TOPIC 6: ORHANISMS RESPOND TO CHANGE IN THEIR INTERNAL AND EXTERNAL ENVIRONMENTS Flashcards

1
Q

Stimulus

A

Detectable change in the
environment
detected by cells called
receptors

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2
Q

Nervous system
structure

A

Central nervous system = brain
and spinal cord
peripheral nervous system =
receptors, sensory and motor
neurones

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3
Q

Simple reflex
arc

A

Stimulus (touching hot object)
-> receptor
-> sensory neurone
-> coordinator (CNS / relay
neurone
-> motor neurone
-> effector (muscle)
-> response (contraction)

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4
Q

Importance of
simple reflexes

A

Rapid - short pathway
only three neurones & few
synapses
autonomic
conscious thought not
involved - spinal cord
coordination
protect from harmful stimuli
e.g., burning

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5
Q

Tropism

A

Response of plants to stimuli
via growth
can be positive (growing
towards stimulus) or negative
(growing away from stimulus)
controlled by specific growth
factors (IAA)

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6
Q

Specific
tropisms

A

Response to light
phototropism
response to gravity
gravitropism
response to water
hydrotropism

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7
Q

Indoleacetic
acid

A

Type of auxin (plant hormone)
controls cell elongation in shoots
inhibits growth of cells in roots
made in tips of roots / shoots
can diffuse to other cells

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8
Q

Phototropism
in shoots

A

Shoot tip produces IAA
diffuses to other cells
IAA accumulates on shaded
side of shoot
IAA stimulates cell elongation
so plant bends towards light
positive phototropism

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9
Q

Phototropism
in roots

A

Root tip produces IAA
IAA concentration increases on
lower (darker) side
IAA inhibits cell elongation
root cells grow on lighter side
root bends away from light
negative phototropism

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10
Q

Gravitropism
in shoots

A

Shoot tip produces IAA
IAA diffuses from upper side to
lower side of shoot in response
to gravity
IAA stimulates cell elongation
so plant grows upwards
negative gravitropism

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11
Q

Gravitropism
in roots

A

Root tip produces IAA
IAA accumulates on lower side
of root in response to gravity
IAA inhibits cell elongation
root bends down towards
gravity and anchors plant
positive gravitropism

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12
Q

Taxis

A

Directional response by simple
mobile organisms
move towards favourable
stimuli (positive taxis) or away
from unfavourable stimuli
(negative taxis)

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13
Q

Kinesis

A

When an organism changes its
speed of movement and rate of
change of direction in response to
a stimulus
if an organism moves to a region
of unfavourable stimuli it will
increase rate of turning to return
to origin
if surrounded by negative stimuli,
rate of turning decreases - move
in straight line

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14
Q

Receptors

A

Responds to specific stimuli
stimulation of receptor leads to
establishment of a generator
potential - causing a response
pacinian corpuscle
rods
cones

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15
Q

Pacinian
corpuscle

A

Receptor responds to pressure
changes
occur deep in skin mainly in
fingers and feet
sensory neurone wrapped with
layers of tissue

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16
Q

How pacinian
corpuscle
detects pressure

A

When pressure is applied,
stretch-mediated sodium ion
channels are deformed
sodium ions diffuse into
sensory neurone
influx increases membrane
potential - establishment of
generator potential

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17
Q

Rod cells

A

Concentrated at periphery of
retina
contains rhodopsin pigment
connected in groups to one
bipolar cell (retinal
convergence)
do not detect colour

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18
Q

Cone cells

A

Concentrated on the fovea
fewer at periphery of retina
3 types of cones containing
different iodopsin pigments
one cone connects to one
neurone
detect coloured light

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19
Q

Rods and cones:
describe
differences in
sensitivity to light

A

Rods are more sensitive to light
cones are less sensitive to light

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20
Q

Rods and cones:
describe
differences in
visual acuity

A

Cones give higher visual acuity
rods have a lower visual acuity

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21
Q

Visual acuity

A

Ability to distinguish between
separate sources of light
a higher visual acuity means
more detailed, focused vision

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22
Q

Rods and cones:
describe
differences in
colour vision

A

Rods allow monochromatic
vision (black and white)
cones allow colour vision

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23
Q

Why rods have
high sensitivity
to light

A

Rods are connected in groups to
one bipolar cell
retinal convergence
spatial summation
stimulation of each individualcell
alone is sub-threshold but
because rods are connected in
groups more likely threshold
potential is reached

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24
Q

Why cones have
low sensitivity
to light

A

One cone joins to one neurone
no retinal convergence / spatial
summation
higher light intensity required
to reach threshold potential

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25
Q

Why rods have
low visual
acuity

A

Rods connected in groups to
one bipolar cell
retinal convergence
spatial summation
many neurones only generate 1
impulse / action potential ->
cannot distinguish between
separate sources of light

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26
Q

Why cones
have high
visual acuity

A

One cone joins to one neurone
2 adjacent cones are
stimulated, brain receives 2
impulses
can distinguish between
separate sources of light

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27
Q

Why rods have
monochromatic
vision

A

One type of rod cell
one pigment (rhodopsin)

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28
Q

Why cones give
colour vision

A

3 types of cone cells with
different optical pigments
which absorb different
wavelengths of light
red-sensitive, green-sensitive
and blue-sensitive cones
stimulation of different
proportions of cones gives
greater range of colour
perception

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29
Q

Myogenic

A

When a muscle (cardiac
muscle) can contract and relax
without receiving signals from
nerves

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30
Q

Sinoatrial
node

A

Located in right atrium and is
known as the pacemaker
releases wave of depolarisation
across the atria, causing
muscles to contract

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31
Q

Atrioventricular
node

A

Located near the border of the
right / left ventricle within atria
releases another wave of
depolarisation after a short
delay when it detects the first
wave from the SAN

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32
Q

Bundle of His

A

Runs through septum
can conduct and pass the wave
of depolarisation down the
septum and Purkyne fibres in
walls of ventricles

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33
Q

Purkyne fibres

A

In walls of ventricles
spread wave of depolarisation
from AVN across bottom of the
heart
the muscular walls of ventricles
contract from the bottom up

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34
Q

Role of nonconductive
tissue

A

Located between atria and
ventricles
prevents wave of depolarisation
travelling down to ventricles
causes slight delay in ventricles
contracting so that ventricles
fill before contraction

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35
Q

Importance of short
delay between SAN
and AVN waves of
depolarisation

A

Ensures enough time for atria to
pump all blood into ventricles
ventricle becomes full

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36
Q

Role of the
medulla
oblongata

A

Controls heart rate via the
autonomic nervous system
uses sympathetic and
parasympathetic nervous
system to control SAN rhythm

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37
Q

Chemoreceptors

A

Located in carotid artery and
aorta
responds to pH / CO2 conc.
changes

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38
Q

Baroreceptors

A

Located in carotid artery and
aorta
responds to pressure changes

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39
Q

Response to high
blood pressure

A

Baroreceptor detects high blood
pressure
impulse sent to medulla
more impulses sent to SAN
along parasympathetic
neurones (releasing
noradrenaline)
heart rate slowed

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40
Q

Response to low
blood pressure

A

Baroreceptor detects low blood
pressure
impulse sent to medulla
more impulses sent to SAN
along sympathetic neurones
(releasing adrenaline)
heart rate increases

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41
Q

Response to
high blood pH

A

Chemoreceptor detects low CO2
conc / high pH
impulse sent to medulla
more impulses sent to SAN
along parasympathetic
neurones (releasing
noradrenaline)
heart rate slowed so less CO2
removed and pH lowers

42
Q

Response to
low blood pH

A

Chemoreceptor detects low CO2
conc / high pH
impulse sent to medulla
more impulses sent to SAN
along sympathetic neurones
(releasing adrenaline)
heart rate increases to deliver
blood to heart to remove CO2

43
Q

Resting
potential

A

The difference between
electrical charge inside and
outside the axon when a neuron
is not conducting an impulse
more positive ions (Na+/K+)
outside axon compared to
inside
inside the axon -70mV

44
Q

How is resting
potential
established

A

Sodium potassium pump
actively transports 3 Na+ out of
the axon, 2 K+ into the axon
membrane more permeable to
K+ (more channels and always
open)
K+ diffuses out down conc.
gradient - facilitated diffusion
membrane less permeable to
Na+ (closed Na+ channels)
higher conc. Na+ outside

45
Q

Action
potential

A

When the neurone’s voltage
increases beyond the -55mV
threshold
nervous impulse generated
generated due to membrane
becoming more permeable to
Na+

46
Q

Action potential:
stimulus

A

Voltage-gated Na+ channels
open - membrane more
permeable to Na+
Na+ diffuse (facilitated) into
neurone down conc. gradient
voltage across membrane
increases

47
Q

Action potential:
depolarisation

A

When a threshold potential is
reached, an action potential is
generated
more voltage-gated Na+
channels open
Na+ move by facilitated
diffusion down conc. gradient
into axon
potential inside becomes more
positive

48
Q

Action potential:
repolarisation

A

Na+ channels close, membrane
less permeable it Na+
K+ voltage-gated channels
open, membrane more
permeable to K+
K+ diffuse out neuron down
conc. gradient
voltage rapidly decreases

49
Q

Action potential:
hyperpolarisation

A

K+ channels slow to close ->
overshoot in voltage
too many K+ diffuse out of
neurone
potential difference decrease to
-80mV
sodium-potassium pump
returns neurone to resting
potential

50
Q

All or nothing
principle

A

If depolarisation does not
exceed -55 mV threshold, action
potential is not produced
any stimulus that does trigger
depolarisation to -55mV will
always peak at the same
maximum voltage

51
Q

Importance of all
or nothing
principle

A

Makes sure animals only
respond to large enough stimuli
rather than responding to every
small change in environment
(overwhelming)

52
Q

Refractory
period

A

After an action potential has
been generated, the membrane
enters a period where it cannot
be stimulated
because Na+ channels are
recovering and cannot be
opened

53
Q

Importance of
refractory period

A

Ensures discrete impulses
produced - action potentials
separate and cannot be
generated immediately
unidirectional - cannot generate
action potential in refractory
region
limits number of impulse
transmissions - prevent
overwhelming

54
Q

Factors affecting
speed of
conductance

A

Myelination (increases speed)
axon diameter (increases
speed)
temperature (increases speed)

55
Q

How
myelination
affects speed

A

With myelination -
depolarisation occurs at Nodes
of Ranvier only -> saltatory
conduction
impulse jumps from node-node
in non-myelinated neurones,
depolarisation occurs along full
length of axon - slower

56
Q

How axon
diameter affects
speed

A

Increases speed of conductance
less leakage of ions

57
Q

How
temperature
affects speed

A

Increases speed of conductance
increases rate of movement of
ions as more kinetic energy
(active transport/diffusion)
higher rate of respiration as
enzyme activity faster so ATP is
produced faster - active
transport faster

58
Q

Saltatory
conduction

A

Gaps between myelin sheath
are nodes of Ranvier
action potential can “jump”
from node to node via saltatory
conduction - action potential
travels faster as depolarisation
across whole length of axon not
required

59
Q

Synapse

A

Gaps between end of axon of
one neurone and dendrite of
another
impulses are transmitted as
neurotransmitters

60
Q

Role of calcium
ions in synaptic
transmission

A

Depolarisation of the presynaptic
knob opens voltage
gated Ca2+ channels and Ca2+
diffuses into synaptic knob.
stimulates vesicles containing
neurotransmitter to fuse with
membrane and release
neurotransmitter into the
synaptic cleft via exocytosis

61
Q

Why are
synapses
unidirectional

A

Receptors only present on the
post-synaptic membrane
enzymes in synaptic cleft break
down excess-unbound
neurotransmitter -
concentration gradient
established from pre-post
synaptic neurone
neurotransmitter only released
from the pre-synaptic neurone

62
Q

Cholinergic
synapse

A

The neurotransmitter is
acetylcholine
enzyme breaking down
acetylcholine = acetylcholineesterase
breaks down acetylcholine to
acetate and choline to be
recycled in the pre-synaptic
neurone

63
Q

Summation

A

Rapid build-up of
neurotransmitters in the
synapse to help generate an
action potential by 2 methods:
spatial or temporal
required because some action
potentials do not result in
sufficient concentrations of
neurotransmitters released to
generate a new action potential

64
Q

Spatial
summation

A

Many different neurones
collectively trigger a new action
potential by combining the
neurotransmitter they release
to exceed the threshold value
e.g., retinal convergence for
rod cells

65
Q

Temporal
summation

A

When one neurone releases
neurotransmitters repeatedly
over a short period of time to
exceed the threshold value
e.g., 1 cone cell signalling 1
image to the brain

66
Q

Inhibitory
synapses

A

Causes chloride ions (Cl-) to
move into post-synaptic
neurone and K+ to move out
makes membrane hyperpolarise
(more negative) so less likely an
action potential will be
propagated

67
Q

Neuromuscular
junction

A

Synapse that occurs between a
motor neurone and a muscle
similar to synaptic junction

68
Q

Myofibril

A

Made up of fused cells that
share nuclei/cytoplasm
(sarcoplasm) and many
mitochondria
millions of muscle fibres make
myofibrils - bringing about
movement

69
Q

Role of Ca2+ in
sliding filament
theory

A

Ca2+ enter from sarcoplasmic
reticulum and causes
tropomyosin to change shape
myosin heads attach to exposed
binding sites on actin forming
actin-myosin cross bridge
activates ATPase on myosin
ATP hydrolysed so energy for
myosin heads to be recocked

70
Q

Role of
tropomyosin in
sliding filament
theory

A

Tropomyosin covers binding
site on actin filament
Ca2+ bind to tropomyosin on
actin so it changes shape
exposes binding site
allows myosin to bind to actin,
forming cross bridge

71
Q

Role of ATP in
myofibril
contraction

A

Hydrolysis of ATP -> ADP + Pi
releases energy
movement of myosin heads
pulls actin - power stroke
ATP binds to myosin head
causing it to detach, breaking
cross bridge
myosin heads recocked
active transport of Ca2+ back to
sarcoplasmic reticulum

72
Q

Role of myosin
in myofibril
contraction

A

Myosin heads (with ADP
attached) attach to binding
sites on actin.
form actin-myosin cross bridge
power stroke - myosin heads
move pulling actin
requires ATP to release energy
ATP binds to myosin head to
break cross bridge so myosin
heads can move further along
actin

73
Q

Phosphocreatine

A

A chemical which is stored in
muscles
when ATP concentration is low,
this can rapidly regenerate ATP
from ADP by providing a Pi
group.
for continued muscle
contraction

74
Q

Slow-twitch
muscle fibres

A

Specialised for slow, sustained
contractions (endurance)
lots of myoglobin
many mitochondria - high rate
aerobic respiration to release
ATP
many capillaries - supply high
concentrations of glucose/O2 &
prevent build-up of lactic acid
e.g. thighs / calf

75
Q

Fast-twitch
muscle fibres

A

Specialised in producing rapid,
intense contractions of short
duration
glycogen -> hydrolysed to
glucose -> glycolysis
higher concentration of
enzymes involved in anaerobic
respiration - fast glycolysis
phosphocreatine store
e.g., eyelids/biceps

76
Q

Homeostasis

A

Maintenance of constant
internal environment via
physiological control systems
control temperature, blood pH,
blood glucose concentration
and water potential within
limits

77
Q

Negative
feedback

A

When there is a deviation from
normal values and restorative
systems are put in place to
return this back to the original
level
involves the nervous system
and hormones

78
Q

Islets of
Langerhans

A

Region in the pancreas
containing cells involved in
detecting changes in blood
glucose levels
contains endocrine cells (alpha
cells and beta cells) which
release hormones to restore
blood glucose levels

79
Q

Alpha cells

A

Located in the islets of
Langerhans
release glucagon
when detect blood glucose
concentration is too low

80
Q

Beta cells

A

Located in the islets of
Langerhans
release insulin
when detect blood glucose
concentration is too high

81
Q

Factors affecting
blood glucose
concentration

A

Eating food containing
carbohydrates -> glucose
absorbed from the intestine to
the blood
exercise -> increases rate of
respiration, using glucose

82
Q

Action of
insulin

A

Binds to specific receptors on
membranes of liver cells
increases permeability of cell
membrane (GLUT-4 channels
fuse with membrane)
glucose can enter from blood by
facilitated diffusion
activation of enzymes in liver
for glycogenesis
rate of respiration increases

83
Q

Action of
glucagon

A

Binds to specific receptors on
membranes of liver cells
activates enzymes for
glycogenolysis
activates enzymes for
gluconeogenesis
rate of respiration decreases
blood glucose concentration
increases

84
Q

Role of
adrenaline

A

Secreted by adrenal glands
above the kidney when glucose
concentration is too low
(exercising)
activates secretion of glucagon
glycogenolysis and
gluconeogenesis
works via secondary messenger
model

85
Q

Gluconeogenesis

A

Creating glucose from noncarbohydrate
stores in liver e.g.
amino acids -> glucose
occurs when all glycogen has
been hydrolysed and body
requires more glucose
initiate by glucagon when blood
glucose concentrations are low

86
Q

Glycogenolysis

A

Hydrolysis of glycogen back into
glucose
occurs due to the action of
glucagon to increase blood
glucose concentration

87
Q

Glycogenesis

A

Process of glucose being
converted to glycogen when
blood glucose is higher than
normal
caused by insulin to lower blood
glucose concentration

88
Q

What is a second
messenger model

A

Stimulation of a molecule
(usually an enzyme) which can
then stimulate more molecules
to bring about desired response
adrenaline and glucagon
demonstrate this because they
cause glycogenolysis to occur
inside the cell when binding to
receptors on the outside

89
Q

Second
messenger
model process

A

Adrenaline/glucagon bind to
specific complementary
receptors on the cell membrane
activate adenylate cyclase
converts ATP to cyclic AMP
(secondary messenger)
cAMP activates protein kinase A
(enzyme)
protein kinase A activates a
cascade to break down glycogen
to glucose (glycogenolysis

90
Q

Diabetes

A

A disease when blood glucose
concentration cannot be
controlled naturally

91
Q

Type 1 diabetes

A

Due to body being unable to
produce insulin
starts in childhood
autoimmune disease where
beta cells attacked
treated using insulin injections

92
Q

Type 2
diabetes

A

Due to receptors in target cells
losing responsiveness to insulin
usually develops due to obesity
and poor diet
treated by controlling diet and
increasing exercise with insulin
injections

93
Q

Osmoregulation

A

Process of controlling the water
potential of the blood
controlled by hormones e.g.,
antidiuretic hormone (affects
distal convoluted tubule and
collecting duct)

94
Q

Nephron

A

The structure in the kidney
where blood is filtered, and
useful substances are
reabsorbed into the blood

95
Q

Formation of
glomerular
filtrate

A

Diameter of efferent arteriole is
smaller than afferent arteriole
build-up of hydrostatic pressure
water/glucose / ions squeezed
out capillary into Bowman’s
capsule through pores in
capillary endothelium,
basement membrane and
podocytes
large proteins too large to pass

96
Q

Reabsorption
of glucose by
PCT

A

Co-transport mechanism
walls made of microvilli
epithelial cells to provide large
surface area for diffusion of
glucose into cells from PCT
sodium actively transported out
cells into intercellular space to
create a concentration gradient
glucose can diffuse into the
blood again

97
Q

Counter current
multiplier
mechanism

A

Describes how to maintain a
gradient of Na+ in medulla by
the loop of Henle.
Na+ actively transported out
ascending limb to medulla to
lower water potential
water moves out descending
limb + DCT + collecting duct by
osmosis due to this water
potential gradient

98
Q

Reabsorbtion of
water by DCT /
collecting duct

A

Water moves out of DCT and
collecting duct by osmosis
down a water potential gradient
controlled by ADH which
changes the permeability of
membranes to water

99
Q

Role of
hypothalamus in
osmoregulation

A

Contains osmoreceptors which
detect changes in water
potential
produces ADH
when blood has low water
potential, osmoreceptors shrink
and stimulate more ADH to be
made so more released from the
pituitary gland

100
Q

Anti-diuretic
hormone

A

Produced by hypothalamus,
released by pituitary gland
affects permeability of walls of
collecting duct & DCT to water
more ADH means more
aquaporins fuse with walls so
more water is reabsorbed back
to blood- urine more
concentrated.

101
Q

Role of pituitary
gland in
osmoregulation

A

ADH moves to the pituitary
gland from the hypothalamus
releases ADH into capillaries
travels through blood -> kidney