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Topic 6 Flashcards

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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

Pacinian corpuscle structure

A

-Single sensory neurone wrapped around by layers of connective tissue each layer separated by a gel
-It has special stretch mediated Na+ channels which gets deformed when pressure is applied and causes depolarisation.
-Neurone also contains Schwann cells

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17
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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18
Q

Rod cells

A

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

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19
Q

Cone cells

A

-Concentrated on the fovea
-fewer at periphery of retina
-3 types of cones containing different iodopsin pigments - red,green and blue
-one cone connects to one neurone - Temporal summation
- detect coloured light

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20
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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21
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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22
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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23
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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24
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 individual- cell alone is sub-threshold but because rods are connected in groups more likely threshold potential is reached

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25
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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26
Q

Why rods have low visual acuity

A

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

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27
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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28
Q

Why rods have monochromatic vision

A

One type of rod cell
one pigment (rhodopsin)

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29
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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30
Q

Myogenic

A

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

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31
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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32
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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33
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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34
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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35
Q

Role of non- conductive 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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36
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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37
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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38
Q

Chemoreceptors

A

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

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39
Q

Baroreceptors

A

Located in carotid artery and aorta
responds to pressure changes

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40
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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41
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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42
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

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43
Q

Response to low blood pH

A

-Chemoreceptor detects high CO2
conc / low 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

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44
Q

Structure of mylelinated neurone

A

Dendrites
Axon
Nucleus
Cell body
Myelin sheath
Schwann cells
Axon terminal
Node of ranvier

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45
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

46
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 voltage gated Na+ channels)
-higher conc. Na+ outside

47
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+

48
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

49
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

50
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

51
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

52
Q

Action potential graph

A

Draw and check kerboodle

53
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

54
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)

55
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

56
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

57
Q

Factors affecting speed of conductance

A

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

58
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

59
Q

How axon diameter affects speed

A

Increases speed of conductance
Less leakage of ions

60
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
-diffusion of neurotransmitters is faster due to more kinetic energy

61
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

62
Q

Synapse

A

-Gaps between end of axon of one neurone and dendrite of another
-impulses are transmitted as neurotransmitters
-pre synaptic neurone, synaptic cleft and post synaptic neurone

63
Q

Role of calcium ions in synaptic transmission

A

-Depolarisation of the pre- synaptic 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

64
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 of neurotransmitters established from pre-post synaptic neurone
-neurotransmitter only released from the pre-synaptic neurone

65
Q

Cholinergic synapse

A

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

66
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

67
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

68
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

69
Q

Inhibitory synapses

A

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

70
Q

Neuromuscular junction

A

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

71
Q

Compare the NMJ with a cholinergic synapse (4 difference and 1similatity)

A

NMJ
-Unidirectional - neurotransmitter receptors only on post-synaptic membrane
-Only excitatory
-Connects motor neurones to muscle
-end point tor action potential
-Ach binds to receptors on muscle fibre

Cholinergic synapse:
-Unidirectional - neurotransmitter receptors only on post-synaptic membrane
-excitatory or inhibitory
-connects two neurones (sensory/motor/relay)
-New action potential generated in next neurone
-Ach binds to receptors on post-synaptic membrane

72
Q

Myofibril

A

-Made up of fused cells that share nuclei/cytoplasm (sarcoplasm) and many mitochondria
-millions of myofibrils make up muscle fibre - bringing about movement
- two key proteins - myosin and actin that forms sarcomere

73
Q

Ultra structure of myofibril

A

Draw and check kerboodle
H zone - only actin
A band - H Zone + overlap of actin and myosin
I band - only actin filaments
Z line to another z line is one sarcomere

74
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
-this is at an angle that creates tension leading to the actin being pulled along and in doing so the ADP attached is released
-ATP molecule attaches to myosin head which causes it to detach from the binding site
-ATP hydrolysed by ATPase on myosin which provides energy for myosin heads to return to its normal position

75
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

76
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

77
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

78
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
-restored when muscle is relaxed from atp

79
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

80
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

81
Q

Homeostasis

A

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

82
Q

Islet 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

83
Q

Alpha cells

A

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

84
Q

Beta cells

A

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

85
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

86
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) as it stimulates intracellular chemical which causes vesicles containing glucose channel proteins to fuse with the membrane
-glucose can enter from blood by facilitated diffusion
-activation of enzymes in liver for glycogenesis
-rate of respiration increases

87
Q

Action of glucagon

A

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

88
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

89
Q

Gluconeogenesis

A

-Creating glucose from non- carbohydrate 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

90
Q

Glycogenolysis

A

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

91
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

92
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

93
Q

Second messenger model process

A

-Adrenaline/glucagon bind to specific complementary receptors on the cell membrane
-activate adenyl cyclase for glucagon and protein g for adrenaline
-converts ATP to cyclic AMP (secondary messenger)
-cAMP activates protein kinase A(enzyme)
-protein kinase A causes break down glycogen to glucose (glycogenolysis)

94
Q

Diabetes

A

A disease when blood glucose concentration cannot be controlled naturally

95
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

96
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

97
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)

98
Q

Nephron

A

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

99
Q

Nephron structure

A
  1. Glomerulus and bowman’s capsule :- made of specialised cells called podocytes, capillary made of endothelium.
    filters small solutes from the blood
  2. Proximal convoluted tubule: - lined with epithelial cells and surrounded by many capillaries.
    reabsorbs ions, water, and nutrients; removes toxins and adjusts filtrate pH
  3. Descending loop of Henle:
    allow water to pass from the filtrate into the interstitial fluid
  4. Ascending loop of Henle:
    reabsorbs Na+ and CI- from the filtrate into the interstitial fluid
  5. Distal convoluted tubule:
    selectively secretes and absorbs different ions to maintain blood pH and electrolyte balance
  6. Collecting duct:
    reabsorbs solutes and water from the filtrate
100
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

101
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 epithelial cells into intercellular space to create a concentration gradient
-Na+ now diffuses down concentration gradient from lumen to epithelial cells via co transport protein and this brings glucose along
-glucose diffuses into blood by facilitated diffusion

102
Q

Counter current multiplier mechanism or Reabsorption of water

A

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

103
Q

Reabsorption 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

104
Q

Role of hypothalamus in osmoregulation

A

-Contains osmoreceptors which
detect changes in water
potential
-produces ADH which then passes to posterior pituitary gland from where its secreted into capillaries
-when blood has low water
potential, osmoreceptors shrink
and stimulate more ADH to be
made so more released.

105
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.

106
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

107
Q

Synapse structure

A

Look at notes

108
Q

What happens to parts of sarcomere when muscle contracts

A

H zone narrows or shortens
I band narrows or shortens
A band stays constant
Z line come closer
Overall sarcomere shortens

109
Q

What are the three main proteins involved in sliding filament theory

A

Myosin - made of two proteins - one is fibrous protein which makes up the tail and the other is a globular protein which makes the bulbous head
Actin - globular protein which twist to form a helical shape
Tropomyosin - long thin thread that wounds around actin filament.

110
Q

What happens during muscle relaxation

A

Nervous stimulation ceases and calcium ions are actively transported back into the endoplasmic reticulum using energy from hydrolysis of atp
Causing tropomyosin to change shape and block binding sites of chin again therefore myosin head cannot bind and muscle relaxes
The antagonistic muscles now pulls actin out from between myosin

biology a level (9 decks)

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