'Fluid, Electrolyte, and Acid-Base Balance: Introduction to Body Fluids Essay\r'

' Fluid Compartments\r\n pissing occupies 2 main bland compartments\r\nintracellular fluent (ICF) †somewhat 2 thirds by hoi polloi, contained in cells Extracellular pl blistering (extracellular changeable) †consists of two major subdivisions germ plasm †the fluid role of the squanderer\r\ninterstitial fluid (IF) †fluid in quadricepss among cells\r\nOther extracellular fluid †lymph, cerebrospinal fluid, eyeb completely humors, synovial fluid, serous fluid, and bungletro enteral secernments Extracellular and Intracellular Fluids\r\n piddle is the universal solvent\r\nSolutes atomic number 18 gener totallyy classified into:\r\nElectrolytes †inorganic salts, all red-hots and pocketbooks, and some proteins Electrolytes squ be the chemical and physical reactions of fluids\r\nElectrolytes bugger off greater osmotic power than nonelectrolytes wet campaigns according to osmotic slopes\r\nNonelectrolytes †examples admit glucose, lipids, creatinine, and urea Each fluid compartment of the bole has a distinctive pattern of electrolytes Extracellular fluids ar akin(predicate) ( debar for proud protein content of plasma) atomic number 11 is the chief cation\r\nChloride is the major anion\r\nIntracellular fluids have low sodium and chloride\r\n thousand is the chief cation\r\nPhosphate is the chief anion\r\nProteins, phospholipids, cholesterol, and neutral fats reputation for: 90% of the mass of solutes in plasma\r\n60% of the mass of solutes in interstitial fluid\r\n97% of the mass of solutes in the intracellular compartment\r\nFluid causal agency Among Compartments\r\nCompart mental exchange is regulated by osmotic and hydrostatic closets Net leakage of fluid from the occupation is picked up by lymphatic vessels and returned to the jobstream Exchanges between interstitial and intracellular fluids atomic number 18 complex ascribable(p) to the selective permeability of the cellular membranes Two-way water flow is substantial\r\nIon fluxes atomic number 18 restricted and move selectively by active transport Nutrients, respiratory gases, and wastes move unidirectionally Plasma is the more thanover fluid that circulates passim the be and links external and internal environments Osmolali yokes of all consistence fluids are equal; changes in solute concentrations are quickly followed by osmotic changes\r\n water supply symmetry and ECF Osmolality\r\nTo remain properly hydrated, water uptake essential equal water kayoedput Water intake sources\r\nIngested fluid (60%) and solid food (30%)\r\nmetabolous water or water of oxidation (10%)\r\nWater output\r\nUrine (60%) and feces (4%)\r\nInsensible losings (28%), sweat (8%)\r\nIncreases in plasma osmolality trigger appetency and expose of antidiuretic hormone ( antidiuretic hormone) decree of Water †Homeostaisis\r\nIntake †Hypothalmic Thirst Center\r\nThirst is fill as soon as we begin to boozing water\r\nFeedba ck signals that inhibit the thirst centers include:\r\ndampening of the mucosa of the mouth and throat\r\nActivation of patronage and intestinal stretch receptors\r\n incline and Regulation of antidiuretic hormone\r\nWater resorption in collecting ducts is proportionate to ADH release Low ADH levels elicit dilute pee and reduced volume of body fluids High ADH levels produce concentrated pissing\r\nHypothalamic osmoreceptors trigger or inhibit ADH release\r\nFactors that specifically trigger ADH release include prolonged fever; unreasonable sweating, vomiting, or diarrhea; utter(a) rootage loss; and traumatic burns Disorders of Water correspondence:\r\nDehydration\r\nWater loss exceeds water intake and the body is in negative fluid commensurateness events include: hemorrhage, severe burns, prolonged vomiting or diarrhea, profuse sweating, water deprivation, and diuretic abuse Signs and symptoms: cottonmouth, thirst, dry flushed skin, and oliguria lengthen dehydration ma y lead to weight loss, fever, mental confusion Other consequences include hypovolemic jar and loss of electrolytes Hypotonic Hydration\r\nrenal insufficiency or an extraordinary amount of water ingested quickly throw out lead to cellular overhydration, or water alcohol playiction ECF is diluted †sodium content is pattern hardly prodigality water is present The resulting hyponatremia promotes cyberspace osmosis into tissue cells, causing intumescency These events moldiness be quickly reversed to baffle severe metabolous disturbances, particularly in neurons Edema.\r\nAtypical collecting of fluid in the interstitial space, leading to tissue swelling Caused by anything that adds flow of fluids out of the bloodstream or hinders their return.\r\nFactors that accelerate fluid loss include: increase blood pressure, capillary vessel permeability\r\nIncompetent venous valves, localized blood vessel blockage\r\ncongestive heart hardship, hypertension, gamy blood volume\r\n Hindered fluid return usually reflects an imbalance in colloid osmotic pressures Hypoproteinemia †low levels of plasma proteins\r\nForces fluids out of capillary beds at the arterial ends\r\nFluids fail to return at the venous ends\r\n consequents from protein malnutrition, liver disease, or glomerulonephritis Blocked (or surgically removed) lymph vessels:\r\nCause leaked proteins to accumulate in interstitial fluid\r\n maintain increasing colloid osmotic pressure, which draws fluid from the blood Interstitial fluid accumulation results in low blood pressure and severely impaired circulation sodium in Fluid and Electrolyte Balance\r\n atomic number 11 holds a aboriginal position in fluid and electrolyte balance Sodium salts:\r\nAccount for 90-95% of all solutes in the ECF\r\n wreak 280 mOsm of the total 300 mOsm ECF solute concentration Sodium is the single almost abundant cation in the ECF\r\nSodium is the save cation exerting signifi disregardt osmotic pressure The role of sodium in controlling ECF volume and water distribution in the body is a result of: Sodium being the all cation to exert signifi skunkfult osmotic pressure Sodium ions leaking into cells and being pumped out against their electrochemical gradient Sodium concentration in the ECF ordinarily remains stable\r\nChanges in plasma sodium levels affect:\r\nPlasma volume, blood pressure\r\nICF and interstitial fluid volumes\r\nRenal acid-base control mechanisms are mate to sodium ion transport Regulation of Sodium Balance:\r\nAldosterone\r\nThe renin- angiotonin mechanism triggers the release of aldosterone This is mediated by juxtaglomerular apparatus, which releases renin in result to: Sympathetic nervous musical arrangement stimulant drug\r\nDecreased filtrate osmolality\r\nDecreased stretch due to decreased blood pressure\r\nRenin catalyzes the production of angiotensin II, which prompts aldosterone release Adrenal cortical cells are this instant stimulated to release aldostero ne by elevated K+ levels in the ECF Aldosterone brings about its effects (diminished urine output and increased blood volume) slowly\r\ncardiovascular System Baroreceptors\r\nBaroreceptors alert the oral sex of increases in blood volume (hence increased blood pressure) Sympathetic nervous system impulses to the kidneys decline\r\nAfferent arterioles dilate\r\nglomerular filtration rate rises\r\nSodium and water output increase\r\nThis phenomenon, called pressure diuresis, decreases blood pressure Drops in general blood pressure lead to oppositeness actions and systemic blood pressure increases Since sodium ion concentration determines fluid volume, baroreceptors can be viewed as â€Å"sodium receptors” atrial Natriuretic Peptide (ANP)\r\nReduces blood pressure and blood volume by inhibiting:\r\nEvents that promote vasoconstriction\r\nNa+ and water keeping\r\nIs released in the heart atria as a response to stretch (elevated blood pressure) Has potent diuretic and natriuret ic effects\r\nPromotes evacuation of sodium and water\r\nInhibits angiotensin II production\r\nInfluence of Other Hormones on Sodium Balance\r\nEstrogens:\r\nEnhance NaCl reabsorption by renal tubules\r\nMay get to water computer memory during menstrual cycles\r\nAre responsible for edema during gestation\r\nProgesterone:\r\nDecreases sodium reabsorption\r\nActs as a diuretic, promoting sodium and water loss\r\nGlucocorticoids †enhance reabsorption of sodium and promote edema Regulation\r\nof jet Balance\r\nRelative ICF-ECF kB ion concentration affects a cell’s resting membrane potential exuberant ECF potassium decreases membrane potential\r\n as well as little K+ causes hyperpolarization and nonresponsiveness Hyperkalemia and hypokalemia can:\r\nDisrupt electric conduction in the heart\r\nLead to jerky death\r\nHydrogen ions shift in and out of cells\r\nLeads to corresponding shifts in potassium in the opposite direction Interferes with activity of excitable cel ls\r\nInfluence of Aldosterone\r\nAldosterone stimulates potassium ion discrimination by principal cells In cortical collecting ducts, for each Na+ reabsorbed, a K+ is secreted Increased K+ in the ECF virtually the adrenal cortex causes:\r\nRelease of aldosterone â€>Potassium secretion\r\nPotassium controls its own ECF concentration via feedback regulation of aldosterone release Regulation of Calcium\r\nIonic atomic number 20 in ECF is important for:\r\nBlood coagulate\r\nCell membrane permeability\r\nSecretory demeanour\r\nHypocalcemia: Increases excitability, causes musclebuilder tetany\r\nHypercalcemia: inhibits neurons and muscle cells; cause heart arrhythmias Calcium balance is controlled by parathyroid hormone and calcitonin PTH promotes increase in calcium levels by targeting:\r\nBones †PTH activates osteoclasts to break rectify bone matrix\r\nSmall intestine †PTH enhances intestinal absorption of calcium Kidneys †PTH enhances calcium reabsorption and decreases orthophosphate reabsorption Calcium reabsorption and phosphate excretion go hand in hand Influence of Calcitonin\r\nReleased in response to rising blood calcium levels\r\nCalcitonin is a PTH antagonist, but its contribution to calcium and phosphate homeostasis is minor to negligible sharp Base Balance\r\nIntroduction to Acids and Bases\r\nStrong acids †all their H+ is breakd completely in water wonky acids †dissociate partially in water and are efficient at preventing pH changes Strong bases †dissociate easily in water and quickly tie up H+ Weak bases †accept H+ more slowly (e.g., HCO3¯ and NH3)\r\nNormal pH of body fluids\r\nArterial blood is 7.4\r\nVenous blood and interstitial fluid is 7.35\r\nIntracellular fluid is 7.0\r\nAlkalosis or alkalemia †arterial blood pH rises above 7.45\r\nAcidosis or acidemia †arterial pH drops downstairs 7.35 (physiologic acidosis) Sources of Hydrogen Ions †Most heat content ions originate fr om cellular metabolism Breakdown of phosphorus-containing proteins releases phosphorous acid into the ECF Anaerobic respiration of glucose produces lactic acid\r\nFat metabolism yields organic acids and ketone bodies\r\nTransporting blow dioxide as bi atomic number 6ate releases hydrogen ions Hydrogen Ion Regulation\r\nConcentration of hydrogen ions is regulated sequentially by: Chemical buffer systems †act within seconds\r\nphysiologic buffer systems\r\nThe respiratory center in the brain stem †acts within 1-3 minutes Renal mechanisms †lease hours to days to effect pH changes Chemical archetype Systems\r\nBicarbonate buffer System\r\nA commixture of carbonaceous acid (H2CO3) and its salt, sodium bicarbonate (NaHCO3) (potassium or magnesium bicarbonates dissemble as well) If strong acid is added:\r\nHydrogen ions released combine with the bicarbonate ions and form carboniferous acid (a feeble acid) The pH of the solution decreases only slightly\r\nIf stron g base is added:\r\nIt reacts with the carbonic acid to form sodium bicarbonate (a faint-hearted base) The pH of the solution rises only slightly\r\nThis system is the only important ECF buffer\r\nPhosphate Buffer System\r\nNearly identical to the bicarbonate system\r\nIts components are:\r\nSodium salts of dihydrogen phosphate (H2PO4¯), a weak acid\r\nMonohydrogen phosphate (HPO42¯), a weak base\r\nThis system is an effective buffer in urine and intracellular fluid Protein Buffer System\r\nPlasma and intracellular proteins are the body’s most plentiful and powerful buffers Some amino acids of proteins have:\r\nFree organic acid groups (weak acids)\r\nGroups that act as weak bases (e.g., amino groups)\r\nAmphoteric molecules are protein molecules that can function as both a weak acid and a weak base physiological Buffer Systems\r\nrespiratory Buffer System\r\nThe respiratory system regulation of acid-base balance is a physiological buffering system There is a reversib le counterbalance between:\r\nDissolved carbon dioxide and water\r\n carbonaceous acid and the hydrogen and bicarbonate ions\r\n carbon dioxide + urine â€> H2CO3 â€> H+ + HCO3¯\r\nDuring carbon dioxide unloading, hydrogen ions are structured into water When hypercapnia or rising plasma H+ occurs:\r\nDeeper and more rapid public discussion expels more carbon dioxide\r\nHydrogen ion concentration is reduced\r\nAlkalosis causes slower, more shallow breathing, causing H+ to increase respiratory system impairment causes acid-base imbalance (respiratory acidosis or respiratory alkalosis) Renal Mechanisms of Acid-Base Balance\r\nIntroduction\r\nChemical buffers can tie up excess acids or bases, but they cannot eliminate them from the body The lungs can eliminate carbonic acid by eliminating carbon dioxide Only the kidneys can rid the body of metabolic acids (phosphoric, uric, and lactic acids and ketones) and prevent metabolic\r\nacidosis The ultimate acid-base regulator y organs are the kidneys\r\nThe most important renal mechanisms for regulating acid-base balance are: Conserving (reabsorbing) or generating new bicarbonate ions\r\n elimination bicarbonate ions\r\nLosing a bicarbonate ion is the resembling as gaining a hydrogen ion; reabsorbing a bicarbonate ion is the same as losing a hydrogen ion Hydrogen ion secretion occurs in the PCT\r\nHydrogen ions come from the disassociation of carbonic acid\r\nReabsorption of Bicarbonate\r\n carbon dioxide combines with water in tubule cells, forming H2CO3\r\nH2CO3 splits into H+ and HCO3-\r\nFor each H+ secreted, a Na+ and a HCO3- are reabsorbed by the PCT cells Secreted H+ form H2CO3; thus, HCO3- disappears from filtrate at the same rate that it enters the peritubular capillary blood H2CO3 organize in filtrate dissociates to release CO2 + H2\r\nCO2 then diffuses into tubule cells, where it acts to trigger further H+ secretion Hydrogen Ion Excretion\r\nDietary H+ must be counteracted by generating new HCO3-\r\nThe excreted H+ must bind to buffers in the urine (phosphate buffer system) Intercalated cells actively secrete H+ into urine, which is buffered and excreted HCO3- generated is:\r\nMoved into the interstitial space via a cotransport system\r\nPassively moved into the peritubular capillary blood\r\nIn response to acidosis:\r\nKidneys generate HCO3-and add them to the blood\r\nAn equal amount of H+ are added to the urine\r\nAmmonium Ion (NH4+) Excretion\r\nThis method uses NH4+ produced by the metabolism of glutamine in PCT cells Each glutamine metabolized produces two ammonium ions and two bicarbonate ions HCO3- moves to the blood and ammonium ions are excreted in urine respiratory Acidosis and Alkalosis\r\nResult from failure of the respiratory system to balance pH\r\nPCO2 is the single most important indicator of respiratory inadequacy PCO2 levels †convention PCO2 fluctuates between 35 and 45 mm Hg determine above 45 mm Hg signal respiratory acidosis\r\nValues on a lower floor 35 mm Hg intend respiratory alkalosis\r\nRespiratory acidosis is the most usual cause of acid-base imbalance Occurs when a person breathes shallowly, or gas exchange is hampered by diseases such as pneumonia, cystic fibrosis, or emphysema Respiratory alkalosis is a common result of hyperventilation metabolous Acidosis\r\nAll pH imbalances except those caused by abnormal blood carbon dioxide levels Metabolic acid-base imbalance †bicarbonate ion levels above or below normal (22-26 mEq/L) Metabolic acidosis is second most common cause of acid-base imbalance Typical causes are ingestion of too much alcohol and excessive loss of bicarbonate ions Other causes include accumulation of lactic acid, shock, ketosis in diabetic crisis, starvation, and kidney failure Metabolic Alkalosis\r\nRising blood pH and bicarbonate levels intend metabolic alkalosis Typical causes are:\r\n pass of the acid contents of the stomach\r\nIntake of excess base (e.g., from antacids)\r\nConstipa tion, in which excessive bicarbonate is reabsorbed\r\nRespiratory and Renal Compensations\r\nAcid-base imbalance due to inadequacy of a physiological buffer system is compensated for by the other system The respiratory system go out attempt to correct metabolic acid-base imbalances The kidneys will work to correct imbalances caused by respiratory disease Respiratory Compenstaion\r\nIn metabolic acidosis:\r\nThe rate and depth of breathing are elevated\r\nBlood pH is below 7.35 and bicarbonate level is low\r\nAs carbon dioxide is eliminated by the respiratory system, PCO2 falls below normal In metabolic alkalosis:\r\nCompensation exhibits slow, shallow breathing, allowing carbon dioxide to\r\naccumulate in the blood Correction is revealed by:\r\nHigh pH (over 7.45) and elevated bicarbonate ion levels\r\nRisingPCO2\r\nRenal Compensation\r\nTo correct respiratory acid-base imbalance, renal mechanisms are stepped up Acidosis has high PCO2 and high bicarbonate levels\r\nThe high PCO2 s the cause of acidosis\r\nThe high bicarbonate levels indicate the kidneys are retaining bicarbonate to offset the acidosis Alkalosis has Low PCO2 and high pH\r\nThe kidneys eliminate bicarbonate from the body by failing to reclaim it or by actively secreting it\r\n'