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Biology > Biology - Unit 5 > Flashcards

Biology - Unit 5 Flashcards

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AP® Biology flashcards Biology 101 flashcards
0
Q

What two sources of evidence have led to our understanding of how the brain works?

A

Animal studies and studying human brains

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1
Q

How have brain diseases increased understanding of the brain?

A

What effect damage to different parts of the brain have

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2
Q

How are animals used for brain studies?

A

Effect if removing parts of the brain
Effect of artificially stimulating part of the brain
How the brain develops

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3
Q

What does the frontal lobe do?

A

Emotions
Speech
Decision making
Rational thought

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4
Q

What does the cerebrum do?

A

Integrates impulses in

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5
Q

Function of the parietal lobe

A 
Memory and recognition
Calculation
Movement
Sensation
Orientation
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6
Q

Occipital lobe function

A

Eyesight

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7
Q

Temporal lobes function

A 
Language
Hearing
Smell
Auditory information
Memory
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8
Q

Hypothalamus function

A

Homeostasis

Autonomic nervous system control

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9
Q

Pituitary gland function

A

Keeping water balance by releasing diuretics

Releases hormones like LH and FSH

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10
Q

Basal ganglia function

A

Motor control

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11
Q

Corpus callosum function

A

Connects the two hemispheres

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12
Q

Cerebellum function

A

Body control
Motor memory
Posture and balance

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13
Q

Medulla oblongata function

A

Breathing
Heart rate
Digestion
Sorts information

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14
Q

Olfactory bulb function

A

Sense of smell

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15
Q

Brain stem function

A

Joins to the spinal cord

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16
Q

How do CAT scans work?

A

Thousands of small X-ray beams passed through
Beam attenuated by tissue density
Data put together

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17
Q

What does attenuated mean?

A

Reduced in strength

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18
Q

How does MRI work?

A

Magnetic fields and radio waves passed through

Different tissues respond differently

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19
Q

How do fMRI scans work?

A

Monitors uptake of oxygen as deoxyhaemoglobin absorbs signal

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20
Q

Advantages of fMRI

A

Constant picture

Can see movement of oxygen

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21
Q

How do ultrasound scans work?

A

High frequency sound waves

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22
Q

How do X-rays scans work?

A

X-rays passed through body

Dense matter reflects them

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23
Q

What experiment did Crowley and Katz perform?

A

Injected newborn ferrets with radioactive tracers

Tracers moved from one eye and found in specific bands in visual cortex

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24
Q

Conclusions of Crowley and Katz experiments

A

Neurones ordered in ocular dominance columns from birth

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25
Q

Experiments of Horton and Hocking

A

Prematurely delivered three monkeys
Kept in dark with radioactive tracer in eye
Found fully developed ocular tracers by time would have normally born

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26
Q

Horton and Hocking conclusions

A

Ocular dominance columns formed before birth

Visual cortex development due to genetic factors initially

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27
Q

Experiments of Hubel and Weisel on kittens and monkeys

A

Stitched shut one or both of animals eyes at different ages and for different lengths of time

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28
Q

Hubel and Weisel findings

A

Shut one eye at one week old and uncovered eye worked fine - swap eyes after a few months and animal could not see

If did same at 4 months old, no effect

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29
Q

Findings by Hubel and Weisel

A

Critical windows of development

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30
Q

What are critical windows of development?

A

Periods of time during which vital connections are made in the brain in response to specific stimuli

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31
Q

Visual cortex development

A

Initially, dendrites for both eyes overlap
If both eyes used as much, columns form of equal size for each eye (No overlap)
If one eye used more, its columns are larger

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32
Q

What has been found from studying newborn babies brains?

A

There is discrimination towards paying more attention to biological movement than non-biological
The younger you are the better your face recognition is
Severe sensory deprivation can cause improper brain development

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33
Q

Polks research shows

A

Brain patterns more similar in identical twins than non for face/place recognition
Little difference with regards to word and letter response

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34
Q

Work of Polk

A

Presented fraternal and identical twins with various scrambled images including letters and faces

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35
Q

What is species-characteristic behaviour?

A

Innate behaviour
Seen in every member of a species
Not learned

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36
Q

What is individual-characteristic behaviour?

A

Learned behaviour

Singular members who learn from experience

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37
Q

What is habituation?

A

Animal starts ignoring repeated stimulus as no punishment nor reward

Gills of animal stop retreating when touched

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38
Q

What are conditioned reflexes?

A

Learning to associate new stimuli with an existing unconditioned reflex

Pavlov’s dogs

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39
Q

What is trial-and-error (operant) learning?

A

When an animal learns to associate a piece of trial behaviour with a reward or punishment so repeat or not

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40
Q

What is imprinting?

A

Young animal identifies with another organism and follows it around and relates to other similar objects

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41
Q

What is exploratory (latent) learning?

A

Animal explores new surroundings and learns them without any reward or punishment

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42
Q

What is insight learning?

A

Based on thought and reasoning

Once problem solved, the solution is remembered

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43
Q

How can habituation be shown using a land snail?

A

Poke it and its antennae withdraw

Takes less time to take them out again as the number of pokes increase

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44
Q

What is the cause of Parkinson’s?

A

Nerve cells which produce dopamine die so movement slows as dopamine allows messages to be sent to the brain

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45
Q

What are the risk factors of Parkinson’s?

A 
Genetics
Toxins
Herbicides
Head trauma
Stroke
Age
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46
Q

Why is Parkinson’s difficult to treat?

A

We do not know the risk factors or what causes the dopamine-producing cells to die

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47
Q

What are the symptoms of Parkinson’s?

A

Main symptoms:
Tremors
Slow movement
Stiff and inflexible muscles

Others:
Fatigue
Dementia
Depression

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48
Q

How does L-Dopa work to treat Parkinson’s?

A

It is converted into dopamine in the brain so more dopamine will be produced

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49
Q

What are the benefits of L-Dopa being used to treat Parkinson’s?

A

Greatly relieves stiffness and slowness of movements

Can be combined with carbidopa to improve action and reduce side-effects

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50
Q

What are the problems with using L-Dopa to treat Parkinson’s?

A

Less effective after 4-5 years as brain cells continue to die

Side effects:
Dyskinesia- muscle spasms
Low blood pressure
Arrhythmia

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51
Q

How do dopamine agonists act to treat Parkinson’s?

A

Bind to dopamine receptors in brain synapses and mimic action of dopamine

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52
Q

What are the benefits of using dopamine agonists to treat Parkinson’s?

A

Last longer in the brain than L-Dopa

Effectiveness does not wane over time

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53
Q

What are the problems with using dopamine agonists to treat Parkinson’s?

A

Not as effective as L-Dopa
Cause similar side-effects to L-Dopa
Can cause problems in controlling impulsive and compulsive behaviour

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54
Q

How do MAOB inhibitors work?

A

Block the action of MAOB which breaks down dopamine

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55
Q

What are the benefits of MAOB inhibitors?

A

Slows loss of dopamine

Can be used to make L-Dopa last longer or reduce amount needed

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56
Q

What are the problems with MAOB inhibitors?

A

When combined with L-dopa:
Dyskinesia
Hallucinations

On own:
Headache
Depression
Aching joints

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57
Q

What are the psychological symptoms of clinical depression?

A 
Continuous low mood
Feeling hopeless
Low self-esteem
Guilt ridden
Irritable
Anxiety
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58
Q

What are the physical symptoms of clinical depression?

A 
Slow speaking or slow movement
Change in appetite/weight (Usually decreased)
Constipation
Unexplained aches and pains
Loss of libido
Disturbed Sleep
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59
Q

What is the neurotransmitter involved in depression?

A

Serotonin

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60
Q

What is the role of serotonin in Depression?

A

Low levels result in fewer impulses so reduced brain activity. Low levels related to depression

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61
Q

What are the treatments for Depression?

A 
Talking therapies
Antidepressant drugs:
-SSRIs inhibit re-uptake proteins
-TCAs increase levels of serotonin
-MAO inhibitors prevent neurotransmitter breakdown
Ecstasy
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62
Q

What are the effects of Prozac at synapses?

A

Inhibits re-uptake proteins
More serotonin in synaptic cleft
More impulses travel
Symptoms reduced

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63
Q

What is the effect of ecstasy on the concentration of serotonin in the synaptic cleft?

A

Greater concentration as the re-uptake proteins are inhibited

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64
Q

How does ecstasy work to inhibit the re-uptake proteins?

A

Similar shape to serotonin so blocks them off

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65
Q

Why does taking ecstasy produce a high?

A

More serotonin in the synaptic cleft
Limbic system stimulated more
Feeling of reward

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66
Q

What is pharmacogenomics?

A

The study of how a persons genetics affect their response to drugs

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67
Q

What is the purpose of pharmacogenomics?

A

Can tailor drugs to specific peoples genes so that it has maximum effect and minimum side-effects

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68
Q

What are the responses to drugs?

A

Full response - Beneficial and non-toxic
Partial response - Beneficial but toxic
Non responsive - Not beneficial but non-toxic
Severe adverse reaction - Toxic and not beneficial

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69
Q

What factors influence drug response?

A 
Gender
Age
Weight
Diet
Genetics
Co-medication
Environmental agents (E.g. Smoking)
Disease
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70
Q

How important are genetics in drug response?

A

Account for between 20-95% of variation in response

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71
Q

What are the stages of drug action in the body?

A 
Absorption
Distribution
Target interaction
Metabolism
Excretion
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72
Q

What are the two main gene groups involved in drug response?

A

Pharmacokinetic - Affects how the drug is handled by the body (E.g. Drug metabolising enzymes)
Pharmacodynamic - The drugs effect on the body (E.g. Receptors)

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73
Q

What are SNPs?

A

Single nucleotide polymorphisms
Genetic variants that affect a drugs action
Haplotypes - Combinations of related SNPs

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74
Q

How is pharmacogenomics enhancing the treatment of cancers?

A

Drugs that target the genetics of cancer cells to reduce toxicity and increase efficacy

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75
Q

How does Herceptin act to combat cancers?

A

Targets the chemical which causes massive growth
Block growth factors
Targets Her2 proteins on cancer cells

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76
Q

Why is Herceptin not perceived to be truly based on pharmacogenetics?

A

Targeted for tumour cells genetics not persons genome

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77
Q

What is efficacy?

A

Maximum beneficial response a drug can produce

% of recipients who show a therapeutic response at a given dose

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78
Q

What is toxicity?

A

The extent to which a drug has adverse side effects

% of recipients who show adverse side effects

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79
Q

What is the optimal dose range of a drug?

A

That at which efficacy is greatest and toxicity lowest

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80
Q

Why will pharmacogenomics not replace proper clinical management?

A

Need to choose best drug based on other factors as well

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81
Q

What are the benefits of tailoring drugs?

A

More effective
Lower dosage needed
Less side-effects

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82
Q

Where can pharmacogenomics save lives?

A

Minimising deaths due to severe adverse reactions

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83
Q

Why are microbes frequently used in genetic engineering?

A

Easy and cheap to culture
Reproduce rapidly
Easily identified

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84
Q

How do scientists know which microbes have taken up new genes?

A

Incorporate antibiotic resistance into new genes

Only ones with new genes survive antibiotics

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85
Q

What were the problems with previous methods of getting insulin?

A

Got from animals

  • Immune system attacked the insulin
  • Supply relied on animals being slaughtered
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86
Q

What is humulin?

A

Pure human insulin produced by bacteria

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87
Q

How is humulin produced?

A

One of each of the two polypeptide chains inserted into two bacteria using vectors

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88
Q

How is proinsulin production different to humulin production?

A

Only requires one type of bacteria while humulin requires two

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89
Q

What is the problem with using prokaryotes for drugs?

A

Cannot make complex human proteins

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90
Q

What is the use of bananas in GMOs?

A

Bananas are being developed which contain vaccines or vitamins

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91
Q

What is a crown gall?

A

A tumour which appears on a plant

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92
Q

What is the use of crown galls in transgenic plant technology?

A

It forms on the plant and can be taken and cultured and used to produce new plants containing the genes

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93
Q

What is the method of transgenic plant creation?

A

Ti plasmid removed from A. Tumefaciens bacterium
Gene to be carried inserted into plasmid
Plasmid returned to bacterium
Bacterium inserted into plant
Crown gall develops on plant which can be taken and cultured

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94
Q

What is a tropism?

A

A growth in response to stimulation

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95
Q

What are the stages of plant growth through mitosis?

A 
Division - Mitosis
Assimilation - New material brought in
Elongation - Vacuoles develop
-Cellulose wall stretches
-Large central vacuole forms
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96
Q

Where does the most plant growth occur?

A

At the meristems (Just behind stem and root tips)

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97
Q

What are short-day plants?

A

Plants that flower when nights are long and days are short

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98
Q

What are long-day plants?

A

Plants that flower when nights are short and days are long

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99
Q

What is photoperiodism?

A

A plants ability to flower in response to changes in the photoperiod (Relative lengths of day and night)

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100
Q

What are day-neutral plants?

A

Plants whose flowering is unaffected by the lengths of the day and night

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101
Q

What is the environmental cue for flowering?

A

Length of darkness

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102
Q

What was the work by Hamner and Bonner with regard to critical periods?

A

Long-day plant can flower if in a short day, the long night is interrupted by a flash of light

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103
Q

What are the effects of red light on plant germination?

A

Inhibits short-day
Stimulates Long-day
Stimulates seed germination

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104
Q

What are the effects of far-red light on plant germination?

A

Inhibits seed germination
Inhibits long-day
Stimulates short-day

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105
Q

What is the photosensitive pigment involved in plant germination?

A

Phytochrome

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106
Q

How is Pfr converted into Pr?

A

Darkness - Slow conversion

Far-red light - Rapid conversion

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107
Q

How is Pr (P660) converted into Pfr (P730)?

A

Daylight
White light
Red light

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108
Q

What is etiolation?

A

Rapid growth in an attempt to reach light

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109
Q

What is the effect of Pr build-up/darkness on plant growth?

A 
Tall and thin
Small, pale leaves
Long internodes
Fragile stems
Little chlorphyll
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110
Q

What is the effect of Pfr build-up on plant growth?

A 
Green leaves
Chlorophyll formation
Thick
Strong stem
Shorter internodes
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112
Q

What did the experiments which proved the existence of florigen involve and show?

A

All but one leaf covered, entire plant flowers - Chemical produced which travels across plants
Only flowers if exposed leaf left in place for time - Takes time to synthesise chemical and travel it
Flowers if light-induced plant grafted on - Moves from leaf into plant

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113
Q

What were the experiments which proved the existence of auxin?

A 
Darwin:
-Covering apex
-Removing apex
Boysen-Jenson:
-Effect of inserting mica barrier unilaterally
Paal:
-Tip replaced off-centre
Went:
-Tip incubated on gelatin block. Block replaced off-centre
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114
Q

What is IAA?

A

The first auxin discovered

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115
Q

What is an auxin?

A

The growth substance involved in phototropisms

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116
Q

How are neurones adapted for their function?

A

Long and thin - Take up little space but reach where needed
Not bound to other neurones - Can make and break connections
Flexible - Make connections easily
Chemical messengers to cross synapses

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117
Q

What is the difference between an axon and a dendron?

A

Axons carry impulses away from the nerve cell body while dendrons carry them towards it.

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118
Q

What is the structure of a motor neurone?

A

Cell body with dendrites
Axon
Synaptic bulbs
Effector

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119
Q

What is the structure of a sensory neurone?

A 
Receptor
Dendrites
Dendron
Connection to Cell body
Axon
Synaptic bulbs
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120
Q

What is the structure of a relay neurone?

A 
Dendrites
Dendron
Cell Body
Axon
Synaptic bulbs
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121
Q

What is the structure of a myelin sheath?

A

Schwann cell wrapped around axon multiple times
Cytoplasm and nucleus on outside
Node of Ranvier between adjacent ones

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122
Q

Why are myelin sheaths important?

A

Protect nerves from damage

Speed up transmission of nerve impulse

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123
Q

What was the method used to discover how neurones work?

A

Took giant squid axons
Electrode filled with conducting solution inserted
Electrode attached with wire to amplifier
Two electrodes, one inside axon and one outside detect voltage
Difference amplified and displayed

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124
Q

What is the resting potential of an axon?

A

-70mV

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125
Q

How is the resting potential of an axon maintained?

A

Na+/K+ pump creates concentration gradient

K+ channel allows diffusion out

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126
Q

What is the action potential of an axon?

A

+40mV

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127
Q

How is an action potential formed?

A

Na+ channels open

K+ channels close

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128
Q

What are the stages of the refractory period?

A

Absolute refractory period - Impossible to re-stimulate

Relative refractory period - Threshold has been raised

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129
Q

What is an axons refractory period?

A

Its recovery time following an action potential

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130
Q

How is an action potential conducted along a nerve fibre?

A

The change in potential difference in one section due to the action potential causes a change in potential difference and therefore an action potential in the adjacent section

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131
Q

What is saltatory conduction?

A

The jumping of a nerve impulse from node to node along a myelinated nerve fibre

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132
Q

How are impulses transmitted across synapses?

A 
Calcium ions flow in
Vesicles fuse to pre-synaptic membrane
Neurotransmitter (Acetylcholine) released into synaptic cleft
Neurotransmitter fuses to receptors
Na+ flows in
EPSP or IPSP set up
Cholinesterase breaks down acetylcholine
Acetylcholine re-absorbed
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133
Q

What is an EPSP and IPSP?

A

EPSP (Excitatory post-synaptic potential) - Inside of post-synaptic membrane becomes more positive than resting potential
IPSP (Inhibitory post-synaptic potential) - Inside of post-synaptic membrane becomes more negative than resting potential

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134
Q

What is spatial summation?

A

Multiple action potentials arrive at a synapse at once

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135
Q

What is temporal summation?

A

Two action potentials from the same fibre arrive slightly after one another

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136
Q

What is facilitation?

A

Where multiple small impulses add together to create a larger one which can overcome the threshold

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137
Q

What is accommodation?

A

When neurones stop responding to a repeated stimulus

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138
Q

What is a primary receptor?

A

A dendrite

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139
Q

What is a secondary receptor?

A

A specialised cell which synapses with a sensory neurone

140
Q

What is an exteroreceptor?

A

A receptor which responds to stimuli from outside the body

141
Q

What is an interoreceptor?

A

A receptor which responds to stimuli from inside the body

142
Q

What law do generator potentials not obey?

A

The all-or-nothing law

143
Q

What current and potential are set up in receptors?

A

Generator current and generator potential

144
Q

What is convergence?

A

Where several generator potentials summate and trigger an action potential

145
Q

What is adaptation of receptors?

A

Where a receptor is exposed to a steady stimulus so there is a decline in generator potentials

146
Q

What is the function of the ciliary muscles?

A

Change the shape of the lens

147
Q

What is the function of the conjunctiva?

A

Lubricates eye

Prevents entrance of microbes

148
Q

What is the function of the suspensory ligament?

A

Supports eye

Prevents downward displacement

149
Q

What is the function of the vitreous humour?

A

Maintains the eye shape

150
Q

What is the function of the sclera?

A

Protects the eye

151
Q

What is the function of the retina?

A

Produces images

152
Q

What is the function of the fovea?

A

Causes sharper vision

Area with only rod cells

153
Q

What is the function of the optic nerve?

A

Carries impulses to brain from retina

154
Q

What is the blind spot of the eye?

A

Area of no photoreceptor cells

155
Q

What is the function of the lens?

A

Focuses light onto the retina

156
Q

What is the function of the iris?

A

Muscles which can change size of the pupil

Pigment gives eye its colour

157
Q

What is the function of the pupil?

A

Allows light to enter (size can be changed)

158
Q

What is the function of the cornea?

A

Helps focus light

159
Q

What is the function of the aqueous humour?

A

Maintains pressure - protects eye

Helps focus

160
Q

What type of receptors are the photoreceptors in the retina?

A

Secondary exteroreceptors

161
Q

What are the two types of photoreceptors in the eye and what are their differences?

A 
Rod cells:
-More sensitive, 
-Show black and white and dim light
-Show motion and peripheral
-More of them
-Convergence
Cone cells:
-Colour vision
-Focus
162
Q

What is the layout of the photoreceptors in relation to the retina?

A

Light sensitive part closest
Mitochondria
Synapse

163
Q

What pigment do rod cells contain?

A

Rhodopsin

164
Q

What happens to rhodopsin when bleached?

A

Splits into opsin and retinal
Opsin allows sodium in
Generator potential occurs

165
Q

How is rhodopsin reformed from opsin and retinal?

A

Lack of light stimulation

166
Q

What are light and dark adapted with regards to rhodopsin?

A

Light adapted - Rods bleached and can no longer respond to dim light
Dark adapted - Rhodopsin reformed and eye sensitive to dim light

167
Q

What pigment do cones contain?

A

Iodopsin

168
Q

What are the main features of iodopsin?

A

Three types - each sensitive to one primary colour
Needs more light energy to break down than rhodopsin
Not sensitive to low light intensities
Provides colour vision

169
Q

What is the iris?

A

A muscular diaphragm with the pupil in the middle

170
Q

Why does light only go through the pupil?

A

Pigments in the iris absorb the other light

171
Q

How is amount of light into the eye controlled?

A

By pupil size - Circular and radial muscles

172
Q

How is the pupil widened?

A

The radial muscles contract and circular relax

173
Q

How will pupil size change when it is brighter?

A

Gets smaller

174
Q

What is the mechanism for pupil size changing?

A

Light falls on retina sensory cells
Impulses occur - More light=More action potentials
Control centre in hindbrain detects it
Nerve impulses synapse parasympathetic cranial nerve
Iris effectors stimulated

175
Q

What drugs cause change in pupil size?

A

Pilocarpine - Decreases it

Atropine and adrenaline - Widens it

176
Q

What is another name for the iris’ circular muscles?

A

Sphincter pupillae

177
Q

What is another name for the iris’ radial muscles?

A

Dilator pupillae

178
Q

What does transgenic mean?

A

Taking genes from one organism and inserting into the DNA of another from a different species

179
Q

What is the process of getting an animal to produce a human protein?

A

Copy of human gene and promoter sequence inserted into genetic material of different species’ egg
Egg fertilised and inserted into surrogate mother
Baby born and grown to maturity
Milk of animal with new gene harvested and purified
Human protein extracted from milk

180
Q

How are genes inserted into animals via microinjection?

A

DNA injected into cell by fine micropipette controlled my micromanipulator. Many cells injected before one takes up the DNA successfully

181
Q

How are genes inserted into animals via microprojectiles?

A

DNA shot into cell at high speed carried by gold or tungsten pellets. Some cells survive and accept the DNA

182
Q

How are genes inserted into animals via viruses?

A

Harmless viruses engineered to carry gene and used to infect animals cells

183
Q

How are genes inserted into animals via liposome wrapping?

A

Gene wrapped in liposomes (spheres formed from lipid bilayer). Fuse to and pass through cell membrane to deliver DNA into cytoplasm

184
Q

What are advantages to transgenic animals?

A 
Disease treatments
Alleviate suffering
Continuous supply
Avoids immune response and infection from human diseases
Purer
185
Q

What are disadvantages to transgenic animals?

A

Concerns about safety of animals and of humans who use the product
Expensive to develop

186
Q

Why are promoter sequence used with transgenic animals?

A

So that the gene is expressed in the mammary gland so present in the milk

187
Q

What is striated muscle attached to?

A

The skeleton

188
Q

What is striated muscle involved in?

A

Locomotion

189
Q

Why is striated muscle called that?

A

It appears striped

190
Q

What are muscle fibres made up of?

A

Parallel myofibrils

191
Q

What are myofibrils made up of?

A

Sarcomeres

192
Q

What is the myofibril cytoplasm called?

A

Sarcoplasm

193
Q

What proteins make up sarcomeres?

A

Actin and myosin

194
Q

What does the sarcoplasm contain?

A

Mitochondria

195
Q

What is stored in the sarcoplasmic reticulum?

A

Calcium ions

196
Q

What controls smooth muscle?

A

The involuntary nervous system

197
Q

What is striated muscle also called?

A

Skeletal muscle or voluntary muscle

198
Q

What is smooth muscle also called?

A

Involuntary muscle

199
Q

Where is smooth muscle found?

A

In the gut and blood vessels

200
Q

What is the stamina of striated muscle?

A

Contracts rapidly but fatigues quickly

201
Q

What is the stamina of smooth muscle?

A

Contracts and fatigues slowly

202
Q

Where is cardiac muscle found?

A

In the heart

203
Q

What is myogenic?

A

Generates own contractions with impulses from self

204
Q

What are the properties of cardiac muscle?

A

Striated and myogenic

205
Q

What is the A band?

A

The width of a myosin filament

206
Q

What is the H zone?

A

The gap between two adjacent myosin filaments

207
Q

What is the Z line?

A

The line down the middle of an actin filament

208
Q

What is the M line?

A

The line down the middle of a myosin filament

209
Q

What is the I band?

A

The gap between two adjacent myosin filaments

210
Q

What makes up an actin filament?

A

Actin, troponin and tropomyosin

211
Q

What happens to the muscle fibre in contraction?

A

It gets shorter

212
Q

What is summation?

A

Where multiple contractions are so close they give the appearance of a single larger contraction

213
Q

What is tetanus?

A

Where the muscle fibre becomes fully contracted

214
Q

What are slow twitch muscle fibres adapted for?

A

Steady action over a period of time

215
Q

What is the stamina of slow twitch muscle fibres?

A

Slow contraction and long tetanus

216
Q

What are slow twitch muscle fibres used for?

A

Maintaining body posture and long periods of activity

217
Q

What do slow twitch muscle fibres contain?

A

A rich blood supply, lots of mitochondria and plenty of myoglobin

218
Q

What is myoglobin?

A

A protein similar to haemoglobin which is made of one chain and has a higher oxygen affinity

219
Q

What are slow twitch muscle fibres also called?

A

Oxidative or red muscle fibres

220
Q

What do slow twitch muscle fibres use as fuel?

A

Glucose

221
Q

What is the stamina of fast twitch muscle fibres?

A

Rapidly contract and fatigue quickly

222
Q

What are fast twitch muscle fibres used for?

A

Sudden, rapid bursts of activity

223
Q

What are fast twitch muscle fibres adapted to cope with?

A

Anaerobic conditions

224
Q

What do fast twitch muscle fibres contain little of?

A

Few blood vessels, little myoglobin and a fairly small number of mitochondria

225
Q

What do fast twitch muscle fibres contain lots of?

A

Glycogen and creatine phosphate

226
Q

What is creatine phosphate used for?

A

Forming ATP

227
Q

What are fast twitch muscle fibres also called?

A

Glycolytic or white muscle fibres

228
Q

What is the theory for how muscle contraction occurs?

A

The sliding filament theory

229
Q

What is the method of muscle contraction?

A

Calcium ions are released
Troponin-tropomyosin complex rotates
Actomyosin bridge formed
ADP and phosphate detach from myosin head
Myosin head rotates to shorten sarcomere
ATP binds to head, breaking bridge and shortening sarcomere

230
Q

What is bone made of?

A

Bone cells embedded in a matrix of collagen and calcium salts

231
Q

What properties does bone have?

A

Strong and hard, resistant to compressive forces, light

232
Q

What is cartilage made of?

A

Chrondocytes in a matrix of collagen fibrils

233
Q

What are the two main types of cartilage?

A

Hyaline and white fibrous

234
Q

What are the properties of cartilage?

A

Hard but flexible, elastic, good shock absorber

235
Q

Where is cartilage found?

A

Between bones and in the joints

236
Q

Where is hyaline cartilage found?

A

At the ends of bones

237
Q

Where is white fibrous cartilage found?

A

Between the bones in the joints and it forms the intervertebral discs

238
Q

What are tendons made of?

A

White fibrous tissue

239
Q

What are tendons used for?

A

Joining muscles to bones

240
Q

What are the properties of tendons?

A

Strong but inelastic

241
Q

What do ligaments do?

A

Hold bones together and in the correct alignment

242
Q

What are the properties of ligaments?

A

Elastic

243
Q

What are ligaments made of?

A

Yellow elastic tissue

244
Q

What is the liquid lubricant produced by joints called?

A

Synovial fluid

245
Q

What are joints lined with?

A

A layer of replaceable rubbery cartilage

246
Q

What does Glucose become in the initial step of Glycolysis?

A

A phosphorylated 6C sugar

247
Q

What is formed in the initial step of glycolysis?

A

ADP and a phosphorylated 6C sugar

248
Q

What does the phosphorylated 6C sugar split into in glycolysis?

A

2 3C phosphates

249
Q

What is formed in anaerobic respiration in animals?

A

Lactic acid

250
Q

What occurs when the 2 3C phosphates split into 2 pyruvates in glycolysis?

A

Reduced NAD and ATP are formed

251
Q

What is formed in anaerobic respiration in bacteria and yeast?

A

Ethanol and CO2

252
Q

How much ATP is produced in glycolysis?

A

8 molecules

253
Q

What is the enzyme which regulates the rate of respiration?

A

Phosphofructokinase

254
Q

How is pyruvate converted into acetyl CoA in respiration?

A

By turning NAD into reduced NAD and by forming CO2

255
Q

What are the enzymes which remove CO2 in respiration?

A

Decarboxylases

256
Q

What are the enzymes that remove hydrogen in respiration?

A

Dehydrogenases

257
Q

How is Citrate formed from acetyl CoA in respiration?

A

By combining with a 4C acid

258
Q

How does citrate become a 5C acid in the Kreb’s cycle?

A

By producing CO2 and reduced NAD

259
Q

What is produced in forming a 4C acid from the 5C acid in the Krebs cycle?

A

CO2, ATP, 2 reduced NADs and reduced FAD

260
Q

What is oxidative phosphorylation?

A

Moving electrons down an electron transport chain down the energy levels, phosphorylating ADP and requiring oxygen

261
Q

How many turns of the Krebs cycle are there per glucose molecule?

A

2

262
Q

How many molecules of ATP are formed per molecule of reduced FAD?

A

2

263
Q

How many molecules of ATP are formed per reduced NAD?

A

3

264
Q

What is formed at the end of the electron transport chain?

A

A water molecule

265
Q

Where does glycolysis take place?

A

In the cytoplasm

266
Q

Where does the Krebs cycle take place?

A

Mitochondrion matrix

267
Q

Where is ATP synthesised in respiration?

A

The cristae of the mitochondria

268
Q

What theory says how ATP is produced?

A

The chemiosmotic theory of ATP production

269
Q

What happens to the hydrogen ions left behind by the electrons in respiration?

A

They are actively transported into the space between the inner and outer membranes

270
Q

What gradients are set up between the space and the matrix in respiration?

A

Concentration, pH and electrochemical

271
Q

What happens when the protons travel across the membrane through the pores in respiration?

A

The ATPase enzyme linked to the stalked particles produces ATP

272
Q

How much ATP is produced in respiration?

A

38 molecules

273
Q

What are the electron acceptors involved in respiration?

A

Nicotinamide Adenine Dinucleotide (NAD)Flavine Adenine Dinucleotide (FAD)

274
Q

How does electrical excitation spread through the heart?

A

Sinoatrial node sets up a wave of depolarisation
Atria contracts
Excitation spreads to atrioventricular node
AVN excited and excitation passes to bundle of his
Excitation to purkyne tissue
Depolarisation travels down septum
Ventricles contract

275
Q

What is homeostasis?

A

The maintenance of a steady internal state in the body almost regardless of changes of conditions

276
Q

What are negative feedback systems?

A

Systems which act to oppose a change in conditions

277
Q

What is cardiac output?

A

Cardiac volume X heart rate

278
Q

Where is the cardiovascular control centre?

A

In the medulla of the brain

279
Q

What controls changes to heart rate?

A

The cardiovascular control centre

280
Q

What does most of the nervous control of the heart?

A

The autonomic (involuntary) nervous system

281
Q

What is the autonomic nervous system split into?

A

The sympathetic and parasympathetic systems

282
Q

What does the sympathetic nervous system do to the heart rate?

A

Excites it

283
Q

What does the parasympathetic system do to the heart rate?

A

Inhibits it

284
Q

What does adrenaline do to the heart rate?

A

Increases it

285
Q

Where are to hearts stretch receptors?

A

In the muscle walls

286
Q

How do the stretch receptors register a need to increase the heart rate?

A

They register more blood returning as the muscles squeeze more blood along as they work

287
Q

What do baroreceptors register?

A

Pressure

288
Q

Where are the baroreceptors for heart rate found?

A

In the sinuses of the carotid arteries in the neck

289
Q

How do the heart rates baroreceptors register a need to increase heart rate?

A

The blood vessels dilate as adrenaline is produced so blood pressure falls

290
Q

What is tidal volume?

A

The volume of air entering and leaving the lungs in a normal resting breath

291
Q

What is the inspiratory reserve volume?

A

The maximum air you can breath in after normal breathing

292
Q

What is expiratory reserve volume?

A

The maximum volume of air that can be expelled after a normal expiration

293
Q

What is vital capacity?

A

The total of the tidal volume, and inspiratory and expiratory reserves

294
Q

What is the residual volume?

A

The volume left after the strongest possible expiration

295
Q

What is the total lung capacity?

A

The sum of the vital capacity and the residual volume

296
Q

What is the inspiratory capacity?

A

The tidal volume + the inspiratory reserve volume

297
Q

What gives the stimulus to inhale and exhale?

A

The respiratory centre

298
Q

What controls breathing in?

A

The inspiratory centre

299
Q

What controls breathing out?

A

The expiratory centre

300
Q

How does breathing occur?

A

Inhale
Intercostal muscles and diaphragm contract
Lungs inflate
Stretch receptors in bronchi wall register
Stop breathing in

301
Q

What do chemoreceptors register in regards to breathing?

A

Register CO2 and pH levels

302
Q

How do the chemoreceptors cause increased breath rate?

A

Increased CO2 levels
pH and oxygen levels fall
Chemoreceptors register changes
Breathing increases

303
Q

What is the control of temperature through homeostasis called?

A

Thermoregulation

304
Q

How can temperature tolerance be measured?

A

Via a calorimeter

305
Q

What is the low critical temperature?

A

The point below which the bodys thermoregulatory measures have no effect

306
Q

What is the low lethal temperature?

A

Temperature below which chemical reactions stop in the body

307
Q

What is the high critical temperature?

A

Temperature above which the bodys thermoregulatory measures have no effect

308
Q

How do the superficial blood vessels cool the body down?

A

Vasodilation occurs
Sphincter muscles relax
More blood through superficial capillaries
More heat loss by radiation and conduction

309
Q

How do the superficial blood vessels warm the body up?

A

Vasoconstriction occurs
Entrance to capillaries closes
More blood through shunt vessel
Less blood loss

310
Q

What measures cool the body down?

A

Sweating
More blood closer to skin
Panting

311
Q

What measure are used to warm the body?

A

Shivering
Less blood close to skin
Hairs stand up
More adrenaline produced

312
Q

Where are the heat gain and loss centres?

A

In the hypothalamus

313
Q

Where are the warm and cold receptors?

A

In the skin and hypothalamus

314
Q

What contributes to type two diabetes?

A

Obesity
Lack of exercise
Poor diet

315
Q

What can too much exercise cause?

A

Weakened immune system
Increased risk of upper respiratory tract infections
Less T killer and helper cells
Less B cells and phagocytes

316
Q

What is arrhythmia?

A

Abnormal heart contraction rhythm

317
Q

What is ischaemia?

A

Starvation of the heart of oxygen

318
Q

What can be a heart disorder that is not registered by ECGs?

A

Ischaemia

319
Q

What is atrial fibrillation?

A

An arrhythmia caused by the atria beating too fast and ineffectively

320
Q

What can atrial fibrillation cause?

A

Increased risk of clots
Stroke
Inefficient heart pumping

321
Q

What is tachycardia?

A

Where the heart beats too quickly so the ventricles have no time to empty
Less of a period of no polarity
Muscles and brain may be starved of oxygen

322
Q

What is the P wave?

A

Depolarisation of the SAN and related tissue in the atrium

323
Q

What is the T wave?

A

Rapid repolarisation of the Purkyne tissue in the ventricles

324
Q

What is the QRS in an ECG?

A

Spread of excitation through the ventricles

325
Q

What is ventricular fibrillation?

A

Ventricles contract erratically and weakly
Little blood pumped out of arteries
Small QRS
Starved of blood - can cause heart attack

326
Q

What is rheumatoid arthritis?

A

Immune cells attack membranes lining joints which produce synovial fluid

327
Q

What can rheumatoid arthritis cause?

A

Joint swelling
Stiffness
Pain
Inflammation in nearby tendons, muscles and ligaments

328
Q

What is osteoarthritis?

A

Immune cells attack cartilage

329
Q

What is thought to be the main causes of osteoarthritis?

A

Genetics and as a delayed response to injury

330
Q

What is WADA?

A

World Anti Doping Agency

331
Q

What do anabolic steroids do?

A

Builds muscle mass and increases speed

332
Q

What does EPO do?

A

Increase red blood cell count and amount of oxygen in the blood

333
Q

What do hormone agonists do?

A

Mask or change another hormones action

334
Q

What do drug cheats use diuretics for?

A

Urinate more and so lose weight or remove evidence of illegal substances

335
Q

Why do athletes blood transfuse?

A

Increase oxygen in blood

336
Q

What is gene doping?

A

Attempting to change genes to enhance performance

337
Q

What do stimulants do?

A

Increase heart rate and make you more alert

338
Q

What are narcotics?

A

Painkillers

339
Q

What do beta blockers do?

A

Make heart beat slower

Reduce effect of adrenaline Steadier

340
Q

How do defibrillators work?

A

Depolarise a critical mass of the heart
Terminate arrhythmia
Allowing SAN to reestablish hearts rhythm

341
Q

What do creatine supplements do?

A

Get more creatine phosphate to make ATP

342
Q

What is the action of anabolic steroids?

A

Passes through cell membrane
Binds to receptor molecule
Carried into nucleus
Hormone-receptor complex acts as a transcription factor
Binds to DNA and switches on genes linked to protein synthesis
Produced RNA changed

343
Q

What are anabolic steroids linked to?

A 
Infertility
Impotence
Liver damage
High blood pressure
Agression
344
Q

What is the action of Erythropoietin?

A

Binds to receptor on cell membrane
Activates second messenger
Protein cascade set off
Functional second messenger enters nucleus and acts as transcription factor
Enzyme synthesis genes switched on or off

345
Q

What is EPO linked to?

A

Strokes
Heart attacks
High blood pressure

Biology (5 decks)

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