Exam 4 Review:  Chapter 26:  Acid-Base Homeostasis

buffer - A chemical or mixture of chemicals, usually a weak acid or base and its corresponding salt, which minimizes change in the acidity of a solution, the pH, when an acid or base is added to the solution.

protein buffer system - The most abundant buffer system in cell cytoplasm and in blood plasma; because proteins are composed of amino acids joined in a linear string by peptide bonds, they always possess at least one free amino group (-NH₂) and one free carboxylic acid group (COOH^-) at opposite ends of the strand, and they often possess additional free amino groups and carboxylic acid groups because those groups are present on the R-group side chains of a variety of amino acids; these free amino groups and carboxylic acid groups act as weak acids and bases respectively, and, as a result, can combine with H⁺ ions, reducing the concentration of free H⁺ ions in the solution, a buffering function.

hemoglobin buffer - The property of hemoglobin which allows its various exposed or free amino groups and carboxylic acid groups to act as weak acids and bases respectively, and, as a result, hemoglobin can combine with H⁺ ions, reducing the concentration of free H⁺ ions in the erythrocyte cytoplasm, a buffering function; hemoglobin plays a significant secondary buffering role in the blood, supporting the more important carbonic acid-bicarbonate buffer system found in the plasma; the capacity of hemoglobin to form ionic bonds with H⁺ ions is also related to hemoglobin's ability to transport oxygen because when a hemoglobin molecule ionically bonds with H⁺ ions it tends to favor a consequent dissociation from oxygen; therefore, in the presence of increased hydrogen ions, hemoglobin has less affinity for oxygen and this means that hemoglobin will "unload" oxygen more readily in the capillaries of metabolically active tissues which are liberating H⁺ ions and CO₂, both of which contribute to a more acidic pH environment; this property is known as the Bohr effect.

phosphate buffer system - A secondary buffer system in cell cytoplasm, body fluids and blood plasma; phosphate ions (HPO₄^-2) can form ionic bonds with one or two H⁺ ions, reducing the concentration of free H⁺ ions in the surrounding solution, a buffering function.

carbonic acid-bicarbonate buffer* - Bicarbonate ions can absorb H+ ions to form carbonic acid which can be transported to the lungs where the reaction is reversed, the H+ ions are converted to water molecules and CO₂ is excreted.  [See the chemical equation under carbonic anhydrase below.]  It is an extracellular buffer. The main role of this system is to buffer against the acids produced by fat & protein metabolism or ones produced in oxygen deficiency or starvation; it cannot buffer against the acidity of excess CO₂, which occurs with hypoventilation;  this buffer system is dependent on a functioning respiratory system to excrete the carbon dioxide.  [Note*:   A buffer is a substance which minimizes change in the pH (acidity) of a solution when an acid or base is added to that solution.]

carbonic anhydrase - An enzyme found in erythrocytes and renal tubular epithelial cells which catalyzes the reversible reaction in which carbon dioxide and water combine to form carbonic acid; it is an enzyme with great catalytic efficiency so it can be present in very low concentration and still be effective.  [Note:  Carbonic acid spontaneously dissociates into hydrogen ion and bicarbonate ion at normal body fluid pH.]

                                        (carbonic anhydrase)

    CO₂             +     H₂O <============> H₂CO₃ <============> H⁺         +     HCO₃^-  

carbon dioxide +     water                            carbonic acid                       hydrogen ion + bicarbonate ion 

volatile acid - An alternative name or nickname referring to carbonic acid or the bicarbonate ion which emphasizes the contribution of carbonic acid and the bicarbonate ion to the pH of body fluids and to physiological acid-base balance and emphasizing the fact that this one type of physiological or metabolic acid can be excreted by the lungs into the atmosphere.  [Note: in chemisry, "volatile" means vaporating readily at normal temperatures and pressures.]

fixed acid - An alternative name or nickname referring to any acid other than carbonic acid or the bicarbonate ion, acids which are found in and contributes to the pH of body fluids and to physiological acid-base balance and emphasizing the fact that these physiological or metabolic acids, usually organic acids, cannot be excreted by the lungs into the atmosphere and are, instead, excreted into the urine; examples include lactate, phosphate, sulphate, acetoacetate and beta-hydroxybutyrate.

acidosis - Any abnormal increase in the acidity of the body's fluids (with a corresponding drop in the pH below 7.35), caused either by the accumulation of acids (increase in hydrogen ions) or by depletion of bicarbonate ions which serve as buffers; there are a variety of specific causes which fall into two main groups, respiratory and metabolic.

acidemia - (1) Any situation in which the hydrogen ion concentration in the blood is increased to the degree that the blood pH is < 7.0; it may or may not fall outside of the normal range for blood pH.  (2) A group of relatively rare inherited metabolic disorders in which the absence of a critical enzyme causes the accumulation of a particular organic acid intermediary metabolite in the blood and body fluids; many specific examples are known.  [See the The Organic Acidemia Association.]

respiratory acidosis - A metabolic derangement of acid-base balance in which the blood pH is abnormally low (<7.35) and the cause is improper ventilation, hypoventilation, which leads to the accumulation of carbon dioxide in the blood (pCO₂ > 45 mm Hg), secondary to a variety of disorders including chronic obstructive pulmonary diseases (COPDs), e.g., asthma, emphysema, pulmonary fibrosis, pneumonia, tuberculosis, etc.

metabolic acidosis - A metabolic derangement of acid-base balance in which the blood pH is abnormally low (<7.35) and the cause is anything other than improper ventilation, hypoventilation, and which usually leads to the loss of significant amounts of bicarbonate buffer in the blood (HCO₃^- < 23 mEq/L), secondary to a variety of disorders including hemorrhagic shock, cardiogenic shock, severe dehydration, septicemia, ingestions of toxic chemicals, e.g. methanol, isopropyl alcohol, salicylates (aspirin poisoning), severe diarrhea, alcoholic ketoacidosis, diabetic ketoacidosis, lactic acid, renal failure, etc.

alkalosis - Any abnormal decrease in the acidity of the body's fluids (with a corresponding rise in the pH above 7.45), caused either by the loss of acids (decrease in hydrogen ions) or by the accumulation of bicarbonate ions which serve as buffers; there are a variety of specific causes which fall into two main groups, respiratory and metabolic.

alkalemia - Any situation in which the hydrogen ion concentration in the blood is decreased to the degree that the blood pH is > 7.0; it may or may not fall outside of the normal range for blood pH.

respiratory alkalosis - A metabolic derangement of acid-base balance in which the blood pH is abnormally high (>7.45) and the cause is improper ventilation, hyperventilation, which leads to the loss of carbon dioxide, and therefore of both H⁺ and HCO₃^-, from the blood (pCO₂ < 35 mm Hg), secondary to a variety of disorders including asthma, fever, and emotional hysteria.

metabolic alkalosis - A metabolic derangement of acid-base balance in which the blood pH is abnormally high (>7.45) and the cause is anything other than improper ventilation, hyperventilation, and which usually leads to the accumulation of significant amounts of bicarbonate buffer in the blood (HCO₃^- > 26 mEq/L), secondary to a variety of disorders including prolonged vomiting, diuretic therapy, hyperadrenocortical disease, and the administration of exogenous bases (antiacids, bicarbonate IV, citrate toxicity after massive blood transfusions)

compensation - The increase in size or activity of one part of an organism or organ which makes up for the loss or dysfunction of another part; in terms of acid-base derangements, the first line of defense against disturbances in pH are the intra- and extracellular buffering systems which minimize the change in pH; in more serious situations, additional mechanisms to resist further changes in pH are respiratory adjustments of extracellular fluid (ECF) PCO₂ and renal adjustments of ECF HCO₃^- concentration; such adjustments for acid base imbalance are only partially effective; perfect compensation, without correcting the underlying cause of the pH disturbance, is not possible because it would remove the stimulus for the compensatory mechanisms and the imbalance would be re-established; furthermore the compensatory mechanisms act not only to minimize changes in the pH but also operate, after correcting the cause of the pH disturbance, to restore the body's buffer reserves leaving it more able to cope with repeated episodes of acid-base disturbance.

respiratory compensation - Any change in the rate and depth of ventilation which the body makes in the attempt to resist a derangement of acid-base balance of metabolic origin; hypoventilation will resist a metabolic alkalosis while hyperventilation will resist a metabolic acidosis; perfect or permanent compensation, without correcting the underlying metabolic cause of the pH disturbance, is not possible.

hypoventilation - Abnormally slow or shallow respiration, which results in the retention of carbon dioxide in the blood, the retention of CO₂ may lead to respiratory acidosis.

hyperventilation - Abnormally fast or deep respiration, which results in the loss of carbon dioxide from the blood, thereby causing a fall in blood pressure, tingling of the extremities, and light-headedness, dizziness, and sometimes fainting and chest pain if continued; the loss of CO₂ may lead to respiratory alkalosis.

metabolic compensation - Any change in the secretion of H⁺ or the production and retention (reabsorption) of HCO₃^- by the kidneys, which the body makes in the attempt to resist a derangement of acid-base balance of respiratory origin; reduced H⁺ secretion and reduced HCO₃^- reabsorption will resist a respiratory alkalosis while increased H⁺ secretion and increased HCO₃^- reabsorption will resist a respiratory acidosis; perfect or permanent compensation, without correcting the underlying metabolic cause of the pH disturbance, is not possible.   

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