6. responding to changes in environment P2 Flashcards
1
Q
SURVIVAL AND RESPONSE
explain why plants show positive phototropism
A
- IAA diffuses to shaded side of shoot tip.
- as IAA diffuses down shaded side, it causes active transport of H+ ions into the cell wall
- disruption to H-bonds between cellulose molecules and action of expansions make cell more permeable to water
- cells on shaded side elongate faster due to higher turgor pressure
- shoot bends toward light
2
Q
SURVIVAL AND RESPONSE
explain why roots show positive gravitropism
A
- gravity causes IAA to accumulate on lower side of root
- IAA inhibits elongation of root cells
- cells on upper side of root elongate faster, so the root top bends downwards
3
Q
SURVIVAL AND RESPONSE
define taxis and kinesis
A
taxis: directional movement in response to external stimulus
kinesis: non- directional response to presence and intensity of external stimulus
4
Q
SURVIVAL AND RESPONSE
state the advantage of taxis and kinesis
A
maintain mobile organism in optimum order environment e.g. to prevent dessication.
5
Q
SURVIVAL AND RESPONSE
many organisms respond to temperature and humidity via kinesis rather than taxis. why?
A
less directional stimuli; often no clear gradient from one extreme to the other
6
Q
SYNAPTIC TRANSMISSION
outline what happens in a simple reflex arc
A
receptor detects stimulus —> sensory neuron —> relay neurone in CNS coordinates response —> motor neurone —> response by effector
7
Q
SURVIVAL AND RESPONSE
give the advantages of a simple reflex
A
rapid response to potentially dangerous stimuli since only 3 neurones involved
doesn’t have to be learnt
8
Q
SURVIVAL AND RESPONSE
what features are common to all sensory receptors?
A
act as energy transducers which establish a generator potential
respond to specific stimuli
9
Q
SURVIVAL AND RESPONSE
what features are common to all sensory receptors?
A
act as energy transducers which establish a generator potential
respond to specific stimuli
10
Q
RECEPTORS
describe the basic structure of a Pacinian corpuscle
A
- single nerve fibre surrounded by layers of connective tissue which are separated by viscous gel and contained by a capsule
- stretch-mediated Na+ channels on plasma membrane
- capillary runs along base layer of tissue
11
Q
RECEPTORS
what stimulus does a Pacinian corpuscle respond to and how
A
pressure deforms membrane, causing stretch-mediated Na+ ion channels to open.
if the influx of Na+ raises membrane to threshold potential, a generator potential is produced.
action potential moves along sensory neuron.
12
Q
RECEPTORS
name the two types of receptor cell found in the retina
A
cone cells
rod cells
13
Q
RECEPTORS
where are rod and cone cells located in the retina?
A
Rod: evenly distributed around periphery but not central fovea
cone: mainly central fovea no photoreceptors at blind spot
14
Q
RECEPTORS
compare and contrast rod and cone cells
A
pigment
ROD - rhodopsin
CONE- iodopsin
visual acuity
ROD - many rod cells synapse with one bipolar neuron (low resolution)
CONE - one cone cell synapses with one bipolar neuron (high resolution)
colour sensitivity
ROD- monochromatic: all wavelengths of light detected
CONE - tricolour: red, blue, green wavelengths absorbed by different types of iodopsin
light sensitivity
ROD- very senstitive: spacial summation of subthreashold impulses
CONE- less sensitive: not involved in night vision
15
Q
RECEPTORS
outline the pathway of light from a photoreceptor to the brain
A
photoreceptor —> bipolar neurone —> ganglion cell of optic nerve —> brain
16
Q
RECEPTORS
The fovea of the eye of an eagle had a high density of cones. Explain how the fovea enables an eagle to see its pray in detail
A
high visual acuity as each cone is connected to a single neurone.
comes send separate sets of impulses to brain.
17
Q
RECEPTORS
The retina of an owl has a high density of rod cells, explain how this enables an owl to hunt its prey at night.
A
high visual sensitivity.
several rods connected to a single neurone.
enough neurotransmitter to reach threshold (spacial summation)
18
Q
RECEPTORS
explain how the resting potential of -70mV is maintained in the sensory neurone when no pressure is applied
A
membrane more permeable to potassium ions and less permeable to sodium ions.
sodium ions actively transported/pumped out and potassium ions in.
19
Q
RECEPTORS
explain how applying pressure to the Pacinian corpuscle produces changes in membrane potential
A
pressure causes membrane to become stretched/deformed
sodium ion channels in membrane open and sodium ions move in
greater the pressure, more channels open, more sodium ions enter.
20
Q
RECEPTORS
How would destruction of parts of the myelin sheath result in slower responses to stimuli?
A
Less/no saltatory conduction/ impulse unable to ‘jump’ from node to node.
more depolarisation over length.
21
Q
RECEPTORS
the membrane potential was the same whether medium or heavy pressure was applied. explain why
A
Threshold has been re wedged which causes maximum response (all or nothing principle)
22
Q
CONTROL OF HEART RATE
define myogenic
A
contraction of the heart is initiated within the muscle itself rather than by nerve impulses
23
Q
CONTROL OF HEART RATE
state the name and location of the two nodes involved in heart contraction
A
Sinoatrial node (SAN): within the wall of the right atrium
Atrioventricular node (AVN): near lower end of right atrium in the wall that separates the two atria.
24
Q
CONTROL OF HEART RATE
describe how heartbeats are initiated and coordinated
A
- SAN initiates a wave of depolarisation across both atria
- layer of fibrous, non-conducting tissue delays impulse (prevents it directly going to ventricles) while ventricles fill and valves close.
- impulses travel to AVN, down septum via bundle of His, which carries impulses to the Purkinje fibres.
- Purkinje fibres carry impulse from bottom of heart up both ventricles simultaneously, ventricles contract.
25
**CONTROL OF HEART RATE**
state the formula for cardiac output
cardiac output = stroke volume x heart rate
26
**CONTROL OF HEART RATE**
what is the autonomic nervous system?
system that controls involuntary actions of glands and muscles
2 subdivisions: sympathetic and parasympathetic
27
**CONTROL OF HEART RATE**
state the difference between sympathetic and parasympathetic nervous system
sympathetic involved in ‘fight or flight’ response. stimulates effectors to speed up activity
parasympathetic involved in ‘rest and digest’ response - normal resting conditions. inhibits effectors to slow down activity
28
**CONTROL OF HEART RATE**
name the receptors involved in changing heart rate and state their location pop
**baroreceptors:** detect changes in blood pressure, Carotid artery
**chemoreceptors**: detect changes in PH, e.g. due to an increase of CO2 conc), Carotid artery and aortic body
29
**CONTROL OF HEART RATE**
how does the body respond to an increase in blood pressure?
- Baroreceptors send more impulses to cardio-inhibitory centre in the medulla Oblongata
- more impulses to SAN via parasympathetic nervous system.
- stimulates release of acetylcholine, which decreases heart rate
30
**CONTROL OF HEART RATE**
how does the body respond to decrease in blood pressure?
- Baroreceptors send more impulses to cardioacceleratory centre in medulla oblongata
- more impulses to SAN via sympathetic nervous system
- stimulates release of noradrenaline, which increases heart rate and strength of contraction
31
**CONTROL OF HEART RATE**
how does the body respond to an increase in CO2 concentration?
- Chemoreceptors detect PH decrease and send more impulses to cardioacceleratory centre of medulla oblongata
- more impulses to SAN via sympathetic nervous system
- heart rate increases, so rate of blood flow to lungs increases, so rate of gas exchange increases and ventilation rate increases.
32
**CONTROL OF HEART RATE**
explain how AV valve maintains a unidirectional flow of blood
pressure in atrium is higher than in ventricle causing valve to open
pressure in ventricle is higher than in atrium causing valve to close
33
**CONTROL OF HEART RATE**
suggest how caffeine could account for the results of an increase in heart rate
more impulses/ APs along the sympathetic nervous system pathway to SAN increasing the heart rate
34
**CONTROL OF HEART RATE**
Exercise causes an increase in heart rate. Describe the role of receptors and the nervous system in this process [4]
Chemoreceptors detect a rise in CO2/ fall in PH.
sends impulses to medulla,
more impulses to SAN
by sympathetic nervous system.
OR
Baroreceptors detect rise in blood pressure, sends impulses to medulla, more impulses to san by parasympathetic pathway.
35
**CONTROL OF HEART RATE**
when the heart beats, both ventricles contract at the same time.
explain how this is coordinated in the heart after initiation of the heartbeat by the SAN.
electrical activity only through Bundle of His/ AVN
wave of electrical activity/impulses passes over both ventricles at the same time.
36
**CONTROL OF HEART RATE**
suggest why a syndrome causes heart rate irregularities
fewer impulses along sympathetic/parasympathetic nervous pathway from medulla to SAN.
37
**NERVOUS COORDINATION**
describe the general structure of a motor neurone
**cell body**- contains organelles and high proportion of RER
**dendrons** - branch into dentrites which carry impulses toward cell body
**axon**- long, unbranched fibre carries nerve impulses away from cell body
38
**NERVOUS COORDINATION**
describe the additional features of a myelinated motor neuron
**Schwann cells: **wrap around axon many times
**myelin sheath: **made from myelin-rich membranes of Schwann cells.
**nodes of ranvier**: very short gaps between neighbouring Schwann cells where there is no myelin sheath.
39
**NERVOUS COORDINATION**
name 3 processes Schwann cells are involved in
electrical insulation
phagocytosis
nerve regeneration
40
**NERVOUS COORDINATION**
how does an axon potential pass along an unmyelinated neuron?
- stimulus leads to an influx of Na+ ions. first section of membrane depolarises
- local electrical current cause sodium voltage-gated channels further along the membrane to open
- the section behind begins to repolarise
- sequential wave of depolarisation
41
**NERVOUS COORDINATION**
explain why myelinated axons conduct impulses faster than unmyelinated axons
saltatory conduction: impulse ‘jumps’ from one node of ranvier to another. Depolarisation cannot occur where myelin sheath acts as electrical insulator.
so impulse doesn’t travel along entire axon length.
42
**NERVOUS COORDINATION**
what is resting potential?
the voltage across neuron membrane when not stimulated: -70 mV
43
**NERVOUS COORDINATION**
how is resting potential established?
- membrane is more permeable to K+ than Na+
- sodium-potassium pump actively transports 3Na+ out of cell and 2K+ into cell
- establishes electrochemical gradient: cell contents more negative than extracellular environment
44
**NERVOUS COORDINATION**
name the stages in generating an action potential
1. depolarisation
2. Repolarisation
3. Hyperpolarisation
4. return to resting potential
45
**NERVOUS COORDINATION**
what happens during an action potential?
- a stimulus excites the neurone
- This causes voltage-gated Na+ ion channels to open on the axon
- Na+ moves in my f.diff
- this causes the inside of the neurone to become less negatively charged
46
**NERVOUS COORDINATION**
what happens during depolarisation?
a stimulus causes the facilitated diffusion of Na+ ions into cell down electrochemical gradient.
potential difference across the membrane becomes more positive
if the membrane reaches the threshold potential (-50mV), voltage gated Na+ ion channels open.
significant influx of Na+ ions reverses potential difference to +40mV.
47
**NERVOUS COORDINATION**
what happens during repolaristation?
voltage gated Na+ ion channels close and voltage -gated K+ ion channels open.
Facilitated diffusion of K+ ions out of cell down their electrochemical gradient.
the potential difference across the membrane (the neurone) becomes more negative
48
**NERVOUS COORDINATION**
what happens during hyperpolarisation?
an ‘overshoot’ - when K+ ions diffuse out and the p.d becomes more negative than the resting potential.
49
**NERVOUS COORDINATION**
what happens during the refractory period in hyperpolarisation?
no stimulus is large enough to raise the membrane potential to threshold.
voltage-gated K+ channels close and the sodium-potassium pump re-establishes resting potential.
50
**NERVOUS COORDINATION**
explain the importance of the refractory period
no action potentials can be generated in hyperpolarised sections of membrane
this ensures:
- a unidirectional impulse
- discrete impulses
- limits frequency of impulse transmission.
51
**NERVOUS COORDINATION**
what is the ‘all or nothing’ principle?
any stimulus that causes the membrane to reach threshold potential will generate an action potential.
All action potentials have the same magnitude. (larger stimulus won’t result in larger action potential)
52
**NERVOUS COORDINATION**
name the factors that affect the speed of conductance
- myelin sheath
- axon diameter
- temperature
53
**NERVOUS COORDINATION**
how does axon diameter affect the speed of conductance?
greater diameter = faster
less resistance to flow of ions (depolarisation and repolarisation)
less ‘leakage’ of ions (easier to maintain membrane potential)
54
**NERVOUS COORDINATION**
how does temperature affect the speed of conductance?
higher temp = faster
faster rate of diffusion (depolarisation and repolarisation)
faster rate of respiration (enzyme-controlled) = more ATP for active transport to re-establish resting potential
but temp too high- membrane proteins denature
55
**NERVOUS COORDINATION**
Explain how a resting potential is maintained across the axon membrane in a neurone
higher conc of potassium ions inside and higher concentration of sodium ions outside the neurone.
OR
potassium ions diffuse out and sodium ions diffuse in.
membrane is more permeable to potassium ions leaving than sodium ions entering
sodium ions are strictly transported out and potassium ions in
56
**NERVOUS COORDINATION**
Explain why the speed of transmission of impulses is after along a myelinated axon then along a non-myelinated axon.
Myelination provides electrical insulation in saltatory conduction.
in myelinated, depolarisation occurs at the nodes of ranvier.
in non-myelinated, depolarisation occurs along whole length of axon
57
**NERVOUS COORDINATION**
Explain why the resting potential of a neurone changes from -70mV to 0mV when a respiratory inhibited was added.
less ATP produced
less Active transport/sodium potassium pump inhibited
electrochemical gradient not maintained (same conc of sodium and potassium ions on either side of membrane)
58
**SYNAPTIC TRANSMISSION**
how can you detect the strength of a stimulus?
larger stimulus raises membrane to the threshold more quickly after hyperpolarisation due to greater frequency of impulses.
59
**SYNAPTIC TRANSMISSION**
what is the function of synapses?
electrical impulse cannot travel over junction between neurones
neurotransmitters send impulses between neurones/from neurones to effectors
new impulses can be initiated in several different neurones for multiple simultaneous responses
60
**SYNAPTIC TRANSMISSION**
describe the structure of a synapse
presynaptic neurone ends in synaptic knob: contains lots of mitochondria, ER and vesicles of neurotransmitter.
synaptic cleft: gap between neurones.
post synaptic neurone: has complementary receptors to
neurotransmitter.
61
**SYNAPTIC TRANSMISSION**
describe the sequence of events involved in transmission across a synapse
wave of depolarisation travels down presynaptic neurone, causing Ca+ channels to open and calcium ions entering.
This causes the synaptic vesicles to move towards and fuse with the presynaptic membrane and and release acetylcholine neurotransmitter which diffuses across synaptic cleft.
acetylcholine neurotransmitter attaches to receptors in postsynaptic membrane
sodium ions enter leading to depolarisation.
62
**SYNAPTIC TRANSMISSION**
explain why synaptic transmission is unidirectional
only presynaptic neurone contains vesicles of neurotransmitter and only postsynaptic membrane has complementary receptor.
therefore impulse always travels presynaptic —> postsynaptic
63
**SYNAPTIC TRANSMISSION**
define summation and name the two types
neurotransmitter from several sub-threshold impulses accumulates to generate action potential:
-temporal summation
-spacial summation
64
**SYNAPTIC TRANSMISSION**
what is the difference between temporal and spacial summation?
temporal: one presynaptic neuron releases neurotransmitter several times in quick succession
spacial: multiple presynaptic neurones release neurotransmitter
65
**SYNAPTIC TRANSMISSION**
what are Cholinergic synapses?
use acetylcholine as primary neurotransmitter.
Excitatory/ inhibitory.
located at:
- motor end plate (muscle contraction)
-preganglionic neurones (excitation)
- parasympathetic neurones (inhibition
e.g. of heart rate/ breathing rate)
66
**SYNAPTIC TRANSMISSION**
what happens to acetylcholine from the synaptic cleft?
- hydrolysis into acetyl and choline by acetylcholinesterase (AChE)
- acetyl and choline diffuse back into the presynaptic neurone
- ATP is used to reform acetylcholine for storage in vesicles
67
**SYNAPTIC TRANSMISSION**
explain the importance of AChE
prevents overstimulation of skeletal muscle cells
enables acetyl and choline to be recycled
68
**SYNAPTIC TRANSMISSION**
what happens in an inhibitory synapse?
neurotransmitter binds to and opens Cl- channels on postsynaptic membrane and triggers K+ channels to open.
Cl- moves in and K+ moves out via facilitated diffusion.
p.d. becomes more negative (hyperpolarisation)
69
**SYNAPTIC TRANSMISSION**
describe the structure of a neuromuscular junction
synaptic cleft between a presynaptic neuron and a skeletal muscle cell
70
**SYNAPTIC TRANSMISSION**
contrast a cholinergic synapse and a neuromuscular junction
_response_
**cholinergic:** Excitatory or inhibitory
**nmj:**always excitatory
_neurones involved_
**cholinergic:**motor, sensory or relay
**nmj:**only motor
_postsynaptic cell_
**Cholinergic:**another neuron
**nmJ:**skeletal muscle cell
_AChE location_
**cholinergic:** synaptic cleft
**nmj:** postsynaptic membrane
_Action potential_
**cholinergic:** new action potential produced
**nmj:** end of neural pathway
71
**SYNAPTIC TRANSMISSION**
how might drugs increase synaptic transmission?
- inhibit AChE
- Mimic shape of neurotransmitter
72
**SYNAPTIC TRANSMISSION**
how might drugs decrease synaptic transmission?
- inhibit release of neurotransmitter
- decrease permeability of postsynaptic membrane to
ions
- hyperpolarise postsynaptic membrane
73
**SYNAPTIC TRANSMISSION**
A neurotransmitter causes negatively changed chloride ions to enter postsynaptic neurones. Explain how this inhibits postsynaptic neurones.
The inside of postsynaptic neurone becomes more netative/hyperpolarised.
more sodium ions are required to reach threshold/ not enough sodium ions enter to reach threshold.
for depolarisation
74
**MUSCLES**
name the three types of muscle in the body and where they are located
**cardiac:** exclusively found in heart
**smooth:** walls of blood vessels and intestines
**skeletal:** attached to incompressible skeleton by tendons
75
**MUSCLES**
what does the phrase ‘antagonistic pair of muscles’ mean?
pairs of muscles pull in opposite directions to move bones around joints
as one contracts (agonist), the other relaxes (the antagonist)
76
**MUSCLES**
describe the gross structure of skeletal muscles
muscle cells are fused together to form bundles of parallel muscle fibres (myofibrils)
each bundle is surrounded by endomycium: loose connective tissue with many capillaries
77
**MUSCLES**
describe the microscopic structure of skeletal muscles
myofibrils: site of contraction
sarcoplasm: shared nuclei and cytoplasm with lots of mitochondria and ER.
sarcolemma: folds inwards towards sarcoplasm to form transverse (T) tubules.
T tubules are conductive and help carry electrical impulses throughout the sarcoplasm.
78
**MUSCLES**
describe the ultrastructure of a myofibril
Z-line: boundary between sarcomeres
I-band: only actin
A-band: both myosin and actin
H-zone: only myosin
79
**MUSCLES**
how does each band appear under an
optical microscope?
I band: light (actin only)
A band: dark (actin+myosin)
80
**MUSCLES**
How is muscle contraction stimulated?
Neuromuscular junction - wave of depolarisation leading to Ca+ channels to open and Ca+ to move in
causes vesicles to move towards and fuse with presynaptic membrane.
exocytosis of acetylcholine, which diffuses across synaptic cleft.
Acetylcholine binds to receptors on Na+ channel proteins on skeletal muscle cell membrane.
influx of Na+ = depolarisation.
81
**MUSCLES**
explain the role of Ca+ ions in muscle contraction
AP moves through T-tubules in the sarcoplasm = Ca2+ channels in sarcoplasmic reticulum open.
Ca2+ binds to troponin, causing a change in the shape of the troponin molecule.
the troponin pulls on tropomyosin which releases it from the action myosin binding site.
the myosin head is now free to bind to the actin-myosin binding site (forming actin-myosin cross bridge.
82
**MUSCLES**
outline the sliding filament theory
Myosin head with ADP attached forms cross bridge with actin.
during the power stroke, the myosin head changes shape and loses the ADP, pulling actin over myosin.
ATP attaches to myosin head, causing it to detach from actin.
ATP is hydrolysed into ADP and pi so that the myosin head can return to original position.
myosin attaches to actin further along the filament.
83
**MUSCLES**
how does sliding filament action cause a myofibril to shorten?
Myosin heads flex in opposite directions, so actin filaments are pulled towards each other.
Distance between adjacent sarcomere z lines shortens
84
**MUSCLES**
state 4 pieces of evidence that prove the sliding filament theory
H-zone narrows
I-band narrows
Z-lines get closer (sarcomere shortens)
A-zone remains the same width (proves that myosin filaments don’t shorten)
85
**MUSCLES**
what happens during muscle relaxation?
Ca2+ is actively transported back into ER
Tropomyosin once again blocks actin binding site
86
**MUSCLES**
explain the role of phosphocreatine in muscle contraction
it phosphorylates ADP directly to ATP when oxygen for aerobic respiration is limited (e.g. during vigorous exercise)
87
**MUSCLES**
where are slow and fast twitch muscle fibres found in the body?
slow - sites of sustained contraction, e.g. calf muscles.
fast - sites of short-term, rapid, powerful contractions, e.g. biceps
88
**MUSCLES**
explain the role of slow twitch and fast twitch muscle fibres
**slow twitch**- long-duration contraction; well adapted to aerobic respiration to prevent lactate buildup.
**fast twitch**- powerful, short-term contraction; well adapted to anaerobic respiration.
89
**MUSCLES**
explain the structure and properties of slow twitch muscle fibres
glycogen store: many terminal ends can be hydrolysed to release glucose for respiration
contain lots of myoglobin: higher affinity for oxygen than haemoglobin at lower partial pressures.
many mitochondria: aerobic respiration produces more ATP
surrounded by many blood vessels: high supply of oxygen and glucose.
90
**MUSCLES**
explain the structure and properties of fast- twitch muscle fibres
large store of photocreatine
more myosin filaments that are thicker
high conc of enzymes involved in anaerobic respiration
fewer blood vessels, mitochondria and myoglobin
91
**MUSCLES**
contrast slow-twitch and fast-twitch muscle fibres
**slow twitch** is darker in colour as it has higher concentrations of myoglobin **fast twitch** is lighter in colour as it contains less myoglobin and contains lots of glycogen which can be broken down to release ATP (need a lot as anaerobic resp produces little ATP)
**slow-twitch** - contract slowly, slow to fatigue, used for endurance, e.g. long distance running.
**fast-twitch** - contract quickly, fatigue quickly, used for short bursts of speed and powder, e.g. sprinting.
**slow twitch** - energy is released slowly from aerobic respiration
**fast twitch** - energy is released quickly through anaerobic respiration
**slow twitch** - lots of mitochondria to provide ATP and lots of blood vessels to reduce diffusion pathway for O2 and CO2.
**fast twitch** - few mitochondria and blood vessels
92
**MUSCLES**
use your knowledge of how myosin and acting interact to suggest how the myosin molecule moves the mitochondria towards the presynaptic membrane.
myosin head attaches to actin and bends/performs power stroke
this pulls mitochondria past/along the actin.
next myosin head attaches to actin and bends/performs power stroke
93
**MUSCLES**
suggest and explain one advantage of the movement of mitochondria towards the presynaptic membrane.
mitochondria support additional ATP
to move vesicles/ for active transport of ions
94
**MUSCLES**
Explain how a decrease in the concentration of calcium ions within muscles tissues could cause a decrease in the force of muscle contraction
less tropomyosin moved from binding site
less actin-myosin bridges formed
myosin head doesn’t move/ myosin doesn’t pull actin.
95
**MUSCLES**
explain the role of glycogen granules in skeletal muscles
store of glucose
provides ATP for respiration
96
**MUSCLES**
Suggest how low PH of skeletal muscle tissue can lead to a reduction in the ability of calcium ions to stimulate muscle contraction
Low PH changes shape of calcium ion receptors
fewer calcium ions bind to tropomyosin
fewer tropomyosin molecules move away
fewer binding sites on actin revealed, fewer cross-bridges can form.
97
**MUSCLES**
describe the rules of calcium ions and ATP in the contraction of a myofibril
calcium ions diffuse into myofibrils from sarcoplasmic reticulum.
calcium ions causes movement of tropomyosin on actin (when it binds)
this causes exposure of the binding sites on actin
Hydrolysis of ATP on muslin heads causes myosin heads to bend, which pulls actin molecules
attachment of a new ATP molecule to each myosin head causes myosin heads to detach from actin sites.
98
**MUSCLES**
what is the role of ATP in myofibril contraction?
reaction with ATP allows binding of myosin to actin
provides energy to move myosin head
99
**MUSCLES**
Give two ways in which ATP is a suitable energy source for cells to use
- releases relatively small amounts of energy
- phosphorylates other compounds, making them more reactive
- releases energy instantaneously
- can be rapidly re-synthesised
100
**HOMEOSTASIS**
what is homeostasis?
internal environment is maintained within set limits around an optimum.
101
**HOMEOSTASIS**
why is it important that core temperature remains stable?
maintain stable rate of enzyme-controlled reactions and prevent damage to membranes
temperature too low- enzyme and substrate molecules have insufficient kinetic energy.
temperature too high - enzymes denature.
102
**HOMEOSTASIS**
why is it important that blood PH remains stable?
maintain stable rate of enzyme-controlled reactions.
Acidic PH - H+ ions interact with H-bonds and ionic bonds in tertiary structure of enzyme which leads to the shape of the actin site changing, so no ES complexes.
103
**HOMEOSTASIS**
why is it important that blood glucose concentration remains stable?
maintain constant blood water potential: prevents osmotic lysis/ crenation of cells
maintain constant concentration of respiratory substrate: organisms maintains constant level of activity regardless of environmental conditions.
104
**HOMEOSTASIS**
define negative and positive feedback
**negative feedback**- self-regulatory mechanisms return internal environment to optimum when there is a fluctuation.
**positive feedback** - a fluctuation triggers changes that result in an even greater deviation from the normal level.
105
**HOMEOSTASIS**
outline the general stages involved in negative feedback
receptors detect deviation —> coordinator —> corrective mechanism by effector —> receptors detect that conditions have returns to normal.
106
**HOMEOSTASIS**
suggest why separate negative feedback mechanisms control fluctuations in different directions
provides more control, especially in case of ‘over correction’ which could lead to a deviation in the opposite direction from the original one.
107
**HOMEOSTASIS**
suggest why coordinators analyse several inputs from several receptors before sending an impulse to effectors
receptors may send conflicting information
optimum response may require multiple types of effector
108
**BLOOD GLUCOSE**
name the factors that affect blood glucose concentration
amount of carbohydrate digested
rate of glycogenolysis
rate of gluconeogenesis
109
**BLOOD GLUCOSE**
define glycogenesis
liver converts glucose into the storage polymer glycogen.
110
**BLOOD GLUCOSE**
define glycogenolysis
liver hydrolyses glycogen into glucose which can diffuse into blood
111
**BLOOD GLUCOSE**
define Gluconeogenesis
liver converts glycerol and amino acids into glucose.
112
**BLOOD GLUCOSE**
outline what happens when blood glucose concentration increases
- beta cells in the Islets of Langerhans secrete Insulin
- Insulin attaches to receptors on the surface of target cells (Liver and Muscle)
- This changes the tertiary structure of the channel proteins resulting in more glucose being absorbed by f.diff
- vesicles are activated which migrate and fuses with the cell membrane which leads to more channel proteins in the surface membrane, so more glucose is absorbed into the cell.
- Insulin activates enzymes that convert glucose to glycogen (glycogenesis)
- glucose can be transported into the cell through GLUT4 proteins
113
**BLOOD GLUCOSE**
outline what happens when blood glucose concentration decreases
- Alpha cells in the Islets of Langerhans secrete glucagon
- glucagon attaches to receptors in the surface of target cells (liver)
- this causes a protein to be activated into adenylate cyclase and to convert ATP into cAMP
- cAMP activates protein kinase which hydrolyses glycogen into glucose (glycogenolysis)
114
**BLOOD GLUCOSE**
outline the role of adrenaline when blood glucose concentration decreases
adrenal glands produce adrenaline which binds to surface receptors on liver cells and activates enzymes for glycogenolysis
glucose diffuses from liver into bloodstream
115
**BLOOD GLUCOSE**
how does insulin increase permeability of cells to glucose?
increases number of glucose channel proteins
triggers conformational change which opens glucose carrier proteins
116
**BLOOD GLUCOSE**
explain the causes of type 1 diabetes and how it can be controlled
body cannot produce insulin, e.g. due to autoimmune response which attacks b cells of islets of Langerhans
treat by injecting insulin
117
**BLOOD GLUCOSE**
explain the causes of type 2 diabetes and how it can be controlled
glycoprotein receptors are damaged or become less responsive to insulin
poor diet/ obesity
treat by controlling diet and exercise regime.
118
**BLOOD GLUCOSE**
name some signs and symptoms of diabetes
high blood glucose concentration
glucose in urine
sudden weight loss
blurred vision
119
**BLOOD GLUCOSE**
outline how colorimetry could be used to identify the glucose concentration in a sample
- Benedict’s test on solutions of known glucose concentration. Use colorimeter to record absorbance.
- plot calibration curve: absorbance (y-axis), glucose concentration (x-axis)
- Benedict’s test on unknown sample. Use calibration curve to read glucose concentration at its absorbance value.
120
**BLOOD GLUCOSE**
Using your knowledge of the kidney, explain why glucose is found in the urine of a person with untreated diabetes
high concentration of glucose in blood,
not all glucose is reabsorbed at the proximal convoluted tubule
carrier/ co-transport proteins are working at maximum rate
121
**BLOOD GLUCOSE**
describe the role of glucagon in gluconeogenesis
attaches to receptors on target cells and stimulates enzymes.
glycerol/amino acids into glucose
122
**BLOOD GLUCOSE**
explain how increasing a cells sensitivity to insulin will lower the blood glucose concentration
more insulin binds to receptors which stimulates the uptake of glucose by channel proteins/ GLUT 4
activates enzymes which convert glucose to glycogen
123
**BLOOD GLUCOSE**
Explain how inhibiting adenylate cyclase may help to lower the blood glucose concentration
less ATP is converted to cAMP
less protein kinase is activated
less glycogen is converted to glucose/ less glycogenolysis
124
**BLOOD GLUCOSE**
Give two reasons why pancreas transplants are not used for the treatment of type 2 diabetes
usually type 2 produces insulin still
receptors less responsive/sensitive to insulin or faulty insulin receptors
treated/controlled by diet/ exercise
125
**BLOOD GLUCOSE**
Give two ways in which people with type 1 diabetes control their blood glucose conc
- treat with insulin injections
- control diet or sugar intake
126
**BLOOD WATER POTENTIAL**
Define osmoregulation
control of blood water potential via homeostatic mechanisms
127
**BLOOD WATER POTENTIAL**
describe the gross structure of a kidney
**cortex** - outer region consists of Bowman’s capsules, convoluted tubules, blood vessels
**Medulla** - inner region, consists of collecting ducts, loops of henle, blood vessels
**renal pelvis** - collects urine into ureter
**ureter** - tube carries urine to bladder
**renal artery** - supplies kidneys with oxygenated blood
**renal vein** - returns deoxygenated blood from kidney to heart.
128
**BLOOD WATER POTENTIAL**
describe the structure of a nephron
Bowman’s capsule at start
proximal convoluted tubule (PCT)
Loop of Henle
Distal convoluted tubule (DCT)
collecting duct
129
**BLOOD WATER POTENTIAL**
describe the blood vessels associated with a nephron
wide afferent arteriole from renal artery forms glomorelus
narrow efferent arteriole
130
**BLOOD WATER POTENTIAL**
explain how glomerular filtrate is formed (ultrafiltration)
- blood enters glomerulus at high hydrostatic pressure.
- the efferent arteriole being narrower than the afferent helps maintain this high pressure.
- small molecules (water, urea, glucose, mineral ions) are forced out into the lumen of the nephron against osmotic gradient forming the glomerular filtrate.
- basement membrane acts as a filter. Blood cells and large molecules e.g. proteins remain in capillary
131
**BLOOD WATER POTENTIAL**
how are cells of the Bowman’s capsule adapted for ultrafiltration?
- fenestrations between epithelial cells of capillaries
- fluid can pass between and under folded membrane of podocytes.
132
**BLOOD WATER POTENTIAL**
briefly state what happens during selective reabsorption and where it occurs
useful molecules from glomerular filtrate e.g. glucose are reabsorbed into the blood
occurs in proximal convoluted tubule (PCT)
133
**BLOOD WATER POTENTIAL**
describe what happens during selective reabsorption
- Sodium is actively transported out of the cell by the Sodium/Potassium pump. It is carried away by the blood.
- Glucose and amino acids are passively taken up by cotransport with sodium into the epithelial cells.
- This lowers the water potential inside the epithelial cells and so water moves in by osmosis.
- Urea is also reabsorbed by diffusion up to dynamic equilibrium (not all)
- Glucose and amino acids leave the cell by facilitated diffusion and are reabsorbed into the blood.
- Water leaves the cell and moves back into the bloodstream by osmosis.
- Other mineral ions (e.g. K+) travel through the epithelial cell and into the blood by facilitated diffusion.
134
**BLOOD WATER POTENTIAL**
what happens in the loop of Henle?
- active transport of Na+ ions and Cl- out of ascending limb
- accumulation of Na+ ions in medulla decreases water potential.
- Water diffuses out the descending limb by osmosis (ascending limb is impermeable to water)
- water potential of filtrate decreases going down descending limb.
-
135
**BLOOD WATER POTENTIAL**
explain the role of the distal convoluted tubules (DCT)
reabsorption of water by osmosis and mineral ions by active transport
136
**BLOOD WATER POTENTIAL**
state the role of the collecting duct
reabsorption of water from filtrate into interstitial fluid via osmosis through aquaporins
what remains is transported to form urine
137
**BLOOD WATER POTENTIAL**
explain why it’s important to maintain an Na+ gradient
so the filtrate in collecting duct is always beside an area of interstitial fluid that has a lower WP
maintains water potential gradient for maximum reabsorption of water out of DCT/ collecting duct
138
**BLOOD WATER POTENTIAL**
describe the role of the hypothalamus in osmoregulation
Osmoreceptors in hypothalamus detect the osmotic pressure of blood.
Osmosis of water out of osmoreceptors causes them to shrink, which triggers the hypothalamus to produce more ADH. (low blood WP)
inhibits ADH production when blood WP is high (osmoreceptors swell)
139
**BLOOD WATER POTENTIAL**
explain the role of the pituitary gland in osmoregulation
stores and secretes the ADH produced by hypothalamus into the bloodstream
140
**BLOOD WATER POTENTIAL**
Explain the role of ADH in osmoregulation
1. makes cells lining the collecting duct more permeable to water:
- ADH binds to receptors on collecting duct
- This causes vesicles containing aquaporins to fuse with cell membrane.
2. makea cells lining collecting duct more permeable to urea:
- WP in interstitial fluid decreases
- more water is reabsorbed, leading to more concentrated urine
141
**BLOOD WATER POTENTIAL**
Suggest how a disorder that affects kidney glomeruli leads to high quantities of protein in their urine
- damages basement membrane
- proteins can pass into glomerular filtrate
142
**BLOOD WATER POTENTIAL**
describe how ultrafiltration occurs in glomerulus
high hydrostatic pressure leads to small substances (e.g. glucose, water, urea) passing through small pores in capillary endothelium and through basement membrane.
143
**BLOOD WATER POTENTIAL**
Explain why the concentration of filtrate in the loop of Henle increases then decreases.
Concentration rises in descending limb as sodium ions enter and water is lost
concentration falls in ascending limb as sodium ions are actively removed but water remains because it’s walls are impermeable to water
144
**BLOOD WATER POTENTIAL**
give the location of osmoreceptors in the body of a mammal
hypothalamus
145
**BLOOD WATER POTENTIAL**
When a person is dehydrated the cell volume of an osmoreceptor decreases. explain why
water pot of blood will decrease
water moves from osmoreceptors into blood by osmosis
146
**BLOOD WATER POTENTIAL**
Describe and explain how the secretion of ADH affects urine produced by the kidneys
permeability of membrane/cells to water is increases
more water leaves collecting duct
smaller volume of urine
urine becomes more concentrated
