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Semester 3 - Urinary > Session 6 - Acidosis and Alkalosis > Flashcards

Session 6 - Acidosis and Alkalosis Flashcards

1
Q

How do the kidneys control plasma volume?

A

• Filtering and variably recovering salts

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2
Q

How do the kidneys control plasma osmolarity?

A

• Filtering and variably recovering water

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3
Q

How do the kidneys variably control plasma pH?

A

• Filtering and variably recovering hydrogen carbonate and active secretion of hydrogen ions

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4
Q

What is normal pH range?

A

• 7.38 - 7.42

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5
Q

When does alkalaemia occur?

A

> 7.42

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6
Q

When does acidaemia occur?

A

• <7.38

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7
Q

What is normal conc of H+?

A

37-43 nmol/l

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8
Q

Outline what occurs in alkalaemia

A

• Lowers solubility of Ca2+ salts, free Ca2+ binds to proteins. Results in hypocalcaemia
○ Increases excitability of nerves
• Paraesthesia
• Tetany

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9
Q

What is % mortality at pH 7.55?

A

45%

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10
Q

What is % mortality at pH 7.65?

A

80%

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11
Q

Outline what occurs in acidaemia

A

• Hyperkalaemia (heart arrythmias and arrest)
• Affects many enzymes
○ Reduces cardiac and skeletal muscle contractility
○ Reduced glycolysis in many tissues
○ Reduced hepatic function
• Effects severe under 7.1
• Life threatening below pH 7.0

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12
Q

How much HCO3- is required for accurate pH maintenance?

A
  • 20x as much HCO3- as there is CO2
    • pH = pK + log (HCO3-/pCO2 x 0.23)
    • Log 20 (20x higher) = 1.3
    • pK - 6.1 + 1.3 = 7.4
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13
Q

What is CO2 determined by?

A
  • Controlled by chemoreceptors

* Disturbed by respiratory disease

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14
Q

What is HCO3- conc determined by?

A

• Controlled by kidney

Disturbed by metabolic and renal disease

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15
Q

What is HCO3- largely created by?

A

• Red blood cells

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16
Q

What is respiratory acidaemia (acidosis)?

A
  • Hypoventilation leads to hypercapnia
    • Hypercapnia causes plasma pH to fall
    • Less than 20x amount of HCO3-
    • pH <7.35
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17
Q

What is respiratory alkalaemia (alkalosis)?

A
  • Hyperventilation leads to hypocapnia
    • Fall in pCO2 causes pH to rise
    • More than 20x amount of HCO3- than CO2
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18
Q

What is normal pH?

A

7.38 - 7.42

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19
Q

What is normal HCO3-

A

• 22 - 29 mmol/l

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20
Q

What is normal pO2?

A

• 9.8 - 14.2 kPa

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21
Q

What is normal pCO2?

A

• 4.2 - 6.0 kPa

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22
Q

How is pH corrected in respiratory alkalosis/acidosis?

A
  • Central chemoreceptors normally control pCO2 within tight limits
    • Peripheral chemoreceptors enable changes in respiration driven by changes in plasma pH
    • This is CORRECTION - Changing the factor at hand
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23
Q

How is pH compensated in respiratory acidosis/alkalosis

A
  • changes in pCO2 compensated by changes in HCO3-
    • Kidney control HCO3-
    • Respiratory acidosis is compensated by kidneys increasing HCO3-
    • Respiratory alkalosis is compensated by kidneys decreasing HCO3-
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24
Q

What is metabolic acidosis?

A
  • Tissues produce acid (or acid in blood - amino acids)
    • H+ reacts with HCO3-, leading to fall in pH

Metabolic acidosis

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25
How is metabolic acidosis compensated (acidosis means alteration in buffer base!)?
• Compensated by changes in ventilation ○ Peripheral chemoreceptors increase ventilation ○ This lowers pCO2 Restores pH towards normal
26
What is metabolic alkalosis caused by?
* Plasma HCO3- rises (after vomiting for instance) * Plasma pH rises * Metabolic alkalosis
27
How is metabolic alkalosis compensated?
• Partially compensated by decreased ventilation
28
How are respiratory changes in pH changed? (use correct terminology)
* Compensated by kidney | * Corrected by breathing
29
How are metabolic changes in pH modified? (use correct terminology)
* Compensated by breathing (changing factor than other directly changes) * Corrected by kidney
30
What is produced in metabolic acidosis?
* H+ ions which react with HCO3- to produce CO2 in venous blood * CO2 breathed out, proportionally reducing HCO3-
31
Why can metabolic alkalosis only be partially compensated?
* Because can only slightly reduce respiratory to increase CO2 * At risk of hypoxia
32
How much HCO3- filtered per day?
• 4500 mmol
33
How can HCO3- be increased?
• Recover all filtered HCO3- Make new
34
Give two ways in which kidneys synthesise HCO3-
• Amino acids CO2
35
How do the kidneys make new HCO3- from CO2?
* Kidneys produce a lot of CO2 * Combined with water to produced H2CO3- * H+ excreted into water, HCO3- into blood
36
How do the kidneys make new HCO3- from amino acids?
* Glutamine | * Produces NH4- to enter urine, HCO3- excreted into blood
37
Where is HCO3- recovered in kidney?
* 80-90% in PCT | * Remainder in thick ascending limb of loop of henle
38
How is HCO3- recovered in PCT of kidney?
• H+ exported from cell into lumen via Na-H antiporter ○ Up conc grad ○ Energy from movement of Na+ down Conc grad (Na/K+ ATPase on basolateral membrane • H+ reacts with HCO3- in lumen, making CO2 + H20 • CO2 enters cell, reacts with H20 to make HCO3- • HCO3- exported with K+ into ECG
39
How is HCO3- created from amino acids in the PCT?
``` • Glutamine broken down to produced ○ A-ketoglutarate (HCO3-) ○ Ammonium (NH4+) ○ HCO3- into ECF ○ NH4+ into lumen ```
40
What does HCO3- reabsorption look like in PCT?
• DRAW IT NOW
41
What has happened to HCO3- by the time of the DCT?
Has almost all been filtered and recovered
42
How is HCO3- recovered in distal tubule cells?
* CO2 produced and combined with H20 to make H2CO3- * Na+ gradient insufficient to drive H+ secretion * H+ actively transported out of cell via H+ ATPase and H+/K+ antiporter * H+ bound to HPO42- + H+ -> H2PO4- in lumen
43
What happens to K+ when cells export H+?
• K+ is absorbed into blood
44
Why may you end up absorbing a large amount of K+?
• If a large amount of HCO3- needs to be reabsorbed due to respiratory acidosis, large amount of K+ will be reabsorbed with it. May cause hyperkalaemia
45
What is minimum urine pH
4.5
46
What is a titratable acid?
• One which can freely gain H+ ions in an acid/base reaction
47
How is H+ buffered in urine?
* HP04 2- -> H2PO4- | * NH3 -> NH4+(ammonia -> ammonium)
48
What is daily acid secretion?
• 50-100mmol H+
49
How is H+ excretion controlled?
* pH detected by intracellular pH of tubular cells | * Change in rate of HCO3- export to ECF produced by changes in ECF (H+ automatically excreted)
50
How is respiratory acidosis associated with K+?
* Causes hyperkalaemia * HCO3- being generated, H+ being expelled K+ taken in in exchange for H+
51
How is metabolic alkalosis associated with hypokalaemia?
• Hypokalaemia
52
How does hyperkalaemia cause metabolic acidosis?
* As K+ rises, kidneys ability to reabsorb and create HCO3- reduced. * Hyper kalaemia makes intracellular pH alkaline, favouring HCO3- excretion
53
How does hypokalaemia cause metabolic alkalosis?
• Hypokalaemia makes intracellular pH acidic, favouring H+ excretion and HCO3- recovery
54
Draw activities of DCT
NOW
55
Give 4 cellular responses to acidosis
• Enhanced H+/Na+ exchange ○ Full recovery of all filtered HCO3- ○ Enhanced ammonium production in PCT ○ Increased activity of H+ ATPase in distal tubule ○ Increased activity of H+ ATP-ase from tubular cells to ECF
56
What is metabolic acidosis due to?
* Fall in HCO3- | * A gain in H+
57
What is metabolic alkalosis due to?
* Due to rise in HCO3- | * A fall in H+
58
Give an outline of metabolic acidosis
* Acids produced metabolically * Produced from H+ and an anion (lactate, ketones) * H+ reacts with HCO3-, producing CO2 which is breathed out Some HCO3- replaced by anion from acid
59
What happens to HCO3- after vomiting?
* Large increase in HCO3- and as replacement H+ produced * Kidneys cannot excrete HCO3- as they are trying to compensate for dehydration * HCO3- and Na+ recovery is favoured to increase osmolarity of plasma and cause osmotic movement of water * Metabolic alkalosis ensues
60
How can you treat metabolic alkalosis after vomiting?
* Rehydration | * Post rehydration HCO3- will be excreted quickly
61
Why does HCO3- increase after persistent vomiting?
* H+ decreased in stomach * More H+ produced, releases HCO3- into blood * Hypokalaemia ensues
62
Why does hypokalaemia occur as a result of vomiting?
• H+ secretion in kidney stops, so does K+ reabsorption (Antiporter, intercalated cells)
63
Why do side effects of vomiting include hypokalaemia?>
* H+ secretion in kidney stops, so does K+ reabsorption * More K+ lost in urine * Hypokalaemia
64
Give three causes of metabolic acidosis
* Excess metabolic production of acids * Acids are ingested (amino acids) * Problem with the renal excretion of acid
65
What is the anion gap?
• Indicates whether an HCO3- has been replaced with something other than Cl-
66
How is the anion gap calculated?
• Difference between (Na+ + K+) and (Cl- + HCO3-)
67
What is the normal value of the anion gao?
• 10-15 mmol/l
68
When is the anion gap increased?
• If anions from metabolic acid has replaced plasma HCO3-
69
hen can renal problems reduce HCO3- without increasing the anion gap?
If HCO3- replaced with Cl-
70
Give four causes of an increased anion gap metabolic acidosis
* Lactate * Ketoacids * Toxic alcohols * Aspirin
71
What is renal correction of low pH?
• Fall in tubular cell intra-cellular pH stimulates acid secretion and HCO3- recovery, thus raising plasma HCO3-
72
How can metabolic alkalosis occur?
* HCO3- increases after persistent vomiting | * Should be very easy to correct
73
What is the issue with a HCO3- infusion?
• Excreted in kidney immediately
74
Why does vomiting compromise ability to excrete HCO3-?
* Vomiting also causes dehydration * Volume depletion. Capacity to lose HCO3- is less, because high rates of recovery favour HCO3- recovery and H+ secretion
75
How do you treat metabolic alkalosis?
• Rehydrate
76
What is a dangerous effect of metabolic acidosis?
• Hyperkalaemia ○ K+ moves out of cells, in order to control intracellular pH More K+ reabsorbed in distal nephron, as a result of H+ excretio
77
What is a dangerous effect of metabolic alkalosis?
• Hypokalaemia ○ K+ moves into cells Less K+ reabsorption (less H+ excreted in distal nephron
78
How does hypokalaemia cause metabolic alkalosis?
• Make intracellular pH of tubule cells acidic ○ Favours H+ excretion and HCO3- recovery ○ Therefore metabolic alkalosis occurs
79
How does hyperkalaemia cause metabolic acidosis?
• Makes intracellular pH alkaline ○ Favours HCO3- excretion ○ Therefore metabolic acidosis

Semester 3 - Urinary (33 decks)

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