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Biology > Topic 7 Humphries > Flashcards

Topic 7 Humphries Flashcards

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1
Q

Synovial membrane

A

secretes synovial fluid

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2
Q

Fibrous Capsule

A

encloses joints

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3
Q

Pad of Cartilage

A

gives additional protection

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4
Q

Cartilage

A
  • strong, flexible supporting tissue
  • absorbs synovial fluid
  • acts as shock absorber at the ends of bones in joints
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5
Q

Synovial fluid

A
  • viscous fluid, secreted by the synovial membrane

- acts as lubricant (to the joint)

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6
Q

Ligaments

A
  • joins bone to bone
  • control and restrict the amount of movement in the joint
  • strong and slightly elastic
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7
Q

Tendons

A
  • join muscle to bone
  • enable the transmission of forces
  • inelastic but flexible
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8
Q

Joint

A

where 2 bones meet (some moveable - cartileginous or synovial or immoveable - fixed in the skull)

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9
Q

Bones

A

are made of bone cells and bone matrix (collagen and calcium phosphate) and make up our skeleton

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10
Q

Muscles

A

Bring about movement at a joint by contracting and relaxing to flex (shorten) and extend (lengthen). Work in antagonistic pairs across joints for movement; extensors - extend, flexors - flex

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11
Q

Muscles can only…

A

…pull - they shorten (contract) which pulls on the bone and moves the joint

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12
Q

Extensor

A

a muscle that contracts to cause extension

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13
Q

Flexor

A

a muscle that contracts to shorten the joint/ reverse the movement

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14
Q

For a joint to move back and forth…

A

…2 muscles are needed - a pair of muscles that work in this way are antagonistic muscles

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15
Q

Muscle fibre

A

is a muscle cell

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16
Q

Muscle cell

A

is a muscle fibre - long, thin, multi-nucleated cell containing myofibrils

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17
Q

Myofibrils

A

within the muscle fibre, made of a collection of proteins and organised into sarcomeres

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18
Q

Sarcomere

A

repeating contractile unit in a myofibril

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19
Q

Sarcoplasm

A

cytoplasm in the muscle fibre/ cell

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20
Q

Sarcolemma

A

cell membrane in the muscle fibre/ cell

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21
Q

Tropanin

A

protein attached to actin that binds to Ca2+

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22
Q

Tropomyosin

A

protein wrapped around actin, shields myosin binding site on actin

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23
Q

Actin

A

thin filaments

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24
Q

Myosin

A

thick filaments

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25
Q

Z line

A

the ends of each sarcomere

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26
Q

Neuromuscular junction

A

where neurone and muscle meet

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27
Q

Sarcoplasmic reticulum

A

membrane bounds sacs surrounding the myofibrils - release/ secrete Ca2+

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28
Q

Cross-bridges

A

when the myosin head attaches to the actin binding site

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29
Q

Ca2+ (muscle)

A

causes the shape change of troponin and tropomyosin

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30
Q

ATP (muscle)

A

binds to myosin head, causes it to detach from actin

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31
Q

Role of Ca2+ in muscle contraction

A
  • changes shape of actin by binding to troponin
  • this makes tropomyosin change shape to reveal the myosin head binding sites
  • this allows actin-myosin cross-bridges to form
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32
Q

Role of ATP in muscle contraction

A
  • permits detachment of myosin head from actin
  • hydrolysis of ATP (by ADPase on myosin) causes the shape change of the myosin head
  • the shape change of the myosin head allows it to bind to actin again
  • ATP also pumps the Ca2+ back into the Sarcoplasmic reticulum
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33
Q

What happens to the thin and thick filaments during muscle contraction?

A

they slide over each other - they DO NOT SHORTEN

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34
Q

What happens to the sarcomere during muscle contraction?

A

the length of each sarcomere shortens - z lines get closer together

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35
Q

Uses of ATP

A
  • active transport
  • muscle contraction
  • photosynthesis
  • action potential
  • protein synthesis
  • spindle action
  • glycolysis
  • activation of chemicals
  • making proteins/ polysaccharides
  • secretion - to make vesicles
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36
Q

Aerobic respiration equation

A

Oxygen and Glucose –> Carbon Dioxide and Water (+ ATP)

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37
Q

The input of energy into respiration…

A

…is not as great as the energy released when bonds are formed

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38
Q

Substrate level phosphorylation

A

a phosphate group is transferred from a substrate molecule to ADP (e.g. in glycolysis)

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39
Q

Oxidative phosphorylation

A

ATP is made from Pi and ADP. Energy comes from a series of oxidation reactions in the electron transport chain in the mitochondria

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40
Q

Photophosphorylation

A

ATP is made from Pi + ADP (and AMP). Light energy drives the process

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41
Q

What enzyme catalyses both the hydrolysis and phosphorylation of ATP?

A

ATPase

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42
Q

Hydrolysis of ATP

A

ATP is broken down into ADP + Pi + energy

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43
Q

Phosphorylation

A

ATP is made from ADP + Pi (different types of phosphorylation)

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44
Q

Features of a mitochondrion

A
  • DNA loop
  • cristae
  • matrix
  • double membrane (outer and inner)
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45
Q

Glycolysis yields

A

2 molecules of pyruvate, 2 molecules of NADH (reduced NAD) and a net gain of 2 ATP molecules

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46
Q

Where does glycolysis occur?

A

in the cytoplasm (or sarcoplasm)

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47
Q

What phosphorylation is used in glycolysis?

A

substrate level phosphorylation - phosphate’s from intermediate 3C compound used to make ATP

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48
Q

Process of glycolysis

A

glycogen store or food –> glucose (6C) –> 2x intermediate 3C compounds (phosphorylated) –> 2x pyruvate

2ATP put in and converted to 2ADP
2 hydrogen’s released which go to reduce NAD
4ADP + 2Pi converted to 4ATP

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49
Q

What is NAD? What is its purpose?

A

a co-enzyme (along with FAD)

to transport hydrogen

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50
Q

Which stage of respiration is anaerobic?

A

glycolysis - no oxygen is used

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51
Q

For every 1 glucose molecule…

A

…the link reaction and Krebs cycle happens twice

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52
Q

Link Reaction

A

pyruvate from glycolysis –> carbon dioxide + 2 hydrogens + acetyl CoA

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53
Q

Krebs cycle

A
  • Acetyl CoA combines with 4C compound to make a 6C compound
  • 6C compound undergoes decarboxylation and dehydrogenation to form a 5C compound
  • 5C compound undergoes decarboxylation and 1 ATP molecule is formed from substrate level phosphorylation and 6 hydrogens are released in total to reduce the co-enzymes
  • This reforms the 4C compound
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54
Q

What has happened to glucose following link and Krebs cycle? Carbon? Oxygen? Hydrogen?

A
  • it has been completely broken down
  • carbon and oxygen has been released as CO2
  • Hydrogens have been used to reduce co-enzymes NAD and FAD (these transport them to the ETC)
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55
Q

What is an electrochemical gradient?

A

a really positive to really negative environment

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56
Q

Chemiosmosis

A

is a method of storing energy by creating a proton gradient across a membrane

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57
Q

What is oxygen’s role in the ETC?

A

it’s the final electron acceptor

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58
Q

Electron Transport Chain

A
  • reduced NAD and FAD carries proton and electron to ETC
  • electrons pass from one electron carrier to the next in a series of redox reactions
  • This releases energy, pumping protons across the inner membrane into the inter-membrane space
  • There is now a high proton concentration in the inter-membrane space as H+ accumulate there
  • Protons diffuse back into the matrix down electrochemical gradient (through stalked particle)
  • The movement of the proton diffusion allows ATP synthase to catalyse ATP synthesis
  • Protons are collected by 1/2O2 along with electrons forming hydrogen, then water - this is a waste product
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59
Q

What happens if oxygen supply stops?

A
  • no electrons or hydrogen ions accepted so no ATP synthesis from ETC and NADH and FADH can’t deposit electrons at ETC so Krebs cycle and link reaction stops - ATP synthesis stops and ETC stops
  • no electrons moving along electron carriers by redox reactions, no protons pumped across membrane
  • stop cellular processes so no energy source so no muscle contraction
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60
Q

If there’s no O2…

A

…no electron transport chain, reduced NAD can’t be oxidised, most respiration reactions (link, Krebs, ETC) stop in the absence of oxidised NAD

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61
Q

Difference between aerobic and anaerobic glycolysis

A

In aerobic complete oxidation of glucose to produce waste products. In anaerobic incomplete oxidation of glucose to produce lactate –> lactic acid

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62
Q

Anaerobic glycolysis

A

glucose turns into pyruvate after ADP + Pi is phosphorylated to make ATP and 2 hydrogens are released however the ETC has stopped so no NAD and FAD are there to accept hydrogens so pyruvate comes along to accept hydrogens and is reduced making lactate

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63
Q

What happens to lactate?

A
  • Transported to the liver from the muscles in the blood plasma
  • Pyruvate then is completely oxidised via the Krebs cycle (aerobic). This creates an oxygen debt (extra oxygen needed during ‘recovery period’ to ensure complete oxidation of extra pyruvate)
  • Some lactate may be converted into glycogen and stored in the muscle or liver
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64
Q

What happens to lactate if it builds up?

A

can be broken down in the liver or broken down to CO2 and H2O in aerobic respiration

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65
Q

What happens if lactate builds up?

A

The pH of the cell will fall inhibiting enzymes that catalyse glycolysis reactions - can’t continue. Many amino acids that make up an enzyme have negatively or positively charged groups so if hydrogen ions from lactic acid accumulate in the cytoplasm they neutralise negative groups in the active site of the enzyme which means attractive forces between enzyme and substrate will be affected so substrate may no longer bind to active site

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66
Q

Aerobic respiration facts

A
  • glucose broken down completely into water and carbon dioxide
  • up to 38 molecules of ATP produced for each molecule of glucose
  • oxygen required (final electron acceptor)
  • ATP made via oxidative and substrate level phosphorylation
  • glycolysis, Krebs and ETC all working correctly
  • Happens in cytoplasm and mitochondria
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67
Q

Anaerobic respiration facts

A
  • glucose not completely broken down to produce lactate
  • 2ATP molecules produced for each molecule of glucose
  • oxygen not required (only after to break down)
  • substrate level phosphorylation ONLY
  • only glycolysis occurs
  • happens in cytoplasm only
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68
Q

How do we supply energy instantly?

A

-with creatine phosphate

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69
Q

Creatine phosphate

A
  • stored in muscles
  • can be hydrolysed to release energy
  • breakdown begins as soon as exercise begins
  • can be used to regenerate ATP
  • triggered by formation of ATP
  • doesn’t need oxygen
  • can supply energy for about 6-10 seconds
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70
Q

When is creatine phosphate relied upon?/

A

for regeneration of ATP during short bursts of intense energy - at rest creatine phosphate will be regenerated

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71
Q

Creatine phosphate equation

A

Creatine phosphate + ADP –> Creatine + ATP

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72
Q

What is a respirometer used for?

A

measure the rate of respiration

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73
Q

What should a control tube contain when using a respirometer?

A

equal volume of non-respiring material

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74
Q

How does a respirometer work?

A

Small organisms respire; take in O2, CO2 given off, CO2 taken in by soda-lime so pressure in the test tube drops. Due to higher pressure outside, the coloured liquid moves to the left as air is forced in. You can work out the distance moved in a time to get the rate of O2 uptake. Find area to get volume and divide by mass of organisms to get per gram of organism

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75
Q

What is the syringe used for on a respirometer?

A

to reset the experiment and pressure

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76
Q

What should be controlled? How?

A

temperature - place in a water bath or use a U tube respirometer which has a built in control so any external changes affect the pressure in both tubes so effects cancel out

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77
Q

Aerobic capacity

A

the ability to take in, transport and use oxygen

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78
Q

VO2

A

volume (litres) per minute of oxygen consumed

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79
Q

VO2 max

A

maximal aerobic exercise –> volume (litres) of oxygen consumed during maximal aerobic exercise

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80
Q

Factors affecting VO2 max

A
  • Exercise type - depends on individual and type of exercise
  • Gender - men have higher haemoglobin concentration and women have more body fat
  • Heredity - variation attributable to genes
  • Level of training - with training can increase
  • Age - once reached mid twenties, steadily declines
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81
Q

Cardiac output

A

volume of blood pumped by the left ventricle per minute

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82
Q

Stroke volume

A

volume of blood pumped out of left ventricle by each contraction

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83
Q

Heart rate

A

number of times the heart beats per minute

84
Q

Cardiac output equation

A

Cardiac output (dm^3/min) = Stroke volume (dm^3) x Heart rate (bpm)

85
Q

During exercise what will happen to cardiac output, stroke volume and heart rate?

A

they will all increase

86
Q

Venous return

A

blood returned to the heart

87
Q

1dm^3 =

A

1000cm^3 = 1 litre

88
Q

The heart muscle is myogenic

A

can contract without external nervous stimulation

89
Q

How is the intrinsic rhythm of the heart maintained?

A

by a wave of electrical excitation (similar to a nerve impulse)

90
Q

Heart beat stage 1

A

Depolarisation starts at the SAN (sino atrial node aka pacemaker). This is a small area of specialised muscle cells

91
Q

Heart beat stage 2

A

The SAN generates an electrical impulse which spreads across both atria causing them to contract at the same time - ATRIAL SYSTOLE

92
Q

Heart beat stage 3

A

Some of the impulse also travels to the AVN (atrioventricular node) and is delayed here before continuing. It’s delayed to ensure the atria are completely empty and the ventricles are full

93
Q

Heart beat stage 4

A

After this delay the signal reaches the Purkyne fibres which conduct impulses to the apex of the ventricles rapidly. There are right and left groups which collectively are a ‘bundle of His’

94
Q

Heart beat stage 5

A

The purkyne fibres continue around each ventricle and divide into smaller branches that penetrate the ventricular muscle. These branches carry the impulse to the inner cells and from here it spreads through each ventricle

95
Q

Heart beat stage 6

A

The first depolarised ventricular cells are at the apex so the contraction travels upwards towards the atria. The wave of contraction, pushing upwards, pushes blood into the aorta and pulmonary artery - VENTRICULAR SYSTOLE

96
Q

What is an Electrocardiogram (ECG)? What does it show?

A
  • a graphic record of electrical activity of the heart

- measure changes in polarisation of cardiac muscle

97
Q

P wave

A

depolarisation of the atria (leading to atrial systole)

98
Q

QRS complex

A

depolarisation of the ventricles leading to ventricular systole

99
Q

T wave

A

repolarisation of the ventricles (diastole) during heart relaxation

100
Q

PR interval

A

time between atria depolarisation and ventricular depolarisation - time for impulse to be conducted from SAN to AVN

101
Q

Bradycardia

A

slow heart rate (may be fit athletes)

102
Q

Tachycardia

A

fast heart rate

103
Q

What features on a ECG?

A
  • P wave (first bump)
  • QRS complex (big spike)
  • T wave (last bump)
104
Q

How is heart rate controlled?

A

by the cardiovascular control centre in the medulla in the brain

105
Q

Which nervous system controls heart rate?

A

the autonomic nervous system - has sympathetic and parasympathetic nerves so can speed up and slow down heart rate (is involuntary)

106
Q

Effect of sympathetic and parasympathetic nerves on intercostal muscles (between ribs)

A

sympathetic - increases breathing rate

parasympathetic - decreases breathing rate

107
Q

Effect of sympathetic and parasympathetic nerves on the heart

A

sympathetic - increases heart rate and stroke volume

parasympathetic - decreases heart rate and stroke volume

108
Q

Effect of sympathetic and parasympathetic nerves on the gut

A

sympathetic - inhibits peristalsis

parasympathetic - stimulates peristalsis

109
Q

Stimulation of sympathetic nerve will…

A

increase heart rate

110
Q

Stimulation of parasympathetic nerve will…

A

…decrease heart rate

111
Q

What causes adrenaline to be released?

A

fear, excitement and shock

112
Q

What effect does adrenaline have on heart rate?

A

it increases the heart rate because it has a direct effect on the SAN

113
Q

Cardiovascular control centre receives impulses from:

A
  • stretch receptors in muscles and tendons
  • chemoreceptors (sense blood pH/ CO2 concentration) in walls of aorta arch, carotid artery and in the medulla
  • baroreceptors (sense pressure) in the walls of the aortic arch and carotid artery
114
Q

Adrenaline has an effect on heart rate what else does it cause?

A
  • dilation of the arterioles supplying skeletal muscles and constriction of arterioles going to the digestive system - this maximises blood flow to active muscles
  • causes an anticipatory increase in heart rate
115
Q

Tidal volume

A

average volume of air in one breath

116
Q

Vital capacity

A

maximum volume of air in one breath (inhale and exhale)

117
Q

Minute ventilation

A

volume of air taken into the lungs in 1 minute

118
Q

Minute ventilation equation

A

Minute ventilation (dm^3/min) = tidal volume (dm^3) x breathing rate (per min)

119
Q

Breathing rate

A

number of breaths in one minute

120
Q

When exercise begins we can increase our…

A

…breathing rate and depth of breathing (in fit people, singers and wind instrument players their vital capacity may be larger)

121
Q

How are lung volumes measured?

A

using a spirometer

122
Q

Spirometer key principles

A
  • closed system between machine and person; noseclip worn to ensure this
  • soda-lime used to absorb CO2 if O2 uptake is being measured
  • scales on the revolving kymograph must be calibrated so that volumes and times are accurately measured
123
Q

Spirometer safety

A
  • nurse on standby
  • not to be used by subjects with medical problems (breathing/ circulatory difficulties)
  • to be used for max 5 mins with sodalime or 1 min without sodalime (closed system so inhaling air with decreasing O2)
  • combination of vaseline and medical grade O2 potentially explosive
  • ensure lid is refilled with fresh O2 between experiments
  • mouthpiece to be sterilised
124
Q

How is breathing controlled?

A

by the ventilation centre in the medulla of the brain

125
Q

Breathing control

A
  • impulses from ventilation centre to external intercostal muscles and diaphragm along sympathetic nerves
  • muscles contract –> volume of chest cavity increases –> pressure drops –> air drawn in INHALATION
  • stretch receptors in walls of bronchi send impulses to inhibit ventilation centre
  • impulses to breathing muscles stop, therefore muscles relax EXHALATION
126
Q

Slow twitch muscle fibres

A

Specialised for slower, sustained contraction. Cam cope with long periods of exercise. To do this they must be specialised to carry out a large amount of aerobic respiration

127
Q

Fast twitch muscle fibres

A

Specialised to produce rapid and intense contractions. The ATP used in these contractions is produced almost entirely from anaerobic glycolysis

128
Q

What causes a change in breathing rate?

A

carbon dioxide, pH, temperature of the blood

129
Q

What happens when you exercise to the pH?

A

Exercise, more respiration, more CO2, pH decreases –> CO2 dissolves in blood plasma making carbonic acid, carbonic acid dissociates into hydrogen ions and hydrogencarbonate ions, lowering pH

130
Q

How are changes to CO2, pH and temperature in the blood detected?

A

By chemoreceptors and stretch receptors in the medulla, aorta and carotid artery. From here impulses are sent to other parts of the ventilation centre so impulses are sent to stimulate breathing muscles

131
Q

Features of fast twitch muscle fibres

A
  • white
  • few capillaries
  • fatigue easily
  • less myoglobin
  • oxygen debt built up quickly
  • high creatine phosphate level
  • few mitochondria
  • high glycogen content
  • more sarcoplasmic reticulum
  • lots in a sprinter
  • ATP produced via glycolysis
132
Q

Features of a slow twitch muscle fibre

A
  • red
  • lots of capillaries
  • fatigue less easily
  • lots of myoglobin
  • oxygen debt built more slowly
  • less creatine phosphate
  • many mitochondria
  • low glycogen content
  • little sarcoplasmic reticulum
  • lots in marathon runner
  • ATP produced via oxidative phosphorylation (ETC)
133
Q

Myoglobin

A

-protein similar to haemoglobin
-high affinity for O2
-readily accepts O2 from the blood
-acts as an O2 store in the muscles
(-what makes it red)

134
Q

Creatine phosphate

A

supplies energy to produce (regenerate) ATP before extra O2 can be supplied: the third energy system

135
Q

Homeostasis

A

maintains a stable internal environment so cells can function properly

136
Q

Conditions to be controlled

A
  • water levels
  • temperature –> for enzymes
  • ions –> salt
  • CO2 levels
  • blood pH
  • blood glucose
137
Q

Negative feedback

A
  • each condition has a norm value
  • all conditions must be within a narrow limit of this value
  • a deviation from the norm results in a change in the opposite direction
138
Q

Negative feedback process

A
  • receptors detect a deviation from the norm

- receptors connect to a control centre which turns on/off effectors to bring value back to norm value

139
Q

Reasons for range of temperature values

A
  • clothes
  • external conditions
  • genetics (blood circulation)
  • hair for insulation
  • exercise levels
  • illness
  • pregnancy
  • metabolic rate
140
Q

Why is thermoregulation important?

A
  • because it affects reaction rate
  • loss in efficiency in metabolism
  • enzymes not at optimum temperature –> hot, they denature –> cold, not enough successful collisions
141
Q

Examples of negative feedback

A
  • control of metabolic pathway
  • hormone levels: detected by hypothalamus/ pituitary gland/ pancreas/ ovaries so produce more/ less
  • population size: population increases, predation, illness, population drops
142
Q

Positive feedback

A

output from the control centre moves the condition further from the set point
norm value - rise above/ fall below - change detected - effectors act to continue rise/ fall
E.g. blood clotting - damage to endothelium attract platelets which attracts more platelets or pregnancy pressure of baby on uterus, increase contractions, increase pressure

143
Q

Heat loss centre

A

Stimulates: sweat glans to secrete sweat
Inhibits: contraction of arterioles in skin (dilate capillaries in skin), hair erector muscles (relax - hair lies flat), liver (reduces metabolic rate), skeletal muscles (relax - no shivering)

144
Q

Heat gain centre

A

Stimulates: arterioles in the skin to constrict, hair erector muscles to contract, liver to raise metabolic rate, skeletal muscles to contract in shivering
Inhibits: sweat glans

145
Q

Receptors in skin detect…

A

changes in external temperature

146
Q

Receptors in the hypothalamus detect…

A

changes in blood temperature

147
Q

In the hypothalamus there’s…

A

a heat loss and heat gain centre

148
Q

Vasodilation

A 
arteriole muscles relax
arterioles dilate
shunt vessel constricts
blood flowing through capillaries increases
more heat lost through radiation
149
Q

Vasoconstriction

A 
arteriole muscles contract
arterioles constrict
shunt vessel dilates
blood flowing through capillaries decreases
less heat lost through radiation
150
Q

Key points about thermoregulation

A
  • It’s the evaporation of sweat that cools us not the process of sweating
  • Heat is lost from the blood flowing through capillaries near the surface of the skin by radiation
  • This heat loss is controlled by the blood flow through the arterio-venous shunt vessel
  • Muscles in the arteriole walls contract/ relax to alter blood supply to capillaries
  • The capillaries don’t contract or dilate or constrict or relax or MOVE
151
Q

Radiation

A

energy can be radiated from one object to another through air as electromagnetic radiation (vasodilation/ constriction)

152
Q

Conduction

A

involves direct contact between objects and energy transfer between them

153
Q

Convection

A

energy loss by bulk movement of air - is warmed, becomes less dense, so rises, is replaced by cooler air which is then warmed forming a convection current (hair raising)

154
Q

Evaporation

A

energy needed to convert water from liquid to vapour (sweating)

155
Q

Negative effects of exercise

A

Too much –> immune suppression, joint damage

Too little –> increased risk of obesity, CHD and diabetes

156
Q

Moderate exercise effect on immunity

A

Increases the number and activity of natural killer cells which are found in the blood and lymph. They provide non-specific immunity against cells invaded by viruses and cancerous cells

157
Q

How do natural killer cells work?

A

They are activated by cytokines and interferon, they seem to target cells that don’t display self markers. The killer cells release perforin which makes pores in targeted cell membranes. This allows other molecules to enter and cause apoptosis

158
Q

Vigorous exercise effect on immunity

A

During recovery after prolonged, high intensity exercise, the number and activity of some cells in the immune system falls. Including: natural killer cells, phagocytes, B cells, T helper cells. Due to this the specific immune system is temporarily depressed. decrease T helper, decrease cytokines, decrease antibodies, may also be inflammatory response

159
Q

What effect does both psychological stress and physical exercise have on the immune system?

A

they both cause secretion of hormones such as adrenaline and cortisol - both of these suppress the immune system

160
Q

How are joints damaged?

A

due to high forces on joints

can lead to wear and tear or overuse

161
Q

If a joint is damaged you will experience…

A

inflammation and restricted movement of that joint

162
Q

How do you treat a damaged joint?

A
  • rest, ice, compression, elevation
  • anti-inflammatory painkillers
  • if necessary surgical repair
163
Q

Cruciate ligaments

A

are 2 of 4 knee ligaments which connect the femur to the tibia

164
Q

What do the posterior and anterior cruciate ligaments do?

A

Posterior - prevents knee bending too far back

Anterior - prevents the knee being bent too far forward

165
Q

How can the knee joint be damaged?

A
  • cartilage covering each bones surface wears away
  • kneecap doesn’t glide smoothly across femur due to damage of femur’s cartilage
  • sudden twisting or abrupt movements of the knee joint result in damage to the ligaments
  • the bursae (fluid sacs) that cushion the points of contact can swell up with extra fluid
166
Q

The knee joint

A

is a hinge joint held together by 4 ligaments - control joint movement and prevent overstretching

167
Q

Advantages of keyhole surgery

A
  • rapid recovery time
  • less pain
  • less chance of infection
  • less bleeding
  • less invasive
  • shorter hospital stay –> economic benefit
  • less scarring due to less scar tissue (hard and inflexible; needs to be replaced)
168
Q

Keyhole surgery

A

Uses fibre optics or minute video cameras which makes it possible to repair damaged joints or remove diseased organs through small holes. 1/2 small incisions, small camera and light inserted, diagnosis made or confirmed, if surgery needed miniature instruments inserted through incisions

169
Q

Injuries to joint

A

can limit exercise amounts and shorten athlete’s careers. Surgery to repair damage was painful and took a long time until keyhole surgery

170
Q

Cruciate ligament damage

A

can be repaired and knee joint stabilised so further injury less likely - can be treated using keyhole surgery effectively

171
Q

Prostheses

A
  • artificial body part
  • used by someone with a disability to regain some degree of normal function
  • may also be used to replace damaged or diseased joints that haven’t responded to medical or other therapy
172
Q

Negatives of exercising too much

A
  • joint damage
  • immune suppression –> vulnerability to disease and health problems
  • osteoarthritis –> inflammation of joints
  • mental health
  • fatigue –> exhausted for everything else
  • muscle soreness –> overuse
  • overuse injuries
173
Q

Negatives of too little exercise

A
  • arthritis
  • don’t strengthen muscles, tone them, suppleness
  • increases risk of many disease: CHD, high blood pressure, stroke, obesity
174
Q

Transcription (splicing included)

A

Occurs in the nucleus of the cell. Only one strand of DNA is copied, which contains the relevant gene. The copied strand is called pre-mRNA. Transcription requires 2 enzymes; DNA helicase and RNA polymerase. In mRNA the base T is replace by Uracil. The pre-mRNA is then spliced to remove non-coding sequences called introns, creating mRNA. This requires a complex of enzymes called the spliceosome. The resulting mature mRNA exits the nucleus via the nuclear pore. (hydrogen bonds, phosphodiester bonds, sense, antisense strand, template strand, complementary base pairs)

175
Q

Translation

A

The copied strand leaves the nucleus and is decoded at a ribosome which are found in the cytoplasm. This process is known as translation. Each sequence of 3 bases, known as a codon, codes for a particular amino acid which is brought to the ribosome by tRNA molecules. The anticodon on tRNA binds to the complementary codon on mRNA to ensure the correct amino acid is brought over. The amino acids are joined together in a condensation reaction forming a peptide bond, this uses energy from ATP and an enzyme. When a stop codon is reached, translation is terminated and the resulting amino acid chain folds into a protein.

176
Q

triplet code

A

3 bases code for one specific amino acid

177
Q

degenerate

A

each amino acid is coded for by more than on triplet

178
Q

non overlapping

A

no base of one triplet contributes to part of the next triplet

179
Q

Hormones

A
  • chemical messenger, released into blood plasma from endocrine glands
  • released from the cells, in an inactive form, or packed into vesicles
  • modifies activity of target cells
180
Q

2 groups of hormones:

A

peptide and steroid

181
Q

Hormones and function: Pituitary gland

A

Growth hormone - stimulates growth
FSH - controlls testes and ovaries
Antidiuretic hormone - causes reabsorbtion of water in kidneys

182
Q

Hormones and function: thyroid gland

A

Thyroxine - raises basal metabolic rate

183
Q

Hormones and function: adrenal gland

A

Adrenaline - raises basal metabolic rate, dilates blood vessels, prepares the body for action

184
Q

Hormones and function: pancreas

A

Insulin - lowers blood glucose concentration

185
Q

Hormones and function: ovary

A

Oestrogen - promotes development of ovaries and female secondary sexual characteristics

186
Q

Hormones and function: testis

A

Testosterone - promotes development of male secondary sexual characteristics

187
Q

Peptide hormones are…

A

protein based, produced naturally in the body

188
Q

Examples of peptide hormones

A
  • insulin

- human growth hormone

189
Q

Examples of steroid hormones

A

-testosterone

190
Q

How peptide hormones work

A

even though peptide hormones are relatively small, they’re charged

  • Peptide hormones cannot pass through the membrane due to being charged
  • They bind with receptors on the cell membrane
  • This activates another molecule in the cytoplasm called the second messenger
  • Functional second messengers within the cell can directly or indirectly affect gene transcription (go to nucleus) by activating enzymes or transcription factors
191
Q

How steroid hormones work

A
  • Steroid hormones are formed from lipids
  • Therefore they can pass through the cell membrane
  • They bind with receptors within the cell cytoplasm
  • The hormone receptor complex functions as a transcription factor
192
Q

Transcription factors

A

transcription is initiated by an enzyme called RNA polymerase and a number of associated transcription factors binding to DNA

193
Q

What forms from RNA polymerase and transcription factors (proteins)? Where does it go?

A

a transcription initiation complex is formed and this complex binds to the promoter region of the gene - only after this complex has formed and binded to the promoter region will transcription occur

194
Q

Where are transcription factors found?

A

some transcription factors are present in all cells, some are synthesised only in particular cell types - most are created in an inactive form and converted to active by hormones

195
Q

When will the gene become active/ ‘switched on’?

A

the gene will remain inactive until all required transcription factors are present and in active forms

196
Q

How can the transcription be prevented?

A

By protein repressor molecules attaching to DNA of the promoter region. This blocks the attachment sites for transcription factors so the transcription initiation complex can’t form. Alternatively protein repressor molecules can attach to transcription factors directly. Also the transcription factors may be inactive so the gene won’t be transcribed in this cell.

197
Q

What stimulates the binding of the transcription initiation complex?

A

activator molecules

198
Q

The structure and function of a cell is determined by…

A

the genes (in)active/ switched on or off

199
Q

Creatine

A
  • is a nutritional supplement
  • naturally found in meat and fish
  • supplement ingested, absorbed unchanged, carried in the blood to tissues, also synthesised in the body
  • creatine supplements, increase creatine phosphate levels in muscles so there is improvement in repeated, short duration, high intensity exercise
  • sprinting, swimming, rowing improvements - combined with heavyweight training increases muscle mass
200
Q

Side effects of creatine supplements

A
  • diarrhoea
  • nausea
  • vomiting
  • high blood pressure
  • kidney damage
  • muscle cramps
201
Q

Erythropoietin

A
  • is a peptide hormone produced naturally by the kidneys
  • stimulates production of new red blood cells in bone marrow
  • is used to treat anaemia
  • normal blood O2 level, conc. falls, kidney detects fall, releases erythropoietin, which stimulates bone marrow, produces red blood cells, O2 level starts increasing, back to normal
202
Q

Health risks of EPO

A
  • if EPO levels too high, too many red blood cells produced

- risk of thromobosis –> heart attack or stroke

203
Q

Testosterone

A
  • steroid hormone
  • testosterone binds to androgen receptors, which are numerous on cells in target tissues. They modify gene expression to alter development of the cell –> increases anabolic reactions, increases size and strength of muscles
  • used to increase muscle development but is broken down quickly so synthetic anabolic steroids have been made –> chemical modification of testosterone
204
Q

Health risks of anabolic steroids

A
  • high blood pressure
  • liver damage
  • kidney failure
  • heart disease
  • changes in menstrual cycle
  • decrease sperm production and impotence
  • increase aggression
205
Q

Why should performance enhancing drugs be banned

A
  • health risks —> dangerous side effects
  • unfair –> have an advantage
  • don’t make an informed decision –> lack info, peer presssure
206
Q

Why should performance enhancing drugs be not banned

A
  • athletes have a right to decide whether they take the drug or not
  • benefit worth the risk
  • already inequality –> time, resources, training
207
Q

Why are muscles in antagonistic pairs?

A

because muscles can only pull so to be able to go in both directions you need 2 muscles working in opposite directions

Biology (14 decks)

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