Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Urinary > Week 6 - Renal Control of Acid and Base > Flashcards

Week 6 - Renal Control of Acid and Base Flashcards

1
Q

What is the normal range of pH?

A

7.35-7.45

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is alkalaemia and what are its clinical effects?

A

When plasma pH is greater than 7.45

  • Reduces the solubility of calcium salts
  • – Free Ca2+ leaves the ECF, binding to bone and proteins
  • – Hypocalcaemia results
  • – Makes nerves much more excitable, producing paraesthesia and eventually uncontrolled muscle contractions (tetany)
  • If pH > 7.55, 45% of patients die
  • If pH > 7.65, 80% of patients die
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is acidaemia and what are its clinical effects?

A

When plasma pH is lower than 7.35

  • Increases plasma potassium ion concentration
  • – Effects excitability (particularly of cardiac muscle)
  • – Arrhythmia
  • – Increasing [H+] denatures proteins
  • – Disturbs enzymes
  • – Affects muscle contractility, glycolysis, hepatic function
  • Effects are severe pH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the carbon dioxide/hydrogen carbonate buffer system

A
  • The [H+] in ECF is so low, the addition of very small amounts of acid would change the concentration and hence pH dramatically
  • This doesn’t happen because H+ ions are buffered by binding to various sites
  • Most important buffer = CO2/HCO3 system
  • – CO2 + H2O ←→ H+ + HCO3
  • The extent to which the reversible reaction proceeds is determined by the ratio of [dissolved CO2] (determined by plasma pCO2 to [HCO3] (produced by erythrocytes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is respiratory acidaemia?

A
  • Decreased pH, increased pCO2, no change HCO3, decreased pO2
  • Hypoventilation leads to hypercapnia so the ratio is altered and pH will fall
  • Compensated by the kidneys:
  • – Rise in pCO2 so [HCO3-] rises proportionately to restore pH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is respiratory alkalaemia?

A
  • Increased pH, decreased pCO2, no change HCO3, increased/same pO2
  • Hyperventilation leads to hypocapnia, so the ratio is altered and pH will rise
  • Compensated by the kidneys:
  • – Fall in pCO2 so [HCO3-] falls proportionately to restore pH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is metabolic acidosis?

A
  • Decreased pH, same pCO2, decreased HCO3, same pO2, increased anion gap
  • Metabolically produced H+ ions react with HCO3- to produce CO2 in venous blood
  • – This CO2 is breathed out through the lungs, giving a directly proportional reduction in arterial HCO3-
  • – Relatively less H+ ions are buffered so pH decreases
  • Compensated by the lungs
  • – Fall in [HCO3] causes increased ventilation so pCO2 is lowered proportionately
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is metabolic alkalosis?

A
  • Increased pH, same pCO2, increased HCO3, decreased/same pO2
  • If plasma [HCO3-} rises, for example after persistent vomiting, the [HCO3-] : pCO2 ratio will be altered
  • More HCO3 than CO2 so relatively more H+ ions are buffered causing a pH increase
  • – Rise in [HCO3] causes decreased ventilation so pCO2 is raised proportionately
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the cellular mechanisms of reabsorption of HCO3- in the proximal tubule

A
  • 3Na-2K-ATPase sets up a [Na+] gradient in PCT cells
  • H+ ions are pumped out of the apical membrane up their concentration gradient in exchange for Na+
  • The H+ reacts with filtered HCO3 producing CO2, which enters the cell and reacts with water to produce H+
  • The H+ is quickly exported, recreating HCO3- which crosses the basolateral membrane to enter the plasma

80-90% of HCO3 is reabsorbed in the PCT
- Up to 15% is reabsorbed in the TAL of the loop of Henle by a similar method

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the cellular mechanisms of H+ excretion in the distal tubule

A
  • By the DCT most/all of the filtered HCO3 has been recovered
  • The Na+ gradient is also insufficient to drive H+ secretion
  • H+ is pumped across the apical membrane by H+-ATPase
  • When cells export H+, K+ is absorbed into the blood
  • – So by exporting a lot of H+, a lot of K+ will also be absorbed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the mechanism of buffering of H+ in urine

A
  • The minimum pH of urine is 4.5
  • There is no HCO3 as it has all been recovered
  • Some H+ has been buffered by phosphate (titratable)
  • – Titratable means that it can freely gain H+ in an acid/base reaction
  • Some has reacted with ammonia to form ammonium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the effect of metabolic acidosis on plasma [K+]

A

Associated with hyperkalaemia

  • Acidosis causes K+ ions to move out of cells
  • There is more K+ reabsorption in the distal nephron
  • As [K+] rises, the kidney’s ability to reabsorb and create HCO3 is reduced
  • Hyperkalaemia makes intracellular pH alkaline, favouring HCO3 excretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the effect of metabolic alkalosis on plasma [K+]

A

Associated with hypokalaemia

  • K+ ions move into cells
  • Less K+ reabsorption in the nephron
  • Hypokalaemia makes intracellular pH acidic, favouring H+ excretion and HCO3 recovery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the effect of vomiting on acid-base status?

A

[HCO3] can increase after persistent vomiting, causing metabolic alkalosis

  • HCO3 can be rapidly excreted following infusion of HCO3 so is easy to correct
  • Rise in pH of the tubular cells leads to a fall in H+ excretion and a reduction in HCO3 recovery
  • – H+ excretion has stopped so K+ reabsorption has also stopped
  • – Can cause hypokalaemia
  • Problem if there is volume depletion:
  • – Capacity to lose HCO3 is reduced because of high rate of Na+ recovery
  • – Recovering Na+ favours H+ excretion and HCO3 recovery
  • – If you correct the dehydration by giving fluids, HCO3 will be excreted very rapidly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What can cause metabolic acidosis?

A
  • Excess metabolic production of acids (e.g. lactic acidosis, ketoacidosis)
  • Acids are ingested
  • HCO3 is lost
  • A problem with renal excretion of acid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the anion gap?

A

Difference between [Na+] + [K+] and [Cl-] + [HCO3]

  • This gap increases if other anions from metabolic acids replace HCO3
  • If HCO3 is replaced in the plasma by another anion, the gap will increase
17
Q

Why is it important to maintain ECF [K+]?

A
  • It has an effect on the resting membrane potential
  • – The high ICF [K+] and low ECF [K+] creates a gradient for K+ to move out of the cell, resulting in the resting membrane potential
  • – Decreased ECF [K+] increases the gradient and hyperpolarises the cell
  • – Increased ECF [K+] decreases the gradient and depolarises the cell
  • Can affect the excitability of cardiac tissue
  • High [K+] inside cells and inside mitochondria is essential for:
  • – Maintaining cell volume
  • – Regulating pH
  • – Controlling cell enzyme function
  • – DNA and protein synthesis
  • Low ECF [K+] can cause metabolic disturbances:
  • – Inability of the kidney to form concentrated urine
  • – A tendency to develop metabolic alkalosis
  • – Enhancement of renal ammonium excretion
18
Q

Where is K+ secreted and how?

A

Distal tubule and cortical collecting duct (principal cells)

  • Na-K-ATPase activity in the basolateral membrane creates a K+ gradient (high intracellular K+) for secretion
  • Na+ moves from the lumen into the cell down its concentration gradient, creating an electrical gradient
  • Together these create a favourable electrochemical gradient for K+ secretion via apical K+ channels
19
Q

Where is K+ reabsorbed?

A
  • Proximal tubule
  • Thick ascending limb
  • Distal tubule/cortical collecting duct (intercalated cells)
  • – Active process
  • – Mediated by H-K-ATPase in apical membrane
  • Medullary collecting duct (intercalated cells)
20
Q

What factors affect K+ secretion?

A
  • ECF [K+]
  • Aldosterone
  • Acid base status
  • – Acidosis decreases K+ secretion
  • – Alkalosis increases K+ secretion
  • Increased distal tubular flow rate
  • – Washes away luminal flow
  • – Increases K+ loss
  • Increased Na delivery to distal tubule
  • – More Na absorbed, so more K+ is lost
21
Q

What is external potassium balance?

A
  • Adjusts K+ excretion to correct imbalance
  • Much slower to act
  • 6-12 hours to excrete a load of K+
  • Responsible for control of total body potassium content over the longer term
  • The kidneys adjust K+ excretion to match intake by controlling K+ secretion
22
Q

What is internal potassium balance?

A
  • Moves K+ between ICF and ECF
  • Effect is immediate
  • Responsible for moment-moment control
  • Movement of K+ from ECF into cells is mediated by Na-K-ATPase
  • Movement of K+ out of cells into ECF is via K+ channels (ROMK)
23
Q

What stimulates movement of K+ from ECF into cells is mediated by Na-K-ATPase?

A
  • Hormones (insulin, aldosterone, catecholamines)
  • – K+ in splanchnic blood stimulates insulin secretion by pancreas, which stimulates Na-K-ATPase
  • – Aldosterone secretion is stimulated by K+ in the blood, which then stimulates Na-K-ATPase
  • – Catecholamines act via β2- adrenoceptors, which stimulate Na-K-ATPase
  • Increased [K+] in ECF
  • Alkalosis – low ECF [H+]
24
Q

What stimulates movement of K+ out of cells into ECF?

A

It is via K+ channels (ROMK)
- Exercise
— Net release of K+ during recovery phase of action potential
— Skeletal muscle damage releases K+, but there is uptake of K+ by non-contracting tissues
— Also increase catacholamines, which offset ECF [K+] rise
- Cell lysis
— Trauma to skeletal muscle causing muscle cell necrosis
— Intravascular haemolysis
— Cancer chemotherapy – tumour cell lysis
- Increase in ECF osmolarity
— Can be caused by diabetic ketoacidosis
— Increased plasma and ECF tonicity makes water move into ECF
— This increases [K+] in ICF and hence K+ leaves down concentration gradient
- Low ECF [K+]
- Acidosis - increase in ECF [H+]
— Acidosis leads to a shift of H+ into cells and hence a reciprocal shift of K+ out of cells
• Acidosis leads to hyperkalaemia
— Alkalosis leads to a shift of H+ out of cells and a reciprocal shift of K+ into cells
• Alkalosis leads to hypokalaemia

25
Q

Describe common causes of hypokalaemia

A
  • May be due to problems of external balance
    — Excessive loss
    • GI – diarrhoea/bulimia/vomiting
    • Renal loss of potassium (diuretic drugs, osmotic diuresis, high aldosterone levels)
  • May be due to problems of internal balance
    — Shifts of potassium into ICF
    • E.g. metabolic alkalosis
26
Q

How does hypokalaemia affect acid-base status?

A
  • There is a shift of K+ out of cells and hence a reciprocal H+ shift into the cells
  • Causes alkalosis
27
Q

What are the clinical features of hypokalaemia?

A
  • Heart: altered excitability - arrhytmias
  • GI: neuromuscular dysfunction – paralytic ileus
  • Skeletal muscle: neuromuscular dysfunction – muscle weakness
  • Renal: unresponsive to ADH – nephrogenic DI
28
Q

How can you treat hypokalaemia?

A
  • Treat cause
  • Potassium replacement – IV/oral
  • If due to increased mineralocorticoid activity, give K+ sparing diuretics which block action of aldosterone on principal cells
29
Q

How does hyperkalaemia affect acid-base status?

A
  • There is a shift of K+ into cells and hence a reciprocal shift of H+ out of cells
  • Causes acidosis
30
Q

What are some causes of hyperkalaemia?

A
  • May be due to problems of external balance
  • Increased intake of K+
    — Only causes hyperkalaemia if renal dysfunction occurs
    • If there is decreased renal excretion
    • Acute or chronic kidney injury
    • Normal kidneys but drugs which block potassium excretion (e.g. ACEI)
    • Low aldosterone state
    — Unless an inappropriate dose is given IV
  • May be due to internal shifts
    — Diabetic ketoacidosis
    — Cell lysis
    — Metabolic acidosis
    — (Exercise)
31
Q

What are the clinical features of hyperkalaemia?

A
  • Heart = altered excitability
  • – Arrhythmias, heart block
  • GI = neuromuscular dysfunction
  • – Paralytic ileus
  • Acidosis
32
Q

How can you treat hyperkalaemia in an emergency?

A
  • Reduce K+ effect on heart
  • – IV calcium gluconate
  • Shift K+ into ICF by:
  • – Glucose + insulin IV
  • – Nebulised beta agonists
  • Remove excess K+
  • – Dialysis
33
Q

How can you treat hypokalaemia in an emergency?

A
  • Treat cause
  • – Stop medications
  • – Treat diabetic ketoacidosis
  • Reduce intake
  • Measures to remove excess K+
  • – Dialysis
  • – Oral K+ binding resins to bind K+ in gut

Urinary (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions