A Level CIE Biology: 14 Homeostasis

homeostasis

the process of maintaining constant internal body conditions

in order to function properly and efficiently, organisms…

have diff control systems that ensure their internal conditions are kept relatively constant

why is homeostasis important

ensures the maintenance of optimal conditions for enzyme action and cell function

sensory cells

detect information about the conditions inside and outside of the body

6 physiological factors controlled by homeostasis in mammals:

• core body temp

• metabolic waste e.g. co2 and urea

• blood pH

• conc of glucose in blood

• water potential of blood

• conc of respiratory gases (co2 and o2) in blood

how is homeostatic balance (keep factors within certain limits) maintained 

majority of homeostatic control mechanisms in organisms use negative feedback

3 things negative feedback control loops involve

• receptor

• coordination system

• effector

receptor/sensor

detects stimulus that is involved with condition/physiological factorc

coordination system (nervous and endocrine)

transfer information between different parts of body

effector (muscles and glands)

carry out a response

3 outcomes of negative feedback loop:

• factor/stimulus is continuously monitored

• if increase in factor, body responds to make factor decrease

• if decrease in factor, body responds to make factor increase

what 2 coordination systems does homeostasis in mammals rely on to transfer info between diff parts of body

• nervous - info transmitted as electrical impulses that travel along neurones

• endocrine - info transmitted as chemical messengers called hormones that travel in blood

what do metabolic reactions within body produceq

waste products

excretion

removal of waste products (e.g. co2 and urea)

where is urea produced

liver

why is urea produced

excess amino acids, if more protein eaten than required, excess can’t be stored in body.

why does deamination occur

amino acids within protein provides useful energy so amino group must be removed from each amino acid to make energy accessible

deamination 3

• the amino group (-NH2) of an aa is removed, together with an extra hydrogen atom

• these combine to form ammonia (NH3)

• the remaining keto acid may enter the krebs cycle to be respired, be converted to glucose, or converted to glycogen/fat for storage

ammonia features 3

• very soluble

• highly toxic compound

• produced during deamination

why is ammonia damaging if allowed to build up in blood 3

• dissolves in blood to form alkaline ammonium hydroxide, disrupting blood pH

• impacts reactions of cell metabolism e.g. respiration

• interferes with cell signalling processes

why is ammonia converted to urea

urea is less soluble and less toxic than ammonia

how is ammonia converted to urea

combined with co2

kidney 2 functions

• osmoregulatory organ - regulate water content of blood (vital for maintaining blood pressure)

• excretory organ - excrete toxic waste products of metabolism (e.g. urea) and substances in excess of requirements (e.g. salts)

humans have_ kidneys

2

excretory system diagram

structures of excretory system

• renal artery

• renal vein

• kidney

• ureter

• bladder

• urethra

renal artery function

carries oxygenated blood (containing urea and salts) to the kidneys

renal vein function

carries deoxygenated blood (that has had urea and excess salts removed) away from the kidneys

kidney function

regulates water content of blood and filters blood

ureter function

carries urine from the kidneys to the bladder

bladder function

stores urine (temporarily)

urethra function

releases urine outside of the body

fibrous capsule

fairly tough outer layer that surrounds the kidney

3 main kidney parts beneath the fibrous capsule

• the cortex (contains glomerulus as well as Bowman’s capsule, proximal convoluted tubule, and distal convoluted tubule of the nephrons)

• the medulla (contains loop of Henle and collecting duct of the nephrons)

• the renal pelvis (where the ureter joins the kidney)

nephron 3 features

• thousands of tiny tubes in each kidney

• functional unit of the kidney

• responsible for urine formation

network of blood vessels associated with each nephron:

• within bowmans, each nephron = glomerulus

• each glomerulus is supplied w blood by an afferent arterial (which carries blood from renal artery)

• capillaries of the glomerulus rejoin to form efferent arteriole

• blood flows from efferent arteriole into network of caps that run closely alongside rest of nephron

• blood from caps eventually flows into renal vein

2 stages of urine formation in the kidneys

• ultrafiltration

• selective reabsorption

where does ultrafiltration occur

bowman’s capsule

where does selective reabsorption occur

proximal convoluted tubule

ultrafiltration:

small molecules (including aas, water, glucose, urea and inorganic ions) are filtered out of blood caps of glomerulus and into bowman’s capsule to form filtrate known as glomerular filtrate

selective reabsorption

useful molecules are taken back/reabsorbed from the filtrate and returned to the blood as the filtrate flows along the nephron

what happens after selective reabsorption (2)

• after the necessary reabsorption of aa, water, glucose and inorganic ions is complete (even some urea is reabsorbed), the filtrate eventually leaves the nephron and is now referred to as urine

• urine flows out of kidneys, along the ureters and into the bladder, where it is temporarily stored

ultrafiltration: where and why do arterioles branch off 

they branch off the renal artery and lead to each nephron, where they form a knot of capillaries (glomerulus) sitting inside the cup-shaped Bowman’s capsule

ultrafiltration: why is pressure increasing further into the glomerulus

capillaries get narrower and increases pressure on blood moving through which is already at high pressure bc directly from renal artery connected to aorta

ultrafiltration: what is the effect of increasing pressure in glomerulus

smaller molecules being carried in the blood is forced out of caps into bowman’s capsule, where they form filtrate

ultrafiltration: how is the glomerular capillaries separated from the lumen on Bowman’s

by 2 cell layers with a basement membrane:

• first cell layer: endothelium of the capillary - each capillary endothelial cell is perforated by thousands of tiny membrane-lined circular holes

• next layer: basement membrane - made up of network of collagen and glycoproteins

• second cell layer: epithelium of bowman’s capsule - these epithelial cells have many tiny finger-like projections with gaps in between them known as podocytes

ultrafiltration: what happens as blood passes through the glomerular capillaries

the holes in cap endothelial cells and the gaps between podocytes allow substances dissolved in blood plasma to pass into bowman’s capsule

• glomerular filtrate

glomerular filtrate

the fluid that filters through from the blood into bowman’s with main substances passing out:

• amino acids

• water

• glucose

• urea

• inorganic ions (mainly Na+, K+, Cl-)

ultrafiltration: why do red and white blood cells and platelets remain in the blood

too large to pass through the holes in capillary endothelial cells

ultrafiltration: basement membrane

acts as filter as it stops large protein molecules from getting through

ultrafiltration diagram

why does ultrafiltration occur

due to differences in water potential between plasma in the glomerular caps and the filtrate in the bowmans (water moves down water potential gradient, from region of high wp to lower wp. wp increased by high pressure, decreased by solutes)

2 factors affecting water potential

• pressure

• solute concentration

how pressure affects wp in glomerulus and bowmans 

• as afferent arteriole is wider than efferent, bp high in glom caps

• wp of blood plasma in glom caps is raised above wp of filtarte in bowmans

• water moves down wp gradient from blood plasma in glom caps into bowmans

how solute concentration affects wp in glom and bowmans

• basement membs allow most solutes within blood plasma to filter into bowmans, plasma protein mols are too big to get thru and stay in blood

• solute conc in blood plasma in glom caps higher than the filtrate in bowmans capsule

• wp of blood plasma lower than that of filtrate in bowmans

• water moves down wp gradient from bowmans cap into blood plasma in glom caps

the effect of pressure gradient outweighs…

effect of solute gradient, therefore wp of blood plasma in glom > wp of filtrate in bowmans so blood flows thru glom, overall movement of water down wp gradient from blood into the bowmans capsule

selective reabsorption

• many of substances in glomerular filtarte need to be kept in body

• substances reabsorbed into blood as filtrate passes along nephron

• only certain substances reabsorbed

where is glucose reabsorbed

proximal convoluted tubule

lining of proximal convoluted tubule composition

• single layer of epithelial cells

  • microvilli

  • co-transporter proteins

  • high number of mitochondria

  • tightly packed cells

where are water and salts reabsorbed

via loop of henle and collecting duct

4 adaptations of pct epithelial cells

• many microvilli present on luminal membrane (cell surface membrane that faces lumen)

• many co-transporter proteins in luminal membrane

• many mitochondria

• cells tightly packed together

how does many microvilli present help reabsorption

increases s.a. for reabsorption

how does cotransporter proteins help reabsorption

each type of co-transporter protein tarnsports specific solute (e.g. glucose or particular amino acid ) across luminal membrane

how does many mitoch help reabs

provide eneryg for sodium potassium pump proteins in basal membranes of cells

how do cells tightly packed help reabs

no fluid can pass between cells (all suibstances reabsorbed must pas through cells)

how does selective reabs occur

• blood caps located close to outer surface of pct

• as blood in caps comes staright from glomerulus it has very little plasma and has lost much of water, inorganic ions and other small solutes

• basal membs of pct epithelial cells are sections of cell memb that are closest to the blood caps

• na+k pumps in these basal membs move sodium ions of epithelial cells and into blood where they are carried away

• this lowers conc of sodium ions inside epithelial cells so diffuse down conc grad through luminal memb from filtrate through cotarnsporter proteins in membrane

• several cotarnsporters each tarnsports sodium ion and another solute from filtrate e.g. glucose or aa

• once inside epithelial cells these solutes diffuse down conc grads passing thru transport proteins in basal membs into blood

how much glucose is reabs from glom filtrate

ALL reabs into blood so none in urine

what is reabsorbed 

glucose, aa, vitamins, inorganic ions

how is water potential gradient created and what is the effect

movement of all solutes from pct into caps increases wp of filtarte and decreases the wp of the blood in the caps. causes water to move into blood by osmosis

is urea reabsorbed

significant amount. conc of urea in filtrate higher than in caps causing urea to diffuse from filtrate back into blood.

how are salts and water reabs

filtrate drips thru loop of henle, necessary salts reabs back into blood by diffusion and water follows by osmosis and is reabsorbed

water also from colelcting duct in diff amts depending on how much water body needs at that time.

osmoregulation

control of water potential of body fluids, key part of homeostasis

what is involved in osmoregulation

specialised sensory neurones known as osmoreceptors which monitor wp of blood (found in hypothalamus)

what do osmoreceptors do

• detect a decrease in wp of blood

• nerve impulses sent along sensory neurones to posterior pituitary gland (below hypothal)

• stimulate posterior pithuitary gland to release antidiuretic hormone (ADH)

• adh enters blood and travels through body

• adh causes kidneys to reabsorb more water

• reduces loss of water in urine

effect of adh on the kidneys

• water reabsorbed by osmosis from filtrate in nephron

• reabs occurs as filtrate passes thru structures known as collecting ducts

• adh causes luminal membs - those facing lumen of nephron- of collecting duct cells to become more permeable to water

• adh does this by causing increase in no. aquaporins (water-permeable) in the luminal membranes of collecting duct cells

• as the filtrate in nephron travels along the collecting duct, water move from collecting duct (high wp) through aquaporins into tissue fluid and blood plasma in medulla (low wp)

• as filtrate in colelcting duct loses water it becomes more concentrated

• small vol of concentrated urine is produced. flows from kidneys thru ureters and into bladder

how does adh cause increase in no. aquaporins

• collecting duct cells contain vesicles, teh membs of which contain many aquaporins

• adh mols bind to receptor proteins activating signalling cascade that leads to phosphorylation of aquaporin mols

• aquaporins activated = vesicles fuse with the luminalmembs of collecting duct cells

• increases perm of membrane to water

what happens if wp of blood too high

• osmoreceptors in hypothalamus not stimulated

• no nerve impulses sent to posterior pituitary gland

• no adh released

• aquaporins moved out of luminal membranes of collecting duct cells

• collecting diuict cells are no longer permeable to water

• filtrate flows along collecting duct but loses no water as is very dilute

• large vol of dilute urine produced

• flows from kdineys through ureters and into bladder

why may cells not be able to function normally for resp

conc of glucoise in blood decreases below certain level so cells may not have enough glulcose for respirationwhy

why is it bad if conc of gluciose in blood increases above certain level

disrupts normal function of cells potentially causing major problems

what is blood glucose conc controlled by

2 hormones secreted by endocrine tissue in the pancrease made up of group cells = islets of Langerhans

2 cell types of islets of langerhans

• alpha cells that secrete hormone glucagon

• beta cells that secrete hormone insulin

what do alpha and beta cells do

act as receptors and initiate response for controlling blood glucose conc (cell signalling)

what do alpha and beta cells in pancrease do if decrease in blood glucoe conc occurs

• they detect it

• alpha secretes glucagon

• beta stops the secreting of insulin

decrease of insulin conc and increase of glucagon conc effect

• less insulin = reduces use of glucose by liver and muscle cells

• glucagon binds to receptors in cell surface membranes of liver cells

• binding causes conformational change in receptor protein that activates a g protein

• activated g protein activates enzyme adenylyl cyclase

• active adenylyl cyclase catalyses conversion of atp to second messenger = cyclic AMP

• cAMP binds to protein kinase A enzymes, activating them

• active protein kinase A enzymes activate phosphorylase kinase enzymes by adding phosphate groups to them

• active phosphorylase kinase enzymes activate glycogen phosphorylase enzymes

• active glycogen phosphorylase enzymems catalyse breakdown of glycogen to glucose (glycogenolysis)

• amplifies og signal from glucagon and = extra glucose released by liver to increase blood glucose conc to normal level

what happens when blood glucose conc increases above normal range

• detected by beta cells in pancrease

• conc of glucose is high glucose mols enter beta cells by facilitated diffusion

• cells respire glucose and produce atp

• high conc atp causes potassium channels in beta cells to close producing change in membrane potential

• this change in memb potential causes voltage-gated calcium cahnnels to open

• influx of calcium ions so beta cells secrete insuline (insulin containing veiscles move towards csm where release insuiln into caps

• once in blood insulin circulates around body

• stimulates uptake of glucose by muscle cells fat cells and liver

what does insulin do

• increase of uptake of glucose into target cells by binding to sepcific receptors on membranes of these target cells which stimulates the cells to add more glucose transporter proteins to their csm increasing the permeability of the cells to glucose

target cells of insuilin

muscle cells, fat storage cells, adipose tissue, liver cells (all have specific insulin receptors on csm)

glucose transporter proteins

glut proteins

when are glut proteins added

(high blood sugar) when insulin binds to surface receptors, vesicles move to csm and fuse iwth it

when are glut proteins stored

when blood glucose lvls are low, they are stored inside the membranes of vesicles

why does rate of facilitated diffusion of glucose into target cells increase

bc of increased glut proteins

what enzymes do insulin activate and what do they do

• glucokinase - phosphorylates gluciose, trapping it inside cells

• glycogemn synthase - glycogen synthase converts glucose into glycogen in a process knwon as glycogeneiss

what is blood glucose conc reguilated by

negative feedback control mechanisms

what is the pattern for negative feedback systems:

• recepetors detect whether specific level is too low ro too high

• this info communicated thru hormonal or nervous system to effectors

• effectors react to counteract change by bringing level back to normal

conntrol of blood glucose conc as negative feedback

• alpha and beta cells in pancrease act as receptors

• release hormones glucagong secreted by alpha cells and insulin secreted by beta cells

• liver cells act as the effectors in response to glucagon and liver, muscle and fat cells act as the effectors in response to insulin

diabetes

people can’t control their blood glucose conc to remain within normal safe limits

indicator of diabetes

glucose in urine.

if blood conc increases above renal threshold…

not all glucose from filtrate in pct reabsorbed and some left in urine = presence of glucose in urine

what can test for presence of conc of glucose in urine

test strips

what is the test strip made up of

2 enzymes immobilised on small pad at one end of test strip:

• glucose oxidase

• peroxidase