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Renal by Minnie: AH Version > SM 200a/201a - Acid Base > Flashcards

SM 200a/201a - Acid Base Flashcards

1
Q

What is Pendrin?

Which cells contain it?

A

Pendrin is an HCO3-/Cl- exchanger on the apical membrane of beta-intercalated cells of the collecting duct (secrete bicarb), and the basolateral membrane of alpha-intercalated cells of the collecting duct (reabsorb bicarb)

It functions to get HCO3- out of the cell, and Cl- into the cell

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2
Q

What is the effect of angiotensin II on HCO3- reabsorption and acid excretion?

A

Angiotensin II stimulates bicarbonate reabsorption and acid excretion

Angiotensin II -> kidney works to increase pH

(Angiotensin II is secreted in response to signals that indicate low volume; low volume -> hypoperfusion -> lactic acidosis -> decreased serum pH; kidney reacts by retaining bicarb and excreting acid)

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3
Q

What is citrate?

What is its role in acid-base balance?

A

Citrate is an organic anion

Citrate reabsorption is equivalent to base retention

  • Main urinary base
    • Reabsorbed and converted to CO2 and H2O
    • This consumes H+ and generates OH-
  • Chelates Ca2+
    • Prevents precipitation with phosphate and oxalate ->
  • *prevents kidney stones**
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4
Q

How does NH3 get across the membranes of the kidney tubule?

A

Diffusion

  • Proximal convluted tubule
    • Diffuses into the lumen
    • Binds to H+ and becomes trapped
  • Reabsorbed and recycled in the Loop of Henle
  • Medullary collecting duct
    • Diffuses into lumen
    • Binds to H+ and becomes trapped and excreted
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5
Q

What is the differential for anion-gap metabolic acidosis?

A

MUDPILES: Acid add-on state

  • Methanol
  • Uremia
  • Diabetic ketoacidosis (any ketoacidosis)
  • Phenformin, paracetamol/acetaminophen, paraldehyde
  • Iron, Isoniazid, Inborn errors of metabolism
  • Lactic acidosis
  • Ethanol/Ethylene glycol
  • Saliclates/ASA/Aspirin
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6
Q

What is the Henderson-Hasselbach Equation for Biarbonate/Carbonic acid?

A
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7
Q

What acid-base transporters in the cell membrane protect the cell from changes in pH?

A
  • Na+/H+ exchanger
    • Main mechanism
    • Na+ dependent
  • Cl-/HCO3- exhcanger
    • Na+ independent
  • Na+,HCO3-/H+,Cl- exchanger
    • Na+ dependent
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8
Q

What is the effect of hypokalemia on HCO3- reabsorption and acid excretion?

A

Hypokalemia stimulates bicarbonate reabsorption and acid excretion

Hypokalemia -> kidney works to increase serum pH

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9
Q

In which tubules of the kidney is bicarbonate reabsorption driven by the Na+/H+ exhchanger?

A

Proximal tubule

Thick ascending limb of LOH

(Not the collecting tubule, although Na+ indirectly affects H+ secretion in the CT)

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10
Q

Where in the kidney tubule is NH4+ reabsorbed?

A

Loop of Henle

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11
Q

What is the equation for urine anion gap?

How do you use it?

A

[Na+] + [K+] + [NH4+] = [Cl-]

Useful in in ruling in/out RTA as a cause of hyperchloremic (non-AG) metabolic acidosis

  • If [Na+] + [K+] > [Cl-], then there is no NH4+ in the urine
    • If this is true while the patient is acidemic, the kidney tubules are not properly acidifying the urine
  • If [Na+] + [K+] -], then there is NH4+ in the urine
    • This is an indication of acid excretion, which means the metabolic acidosis is not likely to be caused by RTA
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12
Q

Why might does amiloride cause metabolic acidosis?

A

Amiloride blocks Na+ reabsorption in the collecting duct

  • Decreased Na+ reabsorption
  • -> Decreased Na+/H+ exchange
  • -> Decreased H+ secretion
  • -> Metabolic acidosis
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13
Q

Describe the pathophysiology of diabetic ketoacidosis

A

Lack of insulin

  • -> Lipolysis and release of fatty acids
    • -> Accumulation of ketone bodies
      • Acetoacetatic acid and beta-hydroxybutyric acid
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14
Q

What is Type A lactic acidosis?

A

Increased lactic acid generation

  • Due to tissue hypoxia
    • Severe hypotension
    • Cardiac arrest
    • Sepsis

(Type B = decreased utilization of lactic acid)

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15
Q

A state of _______________ leads to the formation of glutamine in the liver

A

A state of metabolic acidosis leads to the formation of glutamine in the liver

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16
Q

What is the most frequent and severe cause of H+ build up in the circulation?

A

Lactic acidosis

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17
Q

Describe the transport of NH4+ (ammonia) in the kidney tubule

A
  • Glutamine –> NH4+ in the proximal tubule
    • Glutamine into PCT epithelial cell through the basolateral membrane
    • Glutamine –> NH4+ –> NH3 + H+
    • H+ is secreted into the tubule via H+/Na+ exchanger
    • NH3 diffuses into the tubule
    • In the tubule, NH3 + H+ –> NH4+
  • NH4+ is reabsorbed in the Loop of Henle
    • ​NH4+/K+ exchanger
    • Na+/NH4+/Na+ exchanger
    • NH4+ channel
  • NH3 diffuses into the medullary collecting duct, binds to H+ and is trapped as NH4+
    • ​Acid (H+) secreted by collecting duct epithelial cells binds to NH3 and becomes trapped as NH4+
    • This is how the body secretes acid while retaining bicarb
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18
Q

What is the differential for non-anion gap (hyperchloremic) metabolic acidosis?

A

USED CARS: Bicarb loss

  • Uretrosigmoidostomy
  • Saline administration (NaCl)
    • In the face of renal dysfunction
  • Endocrine (addison’s), Ethanol
  • Diarrhea
  • Carbonic anhydrase inhibitors
  • Ammonium chloride
  • Renal tublar acidosis
  • Spironolactone
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19
Q

Meatabolic Acidosis is a primary disturbance characterized by _________________

A

Meatabolic Acidosis is a primary disturbance characterized by
a fall in blood bicarbonate levels

This leads to decreased pH

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20
Q

Why do you see hypokalemia in Distal RTA?

A

DRTA = the distal tubule (alpha-intercalated cells) cannot secrete H+

  • Lumen is negatively charged due to Na+ reabsorption
    • Pulls + charge in
  • K+ is secreted instead
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21
Q

Describe the “classic presentation” of Distal RTA

A
  • Hyperchloremic metabolic acidosis
  • Inability to lower urinary pH below 5.5 despite acidemia
    • Due to impaired H+ secretion
  • Hypokalemia
    • Lumen negatively charged due to Na+ reabsorption; if H+ cannot be secreted, K+ is secreted
  • Nephrocalcinosis (increased Ca2+ in the kidney tubule)
    • Lumen negatively charged due to Na+ reabsorption; if H+ cannot be secreted, Ca2+ is secreted
  • Kidney stones
    • Due to increased Ca2+
22
Q

Describe the process of HCO3+ reabsorption in the proximal tubule

A

There is no “bicarbonate transporter” on the apical membrane

Na+ gradient into the cell is necessary to drive H+ secretion in the apical membrane via Na+/H+ exchanger

  • H+ secreted into the lumen is important (Na+/H+ exchanger, H+ pump)
  • HCO3- combines with H+ to form H2CO3
  • H2CO3 breaks down into H2O and CO2 via carbonic anhydrase
  • CO2 diffuses across the basolateral membrane
  • H2O diffuses across the baslolateral membrane via AQP1
  • CO2 combines with H2O to form H2CO3 via carbonic anhydrase
  • H2CO3 dissociates into H+ and HCO3-
  • HCO3-/Na+ cotransporter (NBCe1a) transports Na+ and 3(HCO3-) into the interstitium
    • This is the only difference from HCO3- reabsorption in the TAL
    • The TAL has a HCO3-/Cl- exchanger instead
  • Na+ gradient is maintained by Na+/K+ ATPase
23
Q

What are the major causes of metabolic alkalosis?

A
  • Loss of H+ ions
    • GI
      • Loss of gastric acid secretions
        • Vomiting, NG tube
    • Renal
      • Loop or thiazide diuretics
        • More Na+ delivery to cortical collecting duct stimulates principal cells to reabsorb more Na+
        • This creates a favorble charge gradient for alpha intercalated cells to secrete H+
      • Mineralcorticoid excess
        • Aldosterone stimulates alpha intercalated cells to reabsorb bicarb and secrete H+
      • Bartter and Gitelman syndromes
  • Retention of administered bicarbonate
    • Milk Alkali syndrome
    • Administration of NaHCO3
24
Q

What is the effect of volume depletion on HCO3- reabsorption and acid excretion?

A

Volume depletion stimulates bicarbonate reabsorption and acid excretion

Volume depletion -> kidney works to increase pH

(Is this a response to the decreased perfusion and resulting acidosis associated with volume depletion?)

25
Q

What is the major function of the alpha-intercalated cells in the collecting tubule?

A

Secrete acid (H+)

Reabsorb K+ (H+/K+ exchanger)

26
Q

What are the two main urine buffers?

A

Phosphate (HPO42- )

H+ + HPO42- —> H2PO4-

Ammonia (NH3)

H+ + NH3 —> NH4+

27
Q

What is the effect of volume expansion on HCO3- reabsorption and acid excretion?

A

Volme expansion inhibits bicarbonate reabsorption and acid excretion

Volume expansion -> kidney works to decrease pH

28
Q

Why is ammonia production and excretion in the kidney important?

A

It is important for reabsorbing bicarbonate

29
Q

What is the main pH regulatory transporter that protects the cell from acid load?

A

Na+/H+ exchanger

30
Q

What is type B lactic acidiosis?

A

Decreased utilization of lactic acid

  • Liver failure
  • Drugs
  • Malignancies

(Type A = Increased lactic acid generation)

31
Q

What are the clinical features of proximal RTA?

A
  • Fanconi syndrome
    • Bicarb wasting
    • Glycosuria
    • Phosphauria
    • Hyperuricosuria
    • Aminoaciduria
  • Hypokalemia
  • No nephrocalcinosis or kidney stones
  • Rickets
32
Q

What are the 4 general mechanisms of metabolic acidosis
(a low HCO3 state)?

A
  • Loss of HCO3- externally
    • Diarrhea
    • Proximal RTA
  • Failure of the kidneys to excrete acid
    • Distal RTA
    • CKD
    • Acid retained in the body uses up bicarb
  • Addition of H+ which titrates HCO3-
    • Drinking something with H+
  • H+ buildup in the circulation
    • Lactic acidosis
    • Ketoacidosis
33
Q

Metabolic Alkalosis is an acid-base disorder characterized by ________________

A

Metabolic Alkalosis is an acid-base disorder characterized by a primary increase in blood bicarbonate concentration

Primary = not in response to an acidosis

34
Q

What compensatory mechanisms in the kidney are activated by metabolic alkalosis?

A
  • Reduced bicarbonate reabsorption along the nephron
  • Increased secretion of bicarbonate by beta-intercalated cells
35
Q

What are the major functions of principal cells in the collecting tubule?

A

Reabsorb Na+

Secrete K+

36
Q

If there is an excess bicarbonate load, which section of the kidney is responsible for secreting it?

A

Cortical collecting duct beta-intercalated cells

Secrete bicarb through upregulation of pendrin

37
Q

Describe the process of HCO3+ reabsorption in the thick ascending limb

A

There is no “bicarbonate transporter” on the apical membrane

Na+ gradient into the cell is necessary to drive H+ secretion in the apical membrane via Na+/H+ exchanger

  • H+ secreted into the lumen is important (Na+/H+ exchanger, H+ pump)
  • HCO3- combines with H+ to form H2CO3
  • H2CO3 breaks down into H2O and CO2 via carbonic anhydrase
  • CO2 diffuses across the basolateral membrane
  • H2O diffuses across the baslolateral membrane via AQP1
  • CO2 combines with H2O to form H2CO3 via carbonic anhydrase
  • H2CO3 dissociates into H+ and HCO3-
  • HCO3-/Cl- exchanger transports Cl- into the cell 3(HCO3-) into the interstitium
    • This is the only difference between TAL and PCT (Na+/HCO3- cotransporter in the PCT)
  • Na+ gradient is maintained by Na+/K+ ATPase

This is basically the same in the TAL, except there is a HCO3-/Cl- cotransporter on the basolateral membrane instead of a Na+/HCO3- exchanger

38
Q

What is the effect of aldosterone on HCO3- reabsorption and acid excretion?

A

Aldosterone stimulates bicarbonate reabsorption and acid excretion

Aldosterone -> kidney works to increase pH

(Aldosterone II is secreted in response to signals that indicate low volume; low volume -> hypoperfusion -> lactic acidosis -> decreased serum pH; kidney reacts by retaining bicarb and excreting acid)

39
Q

What process is occuring?

Is it adequately compensated?

  • pH: 7.55 (7.36-7.42)
  • pCO2: 52 (40)
  • HCO3: 44 (NORMAL=24)
A

Metabolic alkylosis

  • Comparing pH and pCO2: yes
    • 55 is about equal to 52
  • Comparing pCO2 and HCO3: yes
    • ΔpCO2 = 12, which is about half of ΔHCO2 (20)
    • Compensation: ΔpCO2 = 0.6 * ΔHCO3
40
Q

How do you treat metabolic alkalosis?

A

Cl- administration

NaCl usually

KCl if the patient is hypokalemic

41
Q

Based on pCO2 and HCO3- levels, how can we tell if an acid/base process is appropriately compensated?

Metabolic acidosis:

Metabolic alkalosis:

Chronic respiratory acidosis:

Chronic respiratory alkalosis:

A

Metabolic

  • Acidosis: pCO2 and HCO3- decrease about the same amount
    • ΔpCO2 = 1.2 * ΔHCO3-
    • Metabolic acidosis = Decreased pH, decreased pCO2
    • Bicarb will be used up to neutralize extra acid?
  • Alkalosis: pCO2 inreases about twice as much as HCO3-
    • ΔpCO2 = 0.6 * ΔHCO3-
    • Metabolic alkalosis = Increased pH, increased pCO2
    • Bicarb will be produced

Respiratory

  • Acidosis: Increase in HCO3- is about twice as much as increase in pCO2
    • ΔHCO3- = 0.4 * ΔpCO2
    • Respiratory acidosis = Decreased pH, increased pCO2
    • Kidney will reclaim bicarb to compensate for low pH
  • Alkalosis: Decrease in HCO3- is about twice as much as decrease in pCO2
    • ΔHCO3- = 0.5 * ΔpCO2
    • Respiratory alkylosis = Increased pH, decreased pCO2
    • Kidney will excrete bicarb to compensate for high pH
42
Q

Why do you see kidney stones in patients with Distal RTA?

A

Distal RTA = problem secreting H+ in the distal convoluted tubule

  • The lumen is negatively charged due to Na+ reabsorption
  • If H+ cannot be secreted, Ca2+ and K+ are secreted instead
  • Increased Ca2+ in the tubule -> kidney stones
43
Q

What percentage of NH4+ produced in the proximal tubule is excreted in the urine?

A

100%

44
Q

What is the major function of the beta-intercalated cells in the collecting tubule?

A

Secrete HCO3- (HCO3-/Cl- exchanger)

Secrete K+

45
Q

How do you calculate the anion gap in an acid-base process?

A

Serum AG = [Na+] - [Cl-] - [HCO3-]

Urine AG = [Na+] + [K+] - [Cl-]
I like to think of this as [Na+] + [K+] + [NH4+] = [Cl-] to remember what it actually means

  • Note on Urine AG
    • If [Na+] + [K+] > [Cl-], then there is no NH4+ in the urine
      • If this is true while the patient is acidemic, the kidney tubules are not properly acidifying the urine
    • If [Na+] + [K+] -], then there is NH4+ in the urine
      • This is an indication of acid excretion
46
Q

Why is Na+ important for protecting the cell from an acid load?

A

The Na+/H+ exchager (main intracellular pH regulator) depends on extracellular Na+ in order to get H+ out of the cell

47
Q

Where in the kidney tubule is NH4+ formed?

A

Proximal tubule

48
Q

Where is metabolic alkalosis generated?

Where is it maintained?

A
  • Generated by the stomach
    • Gastric fluid loss
    • Decreased H+ secretion
  • Maintained by the kidneys
    • Increased bicarbonate reabsorption
49
Q

What are the compensatory responses to metabolic alkalosis?

A
  • Alkalemia is sensed by the peripheral chemoreceptors
  • -> decreased respiration
  • -> CO2 retention
  • -> increased pCO2
    • 0.6 mmHg for every 1 Meq/L increase in HCO3
    • => +10 HCO3 = +6 pCO2

Note: There is a limit to respiratory compensation for metabolic alkylosis because too much of a decrease in ventilation would cause hypoxemia

50
Q

What process allows for both reabsorption of HCO3- and H+ excretion?

A

De Novo Bicarbonate formation in the collecting duct

Requires the action of carbonic anhydrase

NH3 combines with H+ secreted into the lumen and traps it as NH4+ - this allows for H+ excretion without HCO3- excretion

51
Q
A

Renal by Minnie: AH Version (27 decks)

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