Topic 6 -Organisms response to changes in internal/external environments Flashcards

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 stimulus
Positive-towards stimulus
Negative- Away from stimulus

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4
Q

Describe how high conc of Indoleacetic acid (IAA) affects cells in roots and shoots

A

In shoots- A high concentration of IAA stimulates cell elongation
In roots- High concentration of IAA inhibits cell elongation

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5
Q

Explain gravitropism in flowering plants

A

-Cells in tip of the shoot/root produce IAA
-IAA diffuses down the shoot/root and is even initially
-IAA moves down to the lower side of the shoot/root so concentration increases
-In the shoot this stimulates cell elongation whereas in roots this inhibits cell elongation
-So shoot bends aways from gravity whereas roots bend towards gravity

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6
Q

Explain phototropism in flowering plants

A

-Cells in tip shoots/roots produce IAA
-IAA diffuses down shoot-roots and is even initially
-IAA moves to the shaded side of shoot/root
-In shoots this stimulates cell elongation whereas in roots this inhibits cell elongation
-So shoot bends towards light whereas roots bend away from light

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7
Q

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

A

1) Taxis (tactic response)
-Directional response
-Movement towards or away from a directional stimulus
2) Kinesis (kinetic response)
-Non directional response
-Speed of movement or rate of directional change and changes in response to a non-directional stimulus
-depends on intensity of stimulus

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8
Q

Explain the protective effect of simple reflexes

A

-Rapid as only 3 neurones and few synapses
-Autonomic so dosen’t have to be learnt and requires no conscious brain regions
-Protects from harmful stimuli such as predators/prevents body tissue damage

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9
Q

How can the environmental variables of humidity and light be investigated in a chamber choice

A

Humidity- Add a drying agent to one side and a damp filter paper to the other
Light- Shine a light but cover one half with black card
Put the animals in the centre of the platform and cover with a lid

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10
Q

When investigation an environmental variable using a maze, why is it important to clean the petri dish/maze

A

-Animals may leave chemicals/scents
-This will influence the behaviour of other animal

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11
Q

When investigation an environmental variable using a maze, why is it important to not use the same organism more than once

A

-Reduces stress on the maggots
-Prevents chance of learned behaviours

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12
Q

Describe the basic structure of a pacinian corpuscle

A

-Has Lamellae (layers of connective tissue)
-Stretch mediated sodium ion channel (closed)
-Sensory neurone ending
-Sensory neurone axon
-Gel
-Myelin sheath (Schwann cells
-Capsule
-blood capillary

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13
Q

Describe how a generator potential is established in a pacinian corpuscle

A

1) Mechanical pressure deforms lamellae and stretch- mediated sodium ion channels
2) So sodium channels in the membrane open and sodium diffuses into the sensory neurone
-Greater pressure causes more sodium channels to open leading to more sodium ions entering
3) This causes depolarisation, leading to a generator potential
-If generator potential reaches threshold, it triggers an action potential (nerve impulse)

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14
Q

Explain what the pacinian corpuscle illustrates about receptors

A

-Receptors respond only to specific stimuli as pacinian corpuscle only responds to mechanical pressure
-Stimulation of a receptor leads to the establishment of a generator potential and when threshold is reached action potential sent (all or nothing principle)

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15
Q

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

A

Rods are more sensitive to light
-This is because several rod cells are connected to a single sensory neurone in the optic nerve
-Spatial summation reaches the threshold to generate an action potential
-To create a generator potential, pigment in the rod cells must be broken down, there is enough low intensity light to cause this explaining rod cells sensitivity.

Cones are less sensitive to light
-Each cone is connected to a single neurone so the stimulation of a number of cells cannot be combined to exceed thresholds value and create a generator potential- only respond to high intensity light
-No spatial summation, pigment in rod cells requires high light intensity for breakdown only then can generator potential be activated

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16
Q

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

A

Rods give a lower visual acuity
-This is because several rods are connected to a single neuron, as a consequence light received by rod cells sharing the same neuron will only generate a single impulse travelling to the brain regardless of how many neurons are stimulated. This means they cannot distinguish separate sources of light.

Cones give higher visual acuity
-Each cone is connected to a single neuron
-Cones send separate impulses to the brain so the brain can distinguish between 2 separate sources of light.

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17
Q

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

A

-Rods allow monochromatic vision as there is only 1 type of rod and 1 type of pigment
-Cones allow colored vision as there are 3 types- red, green, blue which are sensitive cones
-They have different optical pigments which absorb different wavelengths
-Stimulating different combinations of cones gives range of color perception

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18
Q

What does cardiac muscle being myogenic mean?

A

It can contract and relax without receiving electrical impulses from nerves

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19
Q

Label the SAN, AVN, Bundle of His and Purkyne tissue on a diagram of the heart

A
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20
Q

Describe the myogenic stimulation of the heart how how heart rate is controlled

A

-The sinoatrial node in the right wall of the atrium acts as a pacemaker by sending regular waves of electrical activity across atria causing them to contract simultaneously.
-Non conducting tissue between atria and ventricles (atrioventricular septum) prevents impulse from passing directly to ventricles preventing the immediate contraction of ventricles.
-Waves of electrical activity reach the atrioventricular node which delays the impulse allowing the atria to fully contract and empty before the ventricles contract.
The atrioventricular node send waves of electrical excitation between the ventricles along a series of specialized muscle fibers called purkyne tissue which make up a structure called the Bundle of his. This causes ventricles to contract simultaneously from the base up.

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21
Q

Where are chemoreceptors and pressure receptors located?

A

In the Aorta and Carotid arteries.

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22
Q

How are changes to the heartrate controlled by chemoreceptors

A

Chemoreceptors are sensitive to changes in the pH of blood as a result of changes in CO2 concentration
-Chemoreceptors detect a rise/fall in blood-Co2 conc
-This sends more nervous impulses to the medulla oblangata
-The center increases the frequency of impulses to the sinoatrial node (SAN) along the sympathetic/Para synthetic neurons.
-SA node increases/decreases heartrate
-Increased/decreased flow of blood removes or adds CO2 quicker

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23
Q

Explain how heart rate is controlled by pressure receptors

A

-pressure receptors detect a fall/rise in heart rate
-Pressure receptors transmit more nervous impulses to the center in the medulla oblongata that increases/decreases heart rate
-This sends more frequent impulses to the sinoatrial node along neurons
-This leads to and increase/decrease in heart beats

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24
Q

What is the region of the brain that controls heart rate and what are the two centres in it

A

The medula Oblongata

-Contains a centre that increases heart rate which is linked to the sinotrial node by the sympathetic nervous system
-Contains a centre that decreases heart rate which is linked to the sinotrial node by the parasympathetic nervous system

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25
Describe the different structures in a motor neurone and ther functions
A body cell- Contains all the usula cell organelles including a nucleus and large amounts of rough endoplasmic rectilium wihich is associated with the production of proteins and neurotransmitters. Dendrons- Extension of the cell body which subdivide into smaller bramched fibres called dendrites, that carry nerve impulses towards the body cell Axon- A single long fibre that carries nerve impulses away from the cell body Schwaan cells/myelin sheath- The schwaan cells surround the axon protecting it and providing eletrical insulation, they also carry out phagocytosis(removal of debris) and play a part in nerve regeneration, the myelin sheath is made up of the membranes of the schwaan cells, rich in lipid called myelin Modes of renvier- contrictions between adjacent schwaan cells where there is no myelin sheath
26
Give 4 comparisions of the hormonal system to the nervous system
-H system is communication by chemicals called hormones N system is communication by nerve impulses -H system is transmission by blood system N system is by neurones -H response is slower N response is rapid -H response travells to all parts of the body but only target specific cells N response targets specific parts of the body
27
Describe what a nerve impulse is using definitions of resting potential and action potential
A nerve impulse is a self propogating wave of electrical activity that travels aong the axon memebrane. It causes a temporary reversal of the electrical potential difference across the axon membrane as at resting potential, the axon has a negative charge relative to outside but action potential is the reversal of this (it will be more positive)
28
Explain how a resting potential is established across the axon membrane in a neurone
Na+ ions are actively transported out of the axon whilst K+ ions are actively transported into the axon by the sodium-potassium ion pumps -(3Na+ out of axon and 2 K+ into the axon) -Higher K+ conc inside and higher Na+ conc on the outside (electrochemical gradient) -But there is differential membrane permeability, as K+ begins to move out if the axon by facilitated diffusion whereas, Na+ is less peremable to move back into axon as most of gated channels are closed
29
Explain how changes in membrane permeability lead to depolarisation and the generation of an action potential
-At resting potential the potassium voltage channels are open but the sodium voltage gated channels are closed Stimulus- The energy of the stimulus causes sodium voltage gated channels to open therefore sodium diffuses down electrochemical gradient into the axon reversing potential difference across the membrane, this causes depolarisation Depolarisation- If a threshold is reached an action potential is generated as more voltage gated Na+ channnels open so more Na+ diffuse in rapidly Repolarisation- At about 40mV action potential established and Na+ channels begin to close and potassium ion channels open and potassium diffuses out of the axon. Hyperpolarisation- The K+ channels are slow to close so too many K+ diffuse out (temporary overshoot) Resting potential-Restored by the Na+ and K+ pump
30
Draw/Label a graph showing an action potential
31
Describe the all or nothing principle
For an action to be produced, depolarisation must exceed threshold potential. Action potentials are always the same magnitude/size and peak at the same potentials, bigger stimuli increase frequency of action potentials
32
Explain how the passage of an action along non-myelinated and myelinated axons result in nerve impulses
Non Myelinated -Action potential passes as a wave of depolarisation -The influx of NA+ in one region increases permeability of adjoining region to Na+ by causing voltage-gated Na+ channels to open so adjoinign region depolarises. Myelinated axon -Myelination provides electrical insulation -Depolarisation of axon at nodes of ranvier only resulting in solitary conduction so there is no need for depolarisation along the whole lenghth of the axon
33
How can damage to the myelin sheath lead to slow responses and jerky movement?
-There is no/less solitary conduction so depolarisation occurs along the whole lenght of the axon. -Also ions/depolarisation may leak to other neurones causing the wrong muscle fibres to contract
34
What are the factors that affect the speed an action potential travels?
Myelin sheath- Causes depolarisation at nodes of ranvier only (salatory conduction), jumpos from one node of ranvier to another increasing speed of conductance Diameter of axon- The greater the distnace of an axon, the fater the speed of conductance as there is less resistance to flows of ions in cytoplasm Temperature- Increases rate of diffusion of K+ and Na+ as there is more kinetic energy so nerve impulse is faster. owever above certain temperature, plasma membrane proteins are denatured and impulses fail to be conducted
35
When does the refractory period occur
After an action potemtial has been created in any region of an axon, there is a period afterwards where inward moevement of sodium ions prevented due to closing of voltage gated sodium channels, no futher action potential can be generated, this is the refractory period
36
Explain the purpose/importance of the refractory period and how this is done
-It ensures discrete impulses are produced so action potentials do not overlap. Action potentials can only pass from an active region to a resting region. This is beacause action potentials cannot be propogated in a region that is refractory. -It limits the number of action potentials At a certain intensity to prevent over reaction to a stimulus a higher intensity stimulus causes higher frequency of action potentials but only up to a certain intensity -Ensures action potentials are propageted in one direction as it cannot be propogated in a refractorty region.
37
What is a synapse?
A synapse is the point where one neurone communicates with another neurone or an effector
38
Describe the structure of a synapse
Synapses transfer information between neurons via chemicals called neurotransmitters. Neurones are seperated by a small gap called the synaptic cleft which is 20-30nm wide. Neurone releasing the transmitter is caled the presynaptic neurone.The axon of this neurone ends in a swollen portion called the synaptic knob. Posses many mitochondria and smooth endoplasmic rectilium which manufactyre neuro transmitter. Neuro transmitter is stored in synaptic vesicles
39
Describe and explain the features of synapses
Unidirectional nerve impulses- synapses can only pass information in one direction fron the presynaptic neurone to the postsynaptic neurone, this is because Neurotransmitters are only made in and released from the presynaptic neurone and receptors are only on the post synaptic neurone. Summation- Low frequency action potentials often lead to the release of insufficient concentrations of neurotransmitter to trigger a new action potential in the post synaptic neurone do so by 2 types of summation Spatial summation- A number of different presynaptic neurones together release enough neurostransmitter to exceed the threshold value of the post synaptic neurone and trigger a new action potential Temporal summation- In which a single presynaptic neurone releases neurotransmitter many times over a very short period. If the concentration of neurotransmitter exceeds the threshold value of the postsynaptic neurone, then a new action potential is triggered
40
Describe what inhibitory synapses are and how they operate
They are synapses that make it less likely that a new action potential will be created on the postsynaptic neurone -They as inhibitory neurotransmitters are released and and cause Cl- channels to open and Cl- move into postsynaptic neurone by facilitated diffusion. -Binding of neurotransmitters causes the opening of nearby K+ channels so K+ oves out of the post synaptic into the synapse. -More Na+ is required for depolarisation -This reduces the likelhood of threshold being met and action potential formation at post-synaptic membranes
41
Explain why when walking on the street humans respong to only loud background noise but not the noise of general traffic
In the synapse in the ear the presynaptic neurone is releasing neurotransmitters but at a low frequency so it is not enough to exceed the threshold in postsynaptic and produce an action potential so noise is filtered out, however, when a loud sound is made e.g. a honk, this creates a higher frequncy, more neurotransmitters are released (temporal or spatial summation) enough to bind to receptors in the post synaptic neurone and reach the threshold triggering an action potential so there is a response.
42
Describe transmission across a cholinergic synapse
-An action potential arrives at the end of the presynaptic neurone causes calcium ion protein channels to open and Ca2+ enter the synaptic knob by facilitated diffusion. -The influx of Ca2+ ions in the presynaptic neurone causes synaptic vesicles to fuse with the presynaptic membrane releasing acetylcholine into the synaptic cleft -Acetylcholine molecules diffue quickly across sunaptic cleft to bind to receptors on sodium ion protein channels in membrane of post synaptic neurone causing sodium ion channels to open Na+ diffuse in rapidly along conc gradient -The influx of Na+ in post synaptic knob cause depolarisation, if threshold is met, an action potential is initiated. -The enzyme acetylcholinerterase hydrolyses acetylcholine into choline and ethanol which diffuse back across the synaptic cleft into the presynaptic neuronen the rapid breakdown prevents it form continuously generating action potential so there is discrete transer of information -ATP released by mitochondria is used to recombine choline and ethanol back into acetylcholine which is stored in synaptic vesicles for future use. Sodium ion protein channels close in the absence of acetylcholine in the receptor sites.
43
Describe the structure of a neuromuscular junction in comparison to a synapse
-Receptors are on mucscle fibre instead instead of postsynaptic membrane and there are more. -Muscle fibres form clefts to store enzymes (acetylcholineterase)
44
Compare transmission across cholinergic synapses and neuromuscular junctions
-In both, transmission is unidirectional -CS is neurone to neuron NJ is motor neurone to muscle -Neurotransmitters can be excititory or inhibitory but in NJ they are always excitatory -In CS, action potential may be initiated in postsynaptic neurone but in NJ action potential ends here, its the end of the neural pathway In CS acetylcholine binds to receptors on membrane of post-synaptic neurone but in NJ acetylcholine binds to receptors on membrane of muscle fibre
45
Explain the effect different drugs can potentially have on the nervous sytem and how it has this effect
-Some drugs stimulate the nervous sytem leading to more action potentials, they do this by mimicking the shape of a neurotransmitter, this stimulates the release of more neurotransmitters. Or it inhibits the enzyme that breaks down neurotransmitters so Na+ continues to enter -Some drugs inhibit the nervous system by creating fewer action potentials, it may inhibit the release of neurotransmitters e.g. prevent opening of calcium ion channels or blocks receptors by mimicking the shape of neurotransmitters
46
Describe how muscles work
-They work in antagonistic pairs meaning they pull in opposite directions of one another -When one muscle contracts its the agonist, it pulls on bone producing force -The other that relaxes is the antagonist -skeleton is incompressible so muscle can transmit force to bone.
47
What is an advantage of antagonistic muscle pairs
The second muscle is required to reverse movement caused by the first muscle and contraction of both muscles helps maintain posture.
48
What are muscle fibres made up of?
Myofibrils
49
Describe the structure of myofibrils
Made up of 2 protein filaments: Actin-Thin filament consisting of two strands twisted around one another Myosin- Thicker filament which consists of a long rod-shaped tail with bulbous heads that project to the side
50
Describe the structure of skeletal muscle
-Made of many bundles of muscle fibres packaged together -Attached to bones by tendons Muscle fibres contain: -Sacromella (inward folding cell membrane which folds inwards to form transverse tubules -Sarcoplasm -Multiple nuclei -Many myofibrils -Sarcoplasmic reticulum -Many mitochondria
51
Explain the banding patterns to be seen in myofibrils
I- bands on the left- Light bands containing only thin actin filaments A-bands middle - Dark bands containing thick myosin filaments and some actin filaments H zone in the centre underneath A band- Contains only myosin so its the darkest region containing overlapping actin and myosin
52
What is tropomyosin and its function
It is a protein found in the muscle that forms a fibrous strand around the actin filament. its function is to prevent muscle contraction by establishing a barrier between the actin and myosin filaments that cause muscle contraction.
53
Give an overview of muscle contraction
-Myosin heads slide actin along myosin causing the sarcomere to contract -Simultaneous contraction of many sarcomeres causes myofibrils and muscle fibres to contract -When sarcomeres contract (shorten) -Hzones get shorter -I bands get shorter -A band stays the same -Z lines get closer
54
Describe muscle stimulation
-An action potential reaches a neuromuscular junction simultaneously, causing calcium ion protein channels to open and calcium ions to diffuse into the synaptic knob -The calcium ions cause the synaptic vesicles to fuse with the presynaptic membrane and release their acetylcholine into the synaptic cleft -Acetylcholine diffuses across the synaptic cleft and binds with receptors on the muscle cell surface membrane, causing it to depolarise.
55
Describe how slow twitch muscle fibres are adapted to their role
Slow twitch fibre- They contract more slowly and provide less powerful contractions and are suited to endurance roles for aerobic respiration. Therefore they have: -Large store of myoglobin -Rich supply of blood vessels -Numerous mitochondria for ATP
56
Describe how fast twitch muscle fibres are adapted to their role
The contract rapidly producing more powerful contractions -Thicker with more numerous myosin filaments -Higher concentration of glycogen -High conc of enzymes involved in anaerobic respiration - A store of phosphocreatine, a molecule that can rapidly generate ATP from ADP in anaerobic conditions
57
Describe the role of phosphocreatine in muscle contraction
-A source of inorganic phosphate rapidly phosphorylates ADP to regenerate ATP ADP + phosphocreatine= ATP+ Creatine -Runs out after a few seconds -Anaerobic and alactic
58
Describe muscle contraction
-Depolarisation spreads down sacrolemma via T tubules causing Ca2+ release from sarcoplasmic reticulum, which diffuse to myofibrils. -Calcium ions bind to tropomyosin causing it to move and exposing binding sites on actin -Allowing myosin head with ADP attached to bind to binding sites on actin forming actinomyosin crossbridge -Myosin heads change angle pulling actin along myosin (ADP released) using energy from ATP hydrolysis -New ATP binds to myosin head causing it to detach from binding site -Hydrolysis of ATP by ATP hydrolase activated by Ca2+ releases energy for myosin heads to return to original position -Myosin reattaches to a different site further along actin and this process is repeated as long as calcium ion conc is high. -
59
Describe what happens during muscle relaxation
-Ca2+ actively transported back into the endoplasmic reticulum using energy from ATP -Tropomyosin can then move back to block the myosin binding site again, so no actinomyosin cross bridges
60
Explain the importance of maintaining a stable core temperature
If temperature is too high: -H bonds in tertiary structure of enzymes break -Enzymes denature, active sites change shape and substrates cant bind -Fewer E-S complexes If temperature too low: -Not enough kinetic energy so fewer enzyme-substrate complexes
61
Explain the importance of maintaining stable blood pH
-Above or below optimal H/I bonds in tertiary structure break -Enzymes denature, active sites change shape and substrates cannot bind -Fewer E-S complexes
62
Explain the importance of maintaining stable blood W.P
Changes to the W.P of the blood and tissue fluids may cause cells to shrink and expand as a result of water entering and leaving via osmosis interrupting normal cell function
63
Describe the role of negative feedback in homeostasis
-Receptors detect change from optimum -A coordinator uses operational information to coordinate effectors -Effectors respond to counteract change -Return to optimum
64
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)
65
Describe positive feedback
1) Receptors detect change from normal 2) Effectors respond to amplify that change 3) Produces a greater deviation from normal -This is not involved in homeostasis e.g Onset contractions in childbirth, blood clotting
66
Describe the factors that influence blood glucose concentration
-Consumption of carbohydrates means more glucose absorbed into blood -Rate of respiration of glucose (e.g increases during exercise)
67
Describe the role of the liver in regulating blood sugar
Glycogenesis- The conversion of glucose to glycogen Glycogenolysis- The conversion of glycogen to glucose Gluconeogenesis- Converts amino acids and/or glycerol to glucose
68
Describe and explain the role of the pancreas in regulating blood glucose
In the cells in the pancreas there are hormone producing cells called islets of Langerhans, the cells inside include: a cells- produce hormone glucagon b cells-Produce hormone insulin
69
Explain the action of insulin in decreasing blood glucose concentration
Beta cells in the islets of langerhan detect high blood glucose and secrete insulin -This attaches to specific receptors on cell surface membrane of target cells -This causes more glucose channel proteins to join cell surface membrane increasing permeability to glucose so more glucose can enter by facilitated diffusion -This also activates enzymes involved in glycogenesis, lowering glucose concentration in cells, creating a concentration gradient so glucose enters cell by facilitated diffusion.
70
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 and secrete glucagon -Glucagon attaches to specific receptors on cell surface membranes of target cells -This activates enzymes involved in hydrolysis of glycogen to glucose (glycogenolysis) -Activates enzymes involved in conversion glycerol/amino acids to glucose -This establishes a concentration gradient so glucose enters blood by facilitated diffusion
71
Explain the role of adrenaline in increasing blood glucose concentration
Adrenal glands secrete adrenaline -Attaches to specific receptors on cell surface membranes of target cells--This activates enzymes involved in hydrolysis of glycogen to glucose (glycogenolysis) -This establishes a concentration gradient whereby glucose enters blood by facilitated diffusion
72
Describe the second messenger model of adrenaline and glucagon action
-Adrenaline/glucagon binds to specific receptors on cell membrane -The binding causes the protein to change shape on the inside of the membrane -This change leads to the activation of the enzyme adenyl cyclase which converts ATP to cyclic AMP (cAMP) -cAMP acts as the second messenger that binds to protein kinase enzyme changing its shape and activating it -Protein kinase catalyses the conversion of glycogen to glucose by facilitated diffusion and into the blood through protein channels
73
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) -This can in turn activate many enzymes for rapid increases in glucose
74
Compare the causes of Type I and Type II diabetes
Type I- B cells in islets of langerhans in pancreas produce insufficient insulin, this normally develops in childhood due to autoimmune response destroying b cells of islets of langerhans Type II- Faulty receptor looses sensitivity/ responsiveness to insulin but still produced. -Fewer glucose transport proteins and less uptake of glucose so less conversion of glucose to glycogen risk factor- obesity
75
Describe how Type I diabetes can be controlled
-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 a rise in glucose
76
Suggest why insulin can't be taken as a tablet by mouth
-Insulin a protein -Would be hydrolysed by endopeptidases/ exopeptidases
77
Describe how type II diabetes can be controlled
-Not normally treated with insulin injections but may use drugs which target insulin receptors to increase sensitivity therefore increase glucose uptake -Reduce sugar intake so low glycaemic index so less absorbed -Reduce fat intake so less glycerol converted to glucose -More regular exercise which uses glucose/ fats by increasing respiration -Lose weight-increased sensitivity of receptors to insulin
78
Describe the structure of a nephron an =d the role of different parts
This is the functional unit of the kidneys with two twisted regions it's made up of: Bowman's renal capsule- Formation of glomerular filtrate by ultrafiltration. Proximal convoluted tubule- Reabsorption of water and glucose Loop of Henle- Maintenance of a gradient of Na+ in the medulla Distal convoluted tubule- Reabsorption of water (permeability controlled by ADH) Collecting duct
79
Describe the formation of glomerular filtrate
-High hydrostatic pressure in glomerulus as diameter of afferent arteriole is wider that efferent arteriole -Small substances e.g water, glucose, ions and urea are forced into glomerular fibre and filtered by: Pores Capillary basement membrane Podocytes -Large proteins/ blood cells remain in blood
80
Describe the reabsorption of glucose by the proximal convoluted tubule
-Na+ is actively transported out of epithelial cells to the 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 (co-transport)
81
Describe the reabsorption of water by the proximal convoluted tubule
-Glucose in the capillaries lowers water potential -Water moves by osmosis down a water potential gradient
82
Describe and explain how the features of the cells in the PCT allow the rapid reabsorption of glucose into the blood
Microvilli/folded cell surface membrane- Large SA Many channel/carrier proteins- FOr facilitated diffusion&co-transport Many carrier proteins- For active transport Many mitochondria- Produce ATP for Active transport Many Ribosomes- Produce carrier/ channel proteins
83
suggest why glucose is found in the urine of an untreated diabetic person
-Blood glucose concentration is too high so not all glucose is reabsorbed at the PCT -As glucose carrier/cotransporter proteins are saturated/ working at minimum rate
84
Explain the importance of maintaining a gradient of sodium ions the the medulla
-Water potential decreases down the medulla (compared to the filtering duct) -So a Water potential gradient is maintained between the collecting duct and medulla -To maximise reabsorption of water by osmosis from filtrate
85
Fillin in the blanks The nephron is a structural unit of the kidney. It comprises a cup shaped structure called the _____ that contains a knot of blood vessels called the _____ arteriorle. Th inner wall of this cup-shaped structure is lined with specialsed cells called _____ and from it extends the first or ______ concoluted tube whose walls are lined with _____ that have _____ to increase SA. The next region of the nephron is a hairpin loop called the _____ which then leads onto the second _____ convoluted tubule. This in turn leads onto the _____ which empties into the renal pelvis. Around much of the nephron is a dense network of blood vessels called ____ capillaries
-Renal Bowmans's Capsule -Glomerulus -Afferent -Podocytes -Proximal -Epithelial cells -Microvilli -Loop of Henle -Distsal Collecting duct
86
Describe the role of the loopf of henle in maintaining a gradient of sodium ions in the medulla
-Na+ are actively transported out of the asceding limbof the loop of Henle using ATP from mitochondria in its walls -Creates a lower water potential interstital region, water remains as acending limb is impermable to water due to thick walls. -The walls of the descending limb are very permeable to water so it passes out of the filtrate by osmosis into the interstitial space. This water is reabsorbed by capillaries so filtrate concentration increases -Filtrate progreeively looses water till the lowest point lowest W.P is reached at the tip of the hairpin -At the base of the ascending limb, Na+ diffuse out of the filtrate and as it moves up the ascending limb, these ions are also actively pumped out therefore the filtrate get higher W.P -In the interestial space between the ascending limb and the collecting duct, there is gradient of water with the highest W.P in the cortex and Incresing low in the medulla -The collecting duct is permeable to water so the filtrate moves down it whilst water passes out by osmosis which is carried away by blood vessels -As water passes out of the filtrate, W.P is lowered, W.P is also loweredin the interstitial space so water continues to move out down collecting duct. The counter-current multiplier ensure that there is always water potential gradient drawing water out of the tubule
87
How does water move out of the collecting duct and how can this be controled by ADH?
-Water passes out through osmosis via specific channel proteins (aquaporins) -ADH can alter the number of these channels and so control water loss.
88
Suggest why animals needing to conserve water have long loops of Henle
-More Na+ can move out so Na+ gradient is maintained for longer -W.P gradient maintained for longer -So more water can be reabsorbed from the collecting duct by osmosis
89
Describe the reabsorption of water by the distal convoluted tubule and collecting ducts
-Water moves out of distal convoluted tubule and collecting duct by osmosis down a W.P gradient. -This is controlled by ADH which increases their permeability
90
What is osmoregulation?
The conrol of water potential of the blood (by negative feedback)
91
Describe ways in which the water potential of the blood may be lowered
-Too little water being consumed -Too much sweating occuring -Large amounts of ions (salt e.g) being taken in
92
Describe how the body respnd to a fall in water potential
-Cells called osmoreceptors in the hypothalumus of the brain detect a fall. -When W.P falls these cells shrink due to osmosis -This change causes the hypthalumus to produce ADH which passes to the posterior pituatary gland where it is secreted into the capillaries -ADH passes into the kidneys and attaches to receptors on collecting ducts and distal convoluted tubule -This activates enzyme phosphorylase within the cell stimulating the addition of channel proteins (aquaphorins) into cell-surface membranes and increasing permability of duct and DCT to water. -More water leavies duct by osmosis down a W.P gradient an re enters the blood -Osmoreceptors also send nerve impulses to the thirst centre of the brain to encourage person to drink more water.
93
Describe the role of the posterior pituitary gland in osmoregulation
Secretes more/less ADH inot blood due to signal from the hypothalamus
94
Descrieb the bodys response to a rise in water potential.
-Osmoreceptors in the hypothalamus detect the rise in water potential and increase the frequency of nerve impulses to pituitary gland to reduce its release of ADH -Less ADH via the blood leads to a descrease in the permability of the collecting ducts to water and urea -More dilute urine is produced and the water potential of the blood falls -WHen the water potential of the blood has returned to normal, the osmoreceptors in the hypothalamus cause the pitutary to raise its ADH back to normal levels