Brainscape's Knowledge GenomeTM

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


See full index

RENAL MEDICINE > DISORDERS OF RENAL ACID-BASE REGULATION > Flashcards

DISORDERS OF RENAL ACID-BASE REGULATION Flashcards

1
Q

What is the normal extracellular 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 the main extracellular buffering system in the body?

A

Bicarbonate system

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

How does the body excrete H+ ions?

A

Either as urinary loss associated with a buffer or as ammonium ions (NH+)

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

What is the minimum obtainable pH of the urine?

A

Hydrogen secretion into urine is inhibited below pH 4.4 therefore this is the minimum pH. Of course more hydrogen can be excreted in pHs above this level if they are bound to buffers.

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

What is the major independent urinary buffer?

A

Sodium phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does most acid excretion from the body happen?

A

As a result of ammonium ion excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the name of the enzyme that catalyses the reaction in the bicarbonate system?

A

Carbonic anhydrase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the form of carbonic anhydrase found in the kidney?

A

95% is Type 2 found in the cytosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

HCO3- is freely filtered in the glomerulus. How is it reabsorbed?

A

Secretion of H+ ions interacts with HCO3- and allows it to be reabsorbed in the form of H2CO3. Carbonic anhydrase in the cells of the basal membrane converts it back into HCO3- which can then be transported back into the plasma. Here there is no net acid excretion.

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

When H+ ions are secreted and interact with a urinary buffer such as phosphate, is there net acid excretion?

A

Yes. When secreted H+ ions interact with a urinary buffer (mainly phosphate), the end result is acid excretion. When buffered acid excretion occurs, the new HCO3- ion generated in the renal cells by carbonic anhydrase can now be added to the blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is ammonia produced by the tubular cells of the nephron?

A

Metabolism of glutamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is bicarbonate produced by the tubular cells of the nephron

A

Metabolism of glutamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where in the nephron tubule does most bicarbonate get reabsorbed?

A

80% in the Proximal tubule

15% in the loop of Henle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How are most H+ secreted in the proximal tubule and what is the main purpose of H+ secretion here?

A

Via the NHE3 (sodium hydrogen exchanger)

Secreted to then be reabsorbed as H2CO3 having interacted with HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where in the nephron tubule does most H+ ion secretion ultimately lead to acid excretion?

A

In the distal nephron. Before this stage H+ secretion is used to reabsorb HCO3- from the filtrate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do type A intercalated cells of the cortical collecting duct contribute to acid handling by the kidney?

A

They secrete H+ principally using an apical (lumen side) H+ ATPase, but also using a H/K ATPase similar to that in the stomach. This can therefore be inhibited by omeprazole.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do type B intercalated cells of the cortical collecting duct contribute to acid handling by the kidney?

A

They reabsorb H+ ions into the blood and secrete bicarbonate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the levels of plasma HCO3- in a metabolic acidosis?

A

Low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does the kidney react to a metabolic acidosis (low plasma HCO3-)?

A

Acidosis directly stimulates NH4+ production for excretion and increases H+ secretion to reabsorb more HCO3-.
There is increased synthesis of the apical NHE3 exchanger.
Also increased synthesis of H+ ATPase in the apical membrane of type A intercalated cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does acidosis affect the renin-angiotensin system and thereby affect acid excretion?

A

Stimulates renin release which raises angiotenin II production and aldosterone secretion which promotes H+ ATPase activity in type A intercalated cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the levels of plasma HCO3- in a metabolic alkalosis?

A

High

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does the kidney react to a metabolic alkalosis (high plasma HCO3-)?

A

Inhibits ammonia genesis.

Renal response depends mainly on chloride. Low chloride levels exacerbate alkalosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What effect does aldosterone have on acid handling in the kidney?

A

Increases acid secretion by the H+ ATPase in type A intercalated cells in the distal tubule.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What effect does angiotensin II have on acid handling in the kidney?

A

Promotes H+ secretion by upregulating NHE3. Also promotes HCO3- reabsorption.

25
Q

What is the anion gap and what is the normal anion gap?

A

The difference between the measured cations and the measured anions in the plasma. Plasma is always electrically neutral and therefore the gap is made of unmeasurable anions.

Anion gap = ([Na] + [K]) - ([HCO3] + [Cl]) = normally 6-16 mmol/L

26
Q

What are the unmeasurable anions that make up the anion gap?

A

Proteins
Organic acids
Sulfate
Phosphate

27
Q

What are the two variants of anion gap in metabolic acidosis?

A

Increased anion gap

Normal anion gap

28
Q

When does increased anion gap occur?

A

If new acid is added to the body

29
Q

When does normal anion gap occur in the context of metabolic acidosis?

A

If there is a loss of bicarbonate. This causes compensatory rise in Cl- so anion gap is normal.

30
Q

What are the causes of normal anion gap metabolic acidosis?

A

Gut bicarbonate loss (diarrhoea)
Renal bicarbonate loss (renal tubular acidosis)
Increased sodium chloride intake (excess infusion of saline) - dilutional acidosis.

31
Q

What is dilutional acidosis?

A

This is when there is excessive infusion of saline solution. Because saline is slightly more acidic than plasma there is a drop in pH. Also because of the excess Cl-, the system has to respond to the increase in negativity by releasing protons from the cell. The anion gap stays normal.

32
Q

What are the causes of increased anion gap metabolic acidosis?

A

Addition of acid:
Increased anaerobic metabolism leading to lactic acid build up
Ketoacidosis
Toxic alcohols - methanol and ethylene glycol (antifreeze)
Aspirin overdose

Failure of acid secretion:
Renal failure
Hyperkalaemia

33
Q

Who is particularly susceptible to lactic acidosis?

A

Haemodynamically shocked patients
Septic patients
Liver failure patients

34
Q

What are the symptoms of methanol or ethylene glycol overdose?

A 
Abdominal pain
Vomiting
Headache
Visual disturbances - methanol
Renal failure - ethylene glycol
35
Q

How are patients with metabolic acidosis treated?

A

Correct underlying cuase
IV sodium bicarbonate can be used
Dialysis if renal failure
Correct hyperkalaemia

36
Q

How does hyperkalaemia cause metabolic acidosis?

A

By interfering with NH4+ production

37
Q

What are the two types of metabolic alkalosis and what is the difference?

A

Chloride responsive - urine chloride of less than 20 mEq/L

Chloride resistant - urine chloride of more than 20 mEq/L

38
Q

What are the causes of chloride responsive metabolic alkalosis?

A

Vomiting
Contraction alkalosis as a result of diuretic therapy
Cystic fibrosis

39
Q

How does vomiting cause chloride responsive metabolic alkalosis?

A

Loss of H+ and Cl- ions
Also hypokalaemia and hyponatraemia means that the kidney responds by keeping these ions in exchange for H+ leading to further alkalosis.

40
Q

What is contraction alkalosis?

A

Water is lost, as a result of diuretic therapy, while bicarbonate is retained, the increased concentration of bicarbonate “mops up” more of the hydrogen ions and raises the blood pH.

41
Q

What are the causes of chloride resistant metabolic alkalosis?

A

Hyperaldosteronism
Hypokalaemia
Glycyrrhizinic acid in licorice - causes hypokalaemia
Bicarbonate increase - metabolism of lactate, citrate or acetate from the diet

42
Q

How does hyperaldosteronism cause alkalosis?

A

Increases the activity of NHE3 (sodium-hydrogen exchanger) in the kidney
Increases activity of H+ ATPase in type A intercalated cells of cortical collecting duct
Causes hypokalaemia

43
Q

How does hypokalaemia cause metabolic alkalosis?

A

Renal:
Enhances proximal NH4+ production
Enhances NHE3 (sodium hydrogen exchanger) as potassium follows sodium
Enhances Na/3HCO3- cotransporter
Stimulate H/K ATPase in collecting duct - potassium reabsorption and H+ secretion

Non renal:
Low potassium outside the cell means potassium comes out of cell, H+ ions as a result go in raising pH

44
Q

What are the clinical features of metabolic acidosis?

A

Increased ventilation - Kussmaul’s breathing
Reduced blood pressure - impaired myocardial contraction
Pulmonary oedema
Ventricular arrest
Hyperkalaemia

45
Q

What are the clinical features of metabolic alkalosis?

A 
Muscle cramps
Weakness
Dysrhythmias
Seizures
Hypokalaemia
46
Q

How are patients with metabolic alkalosis treated?

A

Chloride responsive alkalosis responds to chloride and volume replacement - increased chloride promotes bicarbonate secretion.
Hypokalaemia corrected

Chloride resistant alkalosis - block effect of aldosterone with spironolactone or amiloride. Inspiration of CO2 with added oxygen can correct rapidly.

47
Q

What is renal tubular acidosis?

A

An inability of the kidney to excrete acid.

48
Q

What type of acidosis is caused by renal tubular acidosis?

A

Hyperchloremic normal anion gap metabolic acidosis

49
Q

What are the two types of renal tubular acidosis?

A

Type 1 - Distal renal tubular acidosis

Type 2 - Proximal renal tubular acidosis

50
Q

What is type 2 renal tubular acidosis?

A

Proximal renal tubular acidosis occurs when proximal hydrogen ion secretion and bicarbonate reabsorption fail. Often a result of reduced NHE3 activity and NBC (sodium bicarbonate cotransporter). Can be part of Fanconi’s syndrome (generalised proximal tubule dysfunction).
Leads to massive bicarbonate loss in the urine and resulting acidosis.

51
Q

Is type 2 renal tubular acidosis associated with hypokalaemia or hyperkalaemia? Why?

A

Hypokalaemia - not usual for acidosis. High levels of HCO3- in the filtrate traps Na+ and therefore more of both is excreted. The excreted Na+ leads to release of aldosterone which leads to hypokalaemia.

52
Q

How do you treat type 2 renal tubular acidosis?

A

Sodium bicarbonate and potassium supplements or potassium-sparing diuretics. Vitamin D and phosphate supplements may be required.

53
Q

What is type 1 renal tubular acidosis?

A

Distal renal tubular acidosis occurs when secretion of H+ ions in the distal nephron is impaired so the urine cannot be made acidic and the result is a metabolic acidosis.

54
Q

What are the clinical features of type 1 renal tubular acidosis, other than acidosis?

A

The acidosis mobilises bone calcium and causes osteomalacia, nephrocalcinosis and urinary stone formation.

55
Q

Is type 1 renal tubular acidosis associated with hypokalaemia or hyperkalaemia?

A

Can be either depending on whether potassium handling is itself normal. If it is then there will a hypokalaemia because the potassium is secreted instead of H+ during sodium reabsorption. If potassium handling is affected as well as the H+ handling, then there is reduced potassium secretion which worsens the acidosis. This second type can be caused by hypoaldosteronism.

56
Q

How do you treat type 1 renal tubular acidosis?

A

Sodium bicarbonate or sodium citrate administration. Hyperkalaemia is treated with diuretics. Mineralocorticoids may also need replacing.

57
Q

Other than type 1 and type 2 renal tubular acidosis, what other defect might lead to renal tubular acidosis?

A

Defective ammoniagenesis

58
Q

What are the causes of defective ammoniagenesis?

A

Hyperkalaemia
Glucocorticoid deficiency
Loss of renal mass

RENAL MEDICINE (13 decks)

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