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A Level Biology (SNAB) > Topic 7 > Flashcards

Topic 7 Flashcards

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1
Q

What facilitates movement

A

Skeletal muscles, tendons, ligaments & joints

  • skeletal muscles attached to bones by tendons
  • ligaments attach bone to bone
  • skeletal muscles contract/relax to move bones at a joint
  • > e.g. bicep contracts -> tricep relaxes
  • > pulls bone -> arm bends (flexes) at elbow
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2
Q

Antagonistic Pair

A

Muscles that work together to move a bone

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3
Q

Skeletal Muscles

A

ngng

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4
Q

Myofibrils

A

Composed of thin & thick myofilaments

  • thick = myosin (protein)
  • thin = actin (protein)

Composed of many short units = Sarcomeres

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5
Q

Myofibrils viewed under electron miscroscope

A 
Dark band = thick myosin (and a little actin) = A band
Light band = thin actin = I band
End of each sarcomere marked by Z line
- sarcomeres joined lengthways at Z line
Middle of each sarcomere = M line
- middle section (myosin only) = H zone

INSERT DIAGRAM

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6
Q

Sliding Filament theory

A

Myosin + actin slide over one another (remaining the same length)
-> Sarcomeres contract
Simultaneous contraction of sarcomeres
-> myofibrils + muscle fibres -> contract
Sarcomeres return to original length as muscle relaxes

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7
Q

Skeletal muscle

A

= large bundles of long cells known as muscle fibres

- composed of fast & slow twitch muscle fibres (different muscles = different proportions)

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8
Q

Muscle fibres

A

Cell membrane = SARCOLEMMA
- bits of sarcolemma fold inwards across the muscle fibre & into the SARCOPLASM
= Transverse (T) Tubules -> help to spread electrical impulses across the sarcoplasm (reach all of muscle fibre)
- Sarcoplasmic reticulum stores & releases calcium ions (muscle contraction)
- lots of mitochondria (ATP)
- Multinucleated
- lots of long, cylindrical organelles = myofibrils

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9
Q

Sarcoplasmic reticulum

A

Network of internal membranes in the muscle fibre, which stores and releases calcium ions

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10
Q

Transverse (T) tubules

A

Bits of sarcolemma that fold inwards across the muscle fibre & into the sarcoplasm
- they help to spread electrical impulses through the whole muscle fibre (and sarcoplasm)

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11
Q

Myosin filaments

A
  • hinged globular heads (back & forth movement)

- binding sites for Actin & ATP

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12
Q

Actin Filaments

A
  • Actin-myosin binding site = binding site for myosin head
  • Tropomyosin + Troponin (proteins) between filaments
  • T & T are attached to one another & help myofilaments move pass one another
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13
Q

Binding Sites in resting muscles

A

Blocked by Tropomyosin, which is held in place by troponin

- stops the myofilaments sliding (& myosin head entering the site)

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14
Q

Muscle Contraction (process)

A

Triggered by Action Potential

  1. Action potential -> Influx of Calcium Ions
  2. ATP = energy to move myosin head
  3. Breaking of cross bridge
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15
Q

Muscle Contraction: Action potential -> Influx of Calcium Ions

A

Action potential (from motor neurone) stimulates muscle cell
-> depolarises sarcolemma
-> spreads dow T-tubules to the sarcoplasmic reticulum
Sarcoplasmic reticulum releases stored Ca^2+ into sarcoplasm
-> Ca^2+ binds to troponin -> changes shape
-> pulls tropomyosin out of a-m binding site
Exposes site
-> myosin head binds = Actin-myosin cross bridge

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16
Q

Muscle Contraction: ATP = energy to move myosin head

A

Ca^2+ activate ATPase (ATP breakdown -> energy released)

  • > moves myosin head
  • > pulls actin filament along (‘rowing action’)
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17
Q

Muscle Contraction: Breaking of cross bridge

A 
ATP = energy
-> breaks a-m cross bridge
-> myosin head detaches after movement
Myosin head reattaches to different binding site further along
->  new cross bridges -> cycle repeats
Many cross bridges form + break very rapidly
-> pull actin filament along
-> shortens sarcomere
-> muscle contracts

note: cycle continues as long as Ca^2+ is present and bound to troponin

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18
Q

Excitation of motor neurone (for muscle contraction) stops

A 
Ca^2+ leaves binding site on troponin
- moved by active transport back into sarcoplasmic reticulum (uses ATP)
Troponin returns to original shape
-> tropomyosin pulled back 
-> blocks a-m binding site
Muscle fibres no longer contracted as:
- no myosin heads attached
- no cross bridges
Actin filaments slide back to relaxed position
-> lengthens sarcomere
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19
Q

Slow twitch muscle fibres

A
  • contract slowly
  • muscles for posture = high proportion (e.g. back)
  • endurance
  • long working time before tired
  • slow energy release
  • -> aerobic respiration
  • -> lots of mitochondria + blood vessels (good O2 supply)
  • reddish colour = myoglobin rich (red coloured proteins; stores O2)
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20
Q

Fast twitch muscle fibres

A
  • contract quickly
  • muscles for fast movement = high proportion (legs, eyes)
  • short burst of speed + power
  • tire very quickly
  • quick energy release
  • -> aerobic respiration
  • -> glycogen used
  • -> few mitochondria + blood vessels
  • whitish colour (little myoglobin = poor O2 store)
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21
Q

Aerobic Respiration

A

C6H12O6 + 6O2 -> 6CO2 + 6H2O + energy
- glucose splits into CO2 (waste) + H2 (combines with O2 -> H2O)
= metabolic pathway
- energy released is used to phosphorylate ADP
- 4 stages of AR
Coenzymes used:
- NAD + FAD transfer hydrogen from one molecule to another
- Coenzyme A transfers acetate between molecules

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22
Q

Metabolic pathway

A

series of chemical reactions

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23
Q

4 Stages of Aerobic Respiration

A
  1. Glycolysis
  2. Link Reaction
  3. Krebs Cycle
  4. Oxidative Phosphorylation

1 - 3 = Reaction series
4 = reaction series products used to produce ATP

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24
Q

Glycolysis (process)

A 
Glucose (6C) -> 2 x Pyruvate (3C)
Happens in cell cytoplasm
Anaerobic process (no O2)
1. Phosphorylation:
- glucose phosphorylated (2 Pi from 2 ATP molecules)
-> 2 ATP + 2 triose phosphate
2. Oxidation:
- triose phosphate oxidised
-> 2 x pyruvate
- NAD collects H+ -> reduced NAD (used in 4th stage)
- 4 ATP produced (net gain = 2 ATP)
INSERT DIAGRAM
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25
Q

Link Reaction (process)

A 
Occurs twice for every glucose molecule 
Happens in mitochondrial matrix
1. Pyruvate decarboxylated
- one carbon removed
2. NAD reduced
- collects H+ from pyruvate
- pyruvate -> acetate
3. Acetate + CoEnzyme A (CoA) -> acetyl CoA

Note: no ATP produced

  • 2 x acetyl CoA -> stage 3
  • 2 x CO2 = waste
  • 2 x reduced NAD -> stage 4

INSERT DIAGRAM

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26
Q

Krebs Cycle (process)

A 
Cycle = once for each pyruvate
Occurs in mitochondrial matrix
Series of REDOX reactions
1. Acetyl CoA + Oxaloacetate (4C) -> Citrate (6C)
- CoA goes back to stage 2
2. Citrate -> 5C
- decarboxylation (CO2 = waste)
- dehydrogenation 
--> H+ carried by reduced NAD -> stage 4
3. 5C -> Oxaloacetate
- decarboxylation (CO2 = waste)
- dehydrogenation 
--> 2 x H+ carried by reduced NAD -> stage 4
--> 1 x H+ carried by reduced FAD -> stage 4
- ATP produced
--> direct Pi transfer from intermediate group = SUBSTRATE LEVEL PHOSPHORYLATION

INSERT DIAGRAM

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27
Q

Substrate Level Phosphorylation

A

Direct Pi transfer from an an intermediate group

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28
Q

Oxidative Phosphorylation

A

Process where energy carried by electrons from reduced CoEnzymes is used to make ATP

  • occurs in/across mitochondrial membrane
  • made up of two processes:
    • Electron transport Chain
    • Chemiosmosis
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29
Q

How many ATP can be produced from 1 glucose?

A

38

Reduced NAD = 3 ATP (energy release)
Reduced FAD = 2 ATP (energy release)

  1. Glycolysis = 2 ATP + 2 reduced NAD = 8 ATP
  2. Link reaction = 2 reduced NAD = 6 ATP
  3. Krebs Cycle = 2 ATP + 6 reduced NAD + 2 reduced FAD = 24 ATP

Total = 38 ATP

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30
Q

Anaerobic Respiration

A

No O2 used

Lactate fermentation:

  • glucose -> pyruvate (glycolysis)
  • reduced NAD tranfers H+ to pyruvate
  • > lactate + NAD produced
  • NAD recycled for glycolysis
  • -> glycolysis continues with no O2 allowing for small ATP production (2)
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31
Q

Lactic Acid

A

Lactic acid build us through Anaerobic Respiration

Broken down in two ways:

  1. cell convert lactic acid -> pyruvate (re-enters into link reaction)
  2. liver cells convert lactic acid -> glucose = respired or stored
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32
Q

Metabolic poisons target…

A

Electron carriers

  • stop electron & chemiosmosis
  • stops reduced NAD + FAD oxidation
  • -> stops regeneration
  • -> stops Krebs cycle
  • ATP synthesis falls -> fatal
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33
Q

Oxidative Phosphorylation (process)

A
  1. H atoms released from reduced NAD + FAD (-> oxidised back)
    - H -> H+ + e-
  2. Electrons move down electron transport chain (ETC)
    - lose energy at each carrier
  3. Energy used by electron carriers
    -> pumps protons (H+) from the mitochondrial matix -> intermembrane space
  4. Concentration of protons = higher in intermembrane than matrix
    -> electrochemical gradient
  5. protons move down gradient into matrix
    - via ATP synthase
    -> drives synthesis of ATP (Pi + ADP -> ATP)
  6. Movement of H+ across membrane generates ATP
    = Chemiosmosis
  7. End of ETC finishes int the mitochondrial matrix
    - H+ + e- + O2 -> H2O
    - oxygen = final electron acceptor

INSERT DIAGRAM

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34
Q

Chemiosmosis

A

The movement of ions via diffusion across a semi-permeable membrane

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35
Q

Cardiac muscle

A

Is Myogenic

  1. SAN = Sino-atrial node
    - In wall of right atrium
    = pacemaker
    - sets rhythm by sending out impulses to atrial walls
    -> cause right + left atria to contract simultaneously
  2. Band of non-conducting collagen tissue prevents impulse from passing to ventricles
  3. Impulse transferred from SAN to AVN
    - AVN = Atrioventricular node
  4. AVN leaves a slight delay before passing on impulse to Bundle of HIS
    - slight delay allows atria to fully contract & empty
  5. Bundle of HIS = muscle fibre group
    - conducts impulse to Purkyne Fibres
  6. Purkyne fibres carry impulse
    - cause ventricles to simultaneously contract from the bottom u[
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36
Q

Myogenic

A

Contracts & relaxes without requiring a neurone signal

37
Q

Electrocardiograph

A

Records electrical activity of the heart

  • electrodes placed on chest
  • trace produced = ECG (electrocardiogram)
38
Q

Electrocardiogram

A
  1. P wave = contractions of atria (first peak)
  2. QRS complex = contraction of the ventricles (main peaks + troughs either side)
  3. T wave = relaxation of ventricles; repolarisation (last peak)
  4. Height = amount of electrical charge
    - bigger wave = more
    - (higher) P + R = stronger contractions
39
Q

Using ECG’s

A

Can be compared to normal trace -> diagnose health issues

  • too fast = tachycardia
  • too slow = bradycardia
  • ecotopic heartbeat = ‘extra’ heartbeat
  • Fibrilation = v. irregular
40
Q

Tachycardia

A

Too fast heart beat (above 100 bpm)

41
Q

Bradycardia

A

Too slow heart beat (less than 60 bpm)

42
Q

Ecotopic heartbeat

A

Extra heartbeat

  • earlier contraction of atria (P wave)
  • Can be caused by ventricles
  • if occasionally present (in a healthy individual) = not an issue
43
Q

Fibrilation (ECG)

A

Very irregular

  • atria or ventricles completely lose their rhythm
  • stop contracting properly
  • > chest pain, fainting, lack of pulse, death
44
Q

Exercise ->

A
  • more frequent muscle contractions
  • more energy recquired
  • more aerobic respiration
  • -> increased breathing rate + depth (better gas exhange)
  • -> increased heart rate (delivery/removal)
45
Q

Medulla Oblongata

A

MO controls breathing rate via two ventilation centres

  • inspiratory
  • expiratory
46
Q

Medulla Oblongata effect on breathing rate

A
  1. Inspiratory centre sends nerve impulses to the intercostal + diaphram muscles -> contract
  2. Increases lung volume -> lowers the pressure
    - signal also sent to expiratory centre to inhibit
  3. Air enters lungs due to pressure difference
  4. Lungs inflate
    - stretch receptors stimulated
    - nerve impulses sent to MO to inhibit Inspiratory centre
  5. Expiratory centre sends nerve impulse to diaphram and intercostal muscles -> relax
    - lungs deflate -> air expelled
    - stretch receptors become inactive
    - Inspiratory centre no longer inhibited -> cycle restarts
47
Q

Exercise -> decreased blood pH ->

A

Increased breathing rate

  • exercise -> increased CO2 in blood -> decreased pH
  • chemoreceptors in medulla oblongata:
    • aortic bodies + carotid bodies
  • – sensitive to changes in blood pH
  • Change detected -> nerve impulse to MO
  • > more frequent impulses to intercostal muscle and diaphram
  • > increases rate + depth of breathing
  • > gaseous exchange speeds up
  • > CO2 reduced, extra O2 supplied -> blood pH balances
48
Q

Carotid bodies

A

Clusters of receptor cells in the carotid arteries

49
Q

Aortic bodies

A

Clusters of receptor cells in the aorta

50
Q

Ventilation rate + exercise =

A

An increase in ventilation rate due to increased breathing rate + depth

51
Q

Ventilation rate

A

Volume of air breathed in & out in a period of time

52
Q

Medulla Oblongata’s effect on Heart Rate

A

MO unconsciously controls HR via the Cardiovascular Control Centre (CCC) in the MO

  1. CCC controls the rate the SAN fires at (heart beat rythm)
  2. Animals alter HR to respond to internal stimuli
  3. Chemical + pressure receptors detect stimuli in the blood:
    - baroreceptors (aortic + carotid bodies) = high + low blood pressure
    - chemoreceptors (aortic + carotid bodies +& MO) = blood O2 levels; CO2 + pH (secondary indicators)
  4. Receptors send electrical impulses along sensory neurones to the MO
  5. CCC processes information & sends impulses to SAN via sympathetic/parasympathetic neurones
    - release different neurotransmitters onto SAN
    - > sympathetic = increase
    - > parasympathetic = decrease
53
Q

Baroreceptors

A

High Blood pressure:

  • Impulse to CCC -> impulse along parasympathetic neurones
  • > secrete acetylcholine -> binds to SAN
  • > decreased SAN firing -> lowers BP

Low Blood pressure:

  • Impulse to CCC -> impulse along sympathetic neurones
  • > secrete noradrenaline -> binds to SAN
  • > increased SAN firing -> raises BP
54
Q

Chemoreceptors

A

High blood O2/Low CO2/High pH:

  • Impulse to CCC -> impulse along parasympathetic neurones
  • > secrete acetylcholine -> binds to SAN
  • > decreased SAN firing -> lowers HR

Low blood O2/High CO2/Low pH:

  • Impulse to CCC -> impulse along sympathetic neurones
  • > secrete noradrenaline-> binds to SAN
  • > increased SAN firing -> raises HR
55
Q

Cardiac Output (CO)

A

Total volume of blood pumped by a ventricle each minute

56
Q

Stroke Volume (SV)

A

Volume of blood pumped by one ventricle each time it contracts

57
Q

Cardiac Output equation

A

CO (cm^3min^-1) = HR (bpm) x SV (cm^3)

note: CO increases during exercise -> HR + SV increase

58
Q

Inverse Cardiac output equation

A

SV = CO/HR

59
Q

Purkyne Fibres

A

Finer muscle fibres in r/l ventricle walls

60
Q

SAN

A

Sino-atrial node
- in wall of right atrium
= pacemaker

61
Q

AVN

A

Atrioventricular node

62
Q

Cardiac Muscle diagram

A

INSERT DIAGRAM

63
Q

Tidal Volume

A

Volume of air in a normal breath

- around 0.4 dm^3

64
Q

Breathing rate

A

How many breaths taken (per minute)

65
Q

Oxygen consumption

A

Volume of oxygen used by the body (expressed as a rate)

66
Q

Respiratory minute ventilation

A

Volume of gas breathed in/out in a minute

- also known as respiration rate

67
Q

Respiratory minute ventilation equation

A

RMV = tidal volume x breathing rate (breaths per min)

68
Q

Spirometers

A

Measures Ventilation

  1. oxygen filled chamber with movable lid
  2. Person breathes through tube connected to chamber
  3. Breathes in -> chamber lid moves down
    - breathes out -> chamber lid moves up
  4. Movement recorded by a pen attached to the lid
    - > writes on rotating drum = spirometer trace
  5. Total volume of gas in chamber decreases over time -> air breathed out = O2 + CO2 mixture
    - CO2 absorbed by soda lime in tube
    - only O2 in inhalation chamber -> used by respiration -> chamber vol decreases

INSERT DIAGRAM

69
Q

Using Spirometers to investigate the effect of exercise

A
  1. person breathes into spirometer for 1 minute at rest
    - recordings taken
  2. Person exercises for 2 minutes
    - spirometer chamber refilled with O2
  3. immedietly after exercise stops -> breathe into Spirometer again -> recordings taken for a minute
  4. recordings taken before + after compared
70
Q

Spirometer trace

A 
Breathing rate (per min) = number of peaks in trace in a minute
Tidal volume = average difference in the volume of gas between each each peak & trough on the trace
Oxygen consumption = the change in volume of gas in spirometer (read values from troughs)
71
Q

Homeostasis

A

Maintenance of a stable internal environment

  • counteracts impacts of external environment + activity
  • control systems (kept within narrow limits)
  • internal environment = state of dynamic equilibrium
72
Q

Homeostasic blood glucose content

A

usually = 90mg per 100 cm^3 of blood

  • monitored by pancreatic cells
  • essential for constant energy
73
Q

Homeostatic Systems

A

= receptors, communication system + effectors
- effectors counteract change ( to normal)
= negative feedback mechanism

INSERT DIAGRAM

74
Q

Negative Feedback Mechanism

A

Maintains normal levels by counteracting change

  • e.g. temp= 0.5 +/- 37 C
  • only works within certain limits (too large and it cannot counteract)
75
Q

Positive Feedback mechanism

A

Amplifies a change from the normal level

  • effectors respond to further increase
  • useful to rapidly activate
  • can happen when homeostatic systems break down (hypothermia)
  • not part of homeostasis as it does not provide a stable internal environment
76
Q

Platelets & Positive Feedback

A

Platelets activate:

  • > chemical released
  • > triggers more platelets to be activated
  • > quickly form blood clot at injury site
  • > ends with negative feedback (blood clot detected)
77
Q

Reducing body temperature

A

Sweating:
- more secreted -> water evaporates from skin surface -> heat lost -> skin cooled
Hairs lying flat (mammals):
- erector pilli muscles relax -> hair lies flat -> less air trapped -> heat lossed
- layer of hair insulates by trapping air = poor conductor
Vasodilation:
- aterioles near skin surface dilate -> more blood flows via the capillaries to the skins surface -> heat lost via radiation

78
Q

Increasing body temperature

A

Shivering:
- muscles contract in spasms -> shiver -> heat from increased respiration
Reduced sweat:
- reduced secretion
Hairs stand up:
- erector pili muscles contract -> hairs stand up -> more air trapped
Vasoconstriction:
- arterioles near the skin surface constrict -> less blood flows to surface layer of dermis
Hormones:
- adrenaline + thyroxine -> increased metabolism -> more heat produced

79
Q

Hypothalamus

A

Control body temperature = thermoregulation

  • receives info from thermoreceptors
  • thermoreceptors send impulses along sensory neurones -> hypothalamus -> motor neurones -> effectors
  • effectors respond -> counteract to norm
80
Q

Hormones affect on Transcription Factors (inside cells)

A

= Steroid + thyroid hormones
Cross cell membrane -> bind to nucleus -> bind to transcription factors

E.g. normal body temp:

  • thyroid hormone receptor (transcription factor) binds to DNA at start of gene
  • > decreases transcription of gene coding for protein that increases metabolic rate

Cold body temp -> thyroxine released

  • binds to thyroid hormone receptor -> acts as an activator
  • transcription rate increased -> produces more protein -> increases metabolic rate (& temp)
81
Q

Keyhole Surgery

A

Small incision where a tiny video camera and specialised instruments are inserted

  • less blood lost
  • less pain
  • quicker recovery time
  • less scaring
  • shorter hospital stay -> quicker return to normal activities

e. g. cruciate ligaments
- damaged one removed
- replaced with graft (likely from leg tendon)

82
Q

Prostheses

A

Replaces whole or part of a limb
Can include electronic devices that operate the prosthesis by picking up information sent by the nervous system

e. g. Knee joints -> prosthetic
1. Metal device replaces damaged cartilage + bone
2. Joint + end of bones replaced to provide a smooth joint
- cushioning helps to reduce impact
3. Allows people to move around & participate in low impact sport

83
Q

Knee Joint Diagram

A

ngng

84
Q

Performance Enhancing Drugs (For/Against)

A

Absolutionist argument:

  • illegal
  • unfair competition
  • serious health risks (high bp + heart problems)
  • > may not be dully informed

Rationalist argument:

  • have the right to make their own decisions
  • situation dependent
  • overcome inequalities in training, coaches, equipment etc
  • may be necessary to compete at a higher level
85
Q

Anabolic steriods

A

Increased strength, speed + stamina -> increased muscle size

  • allows for harder training
  • side effect: increased aggression
86
Q

Stimulants

A

Speed up reactions & reduce fatigue

- increase aggression

87
Q

Narcotic Analgesics

A

Reduce pain

- injuries reduce performance impact

88
Q

Hormones affect on Transcription Factors (working at cell membrane)

A

= protein hormones
Cannot cross the cell membrane
Bind to receptor in membrane -> activate messenger molecules in cytoplasm of cell
- messenger molecules activate protein kinase (enzyme) -> trigger cascade in cell
- during cascade transcription factors can be activated
-> then affect transcription of genes in cell nucleus

89
Q

Transcription Factors

A

Proteins that control gene transcription within cells

  • bind to DNA sites near the start of a gene
  • > increase/decrease transcription rate

A Level Biology (SNAB) (10 decks)

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