TOPIC 3.6 Flashcards

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1
Q

Define stimulus

A

a detectable change in the environment.

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2
Q

What detects changes in the environment?

A

receptors

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3
Q

How do organisms increase their chance of survival?

A

By responding to stimuli via different response mechanisms.

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4
Q

Define tropism

A

Term given when plants respond, via growth, to stimuli

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5
Q

What are the 2 stimuli that plants respond to?

A

Light and gravity

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6
Q

What is a prime example of a growth factor that controls tropism in plants?

A

IAA (indoleacetic acid)

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7
Q

What is positive/negative tropism in plants?

A

+ve = growing towards stimulus
-ve = growing away from stimulus

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8
Q

What is auxin?

A

A type/family of plant hormones

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9
Q

What is IAA?

A

a type of auxin that controls CELL ELONGATION in shoots and INHIBITS growth of cells in the roots.
It is made in the tip of the roots/shoots but can diffuse to other cells.

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10
Q

What is phototropism?

A

Plants response to light stimulus

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11
Q

Why does responding to light improve the survival chances of shoots in plants?

A

Light is needed for the light dependant reaction in photosynthesis

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12
Q

What is positive phototropism?

A

When plants grow and bend towards the light

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13
Q

Describe the process of positive phototropism

A
  1. Shoot tip cells produce IAA, causing cell elongation
  2. The IAA diffuses to other cells
  3. If theres unilateral light (light on one side), the IAA will DIFFUSE TOWARDS THE SHADED SIDE of the shoot resulting in a higher concentration of IAA there
  4. The cells on the shaded side elongate more and results in the plant bending towards the light source
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14
Q

Describe the process of negative phototropism

A
  1. IAA diffuses away from the light source in the roots
  2. As IAA inhibits growth of cells/elongation in the roots, this causes the root cells to elongate more on the lighter side
  3. Overall the root bends away from the light and grows downwards
    (anchoring the plant)
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15
Q

How does negative phototropism of the roots in plants increase survival?

A

The elongation of the top layer of cells in the roots cause the roots to grow downwards and help anchor the plant deep into the soil and potentially reach more water sources

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16
Q

What is gravitropism?

A

Plants response to gravitational stimuli

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17
Q

Describe the process of negative gravitropism in shoots of plants

A
  1. IAA diffuse from the upper side to the lower side of a shoot
  2. if a plant is vertical, this causes the plant cells to elongate and the plant grows upwards
  3. If the plant is on its side, this will cause the shoot to bend upwards

(against gravity)

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18
Q

Describe the process of positive gravitropism

A
  1. IAA moves to the lower side of roots so that the upper side elongates and the root bends down towards gravity
  2. This anchors the plant in
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19
Q

Define reflex

A

A rapid, automatic response to protect you from danger

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20
Q

What 3 neurones is the reflex arc made of?

A

Sensory neurone, relay neurone and motor neurone

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21
Q

How many synapses are found in the reflex arc?

A

2

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22
Q

Define taxes

A

An organism moving its ENTIRE BODY towards a favourable stimulus or away from an unfavourable stimulus

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23
Q

What is +ve/-ve taxis?

A

+ve taxi = organism move towards a stimulus
-ve taxi = organism moves away from stimulus

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24
Q

Define kinesis

A

An organisms changing the speed of movement and the rate of change of direction.

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25
Q

How does kinesis keep an organisms in its favourable conditions?

A
  1. If an organisms moves from area where theres beneficial stimuli to area with harmful stimuli, its kinesis response will be to INCREASE THE RATE IT CHANGES DIRECTION to return to favourable conditions quickly
  2. If an organises is surrounded by NEGATIvE STIMULI, the RATE FO TURNING DECREASES to keep it moving in a relatively straight line to increase the chances of it finding a new location with favourable conditions.
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26
Q

How to receptors create a response? (broadly speaking)

A

Stimulation of a receptor leads to the establishment of a generator potential which can cause a response.

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27
Q

What stimuli do PACINIAN CORPUSCLE receptors detect?

A

pressure (changes in pressure)

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28
Q

Where are pacinian corpuscle receptors located?

A

deep in the skin, mainly in fingers and feet

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29
Q

How do pacinian corpuscle receptors create a response?

A
  1. membranes of the pacinian corpuscle have stretch-mediated sodium channels
  2. these open and allow Na+ to enter the sensory neurone only when they are STRETCHED AND DEFORMED
  3. when PRESSURE is applied, it deforms the neurone plasma membrane, stretches and widens the Na+ channels
  4. so Na+ diffuses in which leads to the establishment of a generator potential (if enough Na+ ions diffuses in to surpass the threshold, then you have an action potential and a response will occur)
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30
Q

What is the structure of a pacinian corpuscle?

A

It is a sensory neurone wrapped in layers of plasma membrane at the neurone ending. There are STRETCH-MEDIATED SODIUM CHANNELS embedded in the plasma membrane.
(the connective tissue (plasma membrane) has gel in-between each layer.)

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31
Q

What 2 types of photoreceptors are found in the human retina?

A

Rods and cones

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32
Q

What colour images do Rods process?

A

black and white

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33
Q

How are generator potentials formed by rod cells?

A

The pigment of rod cells (RHODOPSIN) must be broken down by light energy.

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34
Q

Why can rod cells detect light of very low intensity?

A

Many rods connect to ONE sensory neurone , known as RETINAL CONVERGENCE. Many rod cells contribute to one sensory neurone to reach the threshold and produce an action potential.

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35
Q

What is a downside to retinal convergency?

A

LOW VISUAL ACUITY. The brain cannot distinguish between the separate sources of light that stimulated it. (bad clarity in vision)

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36
Q

What type of images do cones process?

A

Images of colour

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37
Q

How many types of cones are there and why?

A

3 types which contain different types of IODOPSIN pigment (red, green and blue) which all absorb different wavelengths of light.

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38
Q

What main factor is required for cones to trigger an action potential?

A

Iodopsin is only broken down if there is a HIGH LIGHT INTENSITY, so action potentials can only be generated with enough light.

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39
Q

Why is high light intensity required for cones to trigger an action potential?

A

As one cone cell connects to one bipolar cell, a singular bipolar cell must gather enough light alone to generate the threshold in order to trigger an action potential. This is why we can’t see colour when its dark.

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40
Q

Why do cone cells provide high visual acuity?

A

As each cone is connected to one bipolar cell, the Brian can distinguish between separate sources of light detected and give high clarity and precision.

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41
Q

Why is the distribution of rods and cones in the retina uneven?

A

Because cones require high light intensity so most are located near the FOVEA (which is where receives the highest intensity of light), whereas rods only require low intensities of light so are located further away along the retina (where slightly less light reaches).

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42
Q

Define myogenic

A

(muscle) contracts on its own accord with out any nervous system input

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43
Q

Cardiac muscle is myogenic so contracts on its own but what feature of it remains controlled?

A

The rate of contraction is controlled by wave of electrical activity.

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44
Q

What 4 things are involved in the control of heart rate and whew are they found?

A
  1. Sinoatrial node/SAN (right atrium)
  2. Atrioventricular node/AVN (near the border of the right and left ventricle within the atria still)
  3. Bundle of His (runs through the septum)
  4. Purknye fibres (in the walls of the ventricles)
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45
Q

Describe in detail the process of the control of heart beating

A
  • SAN releases a WAVE OF DEPOLARISATION across the atria, causing it to contract
  • AVN releases another wave of depolarisation when the first one reaches it

(a non-conductive layer between the atria and ventricles prevents the wave of depolarisation travelling down to the ventricles)

  • Instead, the BUNDLE OF HIS conducts the wave of depolarisation down the septum and the purkyne fibres
  • Hence, the apex and the walls of the ventricles contract. Theres a short delay before this happens whilst the AVN transmits the second waves of depolarisation
  • This allows enough time for the atria to pump all the blood into the ventricles.
  • Finally the cells depolarise and the cardiac muscle relaxes
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46
Q

What triggers the rate at which the SAN releases the waves of depolarisation and through what system does this happen?

A

The medulla oblongata in the brain (controls the heart rate) via the autonomic nervous system

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47
Q

What are the 2 parts to the autonomic nervous system?

A
  1. a centre linked to the sinoatrial node to increase the heart rate via SYMPATHEIC nervous system
    (if impulses travel via the sympathetic nervous system (from the medulla oblongata) , it triggers the SAN to release the waves of depolarisation more frequently)
  2. another that decreases heart rate via the PARASYMPATHETIC nervous system
    (if impulses travel via the parasympathetic nervous system (from the medulla oblongata) it triggers the SAN to release the waves of depolarisation less frequently)
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48
Q

What 2 stimuli can change heart rate?

A

pH and blood pressure

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49
Q

What detects changes in pH in the heart and where can this be found?

A

Chemoreceptors in the aorta and carotid artery

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50
Q

What detects changes in blood pressure and where can this be found?

A

Pressure receptors in the aorta and carotid artery

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51
Q

How does the heart respond to change in pH (detailed)?

A
  • pH of blood decreases during times of high respiratory rate due to the production of CO2 or lactic acid.
  • Excess acid must be removed from the blood rapidly to prevent enzymes denaturing
  • This is achieved by increasing the heart rate (more impulses via sympathetic nervous system to SAN), so CO2 can diffuse out into the alveoli more rapidly
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52
Q

How does the heart respond to change in blood pressure?

A
  • if the blood pressure is too high this can cause damage to the walls of the arteries (so must reduce it)
  • this results in more impulses via parasympathetic nervous system to decrease the heart rate
  • if the blood pressure is too low, there may be insufficient supply of oxygenated blood to repairing cells and removal of waste
  • this results in more impulses sent via the sympathetic nervous system to increase the heart rate.
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53
Q

Describe the structure of a myelinated motor neurone and its function

A
  • CELL BODY, of neurone contains the organelles found in a typical animal cell. Proteins and neurotransmitter chemicals are made here
  • DENDRITES carry action potentials to surrounding cells
  • AXON is the conductive, long fibre that carries the nervous impulse along the motor neurone

-SCHWANN CELLS wrap around the icon to form the myelin sheath, which is a lipid and hence doesnt allow charged ions to pass through it.

  • NODES OF RANVIER, gaps in the myelin sheath (not insulated)
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54
Q

What is resting potential?

A

When a neurone isnt conducting an impulse, theres a difference between the electrical charge inside and outside of the neurone which is the resting potential .

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55
Q

What is the voltage of resting potential and why?

A

-70mV, because theres more +ve ions (Na+ and K+) outside compared to inside hence the inside of the neurone is comparatively more negative at the value of -70mV.

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56
Q

How is the resting potential established?

A
  • The resting potential is maintained by a sodium-potassium pump, involving active transport and ATP
  • The pump moved 2K+ ions IN and 3Na+ ions OUT
  • This creates an electrochemical gradient causing K+ to diffuse out and Na+ to diffuse in
  • The membrane is MORE PERMEABLE to K+ so more are moved out resulting in the -70mV
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57
Q

Define action potential

A

When the neurones voltage increases beyond a set point from the resting potential (generating a nervous impulse)

58
Q

Define depolarisation

A

An increase in voltage

59
Q

How/why does depolarisation occur?

A

Due to the neurone membrane becoming more permeable to Na+.

60
Q

How is an action potential generated (in detail)?

A
  • a stimulus provides the energy that can cause the SODIUM ION VOLTAGE-GATED channels in the axon membrane to open
  • this will cause the sodium ions to start diffusing into the axon
  • hence we begin to see an increase in voltage (depolarisation)
  • if the stimulus is large enough to cause enough of these SODIUM ION VOLTAGE-GATED channels to open, then you’ll have enough sodium ions diffusing in to cause an increase beyond the threshold potential
  • once the voltage has reached/surpassed -55mV (threshold voltage) then the remainder of the curve will occur (always have the action potential generated)
  • as voltage increases to a maximum of +35-40mV, it causes the sodium channels to close so no more Na+ are entering
  • but the K+ ions are still moving out the axon as the potassium channels remain opened
  • this causes a decrease in voltage (depolarisation)
  • this induces more potassium channels to open so more k+ ions diffuse out.
  • eventually so many k+ ions diffuse out that it overshoots the resting potential and goes down to -80mV (refractory period)
61
Q

What is the difference between action potentials on myelinated and unmyelinated axons?

A

myelinated = action potentials occur only at every node of ranvier

unmyelinated = action potentials occur on every single position on the axon (as no myelin sheet so it’ll take longer for action potentials to finally reach the end.)

62
Q

What is the all-or-nothing principle?

A

nothing= if depolarisation does not reach/excess -55mV then an action potential and impulse are not produced

all = any stimulus that does trigger depolarisation to -55mV will always peak at the same maximum voltage.

63
Q

How does a bigger stimuli affect action potentials?

A

Bigger stimuli increase the frequency of the action potentials.

64
Q

Why is the all-or-nothing principle important?

A

It ensures that animals only respond to large enough stimuli rather than responding to every slight change in the environment.

65
Q

What happens during the refractory period?

A

the membrane cannot be stimulated as the sodium channels are recovering and can’t be opened

66
Q

Give 3 reasons as to why the refractory period is important.

A
  1. It ensures that discrete impulses are produced. An action potential cannot be generated immediately after another and this makes sure that each is separate.
  2. It ensures that action potentials travel in one direction. This stops the action potential from spreading out in 2 directions which would prevent a response.
  3. It limits the number of impulse transmission. This is important to prevent over reaction to a stimulus.
67
Q

What 3 factors affect the speed of conductance?

A
  1. Myelination and saltatory conduction
  2. Axon diameter
  3. Temperature
68
Q

How does myelination and saltatory conduction affect the speed of conductance?

A

The action potential jumps from node of ranvier to node of ranvier (saltatory conduction), which means the action potential travels along the axon faster.

(the myelin sheath formed from Schwann cells acts as an insulator so ions cannot diffuse all throughout but can only jump to sections with no insulation.)

69
Q

How does axon diameter affect the speed of conductance?

A

A wider diameter increases the speed of conductance as there will be less leakage of ions and the action potential can travel faster.

70
Q

How does temperature affect the speed of conductance?

A
  1. higher temp = greater kinetic energy so ions can diffuse faster
  2. the enzymes involved in respiration work faster (due to greater kinetic energy) so there is MORE ATP for active transport in the sodium/potassium pump.

(surpassing the optimum temperature can decrease the speed)

71
Q

What is a synapse?

A

The gaps between the end of the axon of one neurone and the dendrite of another one.

72
Q

what does an action potential use to pass across different axons?

A

the action potential is transmitted as neurotransmitter that diffuse across the synapse

73
Q

How is an action potential carried across from a synapse to the post synaptic membrane? (in detail)

A
  • the action potential arrives at the synaptic knob (end of the neurone)
  • depolarisation at the synaptic knob leads to calcium ion channels opening and Ca+ ions diffusing into the synaptic knob
  • the Ca+ ions will cause the vesicles containing the neurotransmitters towards the membrane, fuse and release the neurotransmitter into the SYNAPTIC CLEFT (space between synaptic knob and dendrite spine)
  • due to high conc of neurotransmitter where they’ve just been released, they diffuse across to the post synaptic membrane
  • on the post synaptic membrane, there are receptors complimentary to the neurotransmitters to bind to
  • when those neurotransmitters bind to the receptors, it causes the sodium ion channels on the post synaptic membrane to open
  • sodium ions diffuse in
  • if enough neurotransmitters bind, then enough Na+ ions diffuse in (reaching above -55mV threshold) then the post synaptic neurone becomes depolarised
  • action potential is generating in the post synaptic membrane and continues along the axon
74
Q

What happens to the neurotransmitters after the action potential has been regenerated in the post synaptic membrane?

A

Neurotransmitter is degraded and released from the receptors.

The Na+ channels close and the post synaptic neurone can re-establish resting potentials.

The neurotransmitter is transported back into the presynaptic neurone where it is recycled.

75
Q

How is it ensured that the travel of neurotransmitters across a synaptic cleft is UNIDIRECTIONAL?

A
  1. Vesicles containing the neurotransmitters are only found in the pre-synaptic neurone. Because of the concentration gradient, diffusion occurs from the pre to the post synaptic neurone
  2. You only find the receptors complementary in shape to the neurotransmitters on the membrane of the post synaptic neurone
76
Q

What is the neurotransmitter found in the CHOLINERGIC SYNAPSE?

A

Acetylcholine

77
Q

Acetylecholine mustn’t remain bound on the post synapsing membrane otherwise the Na+ ions would continually be open and you would continually be triggering an action potential even if stimulus isnt present anymore.

How is the prevented?

A

An enzyme (acetylcholinesterase) breaks down acetylcholine into acetate + choline which gets reabsorbed into the pre synaptic neurone and reused

78
Q

What is summation?

A

Rapid build up of neurotransmitters in the synapse to help generate an action potential

79
Q

What 2 methods of summation are there? (in detail)

A

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

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

80
Q

How do inhibitory synapses work?

A
  • chloride ions move into the post synaptic membrane
  • different neurotransmitters binding to the receptors
  • causing chloride ion channels to open
  • due to negative ions moving in, this makes the membrane potential decrease to -80mV, (post synaptic membrane undergoes hyper polarisation) and an action potential is highly unlikely.
81
Q

What is a neuromuscular junction?

A

The synapse that occurs between a motor neurone and a muscle.

82
Q

What is the one similarity between the neuromuscular junction and cholinergic synapse?

A

They are both unidirectional due to the neurotransmitter receptors being only on the post synaptic membrane.

83
Q

What is different between the destination of travel of neurotransmitters in neuromuscular junction and cholinergic synapse?

A

NJ= connects motor neurone to muscle (fibres)

CS= connects 2 neurones which could be sensory, relay or motor

84
Q

What is different between the function of neuromuscular junction and cholinergic synapse?

A

NJ= only excitatory

CS= could be excitatory or inhibitory

85
Q

What is the difference between the responses of the action potential of neuromuscular junction and cholinergic synapse?

A

NJ= this is the end point for the action potential

CS= a new action potential is generated in the next neurone

86
Q

What is the difference between the binding of acetylcholine of neuromuscular junction and cholinergic synapse?

A

NJ= acetylcholine binds to receptors on muscle fibre membrane

CS= acetylcholine binds to receptors on post-synaptic membrane on a neurone

87
Q

Define antagonistic pairs in muscles

A

2 different muscles doing opposite things at the same time

88
Q

Describe the structure of muscles

A

They are made from bundles of myofibrils.

Myofibrils are made up of FUSED CELLS (hence they share nuclei and cytoplasm (known as SARCOPLASM)) and theres a high number of mitochondria for ATP from respiration for contraction.

89
Q

What are muscle fibres made up of?

A

Millions of myofibrils

90
Q

What are the 2 proteins that make up myofibrils and hence form the sarcomere?

A

myosin and actin

91
Q

Describe muscles contacting and relaxing using the terms of A band, Z line, M line, I band, H zone etc. (refer to image)

A

Relax= A band is constant, actin and myosin dont overlap much so theres wide I band remaining (non-overlapping actin) and a wide H zone (non-overlapping myosin). Z line (which represents end of sarcomere) are far apart.

Contract= A band is constant, actin and myosin overlap so theres shortened I band (non-overlapping actin reduced), shortened H zone (non-overlapping myosin reduced). Z line are closer together/shortened distance between adjacent Z lines

(M line remains constant, it connects all the perpendicular branching myosin)

A M Z I H

92
Q

Explain the sliding filament theory in detail

A
  1. when an action potential reaches a muscle, it stimulates a response
  2. calcium ions enter and cause the protein tropomyosin to move and uncover the binding sites on actin
  3. whilst ADP is attached to the myosin head, the myosin heads to the actin to form a cross-bridge
  4. the angle created in this cross-bridge creates tension and the actin filament is pulled and slides along the myosin. In doing so the ADP molecule is released
  5. an ATP molecule then binds to the myosin head and causes it to change shape slightly. As a result it detaches from the actin
  6. Within the sarcoplasm, enzyme ATPase, (activated by the calcium ions) hydrolyse the ATP on the myosin head into ADP and releases enough energy for the myosin head to return to its original position
  7. this entire process repeats continually whilst the calcium ions remain high and therefore whilst the muscle remains stimulated by the nervous system.
93
Q

What 2 things are required for the sliding filament theory/active muscle to occur and why?

A

ATP and Phosphocreatine.

Active muscles need a high concentration of ATP.
The chemical phosphocreatine, which is stored in muscles, assist this by providing phosphate to regenerate ATP from ADP.

94
Q

What is the structure of slow-twitch fibres?

A

Contains large store of myoglobin, a rich blood supply and many mitochondria

95
Q

What is the structure of fast-twitch fibres?

A

Thicker and more myosin filaments, a large store of glycogen, a store of phosphocreatine to help make ATP from ADP and a high concentration of enzymes involved in anaerobic respiration

96
Q

Where can slow/fast twitch muscles be found?

A

Slow = calves (endurance)
Fast = Biceps (quick and powerful)

97
Q

What are the general properties of slow-twitch fibres and why?

A

Contract slower and can respire AEROBICALLY for longer periods of time due to the rich bloody supply and myoglobin oxygen store.
These muscles are adapted for endurance work.

98
Q

What are the general properties of fast-twitch fibres and why?

A

Contract faster to provide short burst of powerful contraction. There are adapted for intense exercise such as sprinting or weightlifiting.

99
Q

Define homeostasis

A

A state of balance among all the body systems needed for the body to survive and function correctly.

100
Q

what 2 conditions are controlled/maintained in the human body via homeostasis?

A
  1. stable core temperature
  2. stable blood pH in relation to enzyme activity
101
Q

What is negative feedback?

A

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

102
Q

When do your blood glucose concentration increase/decrease

A

increase : ingestion of food or drink containing carbs

decreases : following exercise or if you haven’t eaten

103
Q

What organ detects changes in blood glucose concentration?

A

Pancreas

104
Q

What enzyme is released to increase/decrease blood glucose levels and by what cells?

A

to decrease blood glucose, insulin is released by the beta cells in Islets of Langerhans (pancreas)

to increase blood glucose, glucagon is released by the alpha cells in Islets of Langerhans (pancreas)

105
Q

A state of balance among all the body systems needed for the body to survive and function correctly.

A
  1. blood glucose levels increases
  2. it gets detected by the beta cells in the islets of langerhans (pancreas)
  3. beta cells release insulin
  4. liver cells become more permeable to glucose and enzymes are activated to convert glucose into glycogen
  5. glucose is removed from the blood and stored as glycogen in cells
106
Q

Describe the process of negative feedback when blood glucose levels decrease

A
  1. blood glucose levels decrease
  2. it gets detected by alpha cells in the islets of lanterns (pancreas)
  3. alpha cells release glucagon and the adrenal gland releases adrenaline
  4. second messenger model occurs to activate enzymes to hydrolyse glycogen
  5. glycogen is hydrolysed to glucose and more glucose is released back into the blood
107
Q

In what 3 ways can insulin decrease blood glucose concentration levels?

A
  1. attaching to receptors on the surfaces of target cells. This changes the tertiary structure of the channel proteins resulting in more glucose being absorbed by facilitated diffusion.
  2. more protein carries are incorporated into cell membranes so that more glucose is absorbed from the blood into cells. (vesicles within the cells hold the protein carriers)
  3. activating enzymes involved in the conversion of glucose to glycogen. This results in glycogenesis in the liver
108
Q

In what 3 ways do glucagon increase the blood glucose concentrations?

A
  1. attaching to receptors on the surfaces of target cells (liver cells)
  2. when glucagon binds it causes a protein to be activated into adenylate cyclase and to convert ATP in a molecule called cyclic AMP (cAMP). cAMP activates an enzyme, protein kinase, that can hydrolyse glycogen into glucose (second messenger model)
  3. activating enzymes involved in the conversion of glycerol and amino acids into glucose
109
Q

Explain the second messenger model

A

Glucagon binds to glucagon receptors (in liver cells)

Once bound it causes a change in tertiary shape of the enzyme adenyl cyclase which activates it

Activated adenyl cyclase enzymes converts ATP into cyclic AMP (cAMP)

cAMP is the ‘second messenger’

cAMP converts inactive protein kinase to active protein kinase which can convert/hydrolyse glycogen into glucose.

(Exact same process occurs for adrenaline)

110
Q

What are the 3 main roles of the liver?

A

glycoGENESIS : converting glucose into glycogen. This occurs in the liver and is catalysed by enzymes there

glycoGENOLYSIS : hydrolysis of glycogen to glucose. This occurs in the liver due to the second messenger model

GLUCONEOgenesis : creation of glucose from other molecules, such as amino acids and glycerol in the liver

111
Q

What is type 1 diabetes and how does this typically occur + treatment?

A

Inability to produce insulin.

Usually starts in childhood and could be the result of an autoimmune disease where the beta cells are attacked.

Treatment involves injection of insulin

112
Q

What is type 2 diabetes and how does this typically occur + treatment?

A

receptors on the target cells lose their responsiveness to insulin.

Usually develops in adults because of obesity and poor diet.

Controlled by regulating intake of carbs, increasing excersise and sometimes insulin injections

113
Q

Define osmoregulation

A

Controlling water potential of the blood

114
Q

What is hypertonic/hypotonic in terms of the water potential in blood?

A

Hypertonic = blood with too low a water potential

Hypotonic = blood with too high a water potential

115
Q

Define crenation in terms of water potential in blood

A

too much water will leave the cells and move into the blood by osmosis. Cells will shrivel

116
Q

Define lysis in terms of water potential in blood

A

too much water will move fro the blood into the cells by osmosis. Cells will burst

117
Q

What can cause hypertonic blood?

A

too much sweating

not drinking enough water

lots of ions in diet (lots of salt)

118
Q

What can cause hypotonic blood?

A

drinking too much water

not enough salt in diet

119
Q

How is hypertonic blood correct?

A

more water is REabsorbed by osmosis into the blood from the tables of the nephrons. This means the urine is more concentrated as less water is lost in the urine

120
Q

How is hypertonic blood corrected?

A

more water is REabsorbed by osmosis into the blood from the tables of the nephrons (found in kidneys). This means the urine is more concentrated as less water is lost in the urine

121
Q

How is hypnotic blood corrected?

A

Less water is reabsorbed by osmosis into the blood from the tubules of the nephrons (found in kidneys). This means the urine is more dilute and more water is lost in the urine.

122
Q

Where does osmoregulation occur?

A

Within the nephrons which are found in the medulla (in the kidneys)

123
Q

Describe the structure of nephrons

A
  1. afferent arteriole leading into the renal capsule which holds the glomerulus (lots and lots of small capillaries bunched)
  2. renal capsule is connected to the proximal convoluted tubule
  3. then connects to the loop of henle
  4. then up to the distal convoluted tubule
  5. then to the collecting ducts
124
Q

What is the general function of the nephron?

A

Creating urine by filtering the blood to remove waste and selectively reabsorb useful substances back into the blood

125
Q

What does urine contain?

A
  • (excess) water
  • dissolved salts (minerals or ions)

-urea

  • other small substances e.g hormones and excess vitamins
126
Q

What 3 substances does urine not contain and why?

A
  • proteins and blood cell
    : too large to be filtered out of the blood
  • glucose
    : all glucose is absorbed at the selective reabsorption stage in the PCT
127
Q

What occurs during ultrafiltration?

A
  1. blood enters through the AFFERENT ARTERIOLE and this splits into smaller capillaries (making up the glomerulus). causing a HIGH HYDROSTATIC PRESSURE of the blood
  2. WATER and small molecules e.g glucose and mineral ions are forced out of the capillaries to make the GLOMERULUS FILTRATE (which enters the renal capsule)
  3. LARGE PROTEINS AND BLOOD CELLS are TOO BIG to fit through the gaps int he capillary endothelium, so remain in the blood.
  4. the remaining blood leaves via the EFFERENT ARTERIOLE
128
Q

What occurs during selective reabsorption in the proximal convoluted tube?

A

(85% of the glomerulus filtrate is reabsorbed)

  1. concentration of Na+ ions in the PCT cell DECREASED as the Na+ ions are ACTIVELY TRANSPORTED out of the PCT cells into the blood in the capillaries
  2. due to conc gradient, Na+ ions DIFFUSE down the gradient from the LUMEN of the PCT into the cells lining the PCT via CO-TRANSPORT, as proteins which transport the Na+ ions in carry glucose with it

(the Na+ ions and glucose are collected from the glomerulus filtrate which passes by the lumen)

  1. the glucose can then DIFFUSE from the PCT epithelial cell into the blood stream

(this is how all the glucose is REabsorbed)

129
Q

What are 2 adaptations of the proximal convoluted tubule for selective reabsorption?

A
  1. microvilli found on the lumen of the tubule to provide a large surface area for reabsorption
  2. lots of mitochondria in the proximal convoluted tubule cells to provide energy for active transport
130
Q

What is the main function of the loop of henle?

A

to maintain a sodium ion gradient, which enables the reabsorption of water

131
Q

What are the 2 different limbs of the loop of henle and how are they different structure wise?

A

ascending limb = walls are impermeable to water as they are much THICKER

descending limb = walls are permeable to water as they are much thinner

132
Q

Describe the process that occurs within the loop of henle

A

1.

133
Q

Describe the process that occurs within the loop of henle

A
  1. MITOCHONDRIA in the walls of the cells provide energy to ACTIVELY TRANSPORT Na+ ions OUT of the ASCENDING limb of the loop of henle
  2. the accumulation of Na+ ions outside the nephron in the medulla LOWERS the water potential
  3. hence, water DIFFUSES out by osmosis into the interstitial space (from the descending limb) and then the water is reabsorbed into the blood
  4. At the base of the ascending limb, some NA+ IONS ARE TRANSPORTED OUT BY DIFFUSION, as there is low concentration of Na+ ions at the base due to a very dilute solution from all the water that has moved out.
134
Q

What do you call the space between the nephron and capillaries?

A

Interstitial space

135
Q

What happens within the distal convoluted tubule and collecting duct?

A
  1. due to all the Na+ ions being actively transported out of the PCT, when the filtrate reaches the TOP of the PCT, it is VERY DILUTE
  2. this filtrate moves into the DISTAL CONVOLUTED TUBULE AND COLLECTING DUCT.

(at this section of the medulla which surrounds these 2 parts of the nephron, it is VERY CONCENTRATED)

  1. hence EVEN MORE WATER DIFFUSES OUT of the DCT and collecting ducts
  2. what remains is transported to and FROMS URINE (urine flows into RENAL PAPILLA)
136
Q

practice question: Suggest how the length of the loop of henle will differ for a desert animal compared to a human

A

Desert animals will have a longer loop of henle.
The longer the loop of henle, the more Na+ ions that are actively transported out and hence an even more negative water potential is created. This results in more water being reabsorbed into the blood and very concentrated urine. (as more Na+ actively transport out this lowers water potential requiring more water to leave via osmosis from the descending limb and hence more water ends up getting reabsorbed by the blood)

137
Q

What 2 things regulates osmoregulation by nephrons?

A

the hypothalamus AND posterior pituitary gland

138
Q

How do hypothalamus and posterity pituitary gland work together to control the water potential in the blood?

A
  1. the HYPOTHALAMUS detects changes in the water potential of blood via OSMORECEPTORS
  • if the water potential of blood is TOO LOW, water LEAVES the osmoreceptors by osmosis and they SHRIVEL. This stimulates the hypothalamus to produce MORE ADH (hormone)
  • if water potential of blood is TOO HIGH, water enters the osmoreceptors by osmosis. This stimulates the hypothalamus to produce LESS ADH (Anti-diuretic hormone).
139
Q

How exactly is ADH released and where is it first produced?

A

ADH is produced in the hypothalamus.

ADH then moves to the POSTERIOR PITUITARY and from here is is RELEASED INTO CAPILLARIES and INTO BLOOD.

ADH travels through the blood to the kidneys (its target organ).

140
Q

How does ADH affect the distal convoluted tube and collecting duct to control the water left in the nephron?

A

ADH causes an increase in permeability of the walls of the DCT and collecting tubule to water.

Causes more water to leave the nephron be reabsorbed into the blood making urine more concentrated.