1 Exchange And Transport Systems Flashcards

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1
Q

Describe the relationship between size and surface area to volume ratio.

A
  • if organism has large volume, its surface area is relatively small, this makes it harder for it to lose heat from its body.
  • if organism is small its relative surface area is large, so heat lost more easily. This means smaller organisms need relatively high metabolic rate in order to generate enough heat to stay warm.
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2
Q

What 3 things to organisms exchange with the environment.

A
  • oxygen
  • waste products
  • heat
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3
Q

Describe adaptations in organisms to aid exchange.

A
  • animals with high SA:volume ratio tend to lose more water as evaporates from their surface. Some small dessert animals have kidney structure adaptations so that produce less urine to compensate.
  • to support high metabolic rates, small organisms living in cold regions need to eat large amounts of high energy foods.
  • larger organisms living in hot regions find hard to keep cool as heat loss relatively slow. Elephants developed large flat ears to increase SA, allowing them to lose more heat.
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4
Q

Describe adaptations of gas exchange surfaces, shown by gas exchange across body surface of singe-celled organism.

A
  • singe-celled organisms absorb and release gases by diffusion through outer surface.
  • have relatively large surface area, thin surface and short diffusion pathway, so no red for gas exchange system.
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5
Q

Describe adaptations of gas exchange surfaces, shown by gas exchange in tracheal system of an insect.

A
  • air enters trachea through pores on surface called spiracles.
  • oxygen diffuses down concentration gradient along trachea
  • trachea branch off into smaller tracheoles with thin, permeable walls and go to individual cells, means oxygen diffuses directly into respiring cells
  • carbon dioxide from cells moves down its own concentration gradient towards spiracles to be released.
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6
Q

Describe adaptations of gas exchange surfaces, shown by gas exchange across gills of fish.

A
  • filaments and lamellae have big surface area, increases efficiency of diffusion
  • lamellae have lots of blood capillaries and thin surface layer of cells so short diffusion distance.
  • blood flows through lamellae in one direction, water flows over in opposite direction. (Counter-current system)
  • maintains high concentration gradient between water and blood.
  • concentration of oxygen in water always higher than that in blood, so as much oxygen as possible diffuses from water into blood.
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7
Q

Describe adaptations of gas exchange surfaces, shown by gas exchange by the leaves of dicotyledonous plants.

A
  • main gas exchange surface is surface of mesophyll cells in leaf. Well adapted as have a large surface area.
  • mesophyll cells are inside leaf. Gases move in and out through stomata.
  • stomata can open to allow exchange of gases, and close to prevent water loss.
  • guard cells control opening and closing of stomata. Water enters Guard cell making it turgid which opens stomata, plant gets dehydrated guard cells lose water become flaccid and closes stomata.
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8
Q

How do insects control water loss.

A
  • if insects losing too much water, they close their spiracles.
  • also have waterproof waxy cuticle all over body and tiny hairs around spiracles, both of which reduce evaporation.
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9
Q

Describe the adaptations of xerophytes for controlling water loss

A
  • stomata sunk in pits that trap moist air, reducing the concentration gradient of water between leaf and air. This reduces amount of water diffusing out of leaf and evaporating away.
  • layer of hairs on epidermis, trap moist air around stomata.
  • curled leaves with stomata inside, protecting them from wind.
  • reduced number of stomata, so fewer places for water to escape.
  • waxy, waterproof cuticles on leaves and stems reduce evaporation.
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10
Q

Describe the structure of the human gas exchange system.

A
  • air enters trachea
  • trachea splits into 2 bronchi, 1 bronchus leading to each lung
  • each bronchus branches off into bronchioles
  • bronchioles end in alveoli.
  • rib cage, intercostal muscles and diaphragm work together to move air in and out.
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11
Q

Explain gaseous exchange in the alveoli.

A
  • huge number of alveoli in lungs, so big surface area for exchanging O2 and CO2
  • alveoli surrounded by network of capillaries
  • O2 diffuses out of alveoli across alveolar epithelium (Only 1 cel thick,short diffusion pathway )and capillary epithelium, and into haemoglobin in blood
  • CO2 diffuses into alveoli from blood, and is breathed out.
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12
Q

Describe inspiration.

A
  • external intercostal + diaphragm muscles contract
  • causing rib cage to move upwards and outwards and diaphragm to flatten, increasing volume of thoracic cavity
  • as volume of thoracic cavity increases, lung pressure decreases
  • air flows from area of high pressure to low pressure so air flows down trachea into lungs
  • inspiration is an active process, requires energy.
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13
Q

Describe expiration.

A
  • external intercostal + diaphragm muscles relax
  • rib cage moves downwards and inwards and diaphragm becomes curved again
  • volume of thoracic activity decreases causing air pressure to increase
  • air forced down pressure gradient and out of lungs
  • normal expiration is passive process, doesn’t require energy.
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14
Q

What occurs during digestion.

A

Large biological molecules are hydrolysed to smaller molecules that can be absorbed across cell membranes.

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15
Q

Explain how carbohydrates are broken down by amylase and membrane-bound disaccharidases.

A
  • enzyme amylase catalysed conversion of starch into smaller sugar maltose. Involves hydrolysis of glycosidic bonds in starch.
  • amylase produced by salivary glands and by pancreas.
  • membrane-bound disaccharidases are enzymes that are attached to cell membranes of epithelial cells lining the ileum. They help to break down disaccharides into monosaccharides, involves hydrolysis of glycosidic bonds.
  • monosaccharides transported across cell membranes of ileum epithelial cells via specific transporter proteins.
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16
Q

Explain how lipids are broken down by lipase.

A
  • enzyme lipase catalysed breakdown of lipids into monoglycerides and fatty acids. Involves hydrolysis of ester bonds in lipids.
  • lipases made in pancreas. Work in small intestine.
  • bile salts produced by liver and emulsify lipids, means they cause lipids to form small droplets.
  • several small lipid droplets have bigger surface area than single large droplet, so formation of small droplets greatly increases surface are of lipid that’s available for lipases to work on.
  • once lipid has been broken down, monoglycerides and fatty acids stick with bile salts to form tiny structures called micelles.
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17
Q

Why are micelles important in absorption of lipids.

A
  • micelles help to move monoglycerides and fatty acids towards epithelium.
  • because micelles constantly break up and reform they ‘release’ monoglycerides and fatty acids, allowing them to be absorbed- whole micelles no taken up across epithelium.
  • monoglycerides and fatty acids are lipid-soluble so can diffuse directly across epithelial cell membrane.
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18
Q

Explain how proteins a broken down by endopeptidases and exopeptidases.

A
  • endopeptidases act to hydrolyse peptide bonds within a protein.
  • exopeptidases act to hydrolyse peptide bonds at the ends of protein molecules. They remove single amino acids from proteins.
  • dipeptidases are exopeptidases that work specifically on dipeptides. They act to separate the 2 amino acids that make up a dipeptide by hydrolysing the peptide bonds between them. Located in cell-surface membrane of epithelial cells in small intestine.
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19
Q

Explain co-transport mechanisms for the absorption of amino acids and of monosaccharides.

A
  • glucose absorbed by active transport with sodium ions via a co-transporter protein. Galactose absorbed in same way using same co-transporter protein
  • fructose absorbed via facilitated diffusion through different transporter protein.
  • sodium ions actively transported out of epithelial cells into ileum. They then diffuse back into cells through sodium-dependent transporter proteins in epithelial cell membranes, carrying amino acids with them.
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20
Q

What are the haemoglobin’s.

A

A group of chemically similar molecules found in many different organisms. Haemoglobin is a protein with a quaternary structure.

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21
Q

Explain how haemoglobin is different in different organisms.

A
  • organisms living in environments with low concentration of oxygen have haemoglobin with higher affinity for oxygen than human human haemoglobin, dissociation curve to left of human one.
  • very active organisms that have high oxygen demand have haemoglobin with a lower affinity for oxygen than human haemoglobin, dissociation curve to right of human one.
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22
Q

Describe the effect of carbon dioxide on the dissociation of oxyhaemoglobin.

A
  • when cells respire they produce CO2 with raises partial pressures of CO2.
  • this increases rate of oxygen unloading i.e. the rate at which oxyhaemoglobin dissociates to form haemoglobin and oxygen. So dissociation curve shifts right.
  • saturation of blood with oxygen is lower for a given partial pressure of O2, meaning more oxygen being released.
  • this called Bohr effect.
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23
Q

Describe the structure of arteries In relation to their function.

A
  • carry blood from heart to rest of body.
  • thick, muscular walls have elastic tissue to stretch and recoil as heart beats, helps maintain high pressure.
  • endothelium folded, allowing artery stretch, helps to maintain high pressure
  • all arteries carry oxygenated blood except for pulmonary artery, which takes deoxygenated blood to lungs
24
Q

Describe the structure of arterioles In relation to function.

A

Blood directed to different areas of demand in body by muscles inside aterioles , which contract to restrict blood flow or relax to allow full blood flow.

25
Q

Describe the structure of veins in relation to function.

A
  • take blood back to heart under low pressure.
  • wider lumen than equivalent arteries, with very little elastic or muscle tissue.
  • contain valves to stop back-flow of blood.
  • blood flow through veins helped by contraction of the body’s muscles surrounding them.
  • carry deoxygenated blood except for pulmonary veins which carry oxygenated blood to heart from lungs.
26
Q

Describe the structure of capillaries and the importance of capillary beds as exchange surfaces.

A
  • always found near cells in exchange tissues, so there’s a short diffusion pathway.
  • walls only one cell thick, shortens diffusion pathway.
  • large number of capillaries, to increase surface area for exchange.
  • networks of capillaries in tissue called capillary beds.
27
Q

Describe how tissue fluid is formed.

A
  • hydrostatic pressure is higher in blood than in tissue fluid.
  • water and small molecules force out forming tissue fluid.
  • large molecules stay inside the capillary.
28
Q

Describe how tissue fluid is returned to the circulatory system.

A
  • water potential in blood becomes lower than water potential in tissue fluid.
  • because proteins remain in blood.
  • water moves into capillary by osmosis.
  • hydrostatic pressure drops in capillary, water moves in down pressure gradient.
  • tissue fluid drains into lymph.
29
Q

Describe the structure of the heart related to it’s function.

A
  • left ventricle thicker + more muscular than right ventricle as needs to contract powerfully to pump blood all way around body.
  • ventricles have thicker walls than atria, as have to push blood out of heart whereas atria need to push blood short distance into ventricles.
  • AV valves link atria to ventricles and stop back-flow of blood into atria when ventricles contract.
  • SL valves link ventricles to pulmonary artery and aorta, stop back flow of blood into heart after ventricles contract.
  • cords attach atrioventricular valves to to ventricles to stop them being forced up into atria when ventricles contract.
30
Q

Describe the xylem.

A

The tissue that transports water in the stem and leaves of plants. Xylem vessels are long tube-like structures formed from dead cells joined end to end.

31
Q

Explain the cohesion’s-tension theory of water transport in the xylem.

A
  • water evaporates from leaves at ‘top’ of xylem.
  • this creates tension, which pulls more water into leaf.
  • water molecules are cohesive so when some are pulled into leaf others follow. This means whole column of water in xylem moves upwards.
  • water enters stem through roots.
32
Q

Describe the phloem.

A

The tissue that transports organic substances in plants.

33
Q

Explain the mass flow hypothesis.

A

Source- high concentration of solute.

  • active transport of solute from companion cell into sieve tube cell
  • this decreases water potential
  • water moves in by osmosis from companion cell and xylem
  • creates high hydrostatic pressure.
  • at sink end, solutes removed from phloem to be used up
  • this increases water potential inside sieve tubes, so water also leaves tubes by osmosis.
  • this lowers pressure inside sieve tubes
  • result is pressure gradient from source end to sink end
  • this gradient pushes solutes along sieve tubes towards sink, when they reach solutes will be used or stored.
34
Q

Explain the first step of the cardiac cycle.

A
  • ventricles relaxed
  • atria contract, decreasing volume of chambers and increasing pressure inside chambers. This pushes blood into ventricles.
  • slight increase in ventricular pressure and chamber volume as ventricles receive the ejected blood from contracting atria.
35
Q

Explain the second step of the cardiac cycle.

A
  • atria relax
  • ventricles contract decreasing their volume, increasing their pressure.
  • pressure becomes higher in ventricles than atria, forces AV valves shut to prevent back-flow
  • pressure in ventricles higher than aorta and pulmonary artery, forces open SL valves and blood forced out into these arteries.
36
Q

Explain the third step in the cardiac cycle.

A
  • ventricles and atria relax.
  • higher pressure in pulmonary artery and aorta closes SL valves
  • blood returns to heart and atria fill again due to higher pressure in vena cava + pulmonary vein. This starts to increase pressure of atria.
  • as ventricles continue to relax, their pressure falls below pressure of atria so AV valves open. Allows blood to flow passively into ventricles for atria. Atria contract and whole process begins again
37
Q

Define tidal volume.

A

The volume of air in each breath.

38
Q

Define ventilation rate.

A

The number of breaths per minute.

39
Q

Define forced expiratory volume.

A

The maximum volume of air that can be breathed out in 1 second

40
Q

Define forced vital capacity

A

Maximum volume of air it is possible to breathe forcefully out of the lungs after a really deep breath in.

41
Q

What is TB ?

A
  • when someone becomes infected with tuberculosis bacteria, immune system cells build a wall around bacteria in lungs. This forms small, hard lumps (tubercles).
  • infected tissue within the tubercles dies+ gaseous exchange surface damaged, so tidal volume decreased
  • tuberculosis also causes fibrosis, which further reduces tidal volume
42
Q

How does TB affect breathing?

A
  • reduced tidal volume means less air can be inhaled with each breath. In order to take in enough oxygen, patients have to breathe faster, ie ventilation rate is increased.
  • common symptoms include: persistent cough, coughing up blood and mucus, chest pains, shortness of breath and fatigue.
43
Q

What is fibrosis?

A
  • it’s the formation of scar tissue in the lungs. Can be the result of an infection or exposure to substances like asbestos or dust.
44
Q

How does fibrosis affect breathing?

A
  • scar tissue is thicker and less elastic than normal tissue
  • means that lungs are less able to expand and so can’t hold as much air as normal, tidal volume reduced and so is FVC
  • reduction in gaseous exchange, diffusion slower across thicker scarred membrane.
  • symptoms: shortness of breath, dry cough, chest pain, fatigue and weakness
  • fibrosis sufferers have faster ventilation rate than normal to get enough air into their lungs to oxygenate their blood
45
Q

What is asthma?

A

A respiratory condition where the airways become inflamed and irritated. Causes vary from case to case but it’s usually because of an allergic reaction to substances such as pollen or dust.

46
Q

How does asthma affect breathing?

A
  • during asthma attack, smooth muscle lining the bronchioles contracts and a large amount of mucus is produced.
  • causes constriction of airways making it difficult for sufferer to breathe properly. Air flow in + out of lunges severely reduced, so less oxygen enters alveoli and moves into blood. Reduced airflow means FEV1 is severely reduced.
  • symptoms: wheezing, tight chest, shortness of breath. During an attack symptoms come on suddenly. Can be relieved by drugs which cause muscle in bronchioles to relax, opening up airways.
47
Q

What is emphysema?

A

A lung disease caused by smoking or long term exposure to air pollution

48
Q

How does emphysema affect breathing?

A
  • foreign particles in smoke or air become trapped in alveoli. Causes inflammation, which attracts phagocytes to the area. Phagocytes produce protein that breaks down elastin
  • elastin is elastic, helps alveoli to return to normal shape after inhaling and exhaling air
  • loss of elastin means alveoli can’t recoil to expel air as well
  • also leads to destruction of alveoli walls, which reduces SA of alveoli, so rate of gaseous exchange decreases
  • symptoms: shortness of breath and wheezing. People with emphysema have increased ventilation rate as they try to increase the amount of air reaching their lungs.
49
Q

Most cardiovascular diseases start with atheroma formation…

A
  • wall of artery made up of several layers
  • endothelium usually smooth and unbroken
  • if damage occurs to endothelium white blood cells and lipids from blood, clump together under lining to form fatty streaks.
  • over time, more white blood cells, lipids and connective tissue build up + harden to form a fibrous plaque called an atheroma.
  • this plaque partially blocks lumen of artery abs restricts blood flow, which causes blood pressure to increase
  • coronary heart disease occurs when coronary arteries have lots of atheroma sin them, which restricts blood flow to heart muscle. Can lead to myocardial infarction.
50
Q

How does atheroma increase risk of aneurysm?

A

Aneurysm- a balloon like swelling of the artery

  • atheroma plaques damage and weaken arteries. They also narrow arteries, increasing blood pressure
  • when blood travels through a weakened artery at high pressure, it may push inner layers of the artery through the outer elastic layers to form aneurysm
  • aneurysm may burst causing a haemorrhage
51
Q

How does atheroma increase risk of thrombosis?

A
  • atheroma plaque can rupture endothelium of an artery
  • this damages artery wall + leaves rough surface
  • platelets and fibrin accumulate are site of damage and form blood clot
  • blood clot can cause complete blockage of artery, or it can become dislodged and block blood vessel elsewhere in body
  • debris from rupture can cause another blood clot to form further down the artery.
52
Q

How does interrupted blood flow to the heart cause a myocardial infarction?

A
  • heart muscle supplied with blood by the coronary arteries
  • this blood contains oxygen needed by heart muscles to carry out respiration
  • if coronary artery becomes completely blocked area of heart will be cut off from its blood supply, receiving no oxygen
  • this causes myocardial infarction (heart attack)
  • heart attack can cause damage and death of heart muscle
  • symptoms: pain in chest and upper body, shortness of breath and sweating.
53
Q

How does high blood cholesterol and poor diet increase risk of cardiovascular disease?

A
  • if blood cholesterol level high, risk of cardiovascular disease increased
  • because cholesterol is one of main constituents of the fatty acids that form atheromas
  • atheromas can lead to increased blood pressure + blood clots
  • this could block flow of blood to coronary arteries, which could cause myocardial infarction
  • diet high in saturated fat associated with high blood cholesterol levels
  • diet high in salt also increases risk of cardiovascular disease because it increases risk of high blood pressure.
54
Q

How does cigarette smoking increase the risk of cardiovascular disease?

A
  • both nicotine and carbon monoxide, found in cigarette smoke, increase risk of cardiovascular disease
  • nicotine increases risk of high blood pressure
  • carbon monoxide combines with haemoglobin and reduces amount of oxygen transported in blood, so reduces amount of oxygen available to tissues
  • if heart muscles don’t receive enough oxygen can lead to heart attack
  • smoking also decreases amount of antioxidants in blood, these important for protecting cells from damage. Fewer antioxidants means cell damage inn coronary artery walls is more likely, this can lead to atheroma formation.
55
Q

How does high blood pressure increase risk of cardiovascular disease?

A
  • high blood pressure increases risk of damage to artery walls
  • damaged walls have an increased risk of atheroma formation, causing further increase in blood pressure
  • atheromas can cause blood clots to form
  • blood clot could block flow of blood to heart muscle, possibly resulting in myocardial infarction
  • so anything that increase blood pressure also increases risk of cardiovascular disease.