Topic 6 - Internal and External Changes Flashcards

1
Q

define a stimulus

A

a change in an organisms internal or external envrionment

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2
Q

why is it important that organisms can respond to stimuli

A

organisms increase their chance of survival by responoding to stimuli

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3
Q

what is IAA’s effect on shoot tissue

A

it stimulates cell division and elongation

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4
Q

what tropisms does IAA cause in shoot tissue

A

a positive phototropic response (phototropism) and negative gravitropic response (geotropism)

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5
Q

what tropisms does IAA cause in root tissue

A

it causes a positive gravitropic response and a negative phototropic response

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6
Q

what is IAA’s effect on root tissue

A

it inhibits cell devision and elongation

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7
Q

define a hormone

A

a chemical messener produced by a gland that travels in the bloodstream which affects a target organ

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8
Q

why is auxin a plant growth factor

A
  • it is produced by a collection of undifferentiated cells called a meristem (not a gland)
  • it diffuses through plant tissue (not transported in the blood)
  • it affects many cells/tissues including the cells that produces it
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8
Q

what is auxin

A

a group of plant growth factors

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9
Q

what auxin do we need to know about

A

IAA

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10
Q

what is a tropisim

A

growth of a plant in response to directional stimulus

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11
Q

what does positive tropism mean

A

growth of a plant towards a stimulus

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12
Q

what does negative tropism mean

A

growth of a plant away from stimulus

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13
Q

what does a clinostat enable

A

for there to be an equal gravitational force on plants when growing

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14
Q

state 3 things that have an impact on growth response

A
  • growth factor
  • concentration of the growth factor
  • tissue responding to the growth factor
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15
Q

what type of concentration of IAA do weed killers have

A

very strong

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16
Q

explain gravitropism in flowering plants

A
  • cells in trip of shoot/root produce IAA
  • IAA diffuses down shoot/root intially evenly
  • IAA moves to lower side of shoot/root so concentration increase
  • cell elongation in shoots is stimulated whereas in roots it inhibits cell elongation
  • shoots bend away from gravity whereas roots bend towards gravity
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17
Q

explain phototropism in flowering plants

A
  • cells in tip of shoot/root produce IAA
  • IAA diffuses down shoot/root evenly initially
  • IAA moves to shaded side of shoot/root so concentration increases
  • in shoots, this stimulates cell elongation whereas in roots, this inhibits cell elongation
  • shoots bend towards light whereas roots bend away from light
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18
Q

how can organisms increase their chance of survivial

A

they can respond to changes in their environment

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19
Q

what is the sympathetic nervous system responsible for

A

it is responsible for the fight or flight response

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20
Q

what is the parasympathetic nervous system response

A

the rest and relax actions - e.g. digestion

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21
Q

what is the autonomic nervous system responsible for

A

for involutary actions e.g. heart beat, pupil dilation

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22
Q

what is the somatic nervous system responsible for

A

responsible for voluntary movements e.g. muscle movements

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23
Q

what does the central nervous system control

A

the brain and spinal cord

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24
Q

what does the peripheral nervous system control

A

the cranial and spinal nerves

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25
Q

what is the central nervous system responsible for

A

sensory activities, storing memories and emotions

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26
Q

what does the peripheral nervous system do

A

it brings messages to and from the CNS to the rest of the body

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27
Q

describe the structure of a motor neurone

A

should have mentioned:
- nucleus
- cytoplasm (in cell body)
- dendron branched into dendrites
- axon (also cytoplasm)
- myelin sheath
- schwann cell (make up the myelin sheath)
- node of ranvier (gap btwn the schwann cells)

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28
Q

describe the structure of a sensory neurone

A
  • axon
  • dendrites
  • dendron
  • cell body (partway along the axon, adjacent)
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29
Q

describe the structure of an intermediate/relay neurone

A
  • axon
  • dendrites
  • dendron
  • cell body is part of the axon and not parallel to it
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30
Q

define nerve impulse

A

a self propagating wave of electrical disturbance that travels along the surface of the axon membrane

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31
Q

describe resting potential

A

the axon cytoplasm is less positively charged compared to the surrounding tissue fluid

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32
Q

explain how a resting potential is established across the axon membrane in a neurone

A
  • Na\k pump actively transports (using ATP) Na out of the axon and K into the axon
  • this causes an electrochemical gradient = higher K conc inside and higher Na conc outside
  • differential membrane permeability = more permeable to K - move by FD. less permeable to Na
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33
Q

what does self propagating mean

A

the previous section causes the next section to become depolarised

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34
Q

what does electrical disturbance mean

A

unequal distribution of positive ions NaK

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35
Q

what does surface of an axon mean

A

only impacts the surface of the phospholipid bilayer = diameter of the neurone can affect the speed of an action potential

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36
Q

describe action potential

A

when the axon cytoplasm becomes more positively charged than the surrounding tissue fluid

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37
Q

how many sodium and potassium ions are pumped out each time

A

3 sodium out for 2 potassium in

Na-OUT and K-in

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38
Q

how is the unequal distribution of Na and K in the cytoplasm and tissue fluid maintained (how is a resting potential maintained)

A
  • the phospholipid bilayer of the axon is impermeable to Na and K
  • intrinsic proteins are found in the phospholipid bilayer: Na voltage gated channels are closed. K voltage gated channels are some are alwaysopen and some are closed when it is resting potential
  • a sodium otassium pump actively transports Na and K across the axon membrane: 3 Na out, 2 K in
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39
Q

what is the approx value of the resting potential

A

-65 mV (milli volts)

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40
Q

what is the peak value of the action potential

A

+40 mV

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41
Q

can you draw/label a graph showing action potential

A

labelled:
- voltage gated Na channels open
- Na channels open
- hyperpolarisation
- resting potential
- stimulus
- depolarisation
- repolarisation
- voltage gated Kchannel open,Na channel closed
- voltage gated K+ channel close

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42
Q

define action potential

A

when a stimulus detected by a receptor and the energy causes a temporary reversal of the charges on the axon membrane

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43
Q

what is the membrane like during action potential

A

depolarised

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44
Q

why does depolarisation occur

A

due to the voltage gated channels

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45
Q

what is the difference between resting and action potential

A

resting - more +ve outside
action - move +ve inside

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46
Q

describe action potential

A

at resting potential:
- some K+ gated channels are open
- all Na+ gated channels are closed
the energy of the stimulus causes some of the Na+ gated channels to open
- Na+ diffuses into the axon along the electrochemical gradient
- this causes a reversal in potential difference across the membrane
Na+ diffuses into the axon
- axon cytoplasm becomes more positive = more Na+ gated channels open
- amplifies the influx of Na+
when the action potential reaches +40mV the Na+ gated channels close
- additonal K+ gated channels open
K+ gated channels are open = electrochemical gradient is reversed
- K+ diffuses out of the axonn = repolarisation of the axon
hyperpolarisation (axon cytoplasm is more negative than usual)
- K+ gated channels close
- NaK pump resores to 65 mV
- axon is replenished

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47
Q

describe the all or nothing principle

A
  • for an action potential to be produced, depolarisation must exceed the threshold potential
  • action potentials produced are always the same magnitude/size at the same potential
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48
Q

what is the effect of bigger stimuli on the action potentials

A

they increase the frequency of action potentials

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49
Q

What happens according to the all or nothing principle when depolarisation is below the threshold

A

NOTHING

no action potential which means that there is no impulse generated

any stimulus whatever the strength below the threshold value will fail to generate an action potential

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50
Q

what happens according to the all or nothing action potential when depolarisation is above the threshold level

A

ALL

action potential generated so the nerve impulse will travel

the action potential are the same size at the same potential and always peak at the same maximum voltage

the strength of a stimulus does not affect the size of action potential

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51
Q

how can an organism perceive the size of a stimulus if all action potentials are the same size

A

number of impulses passing in given time (frequency) - larger stimulus = more impulses generated in a given time

different neurons with different threshold values - brain interprets number/types off neurons that pass impulses as a result of a given stimulus = determines the size

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52
Q

why is the all or nothing principle important

A

ensure animals only respond to large enough stimuli rather than responding to every slight change in the environment which would overwhelm them

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53
Q

describe the nature of the refractory period

A

the time taken to restore the acon to resting potential when no further action potential can be generated as the Na+ channels are closed and will not open

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54
Q

explain the importance of the refractory period

A

ensure discrete impulses are produced - action potentials don’t overlap
limits the frequency of impulse transmission at a certain intensity - prevents over reaction to stimulus
- higher intensity stimulus cuases a higher frequency of action potentials only up to a certain intensity
ensures action potentials travel in one direction

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55
Q

define nerve impulse

A

the transmission of an action potential along an axon

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56
Q

describe the speed an action potential moves

A

0.5 m/s - 120 m/s

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57
Q

suggest how damage to the myelin sheath can lead to slow responses and/or jerky movements

A

less saltatory conduction = depolarisation occurs along the whole length of the axon, so nerve impulses take longer to reach neuromascular junction/delay in muscle contraction

ions/depolarisation may pass/leak to other neurones = wrong muscle fibres contract

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58
Q

describe how the passage of an action potential along non-myelinated axons result in nerve impulse

A

action potential passes as a wave of depolarisation
influx of Na+ in one region increases permeability of adjoining region to Na+ by causing voltage-gated Na+ channels to open so adjoining region depolarises

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59
Q

describe how the passage of an action potential and myelinated axons results in nerve impulses

A

myelination provides electrical insulation
depolarisation of axon at nodes of Ranvier only
results in saltatory conduction [local currents circuits]
so there is no need for depolarisation along the whole length of axon

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60
Q

describe the function of the myelin sheath and how it affects the speed of an action potential

A
  • insulates the axon preventing an action potential from forming in parts of the axon covered in schwann cells
  • results in saltatory conduction where the action potential jumps from one node of ranvier to the next
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61
Q

what is the affect of saltatory conduction in myelinated vs non myelinated neurones

A

triples the speed in myelinated neurones

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62
Q

state 3 factors that affect the speed of an action potential

A

myelin sheath
diameter of the axon
temperature

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63
Q

describe how the diameter of the axon affectts the speed of an action potential

A

greater the diameter of an axon, the faster the speed of conductance due to:
- greater diamater = smaller SA:V = smaller leakage and membrane potential is easier to maintina
- greater diameter = large SA = larger area for attachment of voltage-gated channels = faster diffusion = faster switch in potentiall difference

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64
Q

describe how temperature affects the speed of an action potential

A

causes an increased rate of diffusion therefore action potentials generated more rapidly
active transport of ions by NaK pump requires ATP from respiration which requires enzymes that is affected by temperature
gated channels and NaK pump will denature = control of ion distribution is lost and impulses cannot be conducted

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65
Q

state 5 ways the synapse’s structure has adapted to its function

A
  • bulbous knob giving a large surface area: for attachment of transport proteins to allow rapid facilitated diffusion + active transport
  • small diffusion distance: decreases time taken for an action potential to be created in the post-synaptic neurone
  • mitochondria: ATP to provide energy for synthesis of neurotransmitter/vesicles/proteins
  • RER: synthesis of transport proteins
  • SER: synthesis of neurotransmitter and vesicles
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66
Q

explain how acetylcholine contributes to a synapse being unidirectional

A
  • acetylcholine is released from the presynaptic side
  • receptors in postsynaptic side
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67
Q

why are synapses important

A
  • a single impulse can be transmitted to multiple neurones = single impulse can create multiple responses
  • multiple impulses from multiple receptors can be passed to a single neurone = single response from multiple different stimuli
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68
Q

describe the transmission across a cholinergic synapse in the presynaptic neurone

A
  • depolarisation of pre-synaptic membrane causes the opening of volted-gated Ca2+ channels, diffuse into pre-synaptic knob
  • causes vesicles containing acetylcholine to move and fuse with the pre-synaptic membrane, releasing ACh into the synaptic cleft by exocytosis
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69
Q

describe transmission across a cholinergetic synapse in the postsynaptic neurone

A
  • ACh diffuses across the synaptic cleft to bind to specific receptors on post-synaptic membrane causing Na+ channels to open
  • Na+ diffuse into post-synaptic knob causing depolarisation, if the threshold is met, action potential is initiated
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70
Q

describe what happens to acetylcholine after synaptic transmission

A
  • hydrolysed by acetylcholinesterase
  • products are reabsorbed by presynaptic neurone
    this is to stop overstimulation, if not removed it would keep binding to receptors causing depolarisation
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71
Q

describe temporal summation

A
  • one pre-synaptic neurone releases neurotransmitter many times over a short period of time
  • sufficient NT to reach threshold to trigger an action potential
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72
Q

describe spatial summation

A
  • many pre-synaptic neurones share one post synaptic neurone
  • collectively release sufficient neurotransmitters to reach threshold to trigger an action potential
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73
Q

describe inhibition by inhibitory synapses

A

inhibitory neurotransmitters hyperpolarise postsynaptic membrane:
Cl- channels open (diffuse in) + K+ channels open (diffuse out)
more Na+ required for depolarisation
reduces likelihood of threshold being met and action potential formation at post-synaptic membranes

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74
Q

describe how muscles work

A

they work in antagonistic pairs = pull in opposite directions
- one muscle contracts, pulling on the bone
- one relaxes

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75
Q

what is the advantage of muscles working in antagonistic pairs

A

the second muscle is required to reverse the movement caused by the first and it helps to maintain posture

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76
Q

describe the gross structure of skeletal muscle

A

made up of many bundles of muscle fibres packaged together, they are attached to bones by tendons

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77
Q

what do muscle fibres contain

A

muscle fibres are made up of long cylindrical cells containing many nuclei and myofibrils

  • sarcolemma (cell membrane)
  • sarcoplasm (cytoplasm)
  • sarcoplasmic reticulum (endoplasmic reticulum)
  • multiple nuclei
  • many myofibrils
  • many mitochondria
  • T (transverse) tubles from sarcolemma folding inward
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78
Q

describe the ultrastructure of a myofibril

A

made of two types of long protein filaments arranged in parallel = myosin (thick) and actin (thin)

arranged in functional repeating units called sarcomeres = Z line, M line, H zone

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79
Q

what causes the characteristic banding pattern of myofibrils

A

characteristic banding pattern due to the arrangement of myofilaments

80
Q

what is cross-striations

A

when muscle cells are composed of alternating light and dark bands

81
Q

explain the banding pattern in I bands

A

light band containing only thin actin filaments

82
Q

explain the banding pattern in A bands

A

dark bands containing thick myosin and some actin filaments

83
Q

explain the banding pattern in the H zone

A

it contains only myosin

84
Q

what does A in A band stand for

A

anisotropic

85
Q

what does I in I band stand for

86
Q

why is summation by synapses important

A

low frequency of action potentials release insufficient neurotransmitter to exceed the threshold

87
Q

define excitatory synapse

A

a synapse that increases the likelihood of an action potential in the post-synaptic membrane

88
Q

explain the effect of drugs on a synapse

A
  • stimulate the nervous system leading to more action potentials = similar shape to NT, stimulates the release of more NT, inhibits the enzyme that breaks down the NT = Na+ continues to enter
  • inhibit the nervous system leading to less action potentials = inhibits the release of NT and blocks the receptors mimicking the shape of NT
89
Q

name the gap between the pre-synaptic membrane and post-synaptic membrane

A

synaptic cleft

90
Q

how does myosin and actin interact

A

the myosin head attaches to actin and bends

91
Q

suggest why ATP is needed in the presynaptic membrane

A

active transport of ions, movement of vesicles

92
Q

describe the roles of calcium ions in the contraction of a myofibril

A
  • calcium ions diffuse into myofibrils from sarcoplasmic reticulum
  • calcium ions bind to and cause movement of tropomyosin on the actin, changing the 3D tertiary structure
  • exposure of the binding sites on the actin
  • myosin heads attach to binding sites on actin
93
Q

describe the role of ATP in the contraction of myofibril

A
  • hydrolysis of ATP causes myosin heads to bend
  • pulling the actin molecules
  • attachment of new ATP molecule to each myosin head causes myosin heads to detach from actin sites
94
Q

state how ATP is used in muscle tissue

A
  • “resetting” of the myosin head back to it’s original position, ready for the next power stroke
  • active transport of Ca2+ back into the sarcoplasmic reticulum for tropomyosin to move
  • the active transport of Na+ out of the sarcoplasm in order to restore the normal potential difference of the muscle cell (‘resting potential’)
95
Q

state the similarities between neuromuscular junctions and a cholinergic synapse

A
  • release neurotransmitters that move by diffusion
  • binding of receptors cause an influx of ions into the cell
  • enzymes break down the neurotransmitter
96
Q

state the differences between neuromuscular junctions and a cholinergic synpase

A
  • synapse has sensory, intermediate and motor neurones involved, the junction only invovles motor neurons
  • synapse
  • ACh binds to receptors on sarcolemma not the post-synaptic membrane
  • neuromuscular is excitatory but synapse is excitatory or inhibitory
  • the action potential ends in the NJ but may be produed in the post-synaptic neuron in the cholinergic
  • synpase links neurons to other neurons whereas NJ links neurons to muscle cells
97
Q

what is a motor unit

A

each section of muscle that is depolarised by a motor end plat

98
Q

how are muscle contractions synchronised and pwoerful

A

the motor neuron’s axon will divide into many dendrons and then into many motor end plates to form many neuromuscular junctions

99
Q

what is a sarcomere

A

the unit of measurement for muscle tissue [distance btwn z lines]

100
Q

describe what happens in neuromuscular junctions

A
  • arrival of action potential at the motor end plate causes release of ACh into the neuromuscular junction
  • Ach binds to the sarcolemma, causing muscle fibre to become depolarised
  • depolarisation is propagated into muscle fibre t-tubles
  • depolarisation of t-tubles causes Ca2+ gated channels to open into sarcoplasmic reticulum, releasing Ca2+ into the sarcoplasm
101
Q

state the 3 ways of generating ATP

A
  • aerobic respiration: large amounts of ATP but takes time
  • anaerobic respiration: generates ATP during intense periods
  • phosphocreatine: instanteneous generation of ATP during first few seconds of muscle contraction + only provides a few seconds worth of ATP but allows us to avoid a potentially life-threatening encounter
102
Q

describe the role of phosphocreatine in muscle contraction

A
  • source of inorganic phosphate to rapidly phosphorylate ADP to regerate ATP

ADP + phosphocreatine -> ATP + creatine

  • runs out after a few seconds, used in short bursts of vigrous exercise
  • anaerobic and alactic
103
Q

what are slow twitch muscle fibres suited for

A

endurance activity e.g. running a marathon

104
Q

what are fast twitch muscle fibres suited for

A

intense activity e.g. weight lifting

105
Q

describe the features of slow twich muscle fibres

A
  • adapted for aerobic respiration
  • a rich blood supply to deliver oxygen and glucose
  • contracts slowly over long periods of time
  • possess a large store of myoglobin (bright red molecule that stores oxygen)
  • common in leg muscles (calves) to maintain body in upright position
  • numerous mitochondria
  • less powerful contractions
106
Q

describe the features of fast twitch muscle fibres

A
  • adapted for anaerobic respiration
  • high concentration of enzymes involved in anaerobic respiration
  • common in arm muscle to do short bursts of exercise
  • more powerful contractions
  • thicker and more numerous myosin filmanets
  • higher conc. of glycogen as delivery of glucose by the bloodstream is not fast enough
  • store of phosphocreatine in order to repidly regenerate ATP from ADP
  • contract rapidly over short periods of time
107
Q

what are receptors also called

A

transducers (convert one form of energy into another form of energy)

108
Q

describe the basic structure of a pacinian corpuscle

A
  • lamellae
  • sensory neurone ending
  • sensory neurone axon
  • myelin sheath
  • gel
  • stretch mediated sodium ion channel
109
Q

what does the receptor convert the energy provided by the stimulus into

A

an action potential

110
Q

state the 4 types of receptors

A
  • mechanoreceptors
  • photoreceptors
  • baroreceptors
  • chemoreceptors
111
Q

explain the protective effect of a simple reflex

A
  • rapid as only 3 neurones and a few synapses
  • autonomic = doesn’t have to be learnt
  • protects from harmful stimuli e.g. escapes predators
112
Q

where is the pacinian corpuscle found

A

fingers feet and external genitalia

113
Q

what type of receptor is a pacinian corpuscle

A

mechanoreceptor

114
Q

how is an generator potential generated in a pacinian corpuscle

A
  • mechanical stimulus e.g. force or pressure, deforms the lamellae and the stretch-mediated Na+ channels deform and allow the diffusion of Na+ into the sensory neuron
  • greater pressure causes more Na+ channels to open and more Na+ to enter = depolarisation = generator potential
  • when the generator potential reaches the threshold, it triggers an action potential
115
Q

what does a pacinian copuscle illustrate

A
  • receptor respond only to specific stimuli: pacinian corpuscle only responds to mechanical pressure
  • stimulation of a receptor leads to the establishment of a generator potential = action potential sent when threshold is reached
116
Q

what are the 4 features of a reflex reaction which means they confer a survival advantage

A
  • innate: have them from birth
  • involuntary
  • fast
  • protect us from harm
117
Q

how are images focused

A

the cornea and lens refract light onto the retina

118
Q

explain the differences in sensitivity to light for rods and cones in the retina

A

rods are more sensitive to light than cones
- several rods are connected to a single neurone vs each cone is connected to a single neurone
- spatial summation to reach a threshold to generate an action potential vs cones have no spatial summation

119
Q

what is the fovea

A

where the majority of light is focused

120
Q

what do rods allow us to do

A

to see in the dark

121
Q

how do rods allow us to see in the dark

A
  • rrhodopsin is broken down very easily by light = generator potentials can be produced in very low light conditions
  • many rod cells are connected to a single sensory neurone vis single bipolar cell = retinal convergence
  • rods can work together to produce enough neurotransmitters in v low light conditions to exceed threshold value for generator potential aka summation
122
Q

why are cones needed

A

thay allow us to see in colour and higher detail

123
Q

how do cones allow us to see in high detail and colour

A
  • 3 cone cells: red green blue = trichromatic colour theory
  • iodopsin is only broken down by high light intensities
  • each cone cell is connected to its own bipolar cells + sensory neurone = high visual acuity
124
Q

what does retinal convergence lead to and why

A

low visual acuity
- multoiple rods connected to single senroy neurone via single bipolar cell = brains cannot interpret exactly where light is coming from

125
Q

describe the distribution of rods and cones

A
  • 20:1 rods to cones in retina
  • most cones found in fovea as this is where majority of light is focused = high visual acuity
    – only rods are found at peripheries of retina = low light intensity
126
Q

what is the difference in visual acuity for rods and cones in the retina

A

rods have lower visual acuity, cones have higher visual acuity

127
Q

explain the differences in visual acuity for rods and cones in the retina

A
  • several rods connected to a single neurone vs each cone connected to a single one
  • several rods send a single set of impulses to brain (can’t distinguish btwn diff sources of light) vs cones send separate impulses to brain (can distinguish btwn diff sources of light)
128
Q

what is the difference between in sensitiviy to colour for rods and cones and why

A

rods allow for monochromatic vision (1 type of rod + pigment)
cones allow for colour vision (3 types of cones rgb sensitive w diff optical pigments = absorb diff wavelengths = different combinations of cones = range of colour perception

129
Q

what does it mean is the cardiac muscle is myogenic

A

contract and relax without receiving electrical impulses from the nerves

130
Q

describe where you can find the Sinoatrial node (SAN)

A

wall of right atrium

131
Q

describe where you can find the atrioventricular node (AVN)

A

border of right and left vventricle within the atria still

132
Q

what is the Sinoatrial node known as

A

the pacemaker

133
Q

where can you find the bundle of His

A

it runs through the septum (bit that separates left and right side of heart)

134
Q

where can you find the purkyne fibres

A

in the wall of the ventricles

135
Q

describe myogenic stimulation of heart and transmission of a subsequent wave of electrical activity

A
  • SAN sends regular waves of electrical activity across the atria = atria contract stimultaneously
  • non-conducting tissue btwn atria/ventricles prevents impulse passing directly to ventricles = prevents immediate contraction of ventricles
  • waves of electrical activity reach AVN = delays impulse = atria fully contracts b4 ventricles contract
  • AVN sends wave of electrical activity down bundle of His = conduct wave btwn ventricles to apex where it branches into purkyn tissue = ventricules contract stimultaneously from base up
136
Q

where can you find chemoreceptors and pressure receptors

A

aorta and carotid arteries

137
Q

where is the cardiac control found in the brain

138
Q

what does the sympathetic nerve do

A

increases heart rate and force of contraction

139
Q

what does vagus/parasympathetic nerve do

A

decreases heart rate

140
Q

where does the parasympathetic and sympathetic nerve lead to

141
Q

describe the roll of chemoreceptors + pressure receptors + autonomic nervous system + effectors in increasing heart rate (if you have low blood pressure)

A
  • baroreceptors detect fall in blood pressure/chemoreceptors detect blood rise in blood CO2 conc or fall in blood pH
  • send impulses to medulla/cardiac control centre
  • sends more frequent impulses to SAN along sympathetic neurones
  • more frequent impulses sent from SAN to AVN
  • cardiac muscle contracts more frequently
  • heart rate increases
142
Q

describe the roll of chemoreceptors + pressure receptors + autonomic nervous system + effectors in decreasing heart rate (if you have high blood pressure)

A
  • baroreceptors detect rise in blood pressure/chemoreceptors detect blood fall in blood CO2 conc or rise in blood pH
  • send impulses to medulla oblongata/cardiac control centre
  • sends more frequent impulses to SAN along parasympathetic neurones
  • less frequent impulses sent from SAN to AVN
  • cardiac muscle contracts less frequently
  • heart rate decreases
143
Q

what is the autonomic nervous system invovled in

A

involves the involuntary control of internal muscles and glands

144
Q

what are the functions of the sympathetic nevour system

A
  • stimulates effectors so speeds up any activity
  • helps to deal with stressful situations
  • heightens our awareness and allows more powerful musle contractions
145
Q

what are the functions parasympathetic nervous system

A
  • inhibits effectors so slows down activity
  • controls activity in restful situations
  • concerend with conserving energy, replenishing body reserves
146
Q

how to calculate cardiac output

A

stroke volume x heart rate

147
Q

how to calculate pulmonary ventilation

A

tidal volume x breathing rate

148
Q

what is the typical heart rate of humans

149
Q

what are the efffects of the sympathetic nervous sytem

A
  • pupils dilate
  • cardiac output increases
  • bronchioles dilate
  • pulmonary ventilation rate increases
  • secretion of adrenaline + sweat
  • blood diverted away from digestive system, towards skeletal muscle
150
Q

what are chemoreceptors sensitive to

A

changes in pH which arise from amount of CO2 dissolved in the blood plasma

150
Q

what are the effects of the parasympathetic nervous system

A
  • pupils constrict
  • cardiac output decreases
  • bronchioles constrict
  • pulmonary ventilation rate returns to resting rate
  • blood diverted to digestive system
  • sweat secretion inhibited
151
Q

what forms when CO2 dissolves in the blood plasma

A

carbonic acid = lowers pH

152
Q

what is homeostasis

A

the maintenance of a constant optimal internal environment through negative feedback mechanisms

the maintenance of a stable internal environment within restricted limits by physiological control systems, normally invovle negative feedback

153
Q

what is negative feedback

A

a stimulus produces a response that acts to limit the effect of that stimulus

154
Q

what is positive feedback

A

a reponse to a stimulus that acts to increrase the stimulus

155
Q

why is it importance to maintain a stable core temperature if the temperature if too high

A
  • H bonds in 3* of enzymes break
  • enzymes denature = active sites change shape and substrates can’t bind = e/s complexes cannot form
156
Q

why is it important to maintain stable core temperature if temperature is too low

A
  • not enough kinetic energy so fewer e/s complexes form
157
Q

why is it important to maintain stable blood pH

A
  • above/below optimal pH = ionic and H bonds in 3* break
  • enzymes denature = active sites change shape and substrates can’t bind = fewer substrate complexes
158
Q

why is it important to maintain stable blood glucose concentration if it is too low

A
  • not enough glucose for respiration
  • less ATP produced
  • active transport can’t happen
159
Q

why is it important to maintain stable blood glucose concentration if it is too high

A
  • water potential of blood decreases
  • water lost from tissue to blood via osmosis
  • kidneys can’t absorb all glucose = more water lost in urine = dehydration
160
Q

describe the role of negative feedback in homeostasis

A
  • receptors detect change from optimum
  • effects respond to counteract change
  • resuming levels to optimum/normal
161
Q

describe vasoconstriction

A
  • muscle in the arterioles near the surface of the skin contract and make the lumen smaller
  • restricts blood flow to skin surface = limits amount of heat lost
162
Q

describe vasodilation

A
  • muscle in the arterioles relax making the lumen larger
  • more blood flows to surface of capillaries + extremities increase heat loss
163
Q

state the physiological responses of thermoregulation

A
  • vasodilation & vasoconstriction
  • sweating
  • piloerection
  • shivering
164
Q

describe piloerection

A

contraction of hair erector muscles which raises the body’s hairs = thicker layer of insulating air/water to be trapped against the skin = improves insulation

165
Q

what is the role of the pancreas in blood glucose regulation

A

has islets of langerhans which secretes either insulin [beta] or glycogen [alpha]

166
Q

define glycogen

A

a carbohydrate storage molecule found in animal livers and muscle tissue

167
Q

define glucagon

A

a hormone that stimulates the conversion of glycogen to glucose via the second messegener model

168
Q

define adrenaline

A

a hormone that stimulates the conversino of glycogen to glucose via the second messenger model

169
Q

define insulin

A

a hormone that stimulates the conversion of glucose into glycogen via the second messenger model

170
Q

define glycogenolysis

A

the conversion of glycogen to glucose when blood levels are lower than normal

171
Q

define glycogenesis

A

the conversion of excess glucose to glycogen when blood levels are higher than normal

172
Q

define glyconeogenesis

A

the conversion of a non-carbohydrate molecule to glucose this occurs if all glycogen has been converted to glucose and your body still requires more glucose

173
Q

define glycolysis

A

the splitting of glucose into two 3 carbon molecules releasing atp

174
Q

what is hypoglycaemia

A

when the blood glucose concentration is too low

175
Q

what is hyperglycaemia

A

when the blood glucose concentration is too high

176
Q

why is it important to maintain a stable blood glucose concentration when its too low

A

not enough glucose for respiration = less ATP produced = AT can’t happen = cell death

177
Q

why is it important to maintain a stable blood glucose concentration when it is too high

A

water potential of bblood decreases = water lost from tissue to blood via osmosis = kidneys can’t absorb all glucose = more water lost in urine causing dehydration

178
Q

describe the role of neggative feedback in homeostasis

A
  • receptors detect change from optimum
  • effectors respond to counteract change
  • returns lelvels to optimum/normal
179
Q

describe positive feedback

A

receptors detect change from normal, effectors respond to amplify change = produce greater deviation from normal

180
Q

explain the importance of conditions being controlled by separate mechanisms involving negative feedback

A

departure in different directions from the original state can all be controlled = greater degree of control

181
Q

define hormone

A

a chemical messenger secreted by glands that travels through the bloodstream and bind to target cells

182
Q

describe the second messenger model

A
  • adrenaline/glucagon binds to a transmembrane protein receptor within the cell-surface membrane of a liver cell
  • the binding of the hormone causes the protein to chnge shape on the inside of the mmebrane
  • this changes the protein shape = activation of a membrane-bound enzyme adenyl cyclase
  • adenyl cyclase converts atp into cyclic AMP [cAMP]
  • the active protein kinease catalyses the hydrolysis of glycosidic bonds in a glycogen molecule
  • glucose released from the hydrolysis reaction leaves the liver cell and enters the blood via FD and carrier protein
183
Q

what does the second messenger model do

A

increase permeability of liver cells

184
Q

suggest an advantage of the second messenger model

A

amplifies signal from hormone, each hormone will stimulate production of many molecules of second messenger [cAMP] which can activate many enzymes for rapid increase in glucose

185
Q

what are the signs and symptoms of diabetes

A
  • high blood glucose conc
  • presence of glucose in urine
  • urinate excessively
  • weight loss
  • blurred vision
  • tiredness
  • increased thirst and hunger
  • genital itching or regular thrush episodes
186
Q

what causes diabetes type 1

A

the body is unable to produce insuline due to an autoimmune response - attacks b cells of islets of langerhans

187
Q

what causes diabetes type 2

A

glycoprotein receptors on body cells are losing/have lost their responsiveness to insulin, or an inadquete supply of insulin from the pancreas

188
Q

how is diabetes type 1 treated

A

injections of insulin 2/4 times a day. insulin dose must match the glucose intake. this is moniitored using biosensors

189
Q

how is diabetes type 2 treated

A

drugs to stimulate insulin production/slow down rate of absorption of glucose

190
Q

state 3 factors

A

core temperature, blood pH, blood glucose concentration

191
Q

what is diabetes

A

a metabolic disorder caused by an inability to control blood glucose concentration due to a lack of the hormone insulin/repsonse to insulin

192
Q

state how insulin reduces blood glucose concentration

A
  • causing more glucose channels to be inserted into the cell membrane = increase uptake of glucose by muscle cells
  • increases rate of respiration = more glucose is used
  • activates enzymes involved in the conversion of glucose to glycogen [glycogenesis]
  • causes excess glucose to be concerted to fat
193
Q

where is insulin secreted

A

beta cells in the islets of langerhans

194
Q

where is glucagon secreted

A

alpha cells in the islets of langerhans

195
Q

state how glucagon increases blood glucose concentration

A
  • attaches to receptors on surface of target cells e.g. liver and muscle
  • activating enzymes involved in the conversion of glycoen to glucose [glycogenolysis]
  • activating enzymes invovled in the conversion of glycerol and amino acids into glucose [ gluconeogenesis]
    0 causes body to use more fatty acids in respiration
196
Q

define diabetes mellitus

A

medical condition where a person is unabl to control their blood glucose concentration