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26 : 

26 Fluid, Electrolyte, and Acid-Base Balance

Body Water Content : 

Body Water Content Infants: 73% or more water (low body fat, low bone mass) Adult males: ~60% water Adult females: ~50% water (higher fat content, less skeletal muscle mass) Water content declines to ~45% in old age

Fluid Compartments : 

Fluid Compartments Total body water = 40 L Intracellular fluid (ICF) compartment: 2/3 or 25 L in cells Extracellular fluid (ECF) compartment: 1/3 or 15 L Plasma: 3 L Interstitial fluid (IF): 12 L in spaces between cells Other ECF: lymph, CSF, humors of the eye, synovial fluid, serous fluid, and gastrointestinal secretions

Slide 4: 

Figure 26.1 Total body water Volume = 40 L 60% body weight Extracellular fluid (ECF) Volume = 15 L 20% body weight Intracellular fluid (ICF) Volume = 25 L 40% body weight Interstitial fluid (IF) Volume = 12 L 80% of ECF

Composition of Body Fluids : 

Composition of Body Fluids Water: the universal solvent Solutes: nonelectrolytes and electrolytes Nonelectrolytes: most are organic Do not dissociate in water: e.g., glucose, lipids, creatinine, and urea

Composition of Body Fluids : 

Composition of Body Fluids Electrolytes Dissociate into ions in water; e.g., inorganic salts, all acids and bases, and some proteins The most abundant (most numerous) solutes Have greater osmotic power than nonelectrolytes, so may contribute to fluid shifts Determine the chemical and physical reactions of fluids

Electrolyte Concentration : 

Electrolyte Concentration Expressed in milliequivalents per liter (mEq/L), a measure of the number of electrical charges per liter of solution

Extracellular and Intracellular Fluids : 

Extracellular and Intracellular Fluids Each fluid compartment has a distinctive pattern of electrolytes ECF All similar, except higher protein content of plasma Major cation: Na+ Major anion: Cl–

Extracellular and Intracellular Fluids : 

Extracellular and Intracellular Fluids ICF: Low Na+ and Cl– Major cation: K+ Major anion HPO42–

Extracellular and Intracellular Fluids : 

Extracellular and Intracellular Fluids Proteins, phospholipids, cholesterol, and neutral fats make up the bulk of dissolved solutes 90% in plasma 60% in IF 97% in ICF

Slide 11: 

Figure 26.2 Na+ Sodium K+ Potassium Ca2+ Calcium Mg2+ Magnesium HCO3– Bicarbonate Cl– Chloride HPO42– SO42– Hydrogen phosphate Sulfate Blood plasma Interstitial fluid Intracellular fluid

Fluid Movement Among Compartments : 

Fluid Movement Among Compartments Regulated by osmotic and hydrostatic pressures Water moves freely by osmosis; osmolalities of all body fluids are almost always equal Two-way osmotic flow is substantial Ion fluxes require active transport or channels Change in solute concentration of any compartment leads to net water flow

Slide 13: 

Figure 26.3 Lungs Interstitial fluid Intracellular fluid in tissue cells Blood plasma O2 CO2 H2O, Ions Nitrogenous wastes Nutrients O2 CO2 H2O Ions Nitrogenous wastes Nutrients Kidneys Gastrointestinal tract H2O, Ions

Water Balance and ECF Osmolality : 

Water Balance and ECF Osmolality Water intake = water output = 2500 ml/day Water intake: beverages, food, and metabolic water Water output: urine, insensible water loss (skin and lungs), perspiration, and feces

Slide 15: 

Figure 26.4 Feces 4% Sweat 8% Insensible losses via skin and lungs 28% Urine 60% 2500 ml Average output per day Average intake per day Beverages 60% Foods 30% Metabolism 10% 1500 ml 700 ml 200 ml 100 ml 1500 ml 750 ml 250 ml

Regulation of Water Intake : 

Regulation of Water Intake Thirst mechanism is the driving force for water intake The hypothalamic thirst center osmoreceptors are stimulated by  Plasma osmolality of 2–3% Angiotensin II or baroreceptor input Dry mouth Substantial decrease in blood volume or pressure

Regulation of Water Intake : 

Regulation of Water Intake Drinking water creates inhibition of the thirst center Inhibitory feedback signals include Relief of dry mouth Activation of stomach and intestinal stretch receptors

Slide 18: 

Figure 26.5 (*Minor stimulus) Granular cells in kidney Dry mouth Renin-angiotensin mechanism Osmoreceptors in hypothalamus Hypothalamic thirst center Sensation of thirst; person takes a drink Water absorbed from GI tract Angiotensin II Plasma osmolality Blood pressure Water moistens mouth, throat; stretches stomach, intestine Plasma osmolality Initial stimulus Result Reduces, inhibits Increases, stimulates Physiological response Plasma volume* Saliva

Regulation of Water Output : 

Regulation of Water Output Obligatory water losses Insensible water loss: from lungs and skin Feces Minimum daily sensible water loss of 500 ml in urine to excrete wastes Body water and Na+ content are regulated in tandem by mechanisms that maintain cardiovascular function and blood pressure

Regulation of Water Output: Influence of ADH : 

Regulation of Water Output: Influence of ADH Water reabsorption in collecting ducts is proportional to ADH release  ADH  dilute urine and  volume of body fluids  ADH  concentrated urine

Regulation of Water Output: Influence of ADH : 

Regulation of Water Output: Influence of ADH Hypothalamic osmoreceptors trigger or inhibit ADH release Other factors may trigger ADH release via large changes in blood volume or pressure, e.g., fever, sweating, vomiting, or diarrhea; blood loss; and traumatic burns

Slide 22: 

Figure 26.6 Osmolality Na+ concentration in plasma Stimulates Releases Osmoreceptors in hypothalamus Negative feedback inhibits Posterior pituitary ADH Inhibits Stimulates Baroreceptors in atrium and large vessels Stimulates Plasma volume BP (10–15%) Antidiuretic hormone (ADH) Targets Effects Results in Collecting ducts of kidneys Osmolality Plasma volume Water reabsorption Scant urine

Disorders of Water Balance: Dehydration : 

Disorders of Water Balance: Dehydration Negative fluid balance ECF water loss due to: hemorrhage, severe burns, prolonged vomiting or diarrhea, profuse sweating, water deprivation, diuretic abuse Signs and symptoms: thirst, dry flushed skin, oliguria May lead to weight loss, fever, mental confusion, hypovolemic shock, and loss of electrolytes

Slide 24: 

Figure 26.7a 1 2 3 Excessive loss of H2O from ECF ECF osmotic pressure rises Cells lose H2O to ECF by osmosis; cells shrink (a) Mechanism of dehydration

Disorders of Water Balance: Hypotonic Hydration : 

Disorders of Water Balance: Hypotonic Hydration Cellular overhydration, or water intoxication Occurs with renal insufficiency or rapid excess water ingestion ECF is diluted  hyponatremia  net osmosis into tissue cells  swelling of cells  severe metabolic disturbances (nausea, vomiting, muscular cramping, cerebral edema)  possible death

Slide 26: 

Figure 26.7b 3 H2O moves into cells by osmosis; cells swell 2 ECF osmotic pressure falls 1 Excessive H2O enters the ECF (b) Mechanism of hypotonic hydration

Disorders of Water Balance: Edema : 

Disorders of Water Balance: Edema Atypical accumulation of IF fluid  tissue swelling Due to anything that increases flow of fluid out of the blood or hinders its return  Blood pressure  Capillary permeability (usually due to inflammatory chemicals) Incompetent venous valves, localized blood vessel blockage Congestive heart failure, hypertension,  blood volume

Edema : 

Edema Hindered fluid return occurs with an imbalance in colloid osmotic pressures, e.g., hypoproteinemia ( plasma proteins) Fluids fail to return at the venous ends of capillary beds Results from protein malnutrition, liver disease, or glomerulonephritis

Edema : 

Edema Blocked (or surgically removed) lymph vessels Cause leaked proteins to accumulate in IF  Colloid osmotic pressure of IF draws fluid from the blood Results in low blood pressure and severely impaired circulation

Electrolyte Balance : 

Electrolyte Balance Electrolytes are salts, acids, and bases Electrolyte balance usually refers only to salt balance Salts enter the body by ingestion and are lost via perspiration, feces, and urine

Electrolyte Balance : 

Electrolyte Balance Importance of salts Controlling fluid movements Excitability Secretory activity Membrane permeability

Table 26.1 Causes and Consequences of Electrolyte Imbalances (1 of 2) : 

Table 26.1 Causes and Consequences of Electrolyte Imbalances (1 of 2)

Table 26.1 Causes and Consequences of Electrolyte Imbalances (2 of 2) : 

Table 26.1 Causes and Consequences of Electrolyte Imbalances (2 of 2)

Central Role of Sodium : 

Central Role of Sodium Most abundant cation in the ECF Sodium salts in the ECF contribute 280 mOsm of the total 300 mOsm ECF solute concentration Na+ leaks into cells and is pumped out against its electrochemical gradient Na+ content may change but ECF Na+ concentration remains stable due to osmosis

Central Role of Sodium : 

Central Role of Sodium Changes in plasma sodium levels affect Plasma volume, blood pressure ICF and IF volumes Renal acid-base control mechanisms are coupled to sodium ion transport

Regulation of Sodium Balance : 

Regulation of Sodium Balance No receptors are known that monitor Na+ levels in body fluids Na+-water balance is linked to blood pressure and blood volume control mechanisms

Regulation of Sodium Balance: Aldosterone : 

Regulation of Sodium Balance: Aldosterone Na+ reabsorption 65% is reabsorbed in the proximal tubules 25% is reclaimed in the loops of Henle Aldosterone  active reabsorption of remaining Na+ Water follows Na+ if ADH is present

Regulation of Sodium Balance: Aldosterone : 

Regulation of Sodium Balance: Aldosterone Renin-angiotensin mechanism is the main trigger for aldosterone release Granular cells of JGA secrete renin in response to Sympathetic nervous system stimulation  Filtrate osmolality  Stretch (due to  blood pressure)

Regulation of Sodium Balance: Aldosterone : 

Regulation of Sodium Balance: Aldosterone Renin catalyzes the production of angiotensin II, which prompts aldosterone release from the adrenal cortex Aldosterone release is also triggered by elevated K+ levels in the ECF Aldosterone brings about its effects slowly (hours to days)

Slide 40: 

Figure 26.8 K+ (or Na+) concentration in blood plasma* Stimulates Releases Targets Renin-angiotensin mechanism Negative feedback inhibits Adrenal cortex Kidney tubules Aldosterone Effects Restores Homeostatic plasma levels of Na+ and K+ Na+ reabsorption K+ secretion

Regulation of Sodium Balance: ANP : 

Regulation of Sodium Balance: ANP Released by atrial cells in response to stretch ( blood pressure) Effects Decreases blood pressure and blood volume:  ADH, renin and aldosterone production  Excretion of Na+ and water Promotes vasodilation directly and also by decreasing production of angiotensin II

Slide 42: 

Figure 26.9 Stretch of atria of heart due to BP Atrial natriuretic peptide (ANP) Adrenal cortex Hypothalamus and posterior pituitary Collecting ducts of kidneys JG apparatus of the kidney ADH release Aldosterone release Na+ and H2O reabsorption Blood volume Vasodilation Renin release* Blood pressure Releases Negative feedback Targets Effects Effects Inhibits Effects Inhibits Results in Results in Angiotensin II

Influence of Other Hormones : 

Influence of Other Hormones Estrogens:  NaCl reabsorption (like aldosterone)  H2O retention during menstrual cycles and pregnancy Progesterone:  Na+ reabsorption (blocks aldosterone) Promotes Na+ and H2O loss Glucocorticoids:  Na+ reabsorption and promote edema

Cardiovascular System Baroreceptors : 

Cardiovascular System Baroreceptors Baroreceptors alert the brain of increases in blood volume and pressure Sympathetic nervous system impulses to the kidneys decline Afferent arterioles dilate GFR increases Na+ and water output increase

Slide 45: 

Figure 26.10 Stretch in afferent arterioles Angiotensinogen (from liver) Na+ (and H2O) reabsorption Granular cells of kidneys Renin Posterior pituitary Systemic arterioles Angiotensin I Angiotensin II Systemic arterioles Vasoconstriction Aldosterone Blood volume Blood pressure Distal kidney tubules Adrenal cortex Vasoconstriction Peripheral resistance (+) (+) (+) (+) Peripheral resistance H2O reabsorption Inhibits baroreceptors in blood vessels Sympathetic nervous system ADH (antidiuretic hormone) Collecting ducts of kidneys Filtrate NaCl concentration in ascending limb of loop of Henle Causes Causes Causes Causes Results in Secretes Results in Targets Results in Releases Release Catalyzes conversion Converting enzyme (in lungs) (+) (+) (+) (+) (+) (+) (+) stimulates Renin-angiotensin system Neural regulation (sympathetic nervous system effects) ADH release and effects Systemic blood pressure/volume

Regulation of Potassium Balance : 

Regulation of Potassium Balance Importance of potassium: Affects RMP in neurons and muscle cells (especially cardiac muscle)  ECF [K+]  RMP  depolarization  reduced excitability  ECF [K+] hyperpolarization and nonresponsiveness

Regulation of Potassium Balance : 

Regulation of Potassium Balance H+ shift in and out of cells Leads to corresponding shifts in K+ in the opposite direction to maintain cation balance Interferes with activity of excitable cells

Regulation of Potassium Balance : 

Regulation of Potassium Balance K+ balance is controlled in the cortical collecting ducts by changing the amount of potassium secreted into filtrate High K+ content of ECF favors principal cell secretion of K+ When K+ levels are low, type A intercalated cells reabsorb some K+ left in the filtrate

Regulation of Potassium Balance : 

Regulation of Potassium Balance Influence of aldosterone Stimulates K+ secretion (and Na+ reabsorption) by principal cells Increased K+ in the adrenal cortex causes Release of aldosterone Potassium secretion

Regulation of Calcium : 

Regulation of Calcium Ca2+ in ECF is important for Neuromuscular excitability Blood clotting Cell membrane permeability Secretory activities

Regulation of Calcium : 

Regulation of Calcium Hypocalcemia   excitability and muscle tetany Hypercalcemia  Inhibits neurons and muscle cells, may cause heart arrhythmias Calcium balance is controlled by parathyroid hormone (PTH) and calcitonin

Influence of PTH : 

Influence of PTH Bones are the largest reservoir for Ca2+ and phosphates PTH promotes increase in calcium levels by targeting bones, kidneys, and small intestine (indirectly through vitamin D) Calcium reabsorption and phosphate excretion go hand in hand

Slide 53: 

Figure 16.12 Intestine Kidney Bloodstream Hypocalcemia (low blood Ca2+) stimulates parathyroid glands to release PTH. Rising Ca2+ in blood inhibits PTH release. 1 PTH activates osteoclasts: Ca2+ and PO43S released into blood. 2 PTH increases Ca2+ reabsorption in kidney tubules. 3 PTH promotes kidney’s activation of vitamin D, which increases Ca2+ absorption from food. Bone Ca2+ ions PTH Molecules

Influence of PTH : 

Influence of PTH Normally 75% of filtered phosphates are actively reabsorbed in the PCT PTH inhibits this by decreasing the Tm

Regulation of Anions : 

Regulation of Anions Cl– is the major anion in the ECF Helps maintain the osmotic pressure of the blood 99% of Cl– is reabsorbed under normal pH conditions When acidosis occurs, fewer chloride ions are reabsorbed Other anions have transport maximums and excesses are excreted in urine

Acid-Base Balance : 

Acid-Base Balance pH affects all functional proteins and biochemical reactions Normal pH of body fluids Arterial blood: pH 7.4 Venous blood and IF fluid: pH 7.35 ICF: pH 7.0 Alkalosis or alkalemia: arterial blood pH >7.45 Acidosis or acidemia: arterial pH < 7.35

Acid-Base Balance : 

Acid-Base Balance Most H+ is produced by metabolism Phosphoric acid from breakdown of phosphorus-containing proteins in ECF Lactic acid from anaerobic respiration of glucose Fatty acids and ketone bodies from fat metabolism H+ liberated when CO2 is converted to HCO3– in blood

Acid-Base Balance : 

Acid-Base Balance Concentration of hydrogen ions is regulated sequentially by Chemical buffer systems: rapid; first line of defense Brain stem respiratory centers: act within 1–3 min Renal mechanisms: most potent, but require hours to days to effect pH changes

Acid-Base Balance : 

Acid-Base Balance Strong acids dissociate completely in water; can dramatically affect pH Weak acids dissociate partially in water; are efficient at preventing pH changes Strong bases dissociate easily in water; quickly tie up H+ Weak bases accept H+ more slowly

Slide 60: 

Figure 26.11 (a) A strong acid such as HCI dissociates completely into its ions. (b) A weak acid such as H2CO3 does not dissociate completely. H2CO3 HCI

Chemical Buffer Systems : 

Chemical Buffer Systems Chemical buffer: system of one or more compounds that act to resist pH changes when strong acid or base is added Bicarbonate buffer system Phosphate buffer system Protein buffer system

Bicarbonate Buffer System : 

Bicarbonate Buffer System Mixture of H2CO3 (weak acid) and salts of HCO3– (e.g., NaHCO3, a weak base) Buffers ICF and ECF The only important ECF buffer

Bicarbonate Buffer System : 

Bicarbonate Buffer System If strong acid is added: HCO3– ties up H+ and forms H2CO3 HCl + NaHCO3  H2CO3 + NaCl pH decreases only slightly, unless all available HCO3– (alkaline reserve) is used up HCO3– concentration is closely regulated by the kidneys

Bicarbonate Buffer System : 

Bicarbonate Buffer System If strong base is added It causes H2CO3 to dissociate and donate H+ H+ ties up the base (e.g. OH–) NaOH + H2CO3  NaHCO3 + H2O pH rises only slightly H2CO3 supply is almost limitless (from CO2 released by respiration) and is subject to respiratory controls

Phosphate Buffer System : 

Phosphate Buffer System Action is nearly identical to the bicarbonate buffer Components are sodium salts of: Dihydrogen phosphate (H2PO4–), a weak acid Monohydrogen phosphate (HPO42–), a weak base Effective buffer in urine and ICF, where phosphate concentrations are high

Protein Buffer System : 

Protein Buffer System Intracellular proteins are the most plentiful and powerful buffers; plasma proteins are also important Protein molecules are amphoteric (can function as both a weak acid and a weak base) When pH rises, organic acid or carboxyl (COOH) groups release H+ When pH falls, NH2 groups bind H+

Physiological Buffer Systems : 

Physiological Buffer Systems Respiratory and renal systems Act more slowly than chemical buffer systems Have more capacity than chemical buffer systems

Respiratory Regulation of H+ : 

Respiratory Regulation of H+ Respiratory system eliminates CO2 A reversible equilibrium exists in the blood: CO2 + H2O  H2CO3  H+ + HCO3– During CO2 unloading the reaction shifts to the left (and H+ is incorporated into H2O) During CO2 loading the reaction shifts to the right (and H+ is buffered by proteins)

Respiratory Regulation of H+ : 

Respiratory Regulation of H+ Hypercapnia activates medullary chemoreceptors Rising plasma H+ activates peripheral chemoreceptors More CO2 is removed from the blood H+ concentration is reduced

Respiratory Regulation of H+ : 

Respiratory Regulation of H+ Alkalosis depresses the respiratory center Respiratory rate and depth decrease H+ concentration increases Respiratory system impairment causes acid-base imbalances Hypoventilation  respiratory acidosis Hyperventilation  respiratory alkalosis

Acid-Base Balance : 

Acid-Base Balance Chemical buffers cannot eliminate excess acids or bases from the body Lungs eliminate volatile carbonic acid by eliminating CO2 Kidneys eliminate other fixed metabolic acids (phosphoric, uric, and lactic acids and ketones) and prevent metabolic acidosis

Renal Mechanisms of Acid-Base Balance : 

Renal Mechanisms of Acid-Base Balance Most important renal mechanisms Conserving (reabsorbing) or generating new HCO3– Excreting HCO3– Generating or reabsorbing one HCO3– is the same as losing one H+ Excreting one HCO3– is the same as gaining one H+

Renal Mechanisms of Acid-Base Balance : 

Renal Mechanisms of Acid-Base Balance Renal regulation of acid-base balance depends on secretion of H+ H+ secretion occurs in the PCT and in collecting duct type A intercalated cells: The H+ comes from H2CO3 produced in reactions catalyzed by carbonic anhydrase inside the cells See Steps 1 and 2 of the following figure

Slide 74: 

Figure 26.12 1 CO2 combines with water within the tubule cell, forming H2CO3. 2 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3–). 3a H+ is secreted into the filtrate. 3b For each H+ secreted, a HCO3– enters the peritubular capillary blood either via symport with Na+ or via antiport with CI–. 4 Secreted H+ combines with HCO3– in the filtrate, forming carbonic acid (H2CO3). HCO3– disappears from the filtrate at the same rate that HCO3– (formed within the tubule cell) enters the peritubular capillary blood. 5 The H2CO3 formed in the filtrate dissociates to release CO2 and H2O. 6 CO2 diffuses into the tubule cell, where it triggers further H+ secretion. * CA CO2 CO2 + H2O 2K+ 2K+ * Na+ Na+ 3Na+ 3Na+ Tight junction H2CO3 H2CO3 PCT cell Nucleus Filtrate in tubule lumen Cl– Cl– HCO3– + Na+ HCO3– H2O CO2 H+ H+ HCO3– HCO3– HCO3– ATPase ATPase Peri- tubular capillary 1 2 4 5 6 3a 3b Primary active transport Simple diffusion Secondary active transport Carbonic anhydrase Transport protein

Reabsorption of Bicarbonate : 

Reabsorption of Bicarbonate Tubule cell luminal membranes are impermeable to HCO3– CO2 combines with water in PCT cells, forming H2CO3 H2CO3 dissociates H+ is secreted, and HCO3– is reabsorbed into capillary blood Secreted H+ unites with HCO3– to form H2CO3 in filtrate, which generates CO2 and H2O HCO3– disappears from filtrate at the same rate that it enters the peritubular capillary blood

Slide 76: 

Figure 26.12 1 CO2 combines with water within the tubule cell, forming H2CO3. 2 H2CO3 is quickly split, forming H+ and bicarbonate ion (HCO3–). 3a H+ is secreted into the filtrate. 3b For each H+ secreted, a HCO3– enters the peritubular capillary blood either via symport with Na+ or via antiport with CI–. 4 Secreted H+ combines with HCO3– in the filtrate, forming carbonic acid (H2CO3). HCO3– disappears from the filtrate at the same rate that HCO3– (formed within the tubule cell) enters the peritubular capillary blood. 5 The H2CO3 formed in the filtrate dissociates to release CO2 and H2O. 6 CO2 diffuses into the tubule cell, where it triggers further H+ secretion. * CA CO2 CO2 + H2O 2K+ 2K+ * Na+ Na+ 3Na+ 3Na+ Tight junction H2CO3 H2CO3 PCT cell Nucleus Filtrate in tubule lumen Cl– Cl– HCO3– + Na+ HCO3– H2O CO2 H+ H+ HCO3– HCO3– HCO3– ATPase ATPase Peri- tubular capillary 1 2 4 5 6 3a 3b Primary active transport Simple diffusion Secondary active transport Carbonic anhydrase Transport protein

Generating New Bicarbonate Ions : 

Generating New Bicarbonate Ions Two mechanisms in PCT and type A intercalated cells Generate new HCO3– to be added to the alkaline reserve Both involve renal excretion of acid (via secretion and excretion of H+ or NH4+

Excretion of Buffered H+ : 

Excretion of Buffered H+ Dietary H+ must be balanced by generating new HCO3– Most filtered HCO3– is used up before filtrate reaches the collecting duct

Excretion of Buffered H+ : 

Excretion of Buffered H+ Intercalated cells actively secrete H+ into urine, which is buffered by phosphates and excreted Generated “new” HCO3– moves into the interstitial space via a cotransport system and then moves passively into peritubular capillary blood

Slide 80: 

Figure 25.13 Active transport Passive transport Peri- tubular capillary 2 4 4 3 3 1 1 2 4 3 Filtrate in tubule lumen Transcellular Paracellular Paracellular Tight junction Lateral intercellular space Capillary endothelial cell Luminal membrane Solutes H2O Tubule cell Interstitial fluid Transcellular Basolateral membranes 1 Transport across the luminal membrane. 2 Diffusion through the cytosol. 4 Movement through the interstitial fluid and into the capillary. 3 Transport across the basolateral membrane. (Often involves the lateral intercellular spaces because membrane transporters transport ions into these spaces.) Movement via the transcellular route involves: The paracellular route involves: • Movement through leaky tight junctions, particularly in the PCT.

Ammonium Ion Excretion : 

Ammonium Ion Excretion Involves metabolism of glutamine in PCT cells Each glutamine produces 2 NH4+ and 2 “new” HCO3– HCO3– moves to the blood and NH4+ is excreted in urine

Slide 82: 

Figure 26.14 Nucleus PCT tubule cells Filtrate in tubule lumen Peri- tubular capillary NH4+ out in urine 2NH4+ Na+ Na+ Na+ Na+ Na+ 3Na+ 3Na+ Glutamine Glutamine Glutamine Tight junction Deamination, oxidation, and acidification (+H+) 2K+ 2K+ NH4+ HCO3– 2HCO3– HCO3– (new) ATPase 1 PCT cells metabolize glutamine to NH4+ and HCO3–. 2a This weak acid NH4+ (ammonium) is secreted into the filtrate, taking the place of H+ on a Na+- H+ antiport carrier. 2b For each NH4+ secreted, a bicarbonate ion (HCO3–) enters the peritubular capillary blood via a symport carrier. 3 The NH4+ is excreted in the urine. Primary active transport Simple diffusion Secondary active transport Transport protein 1 2a 2b 3

Bicarbonate Ion Secretion : 

Bicarbonate Ion Secretion When the body is in alkalosis, type B intercalated cells Secrete HCO3– Reclaim H+ and acidify the blood

Bicarbonate Ion Secretion : 

Bicarbonate Ion Secretion Mechanism is the opposite of the bicarbonate ion reabsorption process by type A intercalated cells Even during alkalosis, the nephrons and collecting ducts excrete fewer HCO3– than they conserve

Abnormalities of Acid-Base Balance : 

Abnormalities of Acid-Base Balance Respiratory acidosis and alkalosis Metabolic acidosis and alkalosis

Respiratory Acidosis and Alkalosis : 

Respiratory Acidosis and Alkalosis The most important indicator of adequacy of respiratory function is PCO2 level (normally 35–45 mm Hg) PCO2 above 45 mm Hg  respiratory acidosis Most common cause of acid-base imbalances Due to decrease in ventilation or gas exchange Characterized by falling blood pH and rising PCO2

Respiratory Acidosis and Alkalosis : 

Respiratory Acidosis and Alkalosis PCO2 below 35 mm Hg  respiratory alkalosis A common result of hyperventilation due to stress or pain

Metabolic Acidosis and Alkalosis : 

Metabolic Acidosis and Alkalosis Any pH imbalance not caused by abnormal blood CO2 levels Indicated by abnormal HCO3– levels

Metabolic Acidosis and Alkalosis : 

Metabolic Acidosis and Alkalosis Causes of metabolic acidosis Ingestion of too much alcohol ( acetic acid) Excessive loss of HCO3– (e.g., persistent diarrhea) Accumulation of lactic acid, shock, ketosis in diabetic crisis, starvation, and kidney failure

Metabolic Acidosis and Alkalosis : 

Metabolic Acidosis and Alkalosis Metabolic alkalosis is much less common than metabolic acidosis Indicated by rising blood pH and HCO3– Caused by vomiting of the acid contents of the stomach or by intake of excess base (e.g., antacids)

Effects of Acidosis and Alkalosis : 

Effects of Acidosis and Alkalosis Blood pH below 7  depression of CNS  coma  death Blood pH above 7.8  excitation of nervous system  muscle tetany, extreme nervousness, convulsions, respiratory arrest

Respiratory and Renal Compensations : 

Respiratory and Renal Compensations If acid-base imbalance is due to malfunction of a physiological buffer system, the other one compensates Respiratory system attempts to correct metabolic acid-base imbalances Kidneys attempt to correct respiratory acid-base imbalances

Respiratory Compensation : 

Respiratory Compensation In metabolic acidosis High H+ levels stimulate the respiratory centers Rate and depth of breathing are elevated Blood pH is below 7.35 and HCO3– level is low As CO2 is eliminated by the respiratory system, PCO2 falls below normal

Respiratory Compensation : 

Respiratory Compensation Respiratory compensation for metabolic alkalosis is revealed by: Slow, shallow breathing, allowing CO2 accumulation in the blood High pH (over 7.45) and elevated HCO3– levels

Renal Compensation : 

Renal Compensation Hypoventilation causes elevated PCO2 (respiratory acidosis) Renal compensation is indicated by high HCO3– levels Respiratory alkalosis exhibits low PCO2 and high pH Renal compensation is indicated by decreasing HCO3– levels

Table 26.2 Causes and Consequences of Acid-Base Imbalances (1 of 2) : 

Table 26.2 Causes and Consequences of Acid-Base Imbalances (1 of 2)

Table 26.2 Causes and Consequences of Acid-Base Imbalances (2 of 2) : 

Table 26.2 Causes and Consequences of Acid-Base Imbalances (2 of 2)