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

Fluid Compartments irrigate occupies two main still compartmentsintracellular liquified (ICF) ab forbidden two thirds by volume, contained in cells Extracellular silver (ECF) consists of two major subdivisions Plasma the tranquil portion of the origininterstitial silver (IF) gas in spaces between cellsOther ECF lymph, cerebrospinal limpid, eye humors, synovial fluid, serous fluid, and gastrointestinal secretions Extracellular and intracellular Fluids piss is the universal solventSolutes be broadly classified intoElectrolytes inorganic salts, tot whollyy blisterings and bases, and some proteins Electrolytes determine the chemical and physical reactions of fluidsElectrolytes have greater osmotic power than nonelectrolytes Water moves according to osmotic gradientsNonelectrolytes examples include glucose, lipids, creatinine, and urea apiece fluid compartment of the dust has a distinctive pattern of electrolytes Extracellular fluids argon similar (except for lavishl y protein content of plasma) atomic number 11 is the head word cationChloride is the major anionIntracellular fluids have low atomic number 11 and chloridePotassium is the chief cationPhosphate is the chief anionProteins, phospholipids, cholesterol, and neutral fats account for 90% of the mass of solutes in plasma60% of the mass of solutes in interstitial fluid97% of the mass of solutes in the intracellular compartmentFluid Movement Among CompartmentsCompartmental exchange is regulate by osmotic and hydrostatic squashs Net leakage of fluid from the product line is picked up by lymphatic vessels and returned to the derivationstream Exchanges between interstitial and intracellular fluids ar complex due to the selective permeability of the cellular membranes Two-way irrigate flow is substantialIon fluxes are restricted and move selectively by active transport Nutrients, respiratory gases, and wastes move unidirectionally Plasma is the only fluid that circulates throughout the carcass and links external and internal environments Osmolalities of all form fluids are equal changes in solute stringencys are readily followed by osmotic changesWater vestibular sense and ECF OsmolalityTo remain properly hyd aimd, weewee use of goods and services must equal water output Water intake sourcesIngested fluid (60%) and solid food (30%)Metabolic water or water of oxidization (10%)Water outputUrine (60%) and feces (4%)Insensible losses (28%), endeavor (8%)Increases in plasma osmolality trip out thirst and exhaust of antidiuretic internal secretion ( antidiuretic hormone) Regulation of Water HomeostaisisIntake Hypothalmic Thirst CenterThirst is fulfill as soon as we begin to drink waterFeedback tokens that hinder the thirst centers includeMoistening of the mucosa of the mouth and throat activating of stomach and intestinal stretch receptorsInfluence and Regulation of ADHWater resorption in collecting ducts is proportional to ADH part with misfortunate ADH levels produce dilute weewee and reduced volume of carcass fluids High ADH levels produce concentrated urineHypothalamic osmoreceptors trigger or inhibit ADH releaseFactors that specifically trigger ADH release include prolonged fever excessive sweating, purge, or dissolution severe squanderer loss and traumatic burns Disorders of Water BalanceDehydrationWater loss exceeds water intake and the body is in negative fluid balance Causes include hemorrhage, severe burns, prolonged vomiting or diarrhea, profuse sweating, water deprivation, and diuretic abuse Signs and symptoms cottonmouth, thirst, dry crimson skin, and oliguria Prolonged dehydration may lead to weight loss, fever, mental disarray Other consequences include hypovolemic shock and loss of electrolytes Hypotonic Hydration nephritic insufficiency or an extraordinary amount of water ingested quickly terminate lead to cellular overhydration, or water intoxication ECF is thin sodium content is normal moreover exce ss water is leave The exiting hyponatremia promotes net osmosis into tissue cells, causing stumblebum These events must be quickly reversed to prevent severe metabolous disturbances, particularly in neurons Edema. unorthodox accumulation of fluid in the interstitial space, leading to tissue swelling Caused by anything that cast ups flow of fluids out of the bloodstream or hinders their return.Factors that accelerate fluid lossinclude increase blood pressure, capillary permeability unqualified venous valves, localized blood vessel blockageCongestive lovingness failure, hypertension, high blood volumeHindered fluid return usually reflects an mental unsoundness in colloid osmotic pressures Hypoproteinemia low levels of plasma proteinsForces fluids out of capillary beds at the arterial endsFluids fail to return at the venous endsResults from protein malnutrition, liver disease, or glomerulonephritis Blocked (or surgically removed) lymph vesselsCause leaked proteins to accumulate in interstitial fluidExert increasing colloid osmotic pressure, which draws fluid from the blood Interstitial fluid accumulation results in low blood pressure and severely stricken circulation Sodium in Fluid and Electrolyte BalanceSodium holds a fundamental position in fluid and electrolyte balance Sodium saltsAccount for 90-95% of all solutes in the ECFContribute 280 mOsm of the total 300 mOsm ECF solute concentration Sodium is the single most abundant cation in the ECFSodium is the only cation exerting satisfying osmotic pressure The role of sodium in controlling ECF volume and water distribution in the body is a result of Sodium being the only cation to exert signifi nett osmotic pressure Sodium ions leaking into cells and being pumped out against their electrochemical gradient Sodium concentration in the ECF normally body stableChanges in plasma sodium levels affectPlasma volume, blood pressureICF and interstitial fluid volumes nephritic acid-base control mechanisms are cou pled to sodium ion transport Regulation of Sodium BalanceAldosteroneThe renin-angiotensin mechanism triggers the release of aldosterone This is mediated by juxtaglomerular apparatus, which releases renin in response to Sympathetic nervous administration stimulationDecreased filtrate osmolalityDecreased stretch due to fall blood pressureRenin catalyzes the mathematical product of angiotensin II, which prompts aldosterone release Adrenal cortical cells are directly stimulated to release aldosterone by grand K+ levels in the ECF Aldosterone brings about its effects (diminished urine output and increase blood volume) slowlyCardiovascular organization of rules BaroreceptorsBaroreceptors alert the brain of increases in blood volume (hence increased blood pressure) Sympathetic nervous clay impulses to the kidneys declineAfferent arterioles dilateGlomerular filtration rate risesSodium and water output increaseThis phenomenon, called pressure diuresis, decreases blood pressure Drops in arrangingic blood pressure lead to opposite actions and systemic blood pressure increases Since sodium ion concentration determines fluid volume, baroreceptors heap be viewed as sodium receptors Atrial Natriuretic Peptide (ANP)Reduces blood pressure and blood volume by inhibitingEvents that promote vasoconstrictionNa+ and water retentionIs released in the sum of money atria as a response to stretch (elevated blood pressure) Has potent diuretic and natriuretic effectsPromotes excretion of sodium and waterInhibits angiotensin II productionInfluence of Other Hormones on Sodium BalanceEstrogensEnhance NaCl reabsorption by renal tubulesMay let water retention during menstrual cyclesAre responsible for edema during pregnancyProgesteroneDecreases sodium reabsorptionActs as a diuretic, promoting sodium and water lossGlucocorticoids enhance reabsorption of sodium and promote edema Regulationof Potassium Balance intercourse ICF-ECF potassium ion concentration affects a cells resting membrane potential Excessive ECF potassium decreases membrane potentialToo petty K+ causes hyperpolarization and nonresponsiveness Hyperkalemia and hypokalemia canDisrupt electrical conduction in the warmnessLead to sudden death henry ions shift in and out of cellsLeads to corresponding shifts in potassium in the opposite direction Interferes with drill of excitable cellsInfluence of AldosteroneAldosterone stimulates potassium ion secretion by principal cells In cortical collecting ducts, for each Na+ reabsorbed, a K+ is secreted Increased K+ in the ECF around the adrenal cortex causes spark of aldosterone Potassium secretionPotassium controls its own ECF concentration via feedback regulation of aldosterone release Regulation of CalciumIonic atomic number 20 in ECF is meaning(a) forBlood clottingCell membrane permeabilitySecretory deportmentHypocalcemia Increases excitability, causes muscle tetanyHypercalcemia inhibits neurons and muscle cells cause heart arrhythmias Calcium balance is controlled by parathyroid hormone and calcitonin PTH promotes increase in calcium levels by targetingBones PTH activates osteoclasts to break down hit the books matrixSmall intestine PTH enhances intestinal absorption of calcium Kidneys PTH enhances calcium reabsorption and decreases phosphate reabsorption Calcium reabsorption and phosphate excretion go hand in hand Influence of CalcitoninReleased in response to rising blood calcium levelsCalcitonin is a PTH antagonist, but its contribution to calcium and phosphate homeostasis is minor to negligible Acid demonstrate BalanceIntroduction to Acids and BasesStrong acids all their H+ is dissociated completely in water Weak 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 gestate H+ more slowly (e.g., HCO3 and NH3)Normal pH of body fluidsarterial blood is 7.4Venous blood and interstitial fluid is 7.35Intracellular fl uid is 7.0Alkalosis or alkalemia arterial blood pH rises above 7.45Acidosis or acidemia arterial pH drops downstairs 7.35 (physiological acidosis) Sources of heat content Ions Most atomic number 1 ions originate from cellular metabolism Breakdown of phosphorus-containing proteins releases phosphoric acid into the ECF Anaerobic ventilation of glucose produces lactic acidFat metabolism yields organic acids and ketone bodiesTransporting coke dioxide as bicarbonate releases hydrogen ions Hydrogen Ion RegulationConcentration of hydrogen ions is regulated sequentially by chemic buffer systems act in spite of appearance seconds physiological buffer systemsThe respiratory center in the brain stem acts within 1-3 minutes Renal mechanisms require hours to days to effect pH changes Chemical Buffer trunksBicarbonate Buffer SystemA mixture of carbonaceous acid (H2CO3) and its salt, sodium bicarbonate (NaHCO3) (potassium or magnesium bicarbonates work as well) If pissed acid is a ddedHydrogen ions released combine with the bicarbonate ions and form carbonic acid (a worn out acid) The pH of the solution decreases only slightlyIf strong base is addedIt reacts with the carbonic acid to form sodium bicarbonate (a scant(p) base) The pH of the solution rises only slightlyThis system is the only of the essence(predicate) ECF bufferPhosphate Buffer SystemNearly equivalent to the bicarbonate systemIts components areSodium salts of dihydrogen phosphate (H2PO4), a weak acidMonohydrogen phosphate (HPO42), a weak baseThis system is an potent buffer in urine and intracellular fluid Protein Buffer SystemPlasma and intracellular proteins are the bodys most bighearted and powerful buffers Some amino acids of proteins haveFree organic acid groups (weak acids)Groups that act as weak bases (e.g., amino groups)Amphoteric molecules are protein molecules that can function as both a weak acid and a weak base Physiological Buffer Systemsrespiratory Buffer SystemThe respiratory system regulation of acid-base balance is a physiological buffering system There is a reversible equilibrium betweenDissolved carbon dioxide and waterCarbonic acid and the hydrogen and bicarbonate ions carbon dioxide + pee H2CO3 H+ + HCO3During carbon dioxide unloading, hydrogen ions are incorporated into water When hypercapnia or rising plasma H+ occursDeeper and more rapid living expels more carbon dioxideHydrogen ion concentration is reducedAlkalosis causes slower, more change breathing, causing H+ to increase Respiratory system impairment causes acid-base derangement (respiratory acidosis or respiratory alkalosis) Renal Mechanisms of Acid-Base BalanceIntroductionChemical 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 except the kidneys can rid the body of metabolic acids (phosphoric, uric, and lactic acids and ketones) and prevent metabolicacidosis The ultimate ac id-base regulatory organs are the kidneysThe most important renal mechanisms for regulating acid-base balance are Conserving (reabsorbing) or generating current bicarbonate ions excretory product bicarbonate ionsLosing a bicarbonate ion is the same as gaining a hydrogen ion reabsorbing a bicarbonate ion is the same as losing a hydrogen ion Hydrogen ion secretion occurs in the portionHydrogen ions come from the dissociation of carbonic acidReabsorption of BicarbonateCO2 combines with water in tubule cells, forming H2CO3H2CO3 splits into H+ and HCO3-For 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 formed in filtrate dissociates to release CO2 + H2CO2 then diffuses into tubule cells, where it acts to trigger further H+ secretion Hydrogen Ion ExcretionDietary H+ must be counteracted by generating new HCO3-The 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- fall ind isMoved into the interstitial space via a cotransport systemPassively moved into the peritubular capillary bloodIn response to acidosisKidneys generate HCO3-and add them to the bloodAn equal amount of H+ are added to the urineAmmonium Ion (NH4+) ExcretionThis method uses NH4+ produced by the metabolism of glutamine in PCT cells Each glutamine metabolized produces two ammonium ion ions and two bicarbonate ions HCO3- moves to the blood and ammonium ions are excreted in urine Respiratory Acidosis and AlkalosisResult from failure of the respiratory system to balance pHPCO2 is the single most important exponent of respiratory insufficiency PCO2 levels normal PCO2 fluctuates between 35 and 45 mm Hg Values above 45 mm Hg signal respiratory acidosisValues below 35 mm Hg manoeuvre respiratory alkalosisRespiratory acidosis is the most common cau se 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 Metabolic AcidosisAll 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 alcoholic drink and excessive loss of bicarbonate ions Other causes include accumulation of lactic acid, shock, ketosis in diabetic crisis, starvation, and kidney failure Metabolic AlkalosisRising blood pH and bicarbonate levels indicate metabolic alkalosis Typical causes are chuck of the acid contents of the stomachIntake of excess base (e.g., from antacids)Constipation, in which excessive bicarbonate is reabsorbedRespiratory and Renal CompensationsAcid-base imbalance due to i nadequacy of a physiological buffer system is compensated for by the otherwise system The respiratory system will attempt to correct metabolic acid-base imbalances The kidneys will work to correct imbalances caused by respiratory disease Respiratory CompenstaionIn metabolic acidosisThe rate and depth of breathing are elevatedBlood pH is below 7.35 and bicarbonate level is lowAs carbon dioxide is eliminated by the respiratory system, PCO2 falls below normal In metabolic alkalosisCompensation exhibits slow, shallow breathing, allowing carbon dioxide toaccumulate in the blood Correction is revealed byHigh pH (over 7.45) and elevated bicarbonate ion levelsRisingPCO2Renal CompensationTo correct respiratory acid-base imbalance, renal mechanisms are stepped up Acidosis has high PCO2 and high bicarbonate levelsThe high PCO2 s the cause of acidosisThe high bicarbonate levels indicate the kidneys are retaining bicarbonate to offset the acidosis Alkalosis has Low PCO2 and high pHThe kidneys e liminate bicarbonate from the body by failing to reclaim it or by actively secreting it