • K+ ions and swapped for H+ ions
50
Q

what hormones are used in regulation of acid/base status and how do they work?

A
  • Angiotensin 2 regulates the reabsorption of K+ which affects pH
  • Aldosterone puts Na+ back into the system - If Na+ is put back into the system then we have to swap it for H+ and K+
  • Parathyroid hormone prevents the reabsorption of phosphate buffer (can’t leave the filtrate) – makes sure that H+ stays buffered.
51
Q

what is the henderson hasselbach equation used for?

A

pH of a buffer solution

ratio of conjugate base to acid of the system

m2 (24 decks)

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