Figure 27-1a The Composition of the Human Body.

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Presentation transcript:

Figure 27-1a The Composition of the Human Body. SOLID COMPONENTS (31.5 kg; 69.3 lb) WATER (38.5 kg; 84.7 lb) 15 20 Other 15 Plasma 10 Liters Kg 10 Interstitial fluid 5 5 Proteins Lipids Minerals Carbohydrates Miscellaneous Intracellular fluid Extracellular fluid a The body composition (by weight, averaged for both sexes) and major body fluid compartments of a 70-kg (154-lb) person. For technical reasons, it is extremely difficult to determine the precise size of any of these compartments; estimates of their relative sizes vary widely. p. 1018

Figure 27-1b The Composition of the Human Body. ICF ECF ICF ECF Intracellular fluid 27% Interstitial fluid 18% Intracellular fluid 33% Interstitial fluid 21.5% Plasma 4.5% Other body fluids (≤1%) Plasma 4.5% Solids 50% (organic and inorganic materials) Solids 40% (organic and inorganic materials) Other body fluids (≤1%) Adult males Adult females b A comparison of the body compositions of adult males and females, ages 18–40 years. p. 1018

Figure 27-2 Cations and Anions in Body Fluids (Part 1 of 3). INTRACELLULAR FLUID 200 KEY Na+ HCO3– Cations CI– Na+ K+ 150 Ca2+ Milliequivalents per liter (mEq/L) HPO42– Mg2+ K+ 100 Anions HCO3– SO42– CI– HPO42– 50 SO42– Proteins Organic acid Mg2+ Proteins p. 1019 Cations Anions

Figure 27-2 Cations and Anions in Body Fluids (Part 2 of 3). PLASMA 200 KEY Cations Na+ K+ 150 HCO3– Ca2+ Milliequivalents per liter (mEq/L) Mg2+ 100 Anions HCO3– Na+ CI– CI– HPO42– 50 HPO42– SO42– Org. acid Organic acid K+ Proteins Ca2+ Proteins p. 1019 Cations Anions

Figure 27-2 Cations and Anions in Body Fluids (Part 3 of 3). INTERSTITIAL FLUID 200 KEY Cations Na+ K+ 150 Ca2+ Milliequivalents per liter (mEq/L) HCO3– Mg2+ 100 Anions HCO3– Na+ CI– CI– HPO42– 50 SO42– Organic acid HPO42– SO42– K+ Proteins p. 1019 Cations Anions

p. 1019 © 2015 Pearson Education, Inc. © 2012 Pearson Education, Inc. Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2012 Pearson Education, Inc.

Normal Sodium Concentrations In ECF ~140 mEq/L In ICF ~ 10 mEq/L or less Normal Potassium Concentrations In ICF ~ 160 mEq/L In ECF ~ 3.5–5.5 mEq/L © 2015 Pearson Education, Inc. Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2012 Pearson Education, Inc.

p. 1025 © 2015 Pearson Education, Inc. © 2012 Pearson Education, Inc. Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings

HOMEOSTASIS p. 1025 Normal Na+ concentration in ECF Figure 27-5 The Homeostatic Regulation of Normal Sodium Ion Concentration in Body Fluids (Part 1 of 2). ADH Secretion Increases Recall of Fluids The secretion of ADH restricts water loss and stimulates thirst, promoting additional water consumption Because the ECF osmolarity increased, water shifts out of the ICF, increasing ECF volume and decreasing Na+ concentrations Osmoreceptors in hypothalamus stimulated HOMEOSTASIS RESTORED HOMEOSTASIS DISTURBED Decreased Na+ levels in ECF Increased Na+ levels in ECF HOMEOSTASIS Normal Na+ concentration in ECF Start p. 1025

p. 1025 HOMEOSTASIS Normal Na+ concentration in ECF HOMEOSTASIS Figure 27-5 The Homeostatic Regulation of Normal Sodium Ion Concentration in Body Fluids (Part 2 of 2). HOMEOSTASIS Normal Na+ concentration in ECF Start HOMEOSTASIS DISTURBED HOMEOSTASIS RESTORED Decreased Na+ levels in ECF Increased Na+ levels in ECF Osmoreceptors in hypothalamus inhibited Water loss decreases ECF volume, concentrates ions ADH Secretion Decreases As soon as the osmotic concentration of the ECF decreases by 2 percent or more, ADH secretion decreases, so thirst is suppressed and water losses by the kidneys increase p. 1025

p. 1026 © 2015 Pearson Education, Inc. © 2012 Pearson Education, Inc. Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2015 Pearson Education, Inc. © 2012 Pearson Education, Inc. p. 1026

Increasing ECF volume by fluid gain or fluid and Na+ gain Figure 27-6 The Integration of Fluid Volume Regulation and Sodium Ion Concentration in Body Fluids (Part 1 of 2). Responses to Natriuretic Peptides Combined Effects Increased Na+ loss in urine Decreased blood volume Increasing blood pressure and volume Increased water loss in urine Natriuretic peptides released by cardiac muscle cells Decreased thirst Decreased blood pressure Inhibition of ADH, aldosterone, epinephrine, and norepinephrine release Increased blood volume and atrial distension HOMEOSTASIS DISTURBED HOMEOSTASIS RESTORED Increasing ECF volume by fluid gain or fluid and Na+ gain Decreasing ECF volume HOMEOSTASIS Start Normal ECF volume p. 1026

loss or fluid and Na+ loss Figure 27-6 The Integration of Fluid Volume Regulation and Sodium Ion Concentration in Body Fluids (Part 2 of 2). HOMEOSTASIS Start Normal ECF volume HOMEOSTASIS DISTURBED HOMEOSTASIS RESTORED Decreasing ECF volume by fluid loss or fluid and Na+ loss Increasing ECF volume Decreased blood volume and blood pressure Endocrine Responses Combined Effects Increased renin secretion and angiotensin II activation Increased urinary Na+ retention Decreased urinary water loss Increased aldosterone release Decreasing blood pressure and volume Increased thirst Increased ADH release Increased water intake p. 1026

p. 1031 PCO2 40–45 mm Hg HOMEOSTASIS If PCO2 increases Figure 27-9 The Basic Relationship between PCO2 and Plasma pH (Part 1 of 2). PCO2 40–45 mm Hg HOMEOSTASIS If PCO2 increases When carbon dioxide levels increase, more carbonic acid forms, additional hydrogen ions and bicarbonate ions are released, and the pH decreases. PCO2 pH p. 1031

p. 1031 pH 7.35–7.45 HOMEOSTASIS If PCO2 decreases Figure 27-9 The Basic Relationship between PCO2 and Plasma pH (Part 2 of 2). pH 7.35–7.45 HOMEOSTASIS If PCO2 decreases When the PCO2 decreases, the reaction runs in reverse, and carbonic acid dissociates into carbon dioxide and water. This removes H+ from solution and increases the pH. pH PCO2 p. 1031

Figure 27-10 Buffer Systems in Body Fluids. occur in Intracellular fluid (ICF) Extracellular fluid (ECF) Phosphate Buffer System Protein Buffer Systems Carbonic Acid– Bicarbonate Buffer System Protein buffer systems contribute to the regulation of pH in the ECF and ICF. These buffer systems interact extensively with the other two buffer systems. The phosphate buffer system has an important role in buffering the pH of the ICF and of urine. The carbonic acid– bicarbonate buffer system is most important in the ECF. Hemoglobin buffer system (RBCs only) Amino acid buffers (All proteins) Plasma protein buffers p. 1032

Figure 27-11 The Role of Amino Acids in Protein Buffer Systems. Neutral pH If pH increases If pH decreases In an alkaline medium, the amino acid acts as an acid and releases H+ Amino acid (zwitterion) In an acidic medium, the amino acid acts as a base and absorbs H+ p. 1033

Cells in peripheral tissues Figure 23-23 A Summary of the Primary Gas Transport Mechanisms (Part 4 of 4). HCO3− Chloride shift Cl− H+ + HCO3− Hb H2CO3 Hb H+ CO2 H2O CO2 Hb Hb CO2 Cells in peripheral tissues Systemic capillary CO2 pickup

Cl− Alveolar air space HCO3− Hb H+ + HCO3− Hb H+ H2CO3 CO2 CO2 H2O CO2 Figure 23-23 A Summary of the Primary Gas Transport Mechanisms (Part 3 of 4). Cl− Alveolar air space HCO3− Hb H+ + HCO3− Hb H+ H2CO3 CO2 CO2 H2O CO2 Hb Hb CO2 Pulmonary capillary CO2 delivery

Figure 27-12a The Carbonic Acid–Bicarbonate Buffer System. BICARBONATE RESERVE H2CO3 (carbonic acid) NaHCO3 (sodium bicarbonate) + HCO3– (bicarbonate ion) CO2 CO2 + H2O Na+ HCO3– H+ Lungs Basic components of the carbonic acid–bicarbonate buffer system, and their relationships to carbon dioxide and the bicarbonate reserve a p. 1034

Figure 27-12b The Carbonic Acid–Bicarbonate Buffer System. Fixed acids or organic acids: add H+ Increased H2CO3 Na+ HCO3– CO2 CO2 + H2O H+ + HCO3– NaHCO3 Lungs The response of the carbonic acid–bicarbonate buffer system to hydrogen ions generated by fixed or organic acids in body fluids b p. 1034

Figure 27-13a Kidney Tubules and pH Regulation. The three major buffering systems in tubular fluid, which are essential to the secretion of hydrogen ions 1 2 3 Cells of PCT, DCT, and collecting system 1 Carbonic acid–bicarbonate buffer system 2 Phosphate buffer system Peritubular fluid 3 Ammonia buffer system Peritubular capillary KEY = Countertransport = Reabsorption = Active transport = Secretion = Exchange pump = Cotransport = Diffusion p. 1037

Figure 27-13b Kidney Tubules and pH Regulation. Production of ammonium ions and ammonia by the breakdown of glutamine Tubular fluid in lumen Glutamine Glutaminase Carbon chain KEY = Countertransport = Reabsorption = Active transport = Secretion = Exchange pump p. 1037 = Cotransport = Diffusion

Figure 27-13c Kidney Tubules and pH Regulation. The response of the kidney tubule to alkalosis Tubular fluid in lumen Carbonic anhydrase KEY = Countertransport = Reabsorption = Active transport = Secretion = Exchange pump p. 1037 = Cotransport = Diffusion

CARBONIC ACID–BICARBONATE BUFFER SYSTEM Renal Response to Acidosis Figure 27-14a Interactions among the Carbonic Acid–Bicarbonate Buffer System and Compensatory Mechanisms in the Regulation of Plasma pH. The response to acidosis caused by the addition of H+ a Addition of H+ Start CARBONIC ACID–BICARBONATE BUFFER SYSTEM BICARBONATE RESERVE CO2 CO2 + H2O H2CO3 H+ + HCO3– HCO3– + Na+ NaHCO3 (sodium bicarbonate) (carbonic acid) (bicarbonate ion) Lungs Generation of HCO3– Respiratory Response to Acidosis Other buffer systems absorb H+ Kidneys Renal Response to Acidosis Increased respiratory rate decreases PCO2, effectively converting carbonic acid molecules to water. Kidney tubules respond by (1) secreting H+, (2) removing CO2, and (3) reabsorbing HCO3– to help replenish the bicarbonate reserve. Secretion of H+ p. 1039

CARBONIC ACID–BICARBONATE BUFFER SYSTEM Figure 27-14b Interactions among the Carbonic Acid–Bicarbonate Buffer System and Compensatory Mechanisms in the Regulation of Plasma pH. The response to alkalosis caused by the removal of H+ b Removal of H+ Start CARBONIC ACID–BICARBONATE BUFFER SYSTEM BICARBONATE RESERVE Lungs CO2 + H2O H2CO3 H+ + HCO3– HCO3– + Na+ NaHCO3 (sodium bicarbonate) (carbonic acid) (bicarbonate ion) Respiratory Response to Alkalosis Other buffer systems release H+ Generation of H+ Kidneys Decreased respiratory rate increases PCO2, effectively converting CO2 molecules to carbonic acid. Renal Response to Alkalosis Kidney tubules respond by conserving H+ and secreting HCO3–. Secretion of HCO3– p. 1039

Figure 27-15a Respiratory Acid–Base Regulation Responses to Acidosis Respiratory compensation: Stimulation of arterial and CSF chemo- receptors results in increased respiratory rate. Increased PCO2 Renal compensation: Combined Effects H ions are secreted and HCO3 ions are generated. Respiratory Acidosis Decreased PCO2 Elevated PCO2 results in a fall in plasma pH Buffer systems other than the carbonic acid–bicarbonate system accept H ions. Decreased H and increased HCO3 HOMEOSTASIS DISTURBED HOMEOSTASIS RESTORED HOMEOSTASIS Hypoventilation causing increased PCO2 Plasma pH returns to normal Normal acid–base balance Respiratory acidosis p. 1039 © 2015 Pearson Education, Inc. 27

Figure 27-15b Respiratory Acid–Base Regulation HOMEOSTASIS HOMEOSTASIS DISTURBED HOMEOSTASIS RESTORED Normal acid–base balance Hyperventilation causing decreased PCO2 Plasma pH returns to normal Respiratory Alkalosis Combined Effects Responses to Alkalosis Lower PCO2 results in a rise in plasma pH Increased PCO2 Respiratory compensation: Inhibition of arterial and CSF chemoreceptors results in a decreased respiratory rate. Increased H and decreased HCO3 Renal compensation: Decreased PCO2 H ions are generated and HCO3 ions are secreted. Buffer systems other than the carbonic acid–bicarbonate system release H ions. Respiratory alkalosis p. 1039 © 2015 Pearson Education, Inc. 28

Figure 27-16a Responses to Metabolic Acidosis Respiratory compensation: Stimulation of arterial and CSF chemo- receptors results in increased respiratory rate. Increased H ions Renal compensation: H ions are secreted and HCO3 ions are generated. Metabolic Acidosis Combined Effects Elevated H results in a fall in plasma pH Buffer systems accept H ions. Decreased H and increased HCO3 Decreased PCO2 HOMEOSTASIS DISTURBED HOMEOSTASIS HOMEOSTASIS RESTORED Normal acid–base balance Increased H production or decreased H excretion Plasma pH returns to normal Metabolic acidosis can result from increased acid production or decreased acid excretion, leading to a buildup of H in body fluids. p. 1042 © 2015 Pearson Education, Inc. 29

Figure 27-16b Responses to Metabolic Acidosis HOMEOSTASIS HOMEOSTASIS DISTURBED HOMEOSTASIS RESTORED Normal acid–base balance Bicarbonate loss; depletion of bicarbonate reserve Plasma pH returns to normal Combined Effects Metabolic Acidosis Responses to Metabolic Acidosis Decreased PCO2 Plasma pH falls because bicarbonate ions are unavailable to accept H Respiratory compensation: Stimulation of arterial and CSF chemo- receptors results in increased respiratory rate. Decreased H and increased HCO3 Renal compensation: H ions are secreted and HCO3 ions are generated. Decreased HCO3 ions Buffer systems other than the carbonic acid–bicarbonate system accept H ions. Metabolic acidosis can result from a loss of bicarbonate ions that makes the carbonic acid–bicarbonate buffer system incapable of preventing a fall in pH. p. 1042 © 2015 Pearson Education, Inc. 30

Figure 27-17 Metabolic Alkalosis HOMEOSTASIS DISTURBED HOMEOSTASIS RESTORED HOMEOSTASIS Loss of H; gain of HCO3 Normal acid–base balance Plasma pH returns to normal Metabolic Acidosis Combined Effects Elevated HCO3 results in a rise In plasma pH Increased H and decreased HCO3 Responses to Metabolic Alkalosis Respiratory compensation: Increased PCO2 Stimulation of arterial and CSF chemoreceptors results in decreased respiratory rate. Decreased H ions, gain of HCO3 ions Renal compensation: H ions are generated and HCO3 Ions are secreted. Buffer systems other than the carbonic acid–bicarbonate system donate H ions. p. 1043 © 2015 Pearson Education, Inc. 31

© 2012 Pearson Education, Inc. Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2015 Pearson Education, Inc.

© 2012 Pearson Education, Inc. Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2015 Pearson Education, Inc.

Figure 27-18 The Diagnosis of Acid–Base Disorders (Part 1 of 2). Suspected Acid–Base Disorder Check pH Acidosis pH <7.35 (acidemia) Check PCO2 Metabolic Acidosis Respiratory Acidosis PCO2 normal or decreased PCO2 increased (>50 mm Hg) Primary cause is hypoventilation Check HCO3– Acute Metabolic Acidosis Chronic (compensated) Metabolic Acidosis Chronic (compensated) Respiratory Acidosis Acute Respiratory Acidosis PCO2 decreased (<35 mm Hg) PCO2 normal HCO3– increased (>28 mEq/L) HCO3– normal Reduction due to respiratory compensation Examples • respiratory failure • CNS damage • pneumothorax Examples • emphysema • asthma Check anion gap* *The anion gap is defined as: Na+ concentration – (HCO3– concentration + Cl– concentration) Normal Increased Due to loss of HCO3– or to generation or ingestion of HCl Due to generation or retention of organic or fixed acids Examples • lactic acidosis • ketoacidosis • chronic renal failure p. 1044 Example • diarrhea

Figure 27-18 The Diagnosis of Acid–Base Disorders (Part 2 of 2). Suspected Acid–Base Disorder Check pH Alkalosis pH >7.45 (alkalemia) Check PCO2 Metabolic Alkalosis Respiratory Alkalosis PCO2 increased (>45 mm Hg) PCO2 decreased (<35 mm Hg) (HCO3– will be elevated) Examples • vomiting • loss of gastric acid Primary cause is hyperventilation Check HCO3– Acute Respiratory Alkalosis Chronic (compensated) Respiratory Alkalosis Normal or slight decrease in HCO3– Decreased HCO3– (<24 mEq/L) p. 1044 Examples • fever • panic attacks Examples • anemia • CNS damage

p. 1025 p. 1044 © 2015 Pearson Education, Inc. Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings p. 1044