Homeostasis is the maintenance of a stable internal environment Flashcards
Importance of homeostasis
Changes in external environment can affect your internal environment
Homeostasis involves control systems that keep your internal environment roughly constant
Importance of maintaining stable core temperature
Enzymes work at an optimum temp
If body temperature is too low, there will not be enough Ek, so fewer successful collisions/enzyme-substrate complexes formed
If body temperature is too high enzymes denature as H-bonds in tertiary structure break and the active site changes shape, no longer complementary to substrate so fewer successful collisions/enzyme-substrate complexes formed
Importance of maintaining stable blood pH
Enzymes work at an optimum pH
If the blood pH is too low or high, the enzymes will denature as ionic bonds in tertiary structure break
The active site changes shape so that it is no longer complementary to substrate
Therefore there are fewer successful collisions and enzyme-substrate complexes formed
Importance of maintaining a stable blood glucose concentration
If blood glucose concentration too low (hypoglycaemia) there will not be enough glucose for respiration (particularly brain + nervous system) so less ATP is produced and active transport etc. can’t happen
If blood glucose concentration too high (hyperglycaemia) blood will have a low water potential (as increased solute)
Water will be lost from tissue to blood via osmosis and kidneys can’t absorb all glucose so more water lost in urine, causing dehydration
Negative feedback
Receptors detect levels that are too low/high
Effectors respond to counteract change
Restores levels to normal/original
e.g. regulation of body temperature
Positive feedback
Amplifies a change from the normal level as effectors respond to further increase the level away from normal level
Advantage – rapidly activate something
e.g. blood clot or hypothermia
Not involved in homeostatic system
Role of multiple negative feedback mechanisms in homeostasis
More control over changes in internal environment
Controls departures in different directions from the original state/actively increase or decrease a level to normal
Faster response and greater control with multiple feedback mechanisms
Factors that influence blood
glucose concentration
Eating food containing carbohydrates increases amount of glucose being absorbed from the intestine to the blood (blood glucose concentration rises)
Exercise increases rate of respiration of glucose (blood glucose concentration falls)
Action of insulin in blood glucose concentration
Insulin lowers blood glucose concentration when it is too high
Secreted by beta cells in islets of Langerhans in pancreas
Insulin binds to specific receptors on cell surface membranes of liver/muscle cells (target cells/effectors)
Increases permeability of muscle cell membrane to glucose by increasing number of channel proteins (GLUT4) in cell surface membrane and therefore cells can uptake more glucose from blood by facilitated diffusion
Insulin also activates enzymes in liver/muscle cells that convert glucose to glycogen
The cells are also able to store glycogen in their cytoplasm as an energy source and the process of forming glycogen from glucose is called glycogenesis
Insulin also increases the rate of respiration of glucose
Action of glucagon in blood glucose concentration
Glucagon raises blood glucose concentration when it is too low
Secreted by alpha cells in islets of Langerhans in pancreas
Glucagon binds to specific receptors on cell surface membranes of liver cells (target cells)
Activates enzymes involved in the breakdown of glycogen to glucose (glycogenolysis)
Activates enzymes involved in the conversion of glycerol/amino acids to glucose (gluconeogenesis)
Glucagon decreases the rate of respiration of glucose in cells
Role of adrenaline in blood glucose concentration
Hormone secreted by adrenal glands (above kidneys) when blood glucose concentration is low, or when the body is stressed/exercising
Binds to specific receptors on cell surface membranes of liver cells (target cells)
Activates enzymes involved in the conversion of glycogen to glucose (glycogenolysis)
Inhibits glycogenesis (synthesis of glycogen from glucose)
It also activates secretion of glucagon and inhibits the secretion of insulin
Therefore it increases blood glucose concentration (more glucose for respiration)
Secondary messenger model
Adrenaline and glucagon demonstrate the secondary messenger model because they cause glycogenolysis to occur inside cell even though they bind to receptors on the outside of the cell
- Receptors for adrenaline/glucagon have specific tertiary structures that bind to specific complementary receptors on cell membrane
- Activate the enzyme called adenylate cyclase
- Adenylate cyclase converts ATP into a chemical signal called a ‘second messenger’ i.e. cyclic AMP or cAMP
- cAMP activates an enzyme called protein kinase A
- Protein kinase A activates a cascade to break down glycogen to glucose (glycogenolysis)
Glucose transporters in the control of blood glucose concentration
Skeletal and cardiac muscle cells contain a channel protein called GLUT4
Glucose transporter that is stored in vesicles in the cytoplasm of cells whilst insulin levels are low
When insulin binds to receptors on the cell-surface membrane, it triggers the movement of GLUT4 to the membrane
Glucose can then be transported into the cell through the GLUT4 protein via facilitated diffusion
Diabetes what is it
Diabetes is where blood glucose concentration can’t be controlled properly.
Blood glucose concentration peaks higher and takes longer to decrease and remains high after a meal
Type 1 diabetes cause and effects
Caused by a gene mutation which causes an autoimmune response on beta cells in the islets on Langerhans so the body can’t produce insulin
After eating, blood glucose level rises and stays high (hyperglycaemia)
Type 1 diabetes control: insulin therapy
Injections of insulin (not by mouth as protein is digested) or use of insulin pump
Dose of insulin matched to glucose intake/use biosensors
If too much insulin administered, produces a dangerous drop in glucose levels (hypoglycaemia)
Type 1 diabetes control: diet manipulation
Eating regularly, control carbohydrate intake e.g. carbs which are broken down/absorbed slower in order to avoid a sudden rise in glucose
Type 2 diabetes cause and effects
Caused by a poor diet/lack of exercise/obesity
It occurs when beta cells do not produce enough insulin or when glycoprotein/receptors on cell membranes lose responsiveness to insulin (faulty) and so since the cells are less responsive to insulin, they don’t take up enough glucose
Type 2 diabetes control: insulin therapy
Use of drugs which target insulin receptors/use of insulin so that there is more glucose uptake by cells/tissues
Type 2 diabetes control: diet manipulation
Reduced sugar intake (carbs) in diet/eat food with low glycaemic index so that less sugar is absorbed into blood
Reduced fat intake so that less fat is converted to glucose
More (regular) exercise since it uses glucose/fats by increasing respiration
Lose weight for increased sensitivity of cells to insulin and an increased uptake of glucose by cells
The structure of the nephron
Long tubules (along with the bundle of capillaries) where the blood is filtered are called nephrons
Blood from renal artery enters smaller arterioles in the cortex of the kidney
Each arteriole splits into a glomerulus, a bundle of capillaries looped inside the Bowmans capsule (ultrafiltration takes place here)
Arteriole that takes blood into each glomerulus is called the afferent arteriole (smaller so higher pressure) whereas the arteriole that takes filtered blood away is called the efferent arteriole
High pressure in glomerulus forces liquid and small molecules in the blood out of the capillary and past three layers into the Bowmans capsule
Liquid and small molecules enter the nephron tubules which consists of the capillary wall, a membrane (basement membrane) and the epithelium of the Bowmans capsule
Substances that enter the Bowmans capsule are known as the glomerular filtrate, whereas larger molecules like proteins and blood cells cant pass through, so they stay in the blood
Glomerular filtrate passes along nephron and useful substances are reabsorbed
Finally filtrate flows through the collecting duct and passes out of the kidney along the ureter
Osmoregulation
Osmoregulation is the control of water and salt levels in the body
Controlled by hormones e.g. antidiuretic hormone (ADH) which affect the distal convoluted tubule and collecting duct
Roles of hypothalamus, posterior pituitary and antidiuretic hormone (ADH) in osmoregulation
How the body responds to a decrease in water potential…
- The water content of the blood drops so its water potential drops. This is detected by osmoreceptors in hypothalamus
- Hypothalamus produces more ADH (antidiuretic hormone) via the posterior pituitary gland
- ADH travels in blood to kidney and attaches to receptors on collecting duct/DCT (distal convoluted tubule) of kidney
- ADH increases permeability of cells/walls of the DCT/collecting duct (more aquaporins fuse with cell membrane) to water so more water absorbed is reabsorbed into the blood via osmosis and leaves the DCT/collecting duct
- A small amount of highly concentrated urine is produced and less water is lost
Roles of hypothalamus, posterior pituitary and antidiuretic hormone (ADH) in osmoregulation
How the body responds to an increase in water potential…
- The water content of the blood rises, so its water potential rises. This is detected by osmoreceptors in the hypothalamus
- Hypothalamus produces less ADH as posterior pituitary gland secretes less ADH into blood
- Less ADH travels in blood to kidney and attaches to receptors of collecting duct/ DCT of kidney
- ADH decreases permeability of cells/walls of the DCT/collecting duct to water and urea to water so less water is reabsorbed into the blood via osmosis and leaves the DCT/collecting dust
- A large amount of dilute urine is produced and more water is lost
Role of nephron in osmoregulation
Selective reabsorption takes place after the formation of glomerular filtrate
Flows along the proximal convoluted tubule (PCT), through the loop of Henle, and along the distal convoluted tubule (DCT)
Reabsorption of glucose and water from the glomerular filtrate occurs at the PCT into the blood
Maintenance of a gradient of sodium ions in the medulla by the loop of Henle
Reabsorption of water by the DCT and collecting duct
Formation of glomerular filtrate
Diameter of efferent arteriole smaller than afferent arteriole so that the glomerulus is under higher pressure
Build-up of hydrostatic pressure in glomerulus
Water, glucose, mineral ions squeezed out of capillary/glomerulus into the Bowman’s capsule to form glomerular filtrate
Liquid and small molecules pass through 3 layers to reach the Bowmans capsule; pores in the capillary endothelium, basement membrane and podocytes which act as a filter
Large proteins/blood cells aren’t passed through as too large
Reabsorption of glucose and water by the proximal convoluted tubule (PCT)
- Sodium ions actively transported out of epithelial cell to capillary, lowering the concentration of Na+ in the epithelial cell
- Na+ moves via facilitated diffusion from PCT into epithelial cell down concentration gradient via co-transporting glucose/amino acids/Cl-, which increases concentration of glucose etc. in epithelial cell
- Glucose/amino acids/Cl- move into capillary via facilitated diffusion down concentration gradient (reabsorbed) which lowers the water potential in the capillary
- Water moves via osmosis down the water potential gradient into capillary (reabsorbed)
Maintaining a gradient of sodium ions in the medulla by the loop of Henle
- Loop of Henle acts as a counter current multiplier which maintains the water potential gradient and water can leave collecting duct/DCT by osmosis
- Na+ actively transported out of ascending limb. Ascending limb is impermeable to water so water remains, increasing the concentration of Na+ in medulla, lowering the water potential
- Water moves out of descending limbs/collecting duct by osmosis into medulla and is reabsorbed by capillaries, so the filtrate is more concentrated as it moves down the ‘hairpin’
- Na+ diffuses into descending limb, recycling Na+ in loop of Henle and reduces water potential further
Reabsorption of water by the distal convoluted tubule and collecting ducts
Water moves out of the DCT and collecting duct by osmosis down a water potential gradient
Controlled by ADH which changes their permeability
