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FLUID AND ELECTROLYTE REGULATION AND ACID BASE BALANCE. EXTRACELLULAR VS INTRACELLULAR FLUIDS. EXTRACELLULAR FLUIDS. INTERSTITIAL OR TISSUE FLUID PLASMA LYMPH CEREBROSPINAL FLUID INTRAOCULAR FLUID SYNOVIAL FLUID PERICARDIAL FLUID PLEURAL FLUID PERITONEAL FLUID.
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EXTRACELLULAR FLUIDS • INTERSTITIAL OR TISSUE FLUID • PLASMA • LYMPH • CEREBROSPINAL FLUID • INTRAOCULAR FLUID • SYNOVIAL FLUID • PERICARDIAL FLUID • PLEURAL FLUID • PERITONEAL FLUID
EXTRACELLULAR FLUID COMPOSITION • PLASMA AND TISSUE FLUIDS VERY SIMILAR • SEPARATED BY CAPILLARY WALLS THAT ALLOW FAIRLY FREE EXCHANGE OF LOW MOLECULAR WEIGHT SUBSTANCES
DIFFERENCES • DUE TO FACT PROTEINS CANNOT PASS THROUGH MEMBRANES\ • PROTEINS NORMALLY ANIONS • LEADS TO MORE SODIUM AND LESS CHLORIDE IN PLASMA THAN INTERSTITIAL FLUID
COMPOSITION OF INTRACELLULAR FLUID • SEPARATED FROM EXTRACELLULAR BY CELL MEMBRANE THAT IS RELATIVELY IMPERMEABLE TO PROTEINS • SODIUM POTASSIUM PUMP ACCUMULATES SODIUM TO OUTSIDE AND POTASSIUM TO INSIDE
REGULATION OF THE INTERNAL ENVIRONMENT • WATER • ELECTROLYTES • KIDNEYS PLAY A MAJOR ROLE
SODIUM REGULATION • MAJOR EXTRACELLULAR CATION • MAJOR OSMOTIC EFFECTS • WHERE SODIUM GOES WATER FOLLOWS • GREATLY AFFECTS PLASMA VOLUME AND BLOOD PRESSURE
INGESTION OF SODIUM • REGULATORY COMPONENT • HEDONISTIC COMPONENT • AVERAGE CONSUMPTION IN US IS 10-15 GRAMS PER DAY • 0.5 GRAMS ARE NEEDED
RENAL EXCRETION & REABSORPTION OF SODIUM • KIDNEYS CONTROL BODY’S SODIUM LEVELS • RELATIONSHIP BETWEEN GLOMERULAR FILTRATION RATE OF SODIUM AND THE TUBULAR REABSORPTION RATE DETERMINES SODIUM EXCRETION • SODIUM IS FREELY FILTERED
FACTORS THAT AFFECT GLOMERULAR FILTRATION RATE • ARTERIAL BLOOD PRESSURE • ACTIVITY OF SYMPATHETIC NERVES
CONTROL OF SODIUM REABSORPTION • IMPORTANT IN LONG TERM CONTROL OF SODIUM EXCRETION • ALDOSTERONE • RENIN-ANGIOTENSIN
ALDOSTERONE • STIMULATES SODIUM REABSORPTION • DISTAL CONVOLUTED TUBULES • COLLECTING TUBULES
HIGH ALDOSTERONE LEVELS • ALMOST ALL SODIUM IS REABSORBED • 0.1 GRAM OF SODIUM EXCRETED
LOW ALDOSTERONE LEVELS • AS MUCH AS 30-40 G OF SODIUM CAN BE EXCRETED
REGULATION OF ALDOSTERONE SECRETION • RENIN • PRODUCED BY JUXTAGLOMERULAR COMPLEX
FACTORS THAT LEAD TO RENIN SECRETION • DECREASE IN RENAL ARTERIAL PRESSURE • INCREASE IN ACTIVITY OF SYMPATHETIC NERVES
EFFECTS OF RENIN • CONVERTS ANGIOTENSINOGEN INTO ANGIOTENSIN I
FATE OF ANGIOTENSIN I • PASSES THROUGH LUNGS AND IS CONVERTED INTO ANGIOTENSIN II
EFFECT OF ANGIOTENSIN II • STIMULATES ALDOSTERONE RELEASE FROM ADRENAL GLAND
EFFECT OF ALDOSTERONE • STIMULATES REABSORPTION OF SODIUM FORM DISTAL CONVOUTED TUBULES AND COLLECTNG TUBULES
FACTORS THAT LEAD TO SODIUM EXCRETION • INCREASE IN SYSTEMIC BLOOD PRESSURE • INCREASED NERVE IMPULSES FROM CIRCULATORY PRESSURE RECEPTORS--THIS CAUSES DECREASED ACTIVITY OF SYMPATHETIC NERVES WHICH CAUSES DILATION OF AFFERENT ARTERIOLES • DECREASED RELEASE OF RENIN--DECREASED RELEASE OF ALDOSTERONE • RELEASE OF ATRIAL NATRIURETIC FACTOR
NET EFFECT • INCREASE AMOUNT OF SODIUM IN GLOMERULAR FILTRATE • DECREASE AMOUNT OF SODIUM REABSORBED FROM TUBULES • INCREASED EXCRETION OF SODIUM • BODY LEVELS OF SODIUM DECLINE • WATER FOLLOWS
REGULATION OF WATER CONTENT • INGESTION • THIRST • RENAL EXCRETION
INGESTION • HABIT AND SOCIAL FACTORS USUALLY MORE INFLUENTIAL
THIRST • RESULTS FROM INCREASED OSMOTIC CONCENTATION • REDUCED PLASMA VOLUME • OSMORECEPTORS IN HYPOTHALAMUS MONITOR • MAYBE CIRCULATORY RECEPTORS • ANGIOTENSIN II
EXCRETION OF WATER • RELATIONSHIP BETWEEN GLOMERULAR FILTRATION RATE AND TUBULAR REABSORPTION RATE • WATER IS FREELY FILTERED FROM PLASMA • FACTORS THAT AFFECT GLOMERULAR FILTRATION RATE AFFECTS WATER EXCRETION • SODIUM REGULATION ALSO VERY IMPORTANT • DEPENDENT ON ANTIDIURETIC HORMONE
ANTIDIURETIC HORMONE AND WATER EXCRETION • AFFECTS PERMEABILITY OF COLLECTING TUBULES TO WATER • OSMORECEPTORS IN HYPOTHALAMUS • CIRCULATORY PRESSURE RECPTORS LEFT ATRIUM OF HEART
FACTORS THAT INFLUENCE WATER EXCETION • OSMOTIC PRESSURE OF EXTRACELLULAR FLUID • RARELY SEPARATE FROM FACTORS THAT INFLUENCE SODIUM EXCRETION
POTASSIUM REGULATION • EXTRACELLULAR LEVELS CLOSELY REGULATED • EXCRETION USUALLY EQUALS THE AMOUNT OF INGESTION • FREELY FILTERED INTO FILTRATE • CAN BE SECRETED OR REABSORBED BY TUBULES • USUALLY ALL IS REABSORBED • AMOUNT EXCRETED DEPENDS ON HOW MUCH IS SECRETED
ROLE OF TUBULAR CELLS IN POTASSIUM EXCRETION • HIGH CONCENTRATION IN CELLS -- MORE POTASSIUM SECRETED • LOWER CONCENTRATION IN CELLS -- LESS POTASSIUM SECRETED
ROLE OF ALDOSTERONE IN POTASSIUM EXCRETION • PROMOTES REABSORPTION OF SODIUM BY TUBULES • INCREASED POTASSIUM CONCENTRATION IN EXTRACELLULAR CELLS BATHING ADRENAL CELLS INCREASES ALDOSTERONE SECRETION
REGULATION OF CALCIUM • BONE (CONTAINS 99% OF CALCIUM) • KIDNEYS • GI TRACT
EFFECTS OF PARATHYROID HORMONE • INCREASES PLASMA CALCIUM LEVELS • DECREASES PLASMA PHOSPHATE CONCENTRATIONS • INCREASES MOVEMENT OF CALCIUM AND PHOSPHATE FROM BONE TO EXTRACELLULAR FLUID
OSTEOCLASTS • BREAK DOWN BONE
EFFECTS OF PARATHYROID HORMONE ON KIDNEY • DECREASES THE URINARY EXCRETION OF CALCIUM • INCREASES EXCRETION OF PHOSPHATE • ENHANCES TRANSFORMATION OF VITAMIN D3 TO 1,25 DIHYDROXYCHOLECALCIFEROL
1,25 DIHYDROXYCHOLECALCIFEROL • STIMULATES CALCIUM ABSORPTION BY INTESTINES
CONTOL OF PARATHYROID HORMONE SECRETION • CALCIUM LEVELS THAT BATH CELLS OF PARATHYROID
CALCITONIN AND CALCIUM LEVELS • FROM THYROID GLAND • LOWERS PLASMA LEVELS OF CALCIUM • INHIBITS REMOVAL OF CALCIUM FROM BONE INHIBITS OSTEOCLASTS • LESS IMPORTANT THAN PARATHYROID
CONTROL OF CALCITONIN SECRETION • CALCIUM LEVELS THAT BATH CELLS OF THYROID
RARE DISORDER CAUSES MALNUTRITION ALCOHOLISM REDUCED ABSORPTION RENAL TUBULE PROBLEMS SOME TYPES OF DIURETICS INCREASED NEUROMUSCULAR ACTIVITY IRRITIBILITY INCREASED REFLEXES MUSCLE WEAKNESS TETANY CONVULSIONS HYPOMAGNESMIA
RARE DISORDER CAUSES RENAL FAILURE ANTACIDS CONTAINING MAGNESIUM DEPRESSED SKELETAL MUSCLE CONTRACTIONS DEPRESSED OF NERVE FUNCTION NAUSEA VOMITING MUSCLE WEAKNESS HYPOTENSION BRADYCARDIA REDUCTION IN RESPIRATION HYPERMAGNESMIA
CAUSES RENAL FAILURE SIDE EFFECTS OF CHEMOTHERAPY HYPERPARATHYOIDISM REDUCED PLASMA CALCIUM CONCENTRATION DUE TO CALCIUM PHOSPHATE DEPOSITED IN TISSUES LUNGS KIDNEYS JOINTS HYPERPHOSPHATEMIA
CAUSES REDUCED ABSORPTION OF MAGNESIUM HYPERPARATHYROIDISM INCREASED RENAL EXCRETION OF PHOSPHATE SYMPTOMS REDUCED METABOLIC RATE REDUCED OXYGEN TRANSPORT WHITE BLOOD CELL FUNCTION REDUCED REDUCED BLOOD CLOTTING HYPOPHOSPHATEMIA
ACID BASE REGULATION • ACIDS • BASES • p H OF BLOOD • p H OF INTERSTITIAL FLUIDS • BUFFER SYSTEMS • ROLE OF RESPIRATORY SYSTEM • ROLE OF KIDNEYS
ACIDS • INCREASE HYDROGEN ION CONCENTRATION • PROTON DONORS
BASES • HYROGEN ACCEPTOR • PROTON ACCEPTOR