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Water , Balance

Water , Balance

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Published by: Charlie Falguera on Sep 19, 2012
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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

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
ALSO PRODUCED BY AEROBIC RESPIRATION  ALSO PRODUCED BY CONDENSATION REACTIONS

EXITS BODY

URINARY, DIGESTIVE, RESPIRATORY, & INTEGUMENTARY SYSTEMS

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 TOTAL BODY WATER  FLUID EXCHANGED BETWEEN COMPARTMENTS      CAPILLARY WALLS.

.

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

K.A. DEHYDRATION REACTIONS .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.

EVAPORATES .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.

.

.

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

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

WATER BALANCE REGULATION OF WATER INTAKE  GOVERNED BY THIRST   PROVOKED BY INCREASED PLASMA OSMOLARITY PROVOKED BY BLOOD LOSS RESPONDS TO SIGNS OF DEHYDRATION     THIRST CENTER IN HYPOTHALAMUS  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 COOLS AND MOISTENS MOUTH  DISTENDS STOMACH AND INTESTINES  REHYDRATES BLOOD   THIRST INHIBITED .

.

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   VOLUME DEPLETION (HYOVOLEMIA) DEHYDRATION VOLUME EXCESS HYPOTONIC HYDRATION  FLUID EXCESS    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  MORE WASTES  MORE URINE VOLUME URINE LESS CONCENTRATED GREATER WATER LOSS BY EVAPORATION  IMMATURE KIDNEYS   GREATER SURFACE AREA-TO-VOLUME RATIO  .

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

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 .

“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 ADH HYERSECRETION LACK OF PROPORTIONATE INTAKE OF ELECTROLYTES .WATER BALANCE WATER BALANCE DISORDERS FLUID EXCESS: HYPOTONIC HYDRATION  “WATER INTOXICATION”.

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) .

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

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

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) .ELECTROLYTE BALANCE SODIUM HOMEOSTASIS  0.

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

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

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  CAN CHANGE SODIUM CONCENTRATION INCREASES WATER REABSORPTION   HIGH BLOOD [Na+]  ADH SECRETION  SODIUM CONCENTRATION DECREASED  ADH ALSO STIMULATES THIRST  ALSO HAPPENS IN REVERSE .

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   WATER RETENTION DURING PREGNANCY MENSTRUAL WATER RETENTION REDUCES SODIUM REABSORPTION DIURETIC AEFFECT PROMOTE SODIUM REABSORPTION. EDEMA  PROGESTERONE    GLUCOCORTICOIDS  .

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

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+  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+ .

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 .

ACIDOSIS E.. SUPPLEMENTAL K+ TO RELIEVE MUSCLE CRAMPS .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.. TRANSFUSION WITH OLD BLOOD E.G.G. CAPITAL PUNISHMENT LETHAL INJECTION    SLOW RISE  NERVE/MUSCLE CELLS LESS EXCITABLE (Na+ CHANNELS INACTIVATED)   K+ HAS LEAKED FROM ERYTHROCYTES E..G.G.G. RENAL FAILURE. K+ RELEASED FROM INJURED CELLS E. EUTHANASIA... ALDOSTERONE HYPOSECRETION.

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

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

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

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

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

R.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. .

ELECTROLYTE BALANCE
CALCIUM HOMEOSTASIS  REGULATED BY PTH & CALCITROL

ALSO BY CALCITONIN IN CHILDREN BONE DEPOSITION & REABSORPTION INTESTINAL ABSORPTION URINARY EXCRETION

BLOOD [Ca2+] REGULATED VIA
  

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

RNA) NTPs AND dNTPs (ATP. etc) cAMP PHOSPHOLIPIDS VARIOUS OTHER PHOSPHORYLATED MOLECULES   GENERATED VIA ATP HYDROLYSIS. ETC. dGTP. GTP. EXIST AS MIXTURE OF THREE FORMS    PO43HPO42H2PO4- (PHOSPHATE ION) (MONOHYDROGEN PHOSPHATE ION) (DIHYDROGEN PHOSPHATE ION) . dATP.ELECTROLYTE BALANCE PHOSPHATES  COMPONENTS OF      NUCLEIC ACIDS (DNA.

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 .

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

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 .

.

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 .35 – 7.ACID-BASE BALANCE BLOOD pH  BLOOD AND TISSUE pH 7.

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

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

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 (H2CO3)  WEAK ACID  BICARBONATE ION (HCO3-)  WEAK BASE   CO2 + H20  H2CO3  H+ + HCO3WORKS IN CONCERT WITH RESPIRATORY AND URINARY SYSTEM  THESE SYSTEMS REMOVE CO2 OR HCO3- .

ACID-BASE BALANCE PHOSPHATE BUFFER SYSTEM  DIHYDROGEN PHOSPHATE ION(H2PO4-)  WEAK ACID  MONOHYDROGEN PHOSPHATE ION (HPO42-)  WEAK BASE    H2PO4. H+ + HPO42STRONGER 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  --COOH  -COO.+ H+ --NH3+  -NH2 + H+ AMINO GROUPS  .

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 .

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 .

.

35 = ACIDOSIS pH ABOVE 7. pH INCREASES  .ACID-BASE BALANCE ACID-BASE BALANCE DISORDERS  AT pH 7. 20:1 HCO3-:H2CO3 RATIO  IF [H2CO3] INCREASES.4.45 = ALKALOSIS  IF [HCO3-] INCREASES. pH DROPS  pH BELOW 7.

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

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

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COMA . DISORIENTATION.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.

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CONVULSIONS.ACID-BASE BALANCE ACID-BASE 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. RESPIRATORY PARALYSIS . TETANY.

4  CAN CORRECT pH 7. CANNOT RID BODY OF KETONE BODIES NOT ALL THE WAY TO 7..0 TO 7.3  .2 OR 7.ACID-BASE BALANCE ACID-BASE IMBALANCE COMPENSATION  RESPIRATORY SYSTEM COMPENSATION  ADJUSTS PCO2 IN ECF     EFFECTIVE VS RESPIRATORY ACIDOSIS AND ALKALOSIS NOT VERY EFFECTIVE VS METABOLIC ACIDOSIS AND ALKALOSIS  CO2 EXCESS  INCREASED VENTILATION CO2 DEFICIENCY  DECREASED VENTILATION I.E.

2 WITH EXCESS HCO3  RESPONSE TO ACIDOSIS RENAL TUBULES INCREASE H+ SECRETION H+ IN URINE IS BUFFERED RESPONSE TO ALKALOSIS HCO3.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+     MAY RISE TO 8.CONCENTRATION IN URINE ELEVATED .

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