Homeostasis Flashcards
B cells of pancreas
- Have receptors that detect stimulus of rise in blood glucose concentration
- Secretes hormone insulin into blood plasma
- Body cells have glycoprotein receptors - bind specifically to insulin molecule
- Changes tertiary structure of glucose transport carrier proteins
- Change shape, open, more glucose into cells via facilitated diffusion
B cells loading blood glucose concentration
- Increase rate of glucose absorption into cells e.g muscle cells
- Increase glycogenesis in liver and muscles
- Increase rate of converting glucose to fat
- Increase respiratory rate
- remove glucose from blood, return to optimum conc, causes B cells to reduce insulin secretion = negative feedback
a cells of pancreas
- detect fall in blood glucose concentration, secrete hormone glucagon to blood plasma
- glucagon attach to specific receptor protein on liver cell surface membrane
- activate enzymes to convert glycogen to glucose, convert amino acid + glycerol (glucogeogenesis)
- increase concentration of glucose to optimum, a cells reduce secretion of glucagon (negative feedback)
Role of adrenaline
- increases blood glucose concentration
- produced in adrenal glands
- attach to protein receptors on CSM of target cells
- activate enzymes, breakdown of glycogen to glucose in liver
Second messenger model (adrenaline + glucagon)
- Adrenaline binds to transmembrane receptor within cell surface membrane of liver cell
- Binding causes protein to change shape
- Leads to activation of adenyl Cyclase
- Adenyl cyclase converts ATP to cAMP
- cAMP acts as second messenger binds to kinase enzyme, changes shape + activates
- Kinase catalysed glycogen to glucose
Moves out of liver cell by facilitated diffusion, into blood, via channel protein
Type 1
Insulin dependent
Body unable to produce insulin
Perhaps due to autoimmune response, attacks B cells of the islets of Langerhans
Begins in childhood, develops quickly
Type 2
Insulin independent
Due to glycoprotein receptors on body cells being lost or losing responsiveness to insulin
Or inadequate supply of insulin from pancreas slow development, overweight people are likely
Nephron osmoregulation
1. Formation of glomerular filtrate by ultrafiltration
- diameter of afferent arteriolar is greater than efferent arteriole = build up of hydrostatic pressure within glomerulus
- water, glucose, mineral ions, urea, are squeezed out of the capillary = forms glomerular filtrate, reabsorbed
- blood cells and proteins cannot pass into renal capsule = too large
- resistance is overcome by spaces between padocytes, spaces in endothelium of glomerular capillary
Nephron osmoregulation
2. Reabsorption of glucose and water by the proximal convoluted tubule
Adaption of proximal convoluted tubules or reabsorption
- microvilli
- infoldings at bases
- lots of mitochondria
Process
1. Sodium ions actively transported out of proximal consulted tubule lining cells, to blood capillaries
Sodium ion concentration of theses cells is lowered
- Sodium ions diffuse from lumen into epithelial lining cells of proximal convoluted tubule via concentration gradient, within carrier proteins + facilitated diffusion
- Via co-transport, carrier proteins carry either glucose/amino acids/ chloride ions with sodium ions
- Molecules in cell diffuse into the blood, molecules glucose, water, are absorbed
Nephron osmoregulation
3. Maintenance of a gradient of sodium ions by loop Henle
Descending limb - narrow, thing walls, permeable to water
Ascending limb - wider, thick walls, impermeable to water (doesn’t move out)
- Sodium ions actively transported out of ascending limb of loop Henle. Using ATP from mitochondria
- Creates lower water potential in the interestial region.
Water does not pass out of ascending limb is osmosis bc impermeable - Walls of descending limb are permeable, water leaves via osmosis from filtrate, enters blood capillaries via osmosis + carried away
- Filtrate reaches lowest water potential at the top of the hair pin
- Base of ascending limb, sodium ions diffuse out, moving up, sodium ions actively moved out = higher water potential
- Gradient of water potential between interestial space of collecting duct and ascending limb. Filtrate moves down collecting duct, water leaves by osmosis by osmosis via channel proteins into blood capillaries
- Urine entering bladder = lower potential than blood
Counter current multiplier
Role of hormones in osmoregulation
regulation of water potential of blood
- Hormone acts on distal convoluted tubule + collecting duct
- Rise in solute concentration = little water consumption, sweating, large ions consumption ~ lowers water potential
Process
- Osmoreceptors in hypothalamus detects fall in WP
- Osmorecptors shrink, hypothalamus produce ADH enzyme
- ADH makes cells covering cell surface membrane of distal convoluted tubule + collecting duct more permeable to water
- ADH molecules bind to specific receptors on cells, activates phosphorylase
- Activation of phosphorylase cause vesicles that have water channel proteins inside (aquaporins), fuse with membrane, makes it more permeable to water
- ADH increases permeability of collecting duct, urea passes out more, lowers WP of fluid around
- Combined effect = more water leaves collecting duct via osmosis, down water potential gradient, re-enters blood
Fall in solute concentration = large volume of water consumed, salts used in metabolism and not replaced ~ increase WP
- Osmoreceptors detect rise in WP, increase nerve impulse to pituitary gland, reduce ADH release
- Less ADH, decreases permeability of collecting duct to water and urea
- Less water reabsorbed, more dilute urine, WP of blood falls
- Return to normal levels, ADH release is back to normal levels = negative feedback