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Biology 233 Human Anatomy and Physiology Chapter 27 Lecture Outline FLUID, ELECTROLYTE, & ACID-BASE HOMEOSTASIS FLUID HOMEOSTASIS water is 50-6-% of body mass (varies depending on body fat) dissolves all molecules so reactions can take place FLUID COMPARTMENTS intracellular fluid (ICF) – cytosol extracellular fluid (ECF) – fluid outside cells interstitial fluid – 80% of ECF plasma Fluid Shifts Between Compartments plasma(ECF)/interstitial fluid(ECF) exchange filtration – shift from plasma to interstitial fluid reabsorption – shift from interstitial fluid to plasma net shift depends on: blood hydrostatic pressure (BP) blood colloid osmotic pressure (plasma osmolarity) interstitial fluid(ECF)/intracellular fluid (ICF) exchange shift is due to osmosis normally osmolarity is the same in both compartments = no net shift altering osmolarity of interstitial fluid causes fluid shifts direction depends on concentration gradient produced Note: Water is not actively transported between compartments. Shifts are normally caused by altering osmolarity (solute concentration) in ECF. FLUID BALANCE Water Loss (2500ml/day) urine – 1200 perspiration – 750ml exhaled water vapor – 400ml feces – 150ml Water Gain (2500ml/day) ingestion (drinking and eating) – 2200ml metabolic water – 300ml 1 Dehydration – water loss exceeds water gain (excess perspiration, inadequate drinking, vomiting, diarrhea) causes low blood volume and pressure, and hyperosmolarity of plasma < filtration, > reabsorption = increases interstitial osmolarity osmosis from ICF to interstitial fluid (cells shrink) Body’s Response to Dehydration >ADH secretion – more water reabsorption from urine thirst center stimulated – more drinking RAA pathway activated – thirst, > ADH secretion, Na+ & water reabsorption treatment – give hypotonic fluids Overhydration – water gain exceeds water loss (excessive drinking, inability to eliminate water in urine, excess ADH) causes high blood volume and pressure, and hypoosmolarity of plasma >filtration, < reabsorption = decreases interstitial osmolarity osmosis from interstitial fluid to ICF (cells swell) Body’s Response to Overhydration < ADH secretion – more water excreted in urine natriuretic peptides – reduce thirst, block ADH and aldosterone treatment – diuretics, IV hypertonic fluids IONS (ELECTROLYTES) IN BODY FLUIDS electrolyte – ions from inorganic compound dissolved in water (eg. Na+, Cl-, K+, Ca+2) Main Ions in ECF (plasma and interstitial fluid) Na+, Cl-, plasma protein anions, bicarbonate Main Ions in ICF (cytosol) K+, protein and organic phosphate anions Other Important Ions Ca+2, Mg+2, inorganic phosphate anions (stored in bones) FUNCTIONS OF IONS IN BODY FLUIDS control osmosis between fluid compartments ions are transported across membranes – water follows participate in cell functions action potentials in neurons muscle contraction regulate acid-base balance – eg. bicarbonate ions cofactors for enzymes – eg. Ca+2 in blood clotting 2 SODIUM most abundant cation in ECF (90%) 136-148 mEq/liter in plasma (10mEq in cells) Na/K pumps are responsible for high concentration in ECF accounts for nearly half of ECF osmolarity Sodium gain – diet (usually high) Sodium loss – urine, perspiration blood concentration is usually stable – balanced by osmosis (fluid level regulated mainly by ADH) Sodium Imbalances: hyponatremia – low blood Na+ (due to overhydration) > aldosterone – increases Na+ reabsorption in kidneys < ADH – increases urine production (dilute) causes depressed CNS function – mental impairment, coma death treatment – diuretics, hypertonic NaCl solution hypernatremia – high blood Na+ (due to dehydration) > ADH – decreases urine production, increases thirst causes thirst, tenting of skin, < BP leading to shock treatment – rehydrate with hypotonic fluids POTASSIUM most abundant cation in ICF 140 mEq/liter in cells (3-5 mEq/liter in plasma) Na/K pumps establish this gradient Potassiuim gain – diet Potassium loss – urine blood concentration regulated by kidney secretion Potassium Imbalances: hyperkalemia – high blood K+ (eg. renal failure, acidosis) causes cardiac arrhythmia treatment – hypotonic fluid hypokalemia – low blood K+ (eg. inadequate dietary intake, diuretics) > aldosterone – increases secretion by renal tubules causes weakness, paralysis treatment – administer K+ 3 CALCIUM most abundant mineral in body 99% stored in bones as mineral salts 4.5-5.5 mEq/liter in plasma Calcium gain – diet (depends on calcitriol) Calcium loss – urine, bile (small amounts) Regulation of Blood Calcium parathyroid hormone (PTH) – increases blood calcium increases bone resorption increases reabsorption of Ca+2 in kidneys increases production of calcitriol increases absorption of dietary Ca+2 in GI tract calcitonin (not significant) – decreases blood calcium decreases bone resorption Calcium Imbalances: hypercalcemia – high blood Ca+2 (hyperparathyroidism) causes mental impairment, cardiac arrythmia, kidney stones abnormal tissue calcification treatment – hypotonic fluids, calcitonin hypocalcemia – low blood Ca+2 (reduced intake, hypoparathyroidism) causes muscle spasms, weak heartbeats, osteoporosis treatment – administer Ca+2 and vitamin D CHLORIDE most abundant anion in ECF 100-108 mEq/liter in plasma (3mEq/L in cells) Cl- follows Na+ to balance electrical charges cells exchange Cl- for HCO3- in respiration (chloride shift) chloride pumps form hydrochloric acid in gastric juice ACID-BASE BALANCE acid – dissociates in solution to form H+ (proton) base – dissociates in solution to form OH- or another proton acceptor decreases acidity by binding H+ pH scale measures H+ concentration of a solution 7 = neutral (acid=base) <7 = acidic (more hydrogen ions) >7 = basic or alkaline (fewer hydrogen ions) strong acid – relatively complete dissociation = forms many H+ weak acid – incomplete dissociation = forms few H+ strong base – relatively complete binding of H+ = significantly reduces H+ weak base – incomplete binding of H+ = minor reduction in H+ 4 normal blood pH is 7.35-7.45 vital for normal metabolic functions proteins (structural, enzymes) denature at high or low pH pH changes disrupt cell membranes pH changes alter balance of reversible reactions acidosis – physiological state when pH < 7.35 CNS – disorientation, coma heart – decreases contractility, causes arrhythmias alkalosis – physiological state when pH > 7.45 CNS – convulsions, seizures muscles – spasms, tetanus Sources of Acids in Body metabolism CO2 production – carbonic acid catabolizing proteins – sulfuric acid, phosphoric acid hypoxia – lactic acid starvation – ketone bodies REGULATION OF BODY pH 3 Mechanisms: 1) BUFFER SYSTEMS – molecules that can temporarily bind excess H+ or donate H+ when they are low Protein Buffer System (eg. hemoglobin, plasma proteins, others) amino acids in ECF and ICF amino group (NH2) – weak base binds H+ when acidity increases carboxyl group (COOH) – weak acid donates H+ when acidity decreases Phosphate Buffer System (in ICF) dihydrogen phosphate (H2PO4-) – weak acid donates H+ when acidity is low monohydrogen phosphate (HPO4-2) – weak base binds excess H+ when acidity is high Carbonic Acid – Bicarbonate System (in ECF) carbonic acid (H2CO3) – weak acid donates H+ when acidity decreases bicarbonate (HCO3-) – weak base binds excess H+ when acidity increases 5 2) RESPIRATORY COMPENSATION – altering ventilation to adjust pH indirectly eliminates H+ by binding it in water H+ + HCO3- <----> H2CO3 <----> CO2 + H2O (CO2 diffuses out of blood in lungs and is exhaled) increasing respirations = more CO2 exhaled = blood is less acidic decreasing respirations = less CO2 exhaled = blood is more acidic 3) RENAL COMPENSATION – altering kidney activity to adjust pH proton pumps normally actively secrete excess H+ and reabsorb HCO3secreted H+ is buffered in tubules (prevents H+ gradient forming) ammonia (NH3) ---> ammonium ion (NH4+) monohydrogen phosphate (HPO4-2) ---> H2PO4- ACID – BASE DISTURBANCES Respiratory Acidosis – low pH due to inadequate respiration hypercapnia – high blood PCO2 (>45mmHg) due to respiratory disorders - emphysema, pulmonary edema, asthma, damage to respiratory center cardiac disorders – reduced pulmonary perfusion body’s response to respiratory acidosis buffer systems bind H+ = > pH respiratory compensation (if possible) increased ventilation = <PCO2 = > pH renal compensation – increased H+ secretion = > pH increased HCO3- reabsorption = buffers H+ = >pH Respiratory Alkalosis – high pH due to excessive respiration hypocapnia – low blood PCO2 (<35mmHg) due to hyperventilation – physical or emotional stress, high altitude body’s response to respiratory alkalosis buffers release H+ respiratory compensation (if possible) decreased ventilation = > PCO2 = < pH renal compensation – decreased H+ secretion = < pH increased HCO3- secretion = less buffering of H+ = < pH Metabolic Acidosis – low pH due to altered metabolic processes accumulation of metabolic acids – ketoacidosis, lactic acidosis failure to excrete H+ - renal disorders loss of HCO3- - severe diarrhea body’s response to metabolic acidosis – see respiratory acidosis respiratory compensation is very effective PCO2 is low when respiratory compensation is occurring renal compensation not possible if problem has renal origin 6 Metabolic Alkalosis – high pH due to altered metabolic processes loss of acid – severe vomiting (HCl lost) excess alkaline drugs – antacids body’s response to metabolic alkalosis – see respiratory alkalosis respiratory compensation is very effective PCO2 is high when respiratory compensation is occurring renal compensation not possible if problem has renal origin 7