Acid Base Homeo Flashcards
Three primary systems that regulate H concentration
1 chemical acid-base buffer system of body fluids (combine with acid or base to prevent excessive changes in H concentration) 2 respiratory center (removal of CO2 and carbonic acid) 3 kidneys (excrete and adjust H ion conc)
H concentration is kept at a low level in the ecf bec
All activities of enzyme system in the body are influenced by H.
pH and relationship with H ion
pH is inversely proportional to the H concentration
Low pH High H concentration
High pH Low H concentration
pH =
pH = -log [H]
pH = log 1/[H] = -log[H]
Any substance that can reversibly bind H
Buffer
How are buffers able to minimize H conc
When H conc increases, the reactions goes to the right more H ions binding with buffer to make a weak acid as long as the buffer is available.
When the H concentration decreases, the reaction shifts toward the left and H is released from buffer.
Bicarbonate buffer system 2 ingredients
1 weak acid H2CO3
2 bicarbonate salt NaHCO3
Carbonic acid is formed by reaction
by the enzyme
CO2 + H2O <=> H2CO3
Carbonic anhydrase
Carbonic anhydrase is present in
Walls of lung alveoli
Epithelial cell of renal tubules
H2CO3 is a buffer bec it can ionize quickly to form
H2CO3 <=> H + HCO3
NaHCO3 is also a buffer in the ECF bec it ionizes quickly to form
NaHCO3 <=> Na + HCO3
Bicarbonate buffer system equation
CO2 + H2O <=> H2CO3 <=> H + HCO3 + Na
Weak dissociation of carbonic acid yields few H conc
Adding strong acid to the bicarbonate buffer solution is buffered by
yielding greater amounts of H2O and CO2.
Elimination of CO2 from ECF is by
HCO3
respiration (hypervent)
The opposite occurs if a strong base is added. There will be dec CO2 and inc HCO3 that is compensated by inc renal excretion of HCO3.
Henderson Hasselbach =
pH = 6.1 + log HCO3/0.03xPCO2
Henderson Hasselbach calculates
pH of soln if the molar concentration of HCO3 and PCO2 are known
defines determinants of normal pH regulation and acidbase balance of ECF
Increase in HCO3 causes
Inc in PCO2 causes
pH to rise shifting acid base balance toward alkalosis
pH to decrease shifting acid-base balance toward acidosis
HCO3 is regulated mainly by
PCO2 is controlled by
Kidneys
Rate of respiration
When two components of buffer system are equal, the pH according to the Henderson-Hasselbach is
equal to pK (dissociation constant) 6.1 of bicarbonate buffer system
Buffer power is determined by
Amount and
relative concentration of buffer component
The buffer system is most effective when
region in titration curve
pH is near the pK
center
Most important extracellular buffer
Bicarbonate buffer system
Phosphate buffer system is important in tubular fluids and kidneys and ICF bec
1 phosphate becomes greatly concentrated in tubules inc buffering power of phosphate system
2 tubular fluid has low pH than ECF bringing operating range of buffer close to pK 6.8 of system
In RBCs hemoglobin is a buffer:
H + Hb <=> HHb
60-70% of chemical buffering of body fluids inside the cell is a result of
intracellular protein buffer
but delayed due to slow diffusion of Bicarbonate and H through cell to buffer ECF
Whenever there is change in H concentration in ECF, balance of all buffer systems change at same time.
Isohydric Principle
Any condition changing the balance of one buffer system changes the balance of others bec the buffer actually buffers one another by shifting H back and forth.
Non volatile acids from protein metabolism are so
Bec they are not excreted by lungs not H2CO3
Reduction in ECF H concentration causes failure of kidney to
reabsorb filtered HCO3
inc excretion of HCO3 to raise H conc back to normal
Kidneys regulate ECF H conc through 3 mechanims
secretion of H
reabsorption of filtered HCO3
production of new HCO3
80-90-% bicarb reabsorption and H secretion occurs in
H secretion and bicarb reab occur in all parts of the tubules except
PCT
thin limbs LOH
H is secreted in PCT, thick ascending LOH and early DT by
Na-H counter transport
Secondary active transport
H secretion and HCO3 reabsorption:
CO2 diffuses or formed by metabolism in tubular epithelial cell
CO2 + H2O by carbonic anhydrase into carbonic acid
Then dissociates into H and HCO3
H is secreted from cell into lumen by Na-H exchanger
Na moves into cell and H moves out into lumen
The HCO3 in the cell moves downhill at the basolateral membrane into interstitial fluid and peritubular capillary
Net result: for every H secreted into lumen, a bicarb entes the blood
Transport of bicarbonate across basolateral membrane is facilitated by
1 NaHCO3 co transport in PCT
2 Cl-HCO3 exchange in late segment of PCT abs TAL, CT, CD
Each time a H is formed in tubular epithelial cell,
a bicarb is formed and released back into the blood
During acidosis excess H is buffered in tubules by
phosphate
ammonia
In distal tubule and cd tubular epithelium intercalated cells secretes H by
active transport by H-transporting ATPase
In acidosis, excess H supposedly excreted in the tubule when all HCO3 are exhausted is combined with
Phosphate and ammonia buffers to generate new HCO3 helping replenish lost HCO3
or excreted as Na salt NaH2PO4 carrying excess H
Ammonia in kidney comes from
glutamine
for each molecule of glutamine in PCT two ammonia are secreted in urine and two bicarbonate are reabsorbed into blood
In the collecting duct, ammonia buffering
for each ammonia excreted a new HCO3 is generated and added to the blood
With chronic acidosis, the dominant mechanism by which acid us eliminated is
excretion of ammonia
also most important mechanism of generatinf bicarb in chronic acidosis
Inc H secretion and HCO3 reabsorption
Inc PCO2 inc H Dec HCO3 Dec extracellular fluid Inc angiotensin II Inc aldosterone Hypokalemia
Dec H secretion and HCO3 reabsorption
Dec PCO2 Dec H and Inc HCO3 Inc ECF Dec Angiotensin II Dec Aldosterone Hyperkalemia
In metabolic acidosis, the compensations
1 inc ventilation rate dec PCO2
2 renal comp by adding HCO3 to ECF
In respi alkalosis, primary compensation:
1 reduction in plasma HCO3 by renal excretion
In metabolic alkalosis, primary compensation:
1 dec ventilation raising PCO2
2 inc renal excretion of HCO3
Renal tubular acidosis (Metabolic Acidosis) assoc d/o
1 chronic renal f
2 Addison’s disease dec aldosterone
3 Fanconi
Most frequent cause of metab acidosis
Diarrhea bec of large amounts of sodium bicarb excretion in feces
Ingestion of acids contribute to formation of metabolic acidosis
Aspirin
Methyl alcohol lambanogz
Diuretics except CA inhibitors cause metabolic alkalosis bec
Inc fluid flow in tubule promotes Na reabsorption which is coupled with H sec and inc bicarb reabsorption
Also aldosterone excess (Conn’s)
Anion gap formula
Anion gap = Na - (Cl + HCO3)
Anion gap inc if
unmeasured anions rise (albumin, phosphate, sulfate)
unmeasured cations fall (Ca, Mg, K)
N= 8-16
Metabolic acidosis with Normal Anion Gap 4
diarrhea
renal tubular acidosis
carbonic anhydrase inhibtors
addison’s
Metabolic Acidosis with inc anion gap normochloremia
DM Lactic acidosis Chronic renal failure Aspirin poisoning Methanol poisoning Ethylene glycol Starvation
