Renal Control of Acid-Base Balance Flashcards

1
Q

what are some of the metabolic acid sources

A

Glucose and Fat produce give rise to HCO3- and H+
-eliminated primarily by lungs and is changeable

Glucose anerobicly gives rise to Lactate and H+
Cysteine to H+ and sulfate
Phosphoprotein to H+ and phospate
-these three eliminated by kidneys and is normally a fixed amount

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

what are the four body buffers and what are their pK values

A

HCO3-/H2CO3, bicarbonate
-pK is 6.1

Hb-/HHb hemoglobin
-pK is 7.3

HPO4/H2PO4, phosphate
-6.8

Pr/HPr, plasma proteins
-pK is 6.7

all are instantaneous rates of reaction

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

what are the 4 organs and their mechanisms and rate for body buffer systems

A

Lungs:

  • regulates retention or elimination of CO2 and therfore H2CO3 concentration
  • Minutes to hours rate

Ionic shifts:

  • Exchange of intracellular potassium and sodium for hydrogen
  • 2-4 hours

Kidneys:

  • Bicarbonate reabsorbtion and regeneration, ammonia formation, phosphate buffering
  • hours to days

Bone:

  • exchanges of calcium, phosphate, and release of carbonate
  • hours to days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the pK of a buffer

A

it is the pH at which this buffer, acting as an H+ sponge has sopped up half of the H+ it can hold
-middle of the sigmoidal curve

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

How does the buffering of Extracellular Hydrogen Ion affect potassium

A

also known as the Ionic shifts,

the cell has a high intracellular level of K+ therefore it will exchange K+ for H+ in the extracellular fluid

if it is acidema, low pH in the ECF, the cell will exchange the H+ for the K+ decreasing the H+ in the ECF, increasing the pH and increasing the K+ in the ECF

if it is alkalemia, the cell lets go of H+ into the ECF and picks up K+ from the ECF, pH decreases and ECF K+ concentration decreases but increases ICF K+ concentration

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

How does the buffering of hydrogen ion by the plasma proteins and hemoglobin work

A

CO2 dissolves into the red blood cell and converted to HCO3- and H+

H+ will bind to HHb to absorb the H+ and act as the buffer

the HCO3- will exchange with Cl- and be left in the ECF

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

what is the Henderson-Hasselbalch equation

A

pH= 6.1 + log ([HCO3-]/(0.03 x pCO2))

HCO3- is controlled by kidneys, slow with large capacity

pCO2 is controlled by lungs, fast with limited capacity

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

what happens when you increase rate of ventilation vs decrease rate of ventilation

A

increase rate means there is less pCO2 and the pH increases

decrease rate means there is more pCO2 and more H+ meaning lower pH

but can only hyperventilate or hold breath for so long

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

what is the direction of water flow in the countercurrent exchange

A

moves from high concentration of water to low concentration

in nephron the flow is downward while the osmotic pressure differences are sucking the water sideways

solute concentration always starts slightly higher on the ascending side than on the descending side but will quickly eqiulibrates

the continuous extraction of water from the downward side makes the flow at the tip comparatively sluggish

at top of cortex it is isotonic

at medulla it is hypertonic

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

what are some factors regulating increased H+ secretion/HCO3- reabsorption by the nephron

A

Primary:

  • Decrease in plasma HCO3- concentration (decrease pH)
  • increase in partial pressure of arterial carbon dioxide

Secondary: not directly for maintaining acid-base

  • Increase in filtered load of HCO3- (Proximal tubule)
  • Decrease in ECF volume (proximal tubule)
  • increase in angiotensin II (proximal tubule)
  • increase in aldosterone (collecting duct)
  • Hypokalemia (proximal tubule)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are some factors regulating decreased H+ secretion/HCO3- reabsorption by nephron

A

Primary:

  • Increased plasma HCO3- concentration (increase pH)
  • Decrease in partial pressure of arterial carbon dioxide

Secondary:

  • Decrease in filtered load of HCO3- (proximal tubule)
  • Increase in ECF volume (proximal tubule)
  • Decrease in aldosterone (collecting duct)
  • hyperkalemia (proximal tubule)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how does the phosphate buffering of secreted hydrogen ions work

A

in the tubular cells they take up CO2 from the ECF and convert to HCO3- and H+ via carbonic anhydrase

then H+ is exchanged with Na+ to the tubular lumen and the HPO4- will bind with H+ (make urine acidic)

HCO3- still in the tubular cell will get sent back into the ECF making the body less acidic (increase pH)

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

Production, transport, excretion and excretion of ammonia by the Nephron for generation of New bicarbonate

A

from glutamine, it is converted into NH4 and the carbon is made into 2HCO3- in the tubular cell of the proximal tubule

the NH4+ is sent into the tubular lumen

new 2 HCO3- is sent into the blood and the H+ is sent into the tubular lumen

NH4 is transported via Na/K/2Cl in place of K until it reaches the Collecting duct in where it gets stuck in the ion trap and excreted out in the urine

Overall, new bicarbonate was created during urinary acidification when H+ was buffered by NH3, and phosphate while the bicarbonate was reabsorbed

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

what is the function of the alpha and beta intercalated cells in the collecting ducts

A

alpha will secrete H+ via K+/H+ transporter (absorb K+) and ATPase
-will also reabsorb HCO3- as CO2 from Tubular luumen and convert to HCO3- via the carbonic anhydrase

the Beta intercalated cell will reabsorb H+ and secret HCO3-

  • does this by taking in CO2 from the interstital fluid and convert to HcO3- and H+ via carbonic anhydrase
  • pumps H+ back into the interstitium
  • uses Cl- to exchange with HCO3- back into the tubular fluid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the Net Acid Excretion equation?

A

NAE = [(Unh4+ x V) +(Uta+ x V) - (Uhco3 x V)]

TA = Titrable acids which are salts of primarily phosphate but other constitutents of urine such as creatine.
-accounts for 1/3 of NAE

Ammonium (NH4+) synthesis and secretion is responsible for 2/3 of NAE
-not apart of TA because of the high pK of ammonium (7.4), and can be easily made

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

Renal Tubular acidosis and the 4 types

A

Acidemia + Normal Anion Gap + Normal Serum Creatinine and no Diarrhea

has Type 1, type 2, type 3 and Type 4

Type: 3 is a combination of type 1 and 2

17
Q

Primary defect, Plasma HCO3-, Urine pH, Plasma K, and Common secondary causes of type 1 RTA

A

Classic distal tubules, rare

Primary defect: Impaired distal H+ secretion

Plasma HCO3-: typically less then 15 mEq/L and can be often lower than 10 mEq/L

Urine pH: typically greater than 5.5

Plasma K: usually low but corrected by alkali therapy

Common secondary causes: Autoimmune disorders, kidney transplant, hypercalcuria, sickle cell anemia, cirrhosis of liver, analgesic nephropathy

18
Q

Primary defect, Plasma HCO3-, Urine pH, Plasma K, and Common secondary causes of type 2 RTA

A

Proximal tube tubules

Primary defect: Impaired proximal HCO3- reabsorption

Plasma HCO3-: typically less then 12-20 mEq/L due to distal compensation

Urine pH: typically less than 5.5 and increased by alkali therapy to greater than 7

Plasma K: usually low but worsened by alkali therapy

Common secondary causes: Fanconis syndrome, multiple myeloma, drugs: tenofovir, ifosfamide, gentamicin, tetracycline

19
Q

Primary defect, Plasma HCO3-, Urine pH, Plasma K, and Common secondary causes of type 4 RTA

A

Hyperkalemic: most common

Primary defect: lack of aldo or failure of kidney to respond to it

Plasma HCO3-: typically greater than 17 mEq/L

Urine pH: typically less than 5.5

Plasma K: high

Common secondary causes: Diabetic neuropathy, chronic interstitial nephritis, drugs: ACEIs, ARBs, heparin, NSAIDs, spironolactone

20
Q

Type 1 RTA mechanism

A

more than 5 sites for dysfunction in the distal tubules
-Failure of H+ secretion by the alpha intercalated cells

hypokalemia

severe acidosis

21
Q

Type 2 RTA mechanism

A

Proximal Tubules

acidosis yes not as bad as type 1

Failed HCO3- reabsorption from the urine by the proximal tubular cells

22
Q

Type 4 RTA mechanism

A

mostly adrenal issue

acidosis mild with normal anion gap

hyperkalemia

deficiency of aldosterone