balance - WATER BALANCE NORMAL WATER CONTENT OF BODY 75% AT...

Info iconThis preview shows page 1. Sign up to view the full content.

View Full Document Right Arrow Icon
This is the end of the preview. Sign up to access the rest of the document.

Unformatted text preview: WATER BALANCE NORMAL WATER CONTENT OF BODY 75% AT BIRTH 5560% YOUNG ADULTS 45% IN ELDERLY, OBESE MEN SLIGHTLY HIGHER THAN WOMEN (MORE FAT, LESS WATER) 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. WATER BALANCE TOTAL BODY WATER ENTERS BODY OSMOSIS FROM DIGESTIVE TRACT EXITS BODY ALSO PRODUCED BY AEROBIC RESPIRATION ALSO PRODUCED BY CONDENSATION REACTIONS URINARY, DIGESTIVE, RESPIRATORY, & INTEGUMENTARY SYSTEMS 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 WATER BALANCE WATER BALANCE FLUID GAIN = FLUID LOSS BOTH TYPICALLY ~2500 ML / DAY 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 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 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 WATER BALANCE WATER LOSS OBLIGATORY WATER LOSS RELATIVELY UNAVOIDABLE EXPIRED AIR, CUTANEOUS TRANSPIRATION, SWEAT, FECAL MOISTURE, MINIMUM URINE OUTPUT (~400 ML/DAY) WATER BALANCE REGULATION OF WATER INTAKE GOVERNED BY THIRST THIRST CENTER IN HYPOTHALAMUS PROVOKED BY INCREASED PLASMA OSMOLARITY PROVOKED BY BLOOD LOSS RESPONDS TO SIGNS OF DEHYDRATION ANGIOTENSIN II ANTIDIURETIC HORMONE (ADH) SIGNALS FROM OSMOCENTERS INHIBITS SALIVATION WATER BALANCE REGULATION OF WATER INTAKE INHIBITED SALIVATION DRY MOUTH SENSE OF THIRST INGESTION OF WATER THIRST INHIBITED COOLS AND MOISTENS MOUTH DISTENDS STOMACH AND INTESTINES REHYDRATES BLOOD WATER BALANCE REGULATION OF WATER OUTPUT CONTROLLED VIA ALTERATIONS IN URINE VOLUME URINE VOLUME AFFECTED BY SODIUM REABSORPTION ANTIDIURETIC HORMONE (ADH) WATER FOLLOWS SODIUM REABSORPTION MORE LATER BLOOD VOLUME , [Na+] , OSMORECEPTORS STIMULATED, PITUITARY RELEASES ADH AQUAPORINS PRODUCED IN KIDNEY'S COLLECTING DUCTS FACILITATE REABSORPTION ALSO WORKS IN REVERSE WATER BALANCE WATER BALANCE DISORDERS FLUID DEFICIENCY FLUID EXCESS VOLUME DEPLETION (HYOVOLEMIA) DEHYDRATION VOLUME EXCESS HYPOTONIC HYDRATION FLUID SEQUESTRATION 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 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 WATER BALANCE WATER BALANCE DISORDERS FLUID DEFICIENCY: DEHYDRATION AFFECTS ALL FLUID COMPARTMENTS INFANTS MORE VULNERABLE THAN ADULTS HIGHER METABOLISM MORE WASTES IMMATURE KIDNEYS MORE WASTES MORE URINE VOLUME URINE LESS CONCENTRATED GREATER SURFACE AREATOVOLUME RATIO GREATER WATER LOSS BY EVAPORATION WATER BALANCE WATER BALANCE DISORDERS EFFECTS OF FLUID DEFICIENCY CIRCULATORY SHOCK NEUROLOGICAL DYSFUNCTION DUE TO LOSS OF BLOOD VOLUME DUE TO DEHYDRATION OF BRAIN CELLS WATER BALANCE WATER BALANCE DISORDERS FLUID EXCESS LESS COMMON THAN FLUID DEFICIENCY KIDNEYS ARE TYPICALLY ABLE TO EXCRETE MORE URINE 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 WATER BALANCE WATER BALANCE DISORDERS FLUID EXCESS: HYPOTONIC HYDRATION "WATER INTOXICATION", "POS H 0 2 BALANCE" CAUSED BY RETENTION OF MORE WATER THAN SODIUM TOTAL BODY WATER INCREASED ECF OSMOLARITY DECREASES CAUSES REPLACEMENT OF WATER AND SALT WITH WATER ADH HYERSECRETION LACK OF PROPORTIONATE INTAKE OF ELECTROLYTES WATER BALANCE WATER BALANCE DISORDERS EFFECTS OF FLUID EXCESS PULMONARY EDEMA CEREBRAL EDEMA 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) ELECTROLYTE BALANCE IMPORTANCE OF ELECTROLYTES SALTS MANY ROLES E.G. NaCl, Ca3(PO4)2, ETC. INCLUDE IONS IN DEFINITION INVOLVED IN METABOLISM DETERMINE ELECTRICAL MEMBRANE POTENTIALS AFFECT OSMOLARITY OF BODY FLUIDS AFFECT WATER CONTENT AND DISTRIBUTION ETC. ELECTROLYTE BALANCE SODIUM PRINCIPAL EXTRACELLULAR CATION ROLES 90 95% OF OSMOLARITY FROM SODIUM SALTS DEPOLARIZATION AFFECT TOTAL BODY WATER AFFECT WATER DISTRIBUTION COTRANSPORT MUSCLES, NERVES ETC. GLUCOSE, AMINO ACIDS, CALCIUM, ETC. 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 ELECTROLYTE BALANCE SODIUM HOMEOSTASIS REGULATION BY ALDOSTERONE "SALTRETAINING HORMONE" STEROID HORMONE ALDOSTERONE SECRETION STIMULATED BY: HYPONATREMIA HYPERKALEMIA HYPOTENSION ELECTROLYTE BALANCE SODIUM HOMEOSTASIS REGULATION BY ALDOSTERONE TARGET CELLS TRANSCRIBE GENE FOR Na+K+ PUMP DISTAL CONVOLUTED TUBULE COLLECTING DUCT SODIUM REABSORPTION INCREASES H+ AND K + SECRETION INCREASES URINE pH DROPS 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 ELECTROLYTE BALANCE SODIUM HOMEOSTASIS REGULATION BY ALDOSTERONE INHIBITED BY HYPERTENSION KIDNEYS THEN REABSORB LITTLE Na+ EXCRETION INCREASED TO ~30 G / DAY ELECTROLYTE BALANCE SODIUM HOMEOSTASIS REGULATION BY ADH INDEPENDENTLY MODIFIES SODIUM AND WATER EXCRETION HIGH BLOOD [Na+] ADH SECRETION CAN CHANGE SODIUM CONCENTRATION INCREASES WATER REABSORPTION ALSO HAPPENS IN REVERSE ADH ALSO STIMULATES THIRST SODIUM CONCENTRATION DECREASED 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 ELECTROLYTE BALANCE SODIUM HOMEOSTASIS REGULATION BY OTHER HORMONES ESTROGENS MIMIC ALDOSTERONE PROGESTERONE WATER RETENTION DURING PREGNANCY MENSTRUAL WATER RETENTION REDUCES SODIUM REABSORPTION DIURETIC AEFFECT PROMOTE SODIUM REABSORPTION, EDEMA GLUCOCORTICOIDS ELECTROLYTE BALANCE SODIUM HOMEOSTASIS: IMBALANCES RELATIVELY RARE HYPERNATREMIA HYPONATREMIA CAN RESULT FROM IV SALINE CAUSES WATER RETENTION, HYPERTENSION, EDEMA GENERALLY FROM WATER EXCESS HYPOTONIC HYDRATION CORRECTED BY EXCRETION OF EXCESS WATER ELECTROLYTE BALANCE POTASSIUM PRINCIPAL INTRACELLULAR CATION AFFECTS INTRACELLULAR OSMOLARITY AFFECTS CELL VOLUME ROLES PRODUCES RESTING & ACTION POTENTIALS COTRANSPORT THERMOGENESIS COFACTOR FOR PROTEIN SYNTHESIS ELECTROLYTE BALANCE POTASSIUM HOMEOSTASIS HOMEOSTASIS LINKED TO THAT OF Na+ 90% OF K+ REABSORBED IN PCT K+ AND Na+ COREGULATED BY ALDOSTERONE 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+ 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 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 SLOW RISE NERVE/MUSCLE CELLS LESS EXCITABLE (Na+ CHANNELS INACTIVATED) K+ HAS LEAKED FROM ERYTHROCYTES E.G., ALDOSTERONE HYPOSECRETION, RENAL FAILURE, ACIDOSIS E.G., SUPPLEMENTAL K+ TO RELIEVE MUSCLE CRAMPS 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 ELECTROLYTE BALANCE CHLORIDE MOST ABUNDANT ANION IN ECF ROLES MAJOR CONTRIBUTION TO OSMOLARITY FORMATION OF HCl CHLORIDE SHIFT REGULATION OF BODY pH CO2 LOADING/UNLOADING ELECTROLYTE BALANCE CHLORIDE HOMEOSTASIS Cl STRONGLY ATTRACTED TO SOME CATIONS (E.G., Na+, K+, Ca2+) HOMEOSTASIS ACHIEVED AS AN EFFECT OF Na+ HOMEOSTASIS CANNOT KEEP THEM APART Cl PASSIVELY FOLLOWS Na+ ELECTROLYTE BALANCE CHLORIDE IMBALANCES HYPERCHLOREMIA HYPOCHLOREMIA RESULTS FROM DIETARY EXCESS RESULTS FROM INTERVENOUS SALINE ADMINISTRATION SIDE EFFECT OF HYPONATREMIA SIDE EFFECT OF HYPOKALEMIA ALTERED ACIDBASE BALANCE EFFECTS KIDNEYS RETAIN K+ BY SECRETING Na+, Cl FOLLOWS ELECTROLYTE BALANCE CALCIUM ROLES STRENGTHENS BONE MUSCLE CONTRACTION SECOND MESSENGER FOR HORMONES ACTIVATES EXOCYTOSIS BLOOD CLOTTING 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. ELECTROLYTE BALANCE CALCIUM HOMEOSTASIS REGULATED BY PTH & CALCITROL BLOOD [Ca2+] REGULATED VIA ALSO BY CALCITONIN IN CHILDREN BONE DEPOSITION & REABSORPTION INTESTINAL ABSORPTION URINARY EXCRETION 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 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 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 ELECTROLYTE BALANCE PHOSPHATES COMPONENTS OF GENERATED VIA ATP HYDROLYSIS, ETC. EXIST AS MIXTURE OF THREE FORMS NUCLEIC ACIDS (DNA, RNA) NTPs AND dNTPs (ATP, dATP, GTP, dGTP, etc) cAMP PHOSPHOLIPIDS VARIOUS OTHER PHOSPHORYLATED MOLECULES PO43 HPO42 H2PO4 (PHOSPHATE ION) (MONOHYDROGEN PHOSPHATE ION) (DIHYDROGEN PHOSPHATE ION) 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 ELECTROLYTE BALANCE PHOSPHATE IMBALANCES PHOSPHATE HOMEOSTASIS NOT VERY CRITICAL BODY CAN TOLERATE WIDE VARIATIONS OF PHOSPHATEE CONCENTRATION WITH LITTLE EFFECT ACID-BASE BALANCE ACIDS, BASES, AND pH ACID BASE ANY SUBSTANCE RELEASING H+ [H+] INCREASES (pH DECREASES) ANY SUBSTANCE ACCEPTING H+ [H+] DECREASES (pH INCREASES) A MEASURE OF [H+] LOG [H+] SCALE 0 14, 7 IS NEUTRAL pH ACID-BASE BALANCE WHY IS ACIDBASE 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 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 ACIDBASE BALANCE ACID-BASE BALANCE BUFFERS ANY MECHANISM OF RESISTING SIGNIFICANT CHANGES IN pH ACCOMPLISHED BY CONVERTING: STRONG ACID WEAK ACID STRONG BASE WEAK BASE ACID-BASE BALANCE BUFFERS PHYSIOLOGICAL BUFFER SYSTEM STABILIZING pH BY CONTROLLING BODY'S OUTPUT OF ACIDS, BASES, OR CO2 URINARY SYSTEM RESPIRATORY SYSTEM BUFFERS GREATEST QUANTITY REQUIRES HOURS OR DAYS TO EXERT EFFECT SMALLER EFFECT EXERTS EFFECT WITHIN MINUTES 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 ACID-BASE BALANCE BICARBONATE BUFFER SYSTEM CARBONIC ACID (H CO ) 2 3 BICARBONATE ION (HCO3) WEAK ACID WEAK BASE 2 2 2 3 + 3 CO + H 0 H CO H + HCO WORKS IN CONCERT WITH RESPIRATORY AND URINARY SYSTEM ACID-BASE BALANCE PHOSPHATE BUFFER SYSTEM DIHYDROGEN PHOSPHATE ION(H PO ) 2 4 MONOHYDROGEN PHOSPHATE ION (HPO42) WEAK ACID 2 WEAK BASE 4 + 42 H PO H + HPO STRONGER THAN BICARBONATE BUFFERING SYSTEM MORE IMPARTANT IN BUFFERING ICF AND RENAL TUBULES THAN IN ECF 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 + AMINO GROUPS + 3+ 2 COOH COO + H ACID-BASE BALANCE RESPIRATORY CONTROL OF pH 2 2 2 3 + 3 CO + H 0 H CO H + HCO ADDITION OF CO2 INCREASES [H+] REMOVAL OF CO2 DECREASES [H+] CAN NEUTRALIZE 23 X MORE ACID AS CHEMICAL BUFFERS 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 ACID-BASE BALANCE ACIDBASE BALANCE DISORDERS AT pH 7.4, 20:1 HCO :H CO RATIO 3 2 3 IF [H2CO3] INCREASES, pH DROPS IF [HCO3] INCREASES, pH INCREASES pH BELOW 7.35 = ACIDOSIS pH ABOVE 7.45 = ALKALOSIS ACID-BASE BALANCE ACIDBASE BALANCE DISORDERS RESPIRATORY ACIDOSIS RESPIRATORY ALKALOSIS CO2 PRODUCTION EXCEEDS RESPIRATORY CO2 ELIMINATION CO2 ACCUMULATES IN ECF pH DROPS RESPIRATORY CO2 ELIMINATION EXCEEDS CO2 PRODUCTION EXCESSIVE VENTILATION (HYPERVENTILATION) pH RISES ACID-BASE BALANCE ACIDBASE BALANCE DISORDERS METABOLIC ACIDOSIS INCREASED PRODUCTION OF ORGANIC ACIDS INGESTION OF ACIDIC DRUGS E.G., FERMENTATION LACTIC ACID E.G., ALCOHOLISM, DIABETES MELLITUS KETONE BODIES E.G., ASPIRIN LOSS OF BASE METABOLIC ALKALOSIS E.G., CHRONIC DIARRHEA, OVERUSE OF LAXITIVES RARE OVERUSE OF BICARBONATES LOSS OF STOMACH ACID FROM CHRONIC VOMITING E.G., ANTACIDS ACID-BASE BALANCE ACIDBASE BALANCE DISORDERS ACIDOSIS H+ PASSIVELY DIFFUSES INTO CELLS K+ DIFFUSES OUT H+ BUFFERED BY INTRACELLULAR PROTEINS NET LOSS OF CATIONS FROM CELL MEMBRANE IS NOW HYPERPOLARIZED NERVE & MUSCLE CELLS DIFFICULT TO STIMULATE ELECTRICAL BALANCE MAINTAINED CENTRAL NERVOUS SYSTEM DEPRESSED CONFUSION, DISORIENTATION, COMA ACID-BASE BALANCE ACIDBASE BALANCE DISORDERS ALKALOSIS H+ PASSIVELY DIFFUSES OUT OF CELLS K+ DIFFUSES INTO CELLS MEMBRANE POTENTIAL SHIFTED NERVOUS SYSTEM HYPEREXCITABLE GAIN IN POSITIVE INTRACELLULAR CHARGE NEURONS FIRE SPONTANEOUSLY SKELETAL MUSCLES OVERSTIMULATED MUSCLE SPASMS, TETANY, CONVULSIONS, RESPIRATORY PARALYSIS ACID-BASE BALANCE ACIDBASE IMBALANCE COMPENSATION RESPIRATORY SYSTEM COMPENSATION ADJUSTS PCO IN ECF 2 EFFECTIVE VS RESPIRATORY ACIDOSIS AND ALKALOSIS NOT VERY EFFECTIVE VS METABOLIC ACIDOSIS AND ALKALOSIS CO2 EXCESS INCREASED VENTILATION CO2 DEFICIENCY DECREASED VENTILATION CAN CORRECT pH 7.0 TO 7.2 OR 7.3 I.E., CANNOT RID BODY OF KETONE BODIES NOT ALL THE WAY TO 7.4 ACID-BASE BALANCE ACIDBASE 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+ MAY RISE TO 8.2 WITH EXCESS HCO3 RESPONSE TO ACIDOSIS RENAL TUBULES INCREASE H+ SECRETION H+ IN URINE IS BUFFERED RESPONSE TO ALKALOSIS HCO3 CONCENTRATION IN URINE ELEVATED ...
View Full Document

This note was uploaded on 12/24/2011 for the course STEP 1 taught by Professor Dr.aslam during the Fall '11 term at Montgomery College.

Ask a homework question - tutors are online