ORGANISMS RESPOND TO CHANGES IN THEIR INTERNAL + EXTERNAL ENVIRONMENTS Flashcards
TOPIC 6
STIMULUS
change in internal or external environment
RESPONDING TO ENVIRONMENT HELPS ORGANISMS TO SURVIVE BY
.Animals respond to changes in external environment eg. Avoid harmful environments
.Animals respond to changes in their internal environment to maintain optimal conditions for internal chemical reactions
.Plants show tropisms to grow towards or away from stimuli
RECEPTORS
specialised cells or proteins in cell membranes which detect stimuli – they are specific to one type of stimulus
EFFECTOR
Cells which bring about response to stimulus
SENSORY NEURON
Transmit impulses from receptors to CNS or relay neurone
RELAY NEURON
Transmit impulses from sensory to motor neurones
MOTOR NEURON
Transmit impulses from CNS/relay to effectors
AUTONOMIC NERVOUS SYSTEM
controls unconscious activities eg. reflex responses and response of heart rate to changes in carbon dioxide concentration or pressure
DENDRTIES
Receive and carry impulses towards cell body
CELL BODY
Contains nucleus and granular cytoplasm containing ribosomes grouped together into Nissl granules for making neurotransmitter
AXON
Long, membrane covered cytoplasmic extension which generates action potentials and transmits impulses away from cell body-Has nerve endings which form synapses w/effector
SCHAWANN CELLS
Grow around axon forming myelin sheath around cell membrane
MYELIN SHEATH
electrically insulates neurone, speeding up transmission of impulse
NODES OF RAVNIER
Thin areas between Schwann cells causing gaps in myelin sheath important in speeding rate of transmission of impulse
EXAMPLES OF SIMPLE REFLEXES
.Blinking
.Contraction of pupils when exposed to light.
.Withdrawal of hands when one touches an hot object
.Sneeze reflex when nose is irritated
EXAMPLE OF REFLEX ARC: TOUCHING VERY HOT OBJECT
.Stimulus: hot object
.Receptor: temperature and pain receptors in skin
.Sensory neurone sends an impulse to spinal cord via dorsal root
.Relay neurone connects sensory neurone to motor neurone
.Motor neurone sends impulse to an effector via ventral root
.Effector: arm muscles that contract to move hand away
GIVE THE IMPORTANCE OF REFLEX ARC
1.Rapid
2.Protect against damage to body tissues
3.Do not have to be learnt
4.Help escape from predators
5.Enable homeostatic control
KINESIS
organisms movement is affected by non-directional stimulus eg. humidity
TAXIS
organisms move towards or away from directional stimulus eg. light
positive taxis-Whole organism moves towards favourable stimulus
negative taxis-whole organisms moves away from unfavourable stimulus
ADVANTAGES OF TAXIS + KINESIS TO ORGANISM
.Move them away from other organisms to reduce competition
.Move them away from predators/into better camouflage to avoid predators
.Prevent them from drying out
.Help them find mate
.Ensure organism remains near food source
RP10-EFFECT OF ENVIRONMENTAL VARIABLE USING WOODLICE
10 woodlice for 10 minutes
Dark and dry, dark and damp, light and dry, light and damp by using dark paper to block out to block out light on one half use wet paper towel to make area damp
TROPISM
Response of plants to stimuli via growth
can be positive-towards stimulus or negative-away from stimulus controlled by specific growth factors-IAA
PHOTOTROPISM
If shoot is exposed to an uneven light source, IAA is transported to more shaded part
positive phototropism-eg.leaves so that they can capture more light for photosynthesis
negative phototropism- roots to grow to soil
GRAVITROPISM
growth in response to direction of gravity
positive gravitropism-roots so that they grow into soil to absorb water and mineral ions
AUXINS
growth factors which stimulate growth of shoots by cell elongation-cause cell walls to become ‘loose and stretchy’ so cells elongate and become longer
HOW AUXINS WORK
1.Auxins stimulate proton pumps in cell membrane
2.Protons are pumped into cell wall and activate proteins called expansins
3.Expansins break some of hydrogen bonds between chains of cellulose
4.Cell walls become ‘loose and stretchy’
5. Potassium channels are stimulated and K+ move into cell, reducing water potential of cytoplasm
6.Water moves in by osmosis, increasing cell volume and causing cell to stretch and elongate IAA
IAA
Type of auxin controls cell elongation in shoots inhibits growth of cells in roots made in tips of roots / shoots can diffuse to other cells
HOW IAA WORKS
IAA moves to shaded parts of roots and shoots
increased IAA concentration causes cells in shaded side to elongate so shoot bends towards light
increases amount of light being absorbed for photosynthesis
root, an increased IAA concentration inhibits growth so root bends away from light
ensure roots stay underground and can absorb necessary molecules for growth
IAA EXPLAIN CURVATURE OF SHOOT
tip produces IAA
IAA diffuses
elongation of cells on one side
PHOTOTROPISM IN ROOTS
Root tip produces IAA
IAA concentration increases on lower darker side
IAA inhibits cell elongation root cells grow on lighter side root bends away from light negative phototropism
PHOTOTROPISM IN SHOOTS
Shoot tip produces IAA diffuses to other cells
IAA accumulates on shaded side of shoot
IAA stimulates cell elongation so plant bends towards light positive phototropism
GRAVITROPISM IN SHOOTS
Shoot tip produces IAA
IAA diffuses from upper side to lower side of shoot in response to gravity
IAA stimulates cell elongation so plant grows upwards
negative gravitropism
GRAVITROPISM IN ROOTS
Root tip produces IAA
IAA accumulates on lower side of root in response to gravity IAA inhibits cell elongation root bends down towards gravity and anchors plant positive gravitropism
DARWIN EXPERIMENT CONCLUSION
Light is stimulus and is detected by cells in tip of coleoptile whilst response is carried out by cells elsewhere
Tip of coleoptile ‘communicates’ w/rest of cells causing them to elongate
BOYSEN EXPERIMENT CONCLUSION
Distribution of chemical produced by tip is affected by stimulus of light- moves away from light and then diffuses downwards through rest of plant
Tip produces water-soluble chemical which diffuses through agar from where it is produced in tip to where it is used in lower regions of plant
PAAL EXPERIMENT CONCLUSION
Uneven distribution of chemical produced in tip of plant causes unequal elongation of shoot resulting in bending of shoot
Elongation occurs where there is more of chemical
WENT EXPERIMENT CONCLUSION
Tip of shoot produces IAA which diffuses downwards to other cells
greater concentration of IAA in agar block causes an increase in bending of shoot
IAA + GRAVITROPISM
IAA moves to underside of shoots and roots
Heavy organelles known as amyloplasts are dense and sink to bottom of roots-IAA is actively transported to area where amyloplasts are increasing concentration of IAA on underside of root
root high concentrations of IAA inhibits cell elongation so underside of root grows less than upper side
EXPLAIN UNEVEN DISTRIBUTION OF IAA CAUSE ROOT TO BEND
IAA bottom of root-IAA is high inhibit expansion
IAA top of root-IAA concentration low leads to expansion
DESCRIBE HOW HEARTBEAT IS INITIATED + COORDINATED
1.Sinoatrial node in right atrial wall initiates heartbeat by sending wave of electrical activity -causes atrial contraction
2.Excitation wave cannot pass into ventricular walls as it is blocked by thin layer of non conducting collagen tissue
3.Atrioventricular node at bottom of wall separating atria delays impulse, then relays impulse to septum between ventricles- allows atria to empty completely before ventricles contract
4.Bundle of His muscle fibres running through septum conduct impulse to apex of heart
5.Bundle branches into Purkyne tissue carry wave of excitation upwards through ventricle muscle from base
6.Ventricles contract simultaneously from base upwards, forcing blood up and out of ventricles
ROLE OF SAN
sends out electrical activity
imitates heartbeat
causes atrial contraction
ROLE OF AVN
separates atria-delay impulse + relays electrical impulse down bundle of HIS
ROLE OF PURKNYE FIBRES
carry wave of citation upwards through ventricle muscle from base
IMPORTANCE OF SHORT DELAY IN AVN
allow atria to empty
before ventricles contract
CHEMORECEPTORS
Located in carotid artery and aorta
responds to pH / CO2 concentration changes
BARORECEPTORS
Located in carotid artery and aorta
responds to pressure changes
HOW HIGH BLOOD PRESSURE CREATES RESPONSE TO HEART RATE
uses Baroreceptors -More impulses along parasympathetic neurones which secrete acetylcholine which bind to receptors on SAN effector is cardiac muscles -Heart rate slows to reduce blood pressure back to normal
HOW LOW BLOOD PRESSURE CREATES RESPONSE TO HEART RATE
uses Baroreceptors -More impulses along sympathetic neurones which secrete noradrenaline which bind to receptors on SAN effector is cardiac muscles -Heart rate speeds up to increase blood pressure back to normal
HOW HIGH BLOOD O2/LOW CO2/HIGH PH CREATES RESPONSE TO HEART RATE
uses Chemoreceptors -More impulses along parasympathetic neurones which secrete acetylcholine which bind to receptors on SAN effector is cardiac muscles -Heart rate slows to return O2/CO2/pH back to normal
HOW LOW BLOOD O2/HIGH CO2/LOW PH CREATES RESPONSE TO HEART RATE
uses Chemoreceptors -More impulses along sympathetic neurones which secrete noradrenaline which bind to receptors on SAN effector is cardiac muscles -Heart rate speeds up to return O2/CO2/pH back to normal
DESCRIBE ROLE OF RECEPTORS + NERVOUS SYSTEM IN INCREASE IN HEAERT RATE DURING EXERCISE
1.Chemoreceptors detect rise in CO2
2.Send impulses to medulla
3.More impulses to SAN
4.By sympathetic NS
RESTING POTENTIAL
1.Na/K pump pumps 3Na+ out and 2K+ in
2.Membrane is impermeable to Na + so Na + cannot diffuse back in + Na+ ions are closed at -70mV creating electrochemical gradient
3.membrane is slightly permeable to K + so some K + can diffuse out of axon-as K+ channels slightly open
4.Large negatively charged proteins contribute to less positive charge inside
ACTION POTENTIAL
1.stimulus causes an increase in sodium ions inside axon- inside of neurone becomes less negative and it begins depolarising- voltage increases
2.Action potential/Depolarisation- If potential difference reaches threshold potential, sodium ion channels open membrane is more permeable to sodium ions and sodium ions diffuse rapidly to neurone-makes charge inside neuron more positive
3.Repolarisation-sodium ion channels close and potassium ion channels open membrane is more permeable to potassium ions, potassium ions diffuse out of neurone down the potassium ion gradient-Loss of positive charges makes inside neurone more negative
4.Hyperpolarisation- Potassium ion channels are slow to close so too many potassium ions diffuse out of neurone-potential difference becomes more negative than resting potential
5.Resting potential-Sodium-potassium pump returns membrane to -70mV until there is another stimulus
VOLTAGE GATED NA+ ION CHANNEL
open at -55mV and close at +30/40 mV
VOLTAGE GATED K+ ION CHANNEL
open at +30/40 mV and start closing at -70 mV
ALL OR NOTHING PRINCIPLE
.If threshold potential is not reached, an action potential won’t fire
.action Potentials are always same size- bigger stimulus will cause an increase in frequency of action potentials not bigger action potential
IMPORTANCE OF HYPER-POLARISATION
inside of axon is more negative than resting potential it would require an even greater increase in sodium ion concentration to reach threshold potential-reduces chance of threshold being reached and means cell membrane cannot be excited again
REFRACTORY PERIOD
stubborn or resistant to process terms of action potentials and neurons, neuron is resistant to second action potential during refractory periods
refractory period includes repolarisation and hyper-polarisation stages
REFRACTORY PERIOD-NA+ IONS CANT OPEN
.Action potentials are discrete and do not overlap
.limit to frequency at which nerve impulse can be transmitted
.Action potentials are uni-directional
FACTORS THAT TRANSMISSION OF IMPULSE
myelination- Schwann cells produce myelin and electrically insulate axon-Action potentials can only occur at nodes of Ranvier, gaps in myelin, as ion channels are only located here and not in myelinated region
neurones cytoplasm conducts enough electrical charge to depolarise next node so impulse ‘jumps’ by ‘saltatory conduction’- increases speed of conduction
Increase in diameter of axon: less resistance to flow of ions in cytoplasm
Higher body temperature: Rate of diffusion of ions is faster-higher than 40oC, proteins begin to denature, and speed decreases
SYNAPSES
junctions between neurone and
.Receptor to trigger an action potential
.Neurone to trigger an action potential .Muscle cell to trigger contraction
.Gland cell to cause hormone to be secreted
Synapses use chemicals called neurotransmitters to transmit impulse
cholinergic synapse neurotransmitter is acetylcholine
SYNAPTIC TRANSMISSION
1.Action potential arrives at axon terminal, depolarisation causes presynaptic membrane to become more permeable to Ca2+ as voltage gated Ca2+ ion channels open and Ca2+ enters by diffusion
2.Synaptic vesicles fuse w/presynaptic membrane
3.Neurotransmitter released by exocytosis and diffuses across synaptic cleft
4.Neurotransmitter binds to receptors on post synaptic membrane causing Na+ channels to open on post synaptic membrane
5.Na+ diffuses in through channels and depolarise post synaptic membrane threshold is reached, an impulse is generated
RECYCLING OF NEUROTRASMITTER
neurotransmitter needs too quickly be removed from cleft so that it does not keep binding to receptors and stimulating post synaptic cell-main way to do this is to initially hydrolyse neurotransmitter so it is no longer complementary to receptors
neurotransmitter is broken down by enzymes eg. acetylcholine is broken down by acetylcholinesterase (AChE) and components are then reabsorbed into presynaptic neurone and later resynthesized
NEUROMUSULAR JUNCTIONS
neuromuscular junction is synapse between motor neurone and muscle cell-It is specialist type of excitatory cholinergic synapse-receptors on muscle cells are called nicotinic cholinergic receptors
post synaptic membrane has more acetylcholine receptors than other synapses – increasing chance of Na+ channels opening and causing depolarisation
postsynaptic membrane has lots of folds which store acetylcholinesterase
SIMILARITIES BETWEEN NEUROMUSCULAR JUNCTIONS + CHOLINERGIC SYNAPSES
.Neurotransmitters diffuse across cleft
.Neurotransmitters bind to receptors on post synaptic membrane causing Na+ to diffuse in
.axon returns to resting potential due to sodium potassium pump .Neurotransmitters are broken down by enzymes in cleft
DIFFERENCES BETWEEN NEUROMUSCULAR JUNCTIONS + CHOLINERGIC SYNAPSES
only excitatory VS can be both
action potential ends here VS another action potential may be generates along different neurone
neurones to muscles VS neurones to neurones or other effectors
only motor neurones VS immediate, motor + sensory neurones
receptors on membrane of muscle fibres VS receptors on membrane of post synaptic neurones
DESCRIBE HOW NEUROTRANSMITTER RELEASED INTO CLEFT
- Ca2+ channel to open
- Ca2+ enter by diffusion
- vesicle to fuses w/membrane
UNIDIRECTIONALITY OF SYNAPSE
impulse can only travel in one direction
Transmission across synapse is one-way because: vesicles of neurotransmitter are present only in presynaptic knob - receptors for neurotransmitters only in post-synaptic neurone
SUMMATION AT SYNAPSES
process where neurotransmitters released separately from multiple neurones/or at different times are summed together to produce response
Impulses arriving at synapse do not always result in impulses being generated in next neurone as there is threshold value-generation of an action potential depends on how much Na+ enters post synaptic neurone
SPATIAL SUMMATION
Several impulses from different presynaptic neurons arrive together, each release some neurotransmitters, enough binds, causing enough sodium ions to enter and reach threshold
TEMPORAL SUMMATION
Acetylcholine breaks down in few ms so several impulses in quick succession ensures enough neurotransmitter builds up in cleft to bind to post synaptic membrane and cause it to reach threshold potential neurotransmitter stays in synaptic cleft for long time as there is too much to break down quickly
Increased likelihood of depolarisation of post synaptic membrane
INHIBITION AT SYNAPSES
presynaptic neurones release neurotransmitters that stop impulses
eg. some neurotransmitters stimulate K+ channels to open so K+ flows out hyper-polarising neurone-neurotransmitters eg. GABA, cause chloride channels to open, stimulating Cl- to enter, hyper-polarising neurone
Hyper-polarisation means that more Na+ would be needed to reach threshold for depolarisation, reducing likelihood of an action potential being generated
Post synaptic neurones may have excitatory and inhibitory presynaptic neurones, therefore end result depends on which are stimulated
EXCITATORY
.Stimulate more neurotransmitter
.Mimic normal transmitter as same shape so more receptors are activated
.Inhibit breakdown of transmitter so bind to receptors for longer
.Block uptake back into presynaptic knob
.Increase number of receptors on post synaptic membrane
INHIBITORY
.Inhibit release of neurotransmitter
.prevent Ca2+ entry into presynaptic knob
.Prevent exocytosis release of transmitter from presynaptic knob
.Bind w/receptors on post synaptic membrane blocking them
PACINIAN CORPUSCLE
Receptor responds to pressure changes
occur deep in skin mainly in fingers and feet
sensory neurone wrapped w/layers of tissue
HOW PACINIAN CORPUSCLE WORKS
stimulated lamella become deformed and press on sensory neurone ending
Membrane of sensory neurone stretches causing stretch-mediated Sodium ion channels to open
Sodium ions diffuse to cell, depolarising it and creating generator potential
threshold is reached an action potential will be generated
PHOTORECEPTORS IN EYE
retina of eye contains photoreceptors which can detect light
part of retina opposite pupil is known as fovea – lens focuses light on this region, and it is therefore densely packed w/ photoreceptors
no photoreceptors in blind spot – this contains optic nerve, where sensory neurones converge and carry impulses out of eye to brain
amount of light entering eye is controlled by reflex reaction that changes size of pupil by regulating size of surrounding iris
size of pupil is changed using two antagonistic muscles called radial muscle and circular muscle
PHOTORECEPTORS RESPOND TO LIGHT
1.Light enters eye and hits photoreceptors
2.Light-sensitive pigments in membranes absorb light, causing them to become bleached and break down
3.breakdown of pigments causes cascade of reactions which results in sodium ion channels opening and membrane permeability to sodium ions increasing
4.Sodium ions diffuse in causing generator potential to be created, and if threshold potential is reached, an action potential is generated and transmitted to bipolar neurone and then to sensory neurone
5.impulse is transmitted to the optic nerve, which takes impulse to brain
GENERATOR POTENTAIL
1.stimulus causes membrane of receptor to become more permeable to Na+ how this occurs depends upon type of receptor
2.Sodium ions diffuse down their gradient to receptor causing inside of receptor to become more positive– this change in potential difference due to stimulus is called generator potential
3.If change reaches threshold potential, an action potential is triggered, voltage gated Na+ channels open, Na+ diffuses in causing depolarisation
ROD CELLS
Concentrated at periphery of retina
contains rhodopsin pigment connected in groups to one bipolar cell
do not detect colour
CONE CELLS
Concentrated on fovea fewer at periphery of retina 3 types of cones containing different iodopsin pigments one cone connects to one neurone
detect coloured light
CONE VS ROD CELLS
higher visual acuity VS lower visual acuity
colour vision VS monochromatic vision
less sensitive to light VS more sensitive to light
VISUAL ACUITY
Ability to distinguish between separate sources of light-higher visual acuity means more detailed, focused vision
WHY CONES GIVE COLOUR VISION
3 types of cone cells w/different optical pigments-absorb different wavelengths of light red-sensitive, green-sensitive and blue-sensitive cones stimulation of different proportions of cones gives greater range of colour perception
WHY RODS HAVE MONOCHROMATIC VISION
One type of rod cell
one pigment
WHY CONES HAVE HIGH VISUAL ACUITY
One cone joins to one neurone 2 adjacent cones are stimulated, brain receives 2 impulses can distinguish between separate sources of light
WHY RODS HAVE LOW VISUAL ACUITY
connected in groups to one bipolar cell
retinal convergence
spatial summation
many neurones only generate 1 impulse-cannot distinguish between separate sources of light
WHY RODS HAVE HIGH LIGHT SENSITIVITY
Rods are connected in groups to one bipolar cell
retinal convergence
spatial summation
stimulation of each individual- cell alone is sub-threshold but because rods are connected in groups more likely threshold potential is reached
WHY CONES HAVE LOW LIGHT SENSITIVITY
One cone joins to one neurone no spatial summation
higher light intensity required to reach threshold potential
WHY ROD CELL SYNAPSES W/SAME BIPOLAR CELLS
prevents brain from being able to accurately determine direction from which light was shining exact stimulated receptor cannot be determined as same bipolar cell would be stimulated no matter which receptor generated action potential-mean that rod cells exhibit spatial summation w/bipolar cell
allows low levels of light to result in enough neurotransmitter being released by all rod cells together to trigger an action potential in bipolar cell
make rods able to send impulses in low light levels – they are very sensitive to light
WHY CONE CELLS SYNAPSE W/ONE BIPOLAR CELLS
allows brain to determine exact direct of light as only one cone cell could lead to an action potential in specific area of retina-are in high concentration in fovea this makes this region of retina area w/highest visual acuity
As there is one to one relationship each cone cell must release enough neurotransmitter alone to trigger an action potential in the bipolar cell
means there must be large enough stimulus to trigger high frequency of action potentials in cone cell to build up enough neurotransmitter in cleft to trigger an action potential at post synaptic membrane
means that for cone cells to transmit impulses to brain there must be high level of light-why cone cells have a low sensitivity to light
also why colour vision is diminished in low light conditions because light stimulus is too low to cause propagation of an impulse from cone cells
SKELETAL MUSCULES ACT IN ANAGOSTIC PAIRS
.Skeletal bones are attached to muscles by tendons
.bones are incompressible they act as levers
.Muscles contract and relax in antagonistic pairs to move bones at joint
AGONIST
contracting muscle
ANTAGONIST
relaxing muscle
STRUCTURE OF SKELETAL MUSCLES
.Sarcolemma: cell membrane
.Sarcoplasm: cytoplasm
.T-tubules: inward folds of sarcolemma to help spread electrical impulse throughout sarcoplasm
.Sarcoplasmic reticulum: network of internal membranes throughout sarcoplasm to store and release Ca2+ ions needed for contraction
.Lots of Mitochondria: lots present to provide more ATP for contraction
.Many nuclei: Muscle fibres are multinucleate due to very long length of muscle fibres and allows proteins to produced at any point in cell
.Myofibril: long cylindrical organelles made of proteins, highly specialized for contraction
ACTIN FILAMENT
.made of bundle of actin proteins
.Surrounded by a different protein: tropomyosin
.Many myosin binding sites beneath tropomyosin
.calcium binding sites – important for muscle contraction
.relaxed tropomyosin covers myosin binding sites on actin
MYOSIN FILAMENT
.Made of bundle of myosin molecules
.consists of many “heads” that protrude from surface
.myosin heads point in different directions
WHAT MYODIN CONSIST OF
.ATPase
.Actin binding site
.ATP binding site
heads can move backwards and forwards
myosin and actin filaments are arranged in overlapping units known as sarcomeres
Interaction of these filaments is what causes muscle contraction
MYOFIBRIL STRUCTURE
.Myosin: thick protein myofilament-Forms dark band: A-band: length of myosin
.Actin: thin protein myofilament- Forms light band: I-band: only actin
.Sarcomere: Unit between Z-lines
.M-line: middle of sarcomere, middle of myosin
.H-zone: only myosin
MUSCLE CONTRACTION
.Sarcomere gets shorter: as Z-lines closer to each other
.H-zone gets shorter: more overlap, so less myosin only area
.I-band gets shorter: more overlap, so less actin only area
SLIDING FILAMENT THEORY
1.Muscle cell surface membrane is depolarised, causing calcium ion channels on sarcoplasmic reticulum to open
2.Ca2+ diffuse from sarcoplasmic reticulum into sarcoplasm and then to myofibril
3.Ca2+ bind to calcium binding sites
4.causes tropomyosin to move/change position, exposing myosin binding sites on actin
5.Myosin heads bind to myosin binding sites on actin forming actinomyosin bridge
6.formation of bridges causes myosin heads to spontaneously bend pulling actin filaments towards centre of sarcomere in rowing motion
7.ATP binds to the head, breaking actinomyosin bridge and detaching myosin from actin filament
8.Ca2+ activate ATPase in head, resulting in ATP being hydrolysed to ADP and Pi, releasing energy that moves myosin head back to its original position
9.head is ready to reattach to different binding site and repeat process
ROLE OF ATP
.Hydrolysis of ATP is required for movements of myosin heads allowing them to form actinomyosin bridges
.Binding of ATP breaks actinomyosin bridge, allowing another to be formed further along actin
.Energy from ATP required for active transport of Ca2+ back into sarcoplasmic reticulum
AEROBIC RESPIRATION
Most ATP is generated by stage of aerobic respiration called oxidative phosphorylation-requires at least 2 stages prior to it to generate lots of ATP- occurs in mitochondria, but this takes comparatively longer period of time
ANAEROBIC RESIRATION
ATP made rapidly by one stage called glycolysis-animal cells it creates waste product called lactate which builds up and causes muscle fatigue Anaerobic respiration takes place in cellular cytoplasm and not in mitochondria
ATP-PHOSPHCREATINE
ATP is made by phosphorylating ADP with phosphate from phosphocreatine-PCr is stored inside cells and generates ATP very quickly but runs out after few seconds
PCr system is anaerobic and alactic
SLOW TWITCH FIBRES
.Slow, less powerful contractions over long time
.Endurance work eg. marathon running, maintaining posture or calf muscle used to stand still
.More calcium ions and ATPase for rapid muscle contraction.
.Aerobic respiration-slower ATP production Therefore:
.Does not become fatigued or produce lactate
.large store of oxygen with myoglobin
.Lots of mitochondria
.Many blood vessels
.Less glycogen stores
.Less phosphocreatine stores.
FAST TWITCH FIBRES
.Fast, powerful contractions over short time
.Sprint work eg. Biceps muscle for weight-lifting
.Less calcium ions and ATPase
.Anaerobic respiration-faster ATP production
Therefore:
.Become fatigued quickly as it produces lactic acid
.Less myoglobin
.Less mitochondria
.Less blood vessels
.More glycogen stores
.More phosphocreatine stores
MYOGLOBIN
molecule which binds to oxygen in similar way as haemoglobin
has very high affinity for oxygen, only unloading its oxygen when partial pressure of oxygen in muscle is extremely low-t it acts as storage of oxygen, allowing muscle fibres to aerobically respire at low partial pressures of oxygen
HOMEOSTATISIS
Maintenance of constant internal environment via physiological control systems
control temperature, blood pH, blood glucose concentration and water potential within limits
HOW HOMEOSTASIS CONTROL TEMP,PH + BLOOD GLUCOSE
Core temperature: too high, then enzymes may become denatured- too low, then enzyme activity is reduced- Highest rate at optimum temperature
Blood pH: If too high or too low then enzymes may become denatured
Blood glucose concentration: Cells need glucose for respiratory substrate for energy Glucose concentration also affects water potential of blood-too high concentration, then water moves out of cells by osmosis and cells shrivel up
NEGATIVE FEEDBACK RESTORES SYSTEMS TO THEIR ORIGINAL LEVELS
Receptors: Detect when level is too high or low
Communication system: via nervous system or hormones
Effectors: counteract change bringing levels back to normal
POSITIVE FEEDBACK MECHANISMS AMPFIY CHANGE FROM NORMAL
.Effectors further increase level away from normal level
.Could be used to rapidly activate something eg. Blood clot: platelets become activated and release chemical after an injury- triggers more platelets to become activated to clot
GLYCOGENESIS
formation of glycogen from glucose
GLYCOGENOLYSIS
breakdown of glycogen to glucose
GLUCONEOGENSIS
formation of new glucose molecules from non-carbohydrates
PANCREASE
organ in digestive and endocrine system located in abdominal cavity behind stomach
ISLETS OF LANGERHANS
groups of pancreatic cells secreting insulin and glucagon
GLUCAGON
hormone released when blood sugar levels are too low
EATING + EXERCISE ON GLUCOSE BLOOD CONCENTRATION
cells need constant energy supply from glucose for respiration- Eating increases glucose levels and exercise increases respiration and glucose demand, resulting in decreased glucose levels
INSULIN LOWERING BLOOD GLUCOSE CONCENTRATION
.Secreted by beta cells of Islets of Langerhans
.Travels in blood to effectors where it binds to receptors on cell surface membrane
.increases permeability of muscle cell membranes to glucose by increasing number of GLUT4 channel proteins so cells take up more glucose by facilitated diffusion
.Insulin activates enzymes that convert glucose to glycogen in liver, which is stored
.Lipid formation is stimulated
.Cells store more glycogen as an energy source;
.Insulin also increases rate of respiration in muscle cells
GLUCAGON RAISING BLOOD GLUCOSE CONCETRATION
.Secreted by the alpha cells of the Islets of Langerhans
.Travel in the blood, to effectors where it binds to receptors on cell surface membrane
.activates enzymes that break down glycogen to glucose: glycogenolysis
.Activates enzymes that are involved in formation of glucose from glycerol and amino acids
.Decreases rate of respiration in cells
ADRENALINE RAISING BLOOD GLUCOSE CONCENTRATION
.Binding to receptors on liver cell membranes
.Activating glycogenolysis and inhibiting glycogenesis
.Activating glucagon secretion and inhibiting insulin secretion
ADRENALINE + GLUCAGON ACT BY SECOND MESSENGER
Adrenaline and glucagon are primary messengers-chemicals which trigger an internal response from cell without entering cell themselves- do this this they need chemical messengers within cell stimulating internal response – these are called second messengers
SECOND MESSENGER RESPONSE
.Glucagon/adrenaline bind to receptors on cell surface membrane
.activates enzyme adenylate cyclase to convert ATP into cyclic AMP
.cAMP activates an enzyme called protein kinase A -activates a cascade of reactions to breakdown glycogen into glucose
EXPLAIN HOW INHIBITING ADENYLATE CYCLASE LOWERS BLOOD GLUCOSE
1.less ATP covered to cAMP
2.less kinase activated
3.less glycogen converted to glucose
DIABETES
disease when blood glucose concentration cannot be controlled naturally
TYPE 1 DIABETES
Due to body being unable to produce insulin
starts in childhood autoimmune disease where beta cells attacked
treated using insulin injections
regularly and control simple carbohydrate intake
TYPE 2 DIABETES
Due to receptors in target cells losing responsiveness to insulin usually develops due to obesity and poor diet
treated by controlling diet and increasing exercise with insulin injections
EXPLAIN WHY PANCREAS TRANSPLANT WOULD BE SUITABLE TREATMENT FOR TYPE 2 DIABETES
- type 2 produces insulin
- cells less sensitive to insulin
- controlled by diet/exercise
RP11-DILUTION SERIES OF GLUCOSE SOLUTION
.Make dilution series of glucose using known concentration of glucose and water
.Test w/‘Quantitative Benedict’s solution’
more sugar less blue-more sugar, less absorbance w/colorimeter OR test w/ Benedict’s solution, remove precipitate and test absorbance of remaining solution
.Test unknowns w/Benedict using same volume of solutions and concentrations
of Benedicts solution-Read off
concentration from absorbance
FUNCTION OF KIDNEY
1.Removal of nitrogenous metabolic waste from body
2.Osmoregulation: maintaining balance of water and dissolved solutes
MACRO STRUCTURE OF KIDNEY
.Cortex
.Medulla
.Pelvis
NEPHRON
structure in kidney where blood is filtered, and useful substances are reabsorbed into blood
NEPHRON STRUCTURE
- glomerulus- filters small solutes from blood
- proximal convoluted tubule- reabsorbs ions, water and nutrients removes toxins and adjust filtrate PH
- defending loop of Henle- aquaporins allow water to pass from filtrate into interstitial
- ascending loop of henel- reabsorbs Na+ and Cl- from filtrate into interstitial fluid
- distal convoluted tubule- selectively secretes and absorbs different ions to maintain blood pH and electrolyte balance
- collecting duct- reabsorbs solutes and water from filtrate
OSMOREGULATION
Process of controlling water potential of blood controlled by hormones eg. antidiuretic hormone
SELECTIVE REABSORPTION
reabsorption of specific useful molecules back to blood e.g. glucose, water, salt ion but never urea
LOOP OF HENULE IN MEDULLA FOR REABSORPTION OF WATER
Reduces water potential of tissue fluid in medulla ascending limb is impermeable to water, preventing water moving out -Instead cells actively transport Na+ to tissue fluid of medulla, this reduces water potential of medulla, creating water potential gradient between filtrate and medulla
descending limb cells are permeable to water, as they contain protein channels called aquaporins, this means that water moves out of filtrate by osmosis down water potential gradient into medulla-water then moves from tissue fluid back into blood
ADAPTION OF LOOP HENULE
longer loop would lose more ions and create lower water potential in medulla than other organisms-creates steeper water potential gradient so more water is reabsorbed by osmosis from descending limb duct-organism would produce lower volume of urine w/higher concentration
shorter loop would lose less ions and create higher water potential in medulla than other organisms-reduces water potential gradient, so less water is reabsorbed by osmosis from descending limb duct-organism would produce higher volume of urine w/ lower concentration
HOW BOWMAN CAPSULE + GLOMERULUS ACTS AS MOLECULAR SIEVE
.Capillary endothelial wall has pores
.Pores in basement membrane forms filter between blood and nephron
.Podocytes create filtration slits on epithelial layer of capsule -molecular sieve separates molecules in blood by size: blood cells and large proteins stay in blood as they are too large, small molecules such as water, glucose, urea and salt ions pass through to Bowman’s Capsule as filtrate
DESCRIBE PROCESS OF ULTRAFILTRATION
1.high blood pressure
2.water + glucose passed out
3.through small gaps in capillary endothelium
4.through capillary basement membrane
SELECTIVE REABSORPTION OF USEFUL SUBSTANCES IN PROXIMAL CONVOLUTED TUBLE
ultrafiltration can only separate molecules by size, some useful small molecules are ‘lost’ from blood into filtrate- need to reabsorb back into the blood
Urea is toxic and must be excreted so reabsorption needs to be carefully selected so only targeted specific molecules are taken out of filtrate
WHAT IS ABSORBED IN PROXIMAL CONVOLUTED TUBLE
.All glucose and amino acids are reabsorbed by active transport
.Most of water is reabsorbed by osmosis
.Many salt ions are absorbed by facilitated diffusion and active transport
SELECTIVE REABSORPTION + DIABETES
Diabetes is categorised as chronic high concentration of glucose in blood-means more glucose is filtered out of blood and into filtrate during ultrafiltration- glucose is reabsorbed by cotransport number of cotransport proteins is limiting factor
If there is more glucose than there is co transport proteins, then all of glucose cannot be reabsorbed from filtrate back to blood-Some will remain in filtrate and be excreted in the urine
EXPLAIN WHY GLUCOSE IS FOUND IN URINE OF A PERSON W/UNTREATED DIABETES
1.High concentration of glucose in blood
2.Not all the glucose is absorbed at proximal convoluted tubule
3.Carrier proteins are working at maximum rate
INCREASE IN THICKNESS OF MEDULLA, INCREASES CONCENTRATION OF URINE
1.Thicker medulla means longer loop
2. increase in sodium ion concentration
sodium ion gradient maintained for longer
3. water potential gradient maintained so more water
OSMOREGULATION BY NEGATIVE FEEDBACK USING ADH
distal convoluted tubule and collecting duct have variable permeability which is subject to hormonal control by ADH
permeability is variable as number of aquaporins in their cell membrane can increase or decrease-change is controlled by hormone called ADH – Antidiuretic hormone
ADH makes walls of duct more permeable by causing more aquaporins to be inserted to membrane-result in more water being reabsorbed from filtrate and to medulla
DETECTOR
osmoreceptors in hypothalamus
Water potential of blood is detected- When water potential decreases, water moves out of osmoreceptors by osmosis which sends signal to posterior pituitary
COORDINATOR
posterior pituitary releases varying amounts of ADH into the blood
EFFECTOR
Cells in the collecting duct wall
ADH makes cells more permeable to water, so water enters medulla tissue fluid w/low water potential via osmosis and then blood
DEHYDRATED PERSON IN WATER CONTENT
1.lower water potential of blood is detected by osmoreceptors in hypothalamus
2.pituitary secretes more ADH to blood
3.Cells of collecting duct more permeable to water
4.More water reabsorbed from filtrate back to medulla then blood
5.Urine volume reduced, and concentration increased
