Response to changes in the environment Flashcards
(97 cards)
1
Q
stimulus
A
detectable change in the environment
2
Q
tropism
A
response of plants to stimuli via growth
3
Q
what are tropisms controlled by
A
growth factors e.g. indoleacetic acid (IAA)
4
Q
what does IAA do
A
controls cell elongation in shoots and inhibits the growth of cells in the roots
5
Q
where is IAA made
A
in the tips of roots of shoots and can diffuse to other cells
6
Q
positive phototropism
A
shoot tip cells produce IAA which causes elongation in the shoots
the IAA diffuses towards the shaded side of the shoot which causes the plant to bend towards the light source
7
Q
negative phototropism
A
in roots, IAA inhibits cell elongation
root cells elongate more on the lighter side so the root bends away from light
8
Q
negative gravitropsim
A
in shoots the IAA diffuses from the upper side to the lower side
if the plant is vertical, this causes the plant cells to elongate and the plant grows upwards
is the plant is horizontal, it causes the shoot to bend upwards
9
Q
positive gravitropism
A
in roots the IAA moves to the lower side and inhibits growth so the upper side elongates more and the root bends down
10
Q
taxes
A
organism moves its entire body towards a favourable stimulus (positive taxis) or away from an unfavourable stimulus (negative taxis) in one direction
11
Q
kinesis
A
organism changes its speed of movement and its rate it changes direction
if an organism moves from an area where there is beneficial stimulus to an area of harmful stimulus its response will be to increase the rate it changes direction
12
Q
reflex arc
A
stimulus –> receptor –> coordinator –> effector –> response
13
Q
components of the nervous system
A
peripheral nervous system - receptors, sensory neurones and motor neurones
central nervous system - coordination centres like brain and spine
14
Q
pacinian corpuscle
A
responds to pressure changes
located deep in the skin - mainly in fingers and feet
15
Q
structure of pacinian corpuscle
A
single sensory neurone wrapped with layers of connective tissue which are separated by gel
the sensory neurone has special channel proteins it its plasma membrane
16
Q
how does the pacinian corpuscle establish a generator potential
A
the plasma membranes of the sensory neurones contain channel proteins that allow ion transportation - they are stretch-mediated sodium channels which open and allow sodium ions to diffuse into the sensory neurone when they are stretched and deformed
in the resting state, sodium ion channels are too narrow for sodium ions to diffuse in so the resting potential is maintained
then pressure is applies, the stretch-mediated sodium ion channels are deformed and widen so sodium ions diffuse in and a generator potential is established
17
Q
what light can rods detect
A
they can’t distinguish between different wavelengths of light so process images in black and white
they can detect light of very low intensity as many rods connect to one sensory neurone (retinal convergence)
18
Q
how is a generator potential established in rods
A
the rhodopsin pigment in rods must be broken down by light energy
enough pigment has to be broken down for the threshold to be met in the bipolar cell
spatial summation - threshold can be reached even in low light as many rod cells are connected to a single bipolar cells
19
Q
why do rod cells give low visual acuity
A
retinal convergence means the brain can’t distinguish between the separate sources of light that stimulated it - two close together light sources can’t be seen as separate
20
Q
how can cone cells see colour
A
there are three types of cone cells that have different types of iodopsin pigment (red, green, and blue) which all absorb different wavelengths of light
21
Q
why can cone cells only see in high light intensity
A
iodopsin is only broken down if there is high light intensity so action potentials can only be generated with enough light
only one cone cell connects to a bipolar cell so no spatial summation occurs and cones can only respond to high light intensity - why we can’t see colour in the dark
22
Q
how do cone cells have high visual acuity
A
each cone cell is connected to one bipolar cell so the brain can distinguish between separate source of light
23
Q
distribution of rods and cones in the retina
A
uneven
light is focused by the lens on the retina opposite the pupil (the fovea) this recieves the highest intensity of light so most cone cells are located near the fovea and most rod cells are further away
24
Q
what does it mean when it says that cardiac muscle is myogenic
A
it contracts of its own accord
25
where is the sinoatrial node located
'pacemaker' in the right atrium
26
where is the atrioventricular node located
near the border of the right and left ventricle within the atria
27
where is the bundle of His located
in the septum
28
where are the Purkyne fibres found
in the walls of the ventricles
29
how is the heart stimulated to contract
SAN releases wave of depolarisation across the atria, causing it to contract
the AVN releases another wave of depolarisation when the first reaches it - there is a slight delay the ventricles don't contract before the atria can fully empty
there is a non-conductive layers between the atria and ventricles that prevents the wave of depolarisation from travelling down the ventricles
the Bundle of His runs through the septum and passes the wave of depolarisation to the Purkyne fibres in the walls of the ventricles
the walls of the ventricles contract, from the apex upwards
the cells repolarise and the cardiac muscle relaxes
30
what in the brain controls the heart rate
the medulla oblongata via the automatic nervous system
31
componenets of the automatic nervous system
a centre linked to the sinoatrial nose that increases the heart rate via the sympathetic nervous system and another that decreases heart rate via the parasympathetic nervous system
32
what causes the heart rate to change
pH (detected by chemoreceptors) and blood pressure (detected by baroreceptors) in the aorta and carotid artery
33
what happens is blood pressure is wrong
too high - causes damage to the walls of arteries
too low - insufficient supply of oxygenated blood to respiring cells and waste not removed
34
what happens if pH is wrong
can become too high in times of high respiratory rate due to the production of carbon dioxide and lactic acid - needs to be removed to prevent enzymes denaturing
heart rate is increased so CO2 can diffuse out into alveoli to be removed
35
response to high blood pressure
stimulus - increased pressure
receptor - pressure receptors in wall of aorta and carotid artery stretch if high blood pressure
coordination - more electrical impulses sent to medulla oblongata and impulses sent via parasympathetic nervous system to SAN to decrease the frequency of electrical impulses
effector - cardiac muscle/SAN tissues
response - reduced heart rate
36
response for low blood pressure
stimulus - decreased pressure
receptor - pressure receptors in wall of aorta/carotid are stretched less
coordination - more electrical impulses sent to medulla oblongata and impulses sent via sympathetic nervous system to SAN to increase frequency of electrical impulses
effector - cardiac muscle/SAN tissues
response - increased heart rate
37
response for low pH
stimulus - decreased pH
receptor - chemoreceptor in wall of aorta/carotid
coordination - more electrical impulses sent to medulla oblongata and then impulses sent via sympathetic nervous system to SAN to increase the frequency of electrical impulses
effector - cardiac muscle/SAN tissues
response - increased heart rate
38
structure of a myelinated motor neurone
cell body - contains organelles like nucleus, proteins and neurotransmitter made here
dendrites - branch off cell body, carry action potentials to surrounding cells
axon - long conductive fibre that carries nerve impulse along the neurone
Schwann cells - wrap around axon to form myelin sheath, lipid so doesn't allow charged ions to pass through - they remove debris via phagocytosis and aid regeneration
nodes of Ranvier - gaps in the myelin sheath
39
saltatory conduction
electrical impulse jumps between nodes of Ranvier, increasing transmission speed
40
resting potential
when neurone is not conducting an impulse, there is a difference between the electrical charge inside and outside the neurone - the resting potential
there are more positive ions (Na+ and K+) outside than inside so the inside of the neurone is more negative at -70mV
41
how is the resting potential maintained
by a sodium potassium pump
it moves 2K+ in and 3Na+ out via active transport, using ATP
this creates an electrochemical gradient which results in K+ diffusing out and Na+ diffusing in
because the membrane is more permeable to K+, more is moved out, resulting in -70mV
42
action potential
when the neurone's voltage increases beyond a set point from the resting potential this generates a nervous impulse
an increase in voltage or depolarisation is due to the membrane becoming more permeable to Na+
43
how does a stimulus lead to an action potential
stimulus provides the energy for the sodium voltage-gated channels in the axon membrane to open
this causes sodium ions to diffuse in, increasing the positivity inside the axon
this causes more voltage-gated channels to open so more sodium ions diffuse in
when a threshold of +40mV is reached inside the axon, the voltage-gated sodium channels close
voltage-gates potassium ion channels open so potassium ions diffuse out
the axon is depolarised (becomes more negative again)
the axon temporarily becomes more negative than -70mV and is hyper polarised (refractory period)
the potassium ion gates shut and the sodium potassium pump restores normal activity to reform the resting potential
44
what is the all-or-nothing principle
if depolarisation doesn't exceed -55mV threshold then an action potential is not produced
any stimulus that triggers depolarisation to -55mV will always peak at the same maximum voltage
bigger stimuli increase the frequency of action potentials, not size
45
why is the all-or-nothing principle important
it makes sure animals only respond to large enough stimuli, rather than every slight change in the environment as this would overwhelm them
46
refractory period
after an action potential s generated, the membrane enters a refractory period when it can't be stimulates because the sodium channels are recovering and can't be opened
47
why is the refractory period important
it ensures that discrete impulses are produced, meaning that an action potential can't be generated immediately after another one - each is separate
it ensures that action potentials travel in one direction, stopping the action potential from spreading out in two directions, preventing a response
it limits the number of impulse transmissions to prevent overreaction to a stimulus
48
what factors affect speed of conductance
myelination and saltatory conduction axon diametertemperature
49
how does saltatory conduction lead to faster conductance
the action potential jumps from node to node (nodes of Ranvier) which means that action potentials travel along the axon faster as ut doesn't have to generate an action potential along the entire length, just the nodes of Ranvier
50
how does axon diameter impact the speed of conductance
with a wider diameter the speed of conductance increases as there is less leakage of ions and therefore action potentials travel faster
51
how does temperature impact speed of conductance
higher temp increases speed of conductance
the ions diffuse faster
the enzymes involved in respiration work faster - more ATP for active transport in the sodium potassium pump
52
synapse
gaps between the end of the axon of one neurone and the dendrite of another
53
transmission across a cholinergic synapse (also generalised to any synapse but say neurotransmitter instead of acetylcholine)
action potential arrives at presynaptic knob, depolarising it, leading to the opening of Ca2+ channels and Ca2+ diffusing in
this pushes vesicles containing acetylcholine to move towards and fuse with the presynaptic membrane, releasing acetylcholine into the synaptic cleft
acetylcholine diffuses down a concentration gradient across the synaptic cleft to the postsynaptic membrane
acetylcholine binds to complementary receptors on the surface of the postsynaptic membrane
Na+ channels on the postsynaptic membrane open and Na+ diffuse in
if enough acetylcholine binds, and enough Na+ diffuse in to raise the membrane potential above the -55mV threshold, the postsynaptic neurone is depolarised
the acetylcholine is hydrolysed by acetylcholinesterase into choline and acetate which are released from the receptor, back to the presynaptic neurone where it is recycled
the Na+ channels close and the postsynaptic neurone reestablished the resting potential
54
why are impulses unidirectional
they can only travel in one direction cross the synapse as neurotransmitter is only released from the presynaptic neurone and therefor only diffuses from there to the postsynaptic neurone
additionally, there are only receptors for the neurotransmitter on the postsynaptic neurone
55
what is summation
the rapid build up of neurotransmitters in the synapse to help generate an action potential
56
spatial summation
many different neurones collectively trigger a new action potential by combining the neurotransmitter they release to exceed the threshold
57
temporal summation
one neurone releases neurotransmitters repeatedly over a short period of time in order to exceed the threshold
58
why is summation needed
some action potentials don't result in sufficient concentrations of neurotransmitters being released to generate a new action potential
59
inhibitory synapse
cause chloride ions to move into the postsynaptic neurone and potassium ions to move out
this causes the membrane potential to rise to -80mV (hyper polarisation) an therefore an action potential is almost impossible to trigger
60
neuromuscular junction
the synapse between a motor neurone and a muscle
61
how are neuromuscular junctions and cholinergic synapses similar
they are both unidirectional due to neurotransmitter receptors only being on the postsynaptic membrane
62
differences between neuromuscular junction and cholinergic synapse
neuromuscular are only excitatory whereas cholinergic can be excitatory or inhibitory
nm connects motor neurone to muscles cs connects two neurones which can be sensory, motor, or relay
nm is the end point for an action potential, in cs a new action potential is generated in the next neurone
nm acetylcholine binds to receptors on the muscle fibre membranes, in cs it binds to receptors on the postsynaptic membrane of a neurone
63
how do muscles work (broadly)
in antagonistic pairs against an incompressible skeleton
64
what are myofibrils made up of
fused cells that share nuclei and sarcoplasm - there's a high number of mitochondria
65
the sarcomere
myofibrils are made up of two key types of protein - myosin (thick) and actin (thin) (combined forms the sarcomere)
66
what are the bands of the sarcomere
I band - only thin actin filaments
A band - the edges are very dark as thick myosin and thin actin overlap
H zone - in the middle of the A band, contains thick myosin filaments only
Z lines - vertical down the I band and outlines where the sarcomere starts and finishes
67
sliding filament theory
action potential reaches a muscle
Ca2+ enter and cause the protein tropomyosin (blocking the binding sites on the actin for the myosin heads) to move and uncover the binding sites
whilst ADP is attached to the myosin head, it can bind to the binding site on the actin, forming a cross bridge
the angle in the cross bridge creates tension, pulling the actin filament and causing it to slide along the myosin, causing a molecule of ADP to be released
an ATP molecule can then bind to the myosin head and cause it to change shape/bend, detaching from the actin
in the sarcoplasm, enzyme ATP hydrolase is activated by the Ca2+ and hydrolyses the ATP on the myosin head into ADP
this releases enough energy for the myosin head to turn to its original position
the entire process repeats continually whilst the Ca2+ remain in high concentration in the sarcoplasm, therefore while the muscle remains stimulated by the nervous system
68
what happens when aerobic respiration doesn't create enough ATP to meet the demand for muscle contraction
anaerobic respiration occurs
phosphocreatine, stored in muscles, combats this by providing phosphate to regenerate ATP from ADP
69
comparison of structure of slow and fast twitch fibres
slow twitch fibres contain a large store of myoglobin, a rich blood supply, and many mitochondria
fast twitch fibres are thicker and have more myosin filaments, they have a large store of glycogen, a store of phosphocreatine to help make more ATP from ADP, and a high conc of enzymes involved in anaerobic respiration
70
location examples of fast and slow twitch fibres
slow - calf muscles
fast - biceps
71
comparison of general properties of fast and slow twitch fibres
slow - contract slower and can respire aerobically for longer due to rich blood supply and myoglobin oxygen store, they are adapted for endurance work like marathons
fast - contract faster to provide short bursts of powerful contraction, they are adapted for intense exercise like sprinting or weight-lifting
72
homeostasis
the maintenance of a constant internal environment via physiologic control systems which respond to counteract change
73
what happens if body temp is wrong
too low - insufficient kinetic energy for enzyme controlled reactions
too high - enzymes denature
74
what happens if blood glucose levels wrong
too low - cell death due to lack of respiration
too high - lowers w.p blood and water leaves surrounding cells by osmosis, cells shrivel and die
75
negative feedback
when there is deviation from the normal values and restorative systems are put in place to return this back to the original level
involves the nervous system and usually hormones
76
what causes blood glucose levels to fluctuate
will increase following ingestion of food/drink containing carbohydrates
will fall following exercise or if you haven't eaten
77
control of body temp
rise in temp detected by temperature sensors and the thermoregulatory centre in the hypothalamus
sweat, lower hairs more blood through capillaries
return to normal body temp
decrease in temp detected
no sweat, hairs stand up, less blood through capillaries
78
what happens when blood glucose conc rises
beta cells in islets of Langerhans have receptors that detect rise and secrete insulin
insulin binds with glycoprotein receptors on cell surface membranesincreased rate of glucose absorption in cells as change in tertiary structure of glucose transport carrier proteins so more glucose can enter via facilitated diffusion, also can cause more channels to formincreased respiratory rate so glucose is used upenzymes activated so glucose converted to glycogen in glycogenesis in the liver and muscles glucose converted to fat
79
what happens when blood glucose conc lowers
alpha cells in the islets of Langerhans detect fall in blood glucose and secrete glucagon into the blood plasma
they attach to specific receptors on the cell surface membrane of liver cells activates enzymes involved in hydrolysis of glycogen to glucose (glycogenolysis) glucose moves back into blood stream by facilitated diffusionactivates enzymes involved in the conversion of amino acids and glycerol into glucose (gluconeogenesis)results in increase in blood glucose conc
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glycogenesis
process of when excess glucose is converted to glycogen when blood glucose conc is higher than normal
it occurs in the liver
81
glycogenolysis
breakdown of glycogen back into glucose in the liver
occurs when blood glucose is lower than normal
82
gluconeogenesis
process of creating glucose from non-carbohydrate stores (typically amino acids and glycerol) in the liver
occurs if all glycogen has already been hydrolysed back into glucose an your body still needs more glucose
83
how does adrenaline play a role in increasing blood glucose concentration
it is released by the adrenal glands in times of excitement and stress and used to increase blood glucose
it attaches to protein receptors on the cell surface membrane of target cells
this causes G protein to be activated and to convert ARP to cAMP
cAMP activates an enzyme for glycogenolysis
84
second messenger model with adrenaline
involves two hormones: adrenaline and glucagon
adrenaline binds to protein receptor on cell surface membrane of the liver cell
this causes the protein to change shape and activates the enzyme adenylate cyclase which converts ATP to cyclic AMP (cAMP)
this acts as a second messenger than binds to protein kinase enzyme, changing its shape and activating it
the protein kinase enzyme catalyses glycogenolysis
glucose moves out of liver by facilitated diffusion and into the blood
85
type 1 diabetes
body is unable to produce insulin
it starts in childhood and can be the result of an autoimmune disease where the beta cells are attacked
treatment involves injection of insulin
86
type 2 diabetes
due to receptors on target cells losing their responsiveness to insulin
typically develops in adults due to obesity and poor diet
it is controlled by regulating the intake of carbohydrates, increasing exercise, and insulin injections
87
osmoregulation
process of controlling the water potential of the blood
88
structure of the nephron
Bowman's capsule - ultrafiltration occurs here, it has a wider afferent arteriole which enters the glomerulus and a smaller efferent arteriole which leaves the glomerulus
glomerulus - network of capillaries that filter blood, it is lined with endothelial cells and podocytes
proximal convoluted tubule - coiled region after the Bowman's capsule
loop of Henle - hairpin bend
distal convoluted tubule - another coiled region after the loop of Henle
collecting duct - after the DCT
vasa recta - capillaries surrounding the lower bit of the loop of Henle
cortex - upper section of kidney which holds the Bc, the Pct, and the DCT
medulla - lower section of kidney which the loop of Henle and collecting duct dip into
89
ultrafiltration of blood
blood enters glomerulus through afferent arteriole and leaves via efferent arteriole, which is narrower - the maintains high hydrostatic pressure
the high pressure forces small molecules like water, ions, and small solutes out of fenestrations in the endothelium of the capillary
the molecules move through the basement membrane of the Bowman's capsule - it has collagen fibres which act as a selective filter, preventing larger molecules and blood cells from passing into the Bowman's capsule
the epithelium of the Bowman's capsule has podocytes with extensions that wrap around capillaries and aid in filtering the blood
filtered fluid collects in the Bowman's capsule
90
how are cells lining the PCT adapted for selective reabsorption
microvilli - larger surface area
channel/carrier proteins - facilitated diffusion/co-transport
carrier proteins - active transport
mitochondria - ATP for active transport
ribosomes - produce channel/carrier proteins
91
selective reabsorption in the PCT
many ions, small molecules, and water molecules are reabsorbed from the ultra filtrate back into the capillaries surrounding the proximal convoluted tubule
92
what substances are/aren't reabsorbed in the PCT
water - most reabsorbed - by osmosis
glucose - all reabsorbed - by co-transport (some active transport, some facilitated diffusion)
amino acids - all reabsorbed - by co-transport (some active transport, some facilitated diffusion)
ions - some reabsorbed - by co-transport/facilitated diffusion
small proteins - some reabsorbed - by endocytosis
urea - tiny amount reabsorbed - by diffusion
93
how is a gradient of Na+ maintained in the medulla of the kidney by the loop of Henle
Na+ moves out of the ascending limb by active transport into the interstitial fluid
the increase in Na+ lowers the water potential of the i.f
Na+ diffuses into the descending limb
water moves out of the descending limb by osmosis into the i.f, it then enters the capillaries and is removed
the water potential towards the base of the descending limb is lowered due to the movement of water out by osmosis
Na+ moves out of the base of the ascending limb by diffusion and out of the upper region by active transport, again lowering the water potential of the i.f
a water potential gradient is created in the i.f between the ascending limb and the collecting duct, with water potential lowering further into the medulla
this gradient is maintained by the fact that the ascending limb is impermeable to ater
94
describe the countercurrent multiplier in the medulla
as filtrate moves down the collecting duct, it loses water, decreasing the water potential
due to the concentration gradient of Na+ in the medulla, the water potentials of the surrounding i.f is even lower than in the collecting duct
this allows water to continue to move out of the filtrate down the whole length of the collecting duct
95
how do osmoreceptors work
if water potential of blood is too low, water leaves osmoreceptors and they shrivel
this stimulates the hypothalamus to produce more of the hormone ADH
if water potential is too high, water enters osmoreceptors by osmosis
this stimulates the hypothalamus to produce less ADH
96
role of hypothalamus in regulating water potential
changes in water potential of the blood are detected by osmoreceptors in the hypothalamus
antidiuretic hormone is secreted from the hypothalamus to the posterior pituitary gland where it can be released into capillaries and into the bloodstream to the kidney
97
how does ADH make urine more concentrated
when ADH reaches the kidney, it binds to receptors on the cell membranes of the DCT and the collecting duct
this activates a phosphorylase enzyme in the cells
this causes the vesicles containing aquaporins to fuse with the cell membrane, resulting in more embedded aquaporins - these are protein channels for water to pass through
this means more water leaves the DCT and collecting duct and is reabsorbed into the blood
