6. Renal Acid Base Flashcards
What must pH stay at around 7.4?
AAs have positive and negative charges which can be altered and change protein folding and other protein to protein interactions
Most of the H+ elimination occurs in the lungs while a fixed percent occurs in the kidneys. What happens if there is a change of 0.3 in pH down?
doubles H+ concentration
if pH goes up by 0.3 it will half the H concentration
What is interesting about the pH of urine and what is its range?
4.5 to 8, allow it to concentrate or dilute H+ if needed
What organ regulates retention or elimination of CO2 and therefore H2CO3 concentration in minutes-hours as a cody buffer system?
the lungs
What organ acting as a body buffer system allows bicarbonate reabsorption and regeneration, ammonia formation and phosphate buffering in hours-days?
Kidneys
What organ exchanges calcium, phosphate, and release of carbonate in hours to days to to help with buffering?
Bone
HPO4 has a pK at 6.8 while HCO3 has a pK at 6.1 which are both buffers in the ECF. what occurs at this number?
where this buffer acts as an H+ sponge, sopping up half of the H+ it can absorb
CO2 is transported as CO2 dissolved 7%, 23% HbCO2, and 70% HCO3. How does a majority of the HCO3 get made/transported into the blood?
In the RBC, CO2 and H2o combine to make H2CO3 via CA and then spontaneously breaks down to form H and HCO3, H is then used to bind Hb or is recycled and HCO is transported out of the red blood cell via chloride shift for a Cl- in
Ionoic shifts is another way of buffering (bringing the pH back down or up) the system via Hydrogen being exchanged for Potassium. When there is acidemia (low pH in the ECF), ICF takes in H+ and excretes K+. When there is alkalemia (high pH in the ECF)?
ICF gives H+ to ECF, and takes K+ into ICF
What is the henderson-hasselbalch equation and what is the normal log for pH of 7.4?
pH= 6.1 + log (HCO3-contolled by kidneys)/(H2CO3)
REMEMBER: H2CO3 = 0.3*pCO2 controlled by lungs
when log is equal to 20 = pH 7.4
When log of 1/1 is equal to 0
When you breath fast, theres less CO2 which means less H2CO3 which means less H+ which means higher pH. What happens when you hold your breath?
more CO2, which means more H2CO3, which means more HCO3 and H+ which means more acidic which = lower pH
What is the percentage reabsorbed of bicarbonate in the PCT, TAL, and DC?
PCT = 85%
TAL= 10%
CD= 4.9%
0.1%-1% excreted via urine
By the Na/HATPase, the Na/HCO3 cotransporter and the Cl/HCO3 antiporter in the PCT is where the majority of bicarbonate is reabsorbed. What is the mechanism? (4)
- H+ is secreted into lumen via Na/Hatp
- H+ combines with HCO3, which is then broken down by carbonic anhydrase into CO2 and H20, which freely cross the apical membrane into the cell
- CO2 h2o combine again via CA forming HCO3 and H+ 4. H+ is recycled to go back to lumen and get more HCO3, HCO is transported into the blood against 1 Cl, or 3 HCO3 co transported with 1 Na
The primary factors that regulate increased H secretion and HCO3 reabsorption are a decrease plasma HCO3 (inc pH) and an increase in pressure of CO2. Secondary that regulate Increased H+ secretion and HCO3 reabsorption include? (5)
Increased filtered load of HCO3
Decreased ECF volume
Increased AGTII because Na/Hexchange increases
Increased aldosterone because inc in Na (CD)
Hypokalemia (PCT for all others)
Phosphate buffering of secreted hydrogens helps regenerate lost HCO3 that had been consumed elsewhere when the NaH2PO4 lost an H+ in a less acidic compartment, how?
So the extra H+ is secreted and bound to NaHPO4-, which forms NaH2PO4 which is then secreted in the urine
Ammonia is also commonly used to bind and release H+ to generate new bicarbonate. In the PCT, glutamine is broken down into Nh3 and NH4, which NH3 binds with H+, in the thick ascending loop what occurs?
NH4 takes K’s space in the NKCC2 where the H+ is taken and NH3 diffuses into the CD where it picks up MORE H+ to generate more HCO3 in the CD
In the CD, Aintercalted cells secrete H+ and reabsorb HCO3 whilce B-intercalated cells secrete HCO3 and reabsorb H+. Why does the opposite occur in each cell?
In A-intercalated, the HATPase is on the apical side while the HCO3 transporter is on the basolateral side (go to blood)
In B-intercalated, the HATPase in on the basolateral side, and the HCO3/Cl antiporter is on the apical side, send the HCO3 right into the lumen to be excreted
net acid excretion must equal nonvolatile acid production each day in order to maintain acid-base balance. What is NAE equation?
= (Unh4*V) + (Uta+ * V) - (Uhco3 *V)
Where Uta is salts of primary phosphate but other consitituents of urine such as creatinine do contribute
The normal values for pH, H, Pco2, and HCO3 are 7.4 40mEq/l, 40mmhg, and 24mEq/L respectively. During respiratory acidosis, there is a decrease in pH, increase in H+, large increase in PCO2, and a small increase in HCO3. What occurs in resp alkalosis, and metabolic acidosis/alkalosis?
Respiratory alkalosis: increase, dec, large dec, dec
Metabolic acidosis: dec, inc, dec, Large dec
metabolic alkalosis: inc, dec, inc, large inc
What are the renal and respiratory compensation when there is a loss in HCO3 or a gain in H+ = metabolic acidosis?
Resp: hyperventilation, decrease Pco2, decreasing H+
Renal: Increase acid titration= inc. NH3 / HPO4 made by kidney= H+ secretion increases, increasing serum pH
How do you calculate anion gap to determine metabolic acidosis?
Na - HCO3 - Cl normal is 8-16mEq/L
MUDPILERS is for high anion gap metabolic acidosis causes. What is the mnemonic for non-anion gap metabolic acidosis?
HARDUPS
Renal tubular acidosis (RTA) is due to an accumulation of acid in the body due to failure of the kidneys to properly acidify the urine. Type 4 RTA is the most common best known for?
hyperkalemic
Type 4 RTA occurs in the adrenal cortex, presents with normal anion gap and hyperkalemia. Commonly caused by ACE inhibitors which cause what?
deficiency in aldosterone and or resisitance to its effects due to drugs.
Low aldo causes high K and low synthesis of NH3, which leads to a decrease in HCO3 generation = acidosis
What are the common symptoms associated with metabolic acidosis?
pH less than 7.4, nausea, vomitting, malaise
See long deep breaths at normal rate without dyspnea
What are the renal and respiratory compensations when there is a increase in HCO3 base and a decrease in H+ acid, as seen in metabolic alkalosis?
Resp: decreased breathing to increase CO2 and increase [H+].
Renal: 1. decreased acid titration (less acid secretion), so there is a decreased amount of Nh3 and HPO4, which leads to decreased h+ secretion and decreased HCO3 regeneration
2. dec. tubular reabsorption of bicarbonate, leading to increased excretion of HCO3
The main causes of the loss of H+ is vomitting or hyperaldosteronism (hypokalemia=inc h+ secretion)
The main causes of HCO3 gain is by?
ingetstion of NaHCO3 such as tums
What are the symptoms of metabolic alkalosis?
increased binding of Ca, hypocalemia..
headache, lethargy, neuromuscular excitability , TETANY
Respiratory acidosis is caused by decreased ventilation, increasing Co2, decreasing pH. How does the kidney compensate?
Increasing acid titration, increasing NH3 and HPO4 production to increase the amount of H+ excreted in the urine, increasing HCO3 reabsorption
Acute respiratory acidosis is associated with headache, confusion, anxiety, drowsiness, coma. If acidosis due to COPD can be well tolerated but can present with?
memory loss, sleep problems, personality changes
Respiratory alkalosis is due to increase in ventilation which leads to decrease in CO2, increasing pH. How does the kidney compensate?
decreased acid titration, decreasing amount of H+ lost in urine, decreasing HCO3 absorbed into the blood (due to lack of regeneration).
Acute symptoms of respiratory alkalosis are associated with light headedness, confusion, cramps and syncope. (tachypnea/hyperpnea). Chronic respiratory alkalosis presents as?
usually asymptomatic, no signs at all
What occurs in type 1 renal tubular acidosis?
H+ secretion by A-intercalated cells is impaired in the DCT/CD, which affects HCO3 reabsorption
What occurs in type 2 renal tubular acidosis?
Impaired proximal(CT) HCO3 reabsorption, so more HCO3 is released
High anion gap Metabolic Acidosis:
MUDPILERS… what are the important ones?
Anything acidotic, salicytes/aspirin overdoes, renal failure
NonAnione gap Acidosis:
HARDUPS
RTA
diarrhea
spironolactone
Metabolic alkalosis:
CLEVER PD
Contraction
Vomiting
Diuretics
Respiratory Acidosis:
CANS (acute)
CNS depression Airway obstruction Neuromuscular disorders Severe pneumonia (Chronic: COPD)
Respiratory Alkalosis:
CHAMPS
CNS disease Hypoxia Anxiety ventilators Sepsis
