Acid Base

Front 1

what is henderson-hasselbalch equation?

Back 1

pH= pKa + long salt/acid

Front 2

list sources of gain and loss of H ions

Back 2

GAIN
-generation of H ions from CO2
-production of nonvolatile acids from metabolism of protein and other organic molecules
-gain of H due to loss of bicarbonate in diarrhea or other nongastric GI fluids
LOSS
-utilizaton of H ions in metabolism of various organic anions
-loss of H ions in vomitus
-loss of H ions in urine
-hyperventilation

-volatile acids- eg carbonic acid from aerobic metabolism of fat and carbohydrate, 13000 mEq/day
-nonvolatile acids- eg acids of sulfate, phosphate from protein and phopholipid metabolism and anaerobic CHO metabolism, organic ions, 70 mEq/day

Front 3

describe different chemical buffer systems

Back 3

-bicarbonate H2CO3/NaHCO3; weak buffer, predominant in ECF and proximal tubule but also imp in intracellular fluid; regulated via pulmonary handling of CO2 and renal handling of HCO3-
-phosphate NaH2PO4/Na2HPO4; strong buffer, ICF, distal tubule and collecting duct, not readily regulated or replenished
-proteins- predominant in ICF; eg histidine and hemoglobin

Front 4

describe acid excretion

Back 4

1. volatile acid via pulmonary expiration of CO2
CO2 + H2O = H2CO3 = H + HCO3-
-inc arterial H (PaCO2) activates chemoreceptors to cause hyperventilation leading to dec PaCO2; hypoventilation to a lesser capacity bc significant hypoventilation accompanied by hypoxia stimulates ventilation
2. nonvolatile acid via kidney
80% of HCO3- reabsorbed in proximal tubule by H from carbonic acid transported across luminal membrane by Na/H exchanger (Na in, H out into lumen)

Front 5

describe renal excretion on carbonic acid

Back 5

in lumen- HCO3- + H forms H2CO3 via carbonic anhydrase forms H2O and CO2
-CO2 diffuses into proximal tubule cell and combines with H2O to form carbonic acid which is reabsorbed into blood with Na cotransporter or Cl counter transporter
-H ion in tubular cell sent back into lumen via Na/H exchanger and H ATPase
-in situations of dec acid production, H may be transported back into blood while HCO3- is secreted

Front 6

describe use of phosphate and ammonium as buffers

Back 6

-maximum pH of collecting tubule is 4, remainder of urinary H must be excreted in buffered form, usually phosphate or ammonium
-at pH of 4 only .1% to .2% of daily load of acid can be excreted as non-buffered H
-rest in buffered form
1. phosphate- H of organic acids enters cell as H2O and combines with CO2 to form H and HCO3; H is secreted via H ATPase and combines with phosphate buffer to be excreted
2. NH3 is freely diffusable and enters tubule and recombines with H to form ammonium to be excreted
-eg glutamine broken down to form new HCO3- which is reabsorbed and ammonium which can be secreted via Na coutertransporter (Na in) or by Na/H coutertransporter and NH3 freely diffusing across
- net acid excretion = titratable acidity + NH4+ -urinary HCO3-

Front 7

describe respiratory acidosis

Back 7

-results from alveolar hypoventilation such as in obstructive lung disease and impaired respiratory centers
-causes dec elimination of CO2
-leads to inc PCO2 hypercapnia
-leads to dec arterial pH
-signs/symptoms CNS depression, lethargy, confusion, coma

Front 8

describe respiratory alkalosis

Back 8

-results from alveolar hyperventilation; can be caused by anxiety, nervousness, fever, drugs, hypoxia
-causes inc elimination of CO2
-leads to dec PCO2 hypocapnia
-causes inc in arterial pH
-signs neural excitation, lightheadedness, paresthesias, tetany, convulsion

Front 9

describe metabolic acidosis

Back 9

-HCO3- loss or inc nonvolatile acid load (lactic acid, diabetic ketoacidosis, poisoning, diarrhea) leads to dec arterial pH
-signs CNS depression, lethargy, confusion, coma, compensatory hyperventilation

Front 10

describe metabolic alkalosis

Back 10

-HCO3- retention or less nonvolatile acid load- vomiting, antacid ingestion leads to inc in arterial pH
-signs CNS excitation, lightheadedness, paresthesias, tetany, convulsion, compensatory hypoventilation

Front 11

define the anion gap

Back 11

- 8-16 mEq/L of Na+ charges are not neutralized by Cl and HCO3-
-remaining covered by anions in plasma (phosphate, sulfate, organic acids and proteins) is called anion gap
= concentration of Na - (concentration of Cl + HCO3-)
-range of 8-16 mEq/L

Front 12

describe anion gap metabolic acidosis

Back 12

-metabolic acidosis produced as a result of excess production of organic acids
-diabetic ketoacidosis and lactic acidosis are common eg
-HCO3- consumed mmole per mmole of acid produced and replaced by anion of acid (lactate)
-anion gap inc as a result of dec in HCO3-
-ingestion of substances such as methanol and salicylates can also cause
-chloride remains normal usually
-not always associated with pH less than normal eg prolong vomiting eventual build up of lactic acid with loss of HCl in vomiting exceeding lactic acid production leading to alkalosis but lactic acid production inc anion gap
-normal anion gap (non-anion gap metabolic acidosis) is metabolic acidosis due primarily to NaHCO3 loss- indirect loss of HCO3 as kidneys fail to excrete NH4 and generate new HCO3

Front 13

describe the osmolal gap

Back 13

plasma osmolal gap = measured osmolarity-calculated osmolarity

calculated osmolarity = 2Na mMol/L + BUN/2.8 mg/dl + glucose/18 mg/dl
-osmolal gap suggest some osmotically active material is present in plasma that is not Na or its anions, urea, or glucose; in metabolic acidosis osmoticaly active acid- forming intoxicants such as methanol, ethanol or ethylene glycol

Front 14

describe relationship of plasma H and K

Back 14

-K loss and deficiency promotes metabolic alkalosis
-hypokalemia leads to acidification of principal cells leads to Na/H exchange inc, leads to inc urinary excretion of H
-alkalosis promotes hypokalemia
-alkalemia leads to alkalinization of principal cells leads to inc Na/K exchange leads to inc urinary excretion of K
-hyperkalemia reduces ammonium synthesis and excretion
-acidosis inhibits Na/K exchange adn dec apical K channels