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Year 2 Biology > Topic 7 > Flashcards

Topic 7 Flashcards

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1
Q

7.1 Muscles

A
  • Muscles are effectors, stimulated by nerve impulses by motor neurones
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2
Q

Tendons

A

Tough and inelastic bands of fibrous tissue that attach skeletal muscles to bone.

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3
Q

Skeletal muscles

A
  • muscles attached to bones, they are arranged in antagonistic pairs.
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4
Q

Ligaments

A

elastic tissue that joins bones together and determines the amount of movement possible at a joint.

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5
Q

Joints

A

The area where two bones are attached for the purpose of permitting body parts to move, they’ve made of fibrous connective tissue and cartilage.

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6
Q

Antagonistic muscle pairs

A
  • pairs of muscles which pull in opposite directions - as one muscle contracts, the other relaxes. Extensors act to straighten the joint while flexors act to bend the joint.
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7
Q

Antagonistic muscle pair contraction

A

Triceps and biceps in the arm: when the triceps relaxes, the biceps contracts to lift the arm.

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8
Q

Muscle contraction - markscheme answer

A
  • Tropomyosin is moved by troponin
  • Myosin binding sites on actin are exposed
  • Myosin heads can bind to binding sites
  • Myosin changes shape
  • Actin filaments slide/pulled over myosin
  • therefore muscle fibres/myofibril/sacromere shorten
  • ATP hydrolysed/ ADP and inorganic phosphate/pi released
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9
Q

The role of calcium in muscle contraction

A
  1. Calcium is stored in the sarcoplasmic reticulum
  2. When your brain tells your muscles to contract
  3. Action potentials arrive at the motor end plate
  4. Release acetyl choline
  5. Acetyl choline binds to gated receptors
  6. Causes depolarisation of the sarcoplasmic reticulum
  7. Calcium is released from the sarcoplasmic reticulum into the sarcoplasm
  8. When it’s time to relax again, the calcium is reabsorbed into the sarcoplasmic reticulum by active transport
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10
Q

Sliding filament theory (muscle contraction)

A
  • Action potentials arrive at the motor end plate and release acetyl choline.
  • Acetyl choline binds to gated receptors, causing depolarisation of the sarcoplasmic reticulum.
    1. Calcium is released from the sarcoplasmic reticulum
    2. Calcium binds to troponin
    3. Troponin changes shape
    4. Cause Troponin and Tropomyosin proteins to change position on the actin (thin) filaments
    5. Exposing myosin binding site
    6. Actin forms cross bridges with myosin
    7. The myosin (globular) heads binds with these sites, changes shape and dips forward
    8. Pulling the actin along the myosin
    9. Energy from ATP
    10. Is used to break the cross bridge
    11. Using ATPase enzyme ATP  ADP +Pi
    12. The myosin head is now reset
  • When excitation stops, calcium leaves the troponin molecules
  • Tropomyosin blocks the actin-myosin binding sites
  • Actin slides back to its original position
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11
Q

Muscle Fibre Cells – make up skeletal muscles

A

• Cell membrane = sarcolemma
• Cytoplasm = sarcoplasm
• Endoplasmic reticulum = sarcoplasmic reticulum (SR)
• Bits of the sarcolemma fold & stick into the sarcoplasm, this helps spread electrical impulses throughout the sarcoplasm so they reach all parts of the muscle fibre - called transverse (T) tubules.
• A network of internal membranes runs through the sarcoplasm = sarcoplasmic reticulum
• contains stores of calcium ions
• Sarcomeres sections of filaments made up of myosin and actin, within the muscle
fibre cell
• Muscle fibre cells have lots of mitochondria (outside the sarcomere) and are multinucleated

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12
Q

Why do the muscle fibre cells need to be multinucleated?

A
  • Instruction for protein synthesis available along whole myofibril, no need for transport.
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13
Q

Why are the mitochondria not located within the sarcomere?

A
  • They would be in the way of the contracting / sliding filaments.
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14
Q

The Role of ATP in muscle contraction

A

•Myosin and actin form crossbridges
•ATP binds to the myosin head causing the crossbridges to break
•ATP  ADP + Pi by ATPase releasing energy
•Pi is released from myosin head causing the myosin head to reset
•ADP is released from myosin head after it resets
•ATP is also used for active transport of Ca ions back into the sarcoplasmic reticulum

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15
Q

Myofibrils in a muscle fibre

A

• Located in the sarcoplasm
• Muscle fibre cells have long, cylindrical organelles called myofibrils, made up of two bundles of protein filament :
• Thick myofilaments – myosin
• Thin myofilaments – actin
• arranged in a particular order, creating different types of bands and line.

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16
Q

Muscle fibres - fast twitch

A

• Muscle fibres that contract very quickly
• Used for fast, short burst movements
• For speed and power
• Get tired very quickly – due to the production of lactic acid
• Large amounts of calcium ions present to stimulate contraction
• Energy released quickly through anaerobic respiration using glucose
• Few mitochondria or blood vessels (capillaries)
• Larger store of glycogen to provide glucose for glycolysis
• Lots of creatine phosphate (donates a phosphate group to rapidly turn ADP 􏰀 ATP) only a short term option
• Whitish in colour as they don’t have much myoglobin (used to store oxygen)

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17
Q

What is Myoglobin?

A
  • red pigment molecule that is similar to haemoglobin
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18
Q

Slow twitch muscle fibres

A

• Contract slowly
• Used for posture and endurance activities
• Work for a long time without getting tired - due to less lactate production
• Energy released slowly through aerobic respiration
• Lots of mitochondria
• Lots of blood vessels to supply the muscle with oxygen (denser network or capillaries)
• Smaller store of glycogen due to good blood supply
• Reddish in colour because they’ve got lots of myoglobin (a red coloured protein that stores oxygen)
• High amounts of myoglobin, haemoglobin and mitochondria.

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19
Q

7.3 i) Understand the overall reaction of aerobic respiration as splitting of the respiratory substrate, to release carbon dioxide as a waste product and reuniting of hydrogen with atmospheric oxygen with the release of a large amount of energy.

A

Glucose + oxygen —> carbon dioxide + water + energy

C6H12O6 + 6O2 —> 6CO2 + 6H2O + 2870kJ

The energy released during respiration is used to phosphorylate (add a phosphate) ADP to form ATP.
The ATP provides energy for other biological processes in cells.

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20
Q

ii) Understand that respiration is a many-stepped process with each step controlled and catalysed by a specific intracellular enzyme.

A
  • Glycolysis (cytoplasm)
  • The Link reaction (matrix of mitochondria)
  • The Krebs cycle (matrix of mitochondria)
  • Oxidative phosphorylation (inner membrane of mitochondria)
  • NAD and FAD - coenzymes responsible for transferring hydrogen between molecules
  • depending on whether they give or take hydrogen, they are able to reduce or oxide a molecule
  • Coenzyme A - responsible for the transfer of acetate (acetic acid) from one molecule to another.
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21
Q

Mitrochondria

A

Two phospholipid membranes
Outer membrane
- smooth
- permeable to several small molecules
Inner membrane
- folded (cristae)
- less permeable
- site of the electron transport chain (used in oxidative phosphorylation)
- location of ATP synthase enzymes (used in oxidative phosphorylation)
Intermembrane space
- low pH due to the high concentration of protons
- concentration gradient across inner membrane is formed during oxidative phosphorylation - essential for ATP synthesis
Matrix
- aqueous solution within inner membrane of the mitochondrion
- contains ribosomes, enzymes, and circular mitochondrial DNA necessary to function

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22
Q

First stage - glycolysis

A

Glycolysis (cytoplasm of cells)

Phosphorylation

  • Glucose is phosphorylated by adding 2 phosphates from 2 molecules of ATP.
  • creating 2 molecules of ADP and 2 molecules of triose phosphate

Oxidation

  • Triose phosphate is oxidised (loses hydrogen) forming 2 molecules of pyruvate.
  • NAD collects hydrogen ions, forming 2 reduced NAD
  • 4 ATP produced, 2 were used up in stage one, net gain of 2.
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23
Q

Why is there only a net gain of two ATP molecules during glycolysis?

A

4 ATP molecules were produced during glycolysis, 2 of them used to phosphorylate glucose, therefore a net gain of 2 ATP molecules

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24
Q

Link reaction

A

Mitochondrial matrix (occurs twice for every glucose molecule)

  • pyruvate is decarboxylated (carbon removed) - one c atom removed from pyruvate in the form of CO2
  • NAD is reduced, collects hydrogen form pyruvate, changing pyruvate into acetate.
  • Acetate is combined with coenzyme A to form acetyl coenzyme A (acetylene CoA)
  • no ATP produced in this reaction.

Pyruvate + NAD + CoA —> acetyl CoA + carbon dioxide + reduced NAD

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25
Q

Why will the link reaction and the Krebs Cycle occur twice?

A

Every molecule of glucose produces two Pyruvate molecules, therefore the two steps will occur twice for every molecule of glucose.

Thus, each molecule of glucose will produce

  • 2 molecules of acetyl CoA
  • 2 molecules of CO2
  • 2 molecules of reduced NAD
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26
Q

Krebs cycle (citric acid cycle)

A

• Occurs in the mitochondrial matrix
• Complete oxidation of glucose to carbon dioxide
• Produces 6 reduced NAD, 2 reduced FAD, 4 carbon dioxide and 2 ATP (for each glucose molecule)
• Cycle of Acetyl co A binding to oxaloacetate 4C
• Involves oxidation and decarboxylation reactions (and
dehydrogenation)

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27
Q

Why does the Link Reaction and the Krebs cycle take place in the mitochondria?

A

• The enzymes needed are specific for each stage
• The enzymes for each step are found in the matrix
• So that the products (coenzymes) are available for the next stage (on the inner membrane of the mitochondria)

ENZYMES
•Each stage is catalysed by a different specific enzyme
•The product of each stage becomes the substrate of the next stage

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28
Q

How much ATP from 1 acetyl co A?

A

• Each reduced NAD makes 3 ATP
• reduced FAD makes 2 ATP

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29
Q

Why are enzymes needed in respiration?

A

• Speed up the reactions
• By lowering activation energy
• Each step produces the substrate for the next enzyme
• Enzymes are specific for each stage
• (gene expression) Allows control of each stage of respiration

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30
Q

7.6 Understand how ATP is synthesised by oxidative phosphorylation associated with the electron transport chain in mitochondria, including the role of chemiosmosis and ATP synthase.

A

On stalked particles on the inner mitochondrial membrane.

  1. Hydrogen atoms are released from reduced NAD and reduced FAD as they are oxidised
  2. Hydrogen atoms split into hydrogen ions (protons) and electrons
  3. Electrons move along the electron transport proteins in the inner membrane of the mitochondria, releasing energy at each carrier
  4. This energy is used to pump the Hydrogen ions (protons) into intermembrane space forming an electrochemical gradient
  5. Hydrogen ions move down electrochemical gradient back to matrix via ATP synthase
  6. Chemiosmosis
  7. Movement of Hydrogen ions drives synthesis of ATP from ADP and Pi
  8. Hydrogen ions, electrons and oxygen combine to form water, oxygen is the final
    electron acceptor (2H+ + 1⁄2 O2 + 2e- 􏰀 H20)
  9. 26 ATP molecules are made (so 30 overall – but there is some debate)
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31
Q

Number of ATP Molecules produced during aerobic respiration per glucose molecule

A

NOTION

= 38

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32
Q

Why is oxygen so important for aerobic respiration?

A
  • Oxygen acts as the final electron acceptor.
  • No oxygen = ETC cannot continue as electrons have no place to go.
  • No more ATP is produced via oxidative phosphorylation
  • Oxygen not accepting electrons (and hydrogen ions) reduced coenzymes NADH and FADH2 cannot be oxidised to regenerate NAD and FAD
  • Cannot be used in further hydrogen transport
  • Krebs cycle stops
  • Link reaction also stops
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33
Q

Lactate fermentation

A
  • Reduced NAD transfers hydrogen to pyruvate to form lactate
  • NAD can now be reused in glycolysis
  • Pyruvate is reduced to lactate by enzyme lactate dehydrogenase
  • Pyruvate = hydrogen acceptor
  • Final product lactate can be further metabolised
  • Small amount of ATP produced
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34
Q

7.7 Understand what happens to lactate after a period of anaerobic respiration in animals.

A
  • Can build up in the cells after a period of time
  • Can be oxidised to pyruvate, then channeled into the Krebs cycle for ATP production (needs extra oxygen - oxygen debt - explains why animals breathe deeper and faster after exercise)
  • Can be converted into glucose by the liver cells for use during respiration or for storage (glycogen)
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35
Q

CORE PRACTICAL 16:
Investigate rate of respiration.

A

• C - Either Temperature OR Mass of organisms (temp only up to 40 degrees - ethics of causing harm to an animal), 5 values stated
• O - Germinating Seeds/ Maggots/ Any small respiring organism of same age, clones of each other or have same parents (plants can be cuttings, same genetic makeup) - to eliminate environmental and genetic effects on the results of the investigation
• R – repeat 5 times at each temp/mass, calculate mean and s.d, stats test – Spearman’s rank, correlation coefficient
• M - Change in volume of oxygen / volume of oxygen taken up - by measuring the distance moved by the liquid in the u tube and multiplying it by the cross-sectional area of the u-tube (πr2). Per unit of time. Per gram.
• EG mm3s-1g-1
• S - Either Mass of organisms OR Temperature and then time left to respire, mass of soda lime, equipment used to measure th

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36
Q

Myogenic definition?

A
  • The heart has the ability to initiate its own contraction.
  • The heart can beat without any input from the nervous system as longs as its cells stay alive. This is due to myogenic contraction.
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37
Q

Cardiac Cycle

A

• Sinoatrial Node is the natural pacemaker - sends an electrical impulse
• Sends a wave of depolarization across the walls of the atria
• Atria contract – atrial systole
• Depolarisation passes to the Atrioventricular Node & causes a delay
• Atrioventricular Node is stimulated and passed the stimulation along the bundle of His to the bottom of the ventricles
• Across the Purkyne fibres
• Causes depolarization of the ventricular walls
• Ventricles contract from the apex of the heart up – ventricular systole

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38
Q

Why is there a delay before the AVN is stimulated?

A
  • Means that the ventricles contract after the atria.
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39
Q

7.8 iii) Understand how the use of electrocardiograms (ECGs) can aid the diagnosis of cardiovascular disease (CVD) and other heart conditions.

A
  • The electrical activity of the heart can be monitored by an electrocardiograph.
  • Electrodes that are capable of detecting electric signals are placed on the skin
  • Produce an electrocardiograph (ECG)
  • Shows a number of distinctive electrical waves produced by the activity of the heart
  • Healthy heart produces a distinctive shape in an ECG.
40
Q

ECG

A
  1. P wave - caused by depolarisation of atria = atrial contraction (systole)
  2. QRS complex - depolarisation of ventricles = ventricular contraction (systole)
  3. T wave - repolarisation of ventricles = ventricular relaxation (diastole)
  4. U wave - scientists are still unsure, may be caused by the repolarisation of the Purkyne fibres

The BIGGER the wave, the GREATER the electrical activity passing through the heart, which results in a stronger contraction.

41
Q

Using ECGs to diagnose heart problems

A

Tachycardia - heart beats too fast (>100)
Bradycardia - heart beats too slow (60>)
Ectopic heartbeat - easily heartbeat caused by a pause (due to earlier contraction of the atria or ventricles)
Fibrillation - irregular heartbeat, disrupt rhythm of the heart - atria or ventricles stop contracting properly.

42
Q

Cardiac output

A
  • the volume of blood that is pumped by the heart per unit of time.
    = heart rate x stroke volume
    Cm^3min^-1
43
Q

Heart rate

A

Number of times a heart beats per minute
- beats per minute (bpm)

44
Q

Stroke volume

A

The volume of blood pumped out of the left ventricle during one cardiac cycle. (Cm^3)

45
Q

Artificial pacemakers

A
  • Devices implanted in people whose heart’s electrical conduction system is not working properly.
  • Problems include
    • the SAN not firing
    • and the blockage or disruption of impulses between the SAN and AVN, or in the bundle of His.
  • Pacemakers monitor the heart’s electrical activity, stimulate the ventricles or atria to contract when necessary.
  • Impulses are transmitted down electrodes implanted in the muscular walls.
46
Q

Why does our cardiac output and respiratory minute volume increase during exercise?

A

⚫ More oxygen to muscle cells
⚫ More glucose to muscle cells
⚫ More removal of carbon dioxide
⚫ More removal of lactate

47
Q

Heart rate is controlled by…

A
  • Hormones (adrenaline)
  • Neurotransmitter (Noradrenaline (binds to receptors on the SAN))
  • Nerves (Parasympathetic nervous system, Sympathetic nervous system, Both part of the autonomic nervous system)
48
Q

During exercise the body will accommodate by making the following changes…

A
  • Increase the rate and depth of breathing
  • Increase the heart rate
49
Q

Control of the breathing rate

A
  • controlled by the ventilation centres (respiratory centres) in the medulla oblongata
  • inspiration centre (air into lungs)
  • expiratory centre (air out of the lungs)
50
Q

Inspiratory centre

A

The inspiratory centre in the medulla oblongata has the following effect on breathing:
• It sends nerve impulses along motor neurons to the intercostal muscles of the ribs and diaphragm muscles
• These muscles will contract and cause the volume of the chest to increase
• This lowers the air pressure in the lungs to slightly below atmospheric pressure
• An impulse is also sent to the expiratory centre to inhibit its action
• Due to the difference in pressure between the lungs and outside air, air will flow into the lungs.
• lungs inflate, stretch receptors in lungs are stimulated. SR send nerve impulses back to the medulla oblongata. These impulses inhibit the action of the inspiratory centre.
• The expiratory centre (no longer inhibited) sends nerve impulses to the diaphragm/inter coastal muscles to relax. Causes the lungs to deflate, expelling air. As the lungs deflate, the stretch receptors become inactive. The Inspiratory centre is no longer inhibited and the cycle starts again.

51
Q

Expiratory centre

A

• Nerve impulses are sent back to the medulla oblongata which willinhibit the inspiratory
• The expiratory centre is no longer inhibited and will bring about the following changes:
• It sends nerve impulses to the intercostal and diaphragm muscles
• These muscles will relax and cause the volume of the chest to decrease
• This increases the air pressure in the lungs to slightly above atmospheric pressure
• Due to the higher pressure in the lungs, air will flow out of the lungs
• As the lungs deflate, the stretch receptors become inactive which means that the inspiratory centre is no longer inhibited and the next breathing cycle can begin

52
Q

What are stretch receptors?

A
  • in the lungs
  • are stimulated as they inflate with air
53
Q

Chemoreceptors/Barorecpetors

A

CHEMORECEPTORS

  • detect chemical changes in the composition of the blood, such as pH levels
  • located in the ventilation centre of the medulla oblongata
  • also present as clusters of cells in the aorta (aortic bodies) and carotid arteries (carotid bodies)

BARORECEPTORS

  • found in the aortic and carotid bodies
  • stimulated by high and low blood pressure
54
Q

Ventilation rate

A

The volume of air that moves in and out of the lungs during a set time period (e.g. a minute)
INCREASES during exercise due to the increase in breathing rate and depth.

55
Q

Control of the heart rate

A
  • Cardiovascular control centre in the medulla oblongata unconsciously controls the heart rate, by controlling the rate at which the sinoatrial node (SAN) generates electrical impulses.
56
Q

Parasympathetic nervous system

A

⚫ Inhibits effectors
⚫ Controls actions under resting conditions
⚫ Slows down activity
⚫ Conserves energy
⚫ Releases the neurotransmitter acetyl choline which binds to receptors on the SAN
⚫ decreases the heart rate after exercise

57
Q

Sympathetic nervous system

A

⚫ Stimulates effectors
⚫ Controls conditions under stress or activity
⚫ Speeds us up (fight or flight)
⚫ Secretes noradrenaline
⚫ increase the heart rate during exercise

58
Q

Changes in heart rate stimulus examples

A

HIGH BLOOD PRESSURE

  • detected by baroreceptors which send impulses to cardiovascular control centre
  • sends impulses along parasympathetic neurones which secrete the neurotransmitter acetylcholine
  • Acetylcholine binds to receptors on SAN causing it to fire less frequently
  • Heart rate slows down and blood pressure decreases back to normal
59
Q

Neurotransmitter - Acetylcholine

A

Parasynthetic neurones secrete acetylcholine (neurotransmitter)

High blood pressure, High blood O2, Low CO2, or High pH levels.

60
Q

Neurotransmitter - Noradrenaline

A

Sympathetic neurones secrete noradrenaline (neurotransmitter)

Low blood pressure, Low blood O2, High CO2, or Low pH levels.

61
Q

CORE PRACTICAL 17:
Investigate the effects of exercise on tidal volume, breathing rate, respiratory minute ventilation and oxygen consumption using data from spirometer traces.

A

• C - Time spent performing a specific exercise or type of activity
• O - Human. The same person so that the results don’t vary from different levels of fitness. Perform repeats by allowing the perfromer to fully rest. If multiple people same age, fitness level.
• R – Repeat 5 times at each time/activity, calculate mean and s.d. stats test, time = spearman’s rank, activity – t-test
• M - A spirometer is used to measure the volume of air in an area. The graph then plotted allows measurements on specific areas (See next slide)
• S – Time exercised/activity type, temperature, volume of water consumed

62
Q

Calculating from a Spirometer trace

A

NOTION

63
Q

Homeostasis

A

Physiological control systems maintain the internal environment within restricted limits despite external changes.

The following have to be maintained;
• Body temp
• Blood glucose conc.
• Blood salt conc. / ions
• Water potential of blood
• Blood pressure
• Carbon dioxide conc.

64
Q

7.11 i) Understand what is meant by negative feedback

A

• A change in the internal environment brings about a response that reverses that change

• EG temperature increases, you sweat, temperature decreases
• Change needs to be detected
• Change must be signalled to other cells
• Response to reverse the change

65
Q

Negative feedback pathway

A

Stimulus —> Receptor —> Communication pathway (cell signalling) —> Effector —> Response

66
Q

Using blood glucose and insulin as the example, Write down the negative feedback pathway

A

Blood glucose levels increase —> Chemoreceptors detect a change in the blood (located in the pancreas) —> cell signalling to pancreases glands —> insulin is produced/secreted from the pancreas glands —> blood glucose levels decrease and return back to normal (cells take up glucose and convert glycogen in the liver)

67
Q

Positive feedback

A
  • not common
  • Increases original change detected by receptors
  • Usually harmful
  • E.g. hypothermia body temp falls,
  • enzymes become less active, less heat released, temp continues to fall!
68
Q

Example of positive feedback

A

• Labour!!
• Cervix opens and stretches
• Oxytocin released
• Oxytocin increases contractions
• Cervix stretches more

69
Q

TOO HOT – THERMOREGULATORY CENTRE OF THE HYPOTHALAMUS

A

1.Receptors in hypothalamus detect increase in core temp/temp of blood
—> Also temperature receptors in the skin
2. Heat loss centre stimulated of the thermoregulatory centre
3. VASODILATION of arterioles
4. Arterioles leading to capillaries in the skin dilate
5. SHUNT VESSELS CONSTRICT
6. More blood flows to skin surface (capillaries) / heat loss by RADIATION
7. Heat loss by EVAPORATION of sweat / by using energy.
—> High(er) rate of sweating leads to a low(er) skin temp
8. VOLUNTARY CENTRE: remove clothing / seek cooler area / cold drink

70
Q

TOO COLD – THERMOREGULATORY CENTRE OF THE HYPOTHALAMUS

A
  1. Receptors in hypothalamus detect decrease in core temp/temp of blood
  2. Heat gain centre stimulated
  3. VASOCONSTRICTION of arterioles
  4. Arterioles leading to capillaries in the skin narrow
  5. SHUNT VESSELS DILATE
  6. Less blood flows to skin surface / less heat is lost by RADIATION
  7. Hair raising / greater insulation / humans have less dense hair \ no effect
  8. Shivering / rapid contraction and relaxation of muscles / heat produced by RESPIRATION
  9. Adrenaline INCREASES METABOLIC RATE of cells //Mammals in cold climates can increase secretion of thyroxine / hormone increases metabolic rate on a more permanent basis
  10. VOLUNTARY CENTRE: put on clothes / seek warmer areas / warm drink
71
Q

Vasodilation

A
  • Blood moves to surface so heat can be lost.
  • Shunt vessels constrict.
  • Sphincter muscles in arterioles are relaxed and open.
  • This allows blood to flow to the surface and heat is lost.
72
Q

Shunt vessel

A
  • A blood vessel that links an artery (arteriole) directly to a vein (venuole).
  • Allowing the blood to bypass the capillaries in certain areas.
  • Shunt vessels can control blood flow by constriction and dilation.
73
Q

Hypothalamus

A

Area of the brain that is responsible for controlling many functions in the body, including
- hormones
- sleep
- growth
- body temperature
- blood pressure

74
Q

Moderate Exercise

A

• Increases number and activity of Natural Killer cells.
• These target cells which do not display “self” markers/antigens.
• ( these can be cells invaded by viruses, bacteria and cancer cells)
• They attack the cell membrane by making pores in it
• ( make protein perforin).
• Proteases can invade cell and cause apoptosis.
• Give non-specific protection.

75
Q

Vigorous exercise

A

After exercise the number of these immune system cells falls
• Natural killer
• Macrophages
• B cells
• Helper T cells.
• The specific immune system is depressed.
• Debate about whether physical or psychological.
• Stress of training could release adrenalin and cortisol both known to suppress the immune system.

76
Q

Disadvantages of exercising too much

A
  • wear and tear on joints
  • suppression of the immune system
77
Q

Disadvantages of exercising too little

A
  • Increased risk of obesity
  • Increased risk of CVD
  • Increased risk of diabetes
  • Suppression of the immune system
  • Increased levels of LDLs
78
Q

Joint damage by exercise

A

E.g. knees
• Cartilage worn away
• Patellar tendonitis – kneecap does not move easily over femur
• Bursitis – fluid filled sacs around joints swell up with extra fluid. Inflammation and tenderness.
• Ligament damage.
• Tendon damage

79
Q

Keyhole surgery

A
  • less invasive procedure, only small incisions
  • small video camera inserted into the incision, along with special medical instruments
80
Q

Benefits of keyhole surgery (arthroscopy)

A

• Less tissue damage
• Less bleeding
• Less scarring
• Less pain
• Less anaesthetic
• Lower risk of infection
• Faster recovery rate
• Cheaper
• Faster – so more patients can be treated

81
Q

Prostheses

A

—> EG Dynamic response prosthetic foot.
—> Changes shape with body weight but returns to its original shape when off the ground.
—> Can replace the joint, allow the person to move without pain & potentially play sport again
—> Some prostheses may be connected to electronic devices that can “read” information from the nervous system in order to operate the body part. (E.g. hand prostheses enabling the user to move the fingers)

82
Q

7.15 Be able to discuss different ethical positions relating to whether the use of performance-enhancing substances by athletes is acceptable.

A

Performance enhancing drugs
Anabolic steroids - increase muscle size, increased strength, speed and stamina, may lead to organ damage and increased aggression.
Stimulants - more alert and able to react faster, greater endurance, may lead to aggressive behaviour
Narcotic analgesics - strong painkillers, used to maintain their performance.

83
Q

Ethical positions on the use of performance - enhancing drugs

A

Rationalists - think there may be times when their use is justified.
Absolutists - think that they are morally wrong and should be banned from all sports.

84
Q

Against performance enhancing drugs

A

• Against:
• Damaging effect on synapses
• Leads to abnormal behaviour
• Unfair advantage
• May have long-term side effects on body eg heart disease – cost to NHS
• Poor role model to youngsters

85
Q

For performance enhancing drugs

A

• Individual choice / responsibility;
• Helps you win

86
Q

7.16 Understand how genes can be switched on and off by DNA transcription factors including hormones.
TRANSCRIPTION FACTORS

A

•Transcription factors are proteins that help activate or deactivate specific genes by binding to nearby DNA.
•Activators boost a gene’s transcription.
•Repressors decrease transcription.
•Transcription factors help ensure that the right genes are expressed in the right cells of the body, at the right time.

87
Q

Lipid soluble hormones can act directly on transcription factors as they can cross the membrane (SET ANSWER)

A

• Normal body temperature – thyroid hormone receptor binds to the start of the gene
• Reduces transcription (blocks RNA polymerase)
• Cold temperature causes thyroxine to be released
• Binds to thyroid hormone receptor
• Activates gene
• RNA polymerase binds
• Transcription rate increases
• Making an enzyme which increases metabolism
• More exothermic reactions, so more heat produced
• Body warms up

88
Q

Some hormones can’t cross the membrane eg protein hormones that aren’t lipid soluble, so…

A

• Bind to receptors on the cell membrane
• Activate messenger molecules in the cytoplasm
• Messenger molecules activate enzymes called protein kinases
• A chain of reactions called a cascade is triggered
• Transcription factors are activated by the cascade

89
Q

How may proteins stop the transcription factors?

A

• Preventing them from binding to the DNA;
• Binding and blocking their DNA-binding site
• Promoting the degradation of these proteins

90
Q

Chemiosmosis

A

The movement of ions across a partially permeable membrane, down their electrochemical gradient

91
Q

Oxidative phosphorylation

A

the process in which ATP is formed as a result of the transfer of electrons from reduced NAD or reduced FAD to Oxygen by a series of electron carriers

92
Q

Substrate level phosphorylation

A

production of ATP in glycolysis & Krebs

93
Q

Electron transport chain

A

the movement of electrons down a series of electron carriers

94
Q

ATPsynthase

A
  • The enzyme which makes ATP when H+ ions move through it.
95
Q

Production of lactate in animals

A

• Human cells do this by converting pyruvate to lactate (reduction).
• This reaction uses reduced NAD by oxidising it to NAD once more.
• NAD is now available again to accept electrons and protons so glycolysis continues.
• If NAD was not regenerated, even glycolysis would have to stop
• Pyruvate + reduced NAD Lactate + NAD

96
Q

What happens in anaerobic respiration and why it is important?

A

• Anaerobic respiration occurs mostly in the muscles when oxygen is being used up quicker than it can be supplied,
• In the absence of oxygen glycolysis would usually stop as there would be a build up of reduced NAD.
• For glycolysis to continue, reduced NAD must be converted into NAD.
• This happens when pyruvate takes up hydrogen from reduced NAD to make
lactate.
• Lactate causes reduced pH & fatigue in muscle tissue so this must be removed.
• An oxygen debt occurs.
• Lactate can be oxidised back to pyruvate and enter the Krebs cycle
• Or taken to the liver converted to glucose & stored as glycogen.

Year 2 Biology (4 decks)

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