Topic 3B: More Exchange and Transport Systems Flashcards

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1
Q

What enzymes break down carbohydrates?

A
  • Amylase
  • Membrane-bound disaccharidases
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2
Q

Where are each made and where do they act?

A
  • Amylase - salivary glands, pancreas - mouth, ileum
  • Membrane-bound disaccharidases - cell membranes of epithelial cells in ileum
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3
Q

How would starch be digested?

A
  • amylase - starch –> maltose
  • maltase (MBD) - maltose –> glucose
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4
Q

What bonds are hydrolysed in carbohydrates?

A
  • glycosidic
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5
Q

What enzymes break down lipids?

A
  • lipases
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6
Q

Where are they made and where do they act?

A
  • made in pancreas
  • act in ileum
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7
Q

What other substance helps in digesting lipids?

A
  • bile salts
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8
Q

Where are they made and what do they do?

A
  • liver
  • emulsify fats to smaller drops to have a larger SA:V for a larger area for lipases to work on
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9
Q

What are lipids hydrolysed into?

A
  • monoglycerides and fatty acids
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10
Q

What bonds are hydrolysed in lipids?

A
  • ester
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11
Q

What can the products of lipids then form?

A
  • monoglycerides and fatty acids can stick with bile salts to form micelles
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12
Q

What enzymes break down proteins?

A
  • endopeptidases
  • exopeptidases
  • dipeptidases
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13
Q

What do endopeptidases do?

A
  • hydrolyse peptide bonds within the protein
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14
Q

What are examples of endopeptidases?
Where are they made and where do they act?

A
  • Trypsin, chymotrypsin
  • Made in pancreas and secreted into ileum
  • Pepsin
  • Released into stomach by cells in the stomach lining
  • Only works in acidic conditions - HCL in stomach
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15
Q

What so exopeptidases do?

A
  • Hydrolyse peptide bonds at the end of proteins
  • Remove single amino acids
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16
Q

What do dipeptidases do?

A
  • Exopeptidases that break up dipeptides
  • Hydrolyse the bond on the middle
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17
Q

Where are dipeptidases usually found?

A
  • Cell surface membrane of epithelial cells of ileum
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18
Q

What bonds are hydrolysed in proteins?

A
  • Peptide
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19
Q

How are monosaccharides absorbed?

A
  • Glucose absorbed by active transport with Na+ via cotransporter
  • Galactose absorbed the same with same cotransporter
  • Fructose uses facilitated diffusion with a different transport protein
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20
Q

How are monoglycerides and fatty acids absorbed?

A
  • Micelles help move them to the epithelium
  • Constantly break up and reform - release them to be absorbed
  • Easily move across membrane as they are lipid soluble
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21
Q

How are amino acids absorbed?

A
  • Na+ actively transported out of epithelial cells into blood
  • Makes conc gradient to ileum
  • Na+ diffuse from ileum into epithelial cells through sodium dependent transporter protein
  • Bring amino acids with them
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22
Q

What is the structure of haemoglobin?

A
  • Quaternary structure
  • 4 polypeptide chains
  • Each has a haem group (Fe2+)
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23
Q

How does O2 load to haemoglobin?

A
  • Each haemoglobin molecule can carry 4 O2 molecules
  • Loads in lungs to form oxyhaemoglobin
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24
Q

What is partial pressure?

A
  • Measure of concentration of a gas
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25
Q

How does pO2 affect O2 affinity of haemoglobin?

A
  • Higher pO2 = higher affinity = O2 loads on
  • Lower pO2 = lower affinity = O2 unloads
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26
Q

Where does O2 load and unload and why?

A
  • Loads in lungs - high pO2
  • Unloads at tissues - low pO2
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27
Q

What does a dissociation curve show?

A
  • How saturated the haemoglobin is with O2 at different partial pressures
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28
Q

What does the curve show at low pO2?

A
  • Low affinity
  • O2 released rather than loaded
  • Low O2 saturation
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29
Q

What does the curve show at high pO2?

A
  • High affinity
  • More readily combines than unloads
  • High O2 saturation
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30
Q

What is the shape of the dissociation curve and why?

A
  • S shaped
  • When first O2 molecule joins - shape changes to make it easier for others to load
  • As it gets more saturated - harder again to join
  • Steep bit in the middle - was easy to load
  • Shallow at each end - harder to load
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31
Q

How does CO2 affect O2 unloading?

A
  • Higher pCO2 at cells - lowers O2 affinity for Hb
  • O2 unloads more readily
  • Dissociation curve moves right - lower saturation for that pO2 so more O2 released
32
Q

What is this affect of CO2 called?

A
  • Bohr effect
33
Q

How is haemoglobin different for organisms in low O2 environments?

A
  • Higher affinity
  • Curve moves left
  • Need to load as much O2 as possible - lower pO2
34
Q

How is haemoglobin different in very active organisms?

A
  • High O2 demand
  • Lower affinity
  • Curve shifts left
  • Need to unload more readily to cells to respire
35
Q

Describe arteries

A
  • Thick and muscular walls
  • Elastic tissue - stretch and recoil as heart beats - maintain pressure
  • Folded endothelium - so artery can stretch - maintain pressure
36
Q

Describe arterioles

A
  • Divide off from arteries - direct blood to where it’s needed
  • Muscular walls - can contract - constrict flow or relax to maintain pressure
37
Q

Describe veins

A
  • Low pressure - carry blood back to heart
  • Wide lumen, little muscle or elastic
  • Valves - prevent backflow
  • Flow helped by contraction in body muscles around them
38
Q

Describe capillaries

A
  • Structured for exchange of substances
  • Close to cells - short diffusion pathway
  • One cell thick - short pathway
  • Large number & capillary beds - high SA
  • Narrow lumen - forces blood to slow - inc diffusion time
39
Q

How is tissue fluid formed?

A
  • Arteriole end - high hydrostatic pressure - fluid pushed out
  • Plasma proteins remain - too large to leave
  • Forms high solute conc = low water potential
  • Water does move back in but pressure is so high net movement is out of the capillary
40
Q

What happens to tissue fluid at the venule end?

A
  • Lower hydrostatic pressure and higher osmotic pressure
  • Water reabsorbed by osmosis
  • Useful materials have been taken in by cells and replaced with waste products
  • 90% reabsorbed - rest goes to lymphatic system and drains back into the blood near the heart
41
Q

Describe the atria

A
  • Thinner elastic walls
  • Stretch to collect blood and pump to ventricles
42
Q

Describe the ventricles

A
  • Thicker muscular walls to contract to pump blood
  • Left - thicker and more muscular - has to pump blood to body
  • Same internal volumes
43
Q

What valves are present in the heart?

A
  • Atrioventricular - between atria and ventricles - tricuspid (right) and bicuspid (left)
  • Semi lunar valves - between ventricles and aorta / pulmonary artery
44
Q

How do valves work?

A
  • Open one way
  • When there is a higher pressure behind - forced open
  • When a higher pressure is in front - forced closed - prevent backflow of blood
45
Q

What is the septum?

A
  • Separates left and right sides of the heart
  • Stops oxygenated and deoxygenated blood from mixing
46
Q

Describe diastole

A
  • All relaxed - Semi lunars close - higher pressure in aorta and pulmonary artery
  • Blood fills atria - pressure increases slightly
  • Pressure is greater in atria so AV open
  • Blood flows passively into ventricles
47
Q

Describe atrial systole

A
  • Ventricles are relaxed
  • Atria contract - blood pumped into ventricles as atrial volume dec so pressure inc
  • Ventricular pressure inc slightly as they gain blood
48
Q

Describe ventricular systole

A
  • Atria relax
  • Ventricles contract - dec volume, inc pressure
  • Pressure is higher in ventricles so AV close and SL open
  • Blood pumped out into arteries
49
Q

What makes the heart sounds?

A
  • Lubb - ventricles contract - AV close
  • Dubb - atria contract - SL shut
50
Q

What is the equation for cardiac output?

A

cardiac output = stroke volume x heart rate

51
Q

How does an atheroma form?

A
  • Endothelium of artery is damaged (e.g. by high blood pressure)
  • White blood cells, lipids from the blood clump under lining to make fatty streaks
  • Over time a fibrous plaque forms - WBC, lipids, connective tissue –> this is an atheroma
52
Q

What does an atheroma cause?

A
  • Partially blocks the lumen of the artery
  • Restricts blood flow
  • Blood pressure increases
53
Q

What is an aneurysm?

A
  • After an atheroma - blood at the now high pressures can push through the inner artery layers
  • Pushes through the outer artery to make a balloon-like swelling –> aneurysm
  • Can burst –> haemorrhage
54
Q

What is thrombosis?

A
  • Atheroma ruptures endothelium of the artery - damages the wall - leaves a rough surface
  • Platelets and fibrin collect at the damage - clots –> thrombosis
  • Can block artery
  • Can dislodge and block somewhere else
  • Can break a bit of and form a clot elsewhere
55
Q

What is a myocardial infarction?

A
  • Heart attack
  • Coronary artery blocks - heart O2 supply is stopped
  • Can damage and kills heart tissue
  • Pain in chest & upper body, shortness of breath, sweating
56
Q

How does a high cholesterol diet increase risk of heart disease?

A
  • High cholesterol = higher chance of fatty deposits –> inc blood pressure and risk of clots –> CHD
  • High sat fat diet = high cholesterol = fatty deposits
  • High salt = high blood pressure = high risk
57
Q

How is smoking a risk factor for heart disease?

A
  • Nicotine - increases risk of high blood pressure
  • Carbon monoxide - reduces O2 transport by binding to haemoglobin instead of O2 - reduced O2 = increased heart attack risk
58
Q

How does high blood pressure contribute to risk of heart disease?

A
  • Increased risk of damage to artery walls - increased atheroma risk - even higher blood pressure
  • Can cause clots and even CHD
  • Blood pressure can be increased by being overweight, lack of exercise, alcohol consumption
59
Q

How would you dissect a heart?

A
  • Lab coat, clean, sharp, rust free tools
  • Try to identify chambers of the heart and blood vessels and coronary arteries
  • Cut down right and left ventricles –> compare thicknesses of walls
  • Locate AV and SL valves
  • Wash hands and disinfect surfaces etc
60
Q

What do the xylem transport?

A
  • water and mineral ions
61
Q

What is the structure of the xylem?

A
  • Dead cells
  • End to end with no end walls –> uninterrupted flow
  • Lignin lining - waterproof polymer - provides structure
62
Q

What is transpiration?

A
  • Water evaporation from leaves via stomata - moves down water potential gradient
63
Q

What is cohesion - tension?

A
  • Water evaporates via transpiration
  • Tension is formed to pull water up and into leaves
  • Cohesion and adhesion means water moves up as a column
  • Water then enters the stem via the roots
64
Q

How does light affect transpiration?

A
  • More light = faster transpiration
  • Stomata open in light for gas exchange for photosynthesis
  • In dark - closed so little transpiration
65
Q

How does temperature affect transpiration?

A
  • Higher temperature = faster transpiration
  • Water molecules have more energy so evaporate faster
  • Increased concentration gradient inside and outside the leaf so diffuses out faster
66
Q

How does humidity affect transpiration?

A
  • Lower humidity = faster transpiration
  • Drier so steeper concentration gradient
  • Faster water loss
67
Q

How does wind affect transpiration?

A
  • Higher wind = faster transpiration
  • Air blows away water from around stomata
  • Increased concentration gradient so faster rate of loss
68
Q

How would you do the potometer investigation?

A
  • Cut shoot underwater so no air enters the xylem - cut at a slant for increased SA
  • Assemble the shoot and potometer underwater
  • Remove from the water leaving the end of the capillary tube under
  • Check water and air tight, dry the leaves and let the plant acclimatise then shut the tap
  • Remove the tube end and let a bubble form then put back in and record the starting position of the bubble
  • Start the stopwatch and record the bubble movement in a given time to find rate
69
Q

How would you dissect and observe a plant?

A
  • Use a scalpel to cut a cross section of the stem - thin for a microscope
  • Put in water with tweezers to stop them drying out
  • Stain with TBO to stain lignin
  • Rinse off the stain and put on a slide and observe
70
Q

What does phloem transport?

A
  • Solutes - mostly sugars
71
Q

What is the structure of phloem?

A
  • Sieve tube elements - living - no nucleus and few organelles
  • Companion cells - carry out living processes for them
72
Q

What is translocation?

A
  • Moves solutes source to sink - requires energy
  • Moves high to low conc
  • Source e.g. leaves
  • Sink e.g. meristems, roots, stem
  • Enzymes maintain conc gradient by changing solutes at the sink to something else e.g. sucrose –> starch
73
Q

Describe the mass flow hypothesis

A
  • Active transport solutes from companion cells into sieve tube - lowers water potential - water moves in - increases pressure
  • At sink solutes are removed - higher water potential - water moves out - decreases pressure
  • Solutes move down pressure gradient
74
Q

What evidence is there for mass flow?

A
  • Ringing - bulge forms above ring and has higher sugar conc - shows downward flow of sugars
  • Aphids - leave mouthparts - sap flows out quicker from near leaves - shows pressure gradient
  • Metabolic inhibitor (stops ATP production) - stops translocation - shows active transport is used
75
Q

What evidence is there against mass flow?

A
  • Sugar moves to many sinks not just the one with the highest water potential
  • Sieve plates would be a barrier to flow - would need lots of pressure to move at a reasonable rate
76
Q

What is the investigation using radioactive tracers?

A
  • Can use radioactive CO2 in a leaf - used in photosynthesis - sugars move in phloem
  • Track this using autoradiography - kill plant (freeze in liquid nitrogen) and put on photo film
  • Goes black where the radioactive substance is present
  • Can kill plants at different times to show movement leaves to roots