1
Q
How do baroreceptors detect and respond to a fall in blood pressure ?
A
- baroreceptors detect fall in blood pressure
- increases the frequency of impulses to the cardiac centre / medulla
- increases the frequency of impulses to the SAN via the sympathetic nervous system
- noradrenaline is released at synapse between the sympathetic neurone and the SAN
- increases rate of production of electrical waves by SAN; therefore increases heart rate
2
Q
How do baroreceptors detect and respond to a rise in blood pressure ?
A
- baroreceptors detect rise in blood pressure
- increases the frequency of impulses to the cardiac centre / medulla
- increases the frequency of impulses to the SAN via the parasympathetic nervous
system - acetylcholine is released at synapse between the parasympathetic neurone and SAN
- decreases the rate of production of electrical waves by SAN; therefore decreases heart
rate
3
Q
How do chemoreceptors detect a rise in blood pH / low CO2 blood concentration ?
A
- chemoreceptors (in carotid arteries / aorta) detect fall in CO2 / rise in pH
- increases frequency of impulses to cardiac centre / medulla oblongata
- increases frequency of impulses to the SAN via the parasympathetic nervous system
- acetylcholine is secreted at synapse between parasympathetic neurone and SAN;
(stimulates SAN) - decreased rate of electrical wave by the SAN; lowers heart rate
4
Q
How do chemoreceptors respond to a low pH / high CO2 blood concentration ?
A
- chemoreceptors (in carotid arteries / aorta) detect rise in CO2 / acidity / fall in pH
- increases frequency of impulses to cardiac centre / medulla oblongata
- increases frequency of impulses to the SAN via the sympathetic nervous system
- noradrenaline is secreted at synapse between sympathetic neurone and SAN;
(stimulates SAN) - increases rate of production of electrical waves by SAN; increases heart rate
5
Q
The heart controls and coordinates the regular contraction of the atria and the
ventricles, describe how
A
- SAN initiates heartbeat / acts as a pacemaker / myogenic
- SAN sends wave of electrical activity/depolarisation across atria (atrial contraction)
- AVN releases another wave of depolarisation
- non-conducting tissue prevents immediate contraction of ventricles / prevents impulses
reaching the ventricles - AVN delays (electrical activity / impulses)
- (allowing) atria to empty before ventricles contract / ventricles to fill before they contract
- (AVN) sends wave of electrical activity / impulses down Bundle of His / Purkyne fibres
- causes ventricles to contract from base up / ventricular systole
6
Q
How does an increased heart rate lead to a decrease in the blood conc. of CO2 ?
A
• increased blood flow
• more CO2 removed by the lungs
• conc. returns to normal
7
Q
The cardiac muscle is myogenic, what does myogenic mean?
A
• can contract / relax without receiving electrical impulses from nerves
• rate of contraction is controlled by wave of electrical activity
8
Q
What are baroreceptors stimulated by ?
A
high / low blood pressure
9
Q
What are chemoreceptors stimulated by ?
A
high / low pH
10
Q
What are the carotid arteries?
A
arteries that serve the brain
11
Q
What are the two branches of the autonomic nervous system and their functions?
A
- parasympathetic; inhibits effectors
- sympathetic; stimulates effectors
12
Q
What does AVN stand for?
A
Atrioventricular node
13
Q
What does SAN stand for?
A
sinoatrial node
14
Q
Where are baroreceptors and chemoreceptors located?
A
in the aorta and carotid arteries
15
Q
Where are the purkyne fibres found ?
A
in the walls of the ventricles
16
Q
Where is the AVN located ?
A
near the border of the right and left ventricle within the atria still
17
Q
Where is the bundle of His located ?
A
runs through the septum
18
Q
Where is the SAN located ?
A
right atrium and is known as the pacemaker
19
Q
Which centre of the medulla oblongata decreases heart rate?
A
the one that is linked to the SA node by the parasympathetic nervous system
20
Q
Which centre of the medulla oblongata increase heart rate?
A
the one linked to the SA node via the sympathetic nervous system
21
Q
Which part of the brain modifies heart rate?
A
medulla oblongata via the autonomic nervous system
22
Q
A myelinated axon conducts impulses faster than a non-myelinated axon, explain this difference. MS
[3]
A
(In myelinated) action potential / depolarisation only at nodes of Ranvier;
(In myelinated, nerve impulse) jumps from node to node / saltatory;
(In myelinated) action potential / impulse does not travel along whole length
23
Q
•
Compare transmission across cholinergic synapses compared to neuromuscular junctions MS [5
A
neurone to neurone vs neurone to muscle
action potential in neurone vs no action potential in muscle / sarcolemma
no summation in muscle
muscle response always excitatory (never inhibitory)
some neuromuscular junctions have different neurotransmitters (noradrenaline as opposed to
acetylcholine)
24
Q
Define ‘nerve impulse
A
Self-propagating wave of electrical activity that travels down the axon membrane
25
Describe the processes that occur at a cholinergic synapse. MS [8]
arrival of action potential at the presynaptic knob causes depolarisation of synaptic knob
causes Ca2+ gated channels to open/causes Ca2+ to enter axon
vesicles move to / fuse with presynaptic membrane
neurotransmitter (acetylcholine) is released
and diffuses across synaptic cleft
ACH binds with complementary receptors on the postsynaptic membrane
stimulates Na+ channels to open/ Na+ enters postsynaptic neurone
depolarisation of (postsynaptic) membrane;
if above threshold nerve impulse / action potential produced
26
Explain how a resting potential is established. [5]
Na+-K+ pump ATrans 3 Na out axon & and 2 K into axon
e-tro chem. gradient created
neurone membrane more permeable to K+ (open K+ channels) than Na+ (closed channels)
K+ move out of axon by facilitated diffusion
inside of axon more neg compared to outside = resting potential
27
Explain why energy is required in the maintenance of the resting potential in an axon. [2] MS
ATP / energy required by ion pumps
to move Na+ and K+ by Atrans against concentration gradient
28
Generation of AP: Depolarisation
threshold reached
Na+ channels open
more sodium ions diffuse in by facilitated diffusion (+ve feedback)
stimulates even more Na+ channels to open
potential rises rapidly
P.D peaks around +40mV
29
Generation of AP: Hyperpolarisation
K+ ion channels are slow to close
overshoot of K+
too many diffuse out
P.D becomes more -ve than R.P
30
Generation of AP: Refractory Period
ion channels reset
• NaK pump returns membrane to R.P
• another AP cannot be generated in this time
31
in this time
Generation of AP: Repolarisation
• at 40mV
• Na+ V.G channels close
• all K+ V.G channels open
• K+ diffuse down conc. gradient out of the axon
• inside of membrane becomes less positive
• returns membrane to resting potential
32
What happens to acetylcholine after it has triggered an AP in the post-synaptic membrane? [3]
• Acetylcholinesterase breaks down acetylcholine in the cleft (into acetate + choline)
• These diffuse back into pre-synaptic membrane
• ATP resynthesises + stores back into vesicles (assisted by SER)
33
What is the 'all or nothing' principle?
• AP only occurs when membrane is depolarised to a certain threshold (-55mV)
• stimulus causes enough Na+ channels to open
• if this is not reached, AP will not be triggered
• not enough Na+ channels open = few Na+ diffuses
• a bigger stimulus won't cause a bigger AP, AP is just fired more frequently
34
Describe and explain differences in sensitivity to light between rods and cones. [5]
rods are more sensitive to light
- they are connected in groups to one bipolar neurone
- spatial summation
- stimulation of each individual rod cell is insufficent, however because they are connected in groups the threshold is more likely to be reached/action potential generated
cones are less sensitive to light
- one cone joins to one neurone
- no spatial summation
- threshold not reached during exposure to low levels of light
35
Describe and explain the differences between sensitivity to colour between rods and cones.
rods allow monochromatic vision
- one type of pigment (rodhopsin)
cones allow trichromatic vision
- 3 types of cones
- different optical pigments (opsins) that absorb different wavelengths (red, green and blue) - stimulation of different combinations of cones give a range of colour perception.
36
Describe and explain the differences in visual acuity between rod and cone cells.
rods give lower visual acuity:
- rods connected in groups to one bipolar neurone
- spatial summation
- many neurones generate ONE action potential, regardless of the no. of neurones stimulated. - therefore they cannot distinguish between separate sources of light
cones give a higher visual acuity:
- one cone joins to one neurone
- if 2 adjacent cones are stimulated, the brain receives 2 separate impulses - therefore it can distinguish between 2 separate sources of light.
37
Describe what a pacinian corpuscle looks like ?
A single sensory neurone wrapped with layers of tissue seperated by gel
38
Why do rods process images in black and white ?
Because they cannot distinguish different wavelengths of light
39
Why do cones have high visual activity ?
• each cone is connected to one bipolar cell
• the brain can distinguish between seperate sources of light detected
40
Why can't we see colour when it's dark ?
• one cone cells connects to a bipolar cell
• no spatial summation occurs
• cones can only respond to high light intensity
41
Why can rods detect light of very low intensity ?
• because many rod cells connect to one sensory neurone • retinal convergence
42
Why can cone cells perceive colour images ?
• 3 types of cone cells that contain different types of iodopsin pigment
• they absorb different wavelengths of light
• depending on the proportion of each cone cell that is stimulated we perceive colour images
43
Which part of the retina receives the highest intensity of light ?
light is focused on the fovea (opposite the pupil)
44
Where are rod cells found ?
• further away from the fovea/ in the periphery of the retina
• as they can respond/pigment are broken down at lower light intensities
45
Where are Pacinian Corpuscles present?
• abundant deep in the skin
• occur in joints, ligaments and tendons i.e fingers, feet soles
46
Where are most of the cone cells located ?
• located/concentrated near the fovea
• as they respond to high light intensities/ need bright light to be stimulated
47
When is iodopsin broken down ?
• only when there is a high light intensity
• action potentials can only be generated with enough light
48
What needs to broken down to create a generator potential ?
• the pigment of rod cells (rhodopsin) must be broken down by light energy
• there is enough energy from low-intensity light to cause the breakdown
• enough pigment has to be broken down to reach threshold in the bipolar cell
49
What leads to the establishment of a generator potential ?
• when pressure is applied
• deforms the neurone plasma membrane
• stretches and widens the Na+ channels
• Na+ diffuses in
• leads to the establishment of a generator potential
50
What does the retina contain ?
photoreceptors rods and cones
51
What do sensory neurones in the pacinian corpuscle contain ?
• plasma membranes contain channel proteins
• allows ion transportation
• membranes surrounding sensory neurones have stretch-mediated sodium channels
52
Give ways in which hormonal coordination differs from nervous coordination MS [5]
• chemical (not electrical)
• slower (to take effect / transmission) • longer-lasting
• delivered by blood (not nerves)
• broader targetting
53
Explain how applying pressure ot the Pacinian Corpuscle leads to the generation of an AP. [5]
• Pressure causes membrane / lamellae to become distorted / stretched;
• Stretched-mediated Na+ ion channels open
• Na+ ions diffuse into the neurone; depolarising the membrane and producing a GP • Greater pressure causes more channels to open / more Na+ to enter
• GP creates AP if threshold reached
54
Disadvantage of retinal convergence ?
• brain cannot distinguish between the seperate sources of light that stimulated it • 2 light sources close together cannot be seen as seperate
• rod cells = low visual activity
55
what is the role of ATP in myofibril contraction? MS [3]
hydrolysis of ATP (on myosin heads) causes myosin heads to bend;
(bending) pulling actin molecules; power stroke
attachment of a new ATP molecule to each myosin head causes myosin heads to detach (from actin sites);
recovery stroke
56
what is the role of ATPase in myofibril contraction? MS [3]
what is the role of ATPase in myofibril contraction? MS [3]
1. splitting/breakdown/hydrolysis of ATP into ADP + Pi
2. (muscle) contraction requires energy / ATP
3. use of ATP by myosin (to bend / detach)
57
what is the role of phosphocreatine (PC) in providing energy during muscle contraction? MS
[2]
[2]
1. provides phosphate
2. to make ATP (ADP + CP → ATP + C );
58
what is the difference between myofibrils and sarcomeres?
• myofibrils = contracting units of muscles
• sarcomeres = repeating units of the myofibril
59
what is a sarcomere?
the basic unit of muscle contraction in a myofibril (which is in a muscle cell)
60
what happens to the length of the I band during muscle contraction?
decrease in length
61
what happens to the length of the H zone during muscle contraction?
decrease in length
62
what happens to the length of the A band during muscle contraction?
remains unchanged in length
63
what do active muscles require ?
• high conc of ATP
• not enough ATP created = phosphocreatine (stored in muscles)
• provides phosphate to regenerate ATP from ADP
64
recall what occurs during muscle relaxation. [4]
• Ca2+ ions move by Atrans back to sarcoplasmic reticulum
• uses energy from ATP
• reabsorption of Calcium causes tropomyosin to block actin filament
• myosin heads no longer able to bind
65
recall the structure of skeletal muscles. [5]
• skeletal muscles made up of many fibres called myofibrils
• which are divided into contractual units called sarcomeres
• muscle fibres fused together + shared nuclei and cytoplasm (sarcoplasm)
• myosin + actin filaments overlap, strenghtening the muscle
• sarcoplasm contains sarcoplasmic reticulum + mithcondria
66
recall the adaptations of ST muscle fibres. [3]
• large myoglobin store (stores oxygen)
• rich supply of blood vessels (aerobic respiration)
• numerous mitochondria
67
recall the adaptations of FT muscle fibres. [4]
• thicker, more numerous myofilaments
• lots of Glycogen
• lots of enzyme involved in AnRes, provides ATP rapidly
• stores of phosphocreatine
68
recall how muscular contraction is stimulated when an AP reaches the end of a motor neurone. [6]
• AP arrives at NMJ
• influx of Ca2+ and release of acetyl choline (from presynapse)
• acetylcholine diffuses across cleft; binds to receptor sites on sarcolemma
• influx of Na+, causes AP in sarcolemma
• impulse carried through the muscle fibres through T-tubules
• triggers release of Ca2+ from sarcoplasmic reticulum
69
recall how muscles work in antagonistic pairs. [5]
• muscles can only pull
• they work in opposing pairs (e.g hamstring + quads / biceps + triceps)
• contracting muscle = agonist
• relaxing muscle = antagonist
• muscle contracting becomes 'shorter'
70
how does the function of slow twitch fibres differ from fast twitch fibres? [8]
1. ST contract more slowly; FT contract rapidly
2. ST found in calf muscles; FT found in biceps
3. ST provide less powerful contractions; FT powerfully contract
4. ST contract over longer periods of time = endurance work (no lactic acid); FT adapted for intense
exercise (lactic acid = muscle fatigue)
5. ST has rich blood supply, large store of myoglobin, many mitochondria; FT has large store of
glycogen, store of phosphocreatine and a high conc of enzymes (involved in anerobic respiration)
6. FT is thicker and has more myosin filaments
7. ST = aerobic respiration; FT = anaerobic respiration
8. ST = red due to high myoglobin; FT = white due to less myoglobin
71
describe the roles of calcium ions and ATP in the contraction of a myofibril. [10]
1. Ca2+ diffuse into myofibrils from sarcoplasmic reticulum
2. Ca2+ bind to troponin and cause it to change shape
3. this causes tropomyosin to move to myosin head of actin
4. causes exposure of the binding sites on the actin
5. myosin heads attach to binding sites on actin
6. hydrolysis of ATP into ADP + Pi
7. ADP attatches to myosin heads causing them to bend
8. when ADP is attatched to myosin head it binds to actin filament forming a crossbridge
9. the bending causes pulling actin molecules
10. attachment of a new ATP molecule to each myosin head causes myosin heads to detach from actin
sites
Bio AQA A-Level
flashcards
Decks in class (5)
# Cards
