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Canada (511,354)
KIN 191 (11)
Lecture

133 Electrolytes - Notes.docx

10 Pages
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Department
Kinesiology
Course Code
KIN 191
Professor
Bruce Matheson

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Water, Electrolytes, Acid-Base balance More adipose tissue > smaller proportion of water in body (women have smaller water proportion) Intracellular fluid compartment > all fluid in trillions of body cells, all cells have similar composition, 40% of body weight. Extracellular fluid compartment: all fluid outside cells, 20% of body weight. Divided into sub compartments > Interstitial fluid and Plasma Interstitial fluid: extracellular space outside bvs Plasma: extracellular spaces within bvs Other compartments: lymph, cerebrospinal fluid, synovial fluid (small volumes) Osmotic pressure of most fluid sub compartments is about equal (water/ion exchange occurs between sub compartments), fluid composition is different, large molecules (proteins) are restricted in movement, cannot penetrate membranes that separate fluid sub compartments. Cations – positive charged ions Anions – negative charged ions Intracellular cation – K+ ISF cation – Na+ Plasma cation – Na+ Intracellular anion – phosphate ISF – Cl- Plasma anion – Cl- If composition of one sub compartment is altered, fluid exchange may not be equal. Edema: fluid shifts from plasma to ISF because of> increase in permeability of capillary walls (inflammation), water moves in same direction because of osmosis. Edema can result from change in hydrostatic pressure across capillary walls. Increased hydrostatic pressure in capillaries > blocked veins/heart failure, forces fluid from plasma into IS spaces. Water content regulated so total volume remains constant. Volume of water taken into body = volume lost each day. 1500-3000mL of water enters body a day > 90% from ingested fluids, 10% from cellular metabolism. Water leaving the body > 61% urine, 35% evaporation (perspiration, respiratory passages), 4% feces. Changes in water volume alters > osmolality of body fluids, BP, ISF pressure. 3 sensors for thirst regulation: hypothalamic receptors, arterial baroreceptors, juxtaglomerular apparatuses. Thirst results from increase in osmolality of extracellular fluids/reduction in plasma volume, lowers BP. Cells in supraoptic nucleus in hypothalamus detect changes in extracellular fluid osmolality and initiate activity in neural circuits causing you to “feel thirsty”. Baroreceptors influence thirst sensation > detect decrease in BP, Aps conducted to the brain along sensory neurons to influence thirst feeling. Juxtaglomerular apparatus > detects BP, when BP is low in kidney, release renin, renin increases formation of angiotensin II in circ sytem, Angiotensin II opposes decrease in BP by stimulating thirst sensation in brain > acts on adrenal cortex to increase aldosterone secretion, and bv smooth muscle cells to vasoconstrict. After drinking a little water, thirst sensation temporarily goes away > oral mucosa is wet after being dry, sensory neurons conduct AP to thirst centre of hypothalamus to decrease sensation. ALSO consumed fluid reaches digestive tract, digestive wall stretches, initiates sensory APs in stretch receptors so sensory neurons conduct Aps to thirst centre in hypothalamus temporarily suppress thirst sensation.Prevents person from consuming too much fluid to exceed amt required to reduce blood osmolality. Long term suppression of thirst: when extracellular fluid osmolality and BP are within normal ranges. Learned behaviour > prevents dehydration. Feeling thirsty promotes water consumption > healthy person drinks more thang minimum volume of fluid required to maintain homeostasis > excess is secreted in urine. Kidneys: primary organs to regulate composition and volume of body fluids > control volume/concentration of water in the form of urine. Insensible perspiration > water evaporated off of skin, regulates heat loss. Sweat > secreted by sweat glands, contains solutes, resembles extracellular fluid, sodium chloride major component, contains potassium, ammonia, urea. Volume determined by: neural mechanisms for body temp (exercise, summer day) OR sympathetic stimulation (stress). Sweat is hyposmotic to plasma, loss of large volume of sweat decreases body fluid volume/increases concentration. Fluid is lost from extracellular space, increased extracellular fluid osmolality, reduced plasma volume, increased hematocrit. Large volume of fluid in digestive tract, nearly all reabsorbed under normal conditions. Extracellular fluid osmolality/volume determines whether body needs to get rid of large volume of dilute urine OR small volume of concentrated urine. REGULATION OF EXTRACELLULAR FLUID OSMOLALITY Increase in osmolality of extracellular fluid triggers thirst and ADH secretion (thirst hormone). Consumed water absorbed by intestines/enters extracellular fluid. ADH increases reabsorption of water from filtrate by acting on distal convoluted tubule/collecting ducts of kidneys. More fluid entering extracellular fluid decreases osmolality. Decrease in extracellular fluid osmolality inhibits thirst/ADH secretion. Less water consumed/reabsorbed from filtrate in kidneys. More water is excreted in diluted urine. Increase in osmolality of extracellular fluid. REGULATION IN EXTRACELLULAR FLUID OSMOLALITY Sensory receptors that detect changes in BP are important > carotid sinus/aortic arch baroreceptors monitor BP in large arteries, receptors in juxtaglomerular apparatus monitor in afferent arterioles of kidneys, receptors in walls of atria of heart/large veins monitor slight BP changes in them. Activate mechanisms that regulate ECF volume. 1) Neural mechanisms > When baroreceptors detect increase in arterial/venous BP, frequency of AP’s by sympathetic neurons to afferent arterioles decreases. Afferent arterioles dilate, increases glomerular capillary pressure, increased glomerular filtration rate, increase filtrate volume, increase urine volume. Baroreceptors detect decrease in arterial/venous BP, frequency of AP’s carried by sympathetic neurons to afferent arterioles increases, they constrict, decreases GFR, filtrate, urine volume. 2) Renin-angiotensin-aldosterone > Juxtaglomerular cells detect rise in BP in afferent arterioles, decrease renin secretion, leads to lower conversion rate of angiotensin to angiotensin I, slows conversion of angiotensin I to angiotensin II. Less angiotensin II > decline in aldosterone secretion from adrenal cortex. Lower aldosterone levels > reduce rate of sodium reabsorption from distal convoluted tubules/collecting ducts. More sodium remains in filtrate, fewer are reabsorbed. Water remains, excess sodium in filtrate. Volume of urine goes up, ECF volume is reduced, BP returns to normal. Blood volume goes down, BP lowers, juxtaglomerular cells secrete renin. Increases conversion of angiotensin to angiotensin I, angiotensin I to angiotensin II, increases rate of aldosterone secretion from adrenal cortex. More aldosterone increases rate of sodium reabsorption from distal convoluted tubules/collecting ducts, fewer sodium remain in filtrate, more sodium reabsorbed. Decreased osmolality of filtrate, increases kidney’s ability to reabsorb water/increase ECF volume. Volume of urine decreases, EXF volume/BP increase. 3) Atrial Natriuretic Hormone > Larger than normal blood volume, heart atrial walls are stretched, triggers ANH secretion, reduces sodium reabsorption from distal convoluted tubules/collecting ducts, increases rate of sodium/water loss in urine. Decreases ECF volume/blood volume Does not respond to decrease in blood volume. Decrease in pressure in atria of heart inhibits secretion of ANH, without ANH sodium reabsorption is inhibited in distal convoluted tubules/collecting ducts. Rate of sodium AND water reabsorption increases, reduced urine volume, increased ECF volume. 4) ADH mechanism > Regulates ECF volume response to LARGE BP changes. Inc. BP inhibits ADH secretion, reabsorption from lumens/distal convoluted tubules/collecting ducts decreases, larger volume of dilute urine. Decreases ECF volume/BP Low BP stimulates ADH secretion, reabsorption of water from distal convoluted tubule/collecting ducts increases, smaller volume of concentrated urine, increases ECF/BP Too much aldosterone secreted from enlarged adrenal cortex > increases sodium reabsorption by kidneys, total volume of ECF increases. REGULATION OF INTRACELLULAR FLUID COMPOSITION Plasma membranes separate intracellular/extracellular fluid compartments > selectively permeable (impermeable to proteins/large molecules), proteins remain in intracellular fluid. Electrolytes are actively transported across membrane* their concentrations in intracellular fluid determined by transport processes/electrical charge difference across plasma membrane. Water moves across plasma membrane by osmosis > net mvmnt of water affected by changes in concentration of solutes in extra/intra cellular fluids. Dehydration > concentration in extracellular fluid increases, water moves by osmosis from inter to extra fluid. REGULATION OF SODIUM IONS Dominant extracellular cation > exert substantial osmotic pressure with negative ions associated with them (95%). Regulation base on excretion of excess sodium ingested. Kidneys > major organs to excrete sodium, sodium ions pass from glomeruls into lumen of Bowman’s capsule, present in same concentration in filtrate as plasma. Concentration of sodium ions in urine determined by sodium/water reabsorbed from filtrate in the nephron. If Na reabsorption DECREASES > large quantities excreted in urine, if INCREASES > only small amounts secreted in urine. Sodium transport of distal convoluted tubule/collecting duct controlled by Aldosterone. Aldosterone > increases sodium reabsorption from DCT/collecting duct. When aldosterone is absent, Na reabsorption in the nephron is reduced/more is excreted in urine. Sodium lost through sweat > body temp increases, thermoreceptor neurons in hypothalamus increase rate of sweat production. Higher rate of sweat production> less sodium lost in urine to keep ECC of Na constant. If quantity of sodium increases > osmolality of ECF increases, stimulates ADH secretion, increases water reabsorption in kidneys/thirst, extracellular fluid volume/water conservation increases. Decrease in sodium > ADH secretion decreases, large volume of dilute urine produced, less thirst sensation, extracellular osmolality increases. Regulating ECF osmolality/volume, concentration of sodium in body fluids is maintaine
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