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WATER BALANCE. NORMAL WATER CONTENT OF BODY75% AT BIRTH55-60% YOUNG ADULTSMEN SLIGHTLY HIGHER THAN WOMEN(MORE FAT, LESS WATER)45% IN ELDERLY, OBESE. WATER BALANCE. TOTAL BODY WATER~40 LITERSSEVERAL FLUID COMPARTMENTS65% INTRACELLULAR FLUID (ICF)35% EXTRACELLULAR FLUID (ECF)25% INTERSTITIAL FLUID (TISSUE FLUID)8% BLOOD PLASMA AND LYMPH2% TRANSCELLULAR FLUIDSYNOVIAL, PLEURAL, PERICARDIAL, ETC..

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2. WATER BALANCE NORMAL WATER CONTENT OF BODY 75% AT BIRTH 55-60% YOUNG ADULTS MEN SLIGHTLY HIGHER THAN WOMEN (MORE FAT, LESS WATER) 45% IN ELDERLY, OBESE

3. WATER BALANCE TOTAL BODY WATER ~40 LITERS SEVERAL FLUID COMPARTMENTS 65% INTRACELLULAR FLUID (ICF) 35% EXTRACELLULAR FLUID (ECF) 25% INTERSTITIAL FLUID (TISSUE FLUID) 8% BLOOD PLASMA AND LYMPH 2% TRANSCELLULAR FLUID SYNOVIAL, PLEURAL, PERICARDIAL, ETC.

4. WATER BALANCE TOTAL BODY WATER ENTERS BODY OSMOSIS FROM DIGESTIVE TRACT ALSO PRODUCED BY AEROBIC RESPIRATION ALSO PRODUCED BY CONDENSATION REACTIONS EXITS BODY URINARY, DIGESTIVE, RESPIRATORY, & INTEGUMENTARY SYSTEMS

5. WATER BALANCE TOTAL BODY WATER FLUID EXCHANGED BETWEEN COMPARTMENTS CAPILLARY WALLS, PLASMA MEMBRANES DRIVEN BY TRANSIENT OSMOTIC GRADIENTS OSMOTIC GRADIENTS DEPENDENT ON SOLUTE MOLECULES MOST ABUNDANT SOLUTES ARE ELECTROLYTES WATER BALANCE AND ELECTROLYTE BALANCE ARE CLOSELY RELATED

7. WATER BALANCE WATER BALANCE FLUID GAIN = FLUID LOSS BOTH TYPICALLY ~2500 ML / DAY

8. WATER BALANCE WATER GAIN TYPICALLY ~2500 ML / DAY 1600 ML FROM DRINK 700 ML FROM FOOD 200 ML FROM METABOLISM AEROBIC RESPIRATION CONDENSATION REACTIONS A.K.A. DEHYDRATION REACTIONS

9. WATER BALANCE WATER LOSS TYPICALLY ~2500 ML / DAY 1500 ML EXCRETED AS URINE 200 ML ELIMINATED IN FECES 300 ML EXPIRED IN BREATH 100 ML SECRETED AS SWEAT 400 ML LOST AS CUTANEOUS TRANSPIRATION DIFFUSES THROUGH EPIDERMIS, EVAPORATES

12. WATER BALANCE WATER LOSS CAN VARY GREATLY INCREASED RESPIRATORY LOSS IN COLD WEATHER INCREASED SWEAT LOSS IN WARM WEATHER INCREASED RESPIRATORY AND SWEAT LOSS, DECREASED URINE OUTPUT DURING PHYSICAL EXERTION

13. WATER BALANCE WATER LOSS OBLIGATORY WATER LOSS RELATIVELY UNAVOIDABLE EXPIRED AIR, CUTANEOUS TRANSPIRATION, SWEAT, FECAL MOISTURE, MINIMUM URINE OUTPUT (~400 ML/DAY)

14. WATER BALANCE REGULATION OF WATER INTAKE GOVERNED BY THIRST PROVOKED BY INCREASED PLASMA OSMOLARITY PROVOKED BY BLOOD LOSS THIRST CENTER IN HYPOTHALAMUS RESPONDS TO SIGNS OF DEHYDRATION ANGIOTENSIN II ANTIDIURETIC HORMONE (ADH) SIGNALS FROM OSMOCENTERS INHIBITS SALIVATION

15. WATER BALANCE REGULATION OF WATER INTAKE INHIBITED SALIVATION DRY MOUTH SENSE OF THIRST INGESTION OF WATER COOLS AND MOISTENS MOUTH DISTENDS STOMACH AND INTESTINES REHYDRATES BLOOD THIRST INHIBITED

17. WATER BALANCE REGULATION OF WATER OUTPUT CONTROLLED VIA ALTERATIONS IN URINE VOLUME URINE VOLUME AFFECTED BY SODIUM REABSORPTION WATER FOLLOWS SODIUM REABSORPTION MORE LATER ANTIDIURETIC HORMONE (ADH) BLOOD VOLUME ?, [Na+] ?, OSMORECEPTORS STIMULATED, PITUITARY RELEASES ADH AQUAPORINS PRODUCED IN KIDNEY’S COLLECTING DUCTS FACILITATE REABSORPTION ALSO WORKS IN REVERSE

19. WATER BALANCE WATER BALANCE DISORDERS FLUID DEFICIENCY VOLUME DEPLETION (HYOVOLEMIA) DEHYDRATION FLUID EXCESS VOLUME EXCESS HYPOTONIC HYDRATION FLUID SEQUESTRATION

20. WATER BALANCE WATER BALANCE DISORDERS FLUID DEFICIENCY: HYPOVOLEMIA CAUSED BY PROPORTIONATE LOSS OF WATER AND SODIUM WITHOUT REPLACEMENT TOTAL BODY WATER DECREASED OSMOLARITY UNCHANGED CAUSES HEMORRHAGE SEVERE BURNS CHRONIC VOMITING OR DIARRHEA MAJOR CAUSE OF INFANT MORTALITY

21. WATER BALANCE WATER BALANCE DISORDERS FLUID DEFICIENCY: DEHYDRATION CAUSED BY LOSS OF MORE WATER THAN Na+ TOTAL BODY WATER DECREASED ECF OSMOLARITY INCREASES CAUSES LACK OF DRINKING WATER DIABETES MELLITUS ADH HYPOSECRETION PROFUSE SWEATING OVERUSE OF DIURETICS

22. WATER BALANCE WATER BALANCE DISORDERS FLUID DEFICIENCY: DEHYDRATION AFFECTS ALL FLUID COMPARTMENTS INFANTS MORE VULNERABLE THAN ADULTS HIGHER METABOLISM ? MORE WASTES MORE WASTES ? MORE URINE VOLUME IMMATURE KIDNEYS URINE LESS CONCENTRATED GREATER SURFACE AREA-TO-VOLUME RATIO GREATER WATER LOSS BY EVAPORATION

23. WATER BALANCE WATER BALANCE DISORDERS EFFECTS OF FLUID DEFICIENCY CIRCULATORY SHOCK DUE TO LOSS OF BLOOD VOLUME NEUROLOGICAL DYSFUNCTION DUE TO DEHYDRATION OF BRAIN CELLS

24. WATER BALANCE WATER BALANCE DISORDERS FLUID EXCESS LESS COMMON THAN FLUID DEFICIENCY KIDNEYS ARE TYPICALLY ABLE TO EXCRETE MORE URINE

25. WATER BALANCE WATER BALANCE DISORDERS FLUID EXCESS: VOLUME EXCESS CAUSED BY PROPORTIONATE RETENTION OF EXCESS WATER AND SODIUM TOTAL BODY WATER INCREASED OSMOLARITY UNCHANGED CAUSES ALDOSTERONE HYPERSECRETION RENAL FAILURE

26. WATER BALANCE WATER BALANCE DISORDERS FLUID EXCESS: HYPOTONIC HYDRATION “WATER INTOXICATION”, “POS H20 BALANCE” CAUSED BY RETENTION OF MORE WATER THAN SODIUM TOTAL BODY WATER INCREASED ECF OSMOLARITY DECREASES CAUSES REPLACEMENT OF WATER AND SALT WITH WATER LACK OF PROPORTIONATE INTAKE OF ELECTROLYTES ADH HYERSECRETION

27. WATER BALANCE WATER BALANCE DISORDERS EFFECTS OF FLUID EXCESS PULMONARY EDEMA CEREBRAL EDEMA

28. WATER BALANCE WATER BALANCE DISORDERS FLUID SEQUESTRATION EXCESS FLUID ACCUMULATES IN A PARTICULAR LOCATION TOTAL BODY WATER MAY BE NORMAL CIRCULATING VOLUME MAY DROP EXAMPLES EDEMA (IN INTERSTITIAL SPACES) HEMORRHAGE (LOST TO CIRCULATION) PLEURAL EFFUSION (IN PLEURAL CAVITY)

29. ELECTROLYTE BALANCE IMPORTANCE OF ELECTROLYTES SALTS E.G. NaCl, Ca3(PO4)2, ETC. INCLUDE IONS IN DEFINITION MANY ROLES INVOLVED IN METABOLISM DETERMINE ELECTRICAL MEMBRANE POTENTIALS AFFECT OSMOLARITY OF BODY FLUIDS AFFECT WATER CONTENT AND DISTRIBUTION ETC.

30. ELECTROLYTE BALANCE SODIUM PRINCIPAL EXTRACELLULAR CATION 90 – 95% OF OSMOLARITY FROM SODIUM SALTS ROLES DEPOLARIZATION MUSCLES, NERVES AFFECT TOTAL BODY WATER AFFECT WATER DISTRIBUTION COTRANSPORT GLUCOSE, AMINO ACIDS, CALCIUM, ETC. ETC.

31. ELECTROLYTE BALANCE SODIUM HOMEOSTASIS 0.5 G / DAY DIETARY REQUIREMENT RECEIVE 3 – 7 G / DAY FROM OUR DIET KIDNEYS EXCRETE EXCESS (~5 G / DAY) EXCRETION REGULATED BY 3 HORMONES ALDOSTERONE ANTIDIURETIC HORMONE (ADH) ATRIAL NATRIURETIC FACTOR (ANF)

32. ELECTROLYTE BALANCE SODIUM HOMEOSTASIS REGULATION BY ALDOSTERONE “SALT-RETAINING HORMONE” STEROID HORMONE ALDOSTERONE SECRETION STIMULATED BY: HYPONATREMIA HYPERKALEMIA HYPOTENSION

33. ELECTROLYTE BALANCE SODIUM HOMEOSTASIS REGULATION BY ALDOSTERONE TARGET CELLS DISTAL CONVOLUTED TUBULE COLLECTING DUCT TRANSCRIBE GENE FOR Na+-K+ PUMP SODIUM REABSORPTION INCREASES H+ AND K + SECRETION INCREASES URINE pH DROPS

34. ELECTROLYTE BALANCE SODIUM HOMEOSTASIS REGULATION BY ALDOSTERONE AVERAGE Na+ EXCRETION 5 G / DAY ALDOSTERONE REDUCES TO ~0 WATER REABSRBED PROPORTIONALLY SODIUM CONCENTRATION IN BODY UNCHANGED

35. ELECTROLYTE BALANCE SODIUM HOMEOSTASIS REGULATION BY ALDOSTERONE INHIBITED BY HYPERTENSION KIDNEYS THEN REABSORB LITTLE Na+ EXCRETION INCREASED TO ~30 G / DAY

37. ELECTROLYTE BALANCE SODIUM HOMEOSTASIS REGULATION BY ADH INDEPENDENTLY MODIFIES SODIUM AND WATER EXCRETION CAN CHANGE SODIUM CONCENTRATION HIGH BLOOD [Na+] ? ADH SECRETION INCREASES WATER REABSORPTION SODIUM CONCENTRATION DECREASED ADH ALSO STIMULATES THIRST ALSO HAPPENS IN REVERSE

38. ELECTROLYTE BALANCE SODIUM HOMEOSTASIS REGULATION BY ANF HYPERTENSION ? ANF SECRETION INHIBITS ADH AND RENIN SECRETION INHIBITS SODIUM & WATER REABSORPTION MORE SODIUM AND WATER EXCRETED BLOOD PRESSURE DECREASED

39. ELECTROLYTE BALANCE SODIUM HOMEOSTASIS REGULATION BY OTHER HORMONES ESTROGENS MIMIC ALDOSTERONE WATER RETENTION DURING PREGNANCY MENSTRUAL WATER RETENTION PROGESTERONE REDUCES SODIUM REABSORPTION DIURETIC AEFFECT GLUCOCORTICOIDS PROMOTE SODIUM REABSORPTION, EDEMA

40. ELECTROLYTE BALANCE SODIUM HOMEOSTASIS: IMBALANCES RELATIVELY RARE HYPERNATREMIA CAN RESULT FROM IV SALINE CAUSES WATER RETENTION, HYPERTENSION, EDEMA HYPONATREMIA GENERALLY FROM WATER EXCESS HYPOTONIC HYDRATION CORRECTED BY EXCRETION OF EXCESS WATER

41. ELECTROLYTE BALANCE POTASSIUM PRINCIPAL INTRACELLULAR CATION AFFECTS INTRACELLULAR OSMOLARITY AFFECTS CELL VOLUME ROLES PRODUCES RESTING & ACTION POTENTIALS COTRANSPORT THERMOGENESIS COFACTOR FOR PROTEIN SYNTHESIS

42. ELECTROLYTE BALANCE POTASSIUM HOMEOSTASIS HOMEOSTASIS LINKED TO THAT OF Na+ K+ AND Na+ COREGULATED BY ALDOSTERONE 90% OF K+ REABSORBED IN PCT REMAINDER EXCRETED IN URINE CONTROL IMPARTED IN DCT & COLLECTING DUCT (CD) HIGH [K+] ? SECRETE MORE INTO FILTRATE LOW [K+] ? SECRETE LESS INTO FILTRATE EXCHANGED FOR Na+

43. ELECTROLYTE BALANCE POTASSIUM HOMEOSTASIS REGULATION BY ALDOSTERONE HIGH [K+] ? ALDOSTERONE PRODUCTION Na+-K+ PUMP PRODUCED Na+ AND K+ COREGULATED INCREASE K+ SECRETION DECREASE Na+ SECRETION

44. ELECTROLYTE BALANCE POTASSIUM HOMEOSTASIS: IMBALANCES MOST DANGEROUS ELECTROLYTE IMBALANCES HYPERKALEMIA EFFECTS DEPEND ON SPEED OF CONC RISE QUICK RISE ? NERVE/MUSCLE CELLS VERY EXCITABLE ? CARDIAC ARREST E.G., K+ RELEASED FROM INJURED CELLS E.G., TRANSFUSION WITH OLD BLOOD E.G., EUTHANASIA, CAPITAL PUNISHMENT LETHAL INJECTION K+ HAS LEAKED FROM ERYTHROCYTES SLOW RISE ? NERVE/MUSCLE CELLS LESS EXCITABLE (Na+ CHANNELS INACTIVATED) E.G., ALDOSTERONE HYPOSECRETION, RENAL FAILURE, ACIDOSIS E.G., SUPPLEMENTAL K+ TO RELIEVE MUSCLE CRAMPS

45. ELECTROLYTE BALANCE POTASSIUM HOMEOSTASIS: IMBALANCES HYPOKALEMIA NERVE/MUSCLE CELLS LESS EXCITABLE MUSCLE WEAKNESS, LOSS OF MUSCLE TONE, DEPRESSED REFLEXES, IRREGULAR HEART ACTIVITY E.G., HEAVY SWEATING, CHRONIC VOMITING OR DIARRHEA, EXCESSIVE LAXATIVES, ALDOSTERONE HYPERSECRETION, ALKALOSIS E.G., DEPRESSED APPETITE, BUT RARELY FROM DIETARY INSUFFICIENCY

47. ELECTROLYTE BALANCE CHLORIDE MOST ABUNDANT ANION IN ECF MAJOR CONTRIBUTION TO OSMOLARITY ROLES FORMATION OF HCl CHLORIDE SHIFT CO2 LOADING/UNLOADING REGULATION OF BODY pH

48. ELECTROLYTE BALANCE CHLORIDE HOMEOSTASIS Cl- STRONGLY ATTRACTED TO SOME CATIONS (E.G., Na+, K+, Ca2+) CANNOT KEEP THEM APART HOMEOSTASIS ACHIEVED AS AN EFFECT OF Na+ HOMEOSTASIS Cl- PASSIVELY FOLLOWS Na+

49. ELECTROLYTE BALANCE CHLORIDE IMBALANCES HYPERCHLOREMIA RESULTS FROM DIETARY EXCESS RESULTS FROM INTERVENOUS SALINE ADMINISTRATION HYPOCHLOREMIA SIDE EFFECT OF HYPONATREMIA SIDE EFFECT OF HYPOKALEMIA KIDNEYS RETAIN K+ BY SECRETING Na+, Cl- FOLLOWS EFFECTS ALTERED ACID-BASE BALANCE

50. ELECTROLYTE BALANCE CALCIUM ROLES STRENGTHENS BONE MUSCLE CONTRACTION SECOND MESSENGER FOR HORMONES ACTIVATES EXOCYTOSIS BLOOD CLOTTING

51. ELECTROLYTE BALANCE CALCIUM BINDS TO PHOSPHATE ION CAN FORM Ca3(PO4)2 HIGH CONCENTRATIONS OF BOTH IONS WILL FORM PRECIPITATE CRYSTALS INTRACELLULAR [Ca2+] MUST BE KEPT LOW Ca2+ PUMPED OUT & INTO E.R.

52. ELECTROLYTE BALANCE CALCIUM HOMEOSTASIS REGULATED BY PTH & CALCITROL ALSO BY CALCITONIN IN CHILDREN BLOOD [Ca2+] REGULATED VIA BONE DEPOSITION & REABSORPTION INTESTINAL ABSORPTION URINARY EXCRETION

53. ELECTROLYTE BALANCE CALCIUM IMBALANCES HYPERCALCEMIA REDUCES EMBRANE PERMEABILITY TO Na+ INHIBITS DEPOLARIZATION OF NERVES/MUSCLES ? MUSCULAR WEAKNESS, CARDIAC ARRHYTHMI, ETC. RESULTS FROM ALKALOSIS HYPERPARATHYROIDISM HYPOTHYROIDISM

54. ELECTROLYTE BALANCE CALCIUM IMBALANCES HYPOCALCEMIA INCREASES EMBRANE PERMEABILITY TO Na+ NERVES/MUSCLES OVERLY EXCITABLE ? TETANUS IF CONCENTRATION DROPS TO LOW RESULTS FROM ACIDOSIS VITAMIN D DEFICIECY DIARRHEA PREGNANCY OR LACTATION HYPOPARATHYROIDISM HYPERTHYROIDISM

55. ELECTROLYTE BALANCE PHOSPHATES RELATIVELY CONCENTRATED IN ICF ROLES COMPONENTS OF BONES COMPONENTS OF DNA & RNA COMPONENTS OF PHOSPHOLIPIDS ACTIVATE / DEACTIVATE ENZYMES BUFFER pH OF BODY FLUIDS

56. ELECTROLYTE BALANCE PHOSPHATES COMPONENTS OF NUCLEIC ACIDS (DNA, RNA) NTPs AND dNTPs (ATP, dATP, GTP, dGTP, etc) cAMP PHOSPHOLIPIDS VARIOUS OTHER PHOSPHORYLATED MOLECULES GENERATED VIA ATP HYDROLYSIS, ETC. EXIST AS MIXTURE OF THREE FORMS PO43- (PHOSPHATE ION) HPO42- (MONOHYDROGEN PHOSPHATE ION) H2PO4- (DIHYDROGEN PHOSPHATE ION)

57. ELECTROLYTE BALANCE PHOSPHATE HOMEOSTASIS DIET PROVIDES AMPLE PHOSPHATE READILY ABSORBED BY SMALL INTESTINE REGULATION RENAL TUBULES SITE OF REGULATION PTH INCREASES PHOSPHATE EXCRETION EXCRETION RATE AFFECTED BY URINE pH

58. ELECTROLYTE BALANCE PHOSPHATE IMBALANCES PHOSPHATE HOMEOSTASIS NOT VERY CRITICAL BODY CAN TOLERATE WIDE VARIATIONS OF PHOSPHATEE CONCENTRATION WITH LITTLE EFFECT

59. ACID-BASE BALANCE ACIDS, BASES, AND pH ACID ANY SUBSTANCE RELEASING H+ [H+] INCREASES (pH DECREASES) BASE ANY SUBSTANCE ACCEPTING H+ [H+] DECREASES (pH INCREASES) pH A MEASURE OF [H+] -LOG [H+] SCALE 0 – 14, 7 IS NEUTRAL

60. ACID-BASE BALANCE WHY IS ACID-BASE BALANCE IMPORTANT? METABOLISM REQUIRES NUMEROUS ENZYMES ENZYMES ARE PROTEINS pH AFFECTS PROTEIN STRUCTURE PROTEIN STRUCTURE AFFECTS FUNCTION DEVIATIONS FROM NORMAL pH CAN INACTIVATE ENZYMES AND SHUT DOWN METABOLIC PATHWAYS

62. ACID-BASE BALANCE BLOOD pH BLOOD AND TISSUE pH 7.35 – 7.45 ENZYMES FUNCTION WELL WITHIN THIS RANGE ENZYMES FUNCTION POORLY (OR NOT AT ALL) WHEN SIGNIFICANTLY OUTSIDE OF THIS RANGE THIS RANGE MUST BE MAINTAINED ACID-BASE BALANCE

63. ACID-BASE BALANCE BUFFERS ANY MECHANISM OF RESISTING SIGNIFICANT CHANGES IN pH ACCOMPLISHED BY CONVERTING: STRONG ACID ? WEAK ACID STRONG BASE ? WEAK BASE

64. ACID-BASE BALANCE BUFFERS PHYSIOLOGICAL BUFFER SYSTEM STABILIZING pH BY CONTROLLING BODY’S OUTPUT OF ACIDS, BASES, OR CO2 URINARY SYSTEM BUFFERS GREATEST QUANTITY REQUIRES HOURS OR DAYS TO EXERT EFFECT RESPIRATORY SYSTEM SMALLER EFFECT EXERTS EFFECT WITHIN MINUTES

65. ACID-BASE BALANCE BUFFERS CHEMICAL BUFFER SYSTEM COMBINATION OF WEAK ACID AND WEAK BASE BINDS TO H+ AS [H+] RISES, AND RELEASES H+ AS [H+] FALLS CAN RESTORE NORMAL pH ALMOST IMMEDIATELY THREE MAJOR CHEMICAL BUFFER SYSTEMS BICARBONATE SYSTEM PHOSPHATE SYSTEM PROTEIN SYSTEM

66. ACID-BASE BALANCE BICARBONATE BUFFER SYSTEM CARBONIC ACID (H2CO3) WEAK ACID BICARBONATE ION (HCO3-) WEAK BASE CO2 + H20 ? H2CO3 ? H+ + HCO3- WORKS IN CONCERT WITH RESPIRATORY AND URINARY SYSTEM THESE SYSTEMS REMOVE CO2 OR HCO3-

67. ACID-BASE BALANCE PHOSPHATE BUFFER SYSTEM DIHYDROGEN PHOSPHATE ION(H2PO4-) WEAK ACID MONOHYDROGEN PHOSPHATE ION (HPO42-) WEAK BASE H2PO4- ? H+ + HPO42- STRONGER THAN BICARBONATE BUFFERING SYSTEM MORE IMPARTANT IN BUFFERING ICF AND RENAL TUBULES THAN IN ECF

68. ACID-BASE BALANCE PROTEIN BUFFER SYSTEM PROTEINS ARE MORE CONCENTRATED THAN BICARBONATE AND PHOSPHATE BUFFERS ACCOUNTS FOR ~75% OF ALL CHEMICAL BUFFERING OF BODY FLUIDS BUFFERING ABILITY DUE TO CERTAIN FUNCTIONAL GROUPS OF AMINO ACID RESIDUES CARBOXYL GROUPS --COOH ? -COO- + H+ AMINO GROUPS --NH3+ ? -NH2 + H+

69. ACID-BASE BALANCE RESPIRATORY CONTROL OF pH CO2 + H20 ? H2CO3 ? H+ + HCO3- ADDITION OF CO2 INCREASES [H+] REMOVAL OF CO2 DECREASES [H+] CAN NEUTRALIZE 2-3 X MORE ACID AS CHEMICAL BUFFERS

70. ACID-BASE BALANCE RENAL CONTROL OF pH CAN NEUTRALIZE MORE ACID OR BASE THAN BOTH RESPIRATORY SYSTEM AND CHEMICAL BUFFERS RENAL TUBULES SECRETE H+ H+ EXCRETED IN URINE EXCHANGED FOR SODIUM ION (Na+) ONLY POSSIBLE WHEN [H+] INSIDE TUBULE CELLS IS > [H+] IN TUBULAR FLUID

72. ACID-BASE BALANCE ACID-BASE BALANCE DISORDERS AT pH 7.4, 20:1 HCO3-:H2CO3 RATIO IF [H2CO3] INCREASES, pH DROPS pH BELOW 7.35 = ACIDOSIS IF [HCO3-] INCREASES, pH INCREASES pH ABOVE 7.45 = ALKALOSIS

73. ACID-BASE BALANCE ACID-BASE BALANCE DISORDERS RESPIRATORY ACIDOSIS CO2 PRODUCTION EXCEEDS RESPIRATORY CO2 ELIMINATION CO2 ACCUMULATES IN ECF pH DROPS RESPIRATORY ALKALOSIS RESPIRATORY CO2 ELIMINATION EXCEEDS CO2 PRODUCTION EXCESSIVE VENTILATION (HYPERVENTILATION) pH RISES

74. ACID-BASE BALANCE ACID-BASE BALANCE DISORDERS METABOLIC ACIDOSIS INCREASED PRODUCTION OF ORGANIC ACIDS E.G., FERMENTATION ? LACTIC ACID E.G., ALCOHOLISM, DIABETES MELLITUS ? KETONE BODIES INGESTION OF ACIDIC DRUGS E.G., ASPIRIN LOSS OF BASE E.G., CHRONIC DIARRHEA, OVERUSE OF LAXITIVES METABOLIC ALKALOSIS RARE OVERUSE OF BICARBONATES E.G., ANTACIDS LOSS OF STOMACH ACID FROM CHRONIC VOMITING

76. ACID-BASE BALANCE ACID-BASE BALANCE DISORDERS ACIDOSIS H+ PASSIVELY DIFFUSES INTO CELLS K+ DIFFUSES OUT ELECTRICAL BALANCE MAINTAINED H+ BUFFERED BY INTRACELLULAR PROTEINS NET LOSS OF CATIONS FROM CELL MEMBRANE IS NOW HYPERPOLARIZED NERVE & MUSCLE CELLS DIFFICULT TO STIMULATE CENTRAL NERVOUS SYSTEM DEPRESSED CONFUSION, DISORIENTATION, COMA

78. ACID-BASE BALANCE ACID-BASE BALANCE DISORDERS ALKALOSIS H+ PASSIVELY DIFFUSES OUT OF CELLS K+ DIFFUSES INTO CELLS GAIN IN POSITIVE INTRACELLULAR CHARGE MEMBRANE POTENTIAL SHIFTED NERVOUS SYSTEM HYPEREXCITABLE NEURONS FIRE SPONTANEOUSLY SKELETAL MUSCLES OVERSTIMULATED MUSCLE SPASMS, TETANY, CONVULSIONS, RESPIRATORY PARALYSIS

79. ACID-BASE BALANCE ACID-BASE IMBALANCE COMPENSATION RESPIRATORY SYSTEM COMPENSATION ADJUSTS PCO2 IN ECF CO2 EXCESS ? INCREASED VENTILATION CO2 DEFICIENCY ? DECREASED VENTILATION EFFECTIVE VS RESPIRATORY ACIDOSIS AND ALKALOSIS NOT VERY EFFECTIVE VS METABOLIC ACIDOSIS AND ALKALOSIS I.E., CANNOT RID BODY OF KETONE BODIES CAN CORRECT pH 7.0 TO 7.2 OR 7.3 NOT ALL THE WAY TO 7.4

80. ACID-BASE BALANCE ACID-BASE IMBALANCE COMPENSATION RENAL SYSTEM COMPENSATION SLOWER TO RESPOND CAN FULLY RESTORE NORMAL pH URINE pH NORMALLY 5 – 6 MAY DROP TO 4.5 WITH EXCESS H+ RESPONSE TO ACIDOSIS RENAL TUBULES INCREASE H+ SECRETION H+ IN URINE IS BUFFERED MAY RISE TO 8.2 WITH EXCESS HCO3- RESPONSE TO ALKALOSIS HCO3- CONCENTRATION IN URINE ELEVATED

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