Acid and Bases Flashcards
acid base balance
-maintaining normal H+ concentration in body fluids
-buffers (short term)
-respiratory (short-intermediate term)
-renal (long term)
hydrogen ion concentration
-extremely low -> 40 x 10 ^ -9
-subtle changes are hard to quantity
-pH- logarithmic scale
- -log(40x10^-9) = 7.4 -> neutral
-increase in H+ -> decrease pH
-H concentration and pH is not linear -> logarithmic
-equal changes in pH do not reflect equal changes in H concentration
-acidic range change (<7.4) -> large change in H+ than same change pH in alkaline range (>7.4)**!!
intracellular pH
-7.2
-slightly acidic
-slightly lower than extracellular pH (7.4)
-uses Na-H pump -> alkalinize ICF
-Cl-HCO3 - spit out HCO3- which acidify ICF
acidemia vs alkalemia
-normal- 7.37-7.42
-acidemia- < 7.37
-alkalemia- > 7.42
-6.8-8.0- compatible with life
acid production in body
-arterial pH is alkaline (7.4) even though produces acids
-these present a challenge to normally alkaline pH
-2 forms:
-volatile acid (CO2)- gas that can be exhaled
-nonvolatile- fixed
CO2 volatile acid
-CO2 itself is not an acid
-CO2 is end product of aerobic metabolism
-CO2 + water in the presence of carbonic anhydrase -> carbonic acid -> dissociated into H+ and bicarbonate in venous blood
-high levels of H+ will combine with bicarbonate -> turn into carbonic acid (H2CO3) -> and converts to CO2 and water -> exhaled
-gets rid of additional acids
-exhaling -> increases pH
-TOO MUCH CO2 -> RESPIRATORY ACIDOSIS
-BREATHE OFF TOO MUCH CO2 -> RESPIRATORY ALKALOSIS
nonvolatile acids
-fixed
-catabolism of proteins and phospholipids
-proteins with sulfur-containing amino acids -> generate sulfuric acid
-phospholipids -> generate phosphoric acid
-must be buffered in body fluids until they are excreted by kidneys
-takes longer to rid of these
-beta hydroxybutyric acid and acetoacetic acid are ketoacids- produced with uncontrolled diabetes mellitus
-lactic acid byproduct of anaerobic respiration -during strenuous exercise or hypoxic tissue
-ingestion of acids- salicylic acid (aspirin overdose), formic acid (methanol), glycolic and oxalic acids (ethylene glycol)
-TOO MANY FIXED ACIDS -> METABOLIC ACIDOSIS
buffer
-weak acid and its conjugate base OR
-a weak base and its conjugate acid
-accepts extra H+ or produce extra H+
Henderson-Hasselbalch equation
-acid that gives off H+ and conjugate base that can accept H+
-chemical equilibrium- forward and reverse equation is equal -> no further net change in concentration of HA (weak acid) or conjugate base (A-)
titration curve
-sigmoidal shape
-dependent on acid being used
-pK- equal amounts of acid and base
-linear portion of curve- small changes in pH -> most effective buffering zone
-outside the buffering zone -> drastic changes in pH with addition/removal of H+
-bicarbonate / CO2
SMOR
-same metabolic- pH is low bicarbonate is low (acidotic) ; pH is high bicarbonate is high (alkalotic)
-opposite respiratory- pH is low CO2 is high; pH is high CO2 is low
bicarbonate as a buffer
-A- form is HCO3-
-HA form is CO2
-most important ECF* buffer (better than phosphorous)
-concentration of bicarbonate (A-) is extremely high -> able to accept a lot of H+ without running out of concentration
-works longer!
-CO2 (acid form) can be expired out -> volatile -> fast acting
-also important bc pK is close to pH of ECF (6.1)
-ex. HCl added to ECF -> becomes H2CO3 -> strong acid become a weak acid -> then dissociated to CO2 and H2O -> expire
phosphate as a buffer
-A- form is HPO4-2
-HA form H 2 PO4-
-phosphorous is very low concentration -> only accept certain amount of H+
respiratory compensation
-pK of CO2 buffer is 6.06 -> this is fatal pH
-acidemia stimulates chemoreceptors in carotid bodies -> hyperventilation -> excess CO2 (and more) expired
-drives Pco2 down to lower than normal
-buffering by HCO3- and respiratory compensation -> normal pH! (7.4)
-final touches tweaked by renal
ICF buffers
-organic phosphates and proteins (ATP, ADP, AMP, glucose-1-phosphate, 2,3 DPG) -> accept H+
-HEMOGLOBIN- accepts H+
-in order for buffer to work in ICF H+ on the buffers must get through the cell membrane itself -> 3 mechanisms:
-1. CO2- can cross (ex. respiratory acidosis- CO2 rushes into cell and generates H+ which is buffered by ICF buffers)
-2. if H+ is increased/decreased by fixed acid -> H+ can cross with organic anion (fixed acid) -> (ex. H+ and lactate can cross into cell during metabolic acidosis, preserving electroneutrality
-3. H+ exchange with K+ to preserve electroneutrality (in absence of organic anion)
Ca concentration
-negative groups on plasma proteins (albumin) can bind either H+ or Ca2+
-acidemia- excess H+ -> binds to plasma proteins -> high free Ca concentration
-alkalemia- deficit in H+ -> more Ca2+ is bound -> decrease in free Ca concentration (hypocalcemia)
-respiratory alkalosis- deficit in H+ -> hypocalcemia -> tingling, numbness, tetany
hemoglobin
-most significant ICF buffer
-oxyhemoglobin releases O2 to tissues -> deoxyhemoglobin
-CO2 is added to systemic capillary blood from tissues
-CO2 diffuses into RBC -> combines with H2O -> forms H2CO3 -> dissociates into H+ and HCO3-
-H+ generated is buffered by hemoglobin which is then in the deoxygenated form
-venous blood pH 7.37 -> very good for the amount of acids involved with CO2 dissociation
2 major role of kidneys in acid-base balance
-reabsorption of bicarbonate ions
-excretion of H+ ions
excetion of H+ ions by kidneys
-2 methods:
-1. as titratable acid (buffered by urinary phosphate
-2. as NH4+
-excretion of H+ is accompanied by synthesis and reabsorption of NEW HCO3-
-replenishes the HCO3- stores used in buffering fixed H+
kidneys reabsorption of bicarbonate
-important this ECF buffer isnt excreted into urine
-more than 99.9% is reabsorbed (mostly in proximal tubule 90%)
-*carbonic anhydrase- enzyme that converts CO2 + H2O to H2CO2
-if you add H+ to body -> bicarbonate concentration reduces as it accepts H+ -> breathe out more CO2 -> IMPORTANT TO MAINTAIN BICARBONATE
-body holds on to bicarbonate that is filtered
mechanism of HCO3- reabsorption in proximal tubule
-reabsorbed into blood via Na-HCO3- cotransporter OR Cl-HCO3- countertransporter
-bicarbonate is reabsorbed from tubule as CO2 and water (via brush bored carbonic anhydrase) -> converts back to HCO3- and H+ within the proximal tubule cell -> the H+ is recycled back into nephron -> bicarbonate is reabsorbed into the blood via pumps
-net reabsorption of Na and HCO3-
-no net reabsorption or secretion of H+ (no pH change)
-if we hit saturation -> we excrete bicarbonate -> this probably means we are alkalotic state
-respiratory acidosis-> increase in CO2 -> increase reabsorption of bicarbonate -> helps bring pH up
angiotensin 2: contraction alkalosis
-increased angiotensin 2 produces alkalosis
-ECF volume contraction stimulates isosmotic reabsorption in proximal tubule -> stimulates HCO3- reabsorption
-ECF volume contraction -> angiotensin 2 -> stimulates Na-H+ pump -> stimulating HCO3- reabsorption -> increasing HCO3- blood concentration -> metabolic alkalosis
-CONTRACTION ALKALOSIS
-occurs with tx with loop diuretics or thiazide diuretics
-complicating factor in metabolic alkalosis caused by vomiting
-fix this by infusing isotonic NaCl to restore ECF!!
H+ secretion: 2 ways
-2 ways
-1. secretion as a titratable acid
-2. secretion of H+ with ammonium ions
secreting H+ a titratable acid
-secreted with a urinary buffer (phosphate)
-85% of phosphate is reabsorbed and 15% is excreted as titratable acid (urinary buffer)
-alpha intercalated cells in distal convoluted tubule
-secrete H+ into tubule from H2CO2 -> forms H+ and a new bicarbonate -> bicarbonate is reabsorbed into blood
-phosphate in the tubules accepts the H+ being secreted -> becomes H2PO4 -> excreted
-as HCO3- is being used for buffering for fixed acids it is continuously being replaced
-minimum urine pH is 4.4 and highest is 7.4
aldosterone
-not only acts on principal cells to stimulate Na reabsorption and K secretion but also
-stimulates H+ secretion in alpha intercalated discs
excretion of H+ as NH4+
-3 segments involved- proximal tubule, thick ascending limb, and alpha intercalated discs of collecting ducts
-ONLY proximal and alpha intercalated are involved in secretion of NH3 and H+
-proximal tubule- H+ secreted via Na-H+ pump and combines with NH3 -> NH4
-thick ascending limb- NH4 created by proximal tubule is reabsorbed and deposited into medullary interstitial fluid
-alpha intercalated discs- NH3 reabsorbed from medullary interstitial fluid accept H+ that is secreted -> combine -> NH4
-mechanism in proximal and alpha intercalated -> create NEW bicarbonate
NH4 excretion
-portion excreted directly in urine
-remainder is excreted indirectly -> reabsorbed by thick ascending and deposited in medullary interstitial fluid -> NH3+ secretion from medullary interstitial fluid -> collecting duct -> excretion
-diffusion trapping
hyperkalemia
-K enters and H+ leaves -> increase in intracellular pH
-inhibits and reduce amount of NH3 produced
-reduce NH4 and H+ being excreted
-causes type 4 renal tubular acidosis (RTA)
-hypokalemia vice versa
diabetic ketoacidosis
-fixed H+ production increased
-to excrete extra H+ -> excretion of titratable acid and NH4 increased
-acidosis -> stimulates increase in glutamine metabolism -> increase NH3 synthesis -> more H+ excreted as NH4
chronic renal failure
-causes metabolic acidosis
-pt with CRF and eats high protein diet -> increase fixed acid production
-this disease causes loss of nephrons -> H+ excretion impaired bc:
-1. titratable acid excretion reduced bc GFR is reduced -> decrease filtered load of phosphate -> less urinary buffer
-2. NH4 excretion is reduced bc synthesis of NH3 is impaired in diseased nephrons
what you need to know
-what kind of disturbance -> metabolic or respiratory
-is it with or without compensation -> are you starting to compensate
-H+ and bicarbonate reabsorption and where
-metabolic acidosis - anion gap
normal pH
-can have abnormal CO2 or bicarbonate
-normal pH can be due to compensation for past days or hours
-cant assume!
breaking down problems
-first thing you look at is pH -> if its low -> first look at CO2 -> if CO2 is high -> respiratory acidosis
-did my bicarbonate increase? -> you are attempting to compensate
-if CO2 is NOT high -> look for bicarbonate -> if bicarbonate is low -> metabolic acidosis
-did my CO2 try to go down? -> you are attempting to compensate
-if pH is high -> look at CO2 first -> if CO2 is low -> respiratory alkalosis
-is your bicarbonate starting to decrease? -> If yes, you are starting to compensate
-if CO2 is NOT low -> if bicarbonate is high -> metabolic alkalosis
-is CO2 increasing? -> if yes, you are attempting to compensate
HARDUP
-Hypereleminatation TPN
-Acetazolamide
-Renal tubular Acidosis type 1, 2, and 4
-Diarrhea
-Uretroentestinal fistula
-Pancraeticoduodenal fistula
-causes of metabolic acidosis WITHOUT anion gap
low pH, bicarbonate is low, anion gap is normal
sodium - (bicarbonate+Cl)
-HARDUP- normal anion gap
-MUDPILES- abnormal anion gap
