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Y13 Biology > 6. Responding to Changes in Environment > Flashcards

6. Responding to Changes in Environment Flashcards

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1
Q

What is a stimulus?

A

A change in an organisms internal or external environment

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2
Q

Why is it important that organisms can respond to stimuli?

A

Organisms increase their chance of survival by responding to stimuli

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3
Q

What is a tropism?

A
  • Growth of a plant in response to a directional stimulus
  • Positive tropism = towards a stimulus, negative tropism = away from a stimulus
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4
Q

Summarise the role of growth factors in flowering plants

A
  • Specific growth factors (hormone-like growth substances) e.g auxins (such as IAA) move (via phloem or diffusion) from growing regions e.g shoot/root tips where they’re produced
  • To other tissues where they regulate growth in response to directional stimuli (tropisms)
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5
Q

Describe how IAA affects cells in roots and shoots

A
  • In shoots, high concentrations of IAA stimulates cell elongation
  • In roots, high concentrations of IAA inhibits cell elongation
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6
Q

Explain gravitropism in flowering plants

A
  1. Cells in tip of shoot/root produce IAA
  2. IAA diffuses down shoot/root (evenly initially)
  3. IAA moves to lower side of shoot/root (so concentration increases)
  4. In shoots this stimulates cell elongation whereas in roots this inhibits cell elongation
  5. So shoots bend away from gravity whereas roots bend towards gravity
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7
Q

Explain phototropism in flowering plants

A
  1. Cells in tip of shoot/root produce IAA
  2. IAA diffuses down shoot/root (evenly initially)
  3. IAA moves to shaded side of shoot/root (so concentration increases)
  4. In shoots this stimulates cell elongation whereas in roots this inhibits cell elongation
  5. So shoots bend towards light whereas roots bend away from light
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8
Q

Describe the simple responses that can maintain a mobile organism in a favourable environment

A
  1. Taxes
    - directional response
    - movement towards or away from a directional stimulus
  2. Kinesis
    - non-directional response
    - speed of movement or rate of direction change changes in response to non-directional stimulus
    - depending on intensity of stimulus
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9
Q

Give an example of taxis and kinesis

A

Taxis: woodlice moving away from light to avoid predators
Kinesis: woodlice moving faster in drier environments to increase their chance of moving to an area with higher humidity to prevent drying out

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10
Q

Explain the protective effect of a simple (3 neurone) reflex

A

Receptor —> sensory neurone —> relay neurone —> motor neurone —-> effector
- Rapid as only 3 neurones and a few synapses (synaptic transmission is slow)
- Autonomic (doesn’t involve conscious regions of brain) so doesn’t have to be learnt
- Protects from harmful stimuli e.g escape predators/prevents damage to body tissues

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11
Q

Describe the basic structure of a Pacinian corpuscle

A
  • Sensory neurone ending at the end of sensory neurone axon
  • Myelin sheath (Schwann cells) wrapped around sensory neurone axon
  • Sensory neurone ending wrapped in lamella (layers of connective tissue) and gel
  • Stretch mediated sodium ion channels on the neurone membrane
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12
Q

Describe how a generator potential is established in a Pacinian corpuscle

A
  1. Mechanical stimulus e.g pressure deforms lamellae and stretch-mediated sodium ion channels
  2. So sodium ion channels in membrane open and Na+ diffuses into the sensory neurone
    > greater pressure causes more Na+ channels to open and more Na+ to enter
  3. This causes depolarisation, leading to a generator potential
    > if generator potential reaches a threshold it triggers and action potential
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13
Q

Explain what the Pacinian corpuscle illustrates

A
  • Receptors respond only to specific stimuli
    > Pacinian corpuscle only responds to mechanical pressure
  • Stimulation of a receptor leads to the establishment of a generator potential
    > when threshold is reached, action potential sent (all-or-nothing principle)
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14
Q

Explain the differences in sensitivity to light for rods and cones in the retina

A

RODS ARE MORE SENSITIVE TO LIGHT:
- several rods connected to a single bipolar neurone (converge)
- spatial summation to reach/overcome threshold (as enough neurotransmitter released) to generate an action potential
CONES ARE LESS SENSITIVE TO LIGHT:
- each cone connected to a single bipolar neurone
- no spatial summation

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15
Q

Explain the differences in visual acuity for rods and cones in the retina

A

RODS GIVE LOWER VISUAL ACUITY:
- several rods connected to a single bipolar neurone
- so several rods send a single set of impulses to brain (so cant distinguish between seperate sources of light)
CONES GIVE HIGHER VISUAL ACUITY:
- each cone connected to a single bipolar neurone
- cones send seperate sets of impulses to brain (so can distinguish between 2 seperate sources of light)

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16
Q

Explain the differences in sensitivity to colour for rods and cones in the retina

A

RODS ALLOW MONOCHROMATIC VISION: Rhodopsin
- 1 type of rod/1 pigment
CONES ALLOW COLOUR VISION: Iodopsin
- 3 types of cones —> red, green and blue sensitive
- with different optical pigments - absorb different wavelengths of light
- stimulating different combinations of cones gives range of colour perception

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17
Q

How are impulses sent to the optic nerve?

A

From rod/cone cells —> bipolar neurone —> Ganglion cell —> impulses to optic nerve —> brain

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18
Q

Cardiac muscle is myogenic. What does this mean?

A

It can contract and relax without receiving electrical impulses from nerves.

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19
Q

Describe the myogenic stimulation of the heart and transmission of a subsequent wave of electrical activity

A
  1. Sinoatrial node (SAN) acts as a pacemaker - sends regular waves of electrical activity across atria
    > causing atria to contract simultaneously
  2. Non-conducting collagen tissue between atria/venticles prevents impulse passing directly to ventricles
    > preventing immediate contraction of vesicles
  3. Waves of electrical activity reach atrioventricular node (AVN) which delays impulse
    > allowing atria to fully contract and empty before ventricles contract
  4. AVN sends wave of electrical activity down bundle of His, conducting wave between ventricles to apex where it branches into Purkyne tissue
    > causing ventricles to contract simultaneously from the base up
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20
Q

Where are chemoreceptors and pressure receptors located?

A

Chemoreceptors and pressure receptors are located in the aorta and carotid arteries

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21
Q

Describe the roles of chemoreceptors, pressure receptors, the autonomic nervous system and effectors in controlling heart rate.

A
  1. Baroreceptors detects (fall/rise) in blood pressure and/or chemoreceptors detects blood (rise/fall) in blood CO2 concentration or (fall/rise) in blood pH
  2. Sends impulses to medulla/cardiac control centre
  3. Which sends more frequent impulses to SAN along (sympathetic/parasympathetic) neurones
  4. So (more/less) frequent impulses sent from SAN to/from AVN
  5. So cardiac muscle contracts (more/less) frequently
  6. So heart rate (increases/decreases)
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22
Q

Which nerves are involved in increasing or decreasing heart rate?

A

Sympathetic nerves - increase heart rate
Parasympathetic nerves - decrease heart rate

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23
Q

Describe the structure of a myelinated motor neurone

A
  • Axon
  • Myelin sheath (made of Schwann cells) wrapped around the axon
  • Nodes of Ranvier are gaps of exposed axon
  • Cell body surrounded by dendrites which receive the. nerve impulse
  • Impulse sent along neurone to the axon terminal at the opposite side of the
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24
Q

Describe resting potential

A

Inside of axon has a negative charge relative to outside (as more positive ions outside compared to inside)

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25
Q

Explain how a resting potential is established across the axon membrane in a neurone

A
  • Na+/K+ pump actively transports: 3 Na+ out of axon and 2 K+ into the axon
  • Creating an electrochemical gradient, higher conc of K+ inside and higher conc of Na+ outside
  • Differential membrane permeability: more permeable to K+ (move out by facilitated diffusion & more channels), less permeable to Na+ (closed channels)
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26
Q

Explain how changes in membrane permeability lead to depolarisation and the generation of an action potential

A
  1. STIMULUS:
    - Na+ channels open, membrane permeability to Na+ increases
    - Na+ diffuses into the axon down an electrochemical gradient (causing depolarisation)
  2. DEPOLARISATION:
    - if threshold potential is reached, an action potential is generated
    - as more voltage-gated Na+ channels open (positive feedback effect)
    - so more Na+ diffuses in rapidly
  3. REPOLARISATION:
    - voltage-gated Na+ channels close
    - voltage-gated K+ channels open, K+ diffuses out of axon
  4. HYPERPOLARISATION:
    - K+ channels slow to close so there’s a slight overshoot — too many K+ diffuse out of axon
  5. RESTING POTENTIAL:
    - restored by Na+/K+ pump
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27
Q

Draw/label a graph showing an action potential

A

-70mV = stimulus (Na+ channels open)
-55mV = voltage-gated Na+ channels open
Depolarisation
40mV = voltage-gated Na+ channels close, and voltage-gated K+ channels open
Repolarisation
Hyperpolarisation = voltage-gated K+ channels close
-70mV = resting potential

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28
Q

Describe the all-or-nothing principle

A
  • For an action potential to be produced, depolarisation must exceed threshold potential
  • Action potentials produced are always the same size/peak at the same potential
    > bigger stimuli instead increase frequency of action potentials
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29
Q

Explain how the passage of an action potential along non-myelinated and myelinated axons results in nerve impulses

A

NON-MYELINATED:
- action potential passes as a wave of depolarisation
- influx of Na+ in one region increases permeability of adjoining region to Na+ by causing voltage-gated Na+ channels to open do adjoining region depolarises
MYELINATED:
- myelination provides electrical insulation
- depolarisation of axon at nodes of Ranvier only
- resulting in saltatory conduction
- so there is no need for depolarisation along whole length of axon

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30
Q

Suggest how damage to the myelin sheath can lead to slow responses and/or jerky movement

A
  • Less/no saltatory conduction; depolarisation occurs along whole length of axon
    > so nerve impulses take longer to reach neuromuscular junction, delay in muscle contraction
  • Ions/depolarisation may pass/leak to other neurones
    > causing wrong muscle fibres to contract
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31
Q

Describe the nature of the refractory period

A
  • Time taken to restore axon to resting potential when no further action potential can be generated
  • As Na+ channels are closed/inactive/will not open
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32
Q

Explain the importance of the refractory period

A
  • Ensures discrete impulses are produced (action potentials don’t overlap)
  • Limits frequency of impulse transmission at a certain intensity (prevents overreaction to a stimulus)
    > higher intensity stimulus causes higher frequency of action potentials
    > but only up to a certain intensity
  • Also ensures action potentials travel in one direction (unidirectional) - cant be propagated in refractory region
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33
Q

Describe the factors that affect speed of conductance

A
  1. Myelination:
    - depolarisation at Nodes of Ranvier only —> saltatory conduction
    - impulse doesn’t travel along/depolarise whole length of axon
  2. Temperature:
    - increases rate of diffusion of Na+ and K+ as more kinetic energy
    - but proteins/enzymes could denature at a certain temperature
  3. Axon Diameter:
    - bigger diameter means less resistance to flow of ions in cytoplasm
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34
Q

Describe the structure of a synapse

A

Presynaptic neurone, end of an axon
- vesicle containing neurotransmitter
- voltage-gated calcium ion channels
- axon terminal
Synaptic cleft (gap between 2 neurones)
Postsynaptic neurone, has receptors and sodium ion channels on the membrane

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35
Q

What are cholinergic receptors?

A

Synapses that use the neurotransmitter acetylcholine (ACh)

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36
Q

Describe transmission across a cholinergic synapse

A
  1. Depolarisation of pre-synaptic membrane causes opening of voltage-gated Ca2+ ion channels
    - Ca2+ diffuses into pre-synaptic neurone/knob
  2. Causing vesicles containing ACh to move and fuse with the pre-synaptic membrane
    - Releasing Ach into the synaptic cleft (by exocytosis)
  3. ACh diffuses across synaptic cleft to bind to specific receptors on post-synaptic membrane
  4. Causing Na+ channels to open
    - Na+ diffuse into post-synaptic knob causing depolarisation
    - if threshold is met, an action potential is initiated
37
Q

Explain what happens to ACh after synaptic transmission

A
  • It is hydrolysed by acetylcholinesterase
  • Products are reabsorbed by the presynaptic neurone
  • To stop overstimulation —> if not removed it would keep binding to receptors, causing depolarisation
38
Q

Explain how synapses result in unidirectional nerve impulses

A
  • Neurotransmitter made only in/released from pre-synaptic neurone
  • Receptors only on post-synaptic neurone
39
Q

Explain summation by synapses

A
  • Addition of a number of impulses converging on a single post-synaptic neurone
  • Causing rapid buildup of neurotransmitter
  • So threshold more likely to be reached to generate an action potential
    IMPORTANCE: low frequency action potentials release insufficient neurotransmitter to exceed threshold
40
Q

Describe spatial summation

A
  • Many pre-synaptic neurones share 1 synaptic cleft/post-synaptic neurone
  • Collectively release sufficient NT to reach threshold to trigger an action potential
41
Q

Describe temporal summation

A
  • One presynaptic neurone releases neurotransmitter many times over a short period of time
  • Sufficient NT to reach threshold to trigger an action potential
42
Q

Describe inhibition by inhibitory synapses

A
  • Inhibitory neurotransmitters hyperpolarise postsynaptic membrane as:
  • Cl- channels open —> Cl- diffuse in
  • K+ channel open —> K+ diffuse out
  • More Na+ required for depolarisation
  • Reduces likelihood of threshold being met/action potential formation at post-synaptic membranes
43
Q

Describe the structure of a neuromuscular junction

A

Very similar to a synapse except:
- receptors are on muscle fibre instead of postsynaptic membrane and there are more of them
- muscle fibre forms clefts to store enzyme e.g acetylcholinesterase to break down NT

44
Q

Compare transmission across cholinergic synapses and neuromuscular junctions

A

In both, transmission is unidirectional
CHOLINERGIC:
> neurone to neurone (or effectors or glands)
> neurotransmitters can be excitatory or inhibitory
> action potential may be initiated in postsynaptic neurone
NEUROMUSCULAR:
> (motor) neurone to muscle
> always excitatory
> action potential propagates along sarcolemma down T tubules

45
Q

Use examples to explain the effect of drugs on a synapse

A
  • Some drugs stimulate the nervous system, leading to more action potentials e.g:
    > similar shape to neurotransmitter
    > inhibit enzyme that breaks down neurotransmitter - Na+ continues to enter
    > stimulate release of more neurotransmitter
  • Some drugs inhibit the nervous system, leading to fewer action potentials e.g:
    > inhibit release of neurotransmitter (e.g prevent opening of calcium ion channels)
    > block receptors by mimicking shape of neurotransmitter
46
Q

Describe how muscles work

A
  • Work in antagonistic pairs (pull in opposite directions)
    > one muscle contracts, pulling on bone and the other one relaxes
  • Skeleton is incompressible so muscle can transmit force to bone
47
Q

Describe the gross and microscopic structure of skeletal muscle

A
  • Made of many bundles of muscle fibres (cells) packaged together
  • Attached to bones by tendons
  • Muscle fibres contain:
    > sarcolemma (cell membrane) which folds inwards to form transverse T tubules
    > sarcoplasm (cytoplasm)
    > multiple nuclei
    > many myofibrils
    > sarcoplasmic reticulum (endoplasmic reticulum)
    > many mitochondria
48
Q

Describe the ultrastructure of a myofibril

A
  • Made of 2 types of long protein filaments, arranged in parallel
    > myosin = thick filament
    > actin = thin filament
  • Arranged in functional units called sarcomere
49
Q

Explain the banding pattern to be seen in myofibrils

A

> ends are Z lines
middle is M line
H zone - (contains only myosin)
A band - dark band (contains both actin and thick myosin)
I band - light band (contains only actin)

Darkest region contains overlapping actin and myosin

50
Q

Give an overview of muscle contraction

A
  • Myosin heads slide actin along myosin causing the sarcomere to contract
  • Simultaneous contraction of many sarcomere causes myofibrils and muscle fibres to contract
  • When sarcomere contract (shorten) . . .
    > H zones get shorter
    > I bands get shorter
    > A band stays the same
    > Z lines get closer
51
Q

Describe the roles of actin, myosin, calcium ions, tropomyosin and ATP in myofibril contraction (7)

A
  1. Depolarisation spreads down sarcolemma via T tubules causing Ca2+ release from sarcoplasmic reticulum, which diffuse to myofibrils
  2. Calcium ions bind to tropomyosin, causing it to move —> exposing binding sites on actin
  3. Allowing myosin head, with ADP attached, to bind to binding sites on actin —> forming an actin-myosin crossbridge
  4. Myosin heads change angle, pulling actin along myosin (ADP released), using energy from ATP hydrolysis
  5. New ATP binds to myosin head causing it to detach from binding site
  6. Hydrolysis of ATP (by ATP hydrolase/activated by Ca2+) releases energy for myosin heads to return to original position
  7. Myosin reattaches to a different binding site further along actin, process is repeated as long as Ca2+ concentration is high
52
Q

What happens during muscle relaxation?

A
  • Ca2+ actively transported back into the endoplasmic/sarcoplasmic reticulum using energy from ATP
  • Tropomyosin moves back to block myosin binding site on actin again —> no actinmyosin cross bridges
53
Q

Describe the role of phosphocreatine in muscle contraction

A
  • A source of inorganic phosphate (Pi) —> rapidly phosphorylates ADP to regenerate ATP
    > ADP + phosphocreatine —> ATP + creatine
  • Runs out after a few seconds —> used in short bursts of vigorous exercise
  • Anaerobic and alactic
54
Q

Compare the structure, location and general properties of slow and fast twitch skeletal muscle fibres

A

PROPERTIES:
slow = slow, sustained contractions (e.g posture, long distance running), obtain ATP mostly from aerobic respiration —> release energy slowly, fatigues slowly
fast = brief, intensive contractions (e.g sprinting), obtain ATP mostly from anaerobic respiration —> release energy quickly, fatigues quickly due to high lactate concentration
LOCATION:
slow = high proportion in muscles used for posture e.g back, calves, legs of long distance runners
fast = high proportion in muscles used for fast movement e.g biceps, eyelids, legs of sprinters
STRUCTURE:
slow = high concentration of myoglobin (stores O2 for aerobic respiration), many mitochondria (high rate of respiration), many capillaries (supply high conc of oxygen/glucose for aerobic respiration and prevents build up of lactic acid causing muscle fatigue)
fast = low levels of myoglobin, lots of glycogen (hydrolysed to provide glucose for glycolysis/anaerobic respiration which is inefficient so large quantities of glucose required), high conc of enzymes involved in anaerobic respiration (cytoplasm), store phosphocreatine

55
Q

Describe homeostasis in mammals

A
  • Maintenance of a stable internal environment within restricted limits
  • By physiological control systems (normally involve negative feedback)
56
Q

Explain the importance of maintaining stable core temperature

A
  • If temperature is too high:
    > hydrogen bonds in tertiary structures of enzymes break
    > enzymes denature; active sites change shape and substrates can’t bind
    >so fewer e/s complexes form
  • If temperature is too low:
    > not enough kinetic energy so fewer e/s complexes
57
Q

Explain the importance of maintaining stable blood pH

A
  • Above or below optimal pH, ionic/hydrogen bonds in tertiary structure break
  • Enzymes denature; active sites change shape and substrates can’t bind
  • So fewer e/s complexes form
58
Q

Explain the importance of maintaining stable blood glucose concentration

A

Too low (hypoglycaemia)
- not enough glucose for respiration
- so less ATP produced
- active transport can’t happen —> cell death
Too high (hyperglycaemia)
- water potential of blood decreases
- water lost from tissue to blood via osmosis
- kidneys can’t absorb all glucose —> more water lost in urine causing dehydration

59
Q

Describe the role of negative feedback in homeostasis

A
  1. Receptors detect change from optimum
  2. Effectors respond to counteract change
  3. Returning levels to optimum/normal
60
Q

Explain the importance of conditions being controlled by separate mechanisms involving negative feedback

A
  • Departures in different directions from the original state can all be controlled/reversed
  • Giving a greater degree of control (over changes in internal environment)
61
Q

Describe positive feedback

A
  1. Receptors detect change from normal
  2. Effectors respond to amplify change
  3. Producing a greater deviation from normal
62
Q

Describe the factors that influence blood glucose concentration

A
  • Consumption of carbohydrates —> glucose absorbed into blood
  • Rate of respiration of glucose - e.g increases during exercise due to muscle contraction
63
Q

Describe the role of the liver in glycogenesis, glycogenolysis and gluconeogenesis

A

Glycogenesis : converts glucose —> glycogen
Glycogenolysis : converts glycogen —> glucose
Gluconeogenesis : converts amino acids/glycerol —> glucose

64
Q

Explain the action of insulin in decreasing blood glucose concentration

A

Beta cells in islets of Langerhans in pancreas detect blood glucose concentration is too high —> secrete insulin:
- Attaches to specific receptors on cell surface membranes of target cells e.g liver/muscles
1. This causes more glucose channel proteins to join cell surface membrane
> increasing permeability to glucose
> so more glucose can enter cell by facilitated diffusion
2. Also activates enzymes involved in the conversion of glucose to glycogen (glycogenesis)
> lowering glucose concentration in cells, creating a concentration gradient
> so glucose enters by facilitated diffusion

65
Q

Explain the action of glucagon in increasing blood glucose concentration

A

Alpha cells in the islets of Langerhans in the pancreas detect blood glucose concentration is too low —> secrete glucagon:
- Attaches to specific receptors on cell surface membrane of target cells, e.g liver
1. Activates enzymes involved in the hydrolysis of glycogen to glucose (glycogenolysis)
2. Activates enzymes involved in the conversion of amino acids/glycerol to glucose (gluconeogenesis)
- This establishes a concentration gradient —> glucose enters the blood by facilitated diffusion

66
Q

Explain the role of adrenaline in increasing blood glucose concentration

A

Fear/stress/exercise —> adrenal glands secrete adrenaline:
- Attaches to specific receptors on cell surface membranes of target cells e.g liver
- Activates enzymes involved in the hydrolysis of glycogen to glucose (glycogenolysis)
- This establishes a concentration gradient —> glucose enters blood by facilitated diffusion

67
Q

Describe the second messenger model of adrenaline and glucagon action

A

Adrenaline/glucagon attach to specific receptors on cell membrane which:
1. Activates enzyme adenylate cyclase (changes shape)
2. Which converts many ATP to many cyclic AMP (cAMP)
3. cAMP acts as the second messenger —> activates protein kinase enzymes
4. Protein kinases activate enzymes to break down glycogen to glucose

68
Q

Suggest an advantage of the second messenger model

A
  • Amplifies signal from hormone
  • As each hormone can stimulate production of many molecules of second messenger (cAMP)
  • Which in turn can activate many enzymes for rapid increase in glucose
69
Q

Compare the causes of type I and type II diabetes

A

Both - higher and uncontrolled blood glucose concentration; higher peaks after meals and remains high
TYPE I:
- ß-cells in islets of Langerhans in pancreas produce insufficient insulin
- normally develops in childhood due to an autoimmune response destroying ß cells of islets of Langerhans
TYPE II:
- receptor (faulty) loses responsiveness/sensitivity to insulin (but insulin still produced)
- so fewer glucose transport proteins —> less uptake of glucose —> less conversion of glucose to glycogen
- risk factor = obesity

70
Q

Describe how type 1 diabetes can be controlled

A
  • Injections of insulin
  • Blood glucose concentration monitored with biosensors; dose of insulin matched to glucose intake
  • Eat regularly and control carbohydrate intake e.g those that are broken down/absorbed slower
    > to avoid sudden rise in glucose
71
Q

Suggest why insulin can’t be taken as a tablet by mouth

A
  • Insulin is a protein
  • Would be hydrolysed by endo/exopeptidases
72
Q

Describe how type II diabetes can be controlled

A
  • Not normally treated with insulin injections but may use drugs which target insulin receptors to increase their sensitivity
    > to increase glucose uptake by cells/tissues
  • Reduce sugar intake (carbohydrates)/low glycemic index —> less absorbed
  • Reduce fat intake —> less glycerol converted to glucose
  • More (regular) exercise —> uses glucose/fats by increasing respiration
  • Lose weight —> increased sensitivity of receptors to insulin
73
Q

Describe how you can evaluate the positions of health advisers and the food industry in relation to the increased incidence of type II diabetes

A
  • Health advisers aim —> reduce risk of type II diabetes due to health problems caused (e.g kidney failure)
    > so need to reduce obesity as it is a risk factor
  • Food industry aim —> maximise profit
74
Q

Describe the structure of a nephron

A
  • Nephron = basic structural and functional unit of the kidney (millions in the kidney)
  • Associated with each nephron are a network of blood vessels
  • Located within the cortex and medulla of the kidney
75
Q

Summarise the role of different parts of the nephron

A
  1. Bowman’s/renal capsule - formation of glomerular filtrate (ultrafiltration)
  2. Proximal convoluted tubule - reabsorption of water and glucose (selective reabsorption)
  3. Loop of Henle - maintenance of a gradient of sodium ions in the medulla
    4 & 5. Distal convoluted tubule & Collecting duct - reabsorption of water (permeability controlled by ADH)
76
Q

Describe the formation of glomerular filtrate

A
  1. High hydrostatic pressure in glomerulus
    > as diameter of afferent arteriole (in) is wider than efferent arteriole (out)
  2. Small substances e.g water, glucose, ions, urea forced into glomerular filtrate, filtered by:
    a. pores/fenestrations between capillary endothelial cells
    b. capillary basement membrane
    c. podocytes
  3. Large proteins/blood cells remain in blood
77
Q

Describe the reabsorption of glucose by the proximal convoluted tubule

A
  1. Na+ actively transported out of the epithelial cells to capillary
  2. Na+ moves by facilitated diffusion into epithelial cells down a concentration gradient, brining glucose against it’s concentration gradient
  3. Glucose moves into capillary by facilitated diffusion down its concentration gradient
78
Q

Describe the reabsorption of water by the proximal convoluted tubule

A
  • Glucose etc in capillaries lower water potential
  • Water moves by osmosis down a water potential gradient into the capillaries
79
Q

Describe and explain how features of the cells in the PCT allow the rapid reabsorption of glucose into the blood (5)

A
  • microvilli/folded cell-surface membrane —> provides a large surface area
  • many channel/carrier proteins —> for facilitated diffusion/co-transport
  • many carrier proteins —> for active transport
  • many mitochondria —> produce ATP for active transport
  • many ribosomes —> produces carrier/channel proteins
80
Q

Suggest why glucose is found in the urine of an untreated diabetic person

A
  • Blood glucose concentration is too high so not all glucose is reabsorbed at the PCT
  • As glucose carrier/co-transporter proteins are saturated/working at a maximum rate
81
Q

Explain the importance of maintaining a gradient of sodium ions in the medulla (concentration increases further down)

A
  • So water potential decreases down the medulla (compared to filtrate in collecting duct)
  • So a water potential gradient is maintained between the collecting duct and medulla
  • To maximise reabsorption of water by osmosis from filtrate
82
Q

Describe the role of the loop of Henle in maintaining a gradient of sodium ions in the medulla

A
  1. In the ascending limb:
    > Na+ actively transported out (so filtrate concentration decreases)
    > water remains as ascending limb is impermeable to water
    > this increases concentration of Na+ in the medulla, lowering the water potential
  2. In the descending limb:
    > water moves out by osmosis then reabsorbed by capillaries
    > Na+ ‘recycled’ —> diffuses back in
83
Q

Suggest why animals needing to conserve water have long loops of Henle (thick medulla) (3)

A
  • More Na+ moved out —> Na+ gradient is maintained for longer in medulla/higher Na+ concentration
  • So water potential gradient is maintained for longer
  • So more water can be reabsorbed from collecting duct by osmosis
84
Q

Describe the reabsorption of water by the DCT and collecting ducts

A
  • water moves out of the DCT and collecting duct by osmosis down a water potential gradient
  • controlled by ADH which increases their permeability
85
Q

What is osmoregulation?

A

Control of water potential of the blood (by negative feedback)

86
Q

Describe the role of the hypothalamus in osmoregulation

A
  1. Contains osmoreceptors which detect increase OR decrease in blood water potential
  2. Produces more ADH when water potential is low OR less ADH when water potential is high
87
Q

Describe the role of the posterior pituitary gland in osmoregulation

A

Secretes (more/less) ADH into blood due to signals from the hypothalamus

88
Q

Describe the role of ADH in osmoregulation

A
  1. Attaches to receptors on collecting duct & DCT
  2. Stimulating addition of channel proteins (aquaporins) into cell-surface membranes
  3. So increases permeability of cells of collecting duct & DCT to water
  4. So increases water reabsorption from collecting duct & DCT (back into blood) by osmosis
  5. So decreases the volume of urine and increases the concentration of urine produced
89
Q

What produces and what releases ADH?

A

The hypothalamus produces ADH and the posterior pituitary gland releases it into the blood.

Y13 Biology (4 decks)

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