Acid-Base Regulation (Week 11) Flashcards
pH that is considered acidemia
< 7.4
pH that is considered alkalemia
pH > 7.4
major organs for acid-base regulation
kidney and liver
how does a buffer interact with H+ and how does it affect pH
when H+ is added to a system with a buffer the H+ combines with the buffer; instead of H+ concentration increasing a new compoun is formed and the pH isn’t changed
role of kidneya and lung in bicarbonate buffer system
lungs handle CO2 and kidney handles bicarbonate; if one of these organs isn’t working well then the equation shifts to the side that is functioning
two major acid-base functions of kidney
- reabsorb bicarbonate
- excrete H+
how much bicarbonate is filtered/reabsorped in kidney?
bicaronate is freely filtered (small ion); 100% is reaborbed normally
how is bicarbonate reabsorbed?
bicarbonate combines with H+ and is formed into H20 + CO2 by carbonic anhydrase; crosses apical membrane; bicarbonate reformed in cell and transported across basolateral membrane
urine buffers
phosphate (fixed buffer) and ammonia (regulated buffer)
ammonia production compared to body acid
increased acid in body => increase ammonia production
factors that increase renal H+ excretion (4)
- decrease extracellular pH (increase H+ conc)
- decreased plasma K+
- decreased ECV
- increased aldosterone
kidney response to metabolic acidosis and where it occurs
- proximal tubule cells makes more ammonia; increase Na+/H+ activity
- ATP activity – secreting more H+ to lumen via increase H+ ATPase activity
- Collecting Tubule; Intercalated Cell Type A
kidney response to metabolic alkalosis and where it occurs
Intercalated Cell Type B in collecting tubule
puts bicarbonate into urine and reabsorbs H+
when are intercalated cell tyle B cells activated?
only in metabolic alkalosis; are otherwise dormant
affect of ECV on acid secretion by kidney
decreased ECV increases RAAS
Na+ reabsorbed and H+ secreted in process
increased H+ excretion
summary: decreased ECV can result in metabolic alkalosis
aldosterone affect on H+ excretion
aldosterone induces metabolic alkalosis via increase H+ excretion
- Na+ reabsorbed as H+/K+ excreted
- H+-ATPase pump gets stimulated
- HCO3- /Cl- pump activated
what is the relationship between plasma K+ and renal H+ excretion?
decreased plasma potassium = K+ move out of cells and H+ move into cells
leads to intracellular acidosis in kidney causing a response that leads to metanolic alkalosis
decreased K+ = metabolic alkalosis
hyperkalemia and plasma H+
hyperkalemia causes metabolic acidosis (and metabolic acidosis causes hyperkalemia)
bicarbonate buffer system imbalance in metabolic acidosis
decreased HCO3-
bicarbonate buffer system imbalance in metabolic alkalosis
increased HCO3-
bicarbonate buffer system imbalance in respiratory acidosis
increased PCO2
bicarbonate buffer system imbalance in respiratory alkalosis
decrased PCO2
respiratory compensation for metabolic acidosis
hyperventilation (decreased PCO2)
trying to increase the pH to keep it at 7.4
If CO2 levels high, kidney will compensate by increasing bicarbonate in system
causes of low bicarbonate (metabolic acidosis)
- bicarbonate loss (renal, diarrhea)
- consumption of HCO3- (increased acid in body)
- failure of regeneration (renal failure, RTA distal)
AGMA
anion gap metabolic acidosis,
charge of serum; ratio of cations to anions
serum is electroneutral; the total cations = total anion
equation for anion gap/unmeasured anions
anion gap: Na+ - (Cl-) - HCO3- = unmeasured anions
typical amount of unmeasured anions
12 +- 2 mEq/L
the four “unmeasured” anions
SOAP
Sulfate, Organic acids, Albumin, Phosphate
how does adding non-chloride acid contribute to the anion gap?
as acid is added to system, bicarbonate combines with acid to form water, co2, and an anion – the anion contributes to the anion gap
AH + NaHCO3- <–> H20 + CO2 + NaA
how does adding chloride-containing acid contribute to the anion gap?
bicarbonate combines with the added acid to from water, co2, and salt (NaCl)
chloride is a measured anion, so it does not contribute to the anion gap
magnitude of chloride increase and bicarbonate decrease are same magnitude; cancel each other out
mneumonic for metabolic acidosis
GOLDMARK
glycols, oxoproline, lactate L, lactage D, methanol, aspirin, renal failure, keto-acids
AGMA is considered by an anion gap of what value?
>12
enzyme that converts alcohol to acid
alcohol dehydrogenase
what acid does antifreeze form when converted by alcohol dehydrogenase?
ethylene glycol –> oxalic acid
wood alcohol conversation by alcohol dehydrogenase
methanol –> formic acid
normal osmolar gap
10
common toxic alcohols
ethylene glycol (antifreeze)
methanol (wood alcohol)
how does toxic alcohol affect osmolal gap?
increases it significantly after ingestion; can be seen on lab test of patients osmolality
how to treat ingestion of toxic alcohol?
the acid, not the alcohol, is what is dangerous to the patient; give medication to block alcohol dehydrogenase to prevent conversion from alcohol form to acid form
lactic acidosis type A
AGMA via lactic acid accumulation
due to tissue hypoxia, hypoperfusion
examples: shock, sepsis, hypovolemia
lactic acidosis type B
AGMA from lactic acid accumulation
result of liver disease
where is lactate metabolized?
liver and kidneys
treatment of lactic acidosis
treat the hypoxia, hypoperfusion
can give HCO3- if pH < 7.2
AGMA and NAGMA from renal failure
AGMA: due to excess phosphate and sulfate (would normally be excreted in a healthy kidney)
NAGMA: due to lack of acid excretion leads to accumulation of increased H+; (later stage) decrased NH4+ excretion
treatment of AGMA/NAGMA in renal failure
oral sodium bicarbonate – to give buffer to the system
what happens in untreated NAGMA/AGMA in renal failure?
not enough buffer, acid uses proteins in bones as buffer leading to osteoporosis
Diabetic Ketoacidosis (DKA)
lack of insulin leads to lipolysis and increased fatty acid in liver; increased glucagon leads to conversion of fatty acids to ketoacids in liver
AGMA due to increased B-hydroxybutyric acid and acetoacetic acid
treatment for diabetic ketoacidosis and what happens if left untreated
treatment - insulin and IV fluids
if untreated – death
effects of aspirin ingestion on acid-base balance in body
salicylic acid (aspirin) causes AGMA from acid addition and can cause respiratory alkalosis because aspirin is a direct stimulant of the respiratory centers in our brain – patient hyperventilates
can you have both metablolic/respiratory acidosis/alkalosis?
can have metabolic acidosis and alkalosis at same time; can only have either respiratory acidosis or alkalosis (can’t be hyper and hypoventilating at same time)
Renal Tubular Acidosis: Type 1
primary defect
common example
serum HCO3-
K+ (increased or decreased)
urine pH
decreased distal acidification
amphotericin B, lithium
<10
decreased
always 5.5
Renal Tubular Acidosis: Type 2
primary defect
common example
serum HCO3-
K+ (increased or decreased)
urine pH
decreased proximal HCO3- reabsorbtion
Fanconi Syndrome
12-20
decreased
can be lower
Renal Tubular Acidosis: Type 4
primary defect
common example
serum HCO3-
K+ (increased or decreased)
urine pH
decreased aldosterone
diabetes
17+
increased
can be lower
Gartter Syndrome
genetic defect of transporters in the loop of henle
mimics diuretic – excretion of H+ => metabolic alkalosis
Gittelman Syndrome
genetic defect in transporters in distal tubule
mimics diuretic - excretion of H+ => metabolic alkalosis
post-hypercapnic metabolic alkalosis
chronic hypercapnia leads to kidney to compensate by increasing bicarbonate to keep pH normal –> metabolic alkalosis
milk-alkali syndrome and metabolic alkalosis
increased calcium from ingestion leads to increased HCO3- absorption
mechanism unknown
what is the acid-base result of vomitting and why?
metabolic alkalosis
H+ exits body orally; HCO3- doesn’t have downstream H+ to combo with; increased in HCO3-
what is the acid-base effect of primary mineralocoritcoid excess?
metabolic alkalosis
extra aldosterone –> increased Enac activity in distal tubule
triad of HTN, hypokalemia, metabolic alkalosis
early phase (<3 days) vs. late phase effect of vomitting/gastric suctioning on bicarbonate and urine solute levels
first step in differential diagnosis of metabolic alkalosis
look at urine chloride level
responsive vs. resistant
normal Arterial Blood Gas Levels
The 7 steps of approaching an Arterial Blood Gas result
differentiating between simple vs. mixed acid-base disorder
simple if compensation is adequate; mixed if the compensation is NOT adequate
Last Card!
Good job c:
