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DJ - ESA 3 - Urinary > 6 - Acid Base Balance And Potassium Control > Flashcards

6 - Acid Base Balance And Potassium Control Flashcards

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1
Q

How do the kidneys control plasma volume?

A

Through filtering and variably recovering salts.

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2
Q

How do the kidneys control plasma osmolarity?

A

Through filtering and variably recovering water.

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3
Q

How do the kidneys control pH?

A

Through filtering and variably recovering hydrogen carbonate and active secretion of protons.

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4
Q

What is the normal range of pH?

A

7.38 - 7.42.

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5
Q

What is alkalaemia? How does it affect the body?

A

pH > 7.42. Lowers free Ca2+, increasing excitability of nerves; if pH > 7.45, parasthesia and tetany are symptoms. N.B. pH of 7.65 = 80% mortality rate.

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6
Q

What is acidaemia? How does it affect the body?

A

pH < 7.38. Increases plasma K+ and denatures many enzymes - reduced cardiac & skeletal muscle contractility, glycolysis, hepatic function. N.B. pH < 7 is very much life-threatening.

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7
Q

What is the Henderson-Hasselbalch equation? What is the ratio of HCO3 to dissolved CO2?

A

pH = pKa + log([HCO3-] / (pCO2 x 0.23)) pH = 6.1 + 1.3 (or log20) = 7.4 Ratio is 20:1 HCO3- to CO2.

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8
Q

What is the amount of CO2 determined by?

A

Ultimately the lungs - controlled by chemoreceptors - disturbed in respiratory disease.

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9
Q

What is the amount of HCO3- determined by?

A

The kidneys - disturbed by metabolic and renal diseases.

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10
Q

What is the cause of respiratory acidosis?

A

Hypoventilation which results in hypercapnia. Rise in pCO2 causes pH to fall.

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11
Q

What is the cause of respiratory alkalosis?

A

Hyperventilation which results in hypocapnia. Fall in pCO2 causes pH to rise.

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12
Q

What are chemoreceptors? What do they do?

A

Central: maintain pCO2 within tight limits. respiratory changes correct respiratory disturbances of pH. Peripheral: enable changes in respiration driven by changes in plasma pH.

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13
Q

How can the body compensate for respiratory acidosis?

A

The kidneys will increase the [HCO3-] restoring the ratio - increasing the pH.

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14
Q

How can the body compensate for respiratory alkalosis?

A

The kidneys will decrease the [HCO3-] restoring the ratio - decreasing the pH.

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15
Q

What is a typical cause of metabolic acidosis?

A

Excess acid production (lactic acid, ketoacidosis, sulphuric acid) - HCO3- neutralises this. The decrease in [HCO3-] results in acidosis.

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16
Q

How is metabolic acidosis compensated for?

A

Peripheral chemoreceptors detect fall in plasma pH, leading to increased ventilation - lowering pCO2 - restoring pH to normal.

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17
Q

What is a typical cause of metabolic alkalosis?

A

Persistent vomiting. Alkali tide is produced by the body in preparation for the acidic content from the stomach. Acid is vomited, meaning alkali (HCO3-) remains in the body.

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18
Q

How is metabolic alkalosis compensated for?

A

It can only be partially compensated through decreasing ventilation - but can normally be corrected easily by the kidneys (rise in tubular cell pH, reducing acid secretion, reducing recovery of HCO3-).

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19
Q

What do kidneys need to be able to do in order to regulate [HCO3-]?

A

4500mmol of HCO3- is filtered in a day - so it is easy to lose HCO3- (compensate for an alkalosis). To increase HCO3- (compensate for acidosis) must be able to recover all filtered HCO3- and make new.

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20
Q

How do the kidneys increase [HCO3-]?

A

From CO2 + H2O HCO3- + H+ And amino acids, producing NH4- to enter urine.

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21
Q

How much HCO3- is reabsorbed normally and where?

A

100%: 80-90% reabsorbed in PCT and the remainder in the Thick Ascending Limb of the LOH.

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22
Q

What channels are important in order to reabsorb HCO3- in the PCT? Why are they important?

A

Apical: NHE Basolateral: Na-K-ATPase, HCO3- channel Na+ gradient from tubule –> tubular cell –> ECF NHE moves H+ the other way - tubular cell –> tubule. Tubule: H+ + HCO3- –> H2O + CO2 (which enter the cell) Tubular cell: CO2 + H2O –> H+ + HCO3- (leaves via basolateral membrane to ECF). … H+ moves with NHE etc.

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23
Q

How is HCO3- created in the PCT?

A

Glutamine –> alpha-ketoglutarate –> HCO3- + NH4+ HCO3- –> ECF; NH4+ –> Lumen

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24
Q

How is HCO3- created in the DCT?

A

In DCT all filtered HCO3- reabsorbed and Na+ gradient insufficient to drive H+ secretion. Within the tubular cell: H2O + CO2 (metabolism) –> H+ + HCO3-. H+ is actively secreted into the lumen (H+ ATPase); HCO3- moves out of the basolateral membrane.

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25
What is the minimum pH of urine? How can H+ be buffered in the lumen of the DCT?
4.5 or [H+] = 0.04mmol/L H+ + HPO4 2- --\> H2PO4 - (titrable acid) H+ + NH3 --\> NH4+
26
What is H+ excretion controlled by?
Changes in intracellular pH of tubular cells. Changes in rate of HCO3- export to ECF (due to changes in ECF [HCO3-])
27
What are the cellular responses to acidosis?
Upregulating NHE (full recovery of all filtered HCO3-) Increased NH4+ production in DCT, Increased activity of H+ ATPase, Increased capacity to export HCO3- from tubular cells to ECF.
28
What happens to [HCO3-] when acids are produced through metabolic processes?
Lactic acid, Ketone acids etc. are an anion (lactate) and a H+. Some of these H+ react with HCO3- forming CO2 ... therefore [HCO3-] will decrease.
29
What is the anion gap?
( [Na+] + [K+] ) - ( [Cl-] + [HCO3-] ) = Anion Gap. It is a measure of whether HCO3- has been replaced with any other anions (which are not accounted for).
30
What is the normal anion gap?
10 - 15mmol/L (more cations than anions).
31
When would the anion gap be increased?
If anions from metabolic acid have replaced plasma HCO3-.
32
When might there be reduced [HCO3-] but a normal anion gap?
If all the HCO3- is replaced with Cl- (hyperchloraemic acidosis).
33
How do changes in tubular cell intracellular pH influence acid secretion in the DCT?
Reduced intracellular pH of tubular cells stimulates acid secretion, stimulating HCO3- recovery - increasing plasma [HCO3-].
34
When might metabolic alkalosis be difficult to correct?
Usually due to persistent vomiting - rise in intracellular pH (tubular cells), reduces acid secretion and HCO3- recovery. If there is volume depletion as well it is more complicated, high rates of Na+ reabsorption (to restore ECV) favour HCO3- reabsorption and H+ secretion.
35
How are metabolic acidosis/alkalosis linked with K+ balance?
Metabolic acidosis: hyperkalaemia (K+ moves out of cells; more K+ reabsorption in DCT) Metabolic alkalosis: hypokalaemia (K+ moves into cells, less K+ reabsorption)
36
How does hyper/hypo kalaemia affect intracellular pH of tubule cells?
Hyperkalaemia makes intracellular pH of tubular cells acid: favours H+ excretion and HCO3- recovery --\> metabolic alkalosis. Hypokalaemia: makes intracellular pH of tubular cells alkali: reduce H+ secretion and HCO3- recovery --\> metabolic acidosis.
37
In our bodies we often produce acid, does this affect [HCO3-]?
Normally, no. All filtered HCO3- is recovered. PCT: HCO3- made; trade-off AAs --\> NH4+ (glutamine --\> alpha-ketoglutarate --\> HCO3- + NH4+) DCT: HCO3- and H+ produced (from H2O and CO2 - metabolism) - HCO3- reabsorbed; H+ buffered with phosphate and ammonia.
38
How is a 70kg man's body fluid compartments normally divided?
60%... 42L is total body water 2/3... 28L is ICF 1/3... 14L is ECF.
39
What can ECF be divided into?
ECF is 28L 1/4... 3.5L is plasma; 3/4... 10.5L is interstitial fluid.
40
What are the extracellular and intracellular [K+]? Therefore where is the majority of K+ stored in the body?
Extracellular: 4mmol/L Intracellular: 155mmol/L 98% ICF; 2% ECF; Total body K+ = 3500mmol N.B. only small shifts from ICF --\> ECF of K+ are required to change ECF dramatically.
41
What maintains the difference between [K+] in the ECF and the ICF?
The activity of the Na-K-ATPase.
42
Where exactly in the body is the bulk of the K+ stored?
Skeletal muscle cells. Also liver, RBCs, bone.
43
What is it that creates the resting membrane potential?
The K+ gradient from inside the cell to outside. R.M.P in neuron cells is ~-70mV.
44
How will a high ECF [K+] affect the resting membrane potential? What would a low ECF [K+] cause?
Decrease the K+ gradient from inside to outside - depolarising the cell. Opposite in hypokalaemia - hyperpolarisation of cell. Significantly alters electrical excitability of cardiac and neuromuscular tissues.
45
How does the body deal with hyperkalaemia (high ECF [K+])?
Intracellular buffering plays an important role. Kidneys of little immediate help - cannot excrete K+ quickly.
46
How is K+ absorbed?
In the intestines and the colon. It is immediately absorbed into the ECF - with 4/5 ingested K+ moving into cells within minutes; kidneys begin to excrete K+ slightly later - complete after 6-12 hours.
47
How is [K+] regulated?
External balance: Adjusts renal K+ excretion to match intake - slower. Internal balance: Movement of K+ between ICF and ECF - immediate.
48
What is the average K+ intake? Is all of this absorbed?
100mmol/day. No there is a 5-10% loss in the GI.
49
How do the kidneys regulate [K+]?
They adjust K+ excretion to match intake by controlling K+ secretion. Takes 6-12 hours to be complete; responsible for maintenance of total body K+ content over the longer term.
50
How does the ICF regulate ECF [K+]? What channels are involved?
Depending on ECF [K+] - effect is immediate, responsible for moment-to-moment control. Na-K-ATPase - 2 K+ enters; expels 3 Na+. K+ channels (ROMK channels determine K+ permeability) - K+ expelled from cell.
51
With regards to internal balance of K+, what factors promote the uptake of K+ into cells?
Hormones: insulin, aldosterone, catecholamines Increased [K+] in ECF Alkalosis - low ECF [H+] ... H+ moves out of cell to correct alkalosis, K+ moves the other way (into cells).
52
How does insulin affect uptake of K+ into cells?
K+ in splanchnic blood stimulates insultin secretion from pancreas. Insulin stimulates K+ uptake by upregulating Na-K-ATPase in muscle cells and hepatocytes. IV Insulin used to treat life-threatening hyperkalaemia.
53
How does aldosterone affect uptake of K+ into cells? What drug opposes aldosterone's actions?
K+ in blood stimulates aldosterone secretion. Increases K+ reabsorption in late DCT and CD (upregulates ENaC and Na-K-ATPase).
54
How do catecholamines regulate K+?
Act via B2-adrenoceptors - upregulate Na-K-ATPase stimulating cellular uptake of K+.
55
With regards to internal balance of K+, what factors promote the K+ shift out of cells?
Low ECF [K+], Exercise, Cell lysis, Increase in ECF osmolarity, Acidosis - high ECF [H+] - shift of H+ into cells, K+ goes the other way - out of cells.
56
How does exercise affect K+ balance between ICF and ECF?
Skeletal muscle contraction --\> net release of K+ during recovery phase of action potential. Skeletal muscle damage --\> release of K+ N.B. change in plasma [K+] proportional to level of exercise.
57
How does the body prevent dangerously high K+ levels during exercise?
Non-contracting tissues take K+ up. Exercise increases catecholamine production (B2 - upregulate Na-K-ATPase). Cessation of exercise causes a sharp drop in plasma [K+] - \<3mmol/L.
58
How does cell lysis affect K+ balance between ICF and ECF? What are some causes?
Increases K+ in ECF. Rhabdomyolysis - trauma to skeletal muscle causing muscle cell necrosis. Intravascular haemolysis - inappropriate breakdown of RBCs: Incompatible blood transfustion, G6PD deficient patients treated with certain drugs. Chemotherapy - tumour cell necrosis.
59
How do changes in plasma tonicity affect K+ balance between ICF and ECF?
An increase in plasma & ECF tonicity - e.g. diabetic ketoacidosis will lead to water moving from the ICF into the ECF. This increases relative [K+] in ICF - K+ moves from ICF to ECF because of this.
60
How does acid base disturbances affect K+ balance?
61
How does hypo/hyper kalaemia cause acid base disturbances?

DJ - ESA 3 - Urinary (7 decks)

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