3.6.4 HOMEOSTASIS

Cards (43)

  • Changes in external environment can affect your internal environment. 
    Homeostasis - maintenance of a stable internal environment. 
    Physiological control systems keep internal environment roughly constant - in dynamic equilibrium (fluctuating around a normal level), within restricted limits.
    Vital for cells to function normally and stop them being damaged.
  • Importance of Maintaining a Stable Core Temp and Blood pH: 
    Affect enzyme activity, which controls rate of metabolic reactions. 
  • Temperature
    Increasing temp increases rate of metabolic reactions - more kinetic energy (molecules move faster), substrates more likely to collide with active sites. Increased energy of collisions - more likely to result in reaction. 
    Enzyme’s molecules vibrate more. 
    • Temp too high - reaction stops. Vibration breaks hydrogen bonds holding enzyme in its 3D shape - active site changes shape so enzyme and substrate no longer complementary. Enzyme denatured - doesn’t function. 
    • Temp too low - enzyme activity reduced, slowing rate of metabolic reactions. 
    Highest rate of enzyme activity happens at their optimum temperature — 37 °C in humans.
  • pH
    • If blood pH too high/low (highly alkaline/acidic) enzymes denatured. Ionic and hydrogen bonds holding them in 3D shape broken, so active site shape changed and no longer works as a catalyst. 
    • Highest rate of enzyme activity happens at their optimum pH - when metabolic reactions fastest. 
  • pH calculated based on conc of hydrogen ions (H+). 
    • Greater H+ conc = lower pH (more acidic).
    Work out pH of solution:
    pH = -log10 [H+]
    pH expressed on a logarithmic scale.
  • Importance of Maintaining a Stable Blood Glucose Concentration:
    Availability needed as respiratory substrate for cells, and affects water potential of blood. 
    • If b.g.c too high - water potential of blood reduced - water molecules diffuse out of cells into blood by osmosis. Cells shrivel up and die.
    • If b.g.c too low - cells unable to carry out normal activities - not enough glucose for respiration to provide energy.
  • Negative Feedback
    Homeostatic systems involve receptors, a communication system and effectors. 
    • Receptors detect when a level too high/low, and info communicated via nervous/hormonal system to effectors. 
    • Effectors respond to counteract change — bring level back to normal. 
    Negative feedback mechanisms restore systems to their original level - keep around normal level. 
    • If change too big, effectors may not be able to counteract it.
  • Homeostasis involves multiple negative feedback mechanisms for each thing being controlled. Separate mechanisms for departures in different directions from the original state (e.g. feedback mechanisms to reduce body temperature and also mechanisms to increase it). 
    Gives more control -  
    • If only one negative feedback mechanism, could only turn it on or off. Only be able to actively change a level in one direction so it returns to normal.
  • Positive Feedback -
    Effectors amplify the change away from the normal level. 
    • Not involved in homeostasis - doesn’t maintain stable internal environment. Useful to rapidly activate processes in the body. Can happen when a homeostatic system breaks down.
    • Blood glucose conc must be controlled as all cells need a constant energy supply. 
    • Monitored by cells in pancreas. 
    • Rises after eating food containing carbohydrates, falls after exercise - more glucose used in respiration to release energy.
  • Hormonal Control of Blood Glucose Concentration -
    Hormonal system controls b.g.c using insulin and glucagon. 
    • Are hormones - chemical messengers that travel in blood to their target cells (effectors). 
    • Both secreted by the islets of Langerhans - clusters of cells in pancreas. Contain beta (β) cells and alpha (α) cells. β cells secrete insulin into blood, α cells secrete glucagon into blood. 
    Insulin and glucagon act on effectors, which respond to restore the b.g.c to normal level.
  • Insulin - GLYCOGENESIS
    Lowers b.g.c when too high. 
    • Binds to specific receptors on cell membranes of muscle and liver cells. 
    • Increases permeability of cell membranes to glucose, so the cells take up more glucose. Involves increasing the number of channel proteins in the cell membranes.
    • Also activates enzymes in muscle and liver cells that convert glucose into glycogen (Glycogenesis). Cells able to store glycogen in their cytoplasm, as an energy source. 
    Increases rate of respiration of glucose, especially in muscle cells.
  • Glucagon - GLYCOGENOLYSIS, GLUCONEOGENESIS
    Raises b.g.c when it’s too low. 
    • Binds to specific receptors on cell membranes of liver cells 
    • Activates enzymes that break down glycogen into glucose (Glycogenolysis)
    • Activates enzymes involved in formation of glucose from glycerol and amino acids (Gluconeogenesis). 
    Decreases rate of respiration of glucose in cells.
  • Hormone Response
    Slower (than response by nervous impulses) as hormones travel in blood to target cells. Means responses to hormones can occur all over the body if target cells widespread (nervous impulses localised).
    Effects of hormones last longer - not broken down as quickly as neurotransmitters.
  • Negative Feedback Mechanisms and Glucose Concentration
    Rise in b.g.c:
    • Pancreas detects b.g.c too high
    • β cells secrete insulin, α cells stop secreting glucagon 
    • Insulin binds to receptors on liver and muscle cells (the effectors). Respond to decrease b.g.c:
    • Glycogenesis activated
    • Cells take up more glucose
    • Cells respire more glucose
    • B.g.c falls and returns to normal.
  • Negative Feedback Mechanisms and Glucose Concentration
    Fall in  b.g.c:
    • Pancreas detects b.g.c too low
    • α cells secrete glucagon, β cells stop secreting insulin
    • Glucagon binds to receptors on liver cells (the effectors). Respond to increase b.g.c:
    • Glycogenolysis activated
    • Gluconeogenesis activated
    • Cells respire less glucose. 
    • B.g.c rises and returns to normal.
  • Adrenaline -
    Hormone secreted from adrenal glands when there’s low b.g.c, when stressed and when exercising. Binds to receptors in cell membrane of liver cells and:
    • Activates glycogenolysis (the breakdown of glycogen to glucose).
    • Inhibits glycogenesis (the synthesis of glycogen from glucose).
    To increase blood glucose concentration. 
    Activates glucagon secretion and inhibits insulin secretion, which increases glucose conc. 
    Gets body ready for action by making more glucose available for muscles to respire.
  • Second Messenger Model - adrenaline + glucagon:
    To activate glycogenolysis:
    • Adrenaline and glucagon bind to specific receptors and activate adenylate cyclase. 
    • Which converts ATP into cyclic AMP (cAMP) (a second messenger). 
    • cAMP activates enzyme protein kinase A. 
    • Which activates a cascade (chain of reactions) that breaks down glycogen into glucose (glycogenolysis).
  • Diabetes - Condition where blood glucose concentration can’t be controlled properly. 
  • Type I Diabetes
    Immune system attacks the β cells in the islets of Langerhans so they can’t produce any insulin. 
    • After eating, blood glucose level rises and stays high - can result in death if untreated. 
    • Kidneys can’t reabsorb all this glucose, so some excreted in urine. Test for diabetes - sample of urine tested for (higher concs of) glucose. (Normally concentration of glucose in urine very low).
    • Treated with regular insulin injections/insulin pump to deliver insulin continuously. Carefully controlled - too much can produce dangerous drop in blood glucose levels. 
  • Type II Diabetes
    β cells don’t produce enough insulin/body’s cells don’t respond properly to insulin - insulin receptors on cell membranes don’t work properly, so cells don’t take up enough glucose. 
    Means b.g.c higher than normal.
    • Usually acquired later in life than Type I. Often linked with obesity and more likely in people with family history of it. Other risk factors - lack of exercise, age and poor diet.
    • Can be treated by eating a healthy, balanced diet, losing weight and regular exercise. Glucose-lowering medication can be taken.
  • Responses of food companies to Type II diabetes to reduce risk:
    • Some attempted to make products healthier - eg. sugar alternatives (sweetener) and reducing sugar, fat and salt content.
    • Reluctant to spend money developing healthier alternatives if existing unhealthy products still popular and generating profit. 
  • Responses of health advisors to Type II diabetes to reduce risk:
    • Recommended to eat diet low in fat, sugar and salt. Regular exercise and lose weight if necessary.
    Campaigns eg. ‘Change4Life’, to educate people on healthier diet, lifestyle. 
    Challenge food industry to reduce advertising of junk food, improve nutritional value of products, clearer labelling on products.
    • Blood enters kidney through renal artery
    • Passes through capillaries in cortex (outer layer) of kidneys. Substances filtered out of blood and into long tubules surrounding capillaries (ultrafiltration). 
    • Useful substances, like glucose and right amount of water, reabsorbed back into blood (selective reabsorption). 
    • Remaining unwanted substances pass along to bladder and excreted as urine.
  • Nephrons - Long tubules along with the bundles of capillaries where blood filtered. Around one million nephrons in each kidney. 
  • Nephron Structure/Ultrafiltration
    Blood from the renal artery enters smaller arterioles in cortex of kidney.
    Each arteriole splits into a glomerulus (plural, glomeruli) — a bundle of capillaries inside a hollow ball (Bowman’s capsule). Where ultrafiltration takes place.
    • Afferent arteriole - takes blood into each glomerulus 
    • Efferent arteriole - takes the filtered blood away from glomerulus
  • Ultrafiltration 1
    • Efferent arteriole diameter smaller than afferent, so blood in glomerulus under high pressure - forces liquid and small molecules in blood out of capillary into Bowman’s capsule.
    • Pass through capillary endothelium, basement membrane and epithelium of Bowman’s capsule to get into Bowman’s capsule and enter nephron tubules.
    • Larger molecules like proteins + blood cells can’t pass through so stay in blood. 
  • Ultrafiltration 2
    • Glomerular filtrate (Substances that enter Bowman’s capsule) passes along rest of nephron and useful substances reabsorbed along the way.
    • Filtrate flows through collecting duct and passes out of kidney along ureter.
  • Selective Reabsorption of Useful Substances -
    • Occurs as glomerular filtrate flows along PCT, through loop of Henle, and along DCT. 
    • Useful substances leave tubules of the nephrons and enter capillary network wrapped around them.
    • Useful solutes, like glucose, are reabsorbed along PCT by active transport and facilitated diffusion.
    • Water enters blood by osmosis because water potential of blood is lower than that of filtrate. Water is reabsorbed from the PCT, loop of Henle, DCT and the collecting duct. 
    • The filtrate that remains is urine, which passes along ureter to bladder.
    • Epithelium of PCT wall has microvilli to provide large surface area for reabsorption of useful materials from glomerular filtrate (in tubules) into blood (in capillaries). 
  • PCT - proximal convoluted tubule
    DCT - distal convoluted tubule
  • Urine - Usually made up of water and dissolved salts, urea and other substances such as hormones and excess vitamins. 
    Doesn’t usually contain:
    • Proteins or blood cells - too big to be filtered out of blood.
    • Glucose - actively reabsorbed back into blood.
  • Amount of water in the blood (and so water potential of blood) needs to be kept constant - water is essential to keep body functioning.
    • Mammals excrete urea (and other waste products) in solution - water lost. Also lost in sweat. 
  • Osmoregulation - Control of Blood Water Potential
    • Kidneys regulate w.p of blood (and urine), so body has right amount of water.
    • Water reabsorbed along almost all of nephron, but regulation of w.p mainly occurs in loop of Henle, DCT and collecting duct. Volume of water reabsorbed by DCT and collecting duct controlled by hormones.
  • If water potential of blood: 
    • Too low (dehydration) - more water reabsorbed by osmosis into blood from tubules of nephrons. Means urine more concentrated, so less water lost during excretion.
    • Too high (too hydrated) - less water reabsorbed by osmosis into blood from tubules of nephrons. Means urine more dilute, so more water lost during excretion.
  • The Loop of Henle
    • Located in medulla (inner layer) of kidneys.
    • Made up of two ‘limbs’descending and ascending.
    • Control movement of sodium ions so water can be reabsorbed by blood.
  • Osmoregulation + the Loop of Henle 1
    • Top of ascending limb - Na+ ions actively pumped out into medulla. Ascending limb impermeable to water, so water stays inside tubule. Creates low w.p in medulla (high concentration of ions).
    • As lower w.p in medulla than descending limb, water moves out of descending limb (permeable to water) into medulla by osmosis. Makes glomerular filtrate more concentrated (ions can’t diffuse out - desc. limb not permeable to them). Water in medulla reabsorbed into blood through capillary network. 
  • Osmoregulation + the Loop of Henle 2
    • Bottom of asc. limb - Na+ ions diffuse out into medulla, further lowering w.p in medulla (asc. limb impermeable to water so it stays in tubule).
    • Water moves out of DCTs by osmosis and reabsorbed into blood. 
    • First 3 stages hugely incr. ion conc in medulla, lowering w.p. Causes water to move out of collecting duct by osmosis. Water in medulla reabsorbed into blood through capillary network. 
    • Volume of water reabsorbed into capillaries controlled by changing the permeability of DCT and collecting duct.
  • Water potential of blood monitored by osmoreceptors in hypothalamus (part of brain). 
    • When w.p of blood decreases, water moves out of osmoreceptor cells by osmosis. Causes cells to decrease in volume - sends signal to other cells in hypothalamus, which sends signal to posterior pituitary gland. 
    • Causes posterior pituitary to release antidiuretic hormone (ADH) into blood.