Topic 6 organisms respond to changes in their internal and external environment Flashcards

1
Q

What are taxes?

A

A directional response to a stimuli

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2
Q

What is kinesics?

A

Non-directional movement from an unfavourable area to a more favourable area e.g. in response to humidity
or temperature.

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3
Q

What is a tropism?

A

Directional growth in response to a stimuli.

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4
Q

What is the function of indolacetic acid (IAA)?

A
  • Controls plant cell elongation → increases cell wall plasticity.
  • High concentration of IAA increases cell elongation in shoots (shoots grow towards light → positive
    phototropism).
  • High concentration of IAA inhibits cell elongation in roots (roots bend away from light → negative
    phototropism).
  • Only young cells are able to elongate, mature cells are more rigid and so unable to respond.
  • Transport of IAA is in one direction → away from tip of root or shoot.
  • If root/shoot tips are removed → no response is seen, as source of IAA has been removed.
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5
Q

Explain phototropism in flowering plants

A
  1. Cells in tip of shoot produce IAA, which is evenly
    transported down the shoot.
  2. Light causes movement of IAA from light side to the
    shaded side of the shoot.
  3. Greater concentration of IAA on shaded shade than light
    side.
  4. Shaded side of shoot elongates faster than light side →
    shoot tip bends towards light.
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6
Q

Explain gravitropism in flowering plants

A
  1. Cells in tip of root produce IAA, which is evenly transported to
    all sides of root.
  2. Gravity causes movement of IAA from upper side to the lower
    side of the root.
  3. Results in greater concentration of IAA on lower side of root
    than the upper side.
  4. Cells on the lower side elongate less than cells on the upper
    side, causing the root to bend downwards towards the force of
    gravity (roots display positive gravitropism).
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7
Q

Reflex arc

A
  1. A RECEPTOR detects a STIMULUS.
  2. This generates a nerve impulse in a SENSORY NEURONE
    → passes nerve impulses to spinal cord.
  3. A RELAY NEURONE links the sensory neurone to the
    motor neurone in the spinal cord.
  4. A MOTOR NEURONE carries nerve impulses to an
    EFFECTOR.
  5. The effector (muscle or gland) brings about a RESPONSE.
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8
Q

Structure of the Pacinian corpuscle

A
  • Pacinian corpuscles contain a sensory nerve ending which is wrapped in layers of connective tissue called
    lamellae.
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9
Q

How is a generator potential created when a Pacinian corpuscle is stimulated?

A
  1. Pressure causes the lamellae to become deformed.
  2. Causes the sensory neurone’s cell membrane to stretch, which deforms the stretch-mediated sodium
    ion channels.
  3. The sodium ion channels open and sodium ions diffuse into sensory neurone cell.
  4. The influx of sodium ions depolarises the membrane, creating a generator potential (if generator
    potential reaches the threshold → triggers action potential).
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10
Q

How do photoreceptors convert light into an electrical impulse?

A
  1. Light enters eye and hits photoreceptors (of which there are two types, rods & cones).
  2. Light is absorbed by photosensitive optical pigments:
  • The pigment in rod cells is RHODOPSIN, which must be broken down to create a generator potential → low-
    intensity light transfers enough energy to break down rhodopsin.
  • The pigment in cone cells is IODOPSIN → requires higher intensity of light to breakdown and create a
    generator potential.
    3. The breakdown of the pigments, causes a change in the membrane permeability to sodium ions.
    4. A generator potential is created and if it reaches the threshold, a nerve impulse is sent along a bipolar neurone.
    5. Bipolar neurones connect photoreceptors to the optic nerve, which takes impulses to the brain.
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11
Q

Differences between rods and cones

A
  • Rods are found mainly in peripheral parts of retina, cones are concentrated at the fovea (receives the highest
    intensity of light).
  • Rods give poor visual acuity, cones give good visual acuity.
  • Rods are sensitive to low-intensity lights, cones are not.
  • Only one type of rod, but three types of cone (red, green and blue) → each responds to different wavelengths of
    light. Rod cells produce black and white vision, whereas stimulation of cone cells results in colour vision → colour
    that is seen is dependent on the proportion of each type of cone that is stimulated.
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12
Q

Difference in SENSITIVITY between rods and cones

A
  • RODS are MORE SENSITIVE to light than cones.
  • Rods fire action potentials in dim light because several rods are connected to a single neurone (retinal convergence)
  • So enough neurotransmitter is released to reach the threshold (many weak generator potentials can combine to reach
    the threshold and trigger an action potential) (= spatial summation).
  • Advantage? Still able to see in black and white in low light intensities → increase chance of survival.
  • Cones only fire action potentials in bright light because one cone connects to a single neurone, so more light is required
    to reach the threshold and trigger an action potential.
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13
Q

Difference in VISUAL ACUITY between rods and cones

A
  • CONES give HIGH VISUAL ACUITY whereas rods give low visual acuity.
  • Cones give high visual acuity because one cone connects to a single neurone, so cones send separate impulses to the
    brain.
  • Rods give low visual acuity because several rods connect to the same neurone → light from two points close together can’t
    be distinguished as separate.
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14
Q

How is heart rate controlled?

A
  1. Cardiac muscle is myogenic (= can contract and relax without receiving signals from nerves).
  2. Heart beat is initiated by the sinoatrial node (SAN) [located in the wall of the right atrium].
  3. SAN sends out waves of electrical activity to the atrial walls which cause the right and left atria to contract at
    the same time.
  4. The waves of electrical activity are passed from the SAN to the AVN (atrioventricular node).
  5. AVN passes the electrical activity on to the bundle of His [slight delay before the AVN reacts to ensure the atria
    have emptied before the ventricles contract].
  6. Bundle of His splits into Purkyne tissue, which carries the waves of electrical activity in the walls of the right and
    left ventricles, causing them to contract simultaneously, from the apex up.
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15
Q

High blood pressure

A
  • Baroreceptors detect high blood pressure.
  • Impulses sent to medulla, which sends impulses along PARASYMPATHETIC neurones.
  • Which secrete ACETYLCHOLINE.
  • Binds to specific receptors on SAN.
  • SAN reduces frequency that waves of electrical activity are sent out.
  • Heart rate decreases and blood pressure reduces back to normal.
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16
Q

Low blood pressure

A
  • Baroreceptors detect low pressure.
  • Impulses sent to medulla, which sends impulses along SYMPATHETIC neurones.
  • Which secrete NORADRENALINE.
  • Which binds to specific receptors on the SAN.
  • SAN increases frequency that waves of electrical activity are sent out.
  • Heart rate increases to increase blood pressure back to normal.
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17
Q
  • How does exercise affect heart rate?
A
  • Exercise involves muscle contraction, which requires respiration to produce ATP, therefore, CO2 is released into
    blood.
  • This lowers pH of blood.
  • This is detected by chemoreceptors.
  • Which send impulses to the medulla.
  • Medulla sends impulses to SAN via sympathetic nerves.
  • Sympathetic neurones secrete noradrenaline, which increases the frequency at which SAN sends out waves of
    electrical activity.
  • Causes heart rate to increase.
  • Advantage of this = increased blood flow to lungs to remove CO2 and take in O2.
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18
Q

What is the resting potential?

A
  • The membrane potential of a neurone when it is not being stimulated (approximately -70mV).
  • Results from there being more positively charged ions outside the neurone compared to inside.
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19
Q

How is the resting membrane potential created / re-established?

A
  • Na+/K+ pump actively transports 3 Na ions out of the axon and 2 K ions into the axon
  • K+ leak channels allow K+ ions to diffuse out (membrane more permeable to potassium ions)
  • Inside of axon is negatively charged compared to the outside
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20
Q

Explain the sequence of events that occur during an action potential

A
  1. Sodium ion channels open in response to a stimulus - so sodium ions diffuse INTO the axon. Inside of the
    axon is DEPOLARISED / becomes LESS NEGATIVE.
  2. If the potential difference reaches the THRESHOLD POTENTIAL (around -55mV), MORE sodium ion channels
    open and MORE sodium ions diffuse rapidly into the axon [example of POSITIVE FEEDBACK].
  3. At approx +40mV, sodium ion channels close and potassium ion channels open, so potassium ions diffuse
    OUT OF the axon down the potassium
    concentration gradient. This begins to
    REPOLARISE the membrane.
  4. Potassium ions channels are slow to
    close, so the membrane becomes
    HYPERPOLARISED because too many
    potassium ions diffuse out of the axon, so
    the potential difference becomes more
    negative than the resting potential.
  5. The sodium-potassium pump returns
    the membrane to its resting potential
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21
Q

What is the refractory period and why is it necessary?

A
  • During the refractory period, ion channels are RECOVERING and so CANNOT BE OPENED.
  • This important because it:
    1. Ensures action potentials pass along neurones as DISCRETE IMPULSES (don’t overlap).
    2. Ensures action potentials are UNIDIRECTIONAL.
    (The refractory period also LIMITS the FREQUENCY at which nerves impulses can be transmitted).
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22
Q

How does an action potential move along a neurone?

A
  • As a WAVE OF DEPOLARISATION.
  • Some of the sodium ions that diffuse into the neurone, diffuse sideways resulting in sodium ion channels in the
    next section of membrane to open and more sodium ions to diffuse into the axon.
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23
Q

How does the size of stimuli affect a nerve impulse?

A
  • Does not affect size of action potential → larger stimuli increase the FREQUENCY of action potentials.
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24
Q

What affects speed of nerve impulse?

A
  • TEMPERATURE: as temperature increases, the rate of diffusion of ions increases - faster nerve impulse [BUT
    above 40oC, proteins begin to denature and so speed decreases].
  • AXON DIAMETER: wider diameter, less resistance to the flow of ions → so faster nerve impulse.
  • MYELINATION:
  • Schwann cells wrap around axon forming the myelin sheath → acts as an electrical insulator → prevents
    the movement of ions into or out of the axon.
  • Between Schwann cells are patches of bare
    membrane called nodes of Ranvier.
  • In myelinated neurones, sodium ion
    channels are concentrated at the nodes
    so depolarisation can only happen at the
    nodes → action potentials jump from
    node to node → which speeds up
    transmission of nerve impulses.
  • This process is called saltatory conduction.
  • [action potentials pass along myelinated axon faster than along unmyelinated axons of the same diameter].
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25
Q

What does it mean by synpases are unidirectional?

A
  • Unidirectional = action potential travels in one direction, from pre-synaptic membrane to post-synaptic membrane
    (WHY? Because neurotransmitter only released from pre-synaptic membrane and only post-synaptic
    membrane has the receptors for neurotransmitter).
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26
Q

Describe how acetylcholine transmits a nerve impulse across a cholinergic synapse:

A
  1. Action potential arrives at the synaptic knob of the pre-synaptic neurone.
  2. Depolarisation of presynaptic membrane stimulates voltage-gated calcium ion channels in the pre-synaptic
    membrane to open.
  3. Calcium ions diffuse into synaptic knob (via facilitated diffusion).
  4. Influx of calcium ions causes synaptic vesicles containing acetylcholine to move to the presynaptic membrane,
    where they fuse with the membrane and release acetylcholine into the synaptic cleft by exocytosis.
  5. Acetylcholine diffuses across the synaptic cleft and binds to acetylcholine receptors (which are
    complementary to acetylcholine) on the post-synaptic membrane.
  6. Causes sodium ion channels to open in the post-synaptic membrane.
  7. Influx of sodium ions causes depolarisation of the post-synaptic membrane and an action potential is
    generated if the threshold is reached.
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27
Q

To return to rest: specific enzyme breaks down the neurotransmitter

A
  • e.g. acetylcholinesterase breaks down acetylcholine and the products are reabsorbed back into presynaptic neurone
    (ATP used to reform acetylcholine into vesicles and to actively transport Ca2+ ions out).
  • Acetylcholine must be removed from synaptic cleft to prevent continuous action potentials being fired → this enables
    discrete transfer of information across the synapse.
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28
Q

Temporaral summation

A

EMPORAL SUMMATION = when two or more nerve impulses arrive in quick succession from the
same presynaptic neurone, together resulting in sufficient neurotransmitter to be released into the
synaptic cleft to reach the threshold and trigger an action potential.

29
Q

Spatial summation

A

SPATIAL SUMMATION = many pre-synaptic neurones connect to one post-synaptic neurone,
altogether the neurotransmitter released from each neurone is enough to reach the threshold and trigger
an action potential.

30
Q

What is the difference between excitatory and inhibitory synapses?

A
  • Excitatory synapses cause action potentials, inhibitory synapses prevent action potentials from occurring by
    making the postsynaptic neurone hyperpolarised.
  • Inhibitory neurotransmitters = neurotransmitters which result in hyperpolarisation of the post-synaptic
    membrane e.g.
31
Q

Differences between cholinergic synapse and neuromuscular junctions?

A
  • Cholinergic synapse a synapse between two neurones, neuromuscular junction is a synapse between a motor
    neurone and a muscle cell.
  • Post synaptic membrane of a neuromuscular junction has lots of folds that form clefts. The clefts store
    acetylcholinesterase.
  • Post synaptic membrane of neuromuscular junctions has more receptors than other synapses.
  • Acetylcholine is always excitatory at a neuromuscular junction (whereas, acetylcholine can be inhibitory at e.g.
    cholinergic synapses in the heart).
  • When a motor neurone fires an action potential, it normally triggers a response in the muscle cell - this isn’t always
    the case for a synapse between 2 neurones.
32
Q

Why would a disease that destroys receptors at neuromuscular junctions lead to a weaker the normal muscular
response?

A
  1. Fewer receptors for acetylcholine to bind to.
  2. Fewer sodium channels will open in the post-synaptic membrane.
  3. Making it less likely that the threshold potential will be reached and so less likely that an action
    potential will be generated in the muscle cell.
33
Q

Gross and microscopic structure of a muscle fibre:

A
  • Each muscle is made of large bundles of long cells → muscle fibres → each fibre made up of a bundle of myofibrils.
  • Sarcolemma = cell membrane of a muscle fibre.
  • Sarcoplasm = a muscle cell’s cytoplasm.
  • Sarcoplasmic reticulum runs through the sarcoplasm and stores calcium ions for muscle contraction.
  • T-tubules = folds of the sarcolemma which stick into the sarcoplasm → help to spread electrical impulses through
    the sarcoplasm so they reach all parts of the muscle fibre.
  • Muscle fibres have lots of mitochondria (to provide the ATP for muscle contraction) and are multinucleate
    (contain lots of nuclei).
34
Q

Structure of a myofibril

A
  • Myofibrils contain bundles of thick and thin
    myofilaments.
  • Thick myofilaments are made of myosin.
  • Thin myofilaments are made of actin.
  • A-band: dark bands which contain myosin and some
    overlapping actin filaments.
  • I bands: light bands which contain ONLY actin
    filaments.
  • H-zone: contains only myosin filaments.
  • Myofibrils are made up of many sarcomeres, the ends
    of each sarcomere are marked with a Z-line.
35
Q

How do the lengths of the different bands in a myofibril change during muscle contraction?

A
  • A bands stay the same length.
  • I band gets shorter.
  • H zones get shorter.
  • Z lines move closer together.
36
Q

Sliding filament theory / how an impulse in a motor neurone stimulates contraction of a myofibril:

A
  • Acetylcholine is released from the presynaptic membrane and diffuses across the synapse.
  • Acetylcholine binds to specific receptors on the sarcolemma (post-synaptic membrane).
  • The muscle sarcolemma is depolarised (due to influx of sodium ions).
  • Depolarisation spreads along the muscle fibre.
  • Causes calcium ions to be released from the sarcoplasmic reticulum into the sarcoplasm.
  • Calcium ions displace tropomyosin, and so uncover the myosin binding sites on the actin filaments, which allows
    the myosin heads to bind.
  • This bond is called an actin-myosin cross bridge.
  • Myosin heads bend (releasing a molecule of ADP which was attached to the myosin head) and pull the actin
    filament along, which shortens the sarcomere and contracts the muscle.
  • An ATP molecule attaches to each myosin head, causing it to become detached from the actin filament.
  • Calcium ions activate ATP hydrolase providing the energy for myosin heads to return to their original position.
  • Myosin heads reattach further along the actin filament.
  • The cycle will continue as long as calcium ions are present.
37
Q

Describe the role of Ca2+ ions and ATP in muscle contraction:

A
  • Ca2+ ions cause the tropomyosin to move, exposing myosin-binding sites on actin.
  • Ca2+ ions stimulate ATP hydrolase.
  • ATP causes myosin head to bend / detach.
  • ATP actively transports Ca2+ ions back into sarcoplasmic reticulum when the muscle is relaxed.
38
Q

What happens when the muscle stops being stimulated?

A
  • Calcium ions leave their binding sites and are actively transported back into the sarcoplasmic reticulum.
  • Tropomyosin moves back and blocks the actin-myosin binding sites.
  • Actin filaments slide back to their relaxed position → lengthens the sarcomere.
39
Q

What causes cross-bridges to remain bound in rigor mortis?

A
  • Respiration stops, so no ATP production.
  • ATP is required for separation of the actin and myosin cross bridge.
40
Q

Role of ATP and phosphocreatine in muscle contraction:

A
  • ATP is made by phosphorylating ADP using a phosphate group taken from PCr.
  • Advantages =
  • PCr can be stored inside cells (unlike ATP)
  • ATP-PCr system can generate ATP very quickly.
  • ATP-PCr system is anaerobic (doesn’t need oxygen).
  • ATP-PCr system is alactate (doesn’t produce lactate).
  • Disadvantages = PCr runs out after a few seconds so it can only be used during short bursts of very vigorous
    exercise.
41
Q

Slow twitch muscles

A
  • Contract slowly
  • Muscles used for posture
  • Good for endurance activities
  • Can work for a long time without getting tired
  • Lots of mitochondria and blood vessels for energy to be released slowly through aerobic respiration
  • Reddish colour due to myoglobin - a protein that stores oxygen
42
Q

Fast twitch muscle fibres

A
  • Contract quickly
  • Muscles moved for fast movement
  • Good for short bursts of speed
  • Get tired quickly
  • Few mitochondria or blood vessels so energy is released quickly through anaerobic respiration
  • Whittish in colour don’t have much myoglobin therefore can’t store much oxygen
43
Q

What is homeostasis?

A

Homeostasis = maintaining a constant internal environment in response to changes in the internal and
external environment.

44
Q
  • Why is it important to maintain a stable blood glucose concentration?
A
  • If blood glucose concentration is too high:
  • Water potential of the blood is reduced.
  • Water moves from cells into blood by osmosis.
  • Cells shrivel and die.
  • If blood glucose concentration is too low:
  • Water potential of the blood is increased.
  • Water moves into cells by osmosis.
  • Cells swell and possibly burst.
  • Also, a constant blood glucose level ensures a reliable source of respiratory substrate.
45
Q

What type of cells secrete glucagaon?

A

Alpha cells secrete glucagon into blood

46
Q

What type of cells secrete insullin?

A

Beta cells secrete insullin into blood

47
Q

Glycogenesis

A

Process by which glucose is converted to glycogen

48
Q

Glycogenolysis

A

Process by which glycogen is converted to glucose

49
Q

Gluconeogenesis

A

Process by which glucose is fomed from non-carbohydrates

50
Q

What happens when blood glucose levels are TOO HIGH?

A
  • Islets of Langerhans detect change in blood glucose level.
  • Insulin is released by beta cells and binds to specific receptors on muscle cells and liver cells
  • Causes increase in the permeability of membranes to glucose by increasing the number of channel proteins in
    cell surface membranes of target cells.
  • Activates enzymes which convert glucose into glycogen for storage (glycogenesis).
  • Increases rate of respiration of glucose.
  • Blood glucose concentration decreases → causes the beta cells to reduce secretion of insulin (= negative
    feedback).
51
Q

What happens when blood glucose levels are TOO LOW e.g. after exercise?

A
  • Islets of Langerhans detect change in blood glucose level.
  • Glucagon is released by alpha cells and binds to specific receptors on liver cells (only).
  • This activates enzymes which convert glycogen into glucose (glycogenolysis) AND activates enzymes which
    convert glycerol and amino acids into glucose (gluconeogenesis)
  • Rate of respiration of glucose in cells is decreased.
  • Blood glucose concentration increases → causes alpha cells to reduce the secretion of glucagon (= negative
    feedback).
52
Q

Adrenaline

A
  • Secreted from adrenal glands when blood glucose concentration is low / due to stress / during exercise.
  • Binds to receptors on the cell membrane of liver cells - activates glycogenolysis and inhibits glycogenesis.
  • Activates glucagon secretion and inhibits insulin secretion → increases glucose concentration.
  • Makes more glucose available for muscles to respire → gets the body ready for action.
53
Q

How do glucagon and adrenaline activate glycogenolysis inside the cell, when they bind to receptors on the outside of the cell (Second Messenger Model)?

A
  • Adrenaline and glucagon bind to complementary receptors on cell surface membrane of target cell.
  • Activates adenylate cyclase.
  • Activated adenylate cyclase converts ATP into cAMP, which is a second messenger.
  • cAMP activates protein kinase A.
  • Protein kinase A activates a cascade of reactions that results in glycogenolysis.
54
Q

Type 1 diabetes

A

Type 1 usually diagnosed at young age → beta cells destroyed by an autoimmune disorder so person doesn’t
make insulin (treatment = insulin injections, carbohydrate controlled diet).

55
Q

Type 2 diabetes

A
  • Type 2 normally presents > age 40 → person makes insulin but cells are less sensitive to insulin, caused by
    obesity and poor diet (treatment = carbohydrate controlled diet, exercise, drugs).
56
Q

Structure of the nephron

A
  • Each nephron is made up of a Bowman’s capsule which contains a knot of blood vessels called the glomerulus.
  • Bowman’s capsule is attached to the proximal convoluted tubule (PCT),
  • Which leads to the loop of Henle,
  • Which leads onto the distal
    convoluted tubule (DCT),
  • Which leads to the collecting
    duct.
57
Q

Formation of Glomerular Filtrate

A
  1. Produced by ultrafiltration [filtration assisted by blood pressure].
  2. Blood in the glomerulus is under high hydrostatic pressure because afferent arteriole is wider than the efferent
    arteriole.
  3. This forces liquid and small molecules [such as glucose/ions/urea] in the blood out of pores in the capillary
    endothelium and through the basement membrane into the Bowman’s capsule.
  4. Large proteins and blood cells can’t pass through because they are too large, so they remain in the blood.
58
Q

Site of selective reabsorption

A
  • Site of selective reabsorption = PCT (around 85% of filtrate is reabsorbed in the PCT).
  • When the filtrate reaches the PCT, useful substances [such as glucose, amino acids, vitamins and ions] are
    reabsorbed by facilitated diffusion and active transport into the blood.
59
Q
  • How are the epithelial cells lining the PCT adapted to reabsorb substances?
A
  • Microvilli to provide a large surface area for the reabsorption of substances from the filtrate.
  • Infoldings at their bases to give a large surface area to transfer reabsorbed substances into the capillaries.
  • Many mitochondria to provide ATP for active transport.
  • Many carrier proteins/channel proteins for active transport/co-transport.
60
Q

How are useful substances reabsorbed?

A
  • Sodium ions are actively transported from cells lining the PCT into the blood.
  • This lowers the sodium ion concentration in the cells → sodium ions diffuse from the lumen of the PCT into the
    cells, taking glucose (for example) with them, via co-transport.
  • The glucose concentration increases inside the cell and glucose moves via facilitated diffusion into the blood.
  • The movement of salt/glucose/amino acids into the blood, lowers the water potential of the blood, so water
    follows by osmosis.
61
Q

Why can a high blood glucose concentration cause glucose to be present in the urine of a diabetic person?

A

The high concentration of glucose in the filtrate results in the glucose protein carriers becoming saturated,
therefore not all of the glucose is selectively reabsorbed from the filtrate and some glucose ends up in the urine.

62
Q

Role of loop of Henle in the reabsorption of water:

A
  1. Loop of Henle acts as a counter-current multiplier.
  2. Sodium (and chloride) ions are actively transported out of the ascending limb of the loop of Henle into the
    surrounding medulla (ascending limb is impermeable to water, so water remains in the tubule).
  3. This lowers the water potential of the medulla.
  4. Water moves out of the filtrate in the descending limb by osmosis (because the descending limb is permeable
    to water), into the medulla.
  5. This water is reabsorbed into the blood via capillaries.
63
Q

Different animals have different length loops of Henle

A
  • Animals living in dry environments have longer loops of Henle, to produce a larger countercurrent
    multiplier.
  • Therefore more sodium (and chloride) ions are actively transported out of the filtrate into the medulla.
  • This results in an even more negative water potential in the medulla.
  • Therefore more water is absorbed by osmosis into the blood.
  • Only a small volume of very concentrated urine is produced.
64
Q

If blood water level becomes LOW

A
  • Water potential of blood decreases [hypertonic].
  • Osmoreceptors in hypothalamus shrink.
  • Stimulates the release of ADH from the posterior pituitary gland.
  • ADH stimulates the cells lining the DCT and collecting duct to increase the number of aquaporins (water
    channels), making them more permeable to water.
  • So more water is reabsorbed by osmosis from the DCT/collecting duct into blood.
  • Less water is lost in the urine (smaller volume of more concentrated urine produced).
65
Q

If blood water levels become HIGH

A
  • Water potential of blood increases [hypotonic].
  • Osmoreceptors in hypothalamus swell.
  • Stimulates the posterior pituitary gland to secrete less ADH.
  • DCT and collecting duct become less permeable to water (due to presence of fewer aquaporins).
  • So less water is reabsorbed by osmosis from collecting duct into blood.
  • More water lost in urine (larger volume of more dilute urine produced)
66
Q

What substances are present in the urine?

A

Water, excess ions, urea, hormones, excess vitamins etc.

67
Q

What should NOT be found in the urine under normal circumstances?

A
  1. Proteins and blood cells (too large to be filtered out of the blood)
    * If these are present in blood, suggests damage to basement membrane (caused by e.g. chronic high blood
    pressure)
  2. Glucose (should be actively reabsorbed back into the blood)
    * If present in urine, suggest diabetes (carrier proteins saturated due to high blood glucose levels).
68
Q

Explain how resting potential is maintained?

A

Sodium-potassium pump actively transports 3 sodium ions out of axon and 2 potassium ions into the axon the membrane is more permeable to K ions so they diffuse out of axon

69
Q

What substances are selectively reabsorbed in the PCT?

A

Water and glucose