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A-Level Biology > Responding to Changes to Environment > Flashcards

Responding to Changes to Environment Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

what is a stimulus?

A

a detectable change in the environment

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2
Q

what are taxes?

A
  • simple response in which an organism will move its entire body towards a favourable stimulus (positive taxis) or away from an unfavourable stimulus (negative taxis)
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3
Q

what is kinesis?

A
  • when an organism changes the speed of movement and the rate it changes direction
  • in less favourable conditions = inc rate of change of direction
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4
Q

why may an organism move in a straight line when in favourable conditionss? what is this an example of?

A
  • to inc chance of finding a new area with favourable conditions
  • positive kinesis
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5
Q

what is IAA? what does it do?

A
  • growth hormone (type of auxin)
  • can control cell elongation
  • made in tip of roots/shoots and diffuses to other cells
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6
Q

what is the effect of IAA on shoots?

A

promotes cell elongation/growth

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7
Q

what is the effect of IAA on roots?

A

inhibits cell elongation/growth

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8
Q

explain phototropism in shoots, including the role of IAA

A
  • postively phototropic (grow towards light)
  • need light for LDR
  • shoot tip cells produce IAA, which diffuses to other cells
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9
Q

describe the effect unilateral light would have on a shoot

A
  • if light shines in one direction, IAA diffuses to the shaded side of the shoot
  • causes the cells on shaded side to elongate more so plant bends toward light source
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10
Q

explain phototropism in roots, including the role of IAA

A
  • negatively phototropic (grows away from light)
  • no photosynthesis occurs in roots so light not needed
  • root cells elongate more on the light side (IAA inhibit growth) so root bends away from light
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11
Q

describe gravitropism in shoots, including the role of IAA

A
  • negatively gravitropic (grows away from gravity)
  • IAA diffuse from upper side to lower side
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12
Q

describe gravitropism in roots, including the role of IAA

A
  • positively gravitropic (grows towards gravity)
  • IAA diffuse from lower side to upper side
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13
Q

the cardiac muscle is myogenic. what does myogenic mean?

A

can contract without stimulus

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14
Q

where is the sinoatrial node (SAN) located?

A

right atrium

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15
Q

where is the atrioventricular node (AVN) located?

A

in between the left ventricle and right atrium

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16
Q

where is the Bundle of His located?

A

runs through the septum

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17
Q

where are Purkyne/Purkinje located?

A

in the walls of the ventricles

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18
Q

describe the sequence of events that controls heart rate

A
  • SAN sends impulses which initate heartbeat, as it is the pacemaker
  • impulses spread through the atria, causing it to contract
  • impulse reaches AVN
  • AVN delays the impulse to allow atria to finish contracting
  • impulse spreads down Bundle of His, which splits into branches
  • impulse spreads around Purkinje fibres in the ventricle walls, causing the apex + then walls of the ventricle to contract
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19
Q

what part of the brain contols heart rate via the autonomic nervous system?

A

medulla oblongata

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20
Q

what are the two parts of the nervous system? what effect do they have on heart rate?

A
  • sympathetic (inc hr)
  • parasymathetic (dec hr)
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21
Q

what effect can high blood pressure have on the heart?

A

can cause damage to the walls of the arteries

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22
Q

what effect can low blood pressure have on the heart?

A
  • may be insufficient supply of oxygenated blood to respiring cells
  • may be insufficient removal of waste, resulting in a buildup
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23
Q

what causes a decrease in blood pH? how can it return to normal?

A
  • inc respiration = inc CO2/lactic acid produced = acidic
  • inc HR allows CO2 to diffuse out into the alveoli more rapidly
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24
Q

what type of receptor detects changes in blood pH?

A

chemoreceptor

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25
Q

what type of receptor detects changes in blood pressure?

A

baroreceptor

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26
Q

where are chemoreceptors and baroreceptors found?

A

carotid arteries and aorta

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27
Q

describe what happens when blood pH or pressure decreases

A
  • more electrical impulses sent to medulla oblongata
  • more impulses sent to SAN by sympathetic nervous system
  • heart rate increases
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28
Q

describe what happens when blood pH or pressure increases

A
  • more electrical impulses sent to medulla oblongata
  • more impulses sent to SAN by parasympathetic nervous system
  • heart rate decreases
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29
Q

what kind of images are produced by rod cells? why?

A
  • black and white
  • unable to distinguish between different wavelengths of light (low visual acuity) as many rod cells connect to one sensory neurone
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30
Q

what level of light intensity can be detected by rod cells? why?

A
  • low intensity
  • very sensitive to light as many rod cells connect to one sensory neurone
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31
Q

what chemical must be broken down to create a generator potential in a rod cell?

A

rhodopsin

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32
Q

what kind of images are produced by cone cells? why?

A
  • colour images can be perceived, depenending on the proportion of each cone cell stimulated
  • there are 3 different types of iodopsin pigments that all absorb different wavelengths of light
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33
Q

why do cone cells have high visual acuity?

A
  • no retinal convergence, only one cell connects to each bipolar cell
  • can distinguish between different wavelengths of light
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34
Q

what is the peripheral nervous system (PNS) made up of?

A

receptors, sensiry neurones, motor neurones

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35
Q

what is the central nervous system (CNS) made up of?

A

coordination centres, e.g. brain and spine

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36
Q

what is the role of the pacinian corpuscle?

A

respond to pressure changes

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37
Q

describe the structure of a pacinian corpuscle

A
  • consists of a single sensory neurone wrapped with layers of connective tissues separated by gel
  • has special channel proteins in plasma membrane
  • membranes surrounding the sensory neurones have stretch-mediated sodium ion channels
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38
Q

what happen when pressure is applied to pacinian corpuscle?

A
  • neurone in plasma membrane deformed
  • stretch-mediated Na+ channels widen so Na+ enter
  • generator potential established
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39
Q

how is resting potential maintained in a pacinian corpuscle?

A

in resting state, Na+ channels too narrow for Na+ to diffuse into the sensory neurone

40
Q

briefly state the function of a dendrite

A

carry action potentials to surrounding cells

41
Q

briefly state the function of a cell body of a neurone

A
  • contains organelles found in a typical animal cell
  • proteins and neurotransmitters made here
42
Q

briefly state the function of Schwann cells

A

wrap around the axon to form myelin sheath

43
Q

briefly state the function of the myelin sheath

A
  • lipid
  • does not allow charged ions to pass through
44
Q

what are the gaps between myelin sheath called?

A

nodes of Ranvier

45
Q

what causes the difference in electrical charge between the inside and outside of a neurone when a resting potenial is established? what is the potential difference of the inside of the neuron at this point?

A
  • more positive ions (Na+ and K+) outside compared to the inside of the neurone
  • -70mv
46
Q

outline how a resting potential is maintained

A
  • Na+/K+ pumps in axon actively transports Na+ out of cell and K+ into cell
  • K+ move out of axon through K+ channels along the conc gradient
  • results in lesser conc of pos ions in axon so inside more neg than outside
  • K+ ions pulled back into axon due to electrochemical gradient
  • electrochemical gradients counteract so no net movement of K+, therefore pd of -70mv maintained
47
Q

outline the process of an action potential being generated from resting potential

A
  1. stimulus arrives, causes Na+ channels to open so Na+ enter axon, causing neighbouring voltage gated (VG) channels to open, so even more Na+ diffuse in resulting in an inc of voltage
  2. at 40mv, Na+ VG close and K+ open, causing K+ to leave the axon, decreasing the overall charge
  3. K+ continue diffusing out, causing a temp overshoot of the gradient, resulting in the inside of the axon being more neg than usual (hyperpolarisation)
  4. all closable gates close, so resting potential is restored
48
Q

what is the all or nothing principle?

A
  • if the depolarisation does not exceed -55mv (threshold value) then no action potential will be produced
  • any stimuli that triggers depolarisation to -55mv will always peak at the same maximum voltage
  • larger stimuli do not inc the max voltage, instead inc the frequency of action potentials
49
Q

why is the all or nothing principle important?

A

makes sure only respond to large enough stimuli, rather than every slight change

50
Q

what is the refractory period?

A
  • after an action potential has been generated, the membrane enters a refractory period
  • can’t be stimulated as Na+ channels are recovering + can’t be opened
51
Q

why is the refractory period important?

A
  • ensures discrete impulses are produced - an action potential can’t be generated immediately after another so they are separate (no overlap)
  • ensures action potential only travels forward in one direction - stops an action potential from spreading out in 2 directions which would prevent a response as threshold value not reached
  • limits the number of impulse transmission - prevents over reaction to a stimulus so senses are not oversimulated
52
Q

list 3 factors that affect the speed of an action potential

A
  1. myelination + saltatory conduction
  2. axon diamater
  3. temperature
53
Q

how do myelination + saltatory conduction affect the speed of an action potential?

A
  • action potential jumps from node to node (saltatory conduction)
  • therefore travels along the axon faster as it doesn’t have to generate an action potential along the entire length, just the Nodes of Ranvier
54
Q

how does axon diameter affect the speed of an action potential?

A
  • wider diameter = inc speed of conductance
  • wider diameter = less leakage of ions so action potential travels faster
55
Q

how does temperature affect the speed of an action potential?

A
  • higher temp = faster speed of conductance
  • ions diffuse faster
  • enzymes involved in respiration work faster so more ATP available for active transport in the Na+/K+ pump
56
Q

outline the transmission of a synapse

A
  1. ap arrives at synaptic terminal. depolarisation of terminal leads to opening of Ca2+ channels so Ca2+ diffuse into synaptic knob
  2. vesicles containing neurotransmitter move towards + fuse with presynaptic membrane. neurotransmitter released to synaptic cleft
  3. neurotransmitter diffuses down conc gradient across synaptic cleft to post synaptic membrane + binds to complementary receptors on surface of post synaptic membrane
  4. Na+ ion channels on post synaptic membrane open + Na+ diffuse in. if enough neurotransmitter, enough Na+ diffuse in so above threshold + post synaptic neurone becomes depolarised
  5. neurotransmitter is degraded + released from receptor, Na+ channels close + post synaptic neurone re-establishes resting potential. neurotransmitter transported back to presynaptic neurone where it is recycled
57
Q

what is the neurotransmitter in a cholinergic synapse?

A

acetylecholine (Ach)

58
Q

what is acetylecholine broken down by? into what?

A
  • acetylcholinesterase
  • acetate + choline
59
Q

what are the 2 types of summation?

A
  • spatial
  • temporal
60
Q

why is summation necessary?

A

some action potentials do not result in sufficient concentrations of neurotransmitter being released to generate an action potential

61
Q

what is spatial summation?

A

many different neurones collectively trigger a new action potential by combining the neurotransmitter they release to exceed the threshold value

62
Q

what is temporal summation?

A

one neurone releases neurotransmitter repeatedly over a short period of time to add up enough to exceed the threshold value

63
Q

what are inhibitory synapses? how do they work?

A
  • cause chloride ions to move into post synaptic neurone + potassium ions to move out
  • causes hyperpolarisation so action potential highly unlikely
64
Q

why are inhibitory synapses useful?

A

prevents a response to every single stimulus

65
Q

what are neuromuscular junctions?

A
  • synapses that occur between a motor neurone and a muscle
  • very similar to synaptic junctions
66
Q

give 1 similarity between neuromuscular junctions and a cholinergic synapse

A

both unidirectional as neurotransmitter receptors only on post synaptic membrane

67
Q

list 4 differences between a neuromuscular junction and a cholinergic synapse

A
  • NJ = excitatory only, CS = excitatory or inhibitory
  • NJ connects motor neurone to muscles, CS connects 2 neurones (could be sensory, relay or motor)
  • NJ = end point for ap, CS = new ap generated in the next neurone
  • in NJ, Ach binds to receptors on muscle fibre membranes, vs post synaptic membrane of a neurone in CS
68
Q

put in order from largest to smallest: myofibril, muscle, sarcomere, muscle fibre

A

muscle, muscle fibre, myofibril, sarcomere

69
Q

outline sliding filament theory

A
  • ap arrives
  • Ca2+ enter + cause tropomyosin to move from the actin + expose the binding sites for the myosin heads
  • whilst ADP is attached to the myosin head, it can bind to binding site on actin to form crossbridge
  • angle craeated in crossbridge created tension + as a result the actin filament is pulled + slides along the myosin
  • this causes ADP molecules to be released
  • an ATP molecule can then bind to the myosin head, causing it to change shape slightly so detaches from actin
  • ATPase hydrolyses the ATP, releasing energy for the myosin head to return to original position
  • continues if enough Ca2+ present
70
Q

what is the function of phosphocreatine?

A

-acts as a reserve supply of phosphate so in anaerobic conditions, pi can bind with ADP to continue producing ATP

71
Q

list 5 components of a myofibril

A
  • A band
  • I band
  • H zone
  • M line
  • Z lines
72
Q

what is the A band of a myofibril?

A

entire myosin length

73
Q

what is the I band of a myofibril made of?

A

actin only

74
Q

what is the H zone of a myofibril made of?

A

myosin only

75
Q

what are the Z lines of a myofibril?

A

form boundaries

76
Q

what is the M line of a myofibril?

A

middle line

77
Q

what happens to the A band when the sarcomere contracts?

A

stays same width (myosin does not move)

78
Q

what happens to the I band when the sarcomere contracts?

A

becomes shorter

79
Q

what happens to the H Zone when the sarcomere contracts?

A

becomes shorter

80
Q

what happens to the Z lines when the sarcomere contracts?

A

slide closer together but do not shorten

81
Q

compare fast and slow twitch muscle fibres

A
  • F = thicker, S = thinner
  • F = more myosin filaments, S = large myoglobin store
  • F = large glycogen store, S = rich blood supply
  • F = in biceps, S = in calf muscles
  • F = contract faster for shorter period, S = contract slower for longer
  • F = more powerful, S = less powerful
  • F = intense exercise, S - endurance
  • F = anaerobic, S = aerobic
82
Q

what is negative feedback?

A

when any deviation from the normal values are restored to their original level

83
Q

outline the response when there is a rise in blood glucose levels

A
  • detected by beta cells in the islets of langerhans
  • beta cells release insulin
  • liver cells become more permeable to glucose, enzymes are also activated to convert glucose to glycogen
  • glucose is removed from blood + stored as glycogen in cells
  • BG returns to normal levels
84
Q

outline the response when there is a fall in blood glucose levels

A
  • detected by alpha cells in the islets of langerhans
  • alpha cells release glucagon
  • adrenal gland releases adrenaline
  • 2nd messenger model occurs to activate enzymes to hydrolyse glycogen
  • glycogen is hydrolysed to glucose + so more glucose is released back into blood
  • BG returns to normal levels
85
Q

define glycogenesis

A
  • glucose to glycogen
  • happens when BG is higher than normal, usually occurs in the liver
86
Q

define glycogenolysis

A
  • glycogen to glucose
  • happens when BG lower than normal, in liver
87
Q

define gluconeogenesis

A
  • non-carb stores (e.g. amino acids) to glucose
  • in liver
  • occurs if all glycogen hydrolysed but body still needs more glucose
88
Q

outline how insulin decreases blood glucose

A
  • attaches to receptors on surface of target cells which changes tertiary structure of the channel proteins resulting in more glucose being absorbed by facilitated diffusion
  • more protein carriers are incorporated into cell membranes so that more glucose is absorbed from the blood into cells
  • enzymes involved in the conversion of glucose to glycogen are activated -> results in glycogenesis in the liver
89
Q

outline how glucagon increases blood glucose

A
  • attaches to receptors on surface of target cells (liver cells)
  • when glucagon binds it causes a protein to be activated into adenylate cyclase + to convert ATP into cAMP
  • cAMP activates protein kinase that can hydrolyse glycogen into glucose
  • enzymes involved in conversion of glycerol + amino acids into glucose are activated
90
Q

in the second messenger model, what is the first messenger?

A

glucagon

91
Q

in the second messenger model, what is the second messenger?

A

cAMP

92
Q

outline the second messenger model

A
  • glucagon binds to glucagon receptors
  • once bound, it causes a change in shape to the enzyme adenyl cyclase, which activates it
  • activated adenyl cyclase enzymes convert ATP to cAMP
  • cAMP activates protein kinase, which in turn converts glycogen to glucose
93
Q

describe the role of adrenaline in the second messenger model

A

if BG too low, adrenal glands will secrete adrenaline which will inc BG

94
Q

outline how adrenaline increases blood glucose

A
  • attaches to receptor on the surface of target cells
  • this causes G protein to be activated which converts ATP to cAMP
  • cAMP activates enzyme that can hydrolyse glycogen into glucose
95
Q

what is type 1 diabetes? what could be the cause? how is it treated?

A
  • body unable to produce insulin
  • could be result of autoimmune disease where beta cells attacked
  • treatment involves insulin injections
96
Q

what is type 2 diabetes? what could be the cause? how is it treated?

A
  • receptors on target cells lose responsiveness to insulin
  • usually develops in adults due to obesity + poor diet
  • controlled by regulating intake of carbs, inc exercise + sometimes insulin injections

A-Level Biology (6 decks)

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