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3 - Urinary > deck_1649855 > Flashcards

deck_1649855 Flashcards

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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

•

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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 kidneyDisturbed 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

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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 pHMetabolic 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 pCO2Restores 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 acidsCO2
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 expelledK+ 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 outSome 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 cellsLess 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

3 - Urinary (39 decks)

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