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Biology > Topic 7 > Flashcards

Topic 7 Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

ligaments:

A
  • made of elastic connective tissue
  • hold bones together
  • restrict the movement at a joint ( to enable movement)
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2
Q

tendons:

A

cords of non-elastic fibrous tissue that anchors muscles to bones

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3
Q

cartilage:

A

protects bones within joints- lubricant- no friction

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4
Q

antagonistic pair:

A

pair os muscles that pull in opposite directions

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5
Q

joints:

A

an area where two bones are attached- have fibrous connective tissue

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6
Q

6 functions of the human skeleton:

A

S tructure, support, strength
C ell production (white and red blood cells in bone marrow)
O rgan protection
Mi nerals
Mo vement
F at storage and release

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7
Q

3 joint catagories:

A
  • synovial (e.g. knee)
  • immovable (e.g. cranium)
  • cartilaginous (e.g. spine- in between vertibrae)
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8
Q

6 synovial joints:

A
  • pivot- e.g. between skull and vertebrae
  • hinge- e.g. between humurous and ulna
  • planar- e.g. in hand between metacarpels
  • ball and socket- e.g. hip
  • saddle- e.g. between vertebrae
  • condyloid- e.g. wrist- radius and carpels
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9
Q

motion of synovial joints

A

adduction, rotation, abduction, flexion and extension

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10
Q

extensor:

A

straightens joint when contracted

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11
Q

flexor:

A

bends joint when contracted

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12
Q

thin microfilament:

A

actin

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13
Q

thick microfilament:

A

myosin

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14
Q

sarcomere:

A

the functional unit of a muscle fibre (also called a muscle cell)

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15
Q

the bands on a sarcomere:

A

A band: the whole myosin length on a sarcomere (with or without actin)
I band: only actin
H zone: section of sarcomere with only myosin
Z line: bounadary of 1 sarcomere unit- neighbors next sarcomere
M line: centre of the myosin filament

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16
Q

Sliding filament theory:

A
  1. calcium ions released from the sarcoplasmis reticulum upon nervous stimulation
  2. Calcium ions bind to troponin protein (on actin subunit). Troponin molecules undergo a comformational change to their 3D protein structure, pulling tropomyosin out of position
  3. Myosin binding site on actin subunit is exposed. Myosin heads have an ADP molecule and phosphate bound to them.
  4. Phosphate group released from myosin heads causing myosin to bind to the attachment sites on actin, forming cross-bridges.
  5. ADP released from myosin head causing the ‘power stroke’. Actin filament pulled towards the H zone
  6. ATP binds to the the myosin heads causing them to detatch from actin
  7. ADP is hydrolysed into ADP +Pi. Myosin recover and returns to original position.
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17
Q

what happens to the sarcomere upon contraction?

A

the sarcomere shortens as Z-lines get closer together and H zone disappears. The I band also gets narrower.

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18
Q

cellular respiration provides..

A

ATP for processes within the cell.

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19
Q

3 main stages of aerobic respiration:

A

Glycolysis, Kreb’s cycle, electron transport chain

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20
Q

Where does Glycolysis occur?

A

in the cytoplasm and is therefore used both anaerobically and aerobically.

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21
Q

stages of glycolysis and net products:

A
  • glucose (6C) phosphorelysed to form fructose Bis-phosphate as 2 ATP molecules are broken into 2ADP +2Pi
  • Fructose Bis-phosphate is broken into two triose phosphates
  • 2 triose phosphate converted into 2 pyruvate molecules. Per triose phosphate molecule, 2ADP molecules are phosphorelysed into 2ATP (one phosphate from cytoplasm per molecule- from dephosphorelysed triose molecule)
  • 1NAD is reduced to rNAD/ NADH per molecule
    net products: 2ATP (substrate level phosphorelation), 2NADH
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22
Q

what is substrate level phosphorelation?

A

ADP is phosphorelysed by an enzyme directly from the reaction of glycolysis or Kreb’s cycle

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23
Q

where does the link reaction occur?

A

in the mitochondrial matrix

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24
Q

Stages of the link cycle and net products:

A

-2 pyruvate molecules diffuse into the mitochondrial matrix
- pyruvate is decarboxylated (releasing CO2) and NAD is reduced to NADH
- acetate (2C) is formed and is combined with co-enzyme A (CoA) forming acetyl Co-A (primed to enter the Kreb’s cycle)
- the link reaction happens twice (per pyruvate molecule)
Net products: 2CO2, 2NADH

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25
Q

Where does the Kreb’s cycle occur?

A

in the matrix

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26
Q

stages of the Kreb’s cycle and net products:

A
  • Acetyl Co-A loses enzyme Co-A before entering the cycle and combines with a 4-carbon molecule (oxaloacetate) to form a 6-carbon molecule (citrate)
  • Citrate is decarboxylated (releasing CO2) while NAD is reduced to NADH to form a 5 carbon molecule
  • the 5 carbon molecule is decarboxylated, (releasing CO2) to form a 4 carbon molecule while NAD is reduced to NADH (oxidising the carbon compound)
  • ADP is phosphorelysed to form ATP ( substrate level phosphorelation) oxidising the 4 carbon compound to form another 4 carbon molecule.
  • FAD is reduced to FADH while the 4 carbon compound is oxidised to form another 4 carbon compound
  • NAD is reduced to NADH, oxidising the 4 carbon compound and reforming oxaloacetate.
  • Kreb’s cycle turns twice (per glucose)
    Net products: 6NADH, 2FADH, 2ATP, 4CO2
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27
Q

where does the electron transport chain occur?

A

in the inner mitochondrial membrane.

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28
Q

which molecules enter the ETC and where do they come from?

A
  • 2 NADH from glycolysis
  • 2NADH from the link reaction
  • 6 NADH from the Kreb’s cycle
  • 2 FADH from the Kreb’s cycle
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29
Q

stages of electron transport chain:

A
  • NADH is oxidised to NAD+ releasing 2e- and a H+
  • the electrons are passed through protein carrier molecules through a series of redox reactions
  • this generates energy to pump the protons from the matrix into the inner-membrane space, generating a high proton concentration
  • FADH is oxidised to form FAD, releasing 2 electrons and a H+. Electrons are passed through protein carrier molecules through a series of redox reactions, generating energy to pump the H+ through the membrane.
  • 2H+ combine with 1/2O2 and 2e- (from the ETC) to form a molecule of water.
  • a greater proton concentration is generated in the inner mitochondrial mebrane
  • ATPsynthase converts ADP + Pi into ATP (by oxidative phosphorelation while H+ diffuse down into matrix by chemiosmosis
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30
Q

what is oxidative phosphorelation

A

phosphorelation of ADP to ATP using free energy produced from redox reactions in the ETC

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31
Q

what is the final electon acceptor in the electron tranport chain?

A

oxygen (which is why aerobic respiration requires air)

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32
Q

How many ATP molecules are produced per NADH and FADH enetring?

A

3 ATP- NADH
2 ATP-FADH

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33
Q

How many ATP molecules are produced from the electron transport chain?

A
  • 10 NADH entering therefore 10x3= 30 ATP molecules produced- oxidative phosphorelation
  • 2 FADH entering therefore 2x2=4 ATP molecules produced- oxidative phosphorelation
  • AND, 2 net ATP molecules produced by glycolysis and 2 net ATP molecules produced by the Kreb’s cycle - both substrate level phosphorelation.
  • therefore, the total maximum ATP produced is 38 molecules.
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34
Q

anaerobic respiration:

A
  • without oxygen to use as the terminal electron acceptor; the electron transport chain cannot function.
  • the first stage of anaerobic respiration is glycolysis.
    -The product, pyruvate is then converted to lactate (catalysed by lactate dehydrogenase) while NADH is oxidised to NAD+ (providing 2H+)
  • lactate dehydrogenase dehydrogenates lactate to convert back to pyruvate.
  • the NAD+ produced is then available to accept protons and electrons in order for glycolysis to continue.
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35
Q

lactate and lactic acid:

A

-lactate is a necessary end product of the oxidation of NADH to to regenerate NADH so that glycolysis can continue.
- However, the lactate becomes lactic acid and this lowers blood pH. This causes a reduction in enzyme activity and so the lactate must be removed. Most of it is converted back into pyruvate when oxygen is available again.
-The extra oxygen required to do this is called the oxygen debt.

36
Q

the overall equation for aerobic respiration:

A

C6H12O6 +6O2 —> 6CO2 + 6H2O

37
Q

myogenic:

A

ability to beat (contract) without nervous stimulation from the nervous system.

38
Q

control of the heartbeat:

A
  1. Sinoatrial node generate an action potential (wave of depolarisation)
  2. The wave of depolarisation spreads through the cardiac wall of the atria (from top to bottom)
  3. The layer of non-conducting tissue distributed trhoughout the walls of the heard between the atria and ventricles prevents the wave of depolarisation spreading top to bottom in the ventricles
  4. The action potential reaches the atriventricular node and the AV node conducts the signal to the ventricles.
  5. AP travels down conducting fibres called Purkinjie fibres arranged in the bundle of His (in the septum to the apex of the heart)
  6. Ventricular systole initiated as AP travels up cardiac walls of ventricle from bottom to top.
39
Q

analysing electrocardiograms:
P wave-
QRS cpmplex-
P-R interval-
T wave-

A

P wave- the contraction of the atria (caused by the SAN)
QRS cpmplex- ventricular systole (AVN) impluse
P-R interval- difference between the start of the atrial contraction to the start of ventricular contraction.
T wave- relaxing and repolarising (cardiac diastole)

40
Q

how to calculate heart rate from an electrocardiogram:

A

300 divided by the number of large squares between QRS complexes.

41
Q

arrhthmia:

A

abnormal rhythm of the heart

42
Q

ventricular fibrilation:

A

rhythm is rapid, disorganised, non-distinguishable

43
Q

atrial fibrilation:

A

rhythm is irregular with the atrial rate 350-400 bpm

44
Q

sinus bradycardia:

A

beats are slow (less than 60 bpm)

45
Q

sinus tachycardia:

A

beats are rapid (100-160 bpm)

46
Q

atrial flutter:

A

regular atrial rhythm (250-300 bpm)- ventricular rhythms variable

47
Q

asystole:

A

no rhythm or rate- ‘flat line’ (dead)

48
Q

cardiac output definition:

A

volume of blood pumped by the heart in one minute
- at rest= 5dm3min-1
- during exercise= (can rise to) 30 dm3min-1

49
Q

what is the stroke volume?

A

volume of blood pumped out of the left ventricle in each contraction (cm3)

50
Q

heart rate definition:

A

number of heart beats in one minute
- can be measured in radial or corotid arteries

51
Q

equation of cardiac output:

A

stroke volume x heart rate

52
Q

what happens to the stroke volume when we exercise?

A

increases

53
Q

factors affecting heart rate:

A
  • low pH- increased CO2 concentration- detected by chemoreceptors located in the corotid arteries, aorta and the brain. The receptors send impulses to the medulla oblongata where the cardiovascular centre is located.
  • stretch receptors- located in muscles and tendons- respond to muscle movement
  • decrease in blood pressure
  • adrenaline is a hormone released to stimulate fight or flight response.
  • The relevent receptor sends an impulse to the cardiac control centre in the medulla oblongata. An impulse is sent to the SAN along a sympathetic neurone, depolarisation occurs and noradrenaline is released at the SAN (neurotransmitter). This results in
    an increased heart rate.
  • If the stimulus is the opposite, a nervous impulse travels down the parasympathetic (vagus) neurone.
54
Q

ventilation rate is affected by..

A
  • an increased concentration of CO2 in blood, lowering the pH.
  • impulses from stretch muscle receptors in muscles and tendons caused by exercise
  • voluntary control
55
Q

what is the tidal volume:

A

is the normal breathing volume, about 0.5 dm3

56
Q

inspiratory and expiratory reserve volumes

A

are the maximum amount you can breathe in and out

57
Q

residual volume:

A

is the air which is in the lungs after you have fully breathed out

58
Q

vital capacity:

A

the total volume from fully breathed in to fully breathed out.

59
Q

what is the purpose of soda lime in the spirometry practical?

A
  • it absorbs the carbon dioxide so the subject’s use of oxygen can be accurately measured
  • causes the trace to slope downwards from left to right.
60
Q

respiritory minute ventilation is calculated by:

A

average tidal volume over 1 minute x nuber of breaths over 1 minute

61
Q

Fast twitch versus slow twitch muscles: features of fast twitch muscle-

A

Fast twitch:
- specialised to produce rapid, intense contractions in short bursts
- few mitochondria- ATP comes from anaerobic repsiration (glycolysis)
- little myoglobin and few capillaries- the muscle has a light colour
-fatigues quickly
- high glycogen content- rapid conversion into glucose
- high levels creatine phosphate

62
Q

fast twitch versus slow twitch muscle: features of slow-twitch muscle:

A

-specialised for slower, sustained contraction and can cope with long periods of exercise
- many mitochondria- ATP comes from aerobic respiration (ETC)
- lots of myoglobin (dark red pigment) to store O2 and lots of capillaries to supply O2, this gives the muscle a dark colour
- fatigue resistant
- low glycogen content
- low levels of creatine phosphate.

63
Q

what is myoglobin?

A
  • myoglobin is a protein similar to haemoglobin
  • it has a high affinity for oxygen and only releases it when the concentration of oxygen in the cells falls very low, acting as an oxygen store within muscle cells
64
Q

negative feedback:

A

conteracts the change in the internal conditions and fluctuates within a narrow range.

65
Q

positive feedback:

A

increases the original change in conditions

66
Q

homeostasis:

A

the maintainance of a relatively constant internal environment regardless of the external stimuli

67
Q

the importance of homeostasis and factors affecting enzymes:

A

stable conditions are essential for proteins, enzymes- Intracellular enzymes are sensitive to changes in
PH affects molecular structure:
- hydrogen bonds disrupted
- charge distribution on active sites changes
Temperature:
- rate of reaction of enzymes (low)
- denaturing (high)
Water potential:
- affects water content of cells
- too high will cause swelling and bursting
- too low will cause shrinkage of cells

68
Q

Control mechanims:

A
  • Changes are detected and effectors are stimulated to respond to oppose the change
  • once the set point has been restored, the sensory receptors detect the change back to normal and communicate with the effectors to halt the response
  • (negative feedback)
    mechanism:
    1. deviation- why?
    2. detection- receptors
    3. nervous impulse
    4. coordination- somewhere in the brain
    5. NI/ hormone
    6. response (corrective mechanism)- effectors include muscles and glands
69
Q

examples of positive feedback:

A

-giving birth- contractions lead to more contractions
- blood clotting
-nervous impulse- when action potentials have a small increase, the membrane permeability increases further.

70
Q

thermoregulation definition:

A

the control of core body temperatire through negative feedback

71
Q

what detects changes in temp?

A

thermoreceptors in the skin and thermoreceptors in the hypothalamus (for core body temp)

72
Q

what does the hypothalumus do if your core body temp increases?

A
  • stimulates sweat glands to secrete sweat
  • arterioles relax in the skin (dilates capillaries)
  • hair erector muscles relax- hair lies flat
  • liver reduces metabolic rate
  • skeletal muscles relax- no shivering
73
Q

what does the hypothalamus do when the core body temp decreases?

A

-arterioles in the skin constrict
- hair erector muscles contract
- liver raises metabolic rate
- skeletel muscles contract- shivering

74
Q

possible effects of too little exercise:

A

-reduced physical endurance, stroke volume and maximum heart rate, HDL levels, bone density (therefore increased chance of osteoporosis)
- increased resting heart rate, blood pressure, storage of fat in the body and levels of LDL
- increased risk of coronary heart disease, type 2 diabetes, some cancers, weight gain, obesity
- impaired immune response due to lack of natural T killer cells.

75
Q

Possible effects of too much exercise:

A
  • immune suppression- some cells of the immune system may be decreased as the body recovers from vigorous exercise.
    -increased wear and tear on joints
  • chronic fatigue and poor athletic performance
  • damage to cartilage in synovial joints, leading to inflammation and arthiritis
  • ligaments being damaged because bursae (fluid filled sacks) that cushion parts of the joint can become inflamed and tender.
76
Q

Keyhole surgery:

A

-surgeons can repair cruciate ligaments in the knee using fibre optics to perform keyhole surgery.
- less bleeding and damage to the joint (small hole) and less scarring

77
Q

prosthesis:

A

an artificial body part desgined to regain some degree of normal function and appearance.
- damaged joints can be repeaired with small prosthetic implants to replace the ends of damaged bonds

78
Q

doping:

A

many drugs act as hormones to increase muscle mass or endurance to enhance physical capacities in sport.

79
Q

Hormones:

A
  • hormones act through the control of transciption factors (transcription factors are proteins that bind to DNA)
80
Q

Promoter sequences (a type of transcription factor) ..

A
  • enable the binding of RNA polymerase and therefore promote transcription
81
Q

Repressor sequences:

A

binds to promotor so trancription factors cannot attach and RNA polymerase cannot bind

82
Q

transcription factors … to form the ….

A

clump together to form the transcription initiation complex.

83
Q

steroid hormones versus peptide hormones:

A
  • steroid hormones are lipid soluble. They can enter through the plasma membrane to form a hormone-receptor complex, initiating changes in the nucleus (have a direct effect on transcription)
  • peptide hormones are not lipid soluble (e.g. EPO). they cannot enter the cell directly amd trigger the release of secondary messenger molecules from the cell membrane. The second molecule can enter the nucleus and bring about a change.
84
Q

why would doping be acceptable?

A

athletes have the right to decide for themselves and it may allow the more disadvantaged to take part and compete at a higher level.

85
Q

why is doping not acceptable?

A
  • athletes don’t know the risks
    e.g. excess testosterone can cause liver damage, disrupts menstral cycle, impotence (erectile disfunction), aggression, higher blood pressure
    e.g. EPO can cause more viscous blood (leading to thrombosis and heart workng harder)
  • not a fair playing ground
  • may reinforce unrelaistic standards

Biology (9 decks)

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