Lecture 10: Regulation of Body Fluids PDF

LECTURE 10 Regulation of Body Fluids Reference: Amerman; Chapter 25 Dr. Nancy Haydar School of Science [email protected] 1 2  Worksheet 2 Worksheet 2: Gastrointestinal and Genitourinary System – Opens F...

LECTURE 10 Regulation of Body Fluids Reference: Amerman; Chapter 25 Dr. Nancy Haydar School of Science [email protected] 1 2  Worksheet 2 Worksheet 2: Gastrointestinal and Genitourinary System – Opens Friday 4th of September at 4:00pm – Closes next Friday 11th of October at 11:59pm – Worth 5% of final mark – Available on vUWS in the assessment tab – Assesses knowledge gained from Gastrointestinal lecture 1 (week 6) Gastrointestinal lecture 2 (week 7) Gastrointestinal practical 1 (week 7) Gastrointestinal practical 2 (week 9) Urinary lecture (week 9) Reproductive System lecture (week 10)  Objectives Describe how fluid moves between the different fluid compartments of the body Define the regulation of water intake and output Explain disorders of water balance Describe the various influences of water and electrolyte balance  Body Water Content More testosterone Less skeletal High body fat thus bigger bones muscle mass Low bone mass and muscle mass * Water content declines to ~45% in old age  Fluid Compartments Total body water = 60% of body weight (70kg ~ 42L) Two main fluid compartments: – Intracellular fluid (ICF) compartment: ~26L in cells – Extracellular fluid (ECF) compartment: ~16L outside cells Plasma: ~3 L Interstitial fluid (IF) (spaces between cells): ~13L – Usually considered part of IF: Lymph, CSF, humors of the eye, synovial fluid, serous fluid, and gastrointestinal secretions  Composition of Body Fluids Water: Universal solvent Solutes: What is dissolved in water – Classified as: Non-electrolytes – Do not dissociate in water: e.g., glucose, lipids, creatinine, and urea. * No charged particles created. Electrolytes – Charged particles, e.g. Na+, Cl- – Most abundant solutes in body fluids; determine most chemical and physical reactions – Compounds dissociate into ions in water; e.g., inorganic salts, all acids and bases, some proteins o Ions conduct electrical current – vital roles in nerve function, muscle contractions, maintaining fluid balance. – Greater osmotic power than non-electrolytes o Greater ability to cause fluid shifts Fluid Movement Along Compartments Osmotic and blood hydrostatic pressures regulate continuous exchange and mixing of fluids – Water moves freely along osmotic gradients – All body fluid osmolality (measure of solute concentration) almost always equal (equilibrium) – Change in solute concentration of any compartment leads to net water flow  ECF osmolality → water leaves cell  ECF osmolality → water enters cell Cell Water movement Solute  Fluid Movement Along Compartments Between plasma and IF across capillary walls – Fluid leaks from arteriolar end of capillary, reabsorbed at venule end; lymphatics pick up remaining and return to blood Between IF and ICF across cell membrane – Two-way osmotic flow of water – Ions move selectively; Nutrients, wastes, gases → unidirectional  Water Balance Water intake must = water output = ~ 2500 ml/day Water intake: Beverages, food, and metabolic water Water output: Sensible - Urine (60%) Insensible - Perspiration, respiration and faeces. Maintenance of Body Fluid Osmolality Osmolality is the measure of the number of osmoles (Osm) of solute per kilogram of solvent. Osmolarity is the measure of the number of osmoles of solute per litre of solution (both solvent and solute). Measure of solute concentration~ how much solute in the solvent Osmolality maintained within a small range (~ 280 – 300 mOsm) Rise in osmolality (↑solute concentration) → – Stimulates thirst – Anti-Diuretic Hormone (ADH) released by pituitary gland Decrease in osmolality (↓solute concentration) → – Thirst inhibition – ADH inhibition  Renin-Angiotensin Aldosterone System (RAAS) The RAAS is a hormone system for regulating the body's blood volume and therefore blood pressure – Granular cells of juxtaglomerular complex release renin (enzyme) in response to: Sympathetic nervous system stimulation  filtrate NaCl concentration (detected by macula densa cells - chemoreceptors)  stretch (due to  blood pressure) of granular cells (mechanoreceptors). – Renin catalyses angiotensinogen (a protein made in the liver) into Angiotensin I – Angiotensin I is converted in Angiotensin II by another enzyme – Angiotensin II: A potent vasoconstrictor (which increases BP). Stimulates the release of aldosterone (hormone) from the adrenal/suprarenal gland → leads to an  Na+ reabsorption by kidney tubules (PCT and regulated reabsorption in DCT/Collecting duct) → water follows  3 5 7 4 8– 2 regulated reabsorption of Na+ 6 1  ECF osmolality Plasma volume (5 –10%) Regulation of Water Intake Blood pressure Osmoreceptors Saliva Granular cells in hypothalamus in kidney Thirst mechanism driving force for water intake Renin-angiotensin- Governed by hypothalamic thirst centre Dry mouth aldosterone mechanism – Hypothalamic osmoreceptors detect ECF Angiotensin II osmolality; Activated by  Plasma osmolality of 1 – 2% Hypothalamic – Dry mouth detected from reduced saliva Prevents over-hydrating thirst center – Decreased blood volume or pressure Sensation of thirst; – Angiotensin II or granular cell input person takes a drink Sensation of thirst Water moistens Drinking of water inhibits the thirst centre mouth, throat; stretches stomach, intestine Inhibitory feedback signals include: – Relief of dry mouth Water absorbed from GI tract – Activation of stomach and intestinal stretch Initial stimulus receptors ECF osmolality Plasma volume Physiological response Result Increases, stimulates Reduces, inhibits © 2013 Pearson Education, Inc.  Regulation of Water Output Obligatory water losses – Insensible water loss from lungs and skin – Sensible water loss from faeces and urine Minimum daily sensible water loss of 500 ml in urine to excrete wastes  ECF osmolality Regulation of Water Output Na+ concentration in plasma Influence of ADH Stimulates Plasma volume (5–10%), BP Hormone from pituitary gland Osmoreceptors Inhibits Water reabsorption in collecting ducts proportional to in hypothalamus ADH release Negative feedback inhibits –  ADH → dilute urine (light in colour) and  volume of Stimulates Baroreceptors in atria and large vessels body fluids –  ADH → concentrated urine (darker in colour); Stimulates reabsorption of water →  volume of body fluids Posterior pituitary Releases ADH Hypothalamic osmoreceptors sense ECF solute concentration and regulate ADH accordingly. Antidiuretic hormone (ADH) Other factors may trigger ADH release Targets – Large changes in blood volume or pressure Collecting ducts of kidneys E.g.,  BP →  ADH release due to blood vessel Effects baroreceptors and renin-angiotensin-aldosterone mechanism Water reabsorption Factors lowering blood volume: intense sweating, Results in vomiting, or diarrhea; severe blood loss; traumatic burns; and prolonged fever ECF osmolality Plasma volume Scant urine Short Break  Water Balance disorders - Dehydration ECF water loss due to: Haemorrhage, severe burns, prolonged vomiting or diarrhoea, profuse sweating, water deprivation, diuretic abuse, endocrine disturbances Signs and symptoms: "cottony" oral mucosa, thirst, dry flushed skin, the production of abnormally small amounts of urine May lead to: – Weight loss – Fever – Mental confusion – Hypovolemic shock – Loss of electrolytes Water Balance disorders – Hypotonic hydration Cellular over-hydration, or water intoxication Occurs with renal insufficiency or rapid excess water ingestion ECF osmolality  → hyponatremia (low sodium levels) → net osmosis into tissue cells → swelling of cells → severe metabolic disturbances (nausea, vomiting, muscular cramping, cerebral oedema) → possible death Treated with hypertonic saline (high NaCl ~ extra salty)  Water Balance disorders - Oedema Atypical accumulation of IF → tissue swelling (not cell swelling) Result of  fluid out of blood or  fluid into blood  fluid out of blood caused by: – Increased capillary hydrostatic pressure or permeability Capillary hydrostatic pressure increased by incompetent venous valves, localised blood vessel blockage, congestive heart failure =  blood volume Capillary permeability increased by ongoing inflammatory response  fluid returning to blood result of: – Imbalance in colloid osmotic pressures, Fluids fail to return at venous ends of capillary beds Can be caused by protein malnutrition, liver disease, or glomerulonephritis. – Blocked lymph vessels Cause leaked proteins to accumulate in IF Colloid osmotic pressure of IF draws fluid from blood Increases diffusion distance for nutrients and oxygen Results in low blood pressure and severely impaired circulation  Electrolyte Balance Electrolytes are salts, acids, bases, some proteins Electrolyte balance usually refers only to salt balance Salts control fluid movements; provide minerals for excitability, secretory activity and membrane permeability Salts enter body by ingestion and metabolism; lost via perspiration, faeces, urine and vomit  Central Role of Sodium Most abundant cation (+ charged) in ECF Only cation exerting significant osmotic pressure – Controls ECF volume and water distribution – Changes in Na+ levels affects plasma volume, blood pressure, and ECF and IF volumes Na+ leaks into cells (into ICF); pumped out against its electrochemical gradient (~requires energy) Na+ moves back and forth between ECF and body secretions (e.g., digestive secretions) Renal acid-base control mechanisms are coupled to Na+ transport (Acid/Base Lecture)  Regulation of Sodium Balance No known receptors that monitor Na+ levels in body fluids Na+-water balance is linked to blood pressure and blood volume control mechanisms (baroreceptors and osmoreceptors) Changes in blood pressure or volume trigger neural and hormonal controls to regulate Na+ content  Regulation of Sodium Cortex 65% of filtrate volume Regulated reabsorption Balance - Aldosterone reabsorbed H2O Na+, HCO3−, and Na+ (by aldosterone; Cl− follows) Ca2+ (by parathyroid many other ions hormone) Glucose, amino acids, and other nutrients Aldosterone is a steroid hormone produced by the adrenal gland (aka suprarenal gland) Aldosterone → decreased urinary output; H+ and NH4+ Regulated Some drugs secretion K+ (by increased blood volume aldosterone) – By active reabsorption of remaining Na+ in Outer Regulated reabsorption distal convoluted tubule and collecting medulla H2O (by ADH) Na+ (by duct aldosterone; Cl− follows) – Also causes increased K+ secretion Urea (increased by ADH) Regardless of aldosterone presence Urea Regulated – 65% Na+ reabsorbed in proximal tubules; Inner secretion K+ (by 25% reclaimed in nephron loops medulla aldosterone) – Na + never secreted into filtrate (can be released from sweat and faeces). Water in filtrate follows Na+ if ADH is present Reabsorption Secretion  Regulation of Sodium K+ concentration Body Na+ content Balance - Aldosterone in the ECF triggers renin release, increasing angiotensin II Stimulates Renin-angiotensin aldosterone Adrenal/Suprarenal Glands mechanism main trigger for aldosterone Releases release Angiotensin II Aldosterone – Prompts aldosterone release from Targets adrenal cortex Kidney tubules –  Na+ reabsorption by kidney tubules Aldosterone release also triggered by Effects elevated K+ levels in ECF Aldosterone brings about its effects slowly Na+ reabsorption K+ secretion (hours to days) Restores Homeostatic plasma levels of Na+ and K+  Regulation of Sodium Balance – Atrial Natriuretic Peptide (ANP) Protein hormone Released by atrial myocytes of the heart in response to stretch ( blood pressure) Effects: – Decreases blood pressure and blood volume  ADH, renin and aldosterone production  excretion of Na+ and water Promotes vasodilation directly and also by decreasing production of angiotensin II (vasoconstrictor)  Stretch of atria of heart due to BP Releases Negative Atrial natriuretic peptide feedback (ANP) Targets JG complex Hypothalamus and Adrenal cortex of the kidney posterior pituitary Effects Effects Renin release* ADH release Aldosterone release Angiotensin II Inhibits Inhibits Collecting ducts of kidneys Vasodilation Effects Na+ and H2O reabsorption Results in Blood volume Results in Blood pressure © 2013 Pearson Education, Inc.  Influence of Other Hormones Female sex hormones – Oestrogens:  NaCl reabsorption (like aldosterone) → H2O retention during menstrual cycles and pregnancy – Progesterone:  Na+ reabsorption (blocks aldosterone) Promotes Na+ and H2O loss Glucocorticoids:  Na+ reabsorption and promote oedema  Cardiovascular Baroreceptors Baroreceptors alert brain of increases in blood volume and pressure – Sympathetic nervous system impulses to kidneys decline (thus no longer stimulated to retain sodium and water) → Afferent arterioles dilate → GFR increases → Na+ and water output increase → Reduced blood volume and pressure  Next Week – Week 12 THURSDAY ONLY – Practical 7: Urinary & Reproductive System for THURSDAY classes only. – Topics covered: Anatomy and function of the: » kidneys » ureters » bladder » urethra – Nephrons: the functional units of the kidney – Gross anatomy of the reproductive system – Oogenesis and Spermatogenesis Complete before practical: – Read or listen to Urinary lecture (week 9) & Reproductive lecture (week 10) – Work through your practical notes using the pre-practical activities and answer the short answer questions – Reminder: Print your practical notes and come with lots of questions! MONDAY – Public holiday – No lecture. 31