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
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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
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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

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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.

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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

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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

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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

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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

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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

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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
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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.

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12
Q

RECEPTORS

name the two types of receptor cell found in the retina

A

cone cells

rod cells

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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

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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

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15
Q

RECEPTORS

outline the pathway of light from a photoreceptor to the brain

A

photoreceptor —> bipolar neurone —> ganglion cell of optic nerve —> brain

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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.

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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)

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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.

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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.

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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.

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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)

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22
Q

CONTROL OF HEART RATE

define myogenic

A

contraction of the heart is initiated within the muscle itself rather than by nerve impulses

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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.

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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.
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25
Q

CONTROL OF HEART RATE

state the formula for cardiac output

A

cardiac output = stroke volume x heart rate

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26
Q

CONTROL OF HEART RATE

what is the autonomic nervous system?

A

system that controls involuntary actions of glands and muscles
2 subdivisions: sympathetic and parasympathetic

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27
Q

CONTROL OF HEART RATE

state the difference between sympathetic and parasympathetic nervous system

A

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

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28
Q

CONTROL OF HEART RATE

name the receptors involved in changing heart rate and state their location pop

A

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

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29
Q

CONTROL OF HEART RATE

how does the body respond to an increase in blood pressure?

A
  • 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
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30
Q

CONTROL OF HEART RATE

how does the body respond to decrease in blood pressure?

A
  • 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
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31
Q

CONTROL OF HEART RATE

how does the body respond to an increase in CO2 concentration?

A
  • 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.
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32
Q

CONTROL OF HEART RATE
explain how AV valve maintains a unidirectional flow of blood

A

pressure in atrium is higher than in ventricle causing valve to open

pressure in ventricle is higher than in atrium causing valve to close

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33
Q

CONTROL OF HEART RATE
suggest how caffeine could account for the results of an increase in heart rate

A

more impulses/ APs along the sympathetic nervous system pathway to SAN increasing the heart rate

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34
Q

CONTROL OF HEART RATE
Exercise causes an increase in heart rate. Describe the role of receptors and the nervous system in this process [4]

A

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.

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35
Q

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.

A

electrical activity only through Bundle of His/ AVN

wave of electrical activity/impulses passes over both ventricles at the same time.

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36
Q

CONTROL OF HEART RATE
suggest why a syndrome causes heart rate irregularities

A

fewer impulses along sympathetic/parasympathetic nervous pathway from medulla to SAN.

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37
Q

NERVOUS COORDINATION
describe the general structure of a motor neurone

A

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

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38
Q

NERVOUS COORDINATION

describe the additional features of a myelinated motor neuron

A

**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.

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39
Q

NERVOUS COORDINATION

name 3 processes Schwann cells are involved in

A

electrical insulation

phagocytosis

nerve regeneration

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40
Q

NERVOUS COORDINATION

how does an axon potential pass along an unmyelinated neuron?

A
  • 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
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41
Q

NERVOUS COORDINATION

explain why myelinated axons conduct impulses faster than unmyelinated axons

A

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.

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42
Q

NERVOUS COORDINATION

what is resting potential?

A

the voltage across neuron membrane when not stimulated: -70 mV

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43
Q

NERVOUS COORDINATION

how is resting potential established?

A
  • 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
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44
Q

NERVOUS COORDINATION

name the stages in generating an action potential

A
  1. depolarisation
  2. Repolarisation
  3. Hyperpolarisation
  4. return to resting potential
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45
Q

NERVOUS COORDINATION

what happens during an action potential?

A
  • 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
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46
Q

NERVOUS COORDINATION

what happens during depolarisation?

A

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.

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47
Q

NERVOUS COORDINATION

what happens during repolaristation?

A

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

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48
Q

NERVOUS COORDINATION

what happens during hyperpolarisation?

A

an ‘overshoot’ - when K+ ions diffuse out and the p.d becomes more negative than the resting potential.

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49
Q

NERVOUS COORDINATION

what happens during the refractory period in hyperpolarisation?

A

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.

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50
Q

NERVOUS COORDINATION

explain the importance of the refractory period

A

no action potentials can be generated in hyperpolarised sections of membrane

this ensures:
- a unidirectional impulse
- discrete impulses
- limits frequency of impulse transmission.

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51
Q

NERVOUS COORDINATION

what is the ‘all or nothing’ principle?

A

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)

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52
Q

NERVOUS COORDINATION

name the factors that affect the speed of conductance

A
  • myelin sheath
  • axon diameter
  • temperature
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53
Q

NERVOUS COORDINATION

how does axon diameter affect the speed of conductance?

A

greater diameter = faster

less resistance to flow of ions (depolarisation and repolarisation)

less ‘leakage’ of ions (easier to maintain membrane potential)

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54
Q

NERVOUS COORDINATION

how does temperature affect the speed of conductance?

A

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

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55
Q

NERVOUS COORDINATION
Explain how a resting potential is maintained across the axon membrane in a neurone

A

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

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56
Q

NERVOUS COORDINATION
Explain why the speed of transmission of impulses is after along a myelinated axon then along a non-myelinated axon.

A

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

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57
Q

NERVOUS COORDINATION
Explain why the resting potential of a neurone changes from -70mV to 0mV when a respiratory inhibited was added.

A

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)

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58
Q

SYNAPTIC TRANSMISSION
how can you detect the strength of a stimulus?

A

larger stimulus raises membrane to the threshold more quickly after hyperpolarisation due to greater frequency of impulses.

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59
Q

SYNAPTIC TRANSMISSION

what is the function of synapses?

A

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
Q

SYNAPTIC TRANSMISSION

describe the structure of a synapse

A

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
Q

SYNAPTIC TRANSMISSION

describe the sequence of events involved in transmission across a synapse

A

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
Q

SYNAPTIC TRANSMISSION

explain why synaptic transmission is unidirectional

A

only presynaptic neurone contains vesicles of neurotransmitter and only postsynaptic membrane has complementary receptor.

therefore impulse always travels presynaptic —> postsynaptic

63
Q

SYNAPTIC TRANSMISSION

define summation and name the two types

A

neurotransmitter from several sub-threshold impulses accumulates to generate action potential:

-temporal summation
-spacial summation

64
Q

SYNAPTIC TRANSMISSION

what is the difference between temporal and spacial summation?

A

temporal: one presynaptic neuron releases neurotransmitter several times in quick succession

spacial: multiple presynaptic neurones release neurotransmitter

65
Q

SYNAPTIC TRANSMISSION
what are Cholinergic synapses?

A

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
Q

SYNAPTIC TRANSMISSION
what happens to acetylcholine from the synaptic cleft?

A
  • 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
Q

SYNAPTIC TRANSMISSION

explain the importance of AChE

A

prevents overstimulation of skeletal muscle cells

enables acetyl and choline to be recycled

68
Q

SYNAPTIC TRANSMISSION
what happens in an inhibitory synapse?

A

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
Q

SYNAPTIC TRANSMISSION
describe the structure of a neuromuscular junction

A

synaptic cleft between a presynaptic neuron and a skeletal muscle cell

70
Q

SYNAPTIC TRANSMISSION
contrast a cholinergic synapse and a neuromuscular junction

A

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
Q

SYNAPTIC TRANSMISSION
how might drugs increase synaptic transmission?

A
  • inhibit AChE
  • Mimic shape of neurotransmitter
72
Q

SYNAPTIC TRANSMISSION

how might drugs decrease synaptic transmission?

A
  • inhibit release of neurotransmitter
  • decrease permeability of postsynaptic membrane to
    ions
  • hyperpolarise postsynaptic membrane
73
Q

SYNAPTIC TRANSMISSION
A neurotransmitter causes negatively changed chloride ions to enter postsynaptic neurones. Explain how this inhibits postsynaptic neurones.

A

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
Q

MUSCLES
name the three types of muscle in the body and where they are located

A

cardiac: exclusively found in heart

smooth: walls of blood vessels and intestines

skeletal: attached to incompressible skeleton by tendons

75
Q

MUSCLES

what does the phrase ‘antagonistic pair of muscles’ mean?

A

pairs of muscles pull in opposite directions to move bones around joints

as one contracts (agonist), the other relaxes (the antagonist)

76
Q

MUSCLES
describe the gross structure of skeletal muscles

A

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
Q

MUSCLES
describe the microscopic structure of skeletal muscles

A

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
Q

MUSCLES
describe the ultrastructure of a myofibril

A

Z-line: boundary between sarcomeres

I-band: only actin

A-band: both myosin and actin

H-zone: only myosin

79
Q

MUSCLES
how does each band appear under an
optical microscope?

A

I band: light (actin only)
A band: dark (actin+myosin)

80
Q

MUSCLES
How is muscle contraction stimulated?

A

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
Q

MUSCLES
explain the role of Ca+ ions in muscle contraction

A

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
Q

MUSCLES
outline the sliding filament theory

A

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
Q

MUSCLES
how does sliding filament action cause a myofibril to shorten?

A

Myosin heads flex in opposite directions, so actin filaments are pulled towards each other.

Distance between adjacent sarcomere z lines shortens

84
Q

MUSCLES
state 4 pieces of evidence that prove the sliding filament theory

A

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
Q

MUSCLES
what happens during muscle relaxation?

A

Ca2+ is actively transported back into ER

Tropomyosin once again blocks actin binding site

86
Q

MUSCLES
explain the role of phosphocreatine in muscle contraction

A

it phosphorylates ADP directly to ATP when oxygen for aerobic respiration is limited (e.g. during vigorous exercise)

87
Q

MUSCLES
where are slow and fast twitch muscle fibres found in the body?

A

slow - sites of sustained contraction, e.g. calf muscles.

fast - sites of short-term, rapid, powerful contractions, e.g. biceps

88
Q

MUSCLES
explain the role of slow twitch and fast twitch muscle fibres

A

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
Q

MUSCLES
explain the structure and properties of slow twitch muscle fibres

A

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
Q

MUSCLES
explain the structure and properties of fast- twitch muscle fibres

A

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
Q

MUSCLES
contrast slow-twitch and fast-twitch muscle fibres

A

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
Q

MUSCLES
use your knowledge of how myosin and acting interact to suggest how the myosin molecule moves the mitochondria towards the presynaptic membrane.

A

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
Q

MUSCLES
suggest and explain one advantage of the movement of mitochondria towards the presynaptic membrane.

A

mitochondria support additional ATP

to move vesicles/ for active transport of ions

94
Q

MUSCLES
Explain how a decrease in the concentration of calcium ions within muscles tissues could cause a decrease in the force of muscle contraction

A

less tropomyosin moved from binding site
less actin-myosin bridges formed

myosin head doesn’t move/ myosin doesn’t pull actin.

95
Q

MUSCLES
explain the role of glycogen granules in skeletal muscles

A

store of glucose

provides ATP for respiration

96
Q

MUSCLES
Suggest how low PH of skeletal muscle tissue can lead to a reduction in the ability of calcium ions to stimulate muscle contraction

A

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
Q

MUSCLES
describe the rules of calcium ions and ATP in the contraction of a myofibril

A

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
Q

MUSCLES
what is the role of ATP in myofibril contraction?

A

reaction with ATP allows binding of myosin to actin

provides energy to move myosin head

99
Q

MUSCLES
Give two ways in which ATP is a suitable energy source for cells to use

A
  • releases relatively small amounts of energy
  • phosphorylates other compounds, making them more reactive
  • releases energy instantaneously
  • can be rapidly re-synthesised
100
Q

HOMEOSTASIS
what is homeostasis?

A

internal environment is maintained within set limits around an optimum.

101
Q

HOMEOSTASIS
why is it important that core temperature remains stable?

A

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
Q

HOMEOSTASIS
why is it important that blood PH remains stable?

A

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
Q

HOMEOSTASIS
why is it important that blood glucose concentration remains stable?

A

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
Q

HOMEOSTASIS
define negative and positive feedback

A

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
Q

HOMEOSTASIS
outline the general stages involved in negative feedback

A

receptors detect deviation —> coordinator —> corrective mechanism by effector —> receptors detect that conditions have returns to normal.

106
Q

HOMEOSTASIS
suggest why separate negative feedback mechanisms control fluctuations in different directions

A

provides more control, especially in case of ‘over correction’ which could lead to a deviation in the opposite direction from the original one.

107
Q

HOMEOSTASIS
suggest why coordinators analyse several inputs from several receptors before sending an impulse to effectors

A

receptors may send conflicting information

optimum response may require multiple types of effector

108
Q

BLOOD GLUCOSE
name the factors that affect blood glucose concentration

A

amount of carbohydrate digested

rate of glycogenolysis

rate of gluconeogenesis

109
Q

BLOOD GLUCOSE
define glycogenesis

A

liver converts glucose into the storage polymer glycogen.

110
Q

BLOOD GLUCOSE
define glycogenolysis

A

liver hydrolyses glycogen into glucose which can diffuse into blood

111
Q

BLOOD GLUCOSE
define Gluconeogenesis

A

liver converts glycerol and amino acids into glucose.

112
Q

BLOOD GLUCOSE
outline what happens when blood glucose concentration increases

A
  • 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
Q

BLOOD GLUCOSE
outline what happens when blood glucose concentration decreases

A
  • 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
Q

BLOOD GLUCOSE
outline the role of adrenaline when blood glucose concentration decreases

A

adrenal glands produce adrenaline which binds to surface receptors on liver cells and activates enzymes for glycogenolysis

glucose diffuses from liver into bloodstream

115
Q

BLOOD GLUCOSE
how does insulin increase permeability of cells to glucose?

A

increases number of glucose channel proteins

triggers conformational change which opens glucose carrier proteins

116
Q

BLOOD GLUCOSE
explain the causes of type 1 diabetes and how it can be controlled

A

body cannot produce insulin, e.g. due to autoimmune response which attacks b cells of islets of Langerhans

treat by injecting insulin

117
Q

BLOOD GLUCOSE
explain the causes of type 2 diabetes and how it can be controlled

A

glycoprotein receptors are damaged or become less responsive to insulin

poor diet/ obesity

treat by controlling diet and exercise regime.

118
Q

BLOOD GLUCOSE
name some signs and symptoms of diabetes

A

high blood glucose concentration

glucose in urine

sudden weight loss

blurred vision

119
Q

BLOOD GLUCOSE
outline how colorimetry could be used to identify the glucose concentration in a sample

A
  • 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
Q

BLOOD GLUCOSE
Using your knowledge of the kidney, explain why glucose is found in the urine of a person with untreated diabetes

A

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
Q

BLOOD GLUCOSE
describe the role of glucagon in gluconeogenesis

A

attaches to receptors on target cells and stimulates enzymes.

glycerol/amino acids into glucose

122
Q

BLOOD GLUCOSE
explain how increasing a cells sensitivity to insulin will lower the blood glucose concentration

A

more insulin binds to receptors which stimulates the uptake of glucose by channel proteins/ GLUT 4

activates enzymes which convert glucose to glycogen

123
Q

BLOOD GLUCOSE
Explain how inhibiting adenylate cyclase may help to lower the blood glucose concentration

A

less ATP is converted to cAMP

less protein kinase is activated

less glycogen is converted to glucose/ less glycogenolysis

124
Q

BLOOD GLUCOSE
Give two reasons why pancreas transplants are not used for the treatment of type 2 diabetes

A

usually type 2 produces insulin still

receptors less responsive/sensitive to insulin or faulty insulin receptors

treated/controlled by diet/ exercise

125
Q

BLOOD GLUCOSE
Give two ways in which people with type 1 diabetes control their blood glucose conc

A
  • treat with insulin injections
  • control diet or sugar intake
126
Q

BLOOD WATER POTENTIAL
Define osmoregulation

A

control of blood water potential via homeostatic mechanisms

127
Q

BLOOD WATER POTENTIAL
describe the gross structure of a kidney

A

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
Q

BLOOD WATER POTENTIAL
describe the structure of a nephron

A

Bowman’s capsule at start

proximal convoluted tubule (PCT)

Loop of Henle

Distal convoluted tubule (DCT)

collecting duct

129
Q

BLOOD WATER POTENTIAL
describe the blood vessels associated with a nephron

A

wide afferent arteriole from renal artery forms glomorelus

narrow efferent arteriole

130
Q

BLOOD WATER POTENTIAL
explain how glomerular filtrate is formed (ultrafiltration)

A
  • 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
Q

BLOOD WATER POTENTIAL
how are cells of the Bowman’s capsule adapted for ultrafiltration?

A
  • fenestrations between epithelial cells of capillaries
  • fluid can pass between and under folded membrane of podocytes.
132
Q

BLOOD WATER POTENTIAL
briefly state what happens during selective reabsorption and where it occurs

A

useful molecules from glomerular filtrate e.g. glucose are reabsorbed into the blood

occurs in proximal convoluted tubule (PCT)

133
Q

BLOOD WATER POTENTIAL
describe what happens during selective reabsorption

A
  • 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
Q

BLOOD WATER POTENTIAL
what happens in the loop of Henle?

A
  • 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
Q

BLOOD WATER POTENTIAL
explain the role of the distal convoluted tubules (DCT)

A

reabsorption of water by osmosis and mineral ions by active transport

136
Q

BLOOD WATER POTENTIAL
state the role of the collecting duct

A

reabsorption of water from filtrate into interstitial fluid via osmosis through aquaporins

what remains is transported to form urine

137
Q

BLOOD WATER POTENTIAL
explain why it’s important to maintain an Na+ gradient

A

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
Q

BLOOD WATER POTENTIAL
describe the role of the hypothalamus in osmoregulation

A

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
Q

BLOOD WATER POTENTIAL
explain the role of the pituitary gland in osmoregulation

A

stores and secretes the ADH produced by hypothalamus into the bloodstream

140
Q

BLOOD WATER POTENTIAL
Explain the role of ADH in osmoregulation

A
  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.
  1. makea cells lining collecting duct more permeable to urea:
  • WP in interstitial fluid decreases
  • more water is reabsorbed, leading to more concentrated urine
141
Q

BLOOD WATER POTENTIAL
Suggest how a disorder that affects kidney glomeruli leads to high quantities of protein in their urine

A
  • damages basement membrane
  • proteins can pass into glomerular filtrate
142
Q

BLOOD WATER POTENTIAL
describe how ultrafiltration occurs in glomerulus

A

high hydrostatic pressure leads to small substances (e.g. glucose, water, urea) passing through small pores in capillary endothelium and through basement membrane.

143
Q

BLOOD WATER POTENTIAL
Explain why the concentration of filtrate in the loop of Henle increases then decreases.

A

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
Q

BLOOD WATER POTENTIAL
give the location of osmoreceptors in the body of a mammal

A

hypothalamus

145
Q

BLOOD WATER POTENTIAL
When a person is dehydrated the cell volume of an osmoreceptor decreases. explain why

A

water pot of blood will decrease

water moves from osmoreceptors into blood by osmosis

146
Q

BLOOD WATER POTENTIAL
Describe and explain how the secretion of ADH affects urine produced by the kidneys

A

permeability of membrane/cells to water is increases

more water leaves collecting duct

smaller volume of urine

urine becomes more concentrated