[3.6] Organisms Respond to Changes in their Internal & External Environments Flashcards
Stimuli, Nervous Coordination, Skeletal Muscles & Homeostasis
What is a stimulus?
A change in an organism’s internal or external environment.
Why is it important that organisms can respond to stimuli?
Organisms increase their chance of survival by responding to stimuli.
What is a tropism?
- Growth of a plant in response to a directional stimulus.
- Positive tropism = towards a stimulus; negative tropism = away from stimulus.
Summarise the role of growth factors in flowering plants.
- 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).
Describe how indoleacetic acid (IAA) affects cells in roots and shoots.
- In **shoots*, high concentrations of IAA stimulates cell elongation.
- In roots, high concentrtions of IAA inhbitis cell elongation.
Explain gravitropism in flowering plants.
- Cells in tip of shoot / root produce IAA.
- IAA diffuses down shoot / root (evenly initally).
- IAA moves to lower side of shoot / root (so concentration increases).
- In **shoots* this stimulates cell elongation whereas in roots this inhbits cell elongation.
- So shoots bend away from gravity wheras roots bend towards gravity.
Explain phototropism in flowering plants.
- Cells in tip of shoot / root produce IAA.
- IAA diffuses down shoot / root (evenly initally).
- IAA moves to shaded side of shoot / root (so concentration increases).
- In shoots this stimulates cell elongation whereas in roots this inhibits cell elongation.
- So shoots bend towards light whereas roots bend away from light.
Describe the simple responses that can maintain a mobile organism in a favourable environment.
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Taxes (tactic responses).
- Directional response.
- Movement towards or away from a directional stimulus.
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Kinesis (kinetic responses).
- Non-directional response.
- Speed of movement or rate of direction change changes in response to a non-directional stimulus.
- Dependning on intensity of stimulus.
Explain the protective effect of a simple (e.g. 3 neurone) reflex.
- Rapid as only 3 neurones and few synapses (synaptic transmission is slow).
- Autonomic (doesn’t involve conscipus regions of brain) so doesn’t have to be learnt.
- Protects from harmful stimuli e.g. escape predators / prevents damage to body tissues.
Describe the basic structure of a Pacinian Corpuscle
Describe how a generator potential is established in a Pacinian corpuscle.
- Mechanical stimulus e.g. pressure deforms lamellae and stretch-mediated sodium ion (Na⁺) channels.
- So Na⁺ channels in membrane open and Na⁺ diffuse into sensory neurone.
- Greater pressure causes more Na⁺ channels to open and more Na⁺ to enter.
- This causes depolarisation, leading to a generator potential.
- If a generator potential reaches threshold, it triggers an action potential.
Explain what the Pacinian corpuscle illustrates.
- 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).
Explain the difference in sensitivity to light for rods & cones in the retina.
Rods are more sensitive to light
- Several rods connected to a single neurone.
- Spatial summation to reach / overcome threshold (as enough neurotransmitter released) too generate an action potential.
Cones are less sensitive to light
- Each cone connected to a single neurone.
- No spatial summation.
Explain the difference in visual acuity for rods & cones in the retina.
Rods give lower visual activity
- Several rods connected to a single neurone.
- So several rods send a single set of impulses to brain (so can’t distinguish between separate sources of light).
Cones give higher visual acuity
- Each cone connected to a single neurone.
- Cones send separate (sets of) impulses to brain (so can’t distinguish distinguish between 2 separate sources of light)
Explain the differences in sensitivity to colour for rods & cones in the retina.
Rods allow monochromatic vision
- 1 type of rod / 1 pigment.
Cones allow colour vision
- 3 types of cones - red-, green- and blue-sensitive.
- With different optical pigments -> absorb different wavelengths.
- Stimulating different combinations of cones gives range of colour perception.
The cardiac muscle is myogenic. What does this mean?
- It can contract and relax without receiving electrical impulses from nerves.
Label the sinoatrial node (SAN), atrioventricular node (AVN), Bundle of His and Purkyne tissue on a diagram of the heart.
Describe the myogenic stimulation of the heart and transmission of a subsequent wave of electrical activity.
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Sinoatrial node (SAN) acts as pacemaker -> releases regular waves of electrical activity across atria.
- Causing atria to contract simultaneously.
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Non-conducting tissue between atria / ventricles prevents impulses passing directly to ventricles.
- Preventing immediate contraction of ventricles.
- Waves of electrical activity reach atrioventricular node (AVN) which delays impulse.
- Allowing atria to fully contract and empty before ventricles contract.
- 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.
Where are chemoreceptors and pressure receptors located?
- Chemoreceptors and pressure receptors are located in the atria and carotid arteries.
Describe the role of chemoreceptors, pressure receptors, the autonomic nervous system and effectors in controlling heart rate when a fall in blood pressure OR rise in blood CO2 conc. / fall in blood pH is detected.
- Baroreceptors detect fall on blood pressure and / or chemoreceptors detect blood rise in blood CO2 conc. or fall in blood pH.
- Send impulses to medulla / cardiac control centre.
- Which send more frequent impulses to SAN along sympathetic neurones.
- So more frequent impulses sent from SAN and to / from AVN.
- So cardiac muscle contracts more frequently.
- So heart rate increases.
Describe the role of chemoreceptors, pressure receptors, the autonomic nervous system and effectors in controlling heart rate when a raise in blood pressure OR fall in blood CO2 conc. / rise in blood pH.
- Baroreceptors detect rise on blood pressure and / or chemoreceptors detect blood fall in blood CO2 conc. or rise in blood pH.
- Send impulses to medulla / cardiac control centre.
- Which send more frequent impulses to SAN along parasympathetic neurones.
- So less frequent impulses sent from SAN and to / from AVN.
- So cardiac muscle contracts less frequently.
- So heart rate decreases.
Describe the structure of a myelinated motor neurone.
Describe resting potential.
- Inside of axon has a negative charge relative to outside (-70mV).
- i.e. more positive ions outside compared to inside.
Explain how a resting potential is established across the axon membrane in a neurone.
- Na⁺/K⁺ pump actively transports:
- 3 Na⁺ out of axon AND 2 K⁺ into axon.
- Creating an electrochemical gradient:
- Higher K⁺ concentration inside AND higher Na⁺ concentration outside.
- Differential membrane permeability:
- More permeable to K⁺ -> move out by facilitated diffusion.
- Less permeable to Na⁺ (closed channels).
Explain how changes in membrane permeability lead to deplorisaiton and the generation of an action potential.
- Stimulus.
- Na⁺ channels open; membrane permeability to Na⁺ increases.
- Na⁺ diffusion into axon down electrochemical gradient (causing depolarisation).
- Depolarisation.
- If threshold potential is reached, an action potential is generated.
- As more voltage-gated Na⁺ channels open (positive feedback effect).
- So more Na⁺ diffuse in rapidly.
- Repolarisation.
- Voltage-gated Na⁺ channels close.
- Voltage-gated K⁺ channels open; K⁺ diffuse out of axon.
- Hyperpolorisation.
- K⁺ channels slow to close so there’s a slight overshoot = too many K⁺ diffuse out.
- Resting potential.
- Restored by Na⁺/K⁺ pump.
Draw and label a graph showing an action potential.
Describe the all-or-nothing principle.
- For an action potential to be produced, depolarisation must exceed threshold potential.
- Action potentials produced are always same magnitude / size / peak at same potential.
- Bigger stimuli instead increase frequency of action potentials.
Describe the nature of the refractory period.
- 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.
Explain the importance of the refractory period.
- Ensures discrete impulse are produced (action potentials don’t overlap).
- Limits frequency of impulse transmission at a certain intensity (prevents over reaction to stimulus).
- Higher intensity stimulus causes higher frequency of action potentials.
- But only up to certain intensity.
- Also ensures action potentials travel in one direction - can’t be propagated in a refractory region.
Explain how the passage of an action potential along non-myelinated and myelinated axons result in nerve impulses.
NON-MYELINATED AXON
- Action potential passes as a wave of depolarisation.
- Influx of Na⁺ in one region in increases permeability of adjoining region to Na⁺ by causing voltage-gated Na⁺ channels to open so adjoining region depolarises.
MYELINATED AXON
- Myelination provides electrical insulation.
- Depolarisation of axon at nodes of Ranvier only resulting in saltatory conduction (local currents circuits).
- So there is no need for depolarisation along whole length of axon.
Suggest how damage to the myelin sheath can lead to slow responses and/or jerky movement.
- 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.
Describe the factors that affect speed of conductance.
Myelination
- Depolarisation at nodes of Ranvier only resulting in -> saltatory conduction.
- Impulse doesn’t travel / depolarise whole length of axon.
Axon diameter
- Bigger diameter means less resistance to flow of ions in cytoplasm.
Temperature
- Increases rate of diffusion of Na⁺ and K⁺ as more kinetic energy.
- But proteins / enzymes could denature at a certain temperature.
Describe the structure of a synapse.
What are cholinergic synapses?
- Synapses that use the neurotransmitter acetylcholine (ACh).
Describe transmission across a cholinergic synapse.
At pre-synaptic neurone
- Depolarisation of pre-synaptic membrane causes opening of voltage-gated Ca²⁺ channels.
- Ca²⁺ diffuse into pre-synaptic neurone / knob.
- Causing vesicles containing ACh to move and fuse with pre-synaptic membrane.
- Releasing ACh into the synaptic cleft (by exocytosis).
At post-synaptic neurone
- ACh diffuses across synaptic cleft to bind to specific receptors on post-synaptic membrane.
- Causing Na⁺ channels to open.
- Na⁺ diffuse into post-synaptic knob causing depolarisation.
- If threshold is met, an action potential is initiated.
Explain what happens to acetylcholine after synaptic transmission.
- It is hydrolysed by acetylcholinesterase.
- Products are reabsorbed by the presynatpic neurone.
- To stop overstimulation - if not removed it would keep binding to receptors, causing depolarisation.
Explain how synapses result in unidirectional nerve impulses.
- Neurotransmitter only made in / released from pre-synaptic neurone.
- Receptors only on post-synaptic membrane.
Describe summation by synapses.
- Addition of a number of impulses converging on a single post-synaptic neurone.
- Causing rapid build-up of neurotransmitter (NT).
- So threshold more likely to be reached to generate an action potential.
Describe spatial summation.
- Many pre-synaptic neurones share one synaptic cleft / post-synaptic neurone.
- Collectively release sufficient neurotransmitter to reach threshold to trigger an action potential.
Describe temporal summation.
- One pre-synaptic neurone releases neurotransmitter many times over a short time.
- Sufficient neurotransmitter to reach threshold to trigger an action potential.
Describe inhibition by inhibitory synapses.
- Inhibitory neurotransmitters hyperpolarise postsynaptic memebrane as:
- Cl⁻ channels open -> Cl⁻ diffuse in.
- K⁺ channels open -> K⁺ diffuse out.
- This means inside of axon has more negative charge relative to outside / below resting potential.
- So more Na⁺ required to enter for depolorisation,
- Reduces likelihood of threshold being met / action potential formation at post-synaptic membranes.
Describe the structure of a neuromuscular junction.
- Very similar to a synapse except:
- Receptors are on muscle fibre sarcolemma instead of postsynaptic membrane and there are more.
- Muscle fibre forms clefts to store enzyme e.g. acetylcholinesterase to break down neurotransmitter.
Compare transmission across cholinergic synapses and neuromuscular junctions.
In both: transmission is unidirectional.
CHOLINERGIC SYNAPSE
- Neurone to neurone (or effectors, glands).
- Neurotransmitters can be excitatory or inhibitory.
- Action potential may be initiated in post-synaptic neurone.
NEUROMUSCULAR JUNCTION
- Motor neurone to muscle.
- Always excitatory.
- Action potential propagates along sarcolemma down T tubules.
Use examples to explain the effect of drugs on a synapse.
- Some drugs stimulate the nervous system, leading to more action potentials, e.g.:
- Similar shape to neurotransmitter.
- Stimulate release of more neurotransmitter.
- Inhibit enzyme that break downs neurotransmitter -> Na⁺ continues to enter.
- Some drugs inhibit the nervous system, leading to fewer action potentials.
- Inhibit release of neurotransmitter e.g. prevent opening of calcium ion channel.
- Block receptors by mimicking shape of neurotransmitters.
Describe homeostasis.
- Maintenance of a stable internal environemnt within restricted limits.
- By physiological control systems (normally involve negative feedback).
- Examples: core temperature, blood pH, blood glucose concentration & blood water potential.
Explain the importance of maintaining stable core temperature.
- If temperature is too high:
- Hydrogen bonds in tertiary structure of enzymes break.
- Enzymes denature; active sites change shape and substrates can’t bind.
- So fewer enzyme-substrate complexes.
- If temperature is too low:
- Not enough kinetic energy so fewer enzyme-substrate complexes.
Explain the importance of maintaining stable blood pH.
- Above or below optimal pH, ionic / hydrogen bonds in tertiary structure break.
- Enzymes denature; active sites change shape and substractes can’t bind.
- So fewer enzyme substrate complexes.
Explain the importance of maintaining stable blood glucose concentration.
Too low (hypoglycaemia)
- Not enough glucose for respiration.
- So less ATP produced.
- Active transport etc. 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.
Describe the role of negative feedback in homeostasis.
- Receptors detect change from optimum.
- Effectors respond to counteract change.
- Returning levels to optimum / normal.
- Examples: control of blood glucose concentration, blood pH, core temperature and blood water potential.
Explain the importance of conditions being controlled by separate mechanisms involving negative feedback.
- Departures in different directions from the original state can all be controlled / reversed.
- Giving a greater degree of control (over changes in internal environment).
Describe positive feedback.
- Receptors detect changefrom normal.
- Effectors respond to amplify change.
- Producing a greater deviation from normal.
- Not involved in homeostasis.
- Examples: onset of contractions in childbirth, blood clotting etc.
Describe the structure of a nephron.
- Nephron = basic structural and functional unit of the kidney.
- Associated with each nephron is a network of blood vessels.
Summarise the role of different parts of the nephron.
- **Bowman’s / renal capsule.
- Formation of glomerular filtrate (ultrafiltration).
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Proximal convoluted tubule.
- Reabsorption of water and glucose (selective reabsorption).
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Loop of Henle.
- Maintenance of a gradient of sodium ions in the medulla.
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Distal convoluted tubule & collecting duct.
- Reabsorption of water (permeability controlled by ADH).
Describe the formation of glomerular filtrate.
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High hydrostatic pressure in glomerulus.
- As diameter of afferent arteriole (in) is wider than efferent arteriole (out).
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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.
- Large proteins / blood cells remain in blood.
Describe the reabsorption of glucose and water by the proximal convoluted tubule.
- Na⁺ actively transported out of epithelial cells to capillary.
- Na⁺ moves by facilitated diffusion into epithelial cells down a concentration gradient, bringing glucose against its concentration gradient.
- Glucose moves into capillary by facilitated diffusion down its concentration gradient.
- Glucose etc. in capillaries lower water potential.
- Water moves by osmosis down a water potential gradient.
Describe and explain how features of the cells in the PCT allow the rapid reabsorption of glucose into the blood.
- Microvilli / folded cell-surface membrane -> provides a large surface area.
- Many channel / carrier proteins -> for faciliated diffusion / co-transport.
- Many carrier proteins -> for active transport.
- Many mitochondria -> produce ATP for active transport.
- Many ribosomes -> produce carrier / channel proteins.
Suggest why glucose is found in the urine of an untreated diabetic person.
- Blood glucose concentration is too high so not all glucose is reabsorped at the PCT.
- As glucose carrier / cotransporter proteins are saturated / working at maximum rate.
Explain the importance of maintaining gradient of sodium ions in the medulla (concentration increases further down).
- 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.
Describe the role of the loop of Henle in maintaining a gradient of sodium ions in the medulla.
- 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 water potential.
- In the descending limb:
- Water moves out by osmosis then reabsorbed by capillaries (so filtrate concentration increases).
- Na⁺ ‘recycled’ -> diffuses back in.
Suggest why animals needing to conserve water have long loops of Henle (thick medulla).
- 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.
Describe the reabsorption of water by the distal convoluted tubule.
- Water moves out of distal convoluted tubule & collecting duct by osmosis down a water potential gradient.
- Controlled by ADH which increases their permeability.
What is osmoregulation?
- Control of water potential of the blood (by negative feedback).
Describe the role of the hypothalamus in osmoregulation.
- Contains osmoreceptors which detects increase OR decrease in blood water potential.
- Produces more ADH when water potential is low OR less ADH when water potential is high.
Describe the role of the posterior pituitary gland in osmoregulation.
- Secretes (more / less) ADH into blood due to signals from the hypothalamus.
Describe the role of antidiuretic hormone (ADH) when osmoreceptors detect a decrease in blood water potential due to increasing sweating, reduced water intake and increased salt intake.
- Hypothalamus produces more ADH.
- Attaches to receptors on collecting duct and distal convoluted tubule.
- Stimulating addition of channel proteins (aquaporins) into cell-surface membranes.
- So increases permeability of cells of collecting duct and DCT to water.
- So increases water re absorption from collecting duct / DCT back into blood by osmosis.
- So decreases volume and increases concentration of urine produced.
Describe the role of antidiuretic hormone (ADH) when osmoreceptors detect a increase in blood water potential.
- Hypothalamus produces less ADH.
- Less attaches to receptors on collecting duct and distal convoluted tubule.
- Less addition of channel proteins (aquaporins) into cell-surface membranes.
- So low permeability of cells of collecting duct and DCT remain to water.
- So less water reabsorption from collecting duct / DCT back into blood by osmosis.
- So increases volume and decreases concentration of urine produced.
Describe the factors that influence blood glucose concentration.
- Consumption of carbohydrates -> glucose absorbed into blood.
- Rate of respiration of glucose e.g. increases during exercise due to muscle contraction.
Describe the role of the liver in glycogenesis, glycogenolysis and gluconeogenesis.
GLYCOGENESIS
- Converts glucose -> glycogen.
GLYCOGENOLYSIS
- Converts glycogen -> glucose.
GLUCONEOGENESIS
- Converts amino acids and/or glycerol -> glucose.
Explain the action of insulin in decreasing blood glucose concentration.
- 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.
- This causes more glucose channel proteins to join cell surface membranes of.
- Increasing permeability to glucose.
- So more glucose can enter cell by facilitated diffusion.
- This also activates enzymes involved in conversion of glucose to glycogen (glycogenesis).
- Lowering glucose concentration in cells, creating a concentration gradient.
- So glucose enters cell by facilitated diffusion.
Explain the action of glucagon in increasing blood glucose concentration.
- Alpha cells in islets of Langerhans in pancreas detect blood glucose concentration is too low -> secrete glucagon.
- Attaches to specific receptors on cell surface membranes of target cells e.g. liver.
- Activates enzymes involved in hydrolysis of glycogen to glucose (glycogenolysis).
- Activates enzymes involved in conversion of glycerol / amino acids to glucose (gluconeogenesis).
- This establishes a concentration gradient -> glucose enters blood by facilitated fissuion.
Explain the role of adrenaline in increasing blood glucose concentration.
- 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 hydrolysis of glycogen to glucose (glycogenolysis).
- This establishes a concentration gradient -> glucose enters blood by facilitated diffusion.
Describe the second messenger model of adrenaline and glucagon action.
- Adrenaline / glucagon (‘first messengers’) attach to specific receptors on cell membrane which:
- Activates enzyme adenylate cyclase (changes shape).
- Which converts many ATP to any cyclic AMP (cAMP).
- cAMP acts as the second messenger -> activates protein kinase enzymes.
- Protein kinases activate enzymes to break down glycogen to glucose.
Suggest an advantage of the second messenger model.
- Amplifies signal from hormone.
- As each hormone can stimulate production of many molecules of second messenger (cAMP).
- Which can in turn activate many enzymes for rapid increase in glucose.
Compare the causes of types I and II diabetes.
- Both - higher and uncontrolled blood glucose concentration; higher peaks after meals and remains high.
TYPE I
- Key point = beta cells in islets of Langerhans in pancreas produce insufficient insulin.
- Normally develops in childhood due to autoimmune response destroying beta cells of islets of Langerhans.
TYPE II
- Key point = receptor loses responsiveness / sensitivity to insulin, but insulin still produced.
- So fewer glucose transport proteins -> less uptake of glucose -> less conviction of glucose to glycogen.
- Risk factor = obesity.
Describe how type I diabetes can be controlled.
- Injections of insulin (as pancreas doesn’t produce enough).
- Blood glucose concentration monitored with biosensors; dose of insulin matched to glucose intake.
- Eat regularly and control carbohydrate intake e.g. those that broken down / absorbed slower.
- To avoid sudden rise in glucose.
Suggest why insulin can’t be taken as a tablet by mouth.
- Insulin is a protein.
- Would be hydrolysed by endopeptidases / exopeptidases.
Describe how type II diabetes can be controlled.
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Not normally treated with insulin injections (as pancreas still produces it), but may use drugs which target insulin receptors to increase their sensitivity.
- To increase glucose uptake by cells / tissues.
- Reduce sugar intake (carbohydrates) / low glycaemic 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.
Describe how you can evaluate the positions of health advisors and the food industry in relation to the increased incidence of type II diabetes.
- Consider both sides:
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Health advisers aim - reduce risk of type II diabetes due to health problems caused.
- So need to reduce obesity as it is a risk factor.
- Food industry aim - maximise profit.
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Health advisers aim - reduce risk of type II diabetes due to health problems caused.
