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Renal Week 2 > Lecture 19: Metabolic Alkalosis > Flashcards

Lecture 19: Metabolic Alkalosis Flashcards

1
Q

What is the body’s response to being given a bicarbonate load over 24 hours equal to ECF bicarb content? Significance?

A

Serum bicarb would show no change
All bicarb given over 24 hours will be excreted
Significance: thus, increase in serum bicarb not only requires source of new bicarb but also a change in renal bicarb handling

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2
Q

What questions should one ask when encountering a patient with sustained elevated serum bicarb?

A

What is responsible for GENERATING elevated bicarb serum?

Why is elevation persisting? The maintenance of increased bicarb

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3
Q

What leads to an increase in pH?

A

Loss of H+ or gain of bicarb
Ratio of bicarb:H+ will determine pH
High pH = alkalosis

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4
Q

What are the clinical events that

Increase bicarb level?

A
  1. Associated with volume or chloride
    Depletion
  2. Associated with volume expansion
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5
Q

What are events associated with

Volume/chloride depletion that lead to increased bicarb level?

A
  1. vomiting or loss of gastric contents (via nasogastric tubue)
  2. diuretic therapy
  3. rare tubular disorders that mimic diuretic therapy
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6
Q

What are events associated with volume expansion that lead to increased bicarb level?

A

States of mineralocorticoid excess, primarily due to K depletion

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7
Q

What is the effect of gastric secretion on bicarb/H+ balance?

A

Normal processes = HCl generated in the parietal cells is derived from H2CO3
Thus breakdown of H2CO3 into H and bicarb, leads to H being secreted into the lumen while bicarb is secreted into the blood
Thus, normal there is a NET GAIN
Of bicarb in stomach

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8
Q

What is the effect of pancreas on bicarb/H

Balance?

A 
Pancreas does the same process
As stomach (breakdown H2CO3), but
Secretes bicarb into lumen
Reabsorbs H+ into the blood
Thus, there is one net increase in H+
And this neutralizes bicarb reabsorbed from stomach
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9
Q

How does one generate alkalosis from vomiting/nasogastric suctioning?

A

Loss of HCl and NaCl to external environment
Thus there is no H+ that neutralizes the bicarb that is secreted by the pancreas, leading to more bicarb in lumen of GI tract
More bicarb in GI tract will then get reabsorbed in the GI lumen than H+
Thus, vomiting = alkalosis since you lose H+
Serum bicarb will only stay elevated if there is an impairment in renal bicarb

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10
Q

What is the pathway of reabsorptionof bicarb in the PROXIMAL tubule?

A

Bicarb in proximal lumen combines with H+ to form H2CO3 and then H2O and CO2
H2O andCO2 then diffuse into proximal tubule cell, where it recombines to bicarb
The bicarb intracellulary then is reabsorbed back into the blood

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11
Q

What is the role of sodium reabsorption in proximal tubular bicarb handling?

A

Increased sodium reabsorption = increased bicarb reabsorption
Mechanism: Na is exchanged for H+ ions via Na/H exchanger
Thus more Na reabsorption = more H+ in lumen that can bind with bicarb to form H2CO3/H2O and CO2
Furthermore, Na intracellularly is pumped back to blood through Na/Cl symporter

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12
Q

What happens to reabsorbed bicarb?

A

Can go back into the kidney (where it is usually completely reabsorbed)
Or can be expelled by the lungs

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13
Q

What are the factors that increase rate of proximal tubule bicarb reabsorption?

A
  1. Increased rates of sodium reabsorption
    • which can be caused by extracellular volume depletion
  2. Increased rates of Na/H exchange
    • Na/H exchanger can be stimulated by angiotensin II
  3. Increased intracellular H+ activity

Key points: Volume depletion = increased bicarb reabsorption BECAUSE of sodium reabsorption
Volume depletion can not only raise plasma bicarb but also stimulates angio II activity which stimulates Na/H exchanger

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14
Q

What is angiotensin II’s effect on proximal tubule?

A

Activates apical Na/H exchanger

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15
Q

How is bicarb reabsorbed in the distal nephron?

A

Occurs in ALPHA intercalated cells
In the ALPHA intercalated cell, CO2 and H2O combine to form H2CO3/H+ and bicarb
H+ will be secreted into the collecting duct lumen while bicarb is reabsorbed

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16
Q

How is bicarb secreted in the distal nephron?

A

Via Pendrin, a specialized apical Cl/bicarb transporter located on the BETA intercalate cells
Same process of CO2/H2O combining intracellulary to form bicarb/H+
Only that in beta intercalated cells, bicarb is secreted while H+ is reabsorbed

17
Q

How does chloride depletion lead to impairment of bicarb secretion pathway?

A

Bicarb is secreted in the Beta intercalated cells
The transporter on apical beta-intercalated cells is pendrin, or a Cl/bicarb cotransporter
Thus, no Cl = no Cl for the Cl/bicarb cotransporter

18
Q

What happens to urine after vomiting is over?

A

Volume depletion is present
Body responds by increasing angiotensin and increase Na reabsorption + Na/H exchanger
Thus, ALL filtered bicarb is reabsorbed at proximal tubule
-sodium reabsorption in distal tubule will lead to K and H secretion
Urine will look like:
High acid level (low pH)
High K level (increased K and H+ secretion due to increased sodium reabsorption)
No Na
No Cl

19
Q

How does chloride mitigate bicarb accumulation in the distal tubule?

A

By going out of the Cl/bicarb cotransporter on beta-intercalated cells, thereby helping to secrete bicarb

20
Q

What are the lab manifestations of volume/chloride depletion metabolic alkalosis?

A

Blood = high serum bicarb
-compensatory rise in PCO2
Serum K = low because of increased K secretion from aldosterone activity (volume depeleted patient)
Net effect = elevated blood pH, decreased urine pH
Blood alkalosis and urine acidemia

21
Q

What are the key characteristics of metabolic alkalosis secondary to diuretics?

A

With diuretics, kidney is BOTH generating the alkalosis and maintaining the alkalosis
Mechanism: as diuretics deliver more Na downstream to collecting duct, Na is taken up across lumen of principal cells
-as sodium enters principal cells more rapidly than chloride, a lumen negative electrical potential develops
-this transient negative electric potential promotes further secretion of H+ (thus more reabsorption of bicarb) in the ALPHA intercalated cells
-K+ is also secreted more when you have increased Na reabsorption

22
Q

What are the transporters in the alpha/beta intercalated cells?

A

Alpha intercalated = H+/ATPase and H/K exchanger on apical membrane
-Cl/HCO3 on basolateral membrane
Beta intercalated = Cl/HCO3 on apical membrane
-H+/ATPase and H/K exchanger on basolateral membrane
Thus alpha and beta are mirror images of each other and are said to be expressed based on body’s need

23
Q

What is key to appropriate bicarb secretion by beta intercalated cells?

A

Cl- (because of Cl/HCO3 cotransporter)

24
Q

What is paradoxical urine alkalemic?

A

An alkaline urine in metabolic alkalosis

You would expect urine to be secreting bicarb but instead, no bicarb secretion due to proximal reabsorption

25
Q

What are the factors that promote bicarb formation in distal nephron?

A
  1. Aldosterone
    • by increasing Na reabsorption and favoring H ions in the urine
    • stimulates H pumps directly
    • enhances K secretion and thereby increasing H+ content of cells
  2. Endothelin
    • a direct stimulation of H+ secretion
26
Q

What are the causes that lead to primary renal generation of bicarb by stimulation of H+ secretion?

A
  1. diuretics like thiazides or loop diuretics
    • also acquired salt losing nephropathy
  2. Inherited salt losing nephropathies (act like diuretics)
    i. Bartter (defect in TAL Na reabsorption)
    ii. Gitelman’s (defect in DCT Na reabsorption)
  3. Edematous disorders
    i. CHF
    ii. Cirrhosis
    iii. nephrotic syndrome
27
Q

If alkalosis can be generated by the kidney, why and how is it maintained by the kidney?

A

Through the effects of aldosterone
Also by increased sodium reabsorption at proximal tubule, which, as was stated above, secretes H+ out as part of Na/H antiport, leading to more bicarb uptake in the blood

28
Q

What are the causes of volume REPLETION that can lead to metabolic alkalosis?

A

Primary mineralocorticoid excess

29
Q

What are the mechanisms of maintenance of metabolic alkalosis when kidney is principal source of bicarb generation?

A

Diuretics acting on distal nephron can lead to

a. Continued production of bicarb through enhanced H secretion in distal nephron
b. volume and chloride depletion stimulate same factors that exist in gastric alkalosis
c. K depletion may also play a role by lowering intracellular pH

30
Q

How does hypokalemia acidify cell interior?

A

Hypokalemia means K goes from ICF to ECF
H+ will then move from ECF to ICF to compensate for K secretion
If you have more H in ICF, you have more free bicarb in the serum

31
Q

What is the effect of aldosterone on metabolic alkalosis?

A

Aldosterone will lead to volume EXPANSION
Increased NaCl delivery to distal nephron
Increased Na reabsorption
Leads to increase H/K secretion as well as more bicarb reabsorption
Thus, creates effect like diuretics but patient is volume expanded instead of depleted and typically hypertension
Metabolic alkalosis is usually mild since there is no volume stimulus/chloride depletion to support bicarb levels

32
Q

How does one diagnose metabolic alkalosis?

A 
History = vomiting, diuretics, HTN
Physical = volume depletion or volume excess
	-Tetany due to hypocalcemia
Labs = increased serum bicarb
	-alkalemic pH and arterial blood gas
Metabolic alkalosis = hypocalcemima
33
Q

What is the treatment for metabolic acidosis?

A

Treat volume depletion forms with Na-Cl fluids or KCl
-removes stimulus for proximal bicarb reabsorption
-removes stimulus for secondary hyperaldosteronism
-restores distal tubular bicarb secretion
MUST REPLACE CL and not just volume!!!
Treat volume expanded patients by correcting mineralocorticoid excess and/or K+ deficit
-remove stimuli for excess distal tubular H+ secretion

Renal Week 2 (12 decks)

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